2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

Department of Health and Human Services Centers for Disease Control and Prevention

Contents

Contents
Introduction What’s New in this Report What’s Different in this Report Data Sources and Data Analysis Interpretation of Report Data: Important Factors Chemical and Toxicological Information Acrylamide Acrylamide hemoglobin adducts Glycidamide hemoglobin adducts Cotinine Cotinine N,N-Diethyl-meta-toluamide (DEET) N,N-Diethyl-meta-toluamide (DEET) Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Tribromomethane (Bromoform) Trichloromethane (Chloroform) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2,2-bis[4-Hydroxyphenyl] propane) 4-tert-Octylphenol (4-[1,1,3,3- Tetramethylbutyl] phenol) Triclosan (2,4,4’- Trichloro-2’-hydroxyphenyl ether) Fungicides Pentachlorophenol ortho-Phenylphenol Herbicides Acetochlor Acetochlor mercapturate Alachlor Alachlor mercapturate Atrazine Atrazine mercapturate 2,4-Dichlorophenoxyacetic Acid Metolachlor Metolachlor mercapturate 2,4,5-Trichlorophenoxyacetic Acid Insecticides/Pesticides Carbamate Insecticides Carbofuran Carbofuranphenol Propoxur 1 2 3 4 8 9 11 11 12 15 15 19 19 22 22 23 24 25 27 28 30 34 38 40 40 43 46 47 48 50 51 53 53 57 61 62 64 67 67 68 68 71

Fourth National Report on Human Exposure to Environmental Chemicals

i

Contents

2-Isopropoxyphenol Organochlorine Pesticides Aldrin and Dieldrin Aldrin Dieldrin Chlordane and Heptachlor Oxychlordane Heptachlor Epoxide trans-Nonachlor Dichlorodiphenyltrichloroethane (DDT) p,p’-Dichlorodiphenyltrichloroethane (DDT) p,p’-Dichlorodiphenyldichloroethene (DDE) o,p’-Dichlorodiphenyltrichloroethane Endrin Hexachlorobenzene Hexachlorocyclohexane beta-Hexachlorocyclohexane gamma- Hexachlorocyclohexane (Lindane) Mirex 2,4,5-Trichlorophenol and 2,4,6-Trichlorophenol Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Diethylphosphate (DEP) Dimethylphosphate (DMP) Diethylthiophosphate (DETP) Dimethylthiophosphate (DMTP) Diethyldithiophosphate (DEDTP) Dimethyldithiophosphate (DMDTP) Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos, Chlorpyrifos-methyl 3,5,6-Trichloro-2-pyridinol Coumaphos 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Diazinon 2-Isopropyl-4-methyl-6-hydroxypyrimidine Malathion Malathion dicarboxylic acid Methyl Parathion, Ethyl Parathion para-Nitrophenol Pirmiphos-methyl 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Pyrethroid Pesticides Cyfluthrin 4-Fluoro-3-phenoxybenzoic acid

72 75 77 77 79 81 81 84 86 89 89 91 93 97 100 104 104 106 109 112 117 120 122 124 126 128 130 134 135 135 140 141 143 143 146 146 149 149 153 154 156 159 160

ii

Fourth National Report on Human Exposure to Environmental Chemicals

Contents

Cyfluthrin, Cypermethrin, Permethrin cis-3-(2,2-Dichlorovinyl)-2,2-dimethylcyclopropane carboxylic acid trans-3-(2,2-Dichlorovinyl)-2,2-dimethylcyclopropane carboxylic acid Deltamethrin cis-3-(2,2-Dibromovinyl)-2,2-dimethylcyclopropane carboxylic acid Cyhalothrin, Cypermethrin, Deltamethrin, Fenpropathrin, Permethrin, Tralomethrin 3-Phenoxybenzoic acid Metals Antimony Arsenic Arsenic, Total Arsenic (V) Acid Arsenobetaine Arsenocholine Arsenous (III) Acid Dimethylarsinic Acid Monomethylarsonic Acid Trimethylarsine oxide Barium Beryllium Cadmium Cesium Cobalt Lead Mercury Molybdenum Platinum Thallium Tungsten Uranium Perchlorate Perchlorate Perfluorochemicals Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctanoic acid (PFOA) Perfluorooctane acid (PFOS) Perfluorooctane sulfonamide (PFOSA) 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH)

163 163 165 168 169 172 173 176 176 180 180 182 184 186 187 188 189 190 193 196 199 205 208 212 218 227 230 233 236 239 243 243 247 248 249 251 251 252 252 253 253 254 254

Fourth National Report on Human Exposure to Environmental Chemicals

iii

Contents

2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluoroundecanoic acid (PFUA) Phthalates Benzylbutyl Phthalate Mono-benzyl phthalate (MBzP) Dibutyl Phthalates Mono-isobutyl phthalate (MiBP) Mono-n-butyl phthalate (MnBP) Dicyclohexyl Phthalate Mono-cyclohexyl phthalate (MCHP) Diethyl Phthalate Mono-ethyl phthalate (MEP) Di-2-ethylhexyl Phthalate Mono-2-ethylhexyl phthalate (MEHP) Mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP) Mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP) Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Di-isononyl Phthalate Mono-isononyl phthalate (MiNP) Dimethyl Phthalate Mono-methyl phthalate (MMP) Di-(n-octyl) Phthalate Mono-(3-carboxypropyl) phthalate (MCPP) Mono-n-octyl phthalate (MOP) Phytoestrogens Daidzein O-Desmethylangolensin Enterodiol Enterolactone Equol Genistein Polybrominated Diphenyl Ethers and 2,2’,4,4’,5,5’-Hexabromobiphenyl (BB-153) 2,2’,4-Tribromodiphenyl ether (BDE 17) 2,4,4’-Tribromodiphenyl ether (BDE 28) 2,2’,4,4’-Tetrabromodiphenyl ether (BDE 47) 2,3’,4,4’-Tetrabromodiphenyl ether (BDE 66) 2,2’,3,4,4’-Pentabromodiphenyl ether (BDE 85) 2,2’,4,4’,5-Pentabromodiphenyl ether (BDE 99) 2,2’,4,4’,6-Pentabromodiphenyl ether (BDE 100) 2,2’,4,4’,5,5’-Hexabromodiphenyl ether (BDE 153) 2,2’,4,4’,5,6’-Hexabromodiphenyl ether (BDE 154) 2,2’,3,4,4’,5’,6-Heptabromodiphenyl ether (BDE 183) 2,2’,4,4’,5,5’-Hexabromobiphenyl (BB 153)

255 255 258 262 262 265 265 267 270 270 272 272 275 275 277 279 281 284 284 287 287 290 290 292 295 296 298 300 302 304 306 311 312 313 314 314 315 315 316 316 317 317 318

iv

Fourth National Report on Human Exposure to Environmental Chemicals

Contents

Polychlorinated Biphenyls—Non-Dioxin-Like 2,4,4’-Trichlorobiphenyl (PCB 28) 2,2’,3,5’-Tetrachlorobiphenyl (PCB 44) 2,2’,4,5’-Tetrachlorobiphenyl (PCB 49) 2,2’,5,5’-Tetrachlorobiphenyl (PCB 52) 2,3’,4,4’-Tetrachlorobiphenyl (PCB 66) 2,4,4’,5-Tetrachlorobiphenyl (PCB 74) 2,2’,3,4,5’-Pentachlorobiphenyl (PCB 87) 2,2’,4,4’,5-Pentachlorobiphenyl (PCB 99) 2,2’,4,5,5’-Pentachlorobiphenyl (PCB 101) 2,3,3’,4’,6-Pentachlorobiphenyl (PCB 110) 2,2’,3,3’,4,4’-Hexachlorobiphenyl (PCB 128) 2,2’,3,4,4’,5’and 2,3,3’,4,4’,6-Hexachlorobiphenyl (PCB 138 & 158) 2,2’,3,4’,5,5’-Hexachlorobiphenyl (PCB 146) 2,2’,3,4’,5’,6-Hexachlorobiphenyl (PCB 149) 2,2’,3,5,5’,6-Hexachlorobiphenyl (PCB 151) 2,2’,4,4’,5,5’,-Hexachlorobiphenyl (PCB 153) 2,2’,3,3’,4,4’,5-Heptachlorobiphenyl (PCB 170) 2,2’,3,3’,4,5,5’-Heptachlorobiphenyl (PCB 172) 2,2’,3,3’,4,5’,6’-Heptachlorobiphenyl (PCB 177) 2,2’,3,3’,5,5’,6-Heptachlorobiphenyl (PCB 178) 2,2’,3,4,4’,5,5’-Heptachlorobiphenyl (PCB 180) 2,2’,3,4,4’,5’,6-Heptachlorobiphenyl (PCB 183) 2,2’,3,4’,5,5’,6-Heptachlorobiphenyl (PCB 187) 2,2’,3,3’,4,4’,5,5’-Octachlorobiphenyl (PCB 194) 2,2’,3,3’,4,4’,5,6-Octachlorobiphenyl (PCB 195) 2,2’,3,3’,4,4’,5,6’ and 2,2’,3,4,4’,5,5’,6-Octachlorobiphenyl (PCB 196 & 203) 2,2’,3,3’,4,5,5’,6-Octachlorobiphenyl (PCB 199) 2,2’,3,3’,4,4’,5,5’,6-Nonachlorobiphenyl (PCB 206) 2,2’,3,3’,4,4’,5,5’,6,6’-Decachlorobiphenyl (PCB 209) Dioxin-Like Chemicals Polychlorinated Dibenzo-p-dioxins 1,2,3,4,6,7,8-Heptachlorodibenzo-p-dioxin (HpCDD) 1,2,3,4,7,8-Hexachlorodibenzo-p-dioxin (HxCDD) 1,2,3,6,7,8-Hexachlorodibenzo-p-dioxin (HxCDD) 1,2,3,7,8,9-Hexachlorodibenzo-p-dioxin (HxCDD) 1,2,3,4,6,7,8,9-Octachlorodibenzo-p-dioxin (OCDD) 1,2,3,7,8-Pentachlorodibenzo-p-dioxin (PeCDD) 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) Polychlorinated Dibenzofurans 1,2,3,4,6,7,8-Heptachlorodibenzofuran (HpCDF) 1,2,3,4,7,8,9-Heptachlorodibenzofuran (HpCDF) 1,2,3,4,7,8-Hexachlorodibenzofuran (HxCDF)

321 322 326 327 328 330 332 334 336 338 340 342 344 346 348 350 352 354 356 358 360 362 364 366 368 369 370 371 372 373 377 377 378 380 382 384 386 388 390 392 392 394 396

Fourth National Report on Human Exposure to Environmental Chemicals

v

Contents

1,2,3,6,7,8-Hexachlorodibenzofuran (HxCDF) 1,2,3,7,8,9-Hexachlorodibenzofuran (HxCDF) 2,3,4,6,7,8-Hexachlorodibenzofuran (HxCDF) 1,2,3,4,6,7,8,9-Octachlorodibenzofuran (OCDF) 1,2,3,7,8-Pentachlorodibenzofuran (PeCDF) 2,3,4,7,8-Pentachlorodibenzofuran (PeCDF) 2,3,7,8-Tetrachlorodibenzofuran (TCDF) Coplanar Polychlorinated Biphenyls 3,4,4’,5-Tetrachlorobiphenyl (PCB 81) 3,3’,4,4’,5-Pentachlorobiphenyl (PCB 126) 3,3’,4,4’,5,5’-Hexachlorobiphenyl (PCB 169) Mono-ortho-substituted Polychlorinated Biphenyls 2,3,3’,4,4’-Pentachlorobiphenyl (PCB 105) 2,3’,4,4’,5-Pentachlorobiphenyl (PCB 118) 2,3,3’,4,4’,5-Hexachlorobiphenyl (PCB 156) 2,3,3’,4,4’,5’-Hexachlorobiphenyl (PCB 157) 2,3’,4,4’,5,5’-Hexachlorobiphenyl (PCB 167) 2,3,3’,4,4’,5,5’-Heptachlorobiphenyl (PCB 189) Polycyclic Aromatic Hydrocarbons Fluorene 2-Hydroxyfluorene 3-Hydroxyfluorene 9-Hydroxyfluorene Naphthalene 1-Hydroxynaphthalene (1-Naphthol) 2-Hydroxynaphthalene (2-Naphthol) Phenanthrene 1-Hydroxyphenanthrene 2-Hydroxyphenanthrene 3-Hydroxyphenanthrene 4-Hydroxyphenanthrene Pyrene 1-Hydroxypyrene Volatile Organic Compounds (VOCs) Benzene Chlorobenzene Chlorobenzene (Monochlorobenzene) 1,2-Dichlorobenzene (o-Dichlorobenzene) 1,3-Dichlorobenzene (m-Dichlorobenzene) 1,4-Dichlorobenzene (Paradichlorobenzene) 1,2-Dibromo-3-chloropropane (DBCP) 2,5-Dimethylfuran Ethylbenzene

398 400 402 404 406 408 410 412 412 414 416 418 418 420 422 424 426 428 434 436 436 438 440 442 442 444 447 447 449 451 453 455 456 458 458 461 461 462 464 464 466 468 470

vi

Fourth National Report on Human Exposure to Environmental Chemicals

Contents

Halogenated Solvents Dichloromethane (Methylene chloride) Trichloroethene (Trichloroethylene) Tetrachloroethene (Perchloroethylene) Other Halogenated Solvents Dibromomethane 1,1-Dichloroethane 1,2-Dichloroethane (Ethylene dichloride) 1,1-Dichloroethene (Vinylidene chloride) cis-1,2-Dichloroethene trans-1,2-Dichloroethene 1,2-Dichloropropane 1,1,1-Trichloroethane (Methyl chloroform) 1,1,2-Trichloroethane 1,1,2,2-Tetrachloroethane Tetrachloromethane (Carbon tetrachloride) Hexachloroethane Methyl tert-butyl ether (MTBE) Nitrobenzene Styrene Toluene Xylenes o-Xylene m- and p-Xylene Appendices Appendix A. Procedure to Estimate Percentiles Appendix B. Changes and Edits to Results Released in the Third Report Appendix C. References for Biomonitoring Analytical Methods Appendix D. Limit of Detection Table Appendix E. Abbreviations

473 473 474 475 478 478 479 480 481 481 482 482 483 483 484 484 487 489 492 494 497 500 500 501 503 503 506 507 511 519

Fourth National Report on Human Exposure to Environmental Chemicals

vii

Introduction

Introduction
The Fourth National Report on Human Exposure to Environmental Chemicals, 2009 (the Report) provides an ongoing assessment of the exposure of the U.S. population to environmental chemicals by the use of biomonitoring. The Report is cumulative (containing all the results from previous Reports) and provides new data for years 20032004. Data for 75 new environmental chemicals are included for the survey period 2003-2004. The Report website http://www.cdc.gov/exposurereport is also the best source for the most recent update of available data. In each survey period, most chemicals or their metabolites were measured in blood, serum, and urine samples from random subsamples of about 2500 participants from the National Health and Nutrition Examination Survey (NHANES) conducted by the Centers for Disease Control and Prevention’s (CDC’s) National Center for Health Statistics. NHANES is a series of surveys designed to collect data related to the health and nutritional status of the U.S. population. The blood, serum, and urine exposure measurements presented in the Report were made by CDC’s Environmental Health Laboratory (Division of Laboratory Sciences, National Center for Environmental Health) using mass spectrometry methods. The term environmental chemical refers to a chemical compound or chemical element present in air, water, food, soil, dust, or other environmental media (e.g., consumer products). Biomonitoring is the assessment of human exposure to chemicals by measuring the chemicals or their metabolites in such human specimens as blood or urine. A metabolite is a chemical alteration of the original compound produced by body tissues. Blood, serum, and urine levels reflect the amount of a chemical that actually gets into the body by all routes of exposure, including ingestion, inhalation, and dermal absorption. The measurement of an environmental chemical in a person’s blood or urine is an indication of exposure; it does not by itself mean that the chemical causes disease or an adverse effect. Research studies, separate from these data, are required to determine which blood or urine levels are safe and which are associated with disease or an adverse effect. For blood, serum, and urine levels, the Report provides geometric means and percentiles of environmental chemicals by age group, gender and race/ethnicity. More in-depth statistical analysis, including multivariate analysis incorporating health endpoints and other predictive variables, is beyond the scope of this document. We encourage scientists to examine the data further through analysis of the raw data available at http://www.cdc.gov/nchs/nhanes.htm.

Public Health Uses of the Report The overall purpose of the Report is to provide unique exposure information to scientists, physicians, and health officials to help prevent exposure to some environmental chemicals. Specific public health uses of the exposure information in the Report are
• •

• •

• •

To determine which chemicals get into Americans and at what concentrations. For chemicals with a known toxicity level, to determine the prevalence of people with levels above those toxicity levels (e.g., a blood lead level greater than or equal to 10 micrograms per deciliter [≥ 10 µg/dL]). To establish reference values that can be used by physicians and scientists to determine whether a person or group has an unusually high exposure. This information is especially helpful to identify population groups that merit further assessment of exposure sources or health effects. To assess the effectiveness of public health efforts to reduce exposure of Americans to specific chemicals. To determine whether exposure levels are higher among such potentially vulnerable groups as minorities and children. To track, over time, trends in levels of exposure of the population. To set priorities for research on human health effects.

Fourth National Report on Human Exposure to Environmental Chemicals

1

html.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.5'-Tetrachlorobiphenyl (PCB 44) 2. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4'.5.5'.4'-Pentabromodiphenyl ether (BDE 85) 2.2-Dichloroethene trans-1.1.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .6-Pentabromodiphenyl ether (BDE 100) 2.2-Trichloroethane Trichloroethene (Trichloroethylene) m.4. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.3'.1. The process for selection is described at http://www.4.4'-Tribromodiphenyl ether (BDE 28) 2.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.3-Tetramethylbutyl] phenol) Triclosan (2.4-Dichlorobenzene (p-Dichlorobenzene.2'.cdc.5'-Hexabromodiphenyl ether (BDE 153) 2.4'.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.3.4'.2-Dichloroethane (Ethylene dichloride) 1.4.4.4'.6.What’s New in this Report What’s New in this Report In this Fourth Report.2'3.3.3’.4.1-Dichloroethene (Vinylidene chloride) cis-1.2-Dichloropropane 2.3.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.4.5.4’.2-Dichlorobenzene (o-Dichlorobenzene) 1.4'-Tetrabromodiphenyl ether (BDE 66) 2.1.4.2’.2'.2'. Paradichlorobenzene) 1. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4.1-Trichloroethane (Methyl chloroform) 1.2'.2'4.4.5-Pentabromodiphenyl ether (BDE 99) 2.4-Tribromodiphenyl ether (BDE 17) 2.2'.3-Dichlorobenzene (m-Dichlorobenzene) 1.5'-Tetrachlorobiphenyl (PCB 49) 2.2'.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.1.4.3.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4'-Tetrabromodiphenyl ether (BDE 47) 2.1-Dichloroethane 1.5’.2-Dichloroethene Dichloromethane (Methylene chloride) 1.4.4’.5.5.4.6-Heptabromodiphenyl ether (BDE 183) 2.6'-Hexabromodiphenyl ether (BDE 154) 2.2.2'.4'.gov/exposurereport/chemical_selection. Table 1.2'.2'.

Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available.1). Data for other pesticides are included only for 1999-2000 and 2001-2002. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods.. 2003-2004) have been re-computed by use of this improved procedure. 2001-2002. Only slight differences should be noted when one compares the recomputations to previous releases of the Report.4-dichlorophenol and 2. Percentiles for all three NHANES survey periods (1999-2000. Fourth National Report on Human Exposure to Environmental Chemicals 3 . the presence of an interference) that produced results of inadequate quality. five results that all have the value 90. Details of this procedure are provided in Appendix A.g. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. Explanations for each change are provided in Appendix B. and these data will be included in the next release of the Report.What’s Different in this Report What’s Different in this Report The Fourth Report uses a new procedure to estimate percentiles when the percentile estimate falls on a value that is repeated multiple times (e.. urinary 2.g. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e.5-dichlorophenol for the 1999-2002 survey periods.

Otherwise in 2001-2002 and 2003-2004. Serum cotinine and acrylamide adducts were measured in the entire NHANES sample for ages 3 years and older. while organochlorine pesticides and other PCBs were measured in a random one-third subsample of participants aged 12 years and older.gov/exposurereport/chemical_ selection. these chemicals were measured in a random one-third subsample of participants aged 6 years and older. urinary mercury was measured in a random one-third subsample of participants aged 6 years and older. NHANES collects information about a wide range of healthrelated behaviors.htm. in a random one-quarter subsample of people aged 12-59 years in 1999. noninstitutionalized population in the United States based on age. Beginning in 1999. The analytical methods used for measuring the environmental chemicals or their 4 Fourth National Report on Human Exposure to Environmental Chemicals . serum.gov/nchs/nhanes. NHANES became a continuous survey. Most of the environmental chemicals were measured in randomly selected subsamples within specific age groups. and organochlorine pesticides were measured in serum from a random one-third subsample of participants aged 12 years and older in 1999-2000 and 2003-2004. such as risk factors for cardiovascular disease. NHANES is a series of surveys conducted by CDC’s National Center for Health Statistics (NCHS). population annually and releasing the data in 2-year cycles. stratified. blood is obtained by venipuncture from participants aged 1 year and older. selected pesticides. National Center for Environmental Health).cdc. precision. Age groups and sample sizes for each exposure measurement are provided in each of the data tables. furans. The NHANES protocol includes a home interview followed by a standardized physical examination in a mobile examination center. NHANES is unique in its ability to examine public health issues in the U. and in a random one-third subsample of people aged 12 years and older in 2000. sampling the U. and the incremental analytical cost to perform the biomonitoring analysis for the chemical. Different random subsamples include different participants.S. specificity. the availability of a biomonitoring analytical method with adequate accuracy.S. sensitivity. Urinary mercury was measured in women aged 16-49 years in 1999-2002. This subsampling was needed to ensure an adequate quantity of sample for analysis and to accommodate the throughput of the mass spectrometry analytical methods. there have been some exceptions. and throughput. and urine samples from NHANES Biomonitoring measurements for the Report were made in samples from participants in NHANES. probability-cluster design to select a representative sample of the civilian. NHANES is designed to collect data on the health and nutritional status of the U. and metabolites of organophosphate pesticides were measured in a random one-half subsample of children aged 6-11 years in 1999 and 2000. and urine specimens are collected from participants aged 6 years and older. serum and urine exposure measurements in the Report were made by CDC’s Environmental Health Laboratory (Division of Laboratory Sciences. gender. Laboratory Analysis The blood. serum. Environmental chemicals were measured in blood.S. performs physical examinations. Urinary levels of herbicides. Total blood mercury was measured in children aged 1-5 years and in women aged 16-49 years in 1999-2002. Chemicals in the Report were selected on the basis of scientific data that suggested exposure in the U. Though most chemicals in urine were measured in a random one-third subsample of participants aged 6 years and older.cdc. the need to assess the effectiveness of public health actions to reduce exposure to a chemical. The participant ages for which a chemical was measured varied by chemical group. Cotinine is reported only in nonsmokers. and coplanar PCBs were measured in a random one-third subsample of participants aged 20 years and older. Total blood mercury and inorganic blood mercury were measured in all participants aged 1 year and older in 2003-2004. and race/ethnicity.S. dioxins. Additional detailed information on the design and conduct of the NHANES survey is available at http://www. The availability of biomonitoring methods with adequate performance and acceptable cost was a major consideration. or urine specimens collected as part of the examination component of NHANES. population. Dioxins. multistage. furans. Details on the prioritization process for scoring nominated chemicals and the resulting scores are available at http://www.Data Sources and Data Analysis Data Sources and Data Analysis Blood. population. Blood lead and blood cadmium were measured in all participants aged 1 year and older for all survey periods. As part of the examination component. The sampling plan follows a complex. population. the seriousness of health effects known or suspected to result from some levels of exposure. In 20012002. Randomization of subsample selection is built into the NHANES design before sample collection begins. the availability of adequate blood or urine samples.html. polychlorinated biphenyls (PCBs). For the 2003-2004 survey. and collects samples for laboratory tests.

The Report presents descriptive statistics on the blood. including tolerance limits for operational parameters. gender.. if one person has consumed more fluids than another person. This type of distribution is common in the measurement of environmental chemicals in blood or urine.0. Data were analyzed using the statistical software package Statistical Analysis System (SAS) (SAS Institute Inc. results are given for the total population as well as by age group. In each table. and race/ethnicity as defined in NHANES. These compounds are lipophilic and concentrate in the body’s lipid stores.htm.e. probability-cluster design. levels are presented two ways: per volume of urine and per gram of creatinine. serum. Units of measurement are important. including the lipid in serum. but the proportion of the total population represented by other racial/ethnic groups is not large enough to produce valid estimates. or graphite furnace atomic absorption spectrometry.Data Sources and Data Analysis metabolites in blood. Data Analysis Because the NHANES is a complex.g. Ninety-five percent confidence intervals around this Fourth National Report on Human Exposure to Environmental Chemicals 5 . seasons of the year. and urine were based on isotope dilution mass spectrometry. and verification of traceable calibration materials. Table 2. micrograms per liter).cdc. Serum levels reported per gram of total lipid reflect the amount of these compounds that are stored in body fat. proximity to sources of exposure. Other mostly non-lipophilic chemicals measured in serum are expressed per liter of serum (e. Guidelines for the analysis of NHANES data are provided by NCHS at http://www. References for the analytical methods used to measure the different chemicals are provided in Appendix C. population. serum levels are presented per gram of total lipid and per whole weight of serum. Interpretation of creatinine corrected results should also recognize that creatinine correction can also partially adjust for differences in lean body mass or renal function among persons. Gender is coded as male or female. or by use of particular products. state. Age groups are as described for each chemical in each data table. Sample weights also are used to adjust for possible bias resulting from nonresponse and are post-stratified to U. For dioxins. serum. Acrylamide and glycidamide adducts are expressed as the picomoles per gram of blood hemoglobin to which the adduct is bound. inductively coupled plasma mass spectrometry. Units: For chemicals measured in urine. Statistics include unadjusted geometric means and percentiles with confidence intervals. sample weights must be used to adjust for the unequal probability of selection into the survey. generally conforming to those most commonly used in biomonitoring measurements. 2001). Census Bureau estimates of the U. SUDAAN uses sample weights and calculates variance estimates that account for the complex survey design. the measurement of quality control samples in each analytical run to detect unacceptable performance in accuracy or precision. This design does not permit straightforward analysis of exposure levels by non-targeted strata such as locality. The geometric mean is influenced less by high values than is the arithmetic mean. and nonHispanic white. furans. or region. race/ethnicity is categorized based on the sample design as Mexican American. multistage.S. Results are reported here using standard units. Other racial/ethnic groups are sampled. non-Hispanic black. Geometric means were calculated by taking the log of each concentration and then computing the weighted mean of those log-transformed values using SUDAAN software. Laboratory measurements underwent extensive quality control and quality assurance review. and organochlorine pesticides. 2002) and the statistical software package SUDAAN (SUDAAN Release 8. For example. Units of Measurements and Abbreviations Unit liter deciliter milliliter gram milligram microgram nanogram picogram femtogram Abbreviation L dL mL g mg µg ng pg fg Value 10 liters -3 10 liters 10 grams -6 10 grams -9 10 grams -12 10 grams -15 10 grams -3 -1 Geometric means: A geometric mean provides a better estimate of central tendency for data that are distributed with a long tail at the upper end of the distribution. creatinine corrected) adjust for urine dilution.gov/nchs/nhanes/ nhanes2003-2004/analytical_guidelines. Urinary levels are expressed both ways in the literature and used for different purposes.S.. Levels per gram of creatinine (i. Useful unit conversions are shown in Table 2. For these analyses. Other racial/ethnic groups are included in estimates that are based on the entire population sample. or urine levels for each environmental chemical. stratified. his or her urine output is likely higher and the urine more dilute than that of the other person.. PCBs. Serum levels per whole weight of serum are also included to facilitate comparison with studies investigating exposure to these chemicals and reported levels in these units.

The standard error was computed with SUDAAN’s Proc Descript (design=WR). For chemicals measured in urine. LOD calculations were performed using the chemical concentration expressed per amount of lipid. LOD results for urine measurements in each data table and in Appendix D are in units of weight per volume of urine. separate tables are presented for the chemical concentration expressed per volume of urine (uncorrected table) and the chemical concentration expressed per gram of creatinine (creatinine corrected table). separate tables are presented for the chemical concentration expressed per volume of serum (lipid unadjusted table) and the chemical concentration expressed per amount of lipid (lipid adjusted table). For these chemicals. furans. Since the Third Fourth National Report on Human Exposure to Environmental Chemicals . Geometric mean and percentile calculations were performed separately for each of these concentrations. For dioxins. a better ability to detect low levels). and 95th) are given to provide additional information about the shape of the distribution. Percentile estimates (see below) that are less than the LOD for the chemical analysis are reported as “< LOD. and a few other pesticides. five results that all have a value of 90. LOD results for chemicals measured in each data table and in Appendix D are in weight per amount of lipid. The maximum LOD was the highest LOD among all the individual samples analyzed — typically. geometric means were not calculated. The LODs for each chemical and survey period are provided in each data table and collectively in Appendix D. In the creatinine corrected tables. weighted percentile estimates for 1999-2000 and 20012002 data were calculated using SAS Proc Univariate and a proportions estimation procedure. For example. Geometric mean and percentile calculations were performed separately for each of these concentrations. 6 a conservative rule was used for reporting percentiles: if any individual sample LOD in the demographic group was above the percentile estimate.” For most chemicals. Percentiles: Percentiles (50th.e. If the proportion of results below the LOD was greater than 40%. mostly because the sample volume used for analysis differed for each sample. the percentile estimate was not reported. a result for a geometric mean or percentile was reported as < LOD if the corresponding geometric mean or percentile was < LOD in the table using weight per volume of urine. because this concentration determines the analytical sensitivity. the maximum LOD value is provided in each data table and in Appendix D. The degrees of freedom of the t-statistic were determined by subtracting the number of strata from the number of primary sampling units (PSUs) according to the data available from the complex survey design. That is. PCBs. Limit of detection: The limit of detection (LOD) is the level at which the measurement has a 95% probability of being greater than zero (Taylor. Thus. organochlorine pesticides. For the same chemical. because this concentration determines the analytical sensitivity. For chemicals that had individual sample LODs. For chemicals measured in serum lipid. In the lipid unadjusted tables. Concentrations less than the LOD were assigned a value equal to the LOD divided by the square root of 2 for calculation of geometric means. 1987). The same procedure for imputing values below the LOD in calculations of geometric means was used for chemicals with individual LODs for each sample. which uses Taylor series linearization for variance estimation..Data Sources and Data Analysis weighted mean were calculated by adding and subtracting an amount equal to the product of a Student’s t-statistic and the standard error of the weighted mean estimate. In the Third National Report on Human Exposure to Environmental Chemicals. LOD calculations were performed using the chemical concentration expressed per volume of urine. the LOD is constant for each individual specimen analyzed. concentrations less than the individual LOD were assigned a value equal to the individual LOD divided by the square root of 2. if the 50th percentile for males was < LOD in the table using weight per volume of urine. sex and race (e. The weighted geometric mean and its confidence limits were then obtained by taking the antilogs of this weighted mean and its upper and lower confidence limits. 90th. A higher sample volume results in a lower LOD (i. in non-Hispanic white males 12-19 years old. for proper interpretation of LODs in the data tables. For this reason. These analyses have an individual LOD for each sample. each individual sample has its own LOD. One possible consequence is that results may be reported as “< LOD” in the 1999-2000 data but be reported as a concentration value above the LOD in 2001-2002 or 2003-2004 because the analytical method had improved. care must be taken to use the LOD that applies to the survey period. a result for a geometric mean or percentile was reported as < LOD if the corresponding geometric mean or percentile was < LOD in the lipid adjusted table. Percentile estimates and 95% confidence interval estimates that are less than the limit of detection are indicated as <LOD in the data tables.g..1). Assigning a value of the LOD divided by 2 made little difference in geometric mean estimates. LOD values may change over time as a result of improvements to analytical methods. For this reason. 75th. A percentile estimate may fall on a value that is repeated multiple times in a particular demographic group defined by age. it would also be < LOD in the creatinine corrected table. the mean LOD was about 40-50% of the maximum LOD.

Lewis Publishers. 1987. Therefore. This improved procedure makes each repeated value unique by adding a unique negligibly small number to each repeated value. All data from 1999-2004 have been reanalyzed using this new procedure to handle situations where the percentile falls on a repeating value. Appendix A gives the details of the new procedure for estimating percentiles. Boca Raton (FL). occasional percentile estimates may differ slightly in the current Fourth Report than in the Third Report. we have improved the procedure for estimating percentiles to better handle this situation.Data Sources and Data Analysis Report. Taylor JK. Quality Assurance of Chemical Measurements. Fourth National Report on Human Exposure to Environmental Chemicals 7 .

gov/exposurereport/ for a list of these papers. such as lead. soil.cdc. Persistent chemicals (those that stay in the body for a long time) are usually measured in serum as the parent chemical. Not all the chemicals in the Report are measured in the same individuals. use percentiles. Persistent and nonpersistent chemicals. or dust. In this Report. The 95th percentile is helpful for determining whether levels observed in separate public health investigations or other studies are unusual. Concentrations of environmental chemicals in blood or urine are not the same as those in air. However. separate from the Report. water. For example. soil. water. food. 95th) provided for each chemical convey useful information about the upper distribution and range of levels in the population. and how the chemical is distributed in body tissues. for many environmental chemicals. Demographic groups may not be equal in their composition with respect to other variables. serum. soil. and urine levels of a chemical should not be confused with levels of the chemical in air. and eliminated from the body. Therefore. research studies have given us a good understanding of the health risks associated with different blood lead levels. most measurements in urine quantify chemical metabolites of nonpersistent chemicals (those that do not stay in the body a long time). but separate studies of varying exposure levels and health effects are needed to determine whether such blood or urine levels result in disease. food. and urine are determined by how much of the chemical has entered the body through all routes of exposure. water. serum. transformed into metabolites. The higher percentiles (75th. The measurement of an environmental chemical in a person’s blood or urine does not by itself mean that the chemical causes disease. The Fourth Report does not present new data on health risks from different exposures. For more information about exposure to environmental chemicals. comparison of levels between groups of of levels of chemicals in different demographic groups. Levels of a chemical in blood. Levels of chemicals are provided for the demographic groups as stratified by age. 90th. Blood or urine levels may reflect exposure from one or more sources. gender. it is not possible to determine the fraction of all measured chemicals that were found at detectable levels in a given person. and race/ethnicity. Although the levels in the blood. food. including air. a chemical concentration of 10 µg/L in water does not produce a level of 10 µg/L in blood or urine. including ingestion. serum and urine are measures of the amount of a chemical that has entered the body by all routes of exposure. For some environmental chemicals.Interpretation of Report Data: Important Factors Interpretation of Report Data: Important Factors Research studies. Blood. Advances in analytical methods allow us to measure low levels of environmental chemicals in people. the blood or urine level alone does not determine which exposure source or which route of exposure has occurred. are required for determining whether blood or urine levels are safe or are associated with disease or adverse effects. or dust. CDC scientists publish separate scientific papers that make detailed comparisons 8 Fourth National Report on Human Exposure to Environmental Chemicals . and dermal absorption. The results shown in the Fourth Report should help prioritize and foster research on human health risks that result from exposure to environmental chemicals. we need more research to assess health risks from different blood or urine levels. except for some metals. see the section later in this Report titled “Chemical and Toxicological Information”. These studies must also consider other factors such as duration of exposure. See http://www. and dust. which includes Internet reference sites. inhalation.

BEIs can be the blood or urine levels of a chemical that correspond to air-exposure limits for workers set by ACGIH. a private organization that publishes biological exposure indices (BEIs) that “generally indicate a concentration below which nearly all workers may be repeatedly exposed without adverse health effects” (ACGIH.gov/iris) • Office of Prevention.cdc. The information in the text is provided as an overview. CDC is not responsible for the content of an individual organization’s Web pages found at these links.cdc. including documents from national and international agencies and organizations. 2007).htm) U.gov/niosh/database.atsdr. Information about the BEI level is provided here for comparison.atsdr. the U. Separate studies of varying exposure levels and health effects associated with these levels are required to determine whether blood. and comparative blood or urine levels from other studies.html) • Toxic Substances Portal (http://www.htm) • National Institute for Occupational Safety and Health (NIOSH) o Databases and Information Resources (http://www.gov) • National Center for Toxicological Research (http://www. and pathways of human exposure. Links to nonfederal organizations are provided solely as a service to our readers. Food and Drug Administration (FDA) • Center for Food Safety and Applied Nutrition (http://www.S.html) o Registry of Toxic Effects of Chemical Substances (RTECS) (http://www.S. sources.fda. These links do not constitute an endorsement of these organizations or their programs by CDC or the federal government. and public government documents.gov) 9 Fourth National Report on Human Exposure to Environmental Chemicals . For most chemicals in this Report.cdc. Geological Survey (USGS) • (http://www/usgs. Environmental Protection Agency.epa.epa.S. nor do they create guidelines. disposition within the body.Chemical and Toxicological Information Chemical and Toxicological Information The Fourth Report presents biomonitoring data on the exposure of the U. Signature Publications. Cincinnati (OH).gov/substances/index. Where can I find more information? For more information about environmental chemicals.cdc. Generally. American Conference of Government Industrial Hygienists (ACGIH). U. The measurement of an environmental chemical in a person’s blood or urine does not by itself mean that the chemical causes disease or adverse effects.gov/opptsmnt/index.fda. refer to the list of web links below and the references given in the text. Pesticides. Examples of common institutional sources of information include the Agency for Toxic Substances and Disease Registry.cdc. and urine levels result in disease or adverse effects. and it is not intended as a comprehensive review of each chemical. such guidelines are not available. 2007. and the agencies of the World Health Organization. The Fourth Report provides descriptive information about each chemical or chemical group including uses. This organization notes that these values are for workers and that it is not appropriate to apply them to the general population. effects in animals or humans. 2007 TLVs and BEIs. Governmental Sources Centers for Disease Control and Prevention (CDC) Resources: • National Center for Health Statistics (NCHS) (http://www.asp) U. generally recognized guidelines for blood or urine levels are presented in the text. or concordance among multiple scientific papers and sources. peer-reviewed scientific papers obtained from electronic searches.cdc. consensus agreement among experts. Statements are based on common general information.gov/niosh/rtecs) Agency for Toxic Substances and Disease Registry (ATSDR) • Toxicological Profiles and ToxFAQs (http://www.S. not to imply that the BEI is a safety level for general population exposure.gov/nchs) o National Health and Nutrition Examination Survey (NHANES) (http://www. population to environmental chemicals. serum. If available. the information was compiled from many publicly available sources.gov/nctr) U.S. The data and information in the Fourth Report do not establish health effects.gov/toxpro2. Environmental Protection Agency (EPA) • Integrated Risk-Information System (IRIS) (http://www. and Toxic Substances (OPPTS) (http://www.S.cfsan. One exception is the American Conference of Governmental Industrial Hygienists (ACGIH). Some guidelines are from federal agencies. Advances in analytical methods allow us to measure increasingly lower levels of environmental chemicals in people.gov/nchs/nhanes.

nlm.who.gov) National Institutes of Health (NIH) • National Institute for Environmental Health Sciences (NIEHS) (http://www.inchem.nih.html) International Agency for Research on Cancer (IARC) (www.iarc.usda.fr/ENG/Monographs/ allmonos90.fr) • Monographs on the Evaluation of Carcinogenic Risks to Humans (http://monographs.org) International Occupational Safety and Health Information Center • International Chemical Safety Cards (http://www. Toxicology Data Network (http://toxnet.ilo.niehs.edu/pips/ghindex.org/pages/ jmpr.gov) • National Toxicology Program (NTP) (http://ntp.acgih.Chemical and Toxicological Information U.htm) Association of Public Health Laboratories (http://www.S.nih. Department of Agriculture (USDA) • Food Safety and Inspection Service (http://www.htm) The EXtension TOXicology NETwork (EXTOXNET) • Pesticide Information Profiles (http://extoxnet.iarc.gov) • National Library of Medicine (NLM).orst.org/public/english/protection/ safework/cis/products/icsc/dtasht/index.fsis.php) 10 Fourth National Report on Human Exposure to Environmental Chemicals .int/pcs) • Monographs of the Joint FAO/WHO Meeting on Pesticide Residues (http://www.html) World Health Organization International Programme on Chemical Safety (IPCS) (http://www.gov) Professional and Academic Organizations American Conference of Governmental Industrial Hygienists (http://www.org/home.aphl.nih.niehs.

Polyacrylamides are useful water-compatible polymers used in water treatment.0) 85.9 (69.0) 57. In the general population.0-104) 132 (115-151) 223 (194-243) 141 (120-152) 220 (189-237) 164 (147-191) 350 769 1889 2570 1523 3509 3592 03-04 03-04 03-04 61.2) 57. 2006). 2006.6-104) 82. In 1997.2 (75. but are generally above the U. drinking water.4) 57. Foods such as french fries and potato chips can contain acrylamide at levels up to 100 times greater than levels found in cooked fish or poultry (DiNovi and Howard.6-66.6-61.3 (53. Animal studies indicate that acrylamide is well absorbed.S.4 (53.2 (62.8 (91.4 (54.5 (74. as an absorbent in disposable diapers.5 (52.6-65.7 (58.1) 101 (95.7-64. pulp and paper production.8 (52.8 (81.1-57. widely distributed in tissues.5-85. the main source of exposure is from the diet. acrylamide has produced upper airway irritation following inhalation of high levels.0 (53.3) 70.9) 63.3) 86.2-67. 2005).4-83.0-49.2 μg/kg/day (U.5-80. glycidamide.1 (83.0. ocular and dermal irritation from direct contact with acrylamide containing materials. EPA. Natural substances in the food are converted to acrylamide.. Estimated intakes in children are about twice that of adults (DiNovi and Howard.4) 57. and in some cosmetics.9-61.2-118) 98.1) 62. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.5) 66. 1994).2-93.7) 73. interval) 61. but can covalently bind to form adducts with proteins.0 (67.1) 46. and in the synthesis or compounding of dye materials. smoking. EPA reference dose of 0. acrylamide is synthesized and used in the production of polyacrylamide polymer.0 μg/kg for adults (FAO/ WHO.3) 63.3-71. Fennell et al.7) 58.4-60.0-108) 152 (139-175) 126 (111-142) 108 (86.1 (52.7) 54. gels. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.4 (54. EPA.9 (60. Elimination occurs mainly in the urine as mercapturic acid conjugates.5 (44. it was discovered that acrylamide is formed when starch-rich foods.0-66. (NTP-CERHR.6-75.S.2) 57.2-114) 163 (147-191) 96. or to glutathione conjugates (Calleman et al.6) 50. and is either metabolized to the reactive epoxide.6-108) 61. Recently.4) 100 (89. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.9) 75.S. Since acrylamide has limited volatility and high water solubility.0-58.1 (73.9 (54. 2005.0 (57.1 (47. Commercially.5 (79.1 (88.2-70.1) 53.9) 57.6) 90. such as potatoes and some grains. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U..7) 96. 2005).4-89.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. and binding agents. and cosmetics (NTP-CERHR.9) 58.2-77.7-64. Fourth National Report on Human Exposure to Environmental Chemicals 11 .1) 55. 1990.4) Selected percentiles ( 95% confidence interval) Sample 95th 192 (168-217) size 7101 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 54. soil conditioners.4-76. 2005). 2002).4-60.3 (55.2-59.8-55. In humans.7 (65. These estimated intakes are hundreds of times lower than occupational exposures. 2005).0 (69.7 (55. 2004.2 (58. see Data Analysis section) for Survey year 03-04 is 3.9-52. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. FDA.4 (51.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. population from the National Health and Nutrition Examination Survey.6 (81.6 (56.1-64.3-2.9-105) 86. and an average daily intake is estimated as 0. and well below doses known to cause nerve damage or carcinogenicity in animals. are heated at temperatures used for frying and baking. and from dermal contact with products that contain residual acrylamide.7) 75th 79.7-60..6 (51.2-91. People may be exposed to acrylamide from foods.1-64.Acrylamide Acrylamide CAS No. Acrylamide is not thought to accumulate in the body at environmental doses. Survey Geometric mean (95% conf.8 (57. in some sealing grouts.1-61.S.5) 58. FAO/WHO. 217 million pounds of acrylamide were produced commercially in the U.6) 71.8-57. 2005). in permanent press fabrics. Tareke et al. 2004).4 (59.S.6) 73.7 (63. mineral processing.

0-93.. 2002. Puppel et al.0) 118 (103-126) 121 (112-134) 113 (94. Glycidamide has been shown to react with DNA (Doerge et al.2 (56. 2005.2) 65. population from the National Health and Nutrition Examination Survey.1-70..8) 60.2 (72. Acrylamide is clastogenic and can produce dominant lethal mutations. Additional information is available from U..5-92.8-48. interval) 59. 2005.1-56.1 (70.. Schettgen et al. 2005). fetal death. The degree of formation of the more toxic glycidamide and levels of GHA can be influenced by polymorphisms in several of the enzymes that metabolize acrylamide (Duale et al. EPA at: http://www.. After exposure ceases.0.4) 53.2-90.1-60.1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59. Vesper 2005) and smoking (Bergmark. AHA levels have been shown to increase with dietary intake (Hagmar et al. 2005) and sperm DNA adducts (Xie et al. U.5) 75th 85.7-86.4 (57. most non-smokers had levels less than about 100 pmol/gram hemoglobin. Hagmar et al. 2006.4 (61..9-138) 143 (130-159) 96. altered gene expression in testicular tissues (Yang et al.8-49. 2005.7) 61.1 (57.. adrenal.7 (61.9) 87..5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71. Puppel et al.. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.0) 94.0-103) 136 (123-148) 125 (116-135) 126 (119-135) 141 (126-157) 146 (123-169) 187 (169-204) 129 (111-141) 174 (157-197) 159 (143-175) 411 784 1931 2623 1529 3604 3674 03-04 03-04 03-04 64.4 (51.0 (80.7) 60. and cancer (mammary.5 (59.5) 71. Maniere et al. although different analytic methods can affect results. 2005).9 (58.5) 87.3-101) 95.5 (83.8-61. Mucci et al. 1997. NTP-CERHR. 1997. Vesper et al. 2005). 2005.2 (63. dominant lethality).9) 59.. 2006)..3) 59.7 (87. Rice.8 (51. IARC classifies acrylamide as probably carcinogenic to humans.4) 83. 2004).5-66. uterine.0-62.S. EPA. reproductive effects (reduced litter size.4-59.4 (56.3-78.pdf. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.3) 59.int/ ipcs/food/jecfa/summaries/summary_report_64_final. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.9-77.9) 65.9 (57.7 (84.2) 87. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.2-68. 2006).6-62.4 (81.5 (56.4-103) 79..8) 45.. Survey Geometric mean (95% conf. and neuronal DNA reactivity (Doerge et al. male germinal cell injury.9-64. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. In addition. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.0 (52. Axonal degeneration. 2002.6-90.5-64. 2005.7-64.7) 90.epa.. 2003.S. 2005) have been demonstrated in animals.3 (56. 2008). presynaptic nerve terminal binding (LoPachin. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. 2001). 2005. 12 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. thyroid. see Data Analysis section) for Survey year 03-04 is 4.0 (75.4) 46..1 (82.4-98. 2005.7) 74. glycidamide (NTP-CERHR.5) 118 (110-129) 121 (108-140) 136 (124-149) 152 (135-170) 159 (129-204) 172 (157-194) 1841 1954 3044 Limit of detection (LOD.6 (66. 2005).9-62.4-65. Schettgen et al. Levels of AHA and GHA reported the NHANES 20032004 sample are generally similar to those seen in several previous studies of non-occupationally exposed subjects (Bergmark et al..2) 55.2-91.1) 60. and other sites) (FAO/WHO. 2009).7 (57.7-62. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. EPA. U.1 (56.4 (90.S. Animal studies have shown that acrylamide can cause nerve damage (neuropathy). 2005.1) 56.9-76.9 (81.1-62..5 (42. 2006) have been demonstrated after acrylamide dosing. 2004.0 (70.3) 59.9) 75. 2005. scrotal..8 (44.S. Klaunig et al. 2008).3) 85..1) 62.5-94.9-78. 2005.6-64.who.. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.1 (66. respectively) are markers of integrated acrylamide exposure over the preceding few months.6 (90.Acrylamide occupational exposures. probably through its epoxide metabolite.

gov/~dms/acrydata.fda. Malmberg B. Scand J Work Environ Health 2001. Nordander C. 054472. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. da Costa GG. Toxicol Appl Pharmacol 1993. Zhang S. et al. Joint FAO/WHO Expert Committee on Food Additives. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Mutat Res 2005.580(1-2):157-165. Aprea P. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). NIH Publication No. Wirfalt E. Tornqvist M. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Kamendulis LM.gov/chemicals/ acrylamide/Acrylamide_Monograph.Toxicol Appl Pharmacol 1994. Bruze M. Burgess J.3:406-412. Mechanisms of acrylamide induced rodent carcinogenesis.561:21-37. Toxicol Sci 2005. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Available at URL: http://www. AHA levels correlated with a neurologic symptom index and specific physiologic measures in an occupational setting and correlated better with clinical signs and symptoms than urinary excretion of the mercapturic acid metabolite (Calleman et al. Available at URL: http://cerhr. Illinois.120(1):45-54. Food Chem. Rosen I. National Toxicology Program.. Snyder RW.126(2):361-371.580(1-2):131-141. Osterman-Golkar S. Bergmark E.pdf. Biomonitoring studies of acrylamide or glycidamide hemoglobin adducts provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of acrylamide than are found in the general population. Churchwell MI. Italy.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Costa LG. Food and Drug Administration (FDA). Costa LG. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Perez et al. February.pdf. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Hagmar L. Paulsen JE. Laurentie M. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Metabolism and hemoglobin adduct formation of acrylamide in humans. Beland FA.niehs. He F. Calleman CJ. 1999). Guffroy M. Toxicol Sci. Doerge DR. McDaniel LP. DiNovi M and Howard D. Toxicol 2005.27(4):219-226. Calleman CJ. Cheong HK. Farmer PB. July. References Bergmark E. 64th Meeting: Summary and Conclusions (FAO/WHO). Adv Exp Med Biol 2005. et al.56. Summer SCJ. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. 2/3/09 Klaunig JE. Acrylamide intake through diet and human cancer risk. Twaddle NC. et al.43:365–410. 2/3/09 Perez HL.. 1994). Available at URL: http://www. Adv Exp Med Biol 2005. Hagmar et al. 2001). Fennell TR. J Agric Food Chem 2008. In another study.. Chem Res Toxicol 1990. Acrylamide neurotoxicity: neurological. 8-17 February 2005. Wilson KM. Spicer R. Magnusson AL.. Calleman CJ. Churchwell MI. April 13-15. Haugen M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers.who. morphological and molecular endpoints in animal models. Chem Res Toxicol 1997 Jan. Wu Y. Paulsson B. Granath F. Tornqvist M. Doerge DR. and Research Strategies. et al. smoking habits and gender.10(1):78-84. 2009 Jan 8. CFSAN/Office of Plant and Dairy Foods. He F. Survey data on acrylamide in food: individual food products. 2/3/09 Hagmar L. Human exposure and internal dose assessments of acrylamide in food. Godard T. The Updated Exposure Assessment for Acrylamide. Andersen M. et al. Finding a measurable amount of acrylamide or glycidamide hemoglobin adducts in blood does not mean that these levels of acrylamide or glycidamide hemoglobin adducts cause adverse health effects. Duale N. Mutat Res 2005. Uncertainties. Becher G. 6013-6019.561:49-62.Acrylamide In occupational settings.html#u1004.. Bergmark E. Chicago. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. [Epub ahead of print] Dybing E. 2005. 2006. Bjellaas T. Bridson WE. Tian G. Kautiainen A. smokers and nonsmokers. Rome.cfsan.nih. Fennell TR.85:447-459. 2004. Mutat Res 2005. Maniere I. Axmon A.580(1-2):119-129. Yang JS. 2001. 1993. Mucci LA. Bergmark E. Alexander J. LoPachin RM.

et al. EPA). Toxicol Lett 2006. Environmental Protection Agency (U. Schettgen T. Hemoglobin adducts of ethylene oxide. Meyers T. Tareke E. Vesper HW. Available at URL: http://www. Int J Hyg Environ Health 2004. September. Licea-Perez H. Drexler H. revised 1/3/06. Sun H. Chemical Summary for Acrylamide.txt. Washington (DC). Toxicol Lett 2002. Schettgen T. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Drexler H. Angerer J. Fu D.207(6):531-9.S. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Yang HJ. Ingham L. Slimani N. Agudo A. 14 Fourth National Report on Human Exposure to Environmental Chemicals .S. et al. Lee SH. Meyers T. Letzel S. Rossbach B. U.20(6):959-64. Gray JG. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Toxicological effects of acrylamide on rat testicular gene expression profile. Reprod Toxicol 2005.163(2):101-8. Rapid Commun Mass Spectrom 2006.htm. Acrylamide. Rydberg P. Ding X. EPA). Han CH. 1994. Available at URL: http://www. Marko D. Int J Hyg Environ Health 2003. Myers GL. Adv Exp Med Biol 2005. Angerer J.epa. Integrated Risk Information System (IRIS). Puppel N.206(1):9-14. Lee MH. Ospina M. 2/3/09.epa. Schettgen T. Eriksson S. Environmental Protection Agency (U. Broding HC. 2/3/09 Vesper HW. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Anal Biochem 1999. J Agric Food Chem 2002.S.274(1):59-68. Chae C.Acrylamide glycidamide by gas chromatography-mass spectrometry. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Kutting B. Benetou V.580(1-2):71-80.56(15):6046-53. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Liu Y. Mutat Res 2005. Karlsson P. Xie Q. Jin Y. Analysis of acrylamide.gov/iris/subst/0286. Rice JM. Liu K. The carcinogenicity of acrylamide. Tjaden Z. Angerer J. Mutat Res 2005 Feb 7. Smith A. Han DU. U. Ospina M. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Drexler H.561:89-96. J Agric Food Chem 2008.50(17):4998-5006. Hallmans G. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Choi JH.gov/chemfact/s_acryla. Weiss T. a carcinogen formed in heated foodstuffs.580(1-2):3-20. Office of Pollution Prevention and Toxics. Vesper HW.19(4):527-34.S. propylene oxide. Fueller F. Tornqvist M.134(1-3):65-70. Tjønneland A.

188) . and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.96) 2.740-1.260-1.920 (.39) 3.057-. and exacerbated asthma (U.094) .150) .68) 2.077) .02) 1.213) .320) .124 (.66) 1.059-.080-.20 (1.020-.180) .310-1.950 (.060 (.930 (. DHHS.950-1.05) 1.050) .670) .160 (.030 (.400-.990 (.14) . acute respiratory illness.142-.090-.49) 1.50-4.090-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004).66 (1.040 (. Survey Geometric mean (95% conf.75) 1.110-.96-4.625) .12-4.120-.060 (<LOD-.198) * .76 (1.05.062 (.50-1.220) .163 (.120 (.060) .506 (.630 (.32-2.040 (.050 (.533-.38-2.960-1.77 (2.160) . Cigarettes contain about 1.060-.030-.68) .089) Age group 3-11 years 99-00 01-02** 03-04 .080-.770-1. maternal exposure during pregnancy can result in lower birth weight.S. Serum Cotinine Metabolite of nicotine (component of tobacco smoke) Geometric mean and selected percentiles of serum concentrations (in ng/mL) for the non-smoking U.44 (1. DHHS.110 (.12 (2.5% nicotine by weight (Kozlowski et al.20-2.78) 2.620-1.840) 3.32-2.410) .42 (1.164 (.180) .26-1.23 (1. ** In the 2001-2002 survey period.23 (2.108) * .570-1.44 (2.43 (1.580 (.040-.65 (1.053 (<LOD-.70-2. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.130 (.063) .140 (.22) 2.55 (1.23-2.060 (.580-1.054 (.066-.48-3. see Data Analysis section) for Survey years 99-00.63 (2.052 (<LOD-.20) 1.17 (1.087 (.030-.53-4.115-.21-1.145) .310-1. cardiovascular disease.310) .430-1. < LOD means less than the limit of detection.14) .139) * .201) .00) 1. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.77 (1.42-4.33-2.620 (.144 (.310) 90th 1.01 (1.500 (.84-3.110-.050 (<LOD-. Children exposed to ETS are at increased risk for sudden infant death syndrome.660) .047-.48-2.30) * .126) .62 (2.130) .21 (.15) 2.790) .110) .68 (1.120 (.216 (.800 (.580) .050-.308 (.480-.050) .34 (1.080) < LOD < LOD . population from the National Health and Nutrition Examination Survey.015 ng/mL.94) 1.621-1.190-.110 (.570 (.068) .04 (1.137-.120) .360) .070) .21-1.990) .110 (.040 (. and 0.30) 2.770) .086 (.50 (1.Cotinine Cotinine CAS No.110 (.60-2.50) 3.16) .120 (.85 (1.187) .770) .63-2.071 (.28-1.88 (.96 (1.068) .02 (.17) .70) 2.470-.110) .35 (2.05 ng/mL.350-.197) .95) 1. respectively.15 (2.81-2.18-3.052 (<LOD-. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.19) 1.32) 1.17 (.11) .540 (.49) 2241 1878 1707 1333 1602 1704 1950 2847 2500 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02** 03-04 Limit of detection (LOD.710 (.302) .428-.20) .148-.28) . Fourth National Report on Human Exposure to Environmental Chemicals 15 .070 (<LOD-.19-2. and various other disorders (U.89) 1. which may vary for some chemicals by year and by individual sample.30) 2.160 (.066) .075 (.080) < LOD .99) 2.190-.140-.110-.23 (.234) . 486-56-6 Metabolite of nicotine (a component of tobacco smoke) General Information Tobacco use is the most important preventable cause of premature morbidity and mortality in the United States.100-.160) .66-3.131 (.910-1.073) < LOD .060-.220) .164 (.087) < LOD < LOD .820) .280 (.071) .180) .480-1.163) .57) 2. stroke.084) .55-2.54) 1.230) .120-.93) .077) . 1998).175 (.726) .070-.40) . emphysema.12) 1.520 (.061) < LOD .080 (.210 (.87-3.88 (1.050 (<LOD-.120 (. 2006).09-2.076-.997-3.630 (.740-1.140-.350 (.050-.92 (1.180) .S.54 (1.088-.510 (.350-.080-.153-.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .120 (.047-.92) 1174 1415 1252 1773 1902 1783 3052 3502 3285 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 20 years and older Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.240 (. acute respiratory infections.39 (1.040-.111-.154-.00) .106-.137 (.058 (.83-2.20 (.540-.730 (. 2004). 83% of measurements had an LOD of 0.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .47-3.62) 2.150) .050 (<LOD-. ear problems.54 (1.160 (.140 (.99) 2.104-.110 (.79) 3.S.080 (.850 (.220-.690 (.167 (.190-.260) 1.180 (. and 17% had an LOD of 0.505 (.630 (.080-.180) .070) 75th .160-.070) .193) .44) 2.030-.180 (.060-..53 (1.44) 2.087-.77 (1.200) 1.230 (.600-1.02) 1.860 (.49) 1.450-.015.066 (.050 (<LOD-. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.370-.060 (<LOD-.059-.45) 1.14-1. and 03-04 are 0.01) 3.312) .043-.090-.19) .09-3.09-3.300) .900-1.12 (1.

non-Hispanic blacks metabolize cotinine more slowly than do non-Hispanic whites (Benowitz et al.3 to 30 µg/m3. Non-Hispanic blacks had higher serum cotinine concentrations compared with either non-Hispanic whites or Mexican-Americans. Biomonitoring studies of serum cotinine will help physicians Fourth National Report on Human Exposure to Environmental Chemicals . with levels showing similar or slightly higher results (depending on the degree of ETS exposure) than those reported in the previous NHANES (CDC 2005. Children are primarily exposed to ETS by parents and caregivers who smoke. Once absorbed. 2005). However. html. Differences in cotinine concentrations among race/ethnicity and age groups may be influenced by pharmacokinetic differences as well as by ETS exposure (Benowitz et al. Symptoms of 16 nicotine withdrawal include irritability. Over the previous decade. Biomonitoring Information Serum cotinine levels reflect recent exposure to nicotine in tobacco smoke. For an adult. levels of exposure to ETS appeared to decrease since geometric mean cotinine serum concentrations in nonsmokers had fallen by approximately 70% and the rate of detectable cotinine in nonsmokers fell from 88% to 43% when NHANES 1988–1991 was compared to NHANES 1999–2002. Serum cotinine has been measured in many studies of nonsmoking populations.. diarrhea.nida. Iwase et al. 2006). 2006. salivation. 2006).. Wilson et al. (CDC. nausea.Cotinine 1994. Nicotine is also used commercially as an insecticide in its sulfate and alkaloid forms. contains nicotine in larger amounts than other nicotine-containing plants. and increased appetite. craving. Up to 90% of the nicotine delivered in tobacco smoke is absorbed rapidly from the lungs into the blood stream (Armitage et al. 2005.. and peppers. 1975. and death. mean air concentrations typically range from 2 to 14 µg/m3 (NTP. 1999). diaphoresis.. NIOSH guidelines consider ETS to be a potential occupational carcinogen and recommend that exposure be reduced to the lowest feasible concentration. NCI. 1998). urine. chewing tobacco. In homes with one or more smokers. cognitive and sleep disturbances. the primary sources for ETS exposure are in a workplace where smoking occurs and in a residence shared with one or more smokers. nasal sprays. 2004).nih. Nicotine also indirectly causes a release of dopamine in the brain regions that control pleasure and motivation. Measuring cotinine is preferred over measuring nicotine because cotinine persists longer in the body with a plasma half-life of about 16 hours (Benowitz and Jacob. and hair. Nicotine can also be absorbed from the gastrointestinal tract and skin by using snuff.gov/researchreports/nicotine/nicotine. or chewing gum. More information about the effects of smoking and nicotine can be found at: http://www. which include potatoes. vomiting. Nicotiana tabacum.. The Federal Aviation Administration has banned the smoking of tobacco products on both domestic and foreign air carrier flights in the United States. with heavy exposure to ETS producing levels in the 1–10 ng/mL range. Workers who harvest tobacco can be exposed to nicotine and become intoxicated as a result of the transdermal absorption of nicotine contained in the plant. 1999. Acute tobacco or nicotine intoxication can produce dizziness. Nonsmoking is usually defined as a serum cotinine level of less than or equal to 10 ng/mL (Pirkle et al. Cotinine can be measured in serum. Hukkanen et al. Hukkanen et al. Inhaling tobacco smoke from either active or passive (ETS) smoking is the main source of nicotine exposure for the general population. 1999. or skin patches that contain nicotine. is currently regarded as the best biomarker in active smokers and in nonsmokers exposed to ETS. a process involved in the development of addiction. During each previous NHANES survey.. 1996). The IARC and the NTP consider tobacco smoke to be a human carcinogen. the primary metabolite of nicotine. Cotinine. 1998). tomatoes. The serum cotinine levels seen in the NHANES 20032004 appear approximately similar to levels seen in the previous survey period (NHANES 2001-2002) for the total population estimates.. Pirkle et al. Perez-Stable et al... 2005).. 2005). Mean air concentrations of nicotine in public spaces where smoking is allowed range from 0. 1994). Active smokers almost always have levels higher than 10 ng/mL and sometimes higher than 500 ng/mL (Hukkanen et al. Soliman et al. with higher levels measured in restaurants and bars.. The tobacco plant.. nicotine has a half-life in blood plasma of several hours (Benowitz. The overall decline in population estimates of serum cotinine likely reflects decreased ETS exposure among nonsmokers in locations with smoke-free laws (Pickett et al. 1991)... eggplants. variable changes in blood pressure and heart rate. 2005. Higher levels of cotinine have previously been reported for non-Hispanic black smokers (Caraballo et al. the adjusted geometric mean serum cotinine was higher in children (aged 4–11 years) than in adults among both non-Hispanic blacks and non-Hispanic whites (Pirkle et al.. 1996). seizures. 2004). Nicotine stimulates preganglionic cholinergic receptors within peripheral sympathetic autonomic ganglia and at cholinergic sites within the central nervous system. Nonsmokers exposed to typical levels of ETS have serum cotinine levels of less than 1 ng/mL. saliva.

Metabolism and disposition kinetics of nicotine. Jarvis MJ. Third National Report on Human Exposure to Environmental Chemicals. Jacob P. Coordinating Center for Health Promotion. Atlanta (GA): 2005. Nicotine metabolism and intake in black and white smokers. National Institute for Occupational Safety and Hygiene (NIOSH). Jacob III P. Aiba M. Available at URL: http://ntp. Tobacco related exposures. U.4:313-316.gov/ntp/roc/eleventh/profiles/ s176toba.gov/tcrb/monographs/10/. Available at URL: http://monographs. Benowitz NL. 4/13/09 Perez-Stable EJ. Richter PA. cigarette smokers: the Third National Health and Nutrition Examination Survey. Benowitz NL. Am J Public Health 2004. 1988-1991.94(2):314-320. Modin G. References Armitage AK. Int Arch Occup Environ Health 1991. Vogler GP. Bernert JT. Soliman S.15:302-307.surgeongeneral. IARC Monogr Eval Carcinog Risks Hum. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. J Pharmacol Exp Ther 1999. Centers for Disease Control and Prevention. Centers for Disease Control. et al. iarc.S. Tob Control 2006.S. Coordinating Center for Health Promotion. Pirkle JL. DHHS). Pollack HA. Turner DM. Mowery PD.cancer.114(6):853-858. 1999. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. 1988-1991. Maurer KR. Hukkanen J. Summary of Data Reported and Evaluation [online] 1986. Flegal KM. [online]. Jacob P III. Available at URL: http:// cancercontrol. 4/13/09 National Cancer Institute (NCI). Caudill SP. Racial/ethnic differences in serum cotinine levels among adult U. Benowitz NL.niehs. Pechacek TF.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Brody DJ. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. U. Tobacco Smoke and Involuntary Smoking. Clin Pharmacol Ther 1994. population to secondhand smoke: 1988-2002. JAMA 1998. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Pirkle JL.gov/library/ secondhandsmoke/.pdf.niosh. et al.63:139-43. 1999-2002. DHHS). Pickett MA. Benowitz NL. 1991.S. Available at URL: http://monographs. Smoking and Tobacco Control Monograph 10 [online]. Department of Heath and Human Services. Curtin LR. Sosnoff CS. Department of Heath and Human Services. Caraballo R. June.S Department of Health and Human Services (U. Centers for Disease Control and Prevention. and the United States. Summary of Data Reported and Evaluation [online] 2004. Lewis PJ. Trends in the exposure of nonsmokers in the U. Vol 83.280:152-156. Kozlowski LT. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey.fr/ENG/Monographs/ allmonos90. Metabolism of nicotine to cotinine studied by a dual stable isotope method.cdc. Pharmacol Rev 2005. Tobacco Smoke. Etzel RA. Exposure of the U. Brody DJ. Mehta NY. IARC Monogr Eval Carcinog Risks Hum. Warner K. Tob Control 1998.S. Giovino GA.57(1):79115. Cotinine as a biomarker of environmental tobacco smoke exposure. Jacob P III. JAMA 1998. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. 4/13/09 International Agency for Research on Cancer. BMJ 1975. Sweeney CT. Pechacek TF. Herrera B. Respiratory nicotine absorption in non-smoking females during passive smoking.nih.7:369-375. In Report on Carcinogens. Giovino G. 2004. Herrera B. Vol 38.pdf. Absorption and metabolism of nicotine from cigarettes. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Epidemiol Rev 1996. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Kira S.fr/ENG/Monographs/allmonos90.S Department of Health and Human Services (U. Environ Health Perspect 2006. Houseman TH. Available at URL: http://www. 4/13/09 U.php. available at URL: http://mtn. Schober SE. National Center for Chronic Disease Prevention and Health Promotion. 4/13/09 Centers for Disease Control and Prevention (CDC). Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Benowitz NL. Fong I. 4/13/09 Iwase A. Perez-Stable EJ. the United Kingdom. Schwartz SS.iarc. George CF.S.gov/eid/rmca/critdocs/ criteriadoc/33.280:135-140.php. Strauss WJ. Dollery CT. U. National Toxicology Program (NTP). Ethnic differences in N-glucuronidation of nicotine and cotinine. Bernert JT.S.56:483-493.291(3):1196-1203.275:1233-1240.S. JAMA 1996. Office on Smoking and Health [online] 2006. International Agency for Research on Cancer.18:188-204. 11th ed.

2004. 4/13/09 Wilson SE. Kahn RS. Khoury J Lanphear BP. 18 Fourth National Report on Human Exposure to Environmental Chemicals .gov/tobacco/data_statistics/sgr/sgr_2004/index.113(3):362-367. [online]. Office on Smoking and Health. Racial differences in exposure to environmental tobacco smoke among children. Available at URL: http:// www. htm#full.Cotinine Chronic Disease Prevention and Health Promotion. Environ Health Perspect 2005.cdc.

gov/pesticides/.N-Diethyl-meta-toluamide (DEET) CAS No.140-. Survey Geometric mean (95% conf. One survey detected DEET in 74% of sampled streams in the U.100-.120-.130-.S. Its use is recommended for prevention of several vector-borne diseases. 1998). population from the National Health and Nutrition Examination Survey.S.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. DEET is also used in combination with dermal sun screens (U.150) < LOD .130-. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown..100 (<LOD-.220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .S.110 (.120-.140 (. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.epa.110 (.1. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.140) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .. Fourth National Report on Human Exposure to Environmental Chemicals 19 . and they range in concentration from 4% to 100%.N-Diethyl-meta-toluamide (DEET) N. 2002).100-. (U.170 (.240) < LOD . Additional information is available from U.180) < LOD .140) < LOD . DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.100-. < LOD means less than the limit of detection.140) < LOD . Urinary N.100-.130-. 2003).110 (. including seizures and encephalopathy. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.110-.EPA.EPA at: http://www.EPA.210 (.160) < LOD .N.S.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .180 (.220 (.170 (. Sudakin and Trevathan. 2003).270) 688 678 518 700 598 956 Limit of detection (LOD.449 and 0. (Kolpin et al. EPA.130 (.250) < LOD . Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. DEET is not a developmental or reproductive toxicant in animals (U. 1995.130 (.110 (. have been reported as result of self-poisoning by ingestion or excessive dermal application. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.560) < LOD . DEET is not genotoxic.130 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2002).180 (. Neurological effects in humans. DEET has low acute toxicity. 1998). see Data Analysis section) for Survey years 99-00 and 01-02 are 0.110 (<LOD-.. There are over 225 insect repellents brands containing DEET. and it has not been rated by IARC or NTP with respect to human carcinogenicity.110-. DEET is not registered for use on agricultural commodities. 2005).110 (<LOD-. 134-62-3 General Information N. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . DEET can be applied to clothing and the skin to repel biting insects.520) < LOD .140) < LOD .S.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.S.100-.130) < LOD . After absorption.100-.210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130) < LOD .190) < LOD .180 (. About 3-8% of dermally applied DEET is absorbed. which may vary for some chemicals by year and by individual sample.130-.

440) < LOD .150-. population from the National Health and Nutrition Examination Survey.190 (<LOD-. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . Biomonitoring studies on levels of DEET provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEET than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.N.280 (.230) < LOD .300 (..500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .350) < LOD . In this survey period.S. 2005).N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure. representative subsamples from NHANES 2001-2002.250-.290-. 1992).190-.270 (.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.200 (. Urinary N.480 (.410-.230-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.410 (.630) < LOD .190 (. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.500) size 1977 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th . 20 Fourth National Report on Human Exposure to Environmental Chemicals .170-.330 (.140-.500 (.410 (.580) 964 1191 1013 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .320) < LOD . 2007).370) < LOD .250) < LOD .240) < LOD .150) < LOD .190 (.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.320 (.280-1. Urinary DEET levels as high as 5.350-.490) < LOD .270-.240-.250 (.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.350) < LOD . the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.270 (<LOD-.370-.93) < LOD .270) < LOD . Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.130 (<LOD-.230-..640 (.330 (.S.390-.

Available at URL: http://www. 1993-1997. Barr DB.gov/teach/chem_summ/ DEET_summary.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. Page BC. Washington (DC): U.36(6):1202-1211. Centers for Disease Control and Prevention (CDC). Quandt SA. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Osimitz TG. Chemical Summary.S. Smallwood AW. DEET: a review and update of safety and risk in the general population. Fundam Appl Toxicol 1995.EPA. Selim S. Atlanta (GA). Sudakin DL.N-Diethyl-meta-toluamide (DEET) References Arcury TA. Meyer MT. Environ Sci Technol 2002.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. 4/9/09 U. 1999-2000: a national reconnaissance.25:95-100. Hartnagel RE Jr.41(6):831-839.gov/oppsrrd1/REDs/0002red.S. Diethyltoluamide (DEET).2:341352. and excretion of N. Grzywacz JG. pp. et al. U. Int J Toxicol 2002.pdf.S. Barber LB. Veltri JC. streams.S. Chen H. Bell JW. and other organic wastewater contaminants in U. Pharmaceuticals. Environ Health Perspect 2007. Gabriel KL.115(8):1254-1260. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Available at URL: http://www.EPA). Environmental Protection Agency (U. hormones. 2005. J Anal Toxicol 1992.epa. pdf. EPA. EPA 738-R98-010. metabolism. Furlong ET. Schoenig GP.EPA). September 1998. Reregistration Eligibility Decision (RED): DEET. J Toxicol Clin Toxicol 2003. Tapia J. U. DeBord KE. Absorption. Toxicity and Exposure Assessment in Children’s Health. Thurman EM. Environmental Protection Agency (U. N. Third National Report on Human Exposure to Environmental Chemicals.N. 2005 Kolpin DW.S. Human exposures to N.S. Zaugg SD. Trevathan WR.epa.N-diethyl-mtoluamide following dermal application to human volunteers. Lowry LK.S.16(1):10-13. 1-118.

Disinfection By-Products (Trihalomethanes)

Disinfection By-Products (Trihalomethanes)
Bromodichloromethane CAS No. 75-27-4 Dibromochloromethane (Chlorodibromomethane) CAS No. 124-48-1 Tribromomethane (Bromoform) CAS No. 75-25-2 Trichloromethane (Chloroform) CAS No. 57-57-8 General Information Disinfection by-products (DBP) are a class of chemical by-products also referred to as trihalomethanes (THMs), formed when chlorine or bromine interacts with the natural organic materials found in water. DBPs also include other formed products, such as haloacetic acids, haloacetonitriles, haloketones, and chlorophenols. The composition and levels of specific DBPs are determined by water quality, water treatment conditions, and disinfectant type (IPCS, 2000). Primary sources of DBPs are chlorinated drinking water and recreational water bodies, such as swimming pools.

In drinking water, trichloromethane is the predominant DBP, usually found at much higher levels than bromodichloromethane; tribromomethane is the least abundant (Krasner et al., 1989). DBPs are volatile at room temperature and can be detected in ambient air during activities such as showering, bathing, dishwashing, and swimming (Backer, et al., 2000; Gordon et al., 2006). Trichloromethane has industrial applications and is used to produce refrigerants and feedstock. It may be released into the environment where chlorine-based chemicals are used for bleaching and disinfecting processes or disposed at hazardous waste sites (IPCS, 2004; LaRegina, et al. 1986). Tribromomethane has limited industrial uses, mainly in geological assaying, electronics manufacturing, and as a solvent in laboratory analyses (ATSDR, 2005). DBPs tend not to bioaccumulate in aquatic organisms or persist in open or surface waters or soils, but they can remain in water within closed pipe systems. Workplace exposure may occur during the production of trichloromethane or tribromomethane, or in workplaces where DBPs may be generated, such as pulp or paper manufacturing, swimming pools, and water treatment plants (IPCS, 2004). General population exposure to DBPs occurs primarily through ingesting chlorinated water and inhaling the water

Blood Bromodichloromethane
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 2.21 (1.65-2.97)

Selected percentiles
( 95% confidence interval)

50th 2.30 (1.56-3.21) 1.40 (1.10-1.90)

75th 4.63 (3.24-6.20) 3.40 (2.60-4.20)

90th 8.45 (5.86-12.0) 6.20 (5.30-7.00)

95th 12.0 (7.68-19.2) 9.50 (7.00-12.0)

Total Age group 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

1.50 (1.20-1.86)

Sample size 785 1322

01-02 03-04

2.21 (1.65-2.97) 1.50 (1.20-1.86)

2.30 (1.56-3.21) 1.40 (1.10-1.90)

4.63 (3.24-6.20) 3.40 (2.60-4.20)

8.45 (5.86-12.0) 6.20 (5.30-7.00)

12.0 (7.68-19.2) 9.50 (7.00-12.0)

785 1322

01-02 03-04 01-02 03-04

2.19 (1.60-3.00) 1.48 (1.18-1.85) 2.24 (1.66-3.01) 1.51 (1.21-1.90)

2.31 (1.63-3.21) 1.40 (.940-2.00) 2.28 (1.49-3.24) 1.50 (1.10-1.90)

4.64 (3.21-6.08) 3.40 (2.60-4.30) 4.63 (3.09-7.01) 3.30 (2.50-4.20)

7.96 (5.74-15.3) 6.60 (5.40-7.20) 8.62 (5.26-12.9) 6.10 (4.69-7.30)

13.0 (6.93-20.5) 11.0 (7.20-14.0) 11.1 (7.68-25.0) 7.80 (6.40-12.0)

382 650 403 672

01-02 03-04 01-02 03-04 01-02 03-04

3.28 (2.29-4.68) 1.65 (1.15-2.38) 2.32 (1.82-2.94) 1.56 (1.15-2.13) 2.02 (1.42-2.87) 1.42 (1.11-1.81)

3.32 (2.19-4.70) 1.60 (.820-2.80) 2.50 (1.56-3.55) 1.70 (1.10-2.20) 2.16 (1.36-3.09) 1.30 (.850-1.90)

6.81 (3.71-10.4) 3.50 (2.60-4.90) 4.57 (3.60-5.56) 2.90 (2.15-3.80) 4.34 (2.92-6.01) 3.30 (2.30-4.40)

10.8 (8.24-14.7) 7.30 (4.50-10.0) 8.69 (5.63-9.49) 5.10 (3.80-6.60) 7.33 (4.72-15.3) 6.20 (5.20-7.20)

14.7 (11.1-20.5) 10.0 (7.30-11.0) 10.0 (5.89-13.5) 6.60 (4.90-13.0) 11.1 (6.01-26.1) 9.80 (6.70-13.0)

227 244 130 290 365 684

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.233 and 0.62. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds.

22

Fourth National Report on Human Exposure to Environmental Chemicals

Disinfection By-Products (Trihalomethanes)

vapor. Dermal absorption also may occur during bathing and swimming (ATSDR, 1997, 2005; Dick, et al., 1995; Leavens et al., 2007). Each of the DBPs is rapidly absorbed and distributed widely throughout the body. In animals, these chemicals undergo hepatic metabolism to reactive chemicals, which can bind to cell macromolecules and be toxic in large amounts (IPCS, 2000). Ultimately, DBPs are metabolized to carbon dioxide, which is eliminated in exhaled air within a few hours. Only a small amount of each DBP is eliminated unchanged in urine. Elimination halflives for these chemicals are less than four hours (ATSDR, 2005; Leavens et al., 2007). Human health effects from DBPs at low environmental doses or at biomonitored levels from low environmental exposures are unclear or unknown. Humans exposed to massive levels of trichloromethane or tribromomethane develop central nervous system depression and hepatotoxicity (ATSDR, 2005, 1997). Acute animal toxicity studies of each of these chemicals have found central nervous system depression, liver and renal damage or necrosis, and occasionally, cardiac depression and arrhythmias (IPCS, 2000). In studies of rodents chronically fed high doses of either trichloromethane or bromodichloromethane, carcinomas occurred in the liver and kidney; large intestine tumors and

polyps were also noted with bromodichloromethane (NCI, 1976; NTP, 1987). Chronic feeding studies in rodents with either dibromochloromethane or tribromomethane showed inconsistent evidence of carcinogenicity across species and genders. The DBPs did not produce reproductive or developmental effects in animals unless maternal toxicity was present, but bromodichloromethane altered sperm motility (IPCS, 2000). Numerous epidemiologic studies of the relationships between chlorinated water source and various cancers, adverse reproductive outcomes, and cardiovascular disease have been inconclusive (IPCS, 2000). IARC classified trichloromethane and bromodichloromethane as possible human carcinogens, and NTP determined that these chemicals are reasonably anticipated to be human carcinogens. However, IARC found dibromochloromethane and tribromomethane to be unclassifiable regarding human carcinogenicity. The U.S. EPA has established drinking water and environmental standards for “total THMs.” OSHA and ACGIH have established workplace standards and guidelines, respectively, for trichloromethane and tribromomethane. Information about external exposure (i.e., environmental levels) and health effects is available from ATSDR at: http://www.atsdr.cdc.gov/toxpro2.html.

Blood Dibromochloromethane
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) .867 (.521-1.44)

Selected percentiles
( 95% confidence interval)

50th .780 (.340-1.90) < LOD

75th 2.61 (1.22-4.38) 1.30 (1.00-1.80)

90th 5.46 (3.53-9.71) 3.60 (2.70-4.80)

95th 8.96 (5.04-12.9) 7.20 (4.80-8.60)

Total Age group 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

*

Sample size 781 1333

01-02 03-04

.867 (.521-1.44) *

.780 (.340-1.90) < LOD

2.61 (1.22-4.38) 1.30 (1.00-1.80)

5.46 (3.53-9.71) 3.60 (2.70-4.80)

8.96 (5.04-12.9) 7.20 (4.80-8.60)

781 1333

01-02 03-04 01-02 03-04

.850 (.481-1.50) * .884 (.550-1.42) *

.730 (.300-2.25) < LOD .820 (.340-1.69) < LOD

2.66 (.960-4.38) 1.30 (1.00-1.90) 2.54 (1.37-4.31) 1.30 (1.00-1.80)

4.77 (3.33-9.20) 3.70 (2.70-5.70) 6.30 (3.28-10.1) 3.60 (2.50-4.80)

8.06 (4.31-14.6) 7.20 (5.20-8.60) 9.91 (5.02-13.0) 6.60 (3.80-9.20)

371 657 410 676

01-02 03-04 01-02 03-04 01-02 03-04

1.61 (.843-3.06) 1.20 (.963-1.50) 1.03 (.505-2.09) * .736 (.413-1.31) *

1.49 (.670-3.99) 1.10 (.810-1.40) .930 (.530-2.03) < LOD .640 (<LOD-1.93) < LOD

4.59 (1.93-8.89) 2.30 (1.50-4.10) 2.03 (.770-7.06) .970 (.650-1.60) 2.49 (.870-4.27) 1.30 (.950-1.80)

9.26 (5.21-12.1) 5.20 (3.80-6.90) 4.22 (2.01-10.5) 1.90 (1.20-3.20) 4.57 (3.00-7.12) 3.30 (2.50-4.60)

12.0 (9.63-16.1) 7.70 (5.20-11.0) 8.09 (2.80-16.5) 3.20 (1.80-5.20) 6.98 (4.27-11.1) 6.60 (3.70-9.20)

233 256 128 288 357 685

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.271 and 0.62. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Fourth National Report on Human Exposure to Environmental Chemicals

23

Disinfection By-Products (Trihalomethanes)

Biomonitoring Information Levels of blood DBPs reflect recent exposure. Geometric mean blood trichloromethane levels were 0.039 and 0.043 ng/mL among non-smoking and smoking adults, respectively, in a subsample of NHANES 1999-2000 participants (Lin et al., 2008), which were at least twice as high as comparable levels in NHANES 2001-2002 and 2003-2004. In a non-representative sample of NHANES III (1988-1994) participants, the geometric mean and median blood trichloromethane levels, respectively, were 0.043 and 0.023 mg/L (Churchill et al., 2001). Similar median blood trichloromethane levels were reported in smaller studies of U.S adults (Ashley et al., 2005; Backer et al., 2000; Buckley et al., 1997) and in this Report. Immediately following bathing or showering with chlorinated water, median blood levels of trichloromethane, dibromochloromethane, and bromodichloromethane can increase two to four times over baseline levels, and then return to baseline rapidly during the next one to two hours (Ashley et al., 2005; Backer et al., 2000). Finding a measurable amount of one or more of these THMs in blood does not mean that the level of THMs causes an adverse health effect. Biomonitoring studies of blood

THMs can provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of THMs than levels found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Blood Tribromomethane (Bromoform)
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 1.57 (1.07-2.31)

Selected percentiles
( 95% confidence interval)

50th 1.39 (.960-2.02) < LOD

75th 2.78 (1.76-4.63) 1.80 (<LOD-2.80)

90th 6.05 (2.92-29.2) 3.74 (2.30-7.10)

95th 15.5 (3.68-85.4) 6.40 (3.60-14.0)

Total Age group 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

*

Sample size 774 1310

01-02 03-04

1.57 (1.07-2.31) *

1.39 (.960-2.02) < LOD

2.78 (1.76-4.63) 1.80 (<LOD-2.80)

6.05 (2.92-29.2) 3.74 (2.30-7.10)

15.5 (3.68-85.4) 6.40 (3.60-14.0)

774 1310

01-02 03-04 01-02 03-04

1.49 (.944-2.34) * 1.67 (1.17-2.39) *

1.29 (.850-1.98) < LOD 1.46 (1.05-2.21) < LOD

2.65 (1.49-5.05) 1.90 (<LOD-2.87) 2.86 (1.89-4.57) 1.72 (<LOD-2.65)

6.12 (2.26-33.9) 4.00 (2.40-6.80) 5.69 (3.30-27.5) 3.20 (1.93-7.70)

14.9 (2.79-69.9) 6.50 (4.00-13.0) 22.2 (5.09-49.6) 6.10 (3.10-31.0)

374 645 400 665

01-02 03-04 01-02 03-04 01-02 03-04

2.34 (1.15-4.77) * 1.51 (.857-2.67) * 1.47 (.980-2.22) *

1.66 (.990-3.38) 1.60 (<LOD-3.10) 1.47 (.780-3.15) < LOD 1.29 (.840-2.06) < LOD

4.03 (1.42-36.5) 3.30 (<LOD-9.40) 2.58 (1.39-4.64) 1.60 (<LOD-2.30) 2.58 (1.51-4.91) 1.70 (<LOD-2.90)

28.3 (4.39-49.2) 7.60 (3.60-14.0) 4.34 (2.57-8.48) 2.50 (1.80-3.20) 5.69 (2.84-21.2) 3.50 (2.00-7.70)

40.8 (31.5-57.9) 11.0 (5.60-210) 6.27 (3.28-15.2) 3.20 (2.40-6.10) 11.0 (3.30-69.9) 5.90 (3.30-21.0)

234 242 121 289 362 680

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.596 and 1.5. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

24

Fourth National Report on Human Exposure to Environmental Chemicals

Disinfection By-Products (Trihalomethanes)

Blood Trichloromethane (Chloroform)
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 16.6 (13.0-21.1)

Selected percentiles
( 95% confidence interval)

50th 16.1 (11.9-22.2) 10.0 (8.50-13.0)

75th 31.7 (23.9-40.4) 20.0 (17.0-24.0)

90th 55.5 (44.5-68.6) 35.0 (29.0-40.0)

95th 72.1 (57.3-105) 50.0 (37.0-65.0)

Total Age group 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

10.2 (8.56-12.2)

Sample size 744 1222

01-02 03-04

16.6 (13.0-21.1) 10.2 (8.56-12.2)

16.1 (11.9-22.2) 10.0 (8.50-13.0)

31.7 (23.9-40.4) 20.0 (17.0-24.0)

55.5 (44.5-68.6) 35.0 (29.0-40.0)

72.1 (57.3-105) 50.0 (37.0-65.0)

744 1222

01-02 03-04 01-02 03-04

16.8 (12.0-23.5) 10.1 (8.43-12.1) 16.4 (13.4-20.1) 10.4 (8.41-12.7)

16.1 (11.0-24.8) 10.0 (7.90-14.0) 16.6 (12.0-21.5) 10.0 (8.40-13.0)

34.3 (22.4-48.7) 20.0 (17.0-25.0) 29.2 (24.0-36.5) 20.0 (16.0-23.9)

57.0 (39.9-76.4) 36.8 (29.0-49.0) 53.5 (38.4-68.9) 33.0 (26.0-40.0)

75.2 (54.5-156) 53.0 (36.8-69.0) 69.5 (53.3-104) 46.0 (35.0-65.0)

358 599 386 623

01-02 03-04 01-02 03-04 01-02 03-04

17.0 (10.5-27.6) 9.17 (7.45-11.3) 19.1 (12.9-28.1) 11.8 (9.54-14.6) 15.6 (12.0-20.2) 9.84 (8.09-12.0)

14.5 (10.0-32.7) 9.30 (7.60-11.0) 20.9 (9.28-37.4) 12.0 (8.90-15.0) 15.2 (11.2-20.5) 10.0 (8.10-13.0)

35.1 (18.6-57.6) 19.0 (15.0-24.0) 38.4 (27.7-46.0) 20.0 (15.0-30.0) 26.8 (20.4-39.5) 20.0 (16.0-23.0)

60.7 (41.5-100) 34.0 (24.0-44.4) 55.9 (45.5-69.8) 35.0 (28.0-59.0) 53.5 (35.3-72.1) 33.8 (27.0-40.0)

93.0 (49.7-243) 44.4 (30.0-59.0) 68.9 (51.9-74.0) 61.0 (34.0-100) 69.5 (53.5-105) 47.0 (35.0-67.0)

223 225 116 272 348 630

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 2.37 and 2.11. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds.

Fourth National Report on Human Exposure to Environmental Chemicals

25

Disinfection By-Products (Trihalomethanes)

References Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for chloroform update. 1997 [online]. Available at URL: http://www.atsdr.cdc.gov/toxprofiles/tp6.html. 4/26/09 Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for bromoform and chlorodibromomethane. 2005 [online]. Available at URL: http://www.atsdr.cdc.gov/ toxprofiles/tp130.html. 4/26/09 Ashley DL, Blount BC, Singer PC, Depaz E, Wilkes C, Gordon S, et al. Changes in blood trihalomethanes concentrations resulting from differences in water quality and water use activities. Arch Environ Occup Health 2005;60(1):7-15. Backer LC, Ashley DL, Bonin MA, Cardinali FL, Kieszak SM, Wooten JV. Household exposures to drinking water disinfection by-products: whole blood trihalomethane levels. J Expo Anal Environ Epidemiol 2000;10(4):321-326. Buckley TJ, Liddle J, Ashley DL, Paschal DC, Burse VW, Needham LL. Environmental and biomarker measurements in nine homes in the lower Rio Grande Valley: multimedia results for pesticides, metals, PAHs and VOCs. Environ Int 1997;23(5):705732. Churchill JE, Ashley DL, Kaye WE. Recent chemical exposures and blood volatile organic compound levels in a large populationbased sample. Arch Environ Health 2001;56(2):157-166. Dick D, Ng KM, Sauder DN, Chu I. In vitro and in vivo percutaneous absorption of 14C-chloroform in humans. Hum Exp Toxicol 1995;14: 260-265. Gordon SM, Brinkman MC, Ashley DL, Blount BC, Lyu C, Masters J, Singer PC. Changes in breath trihalomethane levels resulting from household water-use activities. Environ Health Perspect 2006;114(4):514-521. International Programme on Chemical Safety (IPCS). Environmental Health Criteria 216. Disinfectants and Disinfectant By-Products. 2000 [online]. Available at URL: http://www. inchem.org/documents/ehc/ehc/ehc216.htm.4/26/09 International Programme on Chemical Safety (IPCS). Concise International Chemical Assessment Document 58. Chloroform. 2004 [online]. Available at URL: http://www.inchem.org/ documents/cicads/cicads/cicad58.htm. 4/26/09 Krasner SW, McGuire MJ, Jacaugelo JG, Patania NL, Reagan KM, Aieta EM. The occurrence of disinfection by-products in US drinking water. J Am Water Works Assoc 1989;81:41–53. LaRegina J, Bozzelli JW, Harkov R, Gianti S. Volatility organic compounds at hazardous waste sites and a sanitary landfill in New

Jersey. An up-to-date review of the present situation. Environ Prog 1986;5:18-27. Leavens TL, Blount BC, De Marini DM, Madden MC, Valentine JL, Case MW, et al. Disposition of bromodichloromethane in humans following oral and dermal exposure. Toxicol Sci 2007;99(2):432-445. Lin YS, Egeghy PP, Rappaport SM. Relationships between levels of volatile organic compounds in air and blood from the general population. J Expo Sci Environ Epidemiol 2008;18(4):421-9. National Cancer Institute (NCI). Report on the carcinogenesis bioassay of chloroform (CAS No. 67-66-3). National Cancer Institute Carcinogenesis Technical Report Series March 1, 1976. [online]. Available at URL: http://ntp.niehs.nih.gov/ntp/htdocs/ LT_rpts/trChloroform.pdf. 4/26/09 National Toxicology Program (NTP). Carcinogenesis studies of bromodichloromethane (CAS No. 75-27-4) in F344/N rats and B6C31F mice (gavage studies). Technical Report Series No. 321. 1987 [online]. Available at URL: http://ntp.niehs.nih.gov/ntp/ htdocs/LT_rpts/tr321.pdf. 4/26/09

26

Fourth National Report on Human Exposure to Environmental Chemicals

Environmental Phenols

Benzophenone-3
CAS No. 131-57-7 General Information Benzophenone-3 (2-hydroxy-4-methoxybenzophenone) occurs naturally in some flowering plants. It is commercially synthesized as a sunscreen for use in lotions, conditioners, and cosmetics. It is also used as a UV stabilizer in plastic surface coatings and polymers. Benzophenone-3 is a common ingredient in sun-blocking agents. People may be exposed through dermal application of sunscreens and cosmetic products. Small amounts of benzophenone-3 can be absorbed through human skin and excreted in the urine, mostly as a glucuronidated conjugate (Gonzalez et al., 2006; Gustavsson et al., 2002; Janjua et al., 2004; Ye et al., 2005). After dermal application of a 4% lotion over the entire body daily for 5 days, one study found that 1.2-8.7% of the applied benzophenone-3 amount was recovered in the urine (Gonzalez et al., 2006). Human health effects from benzophenone-3 at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Following dermal application, some cases of photoallergy or allergy to benzophenone-3 have been reported. Male reproductive toxicity has been inconsistently reported in chronic high dose animal studies (Daston et al., 1993; French, 1992). Benzophenone-3 has weak estrogenic activity or weak anti-androgenic activity (French, 1992; Schlecht et al., 2004; Schlumpf et al., 2001; Schreurs et al., 2005). No human hormonal changes were observed during four days of application of 10% benzophenone-3 lotion (Janjua et al., 2004). Benzophenone-3 is not considered mutagenic (Robison et al., 1994). IARC and NTP have no ratings as to human carcinogenicity of benzophenone-3. Biomonitoring Information Urinary benzophenone-3 levels include both conjugated and unconjugated forms and reflect recent exposure to the chemical. The NHANES 2003-2004 levels of urinary benzophenone-3 have been described by Calafat et al. (2008). The analysis showed that female participants had slightly higher urinary levels than males and that nonHispanic whites were more likely than non-Hispanic blacks to have levels above the 95th percentile of the overall population. In a study of 90 U.S. females aged 6-8 years, the median urinary benzophenone-3 level of 14.7 µg/L was comparable to the median level of children 6-11 years of age (17.2 µg/L) in the NHANES 2003-2004 subsample (Calafat

et al., 2008; Wolff et al., 2007). Total benzophenone-3 urinary concentrations were detectable in 90% of a small sample of adults in whom the values ranged up to 3000 μg/L (Ye et al., 2005). Following short-term application of 10% benzophenone-3 lotion, men and women had mean urinary levels of 140 and 60 μg/L, respectively (Janjua et al., 2004). Finding a measurable amount of benzophenone-3 in urine does not mean that the levels of benzophenone-3 cause an adverse health effect. Biomonitoring studies on levels of benzophenone-3 provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of benzophenone-3 than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Fourth National Report on Human Exposure to Environmental Chemicals

27

Environmental Phenols

Urinary Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone)
Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 22.9 (18.1-28.9)

Selected percentiles
( 95% confidence interval)

Sample 95th 1040 (698-1390) size 2517

Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 03-04

50th 18.1 (15.5-23.2)

75th 94.0 (67.5-123)

90th 370 (225-570)

03-04 03-04 03-04

21.2 (16.4-27.3) 22.9 (18.0-29.3) 23.1 (18.0-29.6)

17.2 (14.9-25.9) 20.1 (16.1-25.1) 18.1 (14.7-23.3)

66.7 (38.7-102) 67.1 (45.2-93.8) 109 (72.1-140)

158 (106-246) 170 (137-240) 450 (315-733)

246 (154-618) 407 (183-717) 1220 (769-1750)

314 715 1488

03-04 03-04

16.8 (13.2-21.3) 30.7 (23.7-39.8)

13.7 (11.4-16.8) 26.0 (20.2-34.1)

55.3 (33.2-86.6) 137 (106-172)

178 (134-324) 596 (403-769)

567 (238-1350) 1340 (776-1790)

1229 1288

03-04 03-04 03-04

16.5 (10.9-25.1) 12.8 (9.38-17.4) 27.7 (20.3-37.8)

11.9 (8.50-18.3) 10.2 (7.40-14.4) 24.4 (16.8-32.0)

45.5 (25.9-78.2) 34.3 (22.8-50.6) 121 (83.6-162)

178 (76.4-412) 127 (90.8-176) 507 (316-769)

412 (178-2180) 247 (143-499) 1340 (733-2070)

613 652 1092

Limit of detection (LOD, see Data Analysis section) for Survey year 03-04 is 0.3.

Urinary Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) (creatinine corrected)
Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 22.2 (17.6-28.0)

Selected percentiles
( 95% confidence interval)

Sample 95th 1080 (686-1600) size 2514

Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 03-04

50th 16.2 (12.7-21.6)

75th 82.0 (58.7-108)

90th 415 (283-577)

03-04 03-04 03-04

25.8 (19.5-34.1) 17.2 (13.7-21.5) 22.8 (17.8-29.1)

22.4 (14.4-33.7) 12.9 (10.4-16.5) 16.2 (12.7-21.9)

84.6 (41.0-131) 43.6 (29.5-57.7) 93.2 (66.0-130)

171 (132-365) 136 (91.7-239) 491 (361-700)

427 (171-710) 350 (173-646) 1330 (880-1880)

314 713 1487

03-04 03-04

13.6 (10.8-17.1) 35.5 (27.1-46.4)

10.3 (8.36-12.9) 28.2 (20.2-37.0)

40.0 (24.9-62.5) 144 (101-224)

169 (93.3-316) 686 (491-1130)

381 (229-685) 1850 (1220-2580)

1228 1286

03-04 03-04 03-04

15.1 (9.44-24.0) 8.78 (6.49-11.9) 28.3 (20.6-38.8)

11.1 (6.95-16.0) 6.80 (5.27-9.00) 22.0 (14.6-32.7)

40.7 (18.3-85.8) 19.7 (13.5-33.4) 116 (73.5-175)

158 (87.4-362) 79.8 (46.8-139) 510 (380-760)

595 (118-1860) 185 (79.8-536) 1330 (852-2410)

612 651 1091

28

Fourth National Report on Human Exposure to Environmental Chemicals

Environmental Phenols

References Calafat AM, Wong LY, Ye X, Reidy JA, Needham LL. Concentrations of the sunscreen agent benzophenone-3 in residents of the United States: National Health and Nutrition Examination Survey 2003--2004. Environ Health Perspect 2008;116(7):893-897. Daston GP, Gettings SD, Carlton BD, Chudkowski M, Davis RA, Kraus AL, et al. Assessment of the reproductive toxic potential of dermally applied 2-hydroxy-4-methoxybenzophenone to male B6C3F1 mice. Fundam Appl Toxicol 1993;20(1):120-124. French JE. NTP technical report on the toxicity studies of 2-hydroxy-4-methoxybenzophenone (CAS No. 131-57-7) Adminstered topically and in dosed feed to F344/N Rats and B6C3F1 mice. National Institutes of Health Publication No. 923344, October 1992 (also Toxic Rep Ser. 1992 Oct;21:1-E14). Gonzalez H, Farbrot A, Larko O, Wennberg AM. Percutaneous absorption of the sunscreen benzophenone-3 after repeated whole-body applications, with and without ultraviolet irradiation. Br J Dermatol 2006;154(2):337-340. Gustavsson Gonzalez H, Farbrot A, Larko O. Percutaneous absorption of benzophenone-3, a common component of topical sunscreens. Clin Exp Dermatol 2002;27(8):691-694. Janjua NR, Mogensen B, Andersson AM, Petersen JH, Henriksen M, Skakkebaek NE, et al. Systemic absorption of the sunscreens benzophenone-3, octyl methoxycinnamate, and 3-(4-methylbenzylidene) camphor after whole-body topical application and reproductive hormone levels in humans. J Invest Dermatol 2004;123(1):57-61. Okereke CS, Barat SA, Abdel-Rahman MS. Safety evaluation of benzophenone-3 after dermal administration in rats. Toxicol Lett 1995;80(1-3):61-67. Robison SH, Odio MR, Thompson ED, Aardema MJ, Kraus AL. Assessment of the in vivo genotoxicity of 2-hydroxy 4-methoxybenzophenone. Environ Mol Mutagen 1994;23(4):312317. Schlecht C, Klammer H, Jarry H, Wuttke W. Effects of estradiol, benzophenone-2 and benzophenone-3 on the expression pattern of the estrogen receptors (ER) alpha and beta, the estrogen receptorrelated receptor 1 (ERR1) and the aryl hydrocarbon receptor (AhR) in adult ovariectomized rats. Toxicology 2004;205(12):123-130. Schlumpf M, Cotton B, Conscience M, Haller V, Steinmann B, Lichtensteiger W. In vitro and in vivo estrogenicity of UV screens. Environ Health Perspect 2001;109(3):239-244. Erratum in: Environ Health Perspect 2001;109(11):A517. Schreurs RH, Sonneveld E, Jansen JH, Seinen W, van der Burg B. Interaction of polycyclic musks and UV filters with the estrogen

receptor (ER), androgen receptor (AR), and progesterone receptor (PR) in reporter gene bioassays. Toxicol Sci 2005;83(2):264-272. Ye X, Kuklenyik Z, Needham LL, Calafat AM. Quantification of urinary conjugates of bisphenol A, 2,5-dichlorophenol, and 2-hydroxy-4-methoxybenzophenone in humans by online solid phase extraction-high performance liquid chromatographytandem mass spectrometry. Anal Bioanal Chem 2005;383(4):638644.

Fourth National Report on Human Exposure to Environmental Chemicals

29

Environmental Phenols

Bisphenol A

CAS No. 80-05-7 General Information Bisphenol A is a phenolic chemical which has been used for over 50 years in the manufacture of polycarbonate plastics and epoxy resins; in thermal paper production; and as a polymerization inhibitor in the formation of some polyvinyl chloride plastics. Polycarbonates are used to make products such as compact discs, automobile parts, baby bottles, plastic dinnerware, eyeglass lenses, toys, and impact-resistant safety equipment. Epoxy resins containing bisphenol A are used in protective linings of some canned food containers, wine vat linings, epoxy resin-based paints, floorings, and some dental composites. In recent years, about 5-6 billion pounds of bisphenol were produced annually worldwide. Bisphenol A may enter the environment from industrial sources or from product leaching, disposal, and use. In 1999-2000, bisphenol A was detected in 41.2% of 139 U.S. streams in 30 states (Kolpin et al., 2002). Bisphenol A can be biodegraded and does not bioaccumulate significantly in aquatic organisms. Some invertebrates may be sensitive and show reproductive effects (European Commission, 2003).

component of total exposure estimates (Wilson et al., 2007. In animal and human studies, bisphenol A is well absorbed orally. In humans, little free bisphenol A circulates after oral absorption due to the high degree of glucuronidation by the liver. The glucuronidated bisphenol A is excreted in the urine within 24 hours with no evidence of accumulation (Volkel et al., 2002).

Human health effects from bisphenol A at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Occupational exposure of epoxy workers to bisphenol A dust may produce eye irritation and skin sensitization. In animal studies, bisphenol A has low acute toxicity. It is not considered a teratogen (Kim et al., 2001). Bisphenol A is rated as weakly estrogenic (Matthews et al., 2001). Some reproductive or developmental changes are observed at high doses in standard experimental animal studies (e.g., delayed vaginal opening and preputial separation) (Ema et al., 2001; Tyl et al., 2002; NTPCERHR, 2008). Reproductive and neurodevelopmental effects of bisphenol A at low doses in animals, including environmental doses potentially relevant to humans, have been the subject of ongoing scientific reviews and study (European Commission, 2002; Gray et al., 2004; NTP, 2001; NTP-CERHR, 2007 and 2008; vom Saal and Hughes, 2005 Welshons et al., 2006; Witorsch, 2002). Examples General population exposure to bisphenol A may occur of recent animal studies which suggest possible low dose through ingestion of foods in contact with bisphenol A effects include altered development of the fetal prostate containing materials. For small children, hand-to-mouth and mammary gland, inhibition of postnatal testosterone and direct oral contact with materials containing bisphenol production, and changes in neurodevelopment (Akingbemi A are possible. Exposure from indoor air is a small et al., 2004; Leranth et al., 2008; NTP-CERHR, 2007;

Urinary Bisphenol A (2,2-bis[4-Hydroxyphenyl] propane)
Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 2.64 (2.38-2.94)

Selected percentiles
( 95% confidence interval)

Sample 95th 16.0 (14.4-17.2) size 2517

Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 03-04

50th 2.80 (2.50-3.10)

75th 5.50 (5.00-6.20)

90th 10.6 (9.40-12.0)

03-04 03-04 03-04

3.55 (2.95-4.29) 3.74 (3.31-4.22) 2.41 (2.15-2.72)

3.80 (2.70-5.00) 4.30 (3.60-4.60) 2.60 (2.30-2.80)

6.90 (6.00-8.30) 7.80 (6.50-9.00) 5.10 (4.50-5.70)

12.6 (9.50-15.1) 13.5 (11.8-15.2) 9.50 (8.10-11.3)

16.0 (11.5-23.3) 16.5 (15.2-20.9) 15.2 (12.4-18.1)

314 715 1488

03-04 03-04

2.92 (2.63-3.24) 2.41 (2.11-2.75)

3.20 (2.70-3.60) 2.50 (2.20-2.80)

6.10 (5.40-6.60) 5.00 (4.20-6.20)

10.4 (9.50-11.6) 10.6 (8.70-12.5)

16.0 (12.7-17.6) 15.9 (13.5-20.1)

1229 1288

03-04 03-04 03-04

2.58 (2.15-3.08) 4.24 (3.73-4.82) 2.51 (2.26-2.79)

2.60 (2.10-3.20) 4.30 (3.80-5.10) 2.70 (2.50-3.00)

5.20 (4.40-6.50) 8.20 (7.10-9.80) 5.20 (4.70-5.80)

9.90 (7.30-13.9) 14.2 (11.7-16.9) 9.60 (8.30-10.9)

15.4 (10.2-19.7) 20.6 (14.9-25.2) 15.1 (12.6-16.7)

613 652 1092

Limit of detection (LOD, see Data Analysis section) for Survey year 03-04 is 0.4.

30

Fourth National Report on Human Exposure to Environmental Chemicals

Environmental Phenols

Timms et al., 2005). Bisphenol A is not considered mutagenic and is unlikely to be a carcinogen, although it may form DNA adducts in vitro and inhibit mitotic spindle activity (Haighton et al., 2002). IARC and NTP do not have ratings for bisphenol A with respect to human carcinogenicity. The epoxy resin oligomer, bisphenol A diglycidyl ether, has limited evidence of animal carcinogenicity and is not classifiable as a human carcinogen by IARC. Biomonitoring Information Urinary levels of bisphenol A include both conjugated and unconjugated forms and reflect recent exposure to the chemical. In the participants of NHANES 20032004, prevalent exposure to bisphenol A in the U.S. population was demonstrated with children, females, and lower income strata having slightly higher urinary levels (Calafat et al., 2008). This study confirmed levels seen in an earlier smaller sample of 394 U.S. residents (Calafat et al., 2005). Several previous small studies in Japanese pregnant women, Japanese university students, and Korean residents have found mean urinary bisphenol A levels to be similar or up to several times higher than those in the U.S. representative NHANES 2003-2004 subsample (Fujimaki et al., 2004; Kim et al., 2003; Ouchi and Watanabe, 2002), although one study of 73 Koreans found levels that averaged seven times higher than median levels in the NHANES 2003-2004 subsample (Yang et al., 2003; Calafat et al., 2008). Applications of certain dental sealants were shown to increase urinary levels of bisphenol A for 24

hours (Joskow et al., 2006). Hanaoka et al. (2002) studied workers with exposure to bisphenol A diglycidyl ether and found mean urinary levels of bisphenol A about double that of unexposed workers. Finding a measurable amount of bisphenol A in the urine does not mean that the levels of bisphenol A cause an adverse health effect. Biomonitoring studies on levels of bisphenol A provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of bisphenol A than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Urinary Bisphenol A (2,2-bis[4-Hydroxyphenyl] propane) (creatinine corrected)
Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 2.58 (2.36-2.82)

Selected percentiles
( 95% confidence interval)

Sample 95th 11.2 (9.78-12.4) size 2514

Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 03-04

50th 2.50 (2.31-2.80)

75th 4.29 (3.88-4.75)

90th 7.67 (6.62-8.66)

03-04 03-04 03-04

4.32 (3.63-5.14) 2.80 (2.52-3.11) 2.39 (2.17-2.64)

4.29 (3.63-5.23) 2.74 (2.35-3.22) 2.36 (2.15-2.59)

7.14 (5.83-9.56) 4.74 (4.21-5.09) 3.93 (3.44-4.33)

12.2 (9.84-14.8) 7.79 (6.41-8.87) 6.64 (5.97-7.74)

15.7 (12.2-23.2) 11.8 (8.05-14.2) 10.0 (9.01-11.4)

314 713 1487

03-04 03-04

2.38 (2.15-2.63) 2.78 (2.50-3.08)

2.31 (2.08-2.70) 2.68 (2.40-2.94)

4.19 (3.81-4.64) 4.41 (3.81-5.15)

7.10 (6.41-8.28) 7.93 (6.48-10.2)

9.94 (9.06-11.7) 12.4 (9.29-18.2)

1228 1286

03-04 03-04 03-04

2.34 (2.02-2.71) 2.92 (2.58-3.32) 2.58 (2.37-2.81)

2.38 (2.00-2.65) 2.95 (2.51-3.27) 2.55 (2.32-2.80)

3.85 (3.24-4.55) 4.90 (4.07-6.13) 4.30 (3.93-4.67)

7.09 (5.00-9.04) 8.64 (7.53-9.63) 7.58 (6.32-8.87)

10.9 (8.50-14.3) 11.9 (10.2-13.3) 11.0 (9.34-12.4)

612 651 1091

Fourth National Report on Human Exposure to Environmental Chemicals

31

S. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Environ Health Perspect 2008. Gray GM. Ekong J. Kawamura N. and Hajszan.pdf . Kim CS. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Arakawa C. 2008.niehs. Needham LL. National Toxicology Program. Research Triangle Park. Haighton LA. Cha SW. Joint Research Centre Institute of Health and Consumer Protection.S. Richter CA. Reidy JA. Myers CB. Chem Res Toxicol 2001.780(2):365-370. Serizawa S. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.59(4):403-408. August 2001.pdf. bisphenol A glucuronide. Thomas BF. Hara K. Department of Health and Human Services. Ecotoxicity and the Environment (CSTEE). Human Health. T. September. with estrogen receptors alpha and beta. Furlong ET.145:592-603. Life Sci 2001. Keimowitz AR. streams. Koh WS.137(3):353-362. Environ Sci Technol 2002.36(6):1202-1211. Inhibition of testicular steroidogenesis by the xenoestrogen bisphenol A is associated with reduced pituitary luteinizing hormone secretion and decreased steroidogenic enzyme gene expression in rat Leydig cells. and other organic wastewater contaminants in U. vom Saal FS. Calafat AM. Caudill SP. Kuklenyik Z. Ikka T. Fujii S.Scientific Committee on Toxicity. 4. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). K. Bradley S. 2/4/09 Fujimaki K. Rat two-generation reproductive toxicity study of bisphenol A. In vitro and in vivo interactions of bisphenol A and its metabolite.149:988-994. Kim YH. Hlywka JJ. Lynch BS. Belgium.Environmental Phenols References Akingbemi BT.gov/chemicals/bisphenol/BPAFinalEPVF112607. Ye X. Kiguchi M. Pyo MY. Koulova AI. Italy. Ema M.gov/chemicals/bisphenol/bisphenol. Twomey K.pdf.116(1):39-44. Brine DR. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. niehs. May 22. Rhomberg et al. Han SS.113(4):391-395.14(2):149-157.69(22):2611-2625. Brussels. Tyl RW. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra..europa. 1999-2000: a national reconnaissance. Zaugg SD. Hum Ecol Risk Assess 2004. et al. Cunha G. Leranth. Watanabe C. N. J Chromatogr B Analyt Technol Biomed Life Sci 2002.nih. Ispra. 2007. Sottas CM. Available at URL: http://ntp.S. Doull J.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. J Am Dent Assoc 2006. Barton L.J. Barr JR. European Commission. Barr DB. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Endocrinology 2004.59(9):625-628. Marr MC. U. Hanaoka T. hormones.68(1):121-146. McConnell EE. Yoshinaga J. Pharmaceuticals. Needham LL. Endocrinology 2008. Calafat AM. 2/4/09 Ouchi K.102(19):7014-7019. C. Available at URL: http://cerhr. Regul Toxicol Pharmacol 2002. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). and Hardy MP. Furukawa M. Available at URL: http://ec. Munro IC. 2/4/09 European Commission. Reidy JA. National Institute of Environmental Health Sciences.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. 2003. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection.pdf . Proc Natl Acad Sci USA 2005. Wong LY. et al. Imai H. Howdeshell KL. National Institutes of Health. Calafat AM. Timms BG. Needham LL. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Available at URL: http://ecb. Watanabe S. NC.nih. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Kroes R. Tsugane S.10:875-921.nih. 2002. DirectorateGeneral Health and Consumer Protection.pdf. Kolpin DW. Occup Environ Med 2002.312(2):441-448.35(2 Pt 1):238-254. Meyer MT. Biochem Biophys Res Commun 2003. Available at URL: http://cerhr. et al. Hughes C.. An evaluation of the possible carcinogenicity of bisphenol A to humans. Exposure of the U. Reprod Toxicol 2001. MacLusky. Gender differences in the levels of bisphenol A metabolites in urine. 5: 505-523. Barber LB.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. November 26. Han SY.eu/ health/ph_risk/committees/sct/documents/out156_en. Kim JC. Bisphenol A. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Cohen JT. niehs. Shin HC. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Rubin C. Toxicol Sci 2002.jrc. Thurman EM. Chung MK. Zacharewski TR. Park S. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Klinefelter GR. Harazono A. Yang M. Nippon Eiseigaku Zasshi 2004. Joskow R. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Matthews JB. 32 Fourth National Report on Human Exposure to Environmental Chemicals .. Environ Health Perspect 2005. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Szigeti-Buck.

Fourth National Report on Human Exposure to Environmental Chemicals 33 . Yang M. Biological monitoring of bisphenol a in a Korean population. Kim SY. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration.Environmental Phenols Volkel W. bisphenol-A.44(4):546-51. Hughes C.40(7):905-12. Lee SM. Dekant W. et al. Large effects from small exposures. Jang JY.103(1):9-20. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Colnot T. Vom Saal FS. Environ Res 2007.147(6 Suppl):S56-69. vom Saal FS. Sheldon LS. Chang SS. An observational study of the potential exposures of preschool children to pentachlorophenol. III. Arch Environ Contam Toxicol 2003. Kawamoto T. Csanady GA. Chem Res Toxicol 2002. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Food Chem Toxicol 2002. Witorsch RJ. Welshons WV. Endocrinology 2006. Wilson NK. Filser JG. and nonylphenol at home and daycare. Morgan MK.15:12811287.113(8):926-33. Nagel SC. Chuang JC. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Environ Health Perspect 2005. Lordo RA.

600-1. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.g. 2000.300 (<LOD-. The alkylphenols can bioaccumulate in some fish.50) 1.600-1.20-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. 140-66-9 General Information 4-tert-Octyphenol. In the 1990s.900 (.80 (1.50) .299-. 2000.20-2.20) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th . Bian et al. In 1999-2000. see Data Analysis section) for Survey year 03-04 is 0. including 4-tert-octylphenol.2.00 (. Less frequently.30-2.20 (1.600-1. The alkylphenol ethoxylates enter the environment through human use of products containing them.600) 1.10) 2.80 (1.30 (1..20) 1.300 (<LOD-.50 (1.600) .80) 2.90) 2.507) * < LOD . over 500.389 (.600) .5% of 139 U.60-3. Saito et al.50-2. Indoor and to a lesser extent.30 (1.600-1.30) 2.369 (. Katsuda et al..40) 2. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. Survey Geometric mean (95% conf. Blake and Boockfor. the various alkylphenols have also been used as emulsifiers and modifiers in paints.20-2.268-. is used to manufacture alkylphenol ethoxylates.700-1.60-3. impaired steroidogenesis. industrial cleaners. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (. Several alkylphenols. and was quickly eliminated from the blood (Certa et al.500) .60-3. 1996).60) 1. and from contact with some personal care products and detergents. and some of their degradation products are toxic to aquatic life. which may vary for some chemicals by year and by individual sample. which are anionic surfactants used in detergents.600) ... and some personal care products.400 (. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.300 (<LOD-. testicular atrophy. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. to shorter chain alkylphenol ethoxylates.10) 1.40) 1.200-. 1995.S.20) 2.20-2.60) 613 652 1092 Limit of detection (LOD.40) 2.900 (.800-1.400) 1.20) 314 715 1488 03-04 03-04 * * .70 (1.900 (. During the 1980s and 1990s.70 (1. 2002).10 (.274-.50-3.. In rats.500) 75th . 2004).3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. have demonstrated estrogenic effects particularly when injected at high doses in animals. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.300-.. Ying et al. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).60-3. and through manufacturing waste streams (Warhurst.20-2..500) . did not bioaccumulate.40) * 03-04 03-04 03-04 .50) . an alkylphenol. and the polyethoxy chain may consist of up to 50 ethoxy units. Laws et al.1.00 (.300 (<LOD-. 4-octylphenol monoethoxylate was detected in 43.900 (.40) 1.20-2.00) 1229 1288 03-04 03-04 03-04 * .300 (<LOD-.500-1.500-1. 2002). 1997.500 (.477) . pesticides..Environmental Phenols 4-tert-Octylphenol CAS No. population from the National Health and Nutrition Examination Survey.200-.10-2.300-. 2003.30 (1.30) 90th 1. orally administered 4-tert-octylphenol was well absorbed.00 (1.40 (1.900 (. streams in 30 states (Kolpin et al.30) 1. through sewage. 34 Fourth National Report on Human Exposure to Environmental Chemicals .600-1. textiles.S. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. and to alkylphenoxycarboxylates.50) 1.60-3. < LOD means less than the limit of detection.90) 2..30 (. Disposition in humans has not been studied sufficiently. leading to inhalation as another potential exposure route (Rudel et al. fish) and drinking water. and emulsifiers. altered estrus cycles and reproductive outcomes.497) * .10 (.400 (.60) . and impaired spermatogenesis (e.50) 1.60-3. Urinary 4-tert-Octylphenol (4-[1.30 (1.80 (1.10 (1.3. 2006.500) .600-1.g.000 tons of alkylphenol ethoxylates were produced annually worldwide.357 (.70 (1.. altered neonatal sexual development.70 (1.

470) 75th .03 (1..199-.530) . nonylphenol.269 (. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.640-1. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U..64 (. It is unclear if estrogenic or other effects occur in animals through oral dosing.. or their corresponding ethoxylates with respect to human carcinogenicity.67-2. 2005.260 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.740 (.460 (.06 (2.910 (.630-1. 2004).550-1.54) * 03-04 03-04 03-04 .270-.73) 2.00) 1.10-2.Environmental Phenols Myllymaki et al.41) .00 (.270 (.3.470-1. 2004.540-1.00) 2.11) 1.17 (.770 (. representative subsample of NHANES 2003-2004. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.02-4.349) * < LOD .00) 2.160-.270 (.08) 1.78) 1228 1286 03-04 03-04 03-04 * . Fourth National Report on Human Exposure to Environmental Chemicals 35 .276 (.560) .890-2.450) 1.05-2.S.320 (<LOD-..50 (2.620-1.850 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.15) 1.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.280-.620) .450) . Biomonitoring studies on levels of 4-tert-octylphenol provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 4-tert-octylphenol than are found in the general population.40 (1. Kawaguchi et al.. Urinary 4-tert-Octylphenol (4-[1. IARC and NTP have not rated octylphenol.170-. Calafat et al.570) .410 (.76 (2.470-1.36-3.85 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.59) 1. Survey Geometric mean (95% conf.62 (1.78) 3.62) .68-2.. In a small number of adult Japanese volunteers.71) 2.25-2.22) . 4-tert-Octylphenol is not considered directly genotoxic.610) .435 (.31 (1.53-3.00 (.68) 2.384) * .3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.03-6.40-4.400) .18-4.43) 1.25) 90th 1.420) .S.43) 1.370 (<LOD-.59 (1. Nagao et al. population from the National Health and Nutrition Examination Survey.740 (.78 (1.03 (1. Yoshida et al.60 (1.29) 2.1.730-1.33) 3. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect.300 (<LOD-.11) 2. Tyl et al.20 (1.207-.96-4.500-1. 2001.380 (<LOD-.65-3. Sweeney et al.31-2.11-2.62 (1. 2003. at lower or environmentally relevant doses (Blake et al. 1999).00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .33 (2.25) 2.43-3. 2000.337-.81 (1.860 (. 2001).14) 314 713 1487 03-04 03-04 * * .

Two-generation reproduction study with para-tert-octylphenol in rats. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. McCoy GL. Nakagomi M. Maekawa A. Muller AM. Makino T. Ito R.141(7):2667-2673. 2/4/09 Ying GG. alkylphenols. Izumi S. Haavisto TE. Nicol L. Wiegand HJ. et al. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats.pdf. Toppari J. polybrominated diphenyl ethers. et al. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Usumi K. Myers CB. prolactin. Xu L. Zaugg SD. Kookana R. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Kawaguchi M. Stir bar sorptive extraction and thermal desorption-gas chromatography-mass spectrometry for the measurement of 4-nonylphenol and 4-tert-octylphenol in human biological samples. Brooks AN. Nair-Menon JU. Williams B. Yoshida M. Katsuda S. Laws SC. Inoue K. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Paranko J. Roche JF. Millette CF. Reprod Toxicol 2001. pesticides. Environ Health Perspect 2008. Sakui N.14(5):325-332. Taya K. Needham LL. Horie M. et al. Certa H.57(2):255-266. Kawaguchi M. Carey SA. Cooper RL. Blake CA. Yoshimura Y. Environ Sci Technol 2002. Korn LR. Barber LB. Watanabe G. Nagao T. Qian J.Environmental Phenols References Bian Q. Taya K. Reprod Toxicol 2004.S. Reidy JA. Inoue K. and other organic wastewater contaminants in U. Toxicol Sci 2000. Meyer MT. Tyl RW. bisphenol A and methoxychlor in rats. Indoor air pollution by alkylphenols in Tokyo.799(1):119-125. Toxicol Appl Pharmacol 2000.165(3):217-226. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Wong LY. Pharmaceuticals. Katsuda S. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Saito I. Calafat AM. and testosterone. Thurman EM. nonylphenol. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Bodman GJ. Estrogenic activity of octylphenol. Ye X.28(3):215-226. Marr MC.uk/resource/reports/ethoxylates_alkylphenols. 2003. Song L.71(1-2):112-122. Boockfor FR. Raychoudhury SS. Environ Int 2002.S. 1999-2000: a national reconnaissance. 1995. Takenaka A.15(6):683-692. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Available at URL: http:// www. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Regul Toxicol Pharmacol 1999.54(1):154-167. Yoshimura S.207(1):59-68. Food Chem Toxicol 2006. Bolt HM. Takai N. Boockfor FR. hormones. Yoshida M. Wang X. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.co. Chen J. An environmental assessment of alkylphenol ethoxylates and alkylphenols. et al. Myllymaki SA. Anal Chim Acta 486:41-50.44(8):1355-1361. Seto H. Saito Y.121(1):21-33. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Biol Reprod 1997. Spengler JD. Blake CA. Fedtke N. Sweeney T. Warhurst AM. testis size. Camann DE.37(20):4543-53. Ferrell JM. Seely JC. Karjalainen M. Rudel RA.folliclestimulating hormone. Phthalates. Brine DR.foe.36(6):1202-1211. Ono H. Fail PA. Environ Sci Technol 2003. and sertoli cell number. Brody JG. Maekawa A. Arch Toxicol 1996. Endocrinology 2000.18(1):43-51. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. streams. Onuki A. Toxicol Appl Pharmacol 2005. Watanabe G. Exposure of the U. Furlong ET.116(1):39-44. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Okada F.30(2 Pt 1):81-95. and other endocrine-disrupting compounds in indoor air and dust. Kolpin DW. Toxicol Lett 2001. Indoor Air 2004.

the median urinary triclosan level of 7.. IARC and NTP do not have ratings with respect to human carcinogenicity. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. In the body it is conjugated to glucuronides and sulfates (Bodey et al. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al.. 1996. In animal and human studies. 1988. 2004).. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent. deodorants. Triclosan is not considered teratogenic at maternally toxic doses. Moss et al. In a U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In a study of 90 U.S. Some reports show endocrine effects are observed in amphibians and fish (Foran et al. a process that can result in the formation of small amounts of 2. Triclosan has a low bioaccumulation potential in fish. toothpastes. 2007. 2005. (Sandborgh-Englund et al... streams sampled in 30 states (Kolpin et al. 2007). 2007. mouthwashes. Mezcua et al. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. but not by race/ethnicity and sex.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. 2000). Triclosan can be absorbed across skin into the blood stream. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. In animal studies. Biomonitoring studies on levels of triclosan provide physicians and public health officials with a reference values so that they can determine whether people have been exposed to higher levels of triclosan than are found in the general population. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2000. Biomonitoring Information Urinary triclosan levels reflect recent exposure. 2008 has shown higher levels during the third decade of life and among people with the highest household income. toys. young girls. Matsumura et al. and medical devices.S. Triclosan enters the aquatic environment mainly through residential wastewaters. It can be photochemically and biologically degraded.S.8-dichlorodibenzo-p-dioxin (Aranami et al. Veldhoen et al. Fourth National Report on Human Exposure to Environmental Chemicals 37 . Triclosan has been added to soaps.. 2002).. and has also been impregnated into some kitchen utensils.. Calafat et al. 2007). it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. triclosan was found in 57.. It acts by inhibiting bacterial fatty acid synthesis. 1987). acne medications.. Triclosan formulations may rarely cause skin irritation..Environmental Phenols Triclosan CAS No. 2006). and wound disinfection solutions. it has low acute toxicity. 1969).. 1976. General population exposure results from dermal and oral use of products containing triclosan. 2008). representative subsample of NHANES 2003-2004..2 µg/L was comparable to the median level (8..6% of 139 U. In 1999-2000.. Lyman and Furia. Calafat et al.

4 (38.74 (5.3 (26.32-14.20-10.8) 116 (39.48-10.16 (6.93 (7. Survey Geometric mean (95% conf.4-19.8-112) 30.0-19.0-15.2 (11.2) 12.4) 357 (225-456) 203 (87.40-17.1) 9.6-15.7 (9.30-14.20-11.4.4) 7.1) 9.2 (10.43-13.4) 51.4 (11.00 (4.9-61.4) 73. Urinary Triclosan (2.00-8.22-10.3 (11.6-14.6) 31.2 (25.1 (15.8-60.9) 7.S.80 (5.0) 65.45-10.6 (9.60 (8.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.7) 123 (36.2-58.4.3.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.40-11.6) 10.4 (12.45 (5.1) 9.10) 84.94 (7.0-15.4) 90th 249 (188-304) 03-04 03-04 03-04 8.2-46. interval) 13.5) 20.4 (32.20 (7.86-12.1) 11.0 (36.S.48 (8.3-35.2 (37.0) 9.6 (10.1) 13.7) 10.5-14.9 (50.6) 90th 212 (172-241) 03-04 03-04 03-04 9.7 (14.6-111) 33. population from the National Health and Nutrition Examination Survey.20-13.0 (34.0 (8.21 (6.3) 10.9 (33.60 (6.2-58.7 (11.89-11.2) 13.3) 47.6 (12.0 (11.1) 14.0-73. interval) 12.1) 50.90-10.1) 7.9-236) 193 (90.9 (8.6-37.3 (9.1) Selected percentiles ( 95% confidence interval) Sample 95th 368 (294-463) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.2) 9.4-18.9) 75th 47.9) 8.4) 25.1 (45.5) 11.70-16.7 (28.8-85. Survey Geometric mean (95% conf.3 (8.8-63.7) 292 (151-432) 132 (78.6-20.0-213) 213 (160-272) 453 (263-1150) 260 (127-513) 358 (276-480) 612 651 1091 38 Fourth National Report on Human Exposure to Environmental Chemicals .5) 66.54 (8. see Data Analysis section) for Survey year 03-04 is 2.7 (39.3-15.6-14.2-14.50) 10.20 (7.4) 317 (231-433) 144 (96.2 (13.9) 32.18 (5.3-67.8 (21.82 (8.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.0 (26.3-31.92-12.45-13.8) 14.6-65.1) 9.6) 12.8) 7.5-86.3) 6.4) 75th 43.6 (30.38-18.72-13.6) 39.29-12.5 (11.5) 13.9 (11.55 (4. population from the National Health and Nutrition Examination Survey.1-39.1 (8.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.Environmental Phenols Urinary Triclosan (2.50-10.10-9.11-11.8) 9.8-127) 37.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 49.2 (27.

4. Teitelbaum SL. et al. Hong HC. Hernando MD. The oral retention and antiplaque efficacy of triclosan in human volunteers. Kanetoshi A. Windham G. Nagao Y. Hirano M. Mezcua M. Wong LY. Environ Health Perspect 2007. hormones. Pinney SM. Larson EL. Arch Environ Contam Toxicol 1988. Levy SB. Meyer MT. Fernandez-Alba AR. and other organic wastewater contaminants in U.36(6):1202-1211. Moss T.69(20):1861-1873. Evidence of 2. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Environ Sci Technol 2002. Furia T. Reidy JA. Williams PE. Thurman EM. Bennett ER.66:1052-1056. Aquat Toxicol 2006.23(5):579-583. Kolpin DW. Veldhoen N. Pharmacokinetics of triclosan following oral ingestion in humans.524:241-247. et al. Food Chem Toxicol 2000. Wolff MS. Urinary concentrations of triclosan in the U. Anal Chim Acta 1004. Photolytic degradation of triclosan in freshwater and seawater. Bhargava HN. Ferrer I. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Chelimo C. Ishibashi H. Br J Clin Pharmacol 1987.83(1):84.38(4):361370. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Erratum in: Aquat Toxicol 2007. J Toxicol Environ Health A 2006. Pilot study of urinary biomarkers of phytoestrogens.7/2. Wigmore H. Calafat AM. Bodey GP. Ebersole R.4’-trichloro-2’hydroxydiphenyl ether)..24(3):209-218.4. Skirrow RC.S. Watanabe N. Britton JA. Ye X.67(4):532-537.80(3):217-227. Chemosphere 2007. phthalates. Sandborgh-Englund G. Benson WH. Kaneshima H. Okui T. Am J Infect Control 1996. Barber LB. Katsura E.38(2):64-71.115:116-121. Readman JW.28(9):1748-1751. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Percutaneous penetration and dermal metabolism of triclosan (2. streams. Mar Environ Res 2000. Fourth National Report on Human Exposure to Environmental Chemicals 39 . and phenols in girls. Howes D.45 Suppl 2:S137-S147. Needham LL. 4’-trichloro-2’-hydroxydiphenyl ether. Adolfsson-Erici M. Aranami K. Zaugg SD.S. Osachoff H. Gomez MJ. Pharmaceuticals. J Invest Dermatol 1976. Lyman FL. Leonard PA. Toxicology of 2.116(3):303-307. et al.50(1-5):153-156.17(5):637-644. Aguera A. Ogawa H. Environ Health Perspect 2008. Furlong ET.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Foran CM. et al. Biol Pharm Bull 2005. Triclosan: applications and safety. population: 2003-2004. Matsumura N.Environmental Phenols References Aiello AE. Clapson DJ. Gilbert RJ. Shiratsuchi H. Gunderson MP. IMS Ind Med Surg 1969. Ekstrand J. Odham G. Williams FM. 1999-2000: a national reconnaissance.

65 (.480-2.530) 1. After a single dose.350-.960) 1.650) 1. PCP cannot be used on wood in residential or agricultural buildings.350 (.390 (.350-.90) 1. has been restricted.75) 2.350) < LOD .860-2.08-3.350-.890 (.350-. PCP use in the U.58-2.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. ingestion of contaminated food or water.47-3.350-1. Human exposure to PCP has become less common.00 (.350) < LOD . 1986).350) < LOD .33-2.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . PCP is absorbed rapidly and well by all exposure routes.350 (.10) 1.390 (.94 (1.04) 1.83 (2.73 (1.350-. bactericide. Acute. Since 1984.350 (. along with small amounts of tetrachlorohydroquinone and conjugates.30) 1.94 (1.42) 696 680 521 696 603 951 Limit of detection (LOD. so it is relatively non-persistent. water and sediments because of the large amounts that were produced and used historically.350-.350-1.660 (.510-3.350) < LOD < LOD 75th . < LOD means less than the limit of detection.350 (.01 (<LOD-1..350-1.10 (.30 (.850-2. Survey Geometric mean (95% conf. and metabolic acidosis were observed in CAS No. 1976.350 (. other polychlorinated benzenes.350) < LOD . 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.350) < LOD .30 (.5.91 (1.350 (. After absorption. population from the National Health and Nutrition Examination Survey.350 (. 2002.70) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50) 1.90) 2.350 (.350-.350 (.350 (..980 (.350) 90th . plants. 40 Fourth National Report on Human Exposure to Environmental Chemicals . To-Figueras et al.350-.350-.990 (<LOD-2.350-.30) .60) 1. Effects including hyperthermia. PCP has been detected in soils.350 (.10 (1. PCP is distributed to most tissues and is not extensively metabolized.60) 1.09) .98 (1.890-1.10) 1.48-2.67) 1.350 (.500-2. Kohli et al.33) .350-.350) < LOD . are eliminated in the urine. In the environment.18 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.350 (.80) .350-2.350-2.32 (.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350) < LOD .S.00) 1. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.510-5.37 (.53) size 1994 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .350-.350-1.30) 1.37) . Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350-2.680-1.350-. the elimination half-life may be a week or more (Uhl et al.00) 2.350 (.350-2.770 (. 1979).25 and 0.64) 1. and possibly of lindane (IPCS.62 (.350-2.76) .350-.40 (.350) < LOD .350-.350 (. 1997). and dermal contact with PCP-treated products.350) . The parent compound and conjugates. PCP is degraded by sunlight and metabolized rapidly by microorganisms.76) 1. PCP is eliminated over a few days (Braun et al.70) 2. utility poles and fence posts). which may vary for some chemicals by year and by individual sample.30 (1.350-.10 (<LOD-1.650 (.90 (1.350-.630 (.78) 1.45-2. herbicide. General population exposure to PCP may occur by inhalation of contaminated air.47-5. with repeated or chronic exposure.23 (.350) < LOD ..350-.350) < LOD .350 (. and animals.350-. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.48 (.350 (.350-.. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350) < LOD .65 (.S. mollusicide.350 (.350) < LOD .54-2.590-1.350-.350) < LOD . air. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.g.350 (.350 (.58-2.350) < LOD .53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .. and it is used primarily as a preservative for wood to be used outdoors (e.51) 1.00) 1.350) < LOD . hypertension.350-. algaecide and insecticide.350) < LOD .350 (.990-2.

650 (.500-1.25 (1.35) 1.67-2.atsdr...0 mg/L.19) 2.500 (. 2003).780) < LOD .00) 1.75) 1.95) 3.25-2. In NHANES 2001-2002 subsamples.650) 90th 1.380-.570 (.25-1. inhalation..500-. carcinogenic.40) 1.52) 1.78) 1. population from the National Health and Nutrition Examination Survey.430-.430) < LOD .400 (.13 (. chronically administered high doses of PCP were hepatotoxic. respectively) (Becker et al.09-1.470 (.S.6 and 14.290) < LOD .40) 1.21 (.320) < LOD . Death can result from seizures and cardiovascular collapse.950-1. 1989).73 (1.19 (1. In a small sample of U.560) < LOD .90) 1.40) 1.11) 2.94-3. EPA has developed standards for PCP in drinking water and the environment. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.560) < LOD .06 (.25-2.S.82 (1.52 (<LOD-1.34 (.57 (1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.950-1.09 (<LOD-2.84 (1.800-1.48-2.320 (.340-.270-.560-.30) 1.40) 1. van Raaij et al. More information about external exposure (i.40-2.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . In animals.09) size 1994 2527 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .82) 1. Survey Geometric mean (95% conf. the 95th percentile of urinary PCP levels was about fiftyfold higher than that for 6-11 year olds in NHANES 2001-2002 (Hill et al. EPA at: http://www.220-. and the FDA has established a standard for bottled water.950-1.16-1..30-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.510-.html.280) < LOD .610 (.320) < LOD .75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .30 (.370 (.220-.10 (1.67 (1.21-2.18 (1..440 (.51) 1.40) 1.56) 1.. Urinary Pentachlorophenol (creatinine corrected) Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.730) < LOD .360 (.79) 1.92) 1.25) 1.19) 2.420) < LOD .360-.29-3.gov/ pesticides/ and from ATSDR at: http://www. Biomonitoring Information In NHANES 1999-2000 the median urinary PCP levels among children aged 6-11 and 12-19 years were as much as thirteen times lower compared to a sample of German children aged 6-14 years in 1990-1992 (4.300 (.06) 1.760 (.320) < LOD < LOD 75th .250 (.67-3.Fungicides adults and children severely exposed to PCP through ingestion.35-2.00-1. 2003). OSHA has established an occupational standard.850 (.910-1.26 (1.310) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 41 .S.920 (. Urinary PCP levels at the 95th percentile in this Report are approximately half the corresponding 95th percentile values found in German adults evaluated in 1998 (Becker et al.36) . or skin absorption.700-2.94 (1. children in the 1980’s..78) 1.650 (.250 (.510-.EPA.35) 1.990 (. environmental levels) and health effects is available from the U.08 and 5.240-.780-1.330-. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.580-.350) < LOD .94 (1. Among adults in the NHANES 1999-2000 subsample.epa.18) . 1995).10-2.55) 1.30) 1.16 (.290-.300 (. 1991).19) 2.630 (.270-.e.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2004.57 (.26 (1.cdc.300 (.9 mg/L.67 (1.69 (1.52 (1.310-. The U.830) < LOD .800) < LOD 1. respectively) (Seifert et al.06-3.590-1. Pentachlorophenol is not mutagenic or teratogenic. 2000).25 (1.84-4.52 (<LOD-1.490) < LOD .290-.710-1..83 (1.gov/ toxpro2.900-1.67-3.67 (1. and adversely affected thyroid function (U.75 (<LOD-2.00-1. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.84) 1.67 (1.S. 1989). Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.260 (.S.35-2.590) < LOD .67 (1.

International Programme on Chemical Safety (IPCS). Notten WR. Krause C. Arch Toxicol 1986. Can J Biochem 1976. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.4:289296. Chenoweth MB.105(1):78-83. PCP: Human Risk Characterization [online]. Gregg M. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Bragt PC. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. r e g u l a t i o n s . Lindane.inchem. house dust. Dev Toxicol Environ Sci 1979. Seiwert M. Blau GE. Hill RH Jr. Needham LL. Kaus S. et al. Cline RE. Pharmacokinetics of pentachlorophenol in man. EPA). Available at URL: h t t p : / / w w w. Environmental Protection Agency (U. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Shealy DB.10:552-65. 206:15-24. Schulz C. Baker S. Schulz C. Arch Environ Contam Toxicol 1989. Jones D.18:475-481. htm. Holler JS. et al. 2002. Seifert B. Santiago-Silva M. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Hill RH. Engel R. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. U.54(3):203-208. Environ Res 1995. Needham LL. J Expo Anal Environ Epidemiol 2000. 4/21/09 Kohli J. The metabolism of higher chlorinated benzene isomers. Toxicology 1991: 67(1):107-16. urine.71:99108. 4/21/09 van Raaij JA. Pesticide residues in urine of adults living in the United States: reference range concentrations. et al. To T. Arch Environ Contam Toxicol 1989. Barrot C. Braun WH. Helm D.18(4):469-474. Otero R. available at URL: http://www. References Becker K. Fast DM.org/documents/jmpr/jmpmono/2002pr08. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Seiwert M. Rodamilans M. Head SL. Uhl S. 42 Fourth National Report on Human Exposure to Environmental Chemicals . drinking water and indoor air. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Bailey SL. Biomonitoring studies on levels of PCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of PCP than are found in the general population. van den Berg KJ. Becker K. Seifert B.S. Hill RH Jr. Schmid P.58:182-186.S. Schlatter C. Sala M. Smith SJ.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Environ Health Perspect 1997. 11/30/2004. To-Figueras J. Phillips DL. hair. g o v / f d m s p u b l i c / c o m p o n e n t / main?main=DocketDetail&d=EPA-HQ-OPP-2004-0402. Safe A. Int J Hyg Environ Health 2003.

90) . 2006). Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.88) 1. on ornamental plants and turfs.600) < LOD 75th .570 (.07 (. OPP is considered to be moderately toxic after acute oral doses in animal studies.509 (.10) 2.90 (1. inhalational.S.60 (1.76) 1.90) 1.40-5. which may vary for some chemicals by year and by individual sample.860 (. Fourth National Report on Human Exposure to Environmental Chemicals 43 . and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.34) 1. Cnubben et al.3.470 (<LOD-.20 (. sodium ortho-phenylphenate (SOPP).10) .30) 1. In the past.552 (.690-1.00 (1.50-2.10 (1. SOPP is applied topically to the crop and then rinsed off.638) * .570-2.50-3. fungicides.60-3. 2006). population from the National Health and Nutrition Examination Survey.60 (1.33 (.890 (.508 (.92 (.20) 2.30) < LOD .386-.90) 2.28 (.540-2.770 (.636) * .349-.10) 1.S.90 (1.350-1. leaving the chemical residue OPP.760-2.567 (.770 (.20) < LOD 2.EPA.10 (1. and as a wood preservative.590-2. or 2-phenylphenol) and its water-soluble salt.61) 2.389-.22 (.800-3. General population exposure can occur via dermal.645) * . 2002.00) .20) < LOD 1.498 (. but OPP and SOPP are still used on pears and citrus (U.490 (<LOD-. EPA.60-2.20-2.670) 2.30-2.10-2. in paints. 2006).390-.750-2.621) * .860) * 99-00 01-02 99-00 01-02 99-00 01-02 . it was used in home sanitizers for surfaces.90) .85) 2.610-1.830 (. and it has limited water solubility.570-. Both have been used in agriculture to control fungal and bacterial growth on stored crops. such as fruits and vegetables. Workers who manufacture.490 (<LOD-. < LOD means less than the limit of detection.00-2.690) < LOD .91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .560-8.00) .00 (1.840-1.00 (1.490 (<LOD-.550-1.450 (<LOD-. Available evidence suggests that OPP does not accumulate in the body.630) < LOD .890) 1.40-2..09) 2.00 (1.10) .480-1.490 (<LOD-.02) 1. Timchalk et al.570-1.497 (.3 and 0.50) < LOD .970 (. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.493 (.50 (1.85) size 1991 2529 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .80 (2.450 (<LOD-.696) * .402-.14 (<LOD-3. formulate.80-3. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.30) < LOD 1.600) < LOD .624) * .364-. or apply these chemicals may be more highly exposed than the general population. 1998.17 (.600-1.50) < LOD .23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .890 (.50) 1.40-7.. are antimicrobial agents used as bacteriostats.389-. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.27 (.50) .28-3.930 (. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.836) * . Chronic dosing in animals resulted in such systemic effects as weight loss and Urinary ortho-Phenylphenol Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 1998).60 (1.600) < LOD .20 (1.710-2. 90-43-7 General Information Ortho-phenylphenol (OPP.490 (<LOD-.00) < LOD .500-2.EPA.496 (.640) < LOD .370-.. Estimated human intakes have been below recommended intake limits (U.742) * . however.466 (.30) < LOD 90th 1.410-.10) .80) 1.10-1.850 (.10) 1. and sanitizers. OPP is volatile.580-1.740 (.600-1.820 (.370-.780) < LOD .50-4.600) < LOD 1.23) 695 680 520 695 603 953 Limit of detection (LOD.20-3.790) 2.40 (.880-2. 1989).19 (.570 (.80) 1.S. 2006). interval) . OPP is still used as a disinfectant fungicide for industrial applications.520 (.50) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (1.50 (1.S.433-.50 (1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.420 (<LOD-.30-7.450 (<LOD-.370-.610 (. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.600-1.40-5.03) 1.Fungicides ortho-Phenylphenol CAS No.710) 3. Both chemicals degrade within hours to weeks in the environment (U.22) 2. Most agricultural food applications have been revoked.950) < LOD . whereas SOPP is not volatile and is more water soluble.30 (1.

610) < LOD 1. Brusick.96 (1.46) < LOD 1.480-.11-1.473) * .06 (1. but no neurologic.980 (. 1999.810-1.11 (. 2005.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .403-.epa.86 (1. or.500) < LOD .08-2..470) < LOD .640-1. IARC has classified SOPP as a possible human carcinogen.. Detectable levels were seen in over half the U.07) 2.970) 1.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. CDC.508) * ..43 (1.343 (. 1984.21 (.53) 1.44 (1.40-13.33) size 1991 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .690 (.620-1.444 (.385 (.06-5.750 (.656) * . Survey Geometric mean (95% conf.32) 3.08-1.64 (2. Volunteers exposed to 0.910 (<LOD-1..43-2.33) . 2002.33-2.29) 1.11) < LOD 90th 1. 1986). OPP was not found to be mutagenic.291-.32) 1.75 (1.590) * .06-4.74 (1.514 (.980 (<LOD-1.361-.S. or developmental toxicity was observed (Bomhard et al.81) 1.61 (2.75 (1.28 (2.78 (2.89 (1.382 (.800-1. U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.25-6.24-2.910-1.00 (.320 (<LOD-.05-2.58) 2.270-. 1984.Fungicides anemia.420 (<LOD-.96 (1.560-2.93) . population from the National Health and Nutrition Examination Survey.750 (.248-.S.420 (<LOD-.62) .780-14. Kwok et al. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.EPA at: http:// www.550-. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect. Pathak and Roy.02 (. leading to production of two metabolites. 2005).47) .18) 2.EPA 2006).30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 . Biomonitoring studies on levels of OPP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of OPP than are found in the general population.311-.510 (<LOD-. Biomonitoring Information Urinary OPP levels reflect recent exposure.69 (1.13) 1.gov/pesticides/.38-3. U. 1998. 2005). 2002.510-.4) 3.570) < LOD 1.01) 1. 1997. by possible genotoxic mechanisms (Hagiwara et al. Smith et al.650-1.990) < LOD .410 (<LOD-.28 (<LOD-4.11 (.61 (.21-2.S. 2002).840 (.61 (1.580) < LOD .17 (.460-. In high dose animal studies.4 mg dermally had urinary levels of OPP that were several hundred times higher than median levels found in NHANES 1999-2000 and 2001-2002 (Bartels et al.770-2.09-3.08) 1.670 (. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.620-1.17 (.580-1.27) < LOD .12) < LOD 1. reproductive.96-4.91 (1.04-4.791) * . Nakagawa et al. 44 Fourth National Report on Human Exposure to Environmental Chemicals ..560) < LOD 75th .453 (.550) < LOD .84 (1.329-. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Zhao et al. Murata et al. and it has classified OPP as not classifiable with respect to human carcinogenicity.484) * .93) 1.810) < LOD .20) < LOD 3.860 (.600-1.09-6.12-2...11) 4.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.880-1.440 (. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.470 (<LOD-. Bomhard et al.43-2. 1999. Ito et al..940-2.550 (.780 (.750-2.51-3. 1993.38) 1.00 (1.380 (.93 (1. 1992.S.900) < LOD .860 (.670 (.97 (2.17) * 99-00 01-02 99-00 01-02 99-00 01-02 . Additional information is available from U.09 (1.26) 1.43) 3.59) .96) 1.59) 1.31) < LOD .900-1.52 (. less likely.0) 1.360 (<LOD-.496 (.910 (. interval) .S.21) 1.24-2.666) * .29) 1.455-. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.88-4.93) .410 (<LOD-.950) < LOD . 2000.670) < LOD .91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.EPA 2006).353-..568) * .301-.38) 2.17) 2.

Available at URL: http://www. Drugs. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Timchalk C. U. van de Sandt JJ. Hum Exp Toxicol 1998. J Agric Food Chem 2002. Cano M. Eastmond DA. Mendrala AL. Murata M. Richter M.20(5):851-857. Brendler-Schwaab SY. Available at URL: http://ntp. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Mutat Res 1993.(56):399-407. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Bartels MJ.43(7):14311437. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Leser KH. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Elliott GR. 1989. EPA).gov/oppsrrd1/REDs/ phenylphenol_red. Christenson WR. 4/9/09.Fungicides References Appel KE. Coelhan M. Stanley JS. 2006.EPA).54(16):5731-5735. The carcinogenicity of the biocide ortho-phenylphenol. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Toxicol Appl Pharmacol 1998. Xenobiotica 1998. Buchholz BA. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Crit Rev Toxicol 2002.703(12):97-104. Hagiwara A. Bartels MJ. McNett DA.286(2):309-319.32(6):551-625. Narang A. Smith RA. Hakkert BC. Office of Toxic Substances. July 28. et al. Nakagawa Y. Zhao S.28(6):579594. Turteltaub KW. Inoue S. Glas K. EPA-560/5-89-003. Ito N. U. Christenson WR. Environmental Protection Agency (U. Toxicol Appl Pharmacol 1999. Food Chem Toxicol 1984. National Toxicology Program (NTP). Environ Mol Mutagen 2005. Gierthy J. Shirai T.17(8):411-417. rat and man.22(10):809-814. Shibata M. J Agric Food Chem 2006.pdf. Centers for Disease Control and Prevention (CDC). Cnubben NH.nih.gov/ntp/htdocs/LT_ rpts/tr301. Carcinogenesis 1999. Moriya K.50(11):3351-3358. Arnold LL. Sangha GK. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Fukushima S. Comparative metabolism of orthophenylphenol in mouse. Moore GA. 2005. Regul Toxicol Pharmacol 2002. Hirose M. IARC Sci Publ 1984. Bartels MJ. Kwok ES. Tayama S. 90-43-7) in Swiss CD-1 mice (dermal studies). Timchalk C. Imaida K. 4/13/09 Onstot JD. Eadon G. Third National Report on Human Exposure to Environmental Chemicals.45(5):460-481. Identification of SARA compounds in adipose tissue. Bromig KH. food additives and natural products as promoters in rat urinary bladder carcinogenesis.. Roy D. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol.S. Fourth National Report on Human Exposure to Environmental Chemicals 45 .S. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol.epa. Brusick D. St John MK. Herbold BA.159(1):18-24.74(2):61-71. March 1986. Ito N. Pathak DN. Arch Toxicol 2000. Meuling WJ. Atlanta (GA). J Chromatogr B Biomed Sci Appl 1997. EPA 739 R-06004.S. Brzak KA. Vogel JS. et al.pdf. Bormett GA. Roberts AL. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Kawanishi S.150(2):402-413.35(2 Pt 1):198-208. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Fukushima S. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Biochem Pharmacol 1992. Selim S. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Bartels MJ. Moldeus P. Hagiwara A. Environmental Protection Agency (U. Sangha G.S. O-phenylphenol and its sodium and potassium salts: a toxicological assessment.niehs. Bomhard EM. Freyberger A.

2004). Environmental Protection Agency (U. from residues on food. or from contamination of drinking water.S. drinking water and other environmental media.pdf. Reference U. U. May. Available at URL: http://www. and aquatic environments.S. or agricultural applications.EPA). or apply these chemicals have greater exposure to herbicides than others. during 2001 (U. S. Pesticide industry sales and usage . 3/17/09 46 Fourth National Report on Human Exposure to Environmental Chemicals . The herbicides discussed in this Report can be classified into the following categories: chlorophenoxy acids. and OSHA have developed criteria for the allowable levels for many of these chemicals in foods. residential.Herbicides Herbicides Herbicides are used to control undesirable weeds and plants in agricultural. formulate. and the workplace. forestal.S. and atrazine. respectively.EPA. Washington (DC): U.EPA. 2004. gov/oppbead1/pestsales/01pestsales/market_estimates2001.EPA. with about 553 million pounds of herbicides used in the U. Office of Prevention Pesticides and Toxic Substances. The FDA. General population exposure may result from herbicides used in residential.S.S. chloroacetanilides.2000 and 2001 market estimates.epa. Workers who manufacture. More herbicides are used annually than insecticides.

2006).. EPA at: http://www. 2000). 2000. Acetochlor is microbiologically degraded. Hladik et al. 1994.0 μg/L (Curwin et al.epa. including one that produces 2-methyl-6ethylaniline and its reactive metabolite. but it has produced testicular atrophy.EPA 2000. Kolpin et al. Acetochlor is not mutagenic. 2000. Feng and Wratten.S. and it is unlikely to be genotoxic at relevant doses (Ashby et al. but other pathways occur. which are often more prevalent in the environment. Acetochlor is moderately toxic to fish and honey bees. 2005). 2005). in some species and at doses above maximum tolerated doses. CAS No.EPA. 2-hydroxyethyl-6-methylaniline. Estimated human intakes of acetochlor have been below recommended limits (U.gov/ pesticides/. Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC.. and thyroid (U. mainly corn.S.EPA.e. Additional information about external exposure (i.. U. Urinary acetochlor mercapturate levels of 0. and neurologic movement abnormalities (U. 2000. and has been detected in watersheds of agricultural lands (Battaglin et al. 1996). Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2007)..S. animals have demonstrated tumors of the lung.. 2006).EPA considers acetochlor likely to be carcinogenic in humans. Fourth National Report on Human Exposure to Environmental Chemicals 47 . Acetochlor has low acute toxicity. General population exposure to acetochlor may occur through diet or drinking water. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8. environmental levels) is available from U.. renal injury.. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies. 1998). and hydroxymethyl ethyl aniline (U. People exposed to acetochlor will excrete acetochlor mercapturate in their urine..EPA. a major pathway for acetochlor metabolism involves mercapturate conjugation. 2006). 2005. 34256-82-1 General Information Acetochlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural crop land.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al.S. In animals.S. 1989. nasal epithelia. Plants can degrade acetochlor to 2-ethyl-6-methylaniline.. remains in soils for up to 3 months.Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure. the latter which may account for some observed effects (Coleman et al. NTP and IARC do not have ratings regarding human carcinogenicity. however.. It is absorbed by plants and inhibits plant protein synthesis. However. Biomonitoring studies on levels of acetochlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of acetochlor than are found in the general population. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid. Davison et al.S. 2006). this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. Jefferies et al.

see Data Analysis section) for Survey year 01-02 is 0. 48 Fourth National Report on Human Exposure to Environmental Chemicals . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2500 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 576 819 1105 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1178 1322 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 678 672 952 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2501 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 576 820 1105 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1178 1323 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 678 673 952 Limit of detection (LOD.1. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey. Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. which may vary for some chemicals by year and by individual sample.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Third National Report on Human Exposure to Environmental Chemicals. epa.Herbicides References Ashby J.pdf. Larsen GL. Atlanta (GA). Burkhardt MR. Dialkylquinonimines validated as in vivo metabolites of alachlor.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. and other herbicides in rivers. Roberts AL. Environmental Protection Agency (U.111(5):749-756. Volume 65. J Expo Anal Environ Epidemiol 2005. et al.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Curwin BD. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Chem Res Toxicol 1998.15(6):500-508. pages 3682-3690. Coleman S. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Barr DB. Casida JE. Kinney PL. Xenobiotica 1994. Available at URL: http://www. J Agri Food Chem 1989. Barr JR. 5/30/06. Linhart SM. Fourth National Report on Human Exposure to Environmental Chemicals 49 .S. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. EPA). Acetochlor (Harness) Pesticide Petition Filing 1/00.17(6):559-566. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.37(4):10881093. U. acetochlor. Tinwell H.24(10):1003-1012. Alavanja MC. Thurman EM. reservoirs and ground water in the Midwestern United States. Wilson AG. Kier L. Environ Health Perspect 2003.html. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Camann DE.11(4):353359. Whyatt RM. Deddens JA. Feil VJ. March 2006. J Expo Sci Environ Epidemiol 2007. Hodgson E. 5/30/06 U. Centers for Disease Control and Prevention (CDC). Wratten SJ. Kolpin DW.15(9):702-735. Feng PCC. Furlong ET.39(17):6561-6574. Green T. Reynolds SJ.S. Peter CJ. Olsson AO. Andrews HF. Rose RL. Jefferies PR. Hines CJ.cce. Lefevre PA. Federal Register: January 24. Striley CA. Ward EM.S. Bravo R. Barr DB. Hein MJ. et al.EPA): http://pmep.cornell.108(12):1151-1157. 1998. Quistad GB.S.S. 2005. and metolachlor herbicides in rats. EPA). Sanderson WT. Sci Total Environ 2000. Hum Exp Toxicol 1996. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Hsiao JJ. Hladik ML. Comparative metabolism and elimination of acetanilide compounds by rat. Number 15. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. et al. Occurrence of sulfonylurea. imidazolinone. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.248(2-3):123-133. Barr DB. Davison KL. Available at URL(non U. Environ Health Perspect 2000. EPA 738-R-00-009. Environmental Protection Agency (U.248(2-3):115-122. Linderman R. Environ Sci Technol 2005. sulfonamide. Battaglin WA. 2000. Heederik D. Sci Total Environ 2000.

but another metabolic pathway can produce 2. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. formulators. Tessier and Clark. about 20-25% of the U. Alachlor and its degradates are leachable from agricultural soils and have been detected in watersheds of agricultural land including ground and surface waters (Battaglin et al. corn cropland was treated with alachlor. It is absorbed by plants and inhibits plant protein synthesis.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. WHO. 1999 and 2007.. IPCS. soybeans. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. U. 15972-60-8 General Information Alachlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural cropland. the dermal exposure route is potentially significant for applicators. Alachlor itself is not considered mutagenic. but shows little bioaccumulation. 1997. ranged from 0. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. 1996). 1998. but not likely at low doses. Hladik et al. 1995). the latter may account for some observed effects (Davison et al. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. mean values of urinary concentrations of alachlor metabolites. 2005). Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. 2003). U. 1998. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. In 1993-1995. 1994. alachlor has demonstrated hepatotoxicity.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. 1996. 1998). mercapturate conjugates were predominant metabolites.epa. (2003) showed that 2. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates.6-diethylaniline and its reactive metabolite. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. 2003). 1989. In a study of applicators and workers exposed to alachlor. U.. Alachlor has a soil half-life of a few weeks. 2000. In chronic animal testing. Additional information about is available from U. 1998). and field workers. Since the late 1980s alachlor use has been declining. 2005..1 mg/L at various collection times (Sanderson et al. EPA at: http://www. 1998. Biomonitoring studies on levels of alachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of alachlor than are found in the general population. Hill et al.S. WHO.S. 50 Fourth National Report on Human Exposure to Environmental Chemicals . 1998). Alachlor has low potential for acute toxicity. and uveal degeneration.S.EPA. 2003). alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. Jefferies et al. In animal studies.. Because it can be absorbed through skin.. hemosiderosis.EPA. 1988.. U. Feng and Wratten. 2003). 2000.S. peanuts and other crops. 1995. Hines et al. stomach. including corn.S. In animals. WHO. whereas 60% of applicators had detectable amounts. Kolpin et al. General population exposure to alachlor may occur through consumption of contaminated food or drinking water..EPA. WHO. USGS.1 to 1.EPA. 1996.EPA. Estimated human intakes have been below recommended limits (U.S. 1999. NTP and IARC do not have ratings regarding human carcinogenicity.gov/pesticides/... as measured through conversion to deethylamine.S.S.EPA considers alachlor to be a probable human carcinogen at high doses. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment.Herbicides Alachlor CAS No. but has not shown developmental or reproductive toxicity in mammalian systems (U. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. and on non-crop land for general weed control.

which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 51 .S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.S. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1942 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 463 662 817 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 992 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 679 507 586 Limit of detection (LOD.18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Urinary Alachlor mercapturate (creatinine corrected) Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. population from the National Health and Nutrition Examination Survey.Herbicides Urinary Alachlor mercapturate Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 99-00 is 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1942 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 463 662 817 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 992 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 679 507 586 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

S. Casida JE. Shealy DB. Environ Sci Technol 2005. WHO/ FAO Data Sheets on Pesticides. Deddens JA. Am Ind Hyg Assoc J 1995. imidazolinone. Atlanta (GA). Sacramento. 2007. Hum Exp Toxicol. revised February 15. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Kimmel EC.395(2-3):159-171. Wilson AG. Camann DE.44(18):1325. U. Shoemaker DA. Hines CJ. Hull RD.S. Tessier DM. Barr JR. and other herbicides in rivers.usgs. 1997. et al. Geological Survey (USGS).43(25):2087-94. Hill RH Jr. J Ag Food Chem 1995. et al. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. World Health Organization (WHO). Casida JE.56(6):853-859. 1999. Kinney PL. Occurrence of sulfonylurea. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Biagini R.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Jefferies PR. Dialkylquinonimines validated as in vivo metabolites of alachlor. Geneva. International Programme on Chemical Safety (IPCS). Martens MA. Furlong ET. Larsen GL. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Brown KK. Whyatt RM. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Xenobiotica 1994. EPA). Alachlor in Drinking-water.S. Quistad GB.pdf. acetochlor. Centers for Disease Control and Prevention (CDC). who. Available at URL: http://www. EPA 738R-98-020. Comparative metabolism and elimination of acetanilide compounds by rat. Barr DB. Thurman EM. Third National Report on Human Exposure to Environmental Chemicals. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. California. 1996. Hladik ML. Tolos W.gov/oppsrrd1/ REDs/0063. Quistad GB. Thelin GP. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Biagini RE. March 2006. December 1998. 86.htm. Hsiao JJ.111(5):749-756. Mutat Res.pdf. Geological Survey (USGS).24(10):1003-1012. Andrews HF. Kolpin DW.Herbicides References Battaglin WA. 1992-2001.37(4):10881093. Driskell WJ.int/water_sanitation_health/dwq/chemicals/en/alachlor. Bull Environ Contam Toxicol 1996. Available at URL: http:// www.php.248(2-3):115-122. Clark JM.S. Sci Total Environ 2000. Heydens WF.56(9):883-889. Kolpin DW. Burkhardt MR. Feng PCC.org/documents/pds/pds/pest86_e. Reregistration Eligibility Decision (RED) Alachlor. Casida JE.epa. Henningsen G. 2/27/09 U. Environ Health Perspect 2003. 98-4245 (by Barbash JE. Sci Total Environ 2000. Environmental Protection Agency (U. Supplemental Technical Information (available on-line only). 4/2/09 U. 1999.11(4):353359. Davison KL. 2003. MacKenzie B. 2005. reservoirs and ground water in the Midwestern United States. Erratum in: Life Sci 1989. Feil VJ.248(2-3):123-133. Gilliom RJ). No. J Agri Food Chem 1989. Identification of a major human urinary metabolite of alachlor by LC-MS/MS.39(17):6561-6574. An evaluation of the carcinogenic potential of the herbicide alachlor to man.inchem. Roberts AL. Sanderson WT. Available at URL: http://water. Brown MA. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals .43(9):2504-2512. Thake DC. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Linhart SM. 2/27/09 Jefferies PR. World Health Organization. Available at URL: http://www. Hill AB. Ann Occup Hyg 2003. and metolachlor herbicides in rats. sulfonamide.18(6):363-391. Background document for development of WHO Guidelines for Drinking-water Quality.47(6):503-517. Chem Res Toxicol 1998. Circular 1291. ALACHLOR. Peter CJ. Life Sci 1988. 1998. Striley CA. Kier LD. Wratten SJ. DNA adduct formation by alachlor metabolites. Hines CJ. Lau H. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor.

S. Atrazine has limited water solubility and is not tightly bound to soil. Hayes et al. metabolized.. but it is leachable into ground and surface waters. but estimates of seasonal intakes from drinking water in a small number of communities have exceeded the recommended limits (U. propazine. atrazine use has progressively been restricted in an effort to reduce surface and ground water contamination.S. 1996. 2002. 2003b). it is one of the more commonly detected pesticides in surface and ground waters (USGS.and post-emergence to agricultural land for crops such as corn and sorghum. 2005.. < LOD means less than the limit of detection. 1993). More than 70 million pounds have been applied annually in recent years. with about 75% of corn cropland receiving treatment. 2003a). Catenacci et al. which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003b).EPA. 1912-24-9 General Information Atrazine is a widely used chlorotriazine herbicide that acts against broadleaf and grassy weeds. U.EPA.S. glutathione conjugation appeared to be the major route of biotransformation. Atrazine may alter the sexual development of frogs at environmental levels (Gammon et al. Applicators of atrazine may be exposed dermally and by inhalation. resulting in atrazine mercapturate and N-dealkylation products (IPCS. and then eliminated in the urine over a few days (Bradway et al. In soils. Atrazine was first registered as an herbicide in 1958.. U..Herbicides Atrazine CAS No. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1878 2477 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 449 568 639 809 790 1100 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 919 1162 959 1315 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 676 498 684 550 918 Limit of detection (LOD. and cyanazine. Urinary Atrazine mercapturate Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. which have half-lives of several months.791 and 0. Atrazine is well absorbed orally. 1993. The dealkylated chloroatrazine metabolites. It has little toxicity in birds and moderate toxicity in some fish and aquatic invertebrates.3.S. Related chlorotriazine herbicides include simazine.. 2007). Atrazine does not bioaccumulate. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Survey Geometric mean (95% conf.. Bacteria and plants can metabolize atrazine to hydroxyatrazine.EPA. For the general population. In regions where atrazine is used. Fourth National Report on Human Exposure to Environmental Chemicals 53 . population from the National Health and Nutrition Examination Survey. Timchalk et al. atrazine is slowly degraded to dealkylated products. In animals and humans. Atrazine mercapturate products accounted for a major proportion of human urinary metabolites (Lucas et al. all of which act by inhibiting plant photosynthesis. It is also used as a non-selective herbicide. 1990). Atrazine is applied pre. drinking water is an infrequent source of atrazine exposure. 1982. As a result.

2002.cdc.epa.. 2003. the dealkylated atrazine metabolites and hydroxyatrazine can occur in the environment from the breakdown of the parent chemical. increased pituitary weight. Stevens et al. Gammon et al. Dealkylated metabolites from atrazine can also result from metabolism of other chlorotriazine pesticides. Additional information is available from U.html. but the effects are difficult to attribute due to lack of exposure markers or due to mixed chemical or pesticide exposures (ATSDR. Laws et al. In mammalian studies... 2005).EPA considers atrazine unlikely to be a human carcinogen.S.. 2004.S.. myocardial muscle degeneration.Herbicides particularly diaminochloroatrazine (the main dealkylated product). delayed onset of puberty. Urinary Atrazine mercapturate (creatinine corrected) Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2000 and 2002. 1997).atsdr. Atrazine and the dealkylated chlorinated metabolites did not have estrogen receptor activity. altered estrus cycles... 1994 and 1999. Atrazine is not considered genotoxic. Chronic high dose toxicity observed in animals includes decreased body weight. Human health effects of atrazine at environmental doses or at biomonitored levels from environmental exposure are unknown. EPA at: http://www. developmental ossification defects. liver toxicity. and reduced levels of luteinizing hormone. but they reduced the pituitary secretion of luteinizing hormone and prolactin and also inhibited aromatase at high doses in some mammalian species (Cooper et al. 1994. 54 Fourth National Report on Human Exposure to Environmental Chemicals .. Eldridge et al.gov/pesticides/ and from ATSDR at: http://www.. impaired fertility. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Sathiakumar and Delzell. U. prolactin... and cyanazine. including simazine. Rayner et al.. 1999).EPA. Estimated human exposures are thousands of times lower than doses that caused effects in animals (Gammon et al. 2003b).S. In addition to being human metabolites of atrazine. 2000 and 2003. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1878 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 449 568 639 808 790 1100 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 919 1162 959 1314 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 676 498 683 550 918 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Atrazine product formulations can be mild skin sensitizers and irritants. IARC considers atrazine not classifiable with respect to human carcinogenicity.S. Survey Geometric mean (95% conf. and testosterone (Gillis et al. 2005. detection of these dealkylated metabolites in a person’s urine may also reflect exposure to these degradates in the environment.gov/toxpro2. may mediate some effects of atrazine (Laws et al. 2005. propazine. Some human ecologic and epidemiologic studies of reproductive and cancer outcomes have shown either positive or no associations. 2003). population from the National Health and Nutrition Examination Survey. atrazine is rated as having low acute toxicity. and U. 2000. Sanderson et al. Stoker et al. Gammon et al. Thus.

Sanborn JR. Available at URL: http:// www. Biological monitoring of human exposure to atrazine. Maroni M.. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Tyrey L. Barr DB. Vonk A. Goodrow MH. Hermaphroditic. Toxicol Sci 2000. 2005. Steroids 1999. Toxicol Sci 2000. The geometric mean of urinary atrazine mercapturate was 1. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Pfeifer KF. Striley CA. Simpkins JW. Moseman RF. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models..html. Bradway DE. Curwin BD. 1996. Ferrell JM.cdc. Environ Health Perspect 2001. Barr DB.org/documents/pds/pds/pest82_e.htm. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Available at URL: http://www. Geneva. Agency for Toxic Substances and Disease Registry (ATSDR). Wetzel LT. J Expo Anal Environ Epidemiol 2005. References Adgate JL. Cooper RL. Pest Manag Sci 2005. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Hines CJ. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products.. Mendoza M. 2000). Ann Occup Hyg 2003. Fleenor-Heyser DG. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L.43(2):155-167. Collins A. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Ferioli A. et al. 82. Lucas AD. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Toxicol Lett 1993. Chen H. Toxicological profile for atrazine. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. et al.30(2):244-247. Stevens JT. Toxicol Sci 2003. Saiz SG. Schmid J.15(6):500-508.atsdr. et al. Gammon DW.58(2):366-376. Shoemaker DA. Brown KK. levels of atrazine mercapturate were generally not detectable (CDC.69(2):217-222.99(8):5476-5480. et al. Breckenridge CB. Eldridge JC. Hein MJ. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. In a small number of field workers. Perry et al. Deddens JA.109(6):583-590. 2001 [online]. 3/11/09 Laws SC. Grzywacz JG. Eldridge JC. WHO/ FAO Data Sheets on Pesticides. In the NHANES 2001-2002 subsample. In a study of 60 farm worker children. Sanderson WT. Hayes TB. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Proc Natl Acad Sci USA 2002. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al.inchem. 2003.76(1):190-200. Catenacci G.. 1993). Centers for Disease Control and Prevention (CDC). atrazine was detected in only four children (Arcury et al. Stuart AA. Environ Health Perspect 2007.43(2):155-167. McElroy WK.. 2005). World Health Organization. Goldman JM. International Programme on Chemical Safety (IPCS). Cooper RL. Clayton CA. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. In small studies of Maryland residents in 19951996 (MacIntosh et al. Heederik D. Aldous CN.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Stoker TE. diamino-S-chlorotriazine and hydroxyatrazine. Bersani M. Reynolds SJ. Quandt SA.gov/toxprofiles/tp153. 2005). Biomonitoring studies on levels of atrazine mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of atrazine than are found in the general population. Stoker TE. Carr WC Jr.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Blewett C. Jones AD. Laws SC. Barbieri F. Gillis JH. 2007). J Agric Food Chem 1982. Atlanta (GA). A risk assessment of atrazine use in California: human health and ecological aspects.64(9):672-678. Third National Report on Human Exposure to Environmental Chemicals. 3/11/09 Arcury TA.47(6):503-517. Lioy PJ. Noriega N. Wetzel LT. Biagini RE. Barr DB. Ferrell JM. ATRAZINE. et al.. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Eberly LE. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. No. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. J Toxicol Environ Health 1994. Cooper RL. Extrom PC. Seiber JN. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. Freeman NC.115(8):1254-1260. Lee M. Gillis JH.53(2):297-307. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. 2001).61(4):331-355. Stoker TE. Cottica D. Tapia J. J Toxicol Environ Health 1994.

Case No. Guidici DL. EPA). Toxicol Sci 2002. 3/11/09 U. Supplemental Technical Information (available on-line only).195(1):23-34. Toxicol Sci 2000.67(2):198-206. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport.9(5):494-501. Kastl PE. White paper on potential developmental effects of atrazine on amphibians. Cooper RL.epa. Delzell E. Stoker TE. Stoker TE. Circular 1291. Needham LL. Wetzel L. A review of epidemiologic studies of triazine herbicides and cancer.usgs.10(7):479. Crit Rev Toxicol 1997. Sanderson JT.S. A risk characterization for atrazine: oncogenicity profile. Rayner JL. Washington (DC). Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Toxicol Appl Pharmacol 2004. Perry M.S. Stevens JT. EPA). Cooper RL. Interim Reregistration Eligibility Decision For Atrazine. Lansbergen GW. March 2006. Available at URL: http://www. Laws SC. U. Guidici DL. J Toxicol Environ Health A 1999.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Tortorelli J. Environmental Fate and Effects Division.S.php. Ryan PB.epa. Christiani D. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Fenton SE.182(1):44-54. Available at URL: http://www. Wood C.Herbicides development of a biomarker of exposure.pdf. A longitudinal investigation of selected pesticide metabolites in urine. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Laws SC. Singzoni B. 2007. MacIntosh DL. Dagenhart D. Pesticides and Toxic Substances. 6/1/09 U. Toxicol Appl Pharmacol 2002.pdf. Breckenridge CB. Geological Survey (USGS). Environmental Protection Agency (U. Osborne DW. Ann Epidemiol 2000. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . EPA Office of Pesticide Programs.27(6):599612. Hammerstrom KA. Environmental Protection Agency (U. Langvardt PW. Toxicology 1990. Pesticides in the Nation’s Streams and Ground Water. Office of Prevention. Timchalk C. Sathiakumar N. 1992-2001.61(1):27-40. J Expo Anal Environ Epidemiol 1999. 2003b. Chem Res Toxicol 1993.56(2):69-109. Urinary biomarkers of atrazine exposure among farm pesticide applicators. May 2003a. Available at URL: http://water.58(1):50-59.S. The Quality of Our Nation’s Waters. Boerma J.6(1):107-116. revised February 15. Dryzga MD. 0062.gov/oppsrrd1/REDs/ atrazine_ired. van den Berg M.S.

07 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.10) < LOD 1.610-.S. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. hypotension.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . it acts as a plant growth hormone.310) < LOD .560-.960-1.690 (.S. 2.4-D were used in the U. < LOD means less than the limit of detection. 1989. 2. the chlorophenoxy herbicide 2.32 (1. General population exposure to 2.610 (..250 (<LOD-.740 (.4-D can be applied either as an aqueous salt or as oil-soluble esters. by direct contact with agricultural and residential areas after applications. but at higher levels they are herbicidal.16) < LOD . Recent estimates of chronic intakes of 2.930-1.350) < LOD < LOD < LOD .230 (<LOD-.670-1. Similar to other chlorophenoxy herbicides.320) 90th . 2.690 (. It is rarely detected in ground waters (USGS.40) 1.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.370-.20 (<LOD-1.08) < LOD .4-D have been below recommended intake limits (U.66) < LOD 1.560-1. 2004). Sauerhoff et al.420) < LOD .00-2.. and mecoprop).10 (<LOD-1.760 (.EPA. population from the National Health and Nutrition Examination Survey.660) 1.4-D may occur during residential applications.260 (<LOD-.43) 1. 1974.27-2.4-D has low acute toxicity. agricultural. 94-75-7 General Information Widely used throughout the United States.70) 1. Survey Geometric mean (95% conf.EPA.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.21) 1.540-.690-1. in 2001 (U.4-D or exposed for prolonged periods.490) < LOD < LOD < LOD .440-1. It is not well absorbed through the skin.4-Dichlorophenoxyacetic Acid CAS No. As much as 62 million pounds of 2.27 (1.S.S. 4-D.51 (1.. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.EPA in 1948. with a half-life of several days to several weeks. and aquatic environments. and by consuming food or drinking water contaminated with 2.420-. dizziness.250 (<LOD-.410) < LOD .13) < LOD .310 (.55 (1.60) 1.910) 1.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. these herbicides can enhance plant growth.230-.210 (<LOD-.952 and 0. Fourth National Report on Human Exposure to Environmental Chemicals 57 .4-D is rapidly absorbed via oral and inhalation routes.690 (.10 (<LOD-1.910) < LOD . It was first registered with U.30 (<LOD-2. Kohli et al. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.80) 1. It is poorly bound in soils. and delayed Urinary 2.05-2.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . nausea. myotonia.20 (. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.22) < LOD .810-1. 2.4-D) controls broadleaf weeds in residential. renal and hepatic injury.550-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.37) size 1977 2413 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD . Once absorbed. At low levels. 2007).490 (.930 (.48) < LOD 1.400) < LOD .03) 695 659 520 668 589 892 Limit of detection (LOD.24 (.730 (.4-dichlorophenoxyacetic acid (2.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210-. MCPA.330 (. abdominal pain.S. 1977).890) < LOD .02-1.Herbicides 2.27 (.890 (.680-1.2. Human health effects from 2. 2005). headache.

2002.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. adrenals and gonads (NTP. Kutz et al. U.08 (.660) < LOD .580-.4-D reflect recent exposure.330-.epa.4-D in farmers were more than 25-fold higher than the 95th percentiles in the NHANES 1999-2000 and 2001-2002 subsamples (Arbuckle et al. 2.850) < LOD .410 (<LOD-.380) < LOD .590 (<LOD-1.570) < LOD ..480 (.810-1.470) < LOD . 2006. Epidemiological studies have reported associations of several types of cancer. 1989).980) < LOD 1.520-.. Additional information is available from U. U.270 (<LOD-. urinary 2. Frank et al. myotonia.. 1994). Post-application levels in farmers and home gardeners were dependent on Urinary 2. 2005).05) . 2005.810-1. and evidence of histological injury to the kidneys. or to contaminants in the herbicide formulations (specifically 2.08 (.08 (.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . 1996. 1996.gov/pesticides/.780) .27-1. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.EPA at: http://www.S.590 (<LOD-1.550-.S.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.13 (. 58 Fourth National Report on Human Exposure to Environmental Chemicals .39) < LOD 1.26) size 1977 2412 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD . Knopp et al..560-.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .780 (.390) < LOD < LOD < LOD .Herbicides neuropathy (Bradberry et al. 1980.670 (<LOD-1. population from the National Health and Nutrition Examination Survey.440 (.7.. 2005. or teratogenic effects in chronic rodent studies (Charles et al. Average post-application urinary levels of 2. 2001.410) 90th ..610-..3.490 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.720 (.340-. U.. 1985.380-. population (Hill et al. 2005).S. Kolmodin-Hedman and Erne.350 (<LOD-.S.740 (.780-1.EPA. Survey Geometric mean (95% conf. 2005. eyes. IOM. U. Biomonitoring Information Urinary levels of 2.41 (1.340 (. developmental.35) < LOD .790) 1.4-D levels were detectable in less than a quarter of the individuals studied.820-1. 2003. 1995).. 2005.4-D are eye irritants.24) 1.990-1.670 (.73) . IPCS.920) < LOD 1. 1995.EPA 2005). IPCS. 2004). The acid and salt forms of 2. Pearce and McLean.700 (. It is unclear whether these associations are related to the chlorophenoxy herbicides. In previous samples of the U.EPA.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .660 (.680) < LOD .17 (.16) 1.560-.670 (.890-1. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. liver.620-.410) < LOD < LOD < LOD .890) < LOD 1. 2002.610-.. in small samples of children (Hill et al. 2005). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Hill et al.S. 1992). IPCS.13 (.EPA. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 2. Acute high doses administered to laboratory animals produced ataxia.32 (<LOD-2.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.410) < LOD 1. 2005).380 (<LOD-. and of adults and children (Baker et al.19) .790) < LOD .930-1. 2000). other exposures.56) .640 (. 1996. 2.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.270-.S. The 95th percentiles of the NHANES 1999-2000 and 2001-2002 subsamples were roughly similar to the 95th percentile values reported in a nonrandom subsample from NHANES III (1988-1994) (CDC.14 (.380 (<LOD-. CDC.4-D production plant workers and a few forestry workers spraying 2. thyroid.4-D does not have significant reproductive.S.

Assessment of exposure to 2. Vet Hum Toxicol 1989. Chapman P. National Toxicology Program (NTP). Alexander BH. International Programme on Chemical Safety-INCHEM (IPCS). Absorption and excretion of 2. Reynolds SJ. Bailey SL. Smith SJ. Ritter L. van Ravenzwaay B.gov/index. Heederik D.4:97-100. Harris et al. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.4:318-321. Stephenson GR.4:427-435. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.71(2):99-108.31 Suppl 1:90-97.37(2):277-291. Crit Rev Toxicol 2002.4-D will result in an adverse health effect. Garabrant DH. Campbell RA. Needham LL. Philbert MA.4-.. Carter-Pokras OD. 2005 Charles JM. Board on Health Promotion and Disease Prevention.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study.org/documents/jmpr/jmpmono/v96pr04. Scand J Work Environ Health 2005.4-D in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2. Available at URL: http://ntp. Harris SA. the amount of pesticide applied. Arnold EK. Atlanta (GA). Forestry workers involved in aerial application of 2. Baker BA.nih. Bus JS. 2005). Developmental toxicity studies in rats and rabbits on 2. Sircar KP. Shealy DB. 2003. Curwin BD. Wilson RD. Kolmodin-Hedman B. Occup Environ Med 1994. Khanna RN. Veterans and Agent Orange: update 2002.4-D): exposure and urinary excretion. Barr DB.edu/catalog. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .4-D than levels found in the general population. Arch Toxicol Suppl 1980.5-T).51(3):152-159.4-dichlorophenoxyacetic acid (2. Gupta BN. Estimation of occupational exposure to phenoxy acids (2. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. geometric mean urinary levels of 2. Sirons G J. Gregg M.4-D were highest in the farmers who applied the 2. Selected pesticide residues and metabolites in urine from a survey of the U. Scand J Work Environ Health 2005. J Expo Anal Environ Epidemiol 2000. Sanderson WT. 914. Erne K. Arch Environ Contam Toxicol 1989. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Third National Report on Human Exposure to Environmental Chemicals. Beasley VR. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Xenobiotica 1974. Hein MJ. Baker S.nap. the number of acres to which it was applied (Curwin et al. Tandon JS. 2. et al. Hanley TR Jr. Mandel et al. Finding a measurable amount of 2.Herbicides the time since application. Kutz FW.4-Dichlorophenoxyacetic Acid).32(4):233-257. Centers for Disease Control and Prevention (CDC).10(6 Pt 2):789-798. Review of 2. Needham LL. Survival and Growth Curves from NTP Toxicity Studies. general population. Head SL.. Dhar MM. J Toxicol Environ Health 1992. 3/17/09 Knopp D. 3/17/09 Institute of Medicine (IOM). Washington (DC): National Academies Press. Dichlorophenoxyacetic acid.18(4):469-474.. Pesticide residues in urine of adults living in the United States: reference range concentrations.31(2):121-125. Biomonitoring for farm families in the farm family exposure study. Tables. References Arbuckle TE.htm. TOX-63 Peroxisone Project (2. TOX-63: TOXICITY REPORT CURVES. and the use of protective clothing or equipment (Arbuckle et al. Driskell WJ. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Cook BT.4-dichlorophenoxyacetic acid and its forms. Arch Environ Contam Toxicol 1985.15(6):500-508.inchem. Cole DC.4-D and 2. Beeson MD.php?record_id=10603.4.4-dichlorophenoxyacetic acid (2.60(1):121-131. Fast DM.27(1):23-38. J Environ Sci Health B 1992. Murphy RS. Baker SE.4-D. Mandel JS. Hill RH Jr.S. Available at URL: http:// www. In farm families. Biomonitoring studies of 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.31 Suppl 1:98-104.4-D). To T.4-dichlorophenoxyacetic acid in man. Honeycutt R. 2005.4-D) epidemiology and toxicology. Solomon KR. Acquavella JF. et al. 1992). Brody D. Environ Res 1995. Pesticides residues in food: 1996 evaluations Part II Toxicology. Toxicol Sci 2001. Barr DB. Hill RH Jr. Ripley BD. J Expo Anal Environ Epidemiol 2005 Nov. Biomonitoring of herbicides in Ontario farm applicators. Available at URL: http:// www. Holler JS.4-D in urine does not mean that the level of the 2. 2005.. Exposure of homeowners and bystanders to 2. et al.niehs. 2006. Frank R. 2005). Kohli JD.4 dichlorophenoxyacetic acid (2. Updated March 7.

gov/oppbead1/pestsales/01pestsales/market_estimates2001. 1992-2001.pdf. Washington (DC): U.4-D) following oral administration to man.S. Environmental Protection Agency (U.S.4-D RED Facts. 2004.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. The fate of 2. Supplemental Technical Information (available on-line only). Toxicology 1977.2000 and 2001 market estimates.EPA). revised February 15. May.8:3-1U. Braun WH. Available at URL: http://www. EPA 738 F-05-002. Gehring PJ. Circular 1291. 3/17/09 U. March 2006.epa. Available at URL: http://www. Blau GE.S. S.S. Available at URL: http://water. June 2005.EPA).usgs. The Quality of Our Nation’s Waters. Office of Prevention Pesticides and Toxic Substances. 60 Fourth National Report on Human Exposure to Environmental Chemicals .4-dichlorophenoxyacetic acid (2.gov/oppsrrd1/ REDs/factsheets/24d_fs. 2007. Pesticide industry sales and usage .S. 4/2/09 U. 2. Geological Survey (USGS). Environmental Protection Agency (U.Herbicides Sauerhoff MW. Pesticides in the Nation’s Streams and Ground Water.php.htm. 3/17/09.EPA.epa.

USGS. metolachlor was quickly absorbed after dermal or oral doses. Hines et al. The geometric mean metolachlor mercapturate was 4. Occasionally in the past. so applicators. Estimated human intakes have been below recommended limits (U. 2005. Jefferies et al. Kolpin et al. Metolachlor has a soil half-life of a few weeks to three months and is degraded microbiologically and photochemically to at least five different products. whereas 60% of applicators had detectable amounts. and convulsions were observed at lethal doses in animal studies. 1995). Salivation. 2003). including corn. in both ground and surface waters (Battaglin et al.EPA. NTP and IARC do not have ratings regarding human carcinogenicity.S.. lacrimation. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. 2007.S. 1995). Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect. and field workers may have significant exposures via this route. 1995. This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment. (2003) showed that 2. 2003).Herbicides Metolachlor available from U.. Gilliom.. soybeans. Hladik et al.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al. though the 95th percentile for males was 0.. Feng and Wratten. Davison et al. sorghum and other crops. U.S. 1999. WHO. In animal studies. 2003). WHO. 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biomonitoring studies on levels of metolachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels metolachlor than are found in the general population.. and it was not mutagenic in mammalian cells (U. Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. Metolachlor has low potential for acute toxicity (U. It is absorbed by plants and inhibits plant protein synthesis.S. but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. 1994. metolachlor levels in water have exceeded lifetime human health advisory levels (U. Metolachlor did not show developmental or reproductive toxicity in chronic animal studies.. EPA.epa. 2005).200 μg/L (CDC. In animals. mercapturate conjugates were the predominant metabolites.EPA. formulators.EPA considers metolachlor to be a possible human carcinogen. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine. Metolachlor is well absorbed dermally.gov/pesticides/.EPA. 1995). Biomonitoring Information CAS No.S. and on non-crop land for general weed control. 2000. 2000. People exposed to metolachlor will excrete metolachlor mercapturate in their urine. EPA at: http://www. 2007. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. Fourth National Report on Human Exposure to Environmental Chemicals 61 .. General population exposure may occur through the consumption of contaminated food or drinking water. Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. and eliminated in urine and feces over two to three days (WHO. 51218-45-2 General Information Metolachlor is a chloroacetanilide type herbicide that is applied for preemergent control of grasses and broadleaf weeds on agricultural crop land. 1989. 1998).

S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .240) 679 701 957 Limit of detection (LOD.2. < LOD means less than the limit of detection.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 62 Fourth National Report on Human Exposure to Environmental Chemicals . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. which may vary for some chemicals by year and by individual sample.440 (<LOD-. see Data Analysis section) for Survey year 01-02 is 0. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.200 (<LOD-.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 831 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.200 (<LOD-.670 (<LOD-.

Kinney PL. usgs. EPA 738R-95-006. reservoirs and ground water in the Midwestern United States.248(2-3):123-133. Sci Total Environ 2000. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Reynolds SJ. imidazolinone.gov/oppsrrd1/ REDs/0001. Dialkylquinonimines validated as in vivo metabolites of alachlor. 4/2/09 U. Xenobiotica 1994. Alavanja MC. Environ Sci Technol 2005. Furlong ET. April 1995. Comparative metabolism and elimination of acetanilide compounds by rat.pdf. Metolachlor in Drinkingwater. Environ Health Perspect 2003.S. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. acetochlor. Hein MJ. Larsen GL. Environmental Protection Agency (U. revised February 15. 1999. 3/26/09 U. Jefferies PR.39(17):6561-6574. Burkhardt MR. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Ward EM. 2003. Wratten SJ. Barr JR. Background document for development of WHO Guidelines for Drinking-water Quality.15(6):500-508. Chem Res Toxicol 1998. Shoemaker DA.pdf 3/30/09 Hines CJ.gov/nawqa/ pnsp/pubs/wrir984245/text.47(6):503-517. Rose RL.41:3409-3414. Gilliom RJ).epa.108(12):1151-1157.usgs. streams and groundwater. Environ Sci Technol 2007. Andrews HF. March 2006. Casida JE. Ann Occup Hyg 2003.who. 2007. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.gov/nawqa/pnsp/pubs/files/051507. Brown KK. Atlanta (GA). and other herbicides in rivers. Camann DE.S. Linderman R. Third National Report on Human Exposure to Environmental Chemicals. Curwin BD. 98-4245 (by Barbash JE. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Feng PCC.248(2-3):115-122. Striley CA. Coleman S. Kolpin DW. J Agri Food Chem 1989. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Peter CJ. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. 1998. R.S.S. J Expo Anal Environ Epidemiol 2005. Sacramento. et al. Available at URL: http://water. Hsiao JJ. Circular 1291.html. Available at URL: http://www.int/water_sanitation_health/dwq/chemicals/ metolachlor. 6/1/09 Whyatt RM. 2005.111(5):749-756. Davison KL. Environ Health Perspect 2000.php. Quistad GB.Herbicides References Battaglin WA. Available at URL: http://water. Deddens JA. Gillion. Feil VJ. et al. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.24(10):1003-1012. World Health Organization (WHO). Available at URL: http://www. EPA). Thelin GP. U. California. Supplemental Technical Information (available on-line only). Hodgson E.ESTfeature_gilliom.pdf. 1992-2001. Sanderson WT. Available at URL: http://water. Hladik ML. Linhart SM.S.11(4):353359. Biagini RE.37(4):10881093. Barr DB. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Roberts AL. Geological Survey (USGS). Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Geological Survey (USGS). Kolpin DW. Reregistration Eligibility Decision (RED) Metolachlor. sulfonamide. Thurman EM. Heederik D. Sci Total Environ 2000. and metolachlor herbicides in rats.usgs. Occurrence of sulfonylurea.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Pesticides in U. Centers for Disease Control and Prevention (CDC). Barr DB.

4. and delayed neuropathy (Bradberry et al.g. 2004).4. 2. 1992. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Human health effects from 2.7. but higher levels are herbicidal.5-Trichlorophenoxyacetic acid (2..5-T degrades to 2.S.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Mohammad and St. abdominal pain.4. 93-76-5 General Information 2.2 and 0. 2. 1974).3.4. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. 2. the general population is unlikely to be exposed to it. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2.4.. Although 2.5-T (Holson et al. 2. 2007).5-T and 2. myotonia.4. Agent Orange). dizziness.5-T in soil varies with conditions. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. The half-life of 2..4. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. Survey Geometric mean (95% conf.5-T use as a herbicide in 1985. headache.4. Given the commercial unavailability of 2.4. Chlorophenoxy herbicides act as plant growth hormones. these herbicides can enhance plant growth. renal and hepatic injury.. hypotension. nausea. Omer. 1992). which may vary for some chemicals by year and by individual sample.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4. Kohli et al.5-T has been rarely detected in ground waters (USGS..4.4.5-trichlorophenol and other degradates. it is not well absorbed through the skin.5T is rapidly absorbed via oral and inhalation routes.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.4. with an elimination half-life of approximately 19 hours (Arnold et al. Epidemiological studies have reported associations of several types of cancer. 64 Fourth National Report on Human Exposure to Environmental Chemicals . 1986. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.4. and concern about contamination with 2.4.5-T. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD.Herbicides 2. < LOD means less than the limit of detection.4-D were used as defoliants in the Vietnam War (e. At low levels. 1989.4.1.. Once absorbed into the body. ranging from several weeks to many months.5-Trichlorophenoxyacetic Acid CAS No. Nelson et al. population from the National Health and Nutrition Examination Survey.5-T was once applied as either an aqueous salt or as an oil-soluble ester. Ester forms of 2.5-T is eliminated mostly unchanged in the urine.

5-T itself is not mutagenic.5-T does not mean that the level will result in an adverse health effect. other exposures.4.EPA at: http://www.3.4.S. 1996. IOM. 1992).5-T than levels found in the general population.4.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. 2005.S.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. 1980). Finding a measurable amount of 2.4.5-T also were below the limit of detection (Kutz et al. or to contaminants in the herbicide formulations (specifically 2. 2002.5-T were generally below the limit of detection. Survey Geometric mean (95% conf. urinary levels of 2.4.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.gov/pesticides/.5-T reflect recent exposure. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey.S. 2005). In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.EPA. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. U. Additional information is available from U. Biomonitoring studies on 2.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. Urinary 2. similar to results of NHANES II (19761980). It is unclear whether these associations are related to the chlorophenoxy herbicides. 2.4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Mean urinary levels of 2.4.epa.. Fourth National Report on Human Exposure to Environmental Chemicals 65 . 2004).7. in which urinary levels of 2.Herbicides or contaminated herbicides.4. IPCS.4. Biomonitoring Information Urinary levels of 2. 2003. Pearce and McLean.

Pearce N. Gaines TB. Dhar MM.edu/catalog.php?record_id=10603.inchem. Khanna RN. Sheehan DM.4. Available at URL: http:// www. Absorption and excretion of 2. Office of Prevention Pesticides and Toxic Substances. May. 2003. Developmental toxicity of 2. Veterans and Agent Orange: update 2002. Atlanta (GA). discussion 5-7. Environmental Protection Agency (U. International Programme on Chemical Safety-INCHEM (IPCS).4-D/2.31 Suppl 1:1825.5-trichlorophenoxyacetic acid (2. Holson JF. gov/oppbead1/pestsales/01pestsales/market_estimates2001. LaBorde JB. McLean D. Multireplicated dose-response studies with technical and analytical grades of 2.EPA. Mohammad FK. Pesticides residues in food: 1996 evaluations Part II Toxicology. Available at URL: http:// www. J Toxicol Environ Health 1992. Nelson CJ. Board on Health Promotion and Disease Prevention. Washington (DC): U. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .37(2):277-91.4.pdf. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Washington (DC): National Academies Press. 2. Behavioral and developmental effects in rats following in utero exposure to 2. Gupta BN.EPA).19(2):286-297. Wolff GL. Arch Int Pharmacodyn Ther 1974. Murphy RS. 3/17/09 Kohli JD. et al. Gaylor DW. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Poisoning due to chlorophenoxy herbicides.4. Tandon JS. Carter-Pokras OD. Toxicol Rev 2004. Pesticide industry sales and usage . Nelson CJ. Kolmodin-Hedman B. Kutz FW.5-trichlorophenoxyacetic acid (2.19(2):298-306.4. Cook BT.8(5):551-60. Review of 2.4-D and 2. Fundam Appl Toxicol 1992. Brody D. Selected pesticide residues and metabolites in urine from a survey of the U.S. Estimation of occupational exposure to phenoxy acids (2. Holson JF.5-T). Garabrant DH.4. 914. Vale JA.5-T in four-way outcross mice. Crit Rev Toxicol 2002. general population. Sircar KP.4-D) epidemiology and toxicology.nap.org/documents/jmpr/jmpmono/v96pr04. Centers for Disease Control and Prevention (CDC). Agricultural exposures and non-Hodgkin’s lymphoma.4:318-21.epa.4-. Arch Toxicol Suppl 1980.htm. Dichlorophenoxyacetic acid. Neurobehav Toxicol Teratol 1986.5-t mixture. Available at URL: http://www. Developmental toxicity of 2. 2005. Vet Hum Toxicol 1989. 210:250-255. Beasley VR. I. Bradberry SM. Third National Report on Human Exposure to Environmental Chemicals.S.2000 and 2001 market estimates. et al.5-T). II.5-trichlorophenoxy acetic acid in man.4-dichlorophenoxyacetic acid (2.5-T).4.4.Herbicides References Arnold EK. U. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Scand J Work Environ Health 2005. S.4. LaBorde JB. St Omer VE.32(4):233-257.S. 3/17/09 Institute of Medicine (IOM). Fundam Appl Toxicol 1992. Proudfoot AT. Erne K. McCallum WF. Philbert MA.31(2):121-125. 2004. Gaines TB.23(2):65-73.

Carbamates do not persist in the environment and have a low potential for bioaccumulation. ornamentals. leading to an increase of acetylcholine in the nervous system. Fourth National Report on Human Exposure to Environmental Chemicals 67 . in nurseries. At high doses. The mechanism of toxicity of carbamate insecticides is similar to that of organophosphate pesticides. from ingesting contaminated foods. weakness. toxic symptoms include nausea. the use of the carbamate insecticides has decreased. paralysis.S. and OSHA. formulation. Carbamate insecticides act by inhibiting acetylcholinesterase enzymes. FDA. thiocarbamates and dithiocarbamates. and throughout the world. or application of these chemicals. Agricultural workers can be exposed when they re-enter areas recently treated. Exposures of workers also can occur during the manufacture. Carbamates have been used on residential lawns.S. the environment. and on golf courses. vomiting. of the carbamate insecticides still used in the U. In agricultural applications. or by ingestion.Carbamate Insecticides Carbamate Insecticides General Information N-methyl carbamate insecticides (carbamates) have been widely used in the U. being replaced by pyrethroid and other insecticides. and the workplace have been developed by the U. U. carbamate insecticides generally are reversible inhibitors of acetylcholinesterase activity. respectively. however. EPA.S. cholinergic signs. Carbamate insecticides are rapidly eliminated from the body. via inhalation. Some other chemical types of carbamates.S. Carbamates can be absorbed through the skin. less commonly. acting for a shorter time than organophosphate pesticides. and seizures. General population exposure to carbamates occurs during contact with residential uses and. Only two metabolites are measured in this Report (metabolites of carbofuran and propoxur). are used as herbicides and fungicides. Criteria for allowable levels of specific carbamates in food.

Carbamate Insecticides

Carbofuran

CAS No. 1563-66-2 General Information Carbofuranphenol is a metabolite of four different carbamate insecticides: benfuracarb; carbofuran; carbosulfan; and furathiocarb. Only carbofuran is registered in the U.S. Carbofuran is a broad spectrum, restricted-use insecticide and nematicide applied to a variety of field, fruit, and vegetable crops for control of beetles, borers, nematodes, weevils, and similar pests. Recently, registered uses of carbofuran were cancelled except for the following: field corn; potatoes; pumpkins; sunflowers; pine seedlings; and spinach grown for seed (U.S.EPA, 2009). About 1 million pounds have been used annually (U.S.EPA, 2007). Carbofuran is not registered for use in residential settings or food-handling establishments. In soils of varying composition, carbofuran has a half-life ranging from one to three months. It can leach into ground waters, but it has been detected only infrequently in either surface or ground waters (Gilliom, 2007; USGS, 2007). Carbofuran

is very highly toxic to fish and aquatic invertebrates, and it is highly toxic to birds where granular applications are used, but such applications have been restricted since 1991 (U.S.EPA, 2007). General population exposure can occur through consumption of food contaminated with carbofuran. Because estimated acute intakes from some dietary components in young children may exceed recommended intake limits, the U.S.EPA is in the process of revoking current regulations that allow carbofuran residues in food (U.S.EPA, 2009). Pesticide handlers and applicators are at greater risk for exposure and a number of incidents of systemic poisoning have been reported. After absorption, carbofuran is metabolized to phenolic metabolites and 3-hydroxycarbofuran, which are quickly eliminated in the urine. Human health effects from carbofuran at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Carbofuran was very highly acutely toxic in animal studies, causing effects related

Urinary Carbofuranphenol
Metabolite of Benfuracarb, Carbofuran, Carbosulfan, and Furathiocarb

Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval)

Selected percentiles
( 95% confidence interval)

Sample 95th .770 (<LOD-1.30) < LOD size 1994 2530

Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

.450 (<LOD-2.20) < LOD .570 (<LOD-1.20) < LOD .840 (<LOD-1.50) < LOD

482 578 681 827 831 1125

99-00 01-02 99-00 01-02

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

.740 (<LOD-1.50) < LOD .840 (<LOD-1.50) < LOD

973 1190 1021 1340

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

.590 (<LOD-2.00) < LOD < LOD < LOD < LOD < LOD

1.90 (<LOD-5.10) < LOD .550 (<LOD-1.60) < LOD .740 (<LOD-1.50) < LOD

696 680 521 696 603 953

Limit of detection (LOD, see Data Analysis section) for Survey years 99-00 and 01-02 are 0.4 and 0.4. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

68

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

to acetylcholinesterase enzyme inhibition. In contrast, carbofuranphenol is not an inhibitor of acetylcholinesterase enzymes. Carbofuran was not teratogenic, but high chronic doses in animals produced nonspecific developmental effects, such as reduced weight gain and pup survival (WHO, 2004). Testicular toxicity at subacute doses was reported in adult rats, rat pups, and dogs (Pant et al., 1995, 1997; WHO, 2004). Carbofuran was found not to be mutagenic or carcinogenic in animals (U.S.EPA, 2007). It is not rated by IARC with regard to human carcinogenicity. Additional information is available from U.S.EPA at: http:// www.epa.gov/pesticides/. Biomonitoring Information Urinary carbofuranphenol levels reflect recent exposure. The level of this metabolite in urine may reflect exposure to carbofuran or to carbofuranphenol as a degradation product in the environment or food. In representative subsamples from NHANES 1999-2000 and 2001-2002, most urinary levels of carbofuranphenol were below the limit of detection (CDC, 2005). In a nonrandom subsample from NHANES III (1988-1994), the 99th percentile level of carbofuranphenol

was 2.1µg/L (Hill et al., 1995). In a previous study of U.S. farmers and their families, carbofuranphenol was detected in 6.7% of urine samples (Shealy et al., 1997); the 95th percentile value in that study was 0.73 µg/L. Urinary levels of carbofuranphenol in two applicators were three and sixfold higher than the detection limit for the NHANES 2003-2004 subsample (Petropoulou et al., 2006). Finding a measurable amount of carbofuranphenol in urine does not mean that the level of carbofuranphenol causes an adverse health effect. Biomonitoring studies on levels of carbofuranphenol provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of carbofuran or related carbamates than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Urinary Carbofuranphenol (creatinine corrected)
Metabolite of Benfuracarb, Carbofuran, Carbosulfan, and Furathiocarb

Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval)

Selected percentiles
( 95% confidence interval)

Sample 95th .780 (<LOD-1.00) < LOD size 1994 2529

Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

.990 (<LOD-2.80) < LOD .480 (<LOD-.850) < LOD .880 (<LOD-1.06) < LOD

482 578 681 826 831 1125

99-00 01-02 99-00 01-02

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

.670 (<LOD-1.08) < LOD .880 (<LOD-1.13) < LOD

973 1190 1021 1339

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

.780 (<LOD-1.94) < LOD < LOD < LOD < LOD < LOD

1.83 (<LOD-4.16) < LOD .700 (<LOD-1.08) < LOD .740 (<LOD-.930) < LOD

696 680 521 695 603 953

< LOD means less than the limit of detection for the urine levels not corrected for creatinine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Fourth National Report on Human Exposure to Environmental Chemicals

69

Carbamate Insecticides

References Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). 2005. Gillion, R. Pesticides in U.S. streams and groundwater. Environ Sci Technol 2007;41:3409-3414. Available at URL: http://water. usgs.gov/nawqa/pnsp/pubs/files/051507.ESTfeature_gilliom. pdf. 4/9/09 Hill RH Jr, Head SL, Baker S, Gregg M, Shealy DB, Bailey SL, et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. Environ Res 1995;71(2):99-108. Pant N, Prasad AK, Srivastava SC, Shankar R, Srivastava SP. Effect of oral administration of carbofuran on male reproductive system of rat. Hum Exp Toxicol 1995;14(11):889-894. Pant N, Shankar R, Srivastava SP. In utero and lactational exposure of carbofuran to rats: effect on testes and sperm. Hum Exp Toxicol 1997;16(5):267-272. Petropoulou SS, Gikas E, Tsarbopoulos A, Siskos PA. Gas chromatographic-tandem mass spectrometric method for the quantitation of carbofuran, carbaryl and their main metabolites in applicators’ urine. J Chromatogr A 2006;1108(1):99-110. Shealy DB, Barr JR., Ashley DL, Patterson DG Jr, Camann DE, Bond AE. Correlation of environmental carbaryl measurements with serum and urinary 1-naphthol measurements in a farmer applicator and his family. Environ Health Perspect 1997;105:510513. U.S. Environmental Protection Agency (U.S.EPA) Carbofuran cancellation process. March 28, 2009. Available at URL: http:// www.epa.gov/pesticides/reregistration/carbofuran/carbofuran_ noic.htm. 4/10/09 U.S. Environmental Protection Agency (U.S.EPA). Reregistration Eligibility Decision for Carbofuran. September 2007. Available at URL: http://www.epa.gov/pesticides/reregistration/REDs/ carbofuran_red.pdf. 4/10/09 U.S. Geological Survey (USGS).The Quality of Our Nation’sWaters: Pesticides in the Nation’s Streams and Ground Water, 1992-2001. Circular 1291. Supplemental Technical Information (available on-line only). March 2006, revised February 15, 2007. Available at URL: http://water.usgs.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.php. 4/2/09 World Health Organization (WHO). Carbofuran in DrinkingWater. Background document for development of WHO Guidelines for Drinking-water Quality. 2004. Available at URL: http://www.who.int/water_sanitation_health/dwq/chemicals/ carbofuran.pdf. 4/9/09

70

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

Propoxur

CAS No. 114-26-1 General Information 2-Isopropoxyphenol is a metabolite of propoxur, a carbamate used to control ants, roaches, hornets, and similar pests in residential areas and around commercial food-handling establishments. Propoxur has also been used in pest strips and pet flea collars. Like several other pesticides, propoxur has been used outside the U.S. as a replacement for DDT in malaria vector control. Propoxur may remain in the environment for weeks to several months, longer than most carbamates (U.S.EPA, 1997b). Despite its mobility in soil and its potential for leaching into groundwater, propoxur has been rarely detected in U.S. surface or ground waters (Gilliom, 2007; USGS, 2007). Although propoxur is toxic to birds and aquatic life, ecologic exposures are unlikely due to current outdoor use restrictions. General population exposure to propoxur through the diet is likely to be limited because of usage restrictions (U.S. EPA, 1997a). Estimated human intakes have been below recommended intake limits (U.S.EPA, 1997b). Pesticide applicators are likely to have the highest exposures. Propoxur can be absorbed through the skin, lungs, and gastrointestinal tract. Propoxur does not accumulate in blood or tissues and is eliminated rapidly from the body (Leenheers et al., 1992; WHO, 2003). In animal and human studies, 2-isopropoxyphenol was one of several urine metabolites (U.S.EPA, 1997b). Human health effects from propoxur at low environmental doses or at biomonitored levels from low environmental exposures are unknown. In animal studies, propoxur has moderate acute toxicity consisting of anticholinesterase effects (U.S.EPA, 1997b). 2-Isopropoxyphenol does not inhibit acetylcholinesterase enzymes. Propoxur is not considered mutagenic, embryotoxic, or teratogenic (WHO, 2003). U.S. EPA considers propoxur to be a probable human carcinogen, based on bladder tumors in male rats (U.S. EPA, 1997b). The human carcinogenic potential of propoxur has not been evaluated by IARC or NTP. Additional information is available from U.S.EPA at: http:// www.epa.gov/pesticides/. Biomonitoring Information Urinary 2-isopropoxyphenol levels reflect recent exposure. The level of this metabolite in urine may reflect exposure to propoxur or to 2-isopropoxyphenol as a degradation product in the environment or food (U.S.EPA, 1997b). In the U.S.

representative subsamples from NHANES 1999-2000 and 2001-2002, most 2-isopropoxyphenol levels in urine were below the limit of detection (CDC, 2005). In a nonrandom subsample from NHANES III (1988-1994), the 95th percentile level of 2-isopropoxyphenol was 1.7 µg/L (Hill et al., 1995). Higher urinary levels of 2-isopropoxyphenol have been measured in a few pesticide applicators, with a range of 45-306 µg/g creatinine (Hardt and Angerer, 1999). Finding a measurable amount of 2-isopropoxyphenol in urine does not mean that the level of 2-isopropoxyphenol causes an adverse health effect. Biomonitoring studies on levels of 2-isopropoxyphenol provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of propoxur than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Fourth National Report on Human Exposure to Environmental Chemicals

71

Carbamate Insecticides

Urinary 2-Isopropoxyphenol
Metabolite of Propoxur

Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval)

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2503

Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

456 574 655 820 806 1109

99-00 01-02 99-00 01-02

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1325

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

664 677 500 696 585 931

Limit of detection (LOD, see Data Analysis section) for Survey years 99-00 and 01-02 are 1.1 and 0.4. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

72

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

Urinary 2-Isopropoxyphenol (creatinine corrected)
Metabolite of Propoxur

Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval)

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2502

Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

456 574 655 819 806 1109

99-00 01-02 99-00 01-02

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1324

99-00 01-02 99-00 01-02 99-00 01-02

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

664 677 500 695 585 931

< LOD means less than the limit of detection for the urine levels not corrected for creatinine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Fourth National Report on Human Exposure to Environmental Chemicals

73

Carbamate Insecticides

References Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). 2005. Gillion, R. Pesticides in U.S. streams and groundwater. Environ Sci Technol 2007;41:3409-3414. Available at URL: http://water. usgs.gov/nawqa/pnsp/pubs/files/051507.ESTfeature_gilliom. pdf. 4/9/09 Hardt J, Angerer J. Gas chromatographic method with massselective detection for the determination of 2-isopropoxyphenol in human urine. J Chromatogr B Biomed Sci Appl 1999;723(12):139-145. Hill RH Jr, Head SL, Baker S, Gregg M, Shealy DB, Bailey SL, et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. Environ Res 1995;71(2):99-108. Leenheers LH, van Breugel DC, Ravensberg JC, Meuling WJ, Jongen MJ. Determination of 2-isopropoxyphenol in urine by capillary gas chromatography and mass-selective detection. J Chromatogr 1992;578(2):189-194. U.S. Environmental Protection Agency (U.S.EPA). RED Facts. Propoxur. August 1997a. EPA 738 F-97-009. Available at URL: http://www.epa.gov/oppsrrd1/REDs/factsheets/2555fact.pdf. 4/9/09 U.S. Environmental Protection Agency (U.S.EPA). Reregistration Eligibility Decision (RED) Propoxur. August 1997b. EPA 738R-97-009. Available at URL: http://www.epa.gov/pesticides/ reregistration/REDs/2555red.pdf. 4/9/09 U.S. Geological Survey (USGS). The Quality of Our Nation’s Waters. Pesticides in the Nation’s Streams and Ground Water, 1992-2001. Circular 1291. Supplemental Technical Information (available on-line only). March 2006, revised February 15, 2007. Available at URL: http://water.usgs.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.php. 4/2/09 World Health Organization (WHO). WHO Specifications and Evaluations for Public Health Pesticides. Propoxur. FAO/WHO Evaluation Report 80/2003. 2003. Available at URL: http:// www.who.int/whopes/quality/en/propoxur_eval_spec_WHO_ October_2005.pdf. 4/9/09

74

Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Organochlorine Pesticides
General Information Organochlorine pesticides, an older class of pesticides, are effective against a variety of insects. These chemicals were introduced in the 1940s, and many of their uses have been cancelled or restricted by the U.S. EPA because of their environmental persistence and potential adverse effects on wildlife and human health. Many organochlorines are no longer used widely in the U.S., but other countries continue to use them. Hexachlorobenzene has been used primarily as a fungicide or biocide. Organochlorine pesticides can enter the environment after pesticide applications, disposal of contaminated wastes into landfills, and releases from manufacturing plants that produce these chemicals. Some organochlorines are volatile, and some can adhere to soil or particles in the air. In aquatic systems, sediments adsorb organochlorines, which can then bioaccumulate in fish and other aquatic mammals. These chemicals are fat soluble, so they are found at higher concentrations in fatty foods. In the general population, diet is the main source of exposure, primarily through the ingestion of fatty foods such as dairy products and fish. Usage restrictions have been associated with a general decrease in serum organochlorine levels in the

U.S. population and other developed countries (Hagmar et al., 2006; Kutz et al., 1991). Contaminated drinking water and air are usually minor exposure sources. Infants can be exposed through breast milk, and the fetus can be exposed in utero via the placenta. Workers can be exposed to organochlorines in the manufacture, formulation, or application of these chemicals. The FDA, U.S. EPA, and OSHA have developed standards for allowable levels of certain organochlorines in foods, the environment, and the workplace, respectively. Attributing human health effects to specific organochlorine chemicals is difficult because exposure to multiple organochlorine chemicals occurs often and these chemicals may have similar actions. The table shows selected parent organochlorines and their metabolites that can be measured in serum or urine. Measurements of these chemicals can reflect either recent or cumulative exposures, or both. Some of the metabolites can be produced from more than one pesticide. The level of a metabolite in a person’s blood or urine may indicate exposure to the parent pesticide as well as to the metabolite itself.

Organochlorine Pesticides and Metabolites in this Report
Organochlorine Pesticide (CAS number) Serum pesticide or metabolite(s) (CAS number) Urinary pesticide or metabolite(s) (CAS number)

Aldrin (309-00-02) Chlordane (12789-03-6)

Aldrin (309-00-02) Dieldrin (60-57-1) Oxychlordane (27304-13-8) trans-Nonachlor (3734-49-4) p,p’-DDT (50-29-3) p,p’-DDE (72-55-9) o,p’-DDT (789-02-6) Dieldrin (60-57-1) Endrin (72-20-8) Heptachlor epoxide (1024-57-3) Hexachlorobenzene (118-74-1) Pentachlorophenol (87-86-5) 2,4,6-Trichlorophenol (88-06-2) 2,4,5-Trichlorophenol (95-95-4) Pentachlorophenol (87-86-5) 2,4,6-Trichlorophenol (88-06-2) 2,4,5-Trichlorophenol (95-95-4)

Dichlorodiphenyltrichloroethanes Dieldrin (60-57-1) Endrin (72-20-8) Heptachlor (76-44-8) Hexachlorobenzene (118-74-1)

Hexachlorocyclohexanes Mirex (2385-85-5) 2,4,5-Trichlorophenol (95-95-4) 2,4,6-Trichlorophenol (88-06-2)

beta-Hexachlorocyclohexane (319-85-7) gamma-Hexachlorocyclohexane (58-89-9) Mirex (2385-85-5)

2,4,5-Trichlorophenol (95-95-4) 2,4,6-Trichlorophenol (88-06-2)

Fourth National Report on Human Exposure to Environmental Chemicals

75

Organochlorine Pesticides

References Hagmar L, Wallin E, Vessby B, Jonsson BA, Bergman A, Rylander L. Intra-individual variations and time trends 1991-2001 in human serum levels of PCB, DDE and hexachlorobenzene. Chemosphere 2006;64(9):507-513. Kutz FW, Wood PH, Bottimore DP. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Rev Environ Contam Toxicol 1991;120:1-82.

76

Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Aldrin

CAS No. 309-00-02

but dieldrin has been detected in meats, dairy products, and in crops grown in soils that have been contaminated, usually by application, manufacturing, or disposal. General population exposure to these chemicals occurs through the diet, and detection of dieldrin residue in foods has decreased over time (FDA, 2008). Inhalation exposure may occur among people living in residences where aldrin was applied historically as a pesticide. Aldrin and dieldrin are absorbed following ingestion, inhalation, and dermal application. After absorption, aldrin is metabolized to dieldrin so rapidly that aldrin is rarely detected. Dieldrin accumulates in fatty tissues, and its metabolites are excreted in bile and feces (ATSDR, 2002). It is also excreted in breast milk and can cross the placenta. The elimination half-life of dieldrin is approximately 1 year (IPCS, 1989; Jorgenson 2001). Human health effects from aldrin and dieldrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. At high doses, aldrin and dieldrin block inhibitory neurotransmitters in the central nervous system (Narahashi et al., 1992). This blocking action can cause abnormal excitation of the brain, leading to symptoms such as headache, confusion, muscle

Dieldrin

CAS No. 60-57-1 Also a Metabolite of Aldrin General Information Aldrin and dieldrin are no longer produced or used in the U.S. From the 1950s to 1970, both chemicals were applied mainly as a soil insecticide or seed dressing for food and commodity crops. Dieldrin was also used for mothproofing clothes and carpets. In tropical countries, dieldrin was used as a residual spray in residential dwellings to control vectorborne diseases such as malaria. The U.S. EPA cancelled agricultural uses of both pesticides in 1970; termiticide uses were cancelled in 1987. Aldrin is readily converted to dieldrin in the environment and in plants that take up the chemical. Aldrin volatilizes after agricultural soil applications or is converted to dieldrin, which volatilizes more slowly. These chemicals persist in the environment and bioaccumulate in foods (Jorgenson 2001; USGS, 2007). Aldrin is rarely detected in plants or animal tissues,

Serum Aldrin (lipid adjusted)
Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval)

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 2275 1946

Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites

years 01-02 03-04

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

01-02 03-04 01-02 03-04

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

756 588 1519 1358

01-02 03-04 01-02 03-04

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

1057 946 1218 1000

01-02 03-04 01-02 03-04 01-02 03-04

* * * * * *

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD < LOD < LOD

559 456 512 485 1045 881

Limit of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 5.94 and 7.8. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Fourth National Report on Human Exposure to Environmental Chemicals

77

In a study of pesticide applicators with occupational exposure to aldrin. the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al. similar to results in a subsample of NHANES II (19761980) (Stehr-Green.. and seizures. the median serum dieldrin level was generally similar to the 90th percentile for females in this Report (Ward et al.Organochlorine Pesticides twitching. 78 Fourth National Report on Human Exposure to Environmental Chemicals ..6% of the subsample had dieldrin levels above the limit of detection (Stehr-Green 1989). 2000). 2000). 2005. both aldrin and dieldrin caused liver enlargement and liver tumors. 2004). Kanthasamy et al. Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al. vomiting. Epidemiologic and animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al.S. and the FDA monitors foods for pesticide residues. dieldrin at higher doses caused irritability. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. tremors.. When dieldrin was fed to pregnant rodents. Serum dieldrin levels at the 95th percentile in NHANES 2001-2002 and 2003-2004 subsamples were approximately ten times lower than the corresponding percentile measured in NHANES II (1976-1980). which may vary for some chemicals by year and by individual sample. The median level in pooled samples from New Zealand adults obtained in 1996-1997 was generally similar to the 90th percentile for adults in this Report (Bates et al. Danish women whose serum was collected in 1976 had a median dieldrin level near the 95th percentile for females in this Report (Hoyer et al..cdc. 1995). Survey Geometric mean (95% conf. nausea.e. 1987). IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity. EPA has established environmental standards for aldrin and dieldrin. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 2275 1946 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 756 588 1519 1358 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1057 946 1218 1000 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 559 456 512 485 1045 881 < LOD means less than the limit of detection for the lipid adjusted serum level.. OSHA has established workplace exposure standards for aldrin and dieldrin. seizures (Smith. 2005). environmental levels) and health effects is available from ATSDR at: http://www. The U. serum aldrin levels were below the limit of detection. In samples obtained between 1973 and 1991 from Norwegian women.html. 1991). Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al. Li et al.. in which only 10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 2004). 1998) and behavioral changes (Carlson and Rosellini.gov/toxpro2.. and occasionally. median levels of dieldrin were more than thirtyfold higher than the 95th percentile Serum Aldrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.. When fed to experimental animals. population from the National Health and Nutrition Examination Survey. Information about external exposure (i. 1989). but no estrogenic effect was noted in a study that used cultured cells (Tully et al.S. 2000...atsdr. 1998).

8-24.2) 14.147 (.4) < LOD < LOD 16.3 (13.100-.8) 14.2-15.4) 21.109-.40-9.1 (18.080-.90) 90th 15.075) < LOD . see Data Analysis section) for survey years 01-02 and 03-04 are 10.9 (12.100) .110-.4) 95th 20.4-18. < LOD means less than the limit of detection.1) 13.5 (<LOD-11.0) < LOD 9. population from the National Health and Nutrition Examination Survey.80-10.Organochlorine Pesticides Serum Dieldrin (lipid adjusted) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.3 (18.130 (.2) 12.S.242) .170) .5 (16.130) .7-19.0-25.083-.062 (.7 (<LOD-15.4) 539 456 484 487 980 885 Limits of detection (LOD.116) .140-.109 (.140 (.149) .182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .0) 19.00-14.40-10.130-.110 (.3 (18.190) .112) 95th .090 (.054-.6-24.096-.5-17.113 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD 9.070-.3-21.120-.160 (.5) 15.0-21.2) 15.4) 14.120 (.110) .139 (.9-23.103 (. Serum Dieldrin (whole weight) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Survey years 01-02 03-04 Geometric mean (95% conf.073-.8) 15.9 (14.9-22.4) 20.130) .5 and 7.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.124) .2) 11.9-38.069) < LOD < LOD .055 (. Survey years 01-02 03-04 Geometric mean (95% conf.80 (<LOD-10.4) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.8) < LOD 8.S.060) .150 (.090 (<LOD-.093) .063-. Fourth National Report on Human Exposure to Environmental Chemicals 79 .058) < LOD .080 (.102 (. population from the National Health and Nutrition Examination Survey.130-.103 (.064) 90th .30 (8.062 (.1) 20.3 (19.086-.1) 14.1-24.8-17.100-.8 (11.147) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .140) .9 (12.80-9.7 (14.10 (<LOD-16.110) .070) .8-19.139 (.5-15.1) 15.50) 15.070 (<LOD-.00 (8.059 (.160 (.138 (.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.130-.090-.110 (.190) .088-.089 (.1-18.6-24.120) .5) 21.138) .6 (15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (15.1-19.8.100 (.8-25.110 (.5-17.062-.120 (.109-.70 (7.5) 19.1) 15.50 (8.098 (.4) 19.054-.054-.4 (12.9 (13.053 (<LOD-.6 (14.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .4-17.077-.049-.090-.1-16.0) 21.130) .117) < LOD .080) . interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD .7) 15.064 (.160) .150 (.1) < LOD 9.6-33.0 (10.158) .180) .180) . which may vary for some chemicals by year and by individual sample.8 (9.100-.3 (14. which may vary for some chemicals by year and by individual sample.8 (18.1) 10.120 (.6) 9.101) .090-.112-.100) .60-10.30 (8.9 (13.4 (12.8-17.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.1 (13.6 (15.6) 19.048 (<LOD-.0 (11.108-.084-.7-22.056-.077 (.7 (15.6) 16.0 (10.

Daniel SE. Soto AM. 4/21/09 Bates MN. Eds. 6/1/09 Ward EM. Kanthasamy AG. United States Geological Survey (USGS). Rosellini RA. 4/21/09 Hoyer AP. Exp Neurol 1998. VT. et al.gov/toxprofiles/ tp1. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Ginsburg KS. Environmental Health Criteria 91.14:95-102. J Toxicol Environ Health 1989. Teta MJ. J Occup Environ Med 2005. Chapin RE. Li AA. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Grandjean P.cfsan. Demographic and seasonal influences on human serum pesticide residue levels. Chlorinated Hydrocarbon Insecticides. Revised Feb.150:263-271. September 2002. Fernandez MG. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Finding a measurable amount of aldrin or dieldrin in serum does not mean that the level of aldrin or dieldrin causes an adverse health effect. Pesticides in the Nation’s Stream and Ground Water. Mann D. 15. Tully DB.html. New York.54:1431-1443. Patterson DG Jr. Jr and Laws ER. 1991. Part A 2000. Six high-priority organochlorine pesticides.352:1816-1820. Ellis H. Hartvig HB. Environ Health Perspect 1995. Psychopharmacology (Berl) 1987. bioaccumulation. Mink PJ. Sanchez-Ramos J. Available at URL: http://www.26:701-719. Neurotoxicol 2005. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Wienburg CL. Narahashi T. Smith AG. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. pp. Frey JM. Aldrin and Dieldrin [online]. Carlson JN. Garrett N. Patterson DG Jr. Anantharam V. Edwards JW. 1992-2001. Vol.htm. either singly or in combination. Toxicological profile for aldrin/dieldrin [online]. Reprod Toxicol 2000. Available at URL: http://www. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Available at URL: http://pubs. Schulte P. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Available at URL: http://www. Academic Press. David VL. Handbook of Pesticide Toxicology. In Hayes WJ. Toxicol Lett 1992. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants.gov/ circ/2005/1291/. Buckland SJ.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Priestly BG.109(Supp1):113-139. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Chemosphere 2004. 731-915. Lancet 1998. McIntosh LJ. Organochlorine exposure and risk of breast cancer. Stehr-Green. Jorgensen T. Environ Health Perspect 2001. References Agency for Toxic Substances and Disease Registry (ATSDR). August 2008. Kanthasamy A.47:1059-1087. Shore RF. and epidemiology in the United States. Andersen A. Sonnenschein C.103(Suppl 7):113-122. No:429-436. Serrano FO.fda. Cancer Epidemiol Biomarkers Prev 2000.27:405-421. 2007 [online]. PA. Mumtaz MM. Facca A. Grajewski B.inchem. Finley B. Song S. are nonestrogenic in transfected HeLa cells. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.91(1):122-126. International Programme on Chemical Safety (IPCS). Basit A. and lymphocyte sister chromatid exchange. Inc. Corrigan FM. Jr. Olea N. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. toxicology.html.cdc. Roy ML. et al. Food and Drug Administration (FDA). Kitzazwa M. 4/21/09 Jorgenson JL. Needham LL. Chung KL. Turner W. J Toxicol Environ Health. 2 Classes of Pesticides.9:1357-1367. 1989. Cox. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress.59:229-234. plasma dieldrin. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.org/documents/ehc/ ehc/ehc91. Int Arch Occup Environ Health 1994.usgs.gov/~dms/ pesrpts.atsdr.66(4):229-234. Biomonitoring studies on levels of aldrin and dieldrin provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of aldrin or dieldrin than are found in the general population. Brock JW.64-65 Spec.

4 (10.1-65.4 (30.0 (16.1 (11. buildings.5.2) 36.7) 28.1-50.3) 18.4) < LOD < LOD < LOD 23.5-13.70 (<LOD-10. see Data Analysis section) for Survey years 99-00.9) 37.6) 49.2 (39.2) 22. foods high in fat such as meat. and in soil. 2007).5) 38.1 (<LOD-12.10-11.9) 17. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.9 (15.4 (31. in addition to trace amounts of numerous other related compounds (ATSDR.9 (11.0) 27.6) 20..3 (20.7-70.7) 31.90 (8.1 (15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-61. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.8 (10.3 (25.10-18.4 (<LOD-12.7-39.6 (9.9 (31.8 (17. heptachlor use has been limited to treatment of fire ants near power transformers.0) 75th 20.8-73.0-33.6) 36.2) < LOD 11.5) 9.4) 39.1 (17.2 (9.9-40.1 (44.7-12.2-28.6) 23.4-51. As a result of the manufacturing process.3 (28.7 (17.6) 9.8 (18.5-65.1) 16.1 (<LOD-12. and 03-04 are 14.0-13. and dairy products are the usual sources of exposure to these chemicals in the general population. 1994.3 (27.0) 41. 01-02. respectively.3 (21.1 (20.4-45.1) 90th 34.2 (10.8 (40. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.6 (43.9) 31.S. which may vary for some chemicals by year and by individual sample.1 (16.8 (42.6) 11.20-11.4 (22.8) 53.1) * 11.36-11.2-56.2 (41.5) 56.5 (33.5) 44.37 (8.1 (40.4-21.9) 39.0 (32.9) 10.8) 52.7-25.5 (<LOD-12.8) 18.3) 10. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.6-24.1 (<LOD-12.5 (8.5) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 11.3-43.5) 10.6-53.5 (41.3) 37.9) 23.1-51.6) 8. Technical grade chlordane had contained 7% trans-nonachlor.S.7 (34.7-14.4 (30.5.1) 30. Both pesticides are persistent in soils and sediments and have been detected in water from agricultural run-off and near production and disposal facilities (ATSDR.3) 18.9 (36.5-47.8-31. Survey Geometric mean (95% conf.7 (<LOD-13.5-32. from the early 1950’s until the mid-1980’s.0) 37.8-33. and 7.0-25.9 (26.6 (9.6 (25.2 (36.5-43.7 (19.3-49.9) 36.6) < LOD 11. Since 1992.82-11.7 (<LOD-32.4) 12.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.9) 47.5-38.74 (<LOD-10.0) 31. 1994).3 (<LOD-19.1) < LOD < LOD < LOD < LOD < LOD 8.3-45.2 (21.4) 37.7-56. fish.0 (37.2-26.0 (26.6) 9.4) 29. population from the National Health and Nutrition Examination Survey.5) 37.4) 22.2) 37.5 (34.2 (28.5-41.6-45.3) 10.8 (10.8-32.3-32.8) 44. 57-74-9 Heptachlor CAS No.9-42.10 (8.7 (34.0 (20.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9) 23.2-49.3-24.9) 11.1 (27.6) 48. Heptachlor and chlordane are somewhat volatile and may be detected in the air and dust of buildings long after treatment for termite or insect control (Whitemore et al.0-12.9-38. 2007).1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12. 10.5) < LOD < LOD < LOD < LOD 13. < LOD means less than the limit of detection.6) 39.9 (18.0 (<LOD-12.9 (26.3 (11.6-24.7 (10.7) 9.7) 35.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.6) 48.9 (21.9 (15. chlordane was used to kill termites and other insects on agricultural crops.Organochlorine Pesticides Chlordane CAS No.1) 22.0) 21.0-67.1-25.5-42.1-19.8-43.9 (17.8) 52. Consequently.8-33. which results in exposure to the fetus and nursing infant Serum Oxychlordane (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.8-42.5-40.8-23. the technical grade product of each chemical contains 10%-20% of the other chemical.7) 19.7) 19.3) 41.7 (32.8-20.30-11.2-21.4 (35.69-10.8) 27.7 (42.0-18.9 (11.4) 18.63 (8.9) 13.S. Fourth National Report on Human Exposure to Environmental Chemicals 81 .5-44.9-21.20-10.6-12.7 (43.2) < LOD 11.9 (29.5 (31. lawns.6-18.2) 46.6 (16.1-25.0-61.9-21.4-40.2 (37.4) < LOD 11.3 (9. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.3 (26.0) 20.89-10.3-45.9) 11.2-49. Chlordane is not currently produced or used in the U.20 (<LOD-11.8 (17.2) * 12.4-14.2) 34.5) < LOD < LOD 9.1 (25.5) 21.8.2) 33.1) 30.1-15. Until 1988.1) * 11.7) 42.

080 (.430) .110-.063 (.063 (.300-.220-.165-.133) 90th .048-.128 (.240-.120-. 2001.120 (.070 (<LOD-. and alterations in immune function of offspring.560) .200-.146) < LOD < LOD .300) .360) .210 (.373) .287) .253-. which may vary for some chemicals by year and by individual sample.073) < LOD < LOD < LOD < LOD .230-.146) .050 (<LOD-.140 (.190-.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .068) .210-.300) .220-.280-.130-..063) .160) .076) < LOD .348) ..170) .149 (.100-.100 (.180) .S.320 (.170) .269 (.104) .140 (.056 (.213) * . 82 Fourth National Report on Human Exposure to Environmental Chemicals . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity. which is also persistent in the body (ATSDR.260-.140 (.315 (.070) < LOD < LOD < LOD < LOD < LOD .057-. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR. Le Marchand et al.203-.310) ..207) .410) .115-.049 (<LOD-.126 (.112 (.070-.331) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .058-.220 (.170-.063) * . 1996.280 (.S.223) .080) . Information Serum Oxychlordane (whole weight) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.210 (.207 (.130 (.450) .130 (.189 (.079) < LOD < LOD < LOD .062) < LOD .070 (<LOD-.070 (<LOD-.315) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.270 (.286 (.230 (.130) .119 (.290-. heptachlor.200-.120-.430) .068-.290-. The major metabolite of heptachlor is heptachlor epoxide.080 (.073 (.070-.370 (. 1981).246-.189-.057) * .066 (<LOD-.055-.260 (.350) .053-.280 (.100 (<LOD-. Chlordane is metabolized primarily to oxychlordane and to a lesser extent. 1977b. neonatal mortality.130-.082 (.300) .070) .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * . Smith.230-. Survey Geometric mean (95% conf. to heptachlor. 2002.260 (.168-.070 (. 1986).090) .070 (<LOD-.071 (.310 (. and inhalation exposure.074-.077) .286 (. EPA has established environmental criteria for chlordane and heptachlor.150-.053-..092) .077) .148-. 2007.110 (<LOD-.350 (.310) .104-. and heptachlor epoxide in foods and bottled water.160) . Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.240-.170) .160) .250 (.270 (. 1991). population from the National Health and Nutrition Examination Survey.300) .230-. 1991.350 (. characterized by seizures and paralysis.077) .140-.057 (.510) .120-.227) < LOD . OSHA has established occupational exposure criteria. and the U.300 (.160 (.320) .242-.091) .340) .330 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.077) .126) .290) . Chlordane and heptachlor are absorbed after oral.200-.225 (.083 (.280-.450) .061-.290 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Acute.370 (.148) .050-.290-.087-.075 (.058 (. chronic doses of heptachlor have produced liver enlargement and injury.440) .180-.258-. Takahashi et al.130-.370 (.240) .090) . IARC.245-.231) . In laboratory animal studies.130 (.302) .290) . FDA established allowable residues of chlordane.090-.069 (<LOD-.115 (.280-. 2006).083) .250 (.271 (. 1986).216-.400) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .130) .150 (.067 (.047 (<LOD-.204 (.060 (<LOD-.066-.180-.066-. The U. 2007).063 (. Shindell and Ulrich. Elimination of all these chemicals from the body occurs over months to years.230 (.140) .320 (.150) .150 (.140 (.320) .190-. dermal.240 (.140-. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.260 (.130-.380) .079) .108-. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.310) .Organochlorine Pesticides (Dallaire et al. 1977a.270 (.258 (.063 (.136) .130-.170) . and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.320 (.080) .068) 75th .320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .280) . IARC considers chlordane and heptachlor as possibly carcinogenic to humans.058-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.070-.065-.150 (.199-.064) < LOD .066 (. and breast milk is a major excretion route in lactating women.320 (.080) .200 (.100-.400) .180) .340) .310-.250-.063-.106-.190-.S.170) . Rogan.230) .208 (.

2006). For the exposed persons drinking milk in the Arkansas episode. 2004).gov/toxpro2. 2002). transnonachlor. respectively. 2001-2002. than the 90th percentile values of NHANES 1999-2000 (Baker. In the Hawaii episode.. In serum samples obtained in between 1994 and1997 from Inuit women in different Arctic countries. Biomonitoring Information Serum oxychlordane and trans-nonachlor levels in NHANES 1999-2000. the mean serum heptachlor epoxide and oxychlordane levels were more than twice as high. respectively.e. A recent assessment of heptachlor is available at: http://www. or heptachlor epoxide in serum does not mean that the level of oxychlordane. Finding a measurable amount of oxychlordane. Serum transnonachlor levels among females in the NHANES 19992001 subsample were about one half the levels obtained between 1994 and 1996 from women in New York (Wolff et al. 2003).. Biomonitoring studies on levels of oxychlordane.. A small sample of Polish women had mean levels of oxychlordane and trans-nonachlor that were about fivefold lower than in females in the NHANES 20012002 subsample (Jaraczweska et al.htm#ref. 1993).atsdr. mean serum heptachlor epoxide and oxychlordane levels were about sevenfold and threefold higher. Biomonitoring data can also help Fourth National Report on Human Exposure to Environmental Chemicals 83 ...Organochlorine Pesticides about external exposure (i. inchem. from ATSDR at: http://www. Two episodes (one each in Arkansas and Hawaii) of inadvertent heptachlor contamination of dairy cattle feed occurred in the early-to-mid 1980’s. or heptachlor epoxide causes an adverse health effect.cdc.. the reported oxychlordane and trans-nonachlor geometric mean levels from Canada and Greenland groups were about threefold to fivefold higher than among females in this Report (van Oostdam et al.. resulting in human exposure to heptachlor epoxide that was excreted into the milk.html.org/documents/cicads/cicads/cicad70. Levels of heptachlor epoxide among females in this Report were approximately one tenth of the corresponding 90th percentile for a cohort of pregnant women in California studied from 1963 to 1967 (James et al. transnonachlor. 2000). environmental levels) and scientists plan and conduct research on exposure and health health effects of chlordane and heptachlor is available effects. trans-nonachlor. 1988). and 2003-2004 subsamples were comparable to levels measured in Swedish women from 1996-1997 (Glynn et al. than the 90th percentile values of NHANES 1999-2000 (Stehr-Green et al. and heptachlor epoxide provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of heptachlor and chlordane than are found in the general population.

9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.S.6 (8.8 (<LOD-23.7 (16.3) 18.9-23.9 (12.0-54.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6 (16.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9-25.8) 19.0-17.8) 21.1-29. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-21.3) 18.5 (11.8-23.7-19.8) 19.50) < LOD < LOD < LOD 17.7-25.4 (<LOD-54.8) 13. Survey Geometric mean (95% conf.4) 18.8) 16.2-27.6 (<LOD-27.2-17.8) 14.6) < LOD < LOD < LOD 27.0-16.9-16.3) 16.6) 22.2-16. respectively.4 (<LOD-19.8-24.3 (13.8 (15.3-18.8-24.1-16.40) 15.1) 13.8 (18.3) 23. 01-02.1) 20.8 (13.7 (10.9 (15.5 (<LOD-32.5) 19.5.3) 10.8 (13.90 (<LOD-9.6 (13.9-29.8-46.6 (16.5) < LOD 14.2) 15.2 (<LOD-62.4 (11.2 (<LOD-25.0) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.3 (<LOD-25. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.2) 26. which may vary for some chemicals by year and by individual sample.6 (12.6.8) 14.6 (14.0-17.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.8) 13. population from the National Health and Nutrition Examination Survey.0) 13.7-18.2-27.5 (10. see Data Analysis section) for Survey years 99-00.7 (13.2 (18.3) 27.5 (11.9) 15. and 7.8) 15. 84 Fourth National Report on Human Exposure to Environmental Chemicals .8-24.6) 14.0-19.3) 18.0 (11.4 (11.8.4) 21.8 (18.3) 22.6 (11.2) 13.1 (16.4 (15.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.6-17.9-29.1 (19.2 (<LOD-16.5 (<LOD-21.6) 13.10-13.8) 20.20 (<LOD-9.1-38.5 (18.0 (15. < LOD means less than the limit of detection.1-15.2) 20.1) 23. and 03-04 are 14. 10.

130 (<LOD-.077-.180) .150 (.101 (.087 (.071-.090-.170 (.090-.111-.130-.310) .077-.130-.130 (.S.120 (<LOD-.113) .117) .180) .082-.100 (.135 (.240) .180 (.067-.135 (.130) .090-.120) .098 (.130-.106-.190) .190) .110-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .090 (.110) . which may vary for some chemicals by year and by individual sample.113-.173) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200 (.Organochlorine Pesticides Serum Heptachlor epoxide (whole weight) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.100-.150 (.096 (.180) .149) .100 (.128 (.310) .108) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .090 (<LOD-.094 (. population from the National Health and Nutrition Examination Survey.173) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .090-.190 (.380) .270) .090-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120-.150 (<LOD-.063) .200) .110 (<LOD-.170) .055 (<LOD-.140-.100 (<LOD-.140) .170 (.110) .094 (.120 (<LOD-.126 (.111) .116) < LOD < LOD < LOD .074-.170) .180) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.130) .100-.069 (.100 (.161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .130-.104) .107-.053-.100 (.133 (.190) .120 (.180 (<LOD-.076-.057 (<LOD-.157) .110-.140) .200) .110 (<LOD-.101 (.108-.063) < LOD < LOD < LOD .170 (<LOD-.170) . Survey Geometric mean (95% conf.220) .097) < LOD .170 (.110 (.108) .110 (.180) . Fourth National Report on Human Exposure to Environmental Chemicals 85 .090-.120) .070-.

5) 26.1) 17.8-90.6) 34.9 (15.5-111) 68.3) 18.8-79.4-23.5-95.8 (11.4) 48.0-143) 112 (68.6) 10.3-57.1-55.7-32.0-93.6-20.4) 19.1) 17.0 (15.0) < LOD < LOD 8.7-17.0 (15.8-90.4 (16.6-82.8) 51.0-20.6 (<LOD-14.3 (56.4-35.2-23.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.9 (28.3-86.6-54.2-16.2-37.9-69.8 (49.6 (15.2-17.6 (50.3) 25.6-22.8 (<LOD-20.7 (30.9) 51.0 (16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5. respectively.3 (45.9 (19.8 (71.4) 59.2) 17.0-24.4 (11.7-160) 86.2 (7.9-45.8-41.2 (59.8 (28. see Data Analysis section) for Survey years 99-00.8-16.7 (74.1-34.1) 17.0) 49.6) 25. and 03-04 are 14.1) 16.1-34.0-23.5 (15.0 (48.8-16.7 (18.0 (42.2) 19. 01-02.6 (16.1) 78.4 (12.6 (52.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.9 (51.0 (62.0 (14.7 (16.7-18.2-18.8-21.3) 32.6) 84.7 (35.7-35.9 (29.1) 62.5) 78.5 (13.3-21.7) 56.2 (14.6 (57.1 (65.5) 35.4) 16.8-67.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.0-22.1-16.8) 19.8 (13.7) 52.2-88. which may vary for some chemicals by year and by individual sample.2) 20.1) 17.9 (<LOD-14.7-113) 68.1) 18.5) 36.4-22.1 (41.5) 30.1) 78.3 (17.2) 39.8-19.8) 80.7) 73.8-19.5 (44.86-13.9-36.2 (27.1 (17.7-34.6) 60.7) 28.4 (67.3) 30.8 (26.5-69.0 (13.1) 17.8.6) 13.0-23.1) 31.4-18.7) 59.8 (16.3 (58.7) 14.2 (25.1-16.5.8 (17.8-110) 59.7 (13.1) 17.0-59.3-50.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.9-35.7 (11.9-58.0 (42.8 (13.3 (14.9 (66.4-36.6) 54.5-19.3) 19.2) < LOD 10.1) 30.6) 82.5) 77.4-62.0) 13.9-64.3) 36.0-93.3 (49.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.7) 15.8 (28.2) 34. population from the National Health and Nutrition Examination Survey.4) 20.0) 33.9 (36.9 (15.7 (59. and 7.9-65.9) 14.9 (51.4 (28.1 (47.5 (15.0 (16.9-65.6 (56.9-40.3-58.8-77.5) 14.3) 16.1) 32.2 (15.5) 48.6-19.4 (45.0-123) 74.7) 78.8 (28.3) 30. interval) 18.5) 9.8 (42.2-21.6 (12.0-37.6-88.2) 30.6 (32.0-113) 68.8 (26.2) 59.8-129) 74.0 (19.S.8) 47.3-30.0) 19.1-51.8 (45.8 (26.5) 19.9) 14.7-29.1) 18.3) 18.3 (14.7-22.9-89.4) 55. 10.70 (<LOD-12.1 (22.4) 107 (84.7 (28. < LOD means less than the limit of detection.7) 35.3) 15.9-22.9 (47.9) < LOD < LOD < LOD 20.0 (60.1) 17.0 (13.5-87.5-36.6) 56.6) 56.2 (36.0 (29.3 (16.5 (25.2 (19.5) 22.2 (60. 86 Fourth National Report on Human Exposure to Environmental Chemicals .0-38.3) 32.1 (48.1-22.2-18.5) 90th 55.8 (19.1-18.7-23.1-20.2 (26.1-28.7-38.10 (<LOD-11.4-67.8 (30.8 (12. Survey Geometric mean (95% conf.7 (59.7) 78.1) 14.0) 18.2 (14.9-20.5-17.7-77.3-39.0) 40.5 (45.1 (10.6-66.0-68.1-126) 67.3-32.5-20.5) 14.7) 17.6 (56.7-20.7-21.2 (64.0) 75th 31.3) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.3-74.5) 20.4 (30.9) 51.9 (16.8 (15.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.4-52.

090 (<LOD-.100-.060-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .420 (.220 (.210 (.109 (.205 (.180-.130) .140) .120 (. Fourth National Report on Human Exposure to Environmental Chemicals 87 .096-.127) < LOD < LOD .114) .490-.242) .520 (.120) .103 (.460-.470-.400 (.237) .220 (.580 (. which may vary for some chemicals by year and by individual sample.409-.470-.116-.105 (.Organochlorine Pesticides Serum trans-Nonachlor (whole weight) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.310) .069) .109 (.191 (.082) .090-.100 (.071 (<LOD-.100-. interval) .390 (.113) < LOD .130) .960) .360-.161-.272-.594) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .288 (.098 (.461 (.090-.490 (.060 (<LOD-.390 (.380 (.684) .068-.340-.420) .690) .310 (.170 (.430-.098 (.400) .069-.087 (.630) .117) .161) .410-.095-.210) .500) .131) .450) .120-. Survey Geometric mean (95% conf.084-.116 (.112 (.124) .108) .930) .128 (.250) .081-.080-.565) .120) .079-.340-.330 (.355 (.177-.840) .085-.340) .594) .20) .395-.310-.220) .110 (.145-.250) .061-.760 (. population from the National Health and Nutrition Examination Survey.070 (.280) .100-.460) .288-.390 (.060) .120) .190-.590) .090-.171-.090-.110 (.186-.104-.085-.460) .310-.324 (.094 (.400-.210) .081 (.103 (.400-.440-.091-.240 (.490) .129) .680) .440) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.260) .078 (.301-.210-.220 (.120-.290-.590 (.240) .270-.130) .120) .285-.510 (.397-.100-.559) .390) .510-.190-.130) .130 (.110 (.041 (<LOD-.106 (.110-.573 (.630) .470 (.520) .576) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 < LOD means less than the limit of detection for the lipid adjusted serum level.220 (.090-.430-.600 (.125) .079-.540) .190-.108) 75th .080 (.130) .220 (.097) .580 (.320-.300-.085-.651) .093-.190-.090 (.310-.600) .480) .310-.090) .130) .106 (.210 (.405) .470 (.202 (.093-.497-.232) .111-.141) .430-.240) .055 (<LOD-.234) .237) .130) .211) 90th .090-.158-.330-.096-.390-.100 (.160 (.630) .490 (.S.125 (.210 (.080-.180-.119) Selected percentiles ( 95% confidence interval) Sample 95th .360-.108 (.400 (.183 (.130 (.210-.092 (.590 (.580 (.190-.092 (.134) .830) .327 (.047-.099-.367) .180-.096) .160-.300) .210) .110) .150) .343 (.120 (.470 (.186 (.317 (.240) .173-.111 (.091) .190-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .150) .054-.113) .122) .260) .104 (.220 (.089 (.098) .120-.093) .110 (.370 (.350-.550 (.120 (.119) < LOD < LOD < LOD .390) .690) .110 (.098-.116) .680 (.110 (.220 (.099-.080-.410-1.330-.520 (.830) .078-.126) .240-.370 (.395) .250) .141) .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .112 (.390 (.106 (.220 (.371) .230 (.080-.135 (.062 (.640 (.279-.093-.350 (.417 (.800) .122) .320-.080) .286-.458 (.414 (.

Drews K. Jr and Laws ER.372:20-31. J Occup Med 1986. In Hayes WJ. Brower S. Charles MJ.150:981-990.html. Voorspoels S. 1993. Hansen JC. 1994-1997 organochlorine compounds. A Report to the Hawaii Heptachlor Research and Education Foundation. Saidein D. Willman E. Available at URL: http://www. Vol. Muckle G. 4/21/09 James RA. Chlorinated Hydrocarbon Insecticides.org/documents/iarc/ vol79/79-12.pdf. Organochlorines in Swedish women: determinants of serum concentrations. 731-915.50(3):108-118. Dewailly E. Glynn AW. Hawaii Med J 1991.htm.259(3):374-377.niehs. Bull Environ Contam Toxicol 1981:27:506-511. Lulek J. Environ Res 2000. Baker DB. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Senie R. gov/toxprofiles/tp12.org/site/foundation/ research/projects2. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Pollutants in breast milk. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Sci Total Environ 2004. Arch Pediatr Adolesc Med 1996. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Siegel BZ. Environ Health Perspect 2002. 9/25/07 International Programme in Chemical Safety (IPCS). Available at URL: http://www. Inc.110(8):835-838. Tartter P.inchem. Toxicological profile for heptachlor and heptachlor epoxide [online]. et al.gov/toxprofiles/tp31. Circumpolar maternal blood contaminant survey. International Agency for Research on Cancer (IARC) . 4/21/09 Dallaire F. Environ Health Perspect 2003. Concise International Chemical Assessment Document 70 Heptachlor [online]. Wong L. et al. Berkowitz GS. Takei G.inchem. Academic Press. 2001. Van Oostdam JC. Ayotte P. 1963-1967. National Toxicology Program (NTP). Gilman A. Available at URL: http://ntp.8:1-123. Loo S. Organochloride pesticide residues in human milk in Hawaii. Shindell S and Ulrich S. Bjerselius R. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Eds. Canada).41:145–148.nih. Laliberte C. Keller JA.84:151-161.111:349355. International Agency for Research on Cancer (IARC). Jaraczewska K. Toxicological profile for chlordane [online]. Environ Health Perspect 2002. 2 Classes of Pesticides.gov/ntp/ htdocs/LT_rpts/tr008. 2006. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Atuma S.html. 6/1/09 National Toxicology Program (NTP). Odland JO. Wohlleb JC. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Wolff MS. Stehr-Green P. Vol. Chlordane and heptachlor [online]. Hertz-Picciotto I. Barker J. Lawrence River (Quebec.Summaries & Evaluations. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.110:617-624.9:1-109. Poland. maternal serum and milk from Wielkopolska region.cdc.heptachlor. Smith AG. 1991 pp.html. Covaci A. KalubaSkotarczak A. Takahashi W.atsdr.atsdr. Dewailly E. Sci Tot Environ 2006. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Mortality of workers employed in the manufacture of chlordane: an update. New York. et al.niehs.28:497501. August 2007. Granath F. Darnerud PO. May 1994. 1986. Bioassay of heptachlor for possible carcinogenicity.330:55-70. LeMarchand L. JAMA 1988. Dendle WH. 79. 4/21/09 Baker DB. Aune M. 6/1/09 Rogan WJ. 1979-1980. Bioassay of chlordane for possible carcinogenicity.org/ documents/cicads/cicads/cicad70. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). et al. Available at URL: http://www. Organochlorine exposures and breast cancer risk in New York City women.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).gov/ntp/ htdocs/LT_rpts/tr009.pdf. Royce W.cdc. Available at URL: http://www. Arch Environ Health. Available at URL: http://ntp. Kolonel LN. Jr.htm. Head SL. Distribution of polychlorinated biphenyls. Chashchin V. Handbook of Pesticide Toxicology. Bleiweiss IJ.nih. Available at URL: http://www.

1’-(2.S. In the body.0-35. which may vary for some chemicals by year and by individual sample.3) 28.70 (8.3 (<LOD-21.7) < LOD 18. although DDT and DDE intakes have decreased over time (FDA.7. DDT is converted in the environment to other more stable chemical forms.50-11.8) 15.10-13.5 (14. or dermal exposure.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.1 (<LOD-39.1) 31.S.1 (33. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR. which is a mixture containing p. air.7 (15.5) 23.5) 25.0 (18.8) 36.0-27.3 (<LOD-31.2) 30.9 (10.0) 19.10 (<LOD-12.3-16.6 (31. inhalation.3) 22.5 (23.5-36.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.1-71.4) < LOD 17. DDT usually refers to the technical product.8-39. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 01-02.5-54. 1991). 2008.3 (27.2-95.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11. The biodegradation half-life of DDT in soil varies from 2 to 15 years.4. DDT is converted to DDE and several other metabolites. Food imported from countries that still use DDT may contain the chemical or its residues. 1991).8.9 (<LOD-20.0) 40.8) 30. see Data Analysis section) for Survey years 99-00.0-37. In the general U. depending on conditions. and dairy products. DDT can be absorbed after ingestion.p’-DDD (4% or less). food. resulting in fetal exposure.0 (10.0-155) 83. It is still used in some countries.6 (25. Both Serum p.0-15. Fourth National Report on Human Exposure to Environmental Chemicals 89 .2) < LOD < LOD 9.5) < LOD < LOD 9. population.7) 677 756 595 1002 1549 1370 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 10.S.9 (10.2) 155 (59.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 12. including 1.8-17.9 (21. 50-29-3 General Information Dichlorodiphenyltrichloroethane (DDT) has been used widely as a broad spectrum insecticide in agriculture and for control of vector-borne diseases.p'-Dichlorodiphenyltrichloroethane (DDT) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.0 (18.2-65. and 7.9 (10.2 (<LOD-40.7) 12.9) 14. p.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2 (11.0-53. Only a small proportion of DDT is metabolized and excreted (Smith.3-590) 293 (104-541) 48. fish.0) 20.7 (19.9) < LOD < LOD 9.1 (23.5 (15.8) 799 1073 959 880 1232 1006 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8. when virtually all use of it was banned. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. sediments. 2002.6 (9. It was produced and used in the U.90 (<LOD-12.6 (22.5 (23.8-26. < LOD means less than the limit of detection. particularly for endemic vector and malaria control.p’-DDT (65%-80%). and 03-04 are 20.7-16. Gunderson. respectively.0 (21.6-33. These chemicals are highly persistent in soil.3) 21. 1988).0) 26.2-bis(p-chlorophenyl) ethane (DDD).1-27.3) 21.p’-DDT (15%-21%).00 (<LOD-10. after World War II until 1972.4 (23.6 (<LOD-25. DDT was used at one time as a treatment for head and body lice. and water. DDT and DDE can cross the placenta.9) 17. as well as in plant and animal tissues.3-236) 24. particularly meat. Smith. and trace amounts of several related compounds. continues to be the primary source of DDT exposure.8-23.1’-dichloro-(2.9-34.9-28. o. 17.4) < LOD < LOD < LOD 61. population from the National Health and Nutrition Examination Survey.9) 29.

130 (<LOD-. 2006. In laboratory animals. 2006).g.150 (<LOD-.120-.105-.530 (.00 (.078 (. 2001).220) .086 (.098-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e..140-.059-.160-.107) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.170-..167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .290) . 1995.150-.p'-Dichlorodiphenyltrichloroethane (DDT) (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Reproductive effects in humans affecting birth weight.150) .p’-DDE can produce anti-androgenic effects (Gray et al.190 (.114-.071-. Beard.180 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 1956).190-1.087 (.250-1.180) ..080-.120 (<LOD-.203) . both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.128 (. 2002.189) 677 756 595 1002 1549 1370 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and seizures. and leukemia have also been inconclusive (ADSDR.313 (.048 (<LOD-.207) 799 1073 959 880 1232 1006 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and o. Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR. fertility.230) .34) .230) . population from the National Health and Nutrition Examination Survey...078-. Mariussen and Fonnum. 2004. Survey Geometric mean (95% conf.420) .140) . lung cancer.075) 1.00) . Animal studies reported reduced fertility. In high dose.079) < LOD < LOD . 1997).095) < LOD . Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. overt signs of acute human toxicity include vomiting.250 (..Organochlorine Pesticides chemicals are excreted in breast milk. 2006).62 (.143) < LOD < LOD .170) . 2002. 1996). 1998). Longnecker et al. 2001). have not been consistently demonstrated (Beard.26) 1. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard. other organochlorines.130-. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.069) .132-.01) .530) . polychlorinated biphenyls.063 (<LOD-. dioxins and furans).130 (<LOD-.065-. and duration of lactation. tremor.071 (.068-..260) . Calle et al.112 (.150 (<LOD-.189-. premature delivery.570-4. 2006. Jusko et al.180) .061) < LOD < LOD < LOD .106) < LOD < LOD .200 (. Studies of DDT exposure and pancreatic cancer.p’-DDD and p.054-. Snedeker.097) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2002. 90 Fourth National Report on Human Exposure to Environmental Chemicals ..400) . Hayes et al..343) < LOD .064 (. and altered behavior after neonatal exposure (Eriksson and Talts. 2002.180 (.. Gladen and Rogan.201 (.. which may vary for some chemicals by year and by individual sample. accidental exposures.150-.146 (.S.146 (.190 (. resulting in exposure to nursing infants (Rogan.627) .240 (.180-.106) .. 2006). Jusko et al.051 (<LOD-. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.106-. DDT may bind to estrogen receptors (Chen et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (.142 (.084 (. 2000.170 (. 2001). A workplace standard for DDT has been established by Serum p.220) .240) .330-4. 2006. reproductive organ abnormalities.108 (.074-.130 (<LOD-. 2001). Gray et al.

More information about external exposure (i. Compared to females in the NHANES 1999-2000 subsample.e. and 03-04 are 18.6 (81. 2005). population declined by about fivefold to tenfold. EPA at: http://www.S. Median DDE levels among a population-based sample of Swedish women in 19961997 were similar to females in the NHANES 1999-2000 subsample (Glynn et al. population from the National Health and Nutrition Examination Survey. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person.. Fourth National Report on Human Exposure to Environmental Chemicals 91 . NTP considers DDT as being reasonably anticipated to be a human carcinogen. 2002. Since the 1970’s. Smith. 2004). mean serum levels of DDT and DDE in the U. IARC classifies DDT (p.gov/ pestcides/ and from ATSDR at: http://www.cdc. 1991). 1998. Survey Geometric mean (95% conf. environmental levels) and health effects is available from the U. In a population-based sample of men and women from eastern Slovakia.S.. 8. 2003.. Declining DDE levels over time have also been observed in the German population. A study of New Zealand adults sampled in 1996-1997 reported median DDE levels that were about threefold higher than the median for adults in the NHANES 1999-2000 subsample (Bates et al. Heudorf et al.p’-DDT) as a possible human carcinogen. Biomonitoring Information DDE persists in the body longer than DDT. 2002.gov/ toxpro2. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. respectively.Organochlorine Pesticides OSHA and a guidance established by ACGIH. and 7. respectively...0-114) 269 (213-323) 285 (249-337) 233 (175-314) 185 (141-237) 213 (172-253) 167 (123-240) 608 (530-693) 695 (595-798) 557 (420-734) 339 (243-479) 319 (282-389) 341 (211-586) 1260 (1030-1550) 1480 (1310-1700) 1270 (877-1800) 528 (339-812) 456 (343-722) 522 (313-1430) 2020 (1520-2730) 2550 (1980-3080) 1990 (1500-2470) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 249 (220-283) 285 (252-323) 235 (193-288) 270 (226-322) 305 (273-341) 241 (193-301) 223 (182-262) 248 (222-285) 200 (164-262) 234 (184-302) 256 (219-297) 207 (161-281) 494 (380-578) 520 (441-627) 466 (331-653) 601 (492-711) 708 (567-844) 539 (386-735) 1010 (789-1130) 1160 (937-1360) 1000 (763-1400) 1350 (1040-1720) 1480 (1410-1710) 1250 (813-1900) 1430 (1080-2160) 1900 (1580-2490) 1610 (1210-2320) 2210 (1570-2810) 2670 (1940-3300) 2010 (1500-2450) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 674 (574-792) 652 (569-747) 444 (362-545) 295 (241-362) 324 (262-400) 262 (233-295) 217 (189-249) 253 (226-284) 208 (165-263) 624 (545-701) 561 (455-690) 373 (283-522) 251 (199-313) 248 (223-296) 216 (173-267) 194 (162-238) 225 (203-254) 177 (148-238) 1350 (1090-1660) 1400 (1050-1950) 875 (608-1170) 668 (492-874) 762 (583-999) 589 (453-747) 438 (355-507) 463 (402-558) 417 (302-564) 3090 (2040-4950) 4110 (2520-6550) 2150 (1520-2470) 1850 (1040-2220) 1620 (1180-2980) 1620 (1130-2310) 825 (647-1010) 1150 (878-1340) 907 (574-1480) 4950 (3070-9350) 7080 (3080-15600) 3290 (2380-9240) 2300 (1560-5680) 3260 (1270-6900) 2860 (1880-3440) 1160 (1010-1350) 1640 (1410-1940) 1490 (909-2300) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites Limit of detection (LOD. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al... see Data Analysis section) for Survey years 99-00. for males and females in the NHANES 19992000 subsample (Pavuk et al.7-119) 113 (100-140) 93. compared to levels observed in this Report (Anderson et al.html. 2003). Stehr-Green.. 1989). 01-02. interval) 260 (226-298) Selected percentiles ( 95% confidence interval) Sample 95th 1830 (1410-2300) 2320 (1830-2780) 1860 (1400-2380) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 226 (184-278) 251 (228-278) 203 (163-275) 75th 537 (476-631) 598 (521-699) 509 (376-655) 90th 1150 (976-1350) 1410 (1210-1500) 1170 (836-1570) 295 (267-327) 238 (195-292) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 118 (102-135) 124 (106-146) 105 (84. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.3. Link et al.p'-Dichlorodiphenyldichloroethene (DDE) (lipid adjusted) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.8.atsdr. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.epa.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.6. In general.S. 2004).

623 (.69 (.18-4.37-10.01-15.40-4.34-11.5) 5.10-5.01-1.6 (8.51) 1.21) 3.32-1.456 (.18-3.75 (8.36-2.965-1.00 (.59 (4.24-17.99) 1. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.81-18.53-15.78 (4.77 (1. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.19) 4.9-17.4 (8.16-1.55-9.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.590 (.57-2.85-10.2 (9.6) 9.91 (6.37 (1.85-4.26 (1.963-1.30 (1.0 (9.83 (1.419-.59) 6.45 (1.63 (1.385-.02 (2.72) 1.870 (.6) 8.06) 1.51-8.5) 7.57-3.75 (4.80) 1.97-4. Survey Geometric mean (95% conf.71) 12.04 (6.14) 2.9-38.25) 8.76) 1.54 (1.82) 1.646) .32-1. 1989).59 (1.52 (1.2 (6.63 (1.39-1.39) 1.6) 13.66) 3. less than one percent had detectable serum levels of o.4 (12. Finding a measurable amount of p.50 (2.68) 2.52 (3.68 (2.5) 16.57 (1.91-3.97 (3.45 (1.88-35.14-9.80 (2.31 (1.00 (6.430-.91-2.66) 4.57 (1.7) 9.29 (1.68-4.28) 1.39-2.53 (2.06) 3.7-48.4) 13.1) 40.680-1.37-1.7) 13.81-5.48 (6.03-1.47 (1.14) 2.60-13.4) 9.57) 2.34 (7.48-4.41 (1.17 (3.534-.30 (1.3 (9.49 (1.1) 12.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.994-2.07) 1.81 (1.96) .65) 1.50-17.796 (.4-19.02) 1.9 (26. or p.. In a subsample of NHANES II (19761980) participants.82 (1.14-1.12 (.19-14.14 (1.22-1.70-3.93 (7.25 (.11 (2.2 (19.500-.56-3.40-8.17-3. In the NHANES 1999-2000.46 (1.860 ng/L) and DDE (about 14.90) 22.3-43.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.8 (13.36-11.46-2.22 (7.76 (2.Organochlorine Pesticides nearby agriculture (Botella et al.25-16.561 (. population from the National Health and Nutrition Examination Survey.54-7.10) . considerably higher than levels in this Report (Smith.91) 3.84 (3.84-3.37-4.557) 1.18-1.520 (.635) 1.6 (9.26) 3.80) 1.02-8.62-6.37-16.56) 2.34) 6.8 (14.2 (9. Serum p.26-10.75) 1.53) 7.27-1. 1991).31-2.2) 19.31-12. 2005).49) 8.75) 2.07) 1.03-4.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.25) 1.43-4.8) 15.07 (5.53) 1.92) 1.32) 1. 1971).58) 1.57-13.01-11.516 (.63 (6.7-20.7 (8.59 (1.56-6.47) 3.8-90.70) 1.34) 2. 2004).51) 3. serum levels of o.55 (2.6 (7..43 (5.05 (3.41-12.01-5.40-4.24 (1.12 (6.01) 1. 2004).18) 1.49 (1.63-15.76-3.01) 1.81) 11.6) 9.600) .18-1.64) 3.4) 14.38 (1.38 (1.3) 13.20 (.01-1.8 (13.3) 16.890-1.0 (12. 309 versus 268 ng/g lipid.46 (1.5) 10.61-2.59) 3.2) 26. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.p’-DDT were below the limits of detection. o.27) 3.25 (1.01-11.36 (3.7-19.25-14.71 (6.66-17.18 (6.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .32 (1.30-1.32-9.66-4.8 (9.3) 10.16 (2.24) 1.90-8.66) 1.66) 1.6) 9.36) 3.13) 4.26-2.69) 8.0) 2.9) 7.34-3.54) 8.81 (7.S.87-16.72) 1.58) 1. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.32 (1.35) 1.49 (6.51 (1.51-49..820-1.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.2-32.09-1.43-8.43-4.80) 3.p'-Dichlorodiphenyldichloroethene (DDE) (whole weight) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.85 (1.00-1.75) 6.0) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites 92 Fourth National Report on Human Exposure to Environmental Chemicals .77 (1.13 (1.40 (3.p’-DDT (Stehr-Green.21) 90th 7.30-1.04-1.12-1.05) 1.69 (2.15-4.726) .11-1.88 (2.10-1.52-6.58) 75th 3.6) 11.10) 2.9) 5.92 (3.64-2.66-2.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.1 (8.611-1. interval) 1.44) 1.22) .p’-DDT.96) 1.6) 12..1 (9.6) 9.33-1.5) 22.71 (5.56-2.3 (8.00) 7. High mean levels of whole blood DDT (about 3.69 (1.57 (3.9 (15.6 (17.36-1.39 (3.13-2. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE than are found in the general population.65 (1.71) 32.87 (5.61 (1.1) 7.92 (3. 2001-2002 and 2003-2004 subsamples.p’-DDT.76) 1.23 (7.51-15.79) 4.488-.7) 16.730) .69) 4.

respectively.S. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 93 . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4. 17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7. 01-02. and 03-04 are 20. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.8.Organochlorine Pesticides Serum o. and 7.

Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.p'-Dichlorodiphenyltrichloroethane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. 94 Fourth National Report on Human Exposure to Environmental Chemicals .Organochlorine Pesticides Serum o.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.

162:890-897.cdc. Davis MD. Sci Tot Environ 2006. Talts U.106(5):279-289. Lancet 2001.85:504508. Chen CW. Drexler H. Darnerud PO. Needham LL. Cerrillo I. and DDD [online]. Olea-Serrano MF. Greenfield TA. Vena JE. Cueto C. Am J Public Health 1995. Bates MN. Beard J. Zhou H. Seiwert M. Epidemiology 2006.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).atsdr. Am J Epidemiol 2002. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Link B. CA Cancer J Clin 2002. Needham LL.7(3):248-264. April 1982 to 1984. Available at URL: http://www.71(6):1200-1209. Environ Health Perspect 1998. Savitz DA. Durham WF. hypospadias. Angerer J. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. September 2002. and HCB residues in human blood in Ahmedabad. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Environ Res 2004. Herrman T. Baker RJ.. Zaidi SS. dichlorodiphenyldichloroethylene. Burse VW. et al. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Rivas A. India. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.111:349355. Ellis H. Willman EJ. et al. Environ Health Perspect 2004.97(2):178192.17(6):692-700. Organochlorines and breast cancer risk. Olson JR. Hurd C. Crespo J. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Koepsell TD. Bhatnagar VK. FDA total diet study. Bjerselius R. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Garrett N.1-dichloro2. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells.112(17):1761-1767. Piechotowski I. DDT and human health. Moysich KB.cfsan. and other chemicals. Klebanoff MA. Environ Res 2005. lindane (g-HCH).52:301-309. HCH. Available at URL: http://www. Glynn AW. Paepke O.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Swanson MK.58:1185-1201. Frumkin H. Levels of DDT. Klebanoff MA. Jusko TA. Wolf CJ. Saiyed HN. Effects of environmental antiandrogens on reproductive development in experimental animals.gov/~dms/ pesrpts. Parks L. Toxicological profile for DDT. Heudorf U. Patterson DG Jr.72:261265. Rogan WJ. Maternal DDT exposures in relation to fetal and 5-year growth.html.fda. Henley SJ. Int J Hyg Environ Health 2002. JAMA 1956. Brock JW. Falk C. August 2008. et al. Organochlorines in Swedish women: determinants of serum concentrations. Jr. Environ Health Perspect 2003.gov/ toxprofiles/tp35. Longnecker MP.155(4):313-322. Hediger ML. Botella B. Kulkarni PK. Thun MJ. Int J Hyg Environ Health 2003. and polythelia among male offspring. Notides AC. Granath F. J Assoc Off Anal Chem 1988. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Chemosphere 2005. Biomonitoring of persistent organochlorine pesticides. et al. Profiles of ortho-polychlorinated biphenyl congeners. Kashyap R. et al. selected elements. Olson J. Bloom MS. Jr. Neurotoxicol 2000. 4/21/09 Gladen BC. et al. Ostby J. Schulz C. Charles MJ. Biochem Pharmacol 1997.53(8):1161-1172. Zhou H. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Gray LE Jr. Brock JW. dietary intakes of pesticides. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Katz SH. et al. DDE. Gladen BC. DDE and shortened duration of lactation in a northern Mexican town. Kaus S. Aune M. Becker K. Hanrahan L. The Great Lakes Consortium. and dichloro(diphenyl)ethylene (DDE).html. Barr DB. Hayes WJ.96:34-40. Vorojeikina DP. Krause C.355:7889. Gray KA. hexachlorobenzene. Needham LL.358:110-114. Zoellner I. Klebanoff MA. Gunderson EL. et al. Eriksson P. Hum Reprod Updat 2001. Bull Environ Contam Toxicol 2004. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Lambright C.54:1431-1443.206:485-491.205:297-308. Atuma S. Furr J. Arnold SF.21(1-2)37-48. Calle EE. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Exposure of women to organochlorine pesticides in Southern Spain. Food and Drug Administration (FDA). Chemosphere 2004. Lepom P. Buckland SJ. et al. 4/21/09 Anderson HA. Gabrio T. Maternal serum level of 1. Longnecker MP. Olea N.

Rey AA. and dieldrin. Deichmann WB. Astolfi E. Jr. Academic Press. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Schecter A. J Toxicol Environ Health 1989. Crit Rev Toxicol 2006.Organochlorine Pesticides Mariussen E. Vol. In Hayes WJ. Lynch CF. 2 Classes of Pesticides. Petrik J. et al. children and newborn infants. 731-915.36:253-589. Inc. Reddy AB. and DDD in male rat liver and cultured rat hepatocytes. 1991 pp. Stehr-Green. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Snedeker SM.27:405-421. Chemosphere 2004. Arch Pediatr Adolesc Med 1996. Jr and Laws ER. Nims R.150:981-990.54:1509-520. Demographic and seasonal influences on human serum pesticide residue levels. Pesticides and breast cancer risk: a review of DDT. J Toxicol Environ Health Part A 1998. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Chovancova J. DDE. New York. Toxicol Appl Pharmacol 1971.20(2):186-193. Lubet R. Rogan WJ. Chlorinated Hydrocarbon Insecticides. Jones CR. Pollutants in breast milk. Radomski JL. Smith AG.109:35-47.53:455-477. DDE. Fonnum F. Environ Health Perspect 2001. Comparative pharmacodynamics of CYP2B induction by DDT. Eds. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. PA. Pavuk M. et al. Cerhan JR. Handbook of Pesticide Toxicology. Fox S. Thomas PE.

a stereoisomer of dieldrin. Kavlock et al. 2008).10 (<LOD-5. inhalation or dermal exposure routes. and occasionally at low levels in sediment and surface waters. 1992). Survey Geometric mean (95% conf. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.S.50) < LOD < LOD < LOD 5. Ketoendrin is a major photodegradation product (IPCS. 1992.20 (<LOD-5. unlike aldrin and dieldrin. Smith. 1991).40) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. In the body.40-5. endrin can persist for years.Organochlorine Pesticides Endrin CAS No. All uses of the pesticide in the U. have been cancelled by the U. rodenticide and avicide. Over time. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. is no longer manufactured in the U. endrin usually is not detected in serum of exposed individuals. and inflammation (Smith. manufactured. Hepatic effects of endrin exposure have included necrosis.S. total diet surveys (FDA.. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. 1987).09 and 7. endrin has been detected with declining frequency in U. population from the National Health and Nutrition Examination Survey.60 (5..40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. EPA. Serum Endrin (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. < LOD means less than the limit of detection. IPCS. unless the dose is high and the exposure is very recent. 1992). 72-20-8 General Information Endrin. anti-12hydroxyendrin.8.S.40 (<LOD-6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. Endrin was used as an insecticide. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used...50) < LOD 5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. or from contact with contaminated soils and sediments in areas where endrin was applied. An epidemic of acute endrin poisoning.70) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. which may vary for some chemicals by year and by individual sample. Endrin is absorbed rapidly after ingestion. endrin is converted rapidly to its major metabolite. 1991). Endrin was not widely used as a termiticide. At high doses. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.20 (<LOD-5.40) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. 1979.S. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. Endrin has been detected in soils. Depending on soil conditions. Because it is metabolized so rapidly.30) < LOD 5. or discarded. 1981). 1992).30 (<LOD-6. Fourth National Report on Human Exposure to Environmental Chemicals 97 .S. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. fatty infiltration.10 (<LOD-5. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Endrin does not accumulate in body tissues (IPCS. 1996.

020 (. Biomonitoring studies on levels of endrin provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of endrin than are found in the general population. IARC has determined that endrin is not classifiable with regard to human carcinogenicity.e. Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples.S. This finding is consistent with other general population studies (Bates et al.html. with the highest value 6.. interval) Selected percentiles ( 95% confidence interval) Sample 95th . population from the National Health and Nutrition Examination Survey.020) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .atsdr.020 (<LOD-.020 (<LOD-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2004. which may vary for some chemicals by year and by individual sample.24 ng/mL (about 6. serum levels of endrin were below the limit of detection.020) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020 (<LOD-. endrin was detected in 9% of serum samples..020) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020) < LOD < LOD < LOD .020) < LOD .S. 2000).020 (<LOD-. 98 Fourth National Report on Human Exposure to Environmental Chemicals .cdc.Organochlorine Pesticides The U. Ward et al.. 2004). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.gov/toxpro2. Survey Geometric mean (95% conf.. Information about external exposure (i.020 (<LOD-. In a small study of Spanish women hospitalized for elective surgery. EPA has established environmental standards for endrin. Workplace exposure standards for endrin have been established by OSHA. environmental levels) and health effects of endrin is available from ATSDR at: http://www.020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level. and the FDA monitors foods for pesticide residues.020 (<LOD-.24 ng/g of serum) (Botella et al. Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect.020) < LOD .020-.

Botella B. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.64-65 Spec. Gray LE. Frey JM. Toxicology 1979. Available at URL: http://www. Gray JA. FDA Pesticide Program Residue Monitoring 1993-2006 [online].html. 731-915. 4/21/09 Bates MN. Liddle J. Grajewski B. Schulte P. Toxicol Lett 1992. Toxicology 1981. et al. Needham LL. August 1996. Fetotoxic effects of prenatal exposure in rats and mice. Exposure of women to organochlorine pesticides in Southern Spain. Food and Drug Administration (FDA).cdc.9:1357-136. Hardjotanojo W. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Fetotoxic effects of prenatal exposure in hamsters. 4/21/09 Kavlock RJ. pp. August 2008. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. et al.fda. Rogers E. Ward EM. Burse VW.96:34-40.org/documents/ehc/ehc/ ehc130. Gray J. Environ Res 2004.atsdr. 2 Classes of Pesticides. Chemosphere 2004. Chlorinated Hydrocarbon Insecticides. Saleem M. Buckland SJ. Rowley DL. Available at URL: http://www. Ellis H. Pediatrics 1987. II.54:1431-1443. Eds. Gray LE. Olea-Serrano MF. Whitehouse DA.gov/~dms/ pesrpts. Olea N. Patterson DG Jr. Turner W. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Cerrillo I. Environmental Health Criteria 130. 1991. Perinatal toxicity of endrin in rodents. I. Perinatal toxicity of endrin in rodents. Vol.13:155-165. et al. Smith AG. In Hayes WJ.cfsan. 1992. Hanisch RC. Toxicological profile for endrin [online]. Endrin [online].htm. Hanisch RC. No:429-436. Andersen A.inchem. Sokal D. Rab MA. Cancer Epidemiol Biomarkers Prev 2000. Narahashi T. New York.79(6):928-934.21:141-150. Jr. Academic Press. Chernoff N. 4/21/09 International Programme on Chemical Safety (IPCS). Handbook of Pesticide Toxicology. Inc. et al. Roy ML.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).html.gov/toxprofiles/tp89. Garrett N. Convulsions caused by endrin poisoning in Pakistan. Jr and Laws ER. Rivas A. Fourth National Report on Human Exposure to Environmental Chemicals 99 . Kavlock RJ. Available at URL: http://www. Patterson DG Jr. Ginsburg KS. Crespo J. Chernoff H.

1 (17.3-20.9 (25. and foods with a high fat content. primarily as a fungicide and seed treatment until the U.0) < LOD < LOD 15.4) < LOD < LOD 19.5-14. or game taken from areas with HCB contamination. 2005).7-16.8 (26.6-44. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.9-17.1 (14.9-15.3 (22. measuring HCB in serum is a specific indicator of exposure to the parent Serum Hexachlorobenzene (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. wildfowl.5) < LOD < LOD 18. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.8) < LOD < LOD 27. breast milk is an additional route of elimination in nursing women.9) < LOD < LOD 20. distributes widely throughout the body. 1988).6) < LOD < LOD 25.4 (22.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.6) < LOD < LOD 26. Although it is not manufactured as an end-product in the U.0 (18.2 (17..9 (25. < LOD means less than the limit of detection. 2008. and 7.3 (20.3 (12. population from the National Health and Nutrition Examination Survey. particularly by consuming fish.4.2-15. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.4) < LOD < LOD 33.1-20.2 (24.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.4-16.9 (23.5-15.1) < LOD < LOD 15.7-16.8 (22.0 (14.0) < LOD < LOD 15.1-16.8.6-TCP) (To-Figueras et al.6-33.4) < LOD < LOD 14.4..9-30. and sediment (Barber et al.7 (27.5 (14.4. The FDA dietary surveys have shown that over time.Organochlorine Pesticides Hexachlorobenzene CAS No.4 (18.3 (14.0-19.4) < LOD < LOD 18.9-32.2-15.6 (24.4) < LOD < LOD 23.7) < LOD < LOD 24.6-26.3 (22.3-22. Therefore.0 (18.5-15.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.6) < LOD < LOD 24.4) < LOD < LOD 22. HCB is well absorbed after oral administration.7 (15. 1976).5-33. EPA cancelled its use in 1984.9) < LOD < LOD 19.3 (16.0-16.1 (13.2 (14.0) * * 15. respectively. and 03-04 are 118.4. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.1 (14.0-25. HCB has been detected in fewer foods since the 1980s (FDA. see Data Analysis section) for Survey years 99-00.6 (23. 100 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample.2) < LOD < LOD 29.6-19.7-29.4-15.9-20..8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5-TCP) and 2.2-31.3-26. 1997). and has been detected in soil. and accumulates in fatty tissues where it persists for years.6 (21.2) < LOD < LOD 13.5 (13.8-15.7) * * 14.9) < LOD < LOD 15.7 (19..9-24. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.6) < LOD < LOD 26.S. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.7-21.3) * * 15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9) 19. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.5-18.5-trichlorophenol (2. 01-02.7-15. Urinary metabolites include pentachlorophenol (PCP). 2.1) * * 15.S.9) < LOD < LOD 20.3) < LOD < LOD 29.6-32. Gunderson.3) < LOD < LOD 20.0) < LOD < LOD 24. 2002).5 (13.S.8 (15.4 (11.4.0 (25.6-trichlorophenol (2.S.9) < LOD < LOD 28.0.7-26. and elimination occurs by renal and fecal routes. 31.4 (18. water.9 (14. Survey Geometric mean (95% conf.6) < LOD < LOD 14.0-28.2 (14.3) 24.7-30.7-22. The general population may be exposed to HCB through diet. air.5-14.2 (13.9) < LOD < LOD 16.7 (15. HCB is slowly metabolized.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.

102) < LOD < LOD .083) < LOD < LOD . IARC classifies hexachlorobenzene as possibly carcinogenic to humans.079 (.e. population from the National Health and Nutrition Examination Survey.095 (.088-. acute doses produce central nervous system depression and seizures.163) < LOD < LOD .091-.099) < LOD < LOD .065 (.148-.225 (.094 (. In humans.081-.159-.090 (.132) < LOD < LOD . a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.090-. This condition. arthritis.160 (.073-.223) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * .145-.203) < LOD < LOD .114-.090 (.176-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. EPA has established a drinking water standard.203) < LOD < LOD .064 (. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.123 (.069) * * .125 (.226) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * .118-.. Schmid.090 (.171 (.190 (. thyromegaly.086) < LOD < LOD .092-.epa.095 (.121 (.100) < LOD < LOD .118-.092 (.087 (. EPA at: http://www.088-. which may vary for some chemicals by year and by individual sample.gov/pesticides/ and from ATSDR at: http://www.097 (.097) . very high.123 (.145-.141) < LOD < LOD .107) < LOD < LOD . reproductive and developmental toxicities. Infants were exposed transplacentally and through breast milk.173) < LOD < LOD .113-.Organochlorine Pesticides chemical.191 (.102 (. HCB levels were generally below the limits of detection Serum Hexachlorobenzene (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.218) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.062-. Biomonitoring Information Serum concentrations reflect the body burden of HCB.152) < LOD < LOD . 1982.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .140 (.176) < LOD < LOD .157-.086-.122) < LOD < LOD .129) < LOD < LOD .109) * * . More information about external exposure (i.178-.182 (.097) < LOD < LOD .174-.089-.175) < LOD < LOD . 1960).098 (.077-. and many died before 2 years of age (Peters et al.086-.163-.155) < LOD < LOD . environmental levels) and health effects is available from the U.094) < LOD < LOD .120 (.127-.147-. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.126) .111-.html. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .088-.118) < LOD < LOD . were seen in an epidemic of poisoning in Turkey that occurred from 1955 to 1959 when HCB-treated seed grain was diverted for bread production.107-.143-. immunologic abnormalities.069) < LOD < LOD .196) < LOD < LOD .082-.095) * * .186 (.092 (.169-.123 (.258) < LOD < LOD .gov/toxpro2. HCB interferes with normal heme synthesis.095) < LOD < LOD 75th < LOD < LOD 90th * * .cdc. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen. Fourth National Report on Human Exposure to Environmental Chemicals 101 .147 (.S.111) < LOD < LOD .104 (. The U. and liver and thyroid cancers (ATSDR.115 (.060-.163 (.. and weakness. as well as hypertrichosis.114-. Chronic feeding studies in animals have demonstrated kidney injury.167 (.S.085-.156 (.078 (.atsdr.081 (. anorexia. and the FDA has established a bottled water standard for HCB.085) * * .179 (.092 (.072-.099) < LOD < LOD .099) < LOD < LOD . 2002).130) < LOD < LOD .157 (. Survey Geometric mean (95% conf.S.089-. With chronic exposure.095-.135-. ACGIH has developed workplace exposure limits for HCB.

In a representative sample of the 1998 German adult population. 1986. Ayotte P. Link et al. The metabolism of higher chlorinated benzene isomers. Atuma S. 2005). Hexachlorobenzene in the global environment: emissions. more HCB levels were quantified.17:388–399. selected elements.gov/ toxprofiles/tp90. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al.. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Zoellner I. Laliberte C. HCB levels were directly related to age. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. 2002). Biomonitoring studies on levels of HCB provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of hexachlorobenzene than are found in the general population. Gunderson EL. and other chemicals.fda. Biomonitoring of persistent organochlorine pesticides. Darnerud PO. Lackmann. Bertram et al. 2005). PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Available at URL: http://www. J Exp Sci Environ Epidemiol 2007. Sweetman AJ. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al.58:1185-1201. Dogramaci I. Food and Drug Administration (FDA). August 2008. Seiwert M. Environ Health Perspect 2003. Glynn et al.. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.html. Environ Health Perspect 2002. Sala M. Krause C. 2005. Bertram HP. only 4. Jones D. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Bradman et al. Lawrence River (Quebec.77:173182. Biol Neonate 2002. Lecha M. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. In Spain. Jones KC. IARC Sci Publ 1986. In the 1976-1980 NHANES subsample.. Safe A. Bradman A. the more recent values in these studies were similar to the lipid adjusted limit of detection in NHANES 1999-2000 and 2001-2002 (Dallaire et al. Paepke O. Otero R. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Piechotowski I.81(2):82-85. Lackman. Schulz C. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Herrero C. 2002. FDA total diet study. 2002) and among children (Link et al. 2006). Kaus S. 1999).cdc. Barr DB. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Ozalla D. 2002.atsdr. September 2002. Becker K. 4/21/09 Barber JL. Dallaire F. Chemosphere 2005.. 2002. Eskenazi B. Santiago-Silva M.. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Lepom P. Int J Hyg Environ Health 2002. et al. van Wijk D. 2003). Muller C. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al.71(6):1200-1209. Bryan GT.205:297-308. Cripps DJ. Available at URL: http://www. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Arch Neurol 1982. 2002.54(3):203-208. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher..html. Sci Tot Environ 2005.. Organochlorines in Swedish women: determinants of serum concentrations.111:349355.135(4):400404. Kemper FH. Gabrio T. however.gov/~dms/ pesrpts. Gocmen A. Holland NT.110(8):835-838.. 4/21/09 Glynn AW. HCB detection in serum also was proportional to age. et al. levels. As a result of the lower limit of detection in NHANES 2003-2004. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Lackmann GM.9% of participants had quantifiable levels (Stehr-Green. Link B.. J Assoc Off Anal Chem 1988. Kohli J. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.. Bjerselius R.. Reference values updated. Aune M. Herrman T. Fenster L. Over the past two decades. Dewailly E. Schwartz JM. and the geometric mean concentration of HCB in whole blood was 0. Peters HA. Canada). References Agency for Toxic Substances and Disease Registry (ATSDR). 1989). Arch Dermatol 1999. but overall. April 1982 to 1984. Toxicological profile for hexachlorobenzene update [online]. Can J Biochem 1976. Muckle G.39(12):744-749.cfsan. trends and processes.44 mg/L. respectively. et al.349:144. Granath F. distribution. dietary intakes of pesticides.

Environ Health Perspect 1997. Otero R. N Engl J Med 1960.Organochlorine Pesticides Schmid R.27:405-421. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Santiago-Silva M. et al. J Toxicol Environ Health 1989. Barrot C. Rodamilans M. Sala M. Stehr-Green. Demographic and seasonal influences on human serum pesticide residue levels. To-Figueras J.263:397-398. PA. Cutaneous porphyria in Turkey. Fourth National Report on Human Exposure to Environmental Chemicals 103 .105(1):78-83.

5 (37.1-15.4-73. and 03-04 are 9.0-111) 70. HCH isomers are lipophilic.8-199) 134 (85.7-26.2-55.4 (12. In 2006.8-16.4) < LOD < LOD < LOD 46.1) 12.6) 653 758 589 1240 1533 1370 20 years and older 10.7) 10.4 (50.4) < LOD 9.9 (40. See the section “What’s New” at the beginning of this Report for details.1-27.7) 56.9 (11.5) 90th 42.2 (9.70 (6.0-34.04-10.8) 7.6) 16. and delta.60-13.5) 29.2 (50.9 (50.2-87.4 (8.30-11.9) 81.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.9-81. 2005).2-17. respectively. each result has been multiplied by 1. 58-89-9 General Information Hexachlorocyclohexane (HCH).1 (16.0 (8.0) 35.1 (12.5 (43.2) 9. the U.6-18.6 (10.7) 97.9-56. **In survey period 2001-2002.43 (<LOD-9.2-46.4 (11.8) 39.8-54.5) 22.7) 32.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.46-11.1 (21.0) 41.9-51. which may vary for some chemicals by year and by individual sample. 6.6-47. However.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.50) 8.3) 14.5 (24.6-89.2) 142 (99.1-16.4 (16. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.8) * * * * * * 15.8-87.4 (52.9 (32.9) 45.5) 67.8) 27. EPA cancelled agricultural uses of lindane (ATSDR.3 (26.2-98. formerly referred to as benzene hexachloride.6-62.9-24.7-20.8 (10.1 (11. 01-02.4) 10.8-19.3) 25.9) 15.6 (17. General population Serum beta-Hexachlorocyclohexane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6) 18.5 (8.6-14.7 (62.9-21.4) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD 21. gamma.0 (<LOD-12.7-69.0 (19.2) 36.6) 47.3-38. 104 Fourth National Report on Human Exposure to Environmental Chemicals .9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.1 (9. exists in several isomeric forms.4) 901 1067 952 992 1224 1007 Females 11. so they can accumulate in fatty tissues of animals.2-52.7 (29.1 (18. containing about 64% alpha and 10%-15% gamma isomers. commonly known as lindane.90-8.8) < LOD 10.70-12.0) 7.Organochlorine Pesticides Hexachlorocyclohexane CAS No. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. soil.8 (23.9 (62.S.7) 73.6 (22.8) 95th 68. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey.8) 12.1 (9.5 (14. Technical grade HCH is a mixture of all four isomers.1 (27.7 (35.4) 44.8 (32.87 (9.90-8.6) 36. including alpha. Lindane has a half-life of about two weeks in soils and water. water.2 (18.2-67.0) 17.4-50.2 (48.7 (<LOD-16.80 (6.4-111) 84.6-20.7) 27.7) 23. < LOD means less than the limit of detection.1-32.8 (9. HCH isomers. and sediment as a result of historic production and use.8 (17.7-96.5) 40.8 (21.9 (30.89 (<LOD-9.68 (<LOD-10.2 (31.7 (30.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.0 (14.8 (64.80 (<LOD-14. 608-73-1 beta-Hexachlorocyclohexane CAS No.0-70.3-56. The other isomers can be formed during the synthesis of lindane.7) 10.3) 51.1) 12.2-42.6) 50.2) 62.5) 11.36. interval) 9.1) 13.6 (16.5-29. and 7.1) 71.4) 21.5-123) 49.9) 17.0) 8.4) 27.8-68. It is no longer produced or sold in the U.6) 35.0 (33.3 (62.70-19. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice. 2005).7) 18.5528.3-85.6 (40. see Data Analysis section) for survey years 99-00.76.90) 7.4) 11.3) 37.56-12.9 (26.0-21.2-20. beta.S.7 (13.1) 31.7 (53.0) 71.S.5) 14.1-36.2) 13.8) 52.3 (42.6-42.7-166) 70.5) 16.0 (37.0-70.7 (25.5 (11.4) 51.70 (8. As pesticide applications of HCH were increasingly restricted or eliminated.2 (34.9-14. environmental levels declined.0-20.66-12.9-178) 48.0-23.1-32. and have been used either as fungicides or to synthesize other chemicals.20-16.7-96.9 (9. 319-85-7 gamma-Hexachlorocyclohexane CAS No.8 (33.4-45.61-12.1-37.1 (30.6 (33.7-69.5 (16.1-49.2-22.0 (35.6-37. The gamma isomer.2 (29.3 (13.6-135) 69. particularly alpha and gamma have been detected widely in air.3 (42.3) 34.8.

410 (.220 (. ingestion.064 (.360) .442 (. for lindane.350 (. 1996.310) .100-.370-. resulting in a half-life of about seven years. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.250) .210 (.240 (.100 (.300-.37) 1.118 (.050-.230-. hepatic enzyme induction.410) .294-.190) ..057-.170-.570 (.290 (.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 . and nephropathy developed (IPCS.070 (.103) 90th .062 (.600) .078 (.140) .319) .580 (.191-.067 (.083 (.056-.120 (.150) . IARC classifies Serum beta-Hexachlorocyclohexane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.470) .580-1.250-.057-. 2002).587) 653 758 589 1240 1533 1370 20 years and older .070-.281 (.390-. enlarged livers.308-.092 (.150) .120 (.150 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.910 (.382-.173-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.190-1.350) .047-.210 (.070-.050) .S.390 (.058 (<LOD-.080-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.290) . OSHA and ACGIH have established workplace standards and guidelines.051-.814) .160-.501) .064) .089-.480) . 1983). After dermal application of lindane 1% lotion.098 (..372 (.119) .320 (. Distribution is mainly to fatty tissues. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.089) .150-.100-.140) .174) .057 (<LOD-.048 (<LOD-.680) .065 (.250 (.700) .. the serum half-life was about 20 hours among children (Ginsburg et al.069) .125) < LOD < LOD < LOD .050 (<LOD-.110) . EPA has established a drinking water standard.140 (.240-.068-.130) .080 (.560 (.510) .110-.620-1.040-.083) . Fourth National Report on Human Exposure to Environmental Chemicals 105 .220) .160 (.140) . which may vary for some chemicals by year and by individual sample.170-.200 (.146-.120-.175 (.221-.5528.360-.32) .290) .050 (.01 (.297-.331 (.050-.090 (. 1971.372) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.340) .200-.400) . interval) .144 (.S.086) < LOD < LOD < LOD < LOD < LOD < LOD .067) . from 6% of samples in 1982-1984 to 2% in 1994 (FDA. paresthesias.216 (.120 (.056-.380 (.05) .480 (. See the section “What’s New” at the beginning of this Report for details.080) * * * * * * .280-. respectively.404) .260-.050-.305) . and seizures. and FDA has established a bottled water standard and food residue tolerances for lindane.250 (.287 (.340-.560) .070) .400) .090-.120) .120) .310) .460 (. U. Gunderson 1988). When animals were chronically fed lindane at high doses.080) .091) .077) < LOD .690) .081-.130-.290 (.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th . The U.191-.167 (.050 (.080-.090 (.070 (. Workers who directly handled HCH have complained of headache.450 (. Saxena et al.050-.250 (.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .139 (. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.120-.103-.280-. population from the National Health and Nutrition Examination Survey.250-.070-..620) . 1986).050 (<LOD-.360 (.460) .220-.160) . HCH isomers are absorbed after inhalation.244-.072 (.100 (.200-.120-.103 (.470 (. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown. or dermal exposure.234 (.090 (.210-. tremors.260) .190-.096) .065 (. 1977)..130 (.110) .118-.310 (.290 (.661) 901 1067 952 992 1224 1007 Females .450-. The beta isomer accumulates in fatty tissues and is metabolized more slowly.131-.100-.710) .100) .190) .077) < LOD .222 (.059-.080-.260) .214) .450) .124-. 1981).210) . each result has been multiplied by 1. 2008.051 (<LOD-.S.254) 95th .480 (.270 (. and memory loss (Nigam et al.521 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.330 (.100) .062 (.840) .180-.073-.Organochlorine Pesticides exposure to HCH is through the diet.060) .410) . **In survey period 2001-2002.220-.330-. probably by blocking inhibitory neurotransmitters in the central nervous system.110) .442) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .410-.420-.080 (. ataxia. Rogan.412 (.

5. < LOD means less than the limit of detection. Sturgeon et al.. the 95th percentile of betaHCH levels was twofold to threefold higher than the 95th percentile of 12-19 year olds in the comparable NHANES Serum gamma-Hexachlorocyclohexane (Lindane) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. serum levels of lindane were generally below the limits of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and a diet that includes meat (Becker et al.. see Data Analysis section) for Survey years 99-00. environmental levels) and health effects is available from the U. and 7. In an earlier (1996-1997) sample of German children. Additional factors associated with higher beta-HCH levels include rural residence. male sex.atsdr.. 2004) and India (Bhatnagar et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.gov/pesticides/ and from ATSDR at: http:// www.S. and 03-04 are 14. 1989). More information about external exposure (i. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. 2002). 1991.gov/toxpro2. Kutz et al. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. EPA at: http://www...html. 1998.5. and 2003-2004.S.. 01-02. 2004). beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. In NHANES 1999-2000. 1998). Bates et al. 2002. Kutz et al. which may vary for some chemicals by year and by individual sample.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans.epa. 2004. 10. population from the National Health and Nutrition Examination Survey. In populationbased studies of New Zealand adults and German adults and children.. Link et al.e. 2005. Becker et al. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. Biomonitoring Information Because of its longer half-life. were similar to the 95th percentiles in this Report. aged 9-11 years. In recent years. respectively. 1989..cdc. Survey Geometric mean (95% conf. 106 Fourth National Report on Human Exposure to Environmental Chemicals . 1991. respectively. 1971. Stehr-Green. the maximum and 95th percentile beta-HCH values. Radomski et al.. 2001-2002. Stehr-Green.. 2005. older age.8...

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.. in this Report (Nigam et al.S. In a small study of adults who consumed sport fish from the Great Lakes.. 2005).. 2003). Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Fourth National Report on Human Exposure to Environmental Chemicals 107 . Beta-HCH and lindane levels in workers involved in HCH production have been more than 1000-fold higher than the 95th percentile and limit of detection (lipid adjusted). 1998). A study of Swedish women aged 54 years and older reported a median beta-HCH level that was slightly higher than the geometric mean for women reported in the NHANES 1999-2000 survey period (Glynn et al. Serum gamma-Hexachlorocyclohexane (Lindane) (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Radomski et al... population from the National Health and Nutrition Examination Survey.Organochlorine Pesticides 2001-2002 survey period (Link et al. respectively. which may vary for some chemicals by year and by individual sample. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1971). Biomonitoring studies on levels of HCH isomers provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of HCH isomers than are found in the general population. 1986.

Raju GS. Hanrahan L.atsdr. Absorption of lindane (g benzene hexachloride) in infants and children. Angerer J. Krause C. Krishna Murti CR. Majumder SK. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.9(4):417-424. Stehr-Green.27:405-421. Glynn AW. FDA total diet study.fda. Bhargava AK. 4/21/09 Kutz FW. Arch Pediatr Adolesc Med 1996. Crespo J. Siddiqui MKJ. and other chemicals. Radomski JL. Int Arch Occup Environ Health 1986. J Pediatr 1977. Environ Res 2004. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Rey AA. Paepke O. Organochlorines in Swedish women: determinants of serum concentrations. Piechotowski I.72:261265. et al.54:1431-1443. Environ Health Perspect 1998. Lepom P. Levels of DDT. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Maass R.58:1185-1201. Becker K.html. Sturgeon SR. Deichmann WB. Cancer Causes and Control 1998. available at URL: http://www. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. April 1982 to 1984. Olea N. Wood PH.gov/~dms/pesrpts. Arch Toxicol 1981. Kashyap R. Zaidi SS. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Gunderson EL. Rev Environ Contam Toxicol 1991. Schulz C. dietary intakes of pesticides. 108 Fourth National Report on Human Exposure to Environmental Chemicals .inchem.57(4):315-320.htm. Rogan WJ. Rothman N. Reisch JS. The Great Lakes Consortium.48:127-134. J Toxicol Environ Health 1989. Herrman T. et al. et al. and HCB residues in human blood in Ahmedabad. J Assoc Off Anal Chem 1988. Metabolism of gammahexachlorocyclohexane in man. Astolfi E. Bottimore DP. Garrett N. Int Arch Occup Environ Health 1983. Kaus S. Toxicological profile for hexachlorocyclohexanes update [online]. Olson J. Biomonitoring of persistent organochlorine pesticides.120:1-82. Olea-Serrano MF.106(5):279-289. selected elements. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. PA.20(2):186-193. children and newborn infants. Lowry W. Atuma S.52(1):59-67. et al. Available at URL: http://www. Zoellner I. Pollutants in breast milk. Int J Hyg Environ Health 2002. Needham LL. Potischman N. Seiwert M. International Programme on Chemical Safety (IPCS). Chemosphere 2005. 2002. Kulkarni PK. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. et al. August 2005. Gabrio T. Rivas A.111:349355. org/documents/jmpr/jmpmono/2002pr08.96:34-4Food and Drug Administration (FDA). Brinton LA. Kutty D. Chemosphere 2004. Darnerud PO.205:297-308. August 2008. Bhatnagar VK. et al. Botella B. Placental transfer of pesticides in humans. Link B.cdc. Burse VW.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Bai KM. VI.html.91:998-1000. Bjerselius R. Nigam SK. Patterson DG Jr. Ellis H. Needham LL. Available at URL: http://www. 4/21/09 Ginsburg CM. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.150:981-990. Buckland SJ. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Demographic and seasonal influences on human serum pesticide residue levels.71(6):1200-1209. Saxena MC. Exposure of women to organochlorine pesticides in Southern Spain. HCH. Cerrillo I. Falk C.cfsan. Lindane. Toxicol Appl Pharmacol 1971. Aune M. Environ Health Perspect 2003. Visweswariah K. Heinrich R. Bates MN. 4/21/09 Anderson HA. gov/toxprofiles/tp43. Granath F. Saiyed HN. Brock JW. Bull Environ Contam Toxicol 2004. India. Needham LL. Karnik AB. Occupational exposure to hexachlorocyclohexane. et al. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.

4) < LOD 15.8 (12.S. water. resulting in exposure to newborns and nursing infants.1 (<LOD-65. Mirex binds strongly to soil. respectively.5.6 (<LOD-31.5 (<LOD-115) 153 (30. aquatic organisms.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.S.6-305) 15. and foods.6) 9.7 (12.5-82. In studies conducted in the 1970’s and 1980’s.70-24.. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. where it was applied directly to soil and by aerial spraying.S.2 (7. which may vary for some chemicals by year and by individual sample. 1991).6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.7) 8. and 7. Some states and the U. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. Occupational exposure is limited to workers at sites where mirex contamination is present.7) < LOD 66.8.70 (<LOD-15. animals.S. Formerly. (Kutz et al.5-425) 40.0 (12.8 (<LOD-73. disposal.3-225) 15. Mirex can cross the placenta and be excreted in breast milk.0 (14.0 (<LOD-108) < LOD < LOD 50.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. it is a highly persistent chemical in the environment.70-40. or pesticide application.8) < LOD 15.1) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 16.3 (15.3 (15.5 (9.. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. Mirex is not metabolized in the body.6 (<LOD-23.0) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 19.6. Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental Serum Mirex (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. sediments.10-37.10 (<LOD-15. especially those from persons living in the southeastern U. soil. < LOD means less than the limit of detection.1 (13. mirex was detected in human adipose samples.6) < LOD < LOD < LOD < LOD 71. 10.3) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13. The most likely sources of human exposure to mirex are eating fish from contaminated water or living in areas with soil contaminated by historic mirex manufacturing. 1985.2-230) 13. 1995). 01-02. Fourth National Report on Human Exposure to Environmental Chemicals 109 . Mirex has been detected in air.Organochlorine Pesticides Mirex CAS No.4) < LOD 63. since 1977. population from the National Health and Nutrition Examination Survey. 2385-85-5 General Information Mirex has not been produced or used in the U.1 (8.7 (<LOD-47. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.40 (<LOD-13. see Data Analysis section) for Survey years 99-00. after which it is widely distributed in the body and stored in fat.S.90-29. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-374) 11.5-291) 11.6 (<LOD-108) 9.2) 51. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. where it has a half-life of 12 years.5 (<LOD-42.4-230) 18. Mirex is absorbed through the skin and from the gastrointestinal tract.4 (8. and 03-04 are 14. Survey Geometric mean (95% conf.

73) .7 ng/g of lipid.41) .510) < LOD < LOD . 110 Fourth National Report on Human Exposure to Environmental Chemicals .064 (<LOD-.08 (. The U. 1989).090-1..102) < LOD < LOD < LOD < LOD . IARC classifies mirex as possibly carcinogenic to humans. environmental levels) and health effects is available from the ATSDR at: http://www. Finding a measurable amount of mirex in serum does not mean that the level of mirex causes an adverse health Serum Mirex (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.220) .080-1. The geometric mean mirex levels of the Inuit mothers were 8.100 (<LOD-..atsdr.79) .310 (.92) .170) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.430 (.110 (<LOD-.140 (<LOD-.gov/toxpro2.470) . EPA has established environmental standards for mirex.090 (<LOD-.062-.610) < LOD < LOD < LOD < LOD .106 (.090-1. and 4.174) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.450 (.8.e.470 (.470) .220 (<LOD-. 2004). Biomonitoring Information In the NHANES 1999-2000.080-1.090-1. as well as in a subsample of NHANES II (1976-1980) participants. Smith.079 (<LOD-. 1995.053-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. Laboratory animals fed high doses developed liver enlargement and liver tumors. Fishermen in New York who consumed Great Lakes sport fish had median levels of lipid-adjusted serum mirex that were lower than the 95th percentile value among males the NHANES 2001-2002 subsample (Bloom et al.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .059 (<LOD-. which is approximately twofold to threefold lower than the 90th percentile for females in the NHANES 20012002 subsample but similar to 95th percentile for females in the NHANES 2003-2004 subsample (Van Oostdam et al. 2001-2002.79) ..html.090 (<LOD-. population from the National Health and Nutrition Examination Survey.268) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . In addition. and 2003-2004 subsamples.077 (<LOD-.054 (<LOD-.112 (.02) .052-.635) < LOD . and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue. Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than nonInuit mother from other Arctic regions. More information about external exposure (i.170-3.170) < LOD .410 (. 1991).S. Survey Geometric mean (95% conf.108 (.093 (.215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .106) < LOD .450) 1.100 (<LOD-.089-. 7.055-.S. 2005).084) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .cdc. In samples obtained between 1994 and 1997.690) . serum mirex levels were generally below the limits of detection (Stehr-Green.370 (.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .090 (<LOD-.Organochlorine Pesticides exposures are unknown.070-1.37) .256 (. reproductive toxicity included decreased fertility and testicular damage. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.

120:1-82. J Toxicol Environ Health 1985. 1994-1997 organochlorine compounds. Vol. Chashchin V. Jr and Laws ER. Vena JE. Strassman SC. Available at URL: http://www. J Toxicol Environ Health 1989. Gilman A. Smith AG. Swanson MK. Rev Environ Contam Toxicol 1991. Circumpolar maternal blood contaminant survey. Moysich KB. Biomonitoring studies on levels of mirex provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of mirex than are found in the general population. Demographic and seasonal influences on human serum pesticide residue levels. New York. 731-915.html. Bottimore DP. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Van Oostdam JC. Kutz FW. Odland JO. et al.97(2):178192. PA.Organochlorine Pesticides effect. References Agency for Toxic Substances and Disease Registry (ATSDR). Stroup CR. 4/21/09 Bloom MS. Academic Press.330:55-70. Jr. hexachlorobenzene. 1991 pp. Wood PH. Eds. dichlorodiphenyldichloroethylene. Toxicological profile for mirex and chlordecone [online]. Sci Total Environ 2004.15:385-394. Chlorinated Hydrocarbon Insecticides. Dewailly E.atsdr.gov/toxprofiles/ tp66. Fourth National Report on Human Exposure to Environmental Chemicals 111 .27:405-421.cdc. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kutz FW. Environ Res 2005. Olson JR. Watts DL. Inc. et al. August 1995. Leininger CC. 2 Classes of Pesticides. Stehr-Green. In Hayes WJ. Carra JS. Hansen JC. The human body burden of mirex in the southeastern United States. Handbook of Pesticide Toxicology. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Profiles of ortho-polychlorinated biphenyl congeners.

80 (1.19 (<LOD-6. 2.42 (<LOD-8.20) < LOD 1.72) < LOD 1.0 (3.50-16. which may vary for some chemicals by year and by individual sample.S.4.50 (1. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.4.0) < LOD 11.6-TCP were used as intermediates in the production of certain pesticides.20-71. 112 Fourth National Report on Human Exposure to Environmental Chemicals .9 (<LOD-121) 9.6-TCP in any of the samples (U.6-Trichlorophenol CAS No.3.60 (. public drinking water systems did not detect 2.60) < LOD 8.71 (<LOD-8. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.50 (.00 (2.0 (8.10-3.0 (3.40 (2. 1999).60-8.50) < LOD 1. 2.4.980-3. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.S. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air. are metabolites of several organochlorine chemicals.20) < LOD 90th 5. Both chemicals have been detected in air. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30-11. 1999).27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.40-11.00 (3.4.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.40 (2. population from the National Health and Nutrition Examination Survey.0) < LOD 5.0 (4. Trichlorophenols are no longer manufactured commercially.40 (1.4. usually at herbicide production or waste incineration facilities.80 (2.30-27.90-33.5-TCP) and 2.27) size 1994 2497 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1.20) < LOD 5.50-25.80) < LOD 1.5-trichlorophenol (2.9 and 0.63) 18.0) < LOD 5. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.0) 2.0) < LOD 5.4.5-trichlorophenol.40 (2. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.40 (.0) < LOD 11. may occur by inhalation or dermal routes. other organochlorines.5TCP and 2.0) 5.4.950 (<LOD-1.27) 696 661 521 696 603 939 Limit of detection (LOD.9.920-3.31 (<LOD-9. Formation of 2.940-3. EPA.4.30 (. hexachlorobenzene.0 (4.4.4. Historically.0) 2.900-2.71 (<LOD-8.980-3. Survey Geometric mean (95% conf.8) 21.0) 2.S.0 (5.30) < LOD 4.30-44.6-trichlorophenol (2.0) 2.40) < LOD 4.5-Trichlorophenol CAS No. soils.0) 14.30-3.40 (2.30) < LOD < LOD < LOD < LOD < LOD 1.60-18.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.60 (4. 1976). including hexachlorobenzene and hexachlorocyclohexanes.80-41.4.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.Organochlorine Pesticides 2.4.20-36.0) < LOD 21.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 2.20 (4.40 (1.30-27.00-3.50-63. Occupational exposures. Such workers would probably Urinary 2.6-TCP).50 (2.40 (.00-8.40) < LOD 1.30-40. and sediments. Exposure to trichlorophenols also may result from metabolism of lindane. 2006).00-3. < LOD means less than the limit of detection. and polychlorinated benzenes (Kohil et al.57 (<LOD-15.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.30-27. surface water.42 (<LOD-12. however. recent sampling of U.40-18.0) 2.7.60 (2.40) < LOD 6.7) 24.03) 9. 95-95-4 2..0 (4.0) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.

50) < LOD 2.1 (<LOD-58.e. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.13-13. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.820-2.47-8.Organochlorine Pesticides be exposed to mixtures of chlorophenols.4) 5. The 95th percentiles for 2.49 (1.37-11. environmental levels) and health effects is available from ATSDR at: http://www.. furans.00-29.6-TCP.920-2. NTP classifies 2.11) size 1994 2496 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 2.81 (<LOD-9. 2003.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.4.4 (6.6) 4.0 mg/L.20-6. In the same 2-6 year old children.05-17. in addition to dioxins. animals showed hepatocellular abnormalities.4.15) < LOD 2.28-25.5) < LOD 12.cdc.80 (1.16) < LOD 90th 5.5-TCP or 2..43 (2.24-11.74) 11.4. population from the National Health and Nutrition Examination Survey.36 (1.8) 4.16 (. Radon et al.gov/toxpro2.4.78 (3. leukemias.html. At lower doses.57 (3.3 mg/L reported in German adults aged 18-69 years (Becker et al. Laboratory animals chronically fed high doses of 2.73 (<LOD-8.6-TCP level was approximately eight times higher than the corresponding percentile in a small group of 2-6 year old children living near an herbicide manufacturing facility: 33 versus 4 mg/L (Hill et al.05-8. 1995) were similar.86 (3.8 (5.2) < LOD 5.55 (4.69 (2.53-3.95 (3.4) < LOD 3.32) < LOD 4.9 (5.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).4.. and lymphomas.2) 2. Survey Geometric mean (95% conf.02-3.4. Neither 2.24) < LOD 5.00) < LOD 4.43) < LOD 12.79-4.6-TCP had increased rates of hepatic tumors. However. 2004).83-12.57 (<LOD-7.5-TCP nor 2.5) 11.4.3 (5. 1989). urinary 2.19-4.68-4.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown..2 (2.17) 9. Human health effects from 2.90 (4.0) 7. More information about external exposure (i.6-TCP levels at the 95th percentile were up to eight times higher than 3.78) < LOD 1. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.67 (1. the 95th percentile urinary 2.24 (3.24) < LOD 6.68 (<LOD-8.33) < LOD < LOD < LOD < LOD < LOD 2.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.60-3.37) 16.27-17.1) 2.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.6) 4. 2003).02) < LOD 7.93-11.82 (<LOD-32.6-TCP as reasonably anticipated to be a human carcinogen..44 (.4. Fourth National Report on Human Exposure to Environmental Chemicals 113 .00-19.4) < LOD 3.46 (1.atsdr.6) 4.9) 12.4. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.53-3.67 (1.4.69-18..62-20.24) < LOD 1. as being possibly carcinogenic to humans.5-TCP. IARC classifies combined exposures to polychlorophenols.57 (<LOD-7.7 (4.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.19-12. and other chlorinated compounds.980 (<LOD-1..31) < LOD 2.75 (3. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.5-TCP and limited for 2.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Urinary 2.4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.. which includes trichlorophenols.8) < LOD 9.64 (4.44 (1.29 (1.75 (<LOD-6.78-19.88-16. 1995) and up to 19 times higher than the 95th percentile value of 1.4.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . the 95th percentile urinary 2.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al. 7.4. 1989). 2003). Among 6-11 year old children in NHANES 1999-2000.

53) 4.5-TCP or 2.2 (14.90) 2.40-2.0 (4.9 (11.25-11.7) 33.6-TCP than are found in the general population.00 (1.5-TCP level of 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.28) * 2.70-6.0 (14.5-46.00 (2.95-6.40 (2.0) 14.52-3.99) 6.5-TCP and 2.60 (3. 1998).1-25.85) * 3.6) 26.91-4.4. 2003).. respectively.10-3.85 (2.98-7..0 (20.6-TCP level.8-15.9) size 1989 2503 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.0 (6. interval) 2.0-41.70) 5.60 (3.08 (2. the median urinary 2.40) 4.40-32.0) 19.0 (9.18-3.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.59) 4.0) 13.0-68.0) 19.0 (6.57 (<LOD-2.40-2.0-38.47 (3.92 (2.4.32-4.80 (2.5-TCP (0.90 (3.87-14.0-18.80 (3.67) 4.95 (4.0 (7.9) 13. In harbor workers exposed to chlorophenol-contaminated river silt.45-9.0 and 1.40) 2.63) 90th 15.60-37.70) 5.0) 11.20 (3.4.67-12.54) 6.80-7.10 (5.30-2.09) 15.0-38.00-4.4.1 (10.00-21.6-TCP in urine does not mean that the level of 2.4.89-6.07 (<LOD-3.7 mg/L.74 (2.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.95) 3.65) 15. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.0 (8.72-10.3) 37.4.32) * 3.8) 18. Mean values of 2.80-25.78 (2.89 (3.1 (8.0 (15.04) 2.60-3.6-TCP exposure and health effects. Urinary 2.0) 17.30) 4.7 (13.S.4 (8.90-8.78 (2.73-9.40) 2.70-3.6TCP values.6-TCP levels that were as much as 450 times higher than the median level among adults in the NHANES 1999-2000 subsample (Pekari et al.8) 32.30-11. similar to the limit of detection for this Report (Anderson et al.30-2.10) 2.70) 3.45) < LOD 11.6 (12.0) 10.3) 23.50-5..5-TCP or 2.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.5-TCP or 2.4.00 (4.46-3. for males in NHANES 19992002 (Agramunt et al.79 (5.0 (15. Urinary 2.4.40-14.9 (13.3-17.02) 2.3 (11.55-3.70 (2.23-2. < LOD means less than the limit of detection.3-26.30-33. which may vary for some chemicals by year and by individual sample.40) 3.7-3.59-6.70-6.4.0-43. Biomonitoring studies on levels of 2.40 (2. 2004).20-6.74-3.60) < LOD 5.4.14 (2.8 (9.60) 6.3 (11.5-TCP and to the median 2.4. 114 Fourth National Report on Human Exposure to Environmental Chemicals .60-21. 1991).58 (1.4 (10. Survey Geometric mean (95% conf. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.68 (<LOD-2.36 (1.23) 3.52 (2.23) 2.69 (3.50 (2.70) 1.35-3.10) 6.0 (12.6-TCP (0.0 (20.0) 13.40-7.0 (11.6-22.4 (17.0) 7.0 (6.2) 12.7 (9.2) 25.4.4.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.9) 694 677 519 696 602 931 Limit of detection (LOD.0) 9.0) 13.0 (14.12) 2.84) 2.0 (8.26 (2. Biomonitoring data will also help scientists plan and conduct research about 2..2-0.80-6.10-2.90 (4.31) * 2.4 (9.80-20.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.75 (8.45 (5.0) 15.51-12.80 (2.0-37.80) 1.98-11.44) 75th 4.0-54.0-50.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.0 (16. population from the National Health and Nutrition Examination Survey.66 (8.20 (3.4.5-TCP or 2. Finding a measurable amount of 2.28) 24.0 (13.76) 3.7-16.0) 17.4.1) 16.3) 20.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.70 (2.06) * 2.6-17.10-3.48-26.0) 9.49 (6.20) 4.0) 7.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.24 (2.5-TCP and 2.0) 11.0) 14.0) 13.0 (14.20-23.6 mg/g creatinine) and 2.0) 6.36-5.31 (3.8-13.32) 3.6) 21.7) 21.53) 2.45 (2.4.3.01-6.20-3.4-17.0) 12. 0.33-4.09-7.0) 10.4.40-4.0-44.4.5 mg/g creatinine) were similar to the limit of detection for 2.6 (11.36 mg/g creatinine.58-3.65 (5.6-19.56 (3.4.4.8-24.60 (2. was about six times lower than the median urinary levels for males in this Report (Radon et al.6TCP causes an adverse health effect.

6 (10.02) 3.04-16.35 (3.7) 25.33) * 2.96) < LOD 4.76) 4.91 (3.87 (3.56 (7.33 (7.4) 8.83-6.91 (7.52 (3.33-2.25-17.43-7.82 (3.20-2.78) 90th 12.9) 7.10 (6.87-7.8) 12.22 (1.68) 2.59 (2.0) 10.90) 2.05 (6.76) 2.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.42 (2.99-2.8 (7.68) 2.23 (1.6 (22.89-2.17-4.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4) 4.29-4.88) 4.42) 2.9) 8.52) 2.58 (4.23) 4.11) 10.72) 32. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.81-9.9) 19.24 (1.02 (1.95-2.65) 2.77-4.30-2.7) 6.4.0 (9.9) 8.0 (11.13 (1.3 (9.1-21.18-4.87-6.8 (8. population from the National Health and Nutrition Examination Survey.Organochlorine Pesticides Urinary 2.9-29.6) 13.4 (11.5) 11.2 (13.44 (3.46-14.78 (2.18-2.88) 5.71 (3.63) * 4.29-4.1-32.13-6.63) 4.63-15.50 (2.88-7.87) 2.00) 4.0 (6.10-9.06-2. interval) 2.5 (7.41-6.38 (4.06) 11.75) 75th 4.00 (2.63 (2.53) * 2.1) 14. Survey Geometric mean (95% conf.66-4.83-5.81) 2.6 (5.00 (3.38-5.62-15.4 (12.1) 11.88 (2.88) 1.25 (3.56) < LOD 11.08-2.63 (<LOD-2.88) 4.52 (5.8) 21.22 (3.6-31.40 (2.41 (3.83-6.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.22-2.6) 12.3-23.26 (6.4) 9.5 (10.40 (7.82) 2.22-9.43 (<LOD-2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.76) 1.25-15.15 (6.14-13.52) 2.60 (4.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.49) 4.38) 22.6 (12.05 (3.92) 4.56-5.9-64.9-34.9-32.78) 2.47-5.54 (2.9 (9.43 (2.73) 5.17) 2.73-22.98 (1.6 (9.53) 4.21-11.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.14-2.01 (3.48-2.63-13.6 (6.60-2.1 (8.S.7 (14.15 (1.65) 18.32-19.67-17.90 (1.55-2.29 (6.8) 19.32 (2.28-4.16-10.51) 18.65-2.51 (2.50-8.53-11.17) 13.27-9.2) 19.89) 10.2 (12.82-2.2 (8.9 (9.70-9.94-13.76-8.79-17.5) 9.06) 4.33 (1.5-28.98) 10.72-16.3) 8.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.5) 8. Fourth National Report on Human Exposure to Environmental Chemicals 115 .3-37.25 (3.10) 4.5) 11.38 (2.6 (9.88) * 2.91-2.5) 12.04-2.22 (<LOD-2.0) 8.53 (3.25-2.82 (8.49-3.87) * 2.8) 11.00) 4.6) 8.7-36.19-5.77) 2.1 (13.5 (8.65-21.09-3.2 (7.26-13.83 (3.51-21.

Available at URL: http://www. Environmental Protection Agency (U. Radon K. Safe A. Gregg M. Heinrich-Ramm R. html.cdc. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Kohli J.EPA). Becker K.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Poschadel B. Pekari K. Luotamo M.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Olson J. Int J Hyg Environ Health 2003. To T. Lindroos L. Pesticide residues in urine of adults living in the United States: reference range concentrations.54(3):203-208. Seiwert M. Aitio A. Corbella J. Burse VW. Kaus S.epa. Urinary excretion of chlorinated phenols in saw-mill workers.18(4):469-474. et al. Int Arch Occup Environ Health 1991. Environ Health Perspect 1998.71:99108. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation.atsdr. Hill RH Jr. Wegner R. Hill RH Jr. Head SL.146:83-91. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Baker S. July 1999. Smith SJ. Available at URL: http://www. The Great Lakes Consortium. Baur X. The metabolism of higher chlorinated benzene isomers. Fast DM. Environ Res 1995. Seifert B.63:57-62. Holler JS. Falk C. Needham LL. Can J Biochem 1976. et al. U.106(5):279-289. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. The analysis of occurrence data from the first unregulated contaminant monitoring regulation (UCMR 1) in support of regulatory determinations for the second drinking water contaminant candidate list [online]. 4/21/09 Agramunt MC. Needham LL. Bailey SL. Domingo JL. Schulz C. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Toxicol Lett 2003.pdf. December 2006 Draft. Hanrahan L. Domingo A. Szadkowski D. et al. Arch Environ Contam Toxicol 1989. Shealy DB. Toxicological profile for chlorophenols [online].45:440-445.S. Jarvisalo J. Jones D. 206:15-24. S.gov/toxprofiles/tp107. Anderson HA. Am J Ind Med 2004. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.

. less common routes include inhalation and dermal contact.Dimethylthio. The thiophosphate type organophosphorus insecticides (e.S. most residential uses have been phased out in the United States as a result of implementation of the Food Quality Protection Act of 1996. 1993). with usage declining 45% since 1980 (U. Certain organophosphorus insecticides (e. chlorpyriphos) are initially metabolized to the more toxic “oxon” form. In general. have accounted for a large share of all insecticides used in the United States. 2004). gardeners.S.. General population exposure to organophosphorus insecticides may occur by ingesting contaminated food and from hand-to-mouth contact with surfaces containing organophosphorus insecticides.DimethyldithioDiethylDiethylthio. An estimated 73 million pounds of organophosphorus insecticides (70% of all insecticides) were used in the United States in 2001. slight to moderate water solubility.. Most organophosphorus insecticides undergo hydrolysis with excretion of major hydrolytic metabolites in the urine. Farm workers. malathion.g. florists. which are active against a broad spectrum of insects. Although organophosphorus insecticides are still used for insect control on many food crops. the organophosphorus insecticides have better gastrointestinal than dermal absorption. EPA. pesticide applicators. Approximately 40 organophosphorus insecticides in a wide variety of formulations are registered for use in the United States by the U.g. mosquito control) in the United States. and manufacturers of these insecticides may have greater exposure than the general population. Estimated intakes by the general population are usually considered below regulatory thresholds though concerns have been raised about some organophosphrus insecticides because of unique routes of exposures and intakes in infants and children (NRC. In general. moderate to high soil binding. the various organophosphorus insecticides demonstrate low vapor pressures (with some exceptions).g. Mammalian elimination halflives can range from hours to weeks. widely varying degrees of soil leaching or runoff potential. Many states have programs to monitor Pesticide (CAS number) Azinphos methyl Chlorethoxyphos Chlorpyrifos Chlorpyrifos methyl Coumaphos Dichlorvos (DDVP) Diazinon Dicrotophos Dimethoate Disulfoton Ethion Fenitrothion Fenthion Isazaphos-methyl Malathion Methidathion Methyl parathion Naled Oxydemeton-methyl Parathion Phorate Phosmet Pirimiphos-methyl Sulfotepp Temephos Terbufos Tetrachlorvinphos Dimethyl.Diethyldithiophosphate phosphate phosphate phosphate phosphate phosphate (813-79-5) (1112-38-5) (756-80-9) (598-02-7) (2465-65-8) (298-06-6) • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • Fourth National Report on Human Exposure to Environmental Chemicals 117 .Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Organophosphorus Insecticides: Dialkyl Phosphate Metabolites General Information Organophosphorus insecticides. naled) are also registered for public health applications (e. and a low persistence in the environment. EPA.

1998. Measurement of these metabolites reflects recent exposure. Aprea et al.. 2003.. FDA. Animal studies at high doses generally demonstrate the effects of inhibition of acetylcholinesterase mentioned above for acute poisoning in humans. 1975. cholinergic effects. Rodnitzky et al. Heudorf and Angerer. In some of these occupational studies. without inhibition of acetylcholinesterase). seasonal use of the parent insecticide.. Young et al. reported levels of urinary dialkyl phosphates may exceed levels seen in the general population by up to fiftyfold. For example. though in general. 2005).S. and demonstrate substantial variability when measured Fourth National Report on Human Exposure to Environmental Chemicals . paralysis. 1998). Savage et al. Measurements of dialkyl phosphates in urine have been used to document exposure of farmers. agricultural workers. Takamiya. Franklin et al.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites cholinesterase activity in the blood of pesticide applicators as part of monitoring exposure to organophosphorus insecticides. 1988)..e.. subjects ingesting “organicallygrown” foods were shown to have lower levels of urinary dialkyl phosphates than subjects eating a conventional diet (Curl et al. 2003.. 2006. but are regarded as markers of exposure to organophosphorus insecticides. Fiedler et al.. Pilkington et al. 2006.. PeirisJohn et al. Jamal et al. and therefore. diethylphosphate (DEP).. Dialkyl phosphates may also occur in the environment as a result of degradation of organophosphorus insecticides 118 (Lu et al. chlorpyrifos is metabolized to both diethylphosphate and diethythiophosphate. Also. Mild to severe peripheral neuropathies and residual deficits in neurocognitive functioning can persist following acute poisonings (London et al. Generally.epa. worker levels are only moderately higher.. Urinary levels of dialkyl phosphate metabolites vary with the type of field application. 2002.. Dialkyl phosphate metabolites can be present in urine after low level exposures to organophosphorus insecticides that do not cause clinical symptoms or inhibition of cholinesterase activity (Davies and Peterson. In these studies and the NHANES subsamples. population from NHANES 1999-2000 and 2001-2002 (CDC. Rothlein et al. 1996.. Chronic exposures studied in farmers and insecticide applicators. who have neither past acute poisoning or significant reduction in blood cholinesterase activity.. 2000. Acute symptoms include nausea.gov/toxpro2. Each of the six urinary dialkyl phosphate metabolites can be produced from the metabolism of more than one organophosphorus insecticide. Therefore. 1981). 2001.cdc. the environment. 1987.. predominantly in the previous few days. Daniell et al. urinary levels in children of farm workers and non-farm workers have been reported to correlate weakly with environmental dust levels of particular insecticides in some.. Diet influences the measured levels of urinary dialkyl phosphates. and seizures.. Additional information about insecticides is available from U. 2006). EPA. 2002... vomiting.. Saieva et al. USDA. For example.html. 1997. Krieger and Dinoff. 1997. children have slightly higher levels than adults..S. 2004. 1981. the presence in a person’s urine may reflect exposure to the metabolite itself. diethylthiophosphate (DETP).. The U.S. as well as mechanistically-related neurodevelopmental and reproductive effects (Astroff et al.. Farahat et al. 1997. six urinary dialkyl phosphate metabolites of organophosphorus insecticides are measured in this Report and other research studies: dimethylphosphate (DMP).. 2001.. 2004).gov/pesticides/ and from ATSDR at: http://www. and the workplace. About 75% of registered organophosphorus insecticides are metabolized in the body to measurable dialkyl phosphate metabolites. 1994). 1992. 1995. and others to organophosphorus insecticides (Davies and Peterson.. though various study results are inconsistent (Albers et al. Stephens et al. 2005). The acute high dose effects of the organophosphorus insecticides from intentional and unintentional overdoses or from high-dose worker exposures are well known and include neurological dysfunction that results from the inhibition of the enzyme acetylcholinesterase leading to excess acetylcholine in the central and peripheral nervous systems.... pest-control workers. geometric mean urinary dialkyl phosphate levels were generally lower than levels reported in smaller studies of children and adults in Italy and Germany (Aprea et al. The dialkyl phosphate metabolites do not inhibit acetylcholinesterase and are not considered toxic.. Maizlish et al. 1995. dimethyldithiophosphate (DMDTP). and OSHA have developed criteria on allowable levels of these chemicals in foods. 2003). Stokes et al. 1991. In nationally representative subsamples of the U. Franklin et al. Rosenstock et al. 1998. Engel et al. but not all. studies (Bouvier et al. EPA at: http:// www.S. U. Prendergast et al. have shown possible subtle or subclinical neurological effects. 2000.. Rothlein et al. atsdr. dimethylthiophosphate (DMTP). 2005). Few animal studies have addressed the potential for low environmental doses to produce non-cholinergic effects (i. The table shows the six urinary metabolites and the parent organophosphorus insecticides responsible for these metabolites. and diethyldithiophosphate (DEDTP). Biomonitoring Information Urinary dialkyl phosphate levels reflect recent exposure. 1998a and 1998b. weakness.. the presence of one or more dialkyl phosphate metabolites without additional information cannot be linked to exposure to a specific organophosphorus insecticide. Curl et al.

2005)... population (CDC. 2006.. estimates of dose or intake calculated from urinary dialkyl phosphate levels in studies of pregnant women in one agricultural community (Castorina et al. Estimates of dose or intake for the general U.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites over multiple times of day and over multiple days. 2005).S. 2006). Children and pregnant family members of farm workers were reported to have median levels of many urinary dialkyl phosphates that were either similar or slightly higher (Arcury et al.. Biomonitoring studies of dialkyl phosphate metabolites provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of organophosphorus pesticides than are found in the general population. 2005). which may reflect changes in exposure. Petchuay et al. 2003). Information is limited with regard to associations between levels of urinary dialkyl phosphates and any health effects... and these higher levels were associated with a few subtle neurobehavioral test results (Rothlein et al.. and elimination kinetics (Kissel et al. 2003) and in another study of workers exposed on reentry to treated orchards (Fenske et al. 2005. Summed levels of urinary dialkyl phosphates in prenatal samples from mothers of neonates living in an agricultural community were associated with subtle changes in one of seven domains of neurophysiologic neonatal testing during one restricted postnatal period of time (Young et al. 2002. Also.. 2005) than those presented in U. 2006). 2003) generally did not exceed doses considered to be safe. except for one study in which DMTP levels were up to fourteenfold higher depending on the season and the type of crop application (Lambert et al... Lambert et al. 2005). collection timing. population as calculated from urinary dialkyl phosphate measurements were below environmental dose estimates based on multiple routes of exposure (Duggan et al.. Fourth National Report on Human Exposure to Environmental Chemicals 119 .S. Finding a measurable amount of dialkyl phosphate metabolites in urine does not mean that the level of dialkyl phosphate metabolites causes an adverse health effect. 2005. median urinary levels of DMTP and DMDTP were more than twentyfold higher than median levels in the U. Bradman et al.S. In a study of farm workers. representative subsamples from NHANES 1999-2000 and 2001-2002 (CDC. Koch et al.

2 (9.13 (2.08-2.3) 14.33 (5.40-11.0 (7.36-4.0) 10.70 (4.90-5.20 (.0) 9.740-2.1.53) 4.56 (1. see Data Analysis section) for Survey years 99-00.56-13.2 (7. 120 Fourth National Report on Human Exposure to Environmental Chemicals .16) 4.52) 6.82) 10.35-16.26-8.620-1.0) 6.840-1.0) 5.6) 18.00-7.89) 9.98-12.60) .6) 7.0) 6.26-6.63) 1.58 (3.14) * * .1) 10.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.21 (.10 (2.2 (11.0) 11.60-25.1 (10.2.60-11.0) 5.0-28. and 0.1-23.5-17.61 (3.33-18.30-6.48-7.39 (8. which may vary for some chemicals by year and by individual sample.40-1.2 (14.37 (3.40-14.2 (7.15) 14.0 (4.71-9.9) 952 1187 928 997 1333 1003 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. respectively.23-5.74 (8.28) 1.93-24.7 (14.3) 16.58 (2.12) 4.70) .0 (7.810-1.0 (9.80) 2.530 (<LOD-2.0) 10.40-5.79-7.44-3.0) 10.57-7.42) .80) 2.12-19.757-2.10 (2.15-12.02) 4.0) 20.55-8.95) 5.07-10.34-3.10) < LOD .80-4.13 (2.90-4.599-1.44 (2.93 (4.8 (9.32 (.91) 4.780) < LOD 3.290 (<LOD-1.9) 14.8-32.0 (12.2.90) 3.8 (8.20-30.0) 12.8 (12.890 (<LOD-2.60) < LOD < LOD 4.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.90 (1.80) 4.1-17.0 (5. < LOD means less than the limit of detection.0 (6.8) 19.0) 5.66) * * 1.1 (9.47) * * 1.52) * * 1.7) 11.60 (5.00) 3.290 (<LOD-.60 (1.81) 11.42-3.750-1.0) 11.4) 18.10 (. population from the National Health and Nutrition Examination Survey.4 (7.71 (2.20-4.96-3.717-1.00-19.955 (.5-16.50 (4.74 (8.80) 3.46) 10.47) 5.5) 15.80 (2.61) 4.954 (.0 (8.70-23.80) 2.490-2.30-4.02-5.00-27.76 (2. 01-02.0 (7.45 (2.5) 20.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.39 (3.20 (.2 (7.81) 11.1) 95th 13.80 (4.27-3.0) 10.623-1.00) 3.51) 2.70) < LOD < LOD 75th 3.0 (9.83 (5.80) 11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.73) * * .20 (.9) 8.26 (5.90) 2.00-12.0) 6.8 (14.19) 9.80) .40-16.60-18.1) 13.68-7.3-15.80) .70-14.3) 17.58 (5.830 (<LOD-3.8) 11.98-5.0-27.08-15.54 (3.17-3.2) 14.21) 9.13-2.35-11.50) 2.2 (9.40-19.29) * * 1.80-24.85 (3.27-15.50 (.43-12.40 (.10 (.82-12.4) 17.70 (2.50-36.70-19.4 (7.2) 16.9 (8. 0.0 (8.94) * * .2 (14.S.20 (2.10-7.0) 11.97) 90th 7.16 (2.5 (8.32) 1.700-1.981 (.4 (9.758-1.94) 3.56 (6.600 (<LOD-1.35-12.0) 7.97) 8.00-12.970-2.20 (.70) < LOD < LOD 1.8) 7.11 (.00-27.55-6.0 (6.72) 5.0 (8.08 (<LOD-2.00 (5. and 03-04 are 0.22 (. interval) 1.56 (4.0) 10.99 (5.0) 11.9-18.5 (11.44-38.81) 1.30 (2.2) 16.70-11.30 (4.10) < LOD < LOD 4.05-7.2-20.38-5.20-7.52-11.0) 15.4) 20.670-1.50 (2.00 (1.67) 3.00 (4.03 (.34-7.50-5.860-2.7 (12.2) 471 576 308 664 822 701 814 1122 922 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.0 (7.30 (2.8) 7.01) * * 1.04) < LOD 1.86-15.2) Sample size 1949 2520 1931 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.4 (9.86 (1.80-22.79 (5.579-1.

82-6.80 (7.95) 2.430-1.924 (.8) 7.6) 9.47 (3.00-17.37 (4.710 (<LOD-1.87 (1.750 (<LOD-1.93-5.56) .69-10.28 (4.40) < LOD < LOD 75th 2.533-1.69) 2.43) 2.66-15.61 (1.7 (8.7) 18.0 (8.57 (6.566-1.75) 14.920 (.37) 9.03) 2.500-1.82-14.88) 2.67) 1.773-1.58) * * 1.54-11.40-28.28-9.90-5.780 (<LOD-1.900 (.52) 4.73 (1.40) 4.04-6.88 (5.9 (9.38) .7) 471 576 308 664 821 699 814 1122 921 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .40-12.3) 952 1187 927 997 1332 1001 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.03 (2.87 (3.570-1.42) 12.82-14.8) 6.47 (1.40-14.05 (1.07 (.68-4.61-29.98) 9.855 (.41) Selected percentiles ( 95% confidence interval) Total * * 50th .57) 4.66-34.650-1.608-1.9) 12.4) 4.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.83 (7.1 (8.2 (8.31-14.41) .81 (1.43 (3.88-10.34) < LOD < LOD .5-20.440 (<LOD-2.10-13.2) 9.21-23.71) 10.44 (2.23 (4.54-15.7) 5.60-9.54-4.1 (7.66 (1.00 (4.94-10.932 (.5) 12.68) < LOD < LOD 3.69) 4.94-23.67-19.1 (11.9 (5.818 (.30 (1.1) 4.1) Sample size 1949 2519 1928 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.98) .98) .02 (7.4 (9.5) 8.87-5.560-1.54) .14 (3.09 (.79-3.92-2.1 (6.790 (.5-13.8) 8.31 (3.15-10.94 (2.549-1.2) 13.60) * * .98-5.27) < LOD 2.2 (10.84) 7.9) 16.20-8.45-5.94 (4.79-9.80 (2.34) * * .67) 4.55-20.72) 11.04 (1.574-1.11-6.2) 5.45-11.870-2.84 (5.28) 10.42 (3.77 (6.37-5.25) 6.S.6 (10.996 (.00-13.47) * * .81-5. interval) .7) 12.1-15.30) 2.7) 672 678 472 509 695 577 595 948 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.960 (.1 (10.56) 7.75-7.18 (.5-32.95 (3.94-9.10 (3.75 (7.57 (4.85) 2.51-5.74) 4.75) 2.61 (1.40-5.56-13.2 (6.2) 95th 12.80 (6.5) 7.03) 2.37 (5.35 (1.6) 8.40-3.8 (10.64-5.38 (1.01-2.56) 4.24-3.3) 5.50) 7.8) 12.3) 15.47 (3.620-1.09) 2.90-8.76) < LOD .9 (9.4) 13.3) 12.02-14.82-26.88-15.1) 4.5-16.60) 2.41-12.34 (6.4 (4.34 (6.890 (<LOD-1.5) 11.9-28.02 (2.40 (3.540-1.29) * * .00) 8.35) < LOD < LOD 3.0) 6.61-13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.06-2.29 (2.89-3.98-22.66 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.93) 9.62-5.69 (4.9) 11.6 (9.2) 5.19 (4.93-9.71-2.2) 8.5) 7.78 (2.883 (.890 (<LOD-1.28 (2.36) * * 1.03-6.92-5.26) * * .05 (.4) 4.53-11.05) .00-19. population from the National Health and Nutrition Examination Survey.3) 16.7 (9.02-2.98 (3.6) 13.75 (3.83) 8.45-5.32-12.57-10.89) * * 1. Fourth National Report on Human Exposure to Environmental Chemicals 121 .1 (9.37-3.09-11.820 (.62) .2) 7.25) < LOD .23) 4.74) 90th 7.80) 9.860 (.76-4.0) 7.85 (6.510-1.8) 16.43 (.03 (7.6) 11.53 (6.46-5.66 (5.7 (10.00 (4.53) 9.633-1.94-22.46) 2.39 (2.47) 2.13) 4.54-2.5 (4.960 (<LOD-2.28 (5.830-1.

8-21.0-24.34-10.70-8.580-2.29) < LOD < LOD < LOD < LOD 3.31-12.30) < LOD < LOD .0) 23.75 (3.90 (2.00-4.17 (7.8-20.20 (<LOD-2.8 (12.50) .80 (2. which may vary for some chemicals by year and by individual sample.0) 13.6-19.3) 8.S.37) 2.20-4.80-21.5 (8.15-2.47-6.22 (6.00-4.1) 11.20-8.670 (<LOD-1.0 (9.80-6.00-18.9) 10.00) < LOD .51) < LOD 1.34-5.97-4.92-17.5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .31-7.3 (9.58.80-3.30) 8.0) 9.96) 3.27) 4.6) 14.2) 14.80 (2.70-9.10 (<LOD-1.0 (15.9) 16.89) 2.29-4.00) 7.30) 3.0) 12.98-9.6 (10.0) 7.00-18.95 (2.7-21.0) 9. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .90 (2.30) < LOD < LOD 4.0-29.10-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 6.88) 10.11-6.9-17.8-17.89 (2.52 (6.24-5.5 (9.74) * * * * * 1.25 (2.9) 9. 0.90 (2.27 (3.39-13.5) 21.62-17. see Data Analysis section) for Survey years 99-00.0 (13.34-3.12 (4.5 (8.90) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6) 14.42 (1.00 (.0 (10.18 (3. population from the National Health and Nutrition Examination Survey.1-23.7 (11.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1. and 0.86-10.0) 18.0) 14.78) 5.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.6 (10.20) 3.0 (14.0) 14.90 (6.10) 6.50) 5.00) 3.80-4.80-14.60) < LOD < LOD 2.50) 3.0 (5.99 (3.60 (2.95-9.00-16.7 (10.3) 20.45 (3.37 (3.4 (14.4) 11.82) 8.16-1.31) 1.24 (2.18) * * * * * * * * 1.72) 2.4-17.80-8.0-19.0) 11.670 (<LOD-1.0 (7.06 (2.790 (<LOD-1.7) 22.1 (10.28 (7.5.0) 12.0) 19.670 (<LOD-1.73) 7.81-6.58 (1.27 (7.50-5.3 (9.77-3.70 (1.35 (6.90 (6.10 (.8 (12.5-26.3 (6.04 (3.8) 9.22 (6.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. respectively.8) 8.80) 5.970 (<LOD-2.88) 3.2 (9.0) 13.90 (5.3) 22.90 (1.80 (5.01 (2.35) 4.67-10.3) 10.6) 18.61-32.9 (7. 01-02.90 (6.7-19.20) 3.50-4.20) .1 (10.66-13.41) 3.41-5.67) 3.650-1.61 (3.70) 2. and 03-04 are 0.30) 3.66) 4.00-9.90-15.14 (6.910 (<LOD-2.27) .9-14.7) 14. < LOD means less than the limit of detection.7) 10.3) 14.46-4.46-28.34 (6. 122 Fourth National Report on Human Exposure to Environmental Chemicals .0) 11.4 (10.0 (8.00) 3.0 (10.63-14.3 (7.75 (2.3 (11.80-12.10-10.95 (5.5.96) 90th 7.40 (2.9 (12.70-5.0-24.9-15.670 (<LOD-1.60 (6.27) 9.80) .60 (5.20-18.10-15.680 (<LOD-1.3 (12.40 (2.7) 15.00) 8.22-12.90 (6.49-4.33-11.6) 11.84-4.8-20.90-9.0 (9.92) 9.53 (3.80) .70-9.15-6.39 (5.59-3.35-3.0-33.90-15.6-41.2 (7.4) 7.0) 12.7) 16.40) < LOD < LOD 75th 2.90) 8.67) 4.77-14.4 (10.64) 10.70 (8.22) 8.90-31.9) 95th 14.740 (<LOD-1.

910 (<LOD-1.89-13.91) 3.27) * * * * * * * * 1.68-10.79-9.63 (2.54-5.29 (5.03 (6.83 (6.7) 14.30) 2.73 (5.11-3.690 (.8 (10.00) 2.6 (12.6) 14.12) < LOD < LOD 4.83 (7. Fourth National Report on Human Exposure to Environmental Chemicals 123 .5-17.1 (19.63 (6.69-11.7 (8.25 (4.S.99 (4.42) 7.72-4.89 (3.3 (7.5 (11.760 (<LOD-1.973 (.39-17.7 (10.92 (5.00 (2.86) 9.32) 2.1 (8.2) 12.36 (2.4 (11.82-11.68-19.54 (7.42) 8.810 (<LOD-1.29) 3.1) 20.5) 10.9 (9.50 (6.27-13.34-18.96-10.4) 7.89-10.6) 12.82-8.45) 3.8) 14.74-19.79-6.58 (4.9) 16.7) 15.30-5.6 (11.61 (2.2) 10.06) .45) 6.81 (7.00 (<LOD-1.75-3.7) 14.7 (10.4-16.9-17.95) 90th 8.71 (1.27) 5.94-14.67 (7.3) 6.33-10.5) 8.86 (3.96-11.780-1.2) 19.09-11.00 (5.86-3.5 (15.53-8.6 (10.6 (13.590 (<LOD-.28) 6.48 (2.0 (13.14 (2.21-21.78 (6.34) < LOD < LOD < LOD < LOD 3.07) 2.89) 5.51-10.3-17.7) 9.93-10.6 (11.51-7.2-15.3-34.2) 8.4) 15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70-2.95) 3.38 (2.4-16.97) < LOD .95 (2.2) 15.00 (<LOD-1.19) 3.47-9.78-10.74-4.68-4.1) 13.8) 16.2-30. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .3-15.29 (2.6) 95th 16.0 (10.89-3.38-13.68) .91-9.9 (9.0) 14.50-17.25-9.2 (9.55 (2.89-3.97-4.6) 952 1187 945 997 1331 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * .3-17.15 (1.37) 3.2) 12.6) 13.07-3.6) 6.2) 16.71) < LOD < LOD 2.0-19.70-35.01-5.64-11.59-3.920 (<LOD-1.55) 16.80) 3.85-8.5 (9.67 (1.02-4.00) 8.7-23.1) 10.6-19.28-12.78 (4.3) 8.8 (8.55) . population from the National Health and Nutrition Examination Survey.8) 11.75-3.07) 2.23-3.11 (5.99) 2.89 (2.33) 3.41 (7.18) 2.93 (6.30) 7.21) * * * * * 1.4-18.92) 3.38 (1.620 (<LOD-.00 (7.42-19.88 (1.4) 6.950) .37-5.00 (3.1 (13.16 (3.87 (3.27) < LOD .530-1.6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.7 (11.0-21.15) < LOD < LOD 75th 2.5) 13.06 (<LOD-1.85-17.03) 3.28 (1.4) 7.38 (.78) 4.94 (5.38) 1.93 (2.5 (10.9) 19.03 (2.3) 9.2) 672 678 497 509 694 578 595 948 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.72) 4.890-2.4) 16.4) 7.5) 22.3) 12.5 (8.52-3.0 (11.3-21.93 (<LOD-2.88-7.940) < LOD < LOD 1.7) 12.30) 8.05-3.2) 12.4) 9.27) 1.32-8.77 (2.07 (5.0 (8.2 (9.54) 9.12 (7.20-3.77 (2.9 (9.850 (<LOD-1.6 (13.44-6.04) 9.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .4-15.7-19.6) 7.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9-25.43 (2.16-14.29-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.09-11.77) 3.

86) 3.510 (.160 (<LOD-.850) < LOD .47) 2.340-.398-.960-1.750-1.60) 3.880) < LOD 75th .78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .240 (<LOD-. 124 Fourth National Report on Human Exposure to Environmental Chemicals .20 (1.80) 2.457 (.760 (. which may vary for some chemicals by year and by individual sample.19-1.618) * .80 (2.50 (1.450 (<LOD-.46 (1.45 (1.00-4.597) * .15) 2.29-2.36-4.10-1.910) 1.16-3.10) 3.04) .27 (3.32) 3.30) 1.540 (.740 (.60 (2.570 (<LOD-.10) 1.90) 3.25-1.930 (.580-1.94 (2.80) 3.37-2.45 (1.98 (2.490 (<LOD-.98) .380) .460-.86 (1.94) .30) 2. see Data Analysis section) for Survey years 99-00. respectively.40 (1.780 (.690) .400) .70 (1.10) 1.30 (.510 (<LOD-.22-2.80) 2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.41 (2.690-1.54) .42-2.70-7.16) 2.260 (<LOD-.76 (1.780) .50 (1.910-1.880) < LOD .336-.592) * .700) .1.20) 2.48 (1. 0.58 (1.830 (.30) 4.45-4.690 (.11-3.00 (1.15) 2.89) .740-1.17-4.584) .303-.13) .50-2.20 (1.570 (<LOD-.30-3.18 (. < LOD means less than the limit of detection.90 (1.505 (.03) 1.810) .61 (1.970) 1.01-3.587) * * .880 (.00) 2.14-1.69-4.20) 3.57 (2.560-.22-8.91) 2.32-1.10) 1.65 (2.89) 471 575 296 664 822 690 814 1122 919 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .95 (2.570-1.26) . population from the National Health and Nutrition Examination Survey.20-2.570) * .83 (2.690-.710 (.68-5.41-5.89-6.26 (2.380-.27 (2.21) 3.95) 2.980) 1.820 (.600-1. interval) Selected percentiles ( 95% confidence interval) Total * .95-5.20) 2.20-3.359-.549 (.63 (1.70-2.46) 1.970) .592) * 50th .48 (2.78) .30-1.201-.S.90) 2.30-3.590-.38) 1.20) 1.710 (.730) .570 (.759) * .89) 1.343 (.45 (2.01-1.83 (2.382-.10-1.50) 1.30 (.79) .960) .05-3.54-2.210 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.453 (.64 (1.73 (1.77-2.31-3.720 (.59-2.31) 2.949) .83) .570 (.30 (1.20-1.720-1.04) 1.46-3.50 (1.97 (2.34) 2.22-3.388-.49) 2.76-6.459 (.74-5.47 (1.750) 1.550 (.87-3.70 (1.79) .440-.600 (<LOD-.580-.820 (.96-3.23-3.910 (.34) 2.749 (.720-1.17) 1.930) < LOD .50-2.20-2.550 (.80) 3.940) < LOD .60-4. and 0.350-.700) .94 (3.50 (1.59-6.800 (.46 (2.960) 1.39) 2.98-3.22-3.08 (2.740 (.35) 1.80) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40 (1.31) 95th 2.75 (2.20 (2.350-.96-5.54 (2.585) * * .960 (.930-1.467 (.20) 3.17) 1.32 (1.14 (1.20 (1.455 (.30 (. 01-02.600-.960) .390-.990-1.30) 4.860) < LOD < LOD .280-.500 (<LOD-.930) 1.449 (.75-2.680-1.680-1.73 (2.57 (1.18 (1.01) .74) 3.60) 2.620-1.950) 90th 1.31-3.592-.09 (.88) 1.50 (1.90) 2.22 (1.353-.08 (2.49) .710) .380-.00) 1.657) * * .29) 1.05-2.80 (1.2.70 (1.650-.740-.00-2.33-2.790 (.13) 2.11-3.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20) 1.83) 1.77 (1.840 (.16) 1.390-.73-5.09. and 03-04 are 0.90-4.78) Sample size 1949 2519 1905 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .83) 2.80) 5.780 (.55 (3.425 (.670) .

84 (2.08-3.440-1.67) .13 (1.250 (<LOD-.940-1.38 (2.390) .285-.447 (.250 (<LOD-.47-4.11-2.480-1.43 (1.17) 2.136-.350) .38 (1.07) 1.690) < LOD < LOD .09) .42) .640 (.58) 3.57 (1.710 (. population from the National Health and Nutrition Examination Survey.790 (.23) 3.97 (1.510 (.320-.50 (1.99) 2.50) 1.560 (.22) 1.330 (<LOD-.57-2.380) .07 (.80) 2.08) 1.444-.34 (1.03-1.480) .65) 2.400) .92) 3.552 (.490 (.10) 2.412-.43) 2.76) 1.23) 1.910) < LOD .60 (2.05 (1.64 (2.97) 2.02-6.393 (.400-1.310 (<LOD-.52) 3.318-.33) .43) 2.580) .16) 1.720 (. Fourth National Report on Human Exposure to Environmental Chemicals 125 .Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.630) * .820) .98) 952 1187 906 997 1331 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .61 (3.23 (.540-.84-6.44) 2.72) 1.78) 3.22) 4.485) * * .234 (.520-.920) .560-.530 (.77-3.71) .270-.90) 2.07) 5.82) 2.88) .180 (<LOD-.77 (3.471-.61-3.460 (.550-1.30-2.18-2.19 (1.36) 3.82 (2.470) .22) .42-6.23) 2.55-3.670 (.98) 1.710 (.32-1.680 (.750 (.660-.300 (<LOD-.92-8.72) Sample size 1949 2518 1903 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .89 (1.60) 1.47 (1.81) 2.38-3.460) .760) .550-.950-2.840) .05-2.67-3.930-1.08-2.730) .70 (2.448 (.700 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.42 (.335-.270 (<LOD-.550) .380-1.17-2.640 (.67 (1.710 (.42-8.645) .20) 1.61-3.53) .62 (1.23) 2.S.43) 1.89-3.688) * .02-3.32) 1.08 (.03-2.32 (.377-.63 (1.91 (1.06-2.07-3.22 (2.33 (1.08-2.280 (<LOD-.08-3.69 (1.69 (3.49 (1.20-2.05) < LOD .58-6.980-1.08-3.520 (.60 (1.64 (2.95) 1.590-1.08-3.04) 95th 2.17) 2.52 (1.72-4.08-2.79 (1.66) .22-2.97 (1.28 (1.310-.58 (1.750 (.790) .830 (.590) * 50th .830) 90th 1.05-4.08) 2.870) .45 (1.39 (1.75 (1.67 (1.79) 1.00-3.77-4.70 (3.510 (.470 (<LOD-.870 (.300-.500-.820) 1.57-4.310 (<LOD-.800) < LOD .880) 1.29-4.07) 1.71) 2.14 (2.02-3.305 (.11 (.742) * * .580-.591 (.550-.75-3.535 (.510-.330-.73-3.08 (2.88 (1.348-.44-2.25-3.320-.740) .07-2.31-1.97) 672 678 478 509 694 552 595 948 744 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.700 (.61) 2.32) 2.253-.368) * .403) .230 (<LOD-.05) 1.372 (.11) 1.75) 6.62 (2.990-1.71 (1.67) 1.47 (1.515) * * .07) 1.390-1.39) 2.30) 3.22-3.97) 1.92 (1.66 (2.06) 4.32) 5.41 (.22-3.20-7.04-5.16-2.739) * .99) 1.740) < LOD 1.80) 471 575 296 664 821 689 814 1122 918 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .55 (1.49-4.509 (.94) .73 (2.00-1.57 (3.75 (2.800-1.60) .370-.460-1.840) 1.580 (.720-1.590 (.24) 4.270-.72 (1.640 (.850) 1.00 (3.760) < LOD 75th .380-.560-.597) * .453 (.04-1.900) 1.700 (.16-1.72 (2.45 (2.840) 1.87 (2. interval) Selected percentiles ( 95% confidence interval) Total * .

2-26.20-4.0 (17.70 (.10 (1.7-41.1 (10.3 (12.13 (1.76 (2.9 (19.7 (28.66-5.0-41.18) 14.23-2.1 (11.5-74.71 (4.04-8.83-2.70 (1.10 (1. 0.90 (1.79 (2.1-19.0) 4.42) 1.0 (32.2-27.44-7.9) 17.9) 38.41) 5.8) 39.9) 18.5.70 (7.2-62.06) * 2.2-80.05) * 2.88) 3.70-17.0-92.2-27.5) 30.77 (1.05-3.02 (2.3) 33.79-2.90) 11.3 (23.2 (12.8-24.59 (1.48-2.44) Selected percentiles ( 95% confidence interval) Total * 2.13) 12.19) 2.81-2.6 (15.64-8.50-7.0-260) 34.29) 2.0 (8.43-7.80) .25-3.4 (19.30 (.4 (10.0) 15.8 (12.0-53.40) < LOD 2. interval) 1.86-3.0-47.94 (1.11) 2.06 (1.79 (1.0 (13.17-2.5 (24.72 (1.87-7.80) < LOD 1.19-2.54 (3.4 (15.10) .26 (. < LOD means less than the limit of detection.85 (1.0-52.83 (3.10 (7.50-17.64-3.2) 31.49-2.20 (2.92) * 2.0-62.10 (1.13 (1.96) 5.18.0) 16.4.61-2.2) 16.1) 95th 48.5-20.0-41.10-13.11 (4.2-47.1 (26.1) 18.50-20.10) 39.21 (1.7-22.12 (3.6) 52.0) 13.45) 2.2 (19.0-53.0-69.05) 1.4-22.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0 (8.0-110) 42.53 (1.41) 1.0-39.85) * 2.46-6.98 (1.3 (24.9-21.1 (22.9-51.40) < LOD 1.5) 69.0) 3.1-46.09 (4.0-43.0 (8.50-5.93-3.0) 8.21 (4.0) 28.60 (2.0 (25.81-3.48) 5.90 (1.7) 47.0) 471 575 310 664 822 717 813 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.80) 1.40-16.0) 30.1) 140 (46.0) 45.14) 5.97) 6.8 (12.0-41.0) 28.660-2.0 (38.83-2.83 (1.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.2-33.40) 50th 2.20) 1.7 (12.0) 3.0) 19.00-24.53) 40.0 (20.44) 2.41) 1.91 (4.0-58.8 (22.53) 1.0) 3.41 (1.90-8.21 (3.S.58) 16.7 (12.35-6.8 (26.0) 17.6-54.0) 4.8-21.0) 31.58-2.82 (1.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6-22.31-6.1 (25.30) 4.18) 6.690-3.33 (5.70) 1.9 (23.36-2.5-45.3) 26.0 (38.65 (4.0-49.0 (38.30) 11.99 (2.75-14. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0) 3.29-4.5-27.0) 6.70-6.50-2.830-4.0 (40.92-5.29-9.4) 19.0-110) 34.600-2.60) < LOD 1.0) 18.67 (1. and 0.1) 38. see Data Analysis section) for Survey years 99-00.8) 62.6 (9.70) 5.1-40.10 (1.3) 28.69) 2.71-2.0) 4.0) 20.3 (10.86 (1. which may vary for some chemicals by year and by individual sample.0-29.59 (1.45) 2.0) 33.0) 42.3) 31.44) 3.1 (25.70) 1.0 (24.50 (2.4-76.6 (11.1) 38.70 (1.57-2.80) 90th 38.41-4.0 (21.54 (1.07-5.5-40.0) 15. respectively.0) 5.3 (14.8) 32.470 (<LOD-1.9) 48.1-20.52 (4.40-4.23-2.9 (19.04) 3. 01-02.30-14.0-31.23) 9.4) 38.0 (19.2-39.53) * 2.0 (7.46 (.0) 16.0 (26.00 (.77) 38. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1-25.0) 32.46-2.6-45.830-3.0 (38.04 (<LOD-2.80-2.0-230) 35.0 (38.26) 75th 11.0 (37.16) 2.71) 5.10-4.76 (2.0 (38.0 (11.0-39.78 (1.27-6.80-18.7) 20.0-58.610 (<LOD-1.530-4.88) 1.98) * 2.0 (38.6-27.6 (26.12) 1.0-50.57-2.18) 20. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (20.16) * 1.0) 17.63-6.0 (6.9 (10.00 (.61 (1.0-62.32 (2.3 (12.9 (27.74-2. population from the National Health and Nutrition Examination Survey.78) 9.3) 38. and 03-04 are 0.48-2.1-47.0 (33.8) 41.95 (5.0) 20.

870-3.0) 25.88 (1.0-70.5 (17.12 (1.6-32.70 (1.22-2.4 (25.8) 15.2 (15.60 (.6-49.67 (1.9) 24.63-5.7) 61.6 (24.20-5.1 (33.09 (5.62) 4.5-97.0 (17.75) * 1.0-118) 29.0) 47.5) 70.17-3.57) 4.16 (1.43-2.31) 2.22-3.32 (3.0 (6.19-6.899-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7-19.60) 4.7-47.1 (12.88 (1.930 (<LOD-1.24 (1.0) 3.2-47.36 (4.3 (20.3 (9.14 (.48) 1.5 (13.17) 2.1-63.19-14.25-3.9-36.94-20.1) 52.47 (1.9) 3.00-16.5 (15.4 (11.3-22.06) 75th 9.1 (39.1) 13.96) 2.47-17.0) 952 1187 945 996 1330 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.7-20.38-1.58-2.2-28.7) 23.1) 25.06-1.01 (.8-45.93) 5.2 (9.5 (8.4 (19.0 (19.59-15.4-21.79 (2.36-13.1-22.11-2.00 (4.4 (5.860 (<LOD-1.890-4.83) .32-3.3 (8.0) 48.7 (24.19) 5.34) * 1.1-60.0) 13.75 (1.95) 90th 32.9 (19.07-2.4-34.2) 36.7) 95th 51.16 (1.66 (1.46) 1.38) 5.94) 1.1) 15.11) < LOD 1.00) 6.5) 27.12) 3.5-190) 30.7-109) 22.80 (1.4-67.1) 17.03-2.88 (4.14-8.28) 1.4) 14.7) 30.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.6) 7.27-3.64 (1.40-7.750 (<LOD-1.6-38.30) 28.8) 3.2) 13.7) 66.3-19.4) 3.9-18.4) 12.2-70.5 (6.08) 1.9 (10.7 (10.00) 1.66) 8.83 (.6-51.27) 10.40 (5.7 (11.95-16.23) 37.9 (7.8-26.95 (2.4 (21.18) 3.62 (2.5-36.870-3.4 (12.26-2.1) 36.0 (25.46-6.61 (1.9 (26.51) < LOD 1.1 (34.67-16.03) 1.35) .3-42.58-17.6) 3.2) 4.4-39.3) 28.02) 1.36) 10.82) 1.2) 13.61-22.76-2.9-37.2 (22.6) 19.6) 23.1) 25.97 (1.1 (50.23-1.99-4.46-5.1) 27. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.41 (2.35 (2.50-5.33-5.6 (7.8-34.3) 13.0-40.9 (39.2) 41.1) 27. Fourth National Report on Human Exposure to Environmental Chemicals 127 .22 (2.68) 47.52 (1.18) * 2.56 (2.08 (1.16 (1.7) 26.S.8-43.37-2.5 (15.48 (4.38-5.57 (6.6) 3.27) 50th 2.69-18.22 (.7 (18.33) 2.870-3.0) 30.680-4.8) 32.53) 1.35) 1.06) 1.7 (18.50 (2.9) 3.2-34.45-1.54-15.54-2.21 (4.4 (25.91-2.47 (3.6 (27.7-43.15 (.55 (2.2) 671 678 497 509 694 578 595 947 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2) 471 575 310 664 821 715 813 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.51) .40-4.4 (9.07-2.4-71.0-71.69-5.59-2.56) 1.9 (13.67-3.6 (11.95-16.4) 12.3-27.46-22.5-43.20) Selected percentiles ( 95% confidence interval) Total * 1.0 (23.8) 23.75 (1.8) 11.6) 11.7-38.43) * 2.07) 9.2) 33.8 (7.18-1.96-16.45 (1.2-38.16-2.0 (23.0 (14.02) * 1.61-2.94) 19.68 (1.71-2.0) 10.44) 9.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5 (41.2 (8.43-12.9-52. population from the National Health and Nutrition Examination Survey.75-6.28 (1.2 (16.0 (32.5 (34.72) 2.9-41.1) 13.91 (6.8-37.9) 24.19 (1.90 (.8) 31.29-5.6) 112 (40.84-13. interval) 1.26-4.27 (6.71) 8.33) 1.70-4.33) < LOD 1.19) 5.670-1.39 (1.06) 1.52-4.7) 34.59-2.88 (4.888-1.71 (1.86) * 3.02 (.23) < LOD 2.67 (1.40 (2.80-8.79-17.9) 12.82 (2.7-37.7) 15.9) 54.9-95.0 (39.1 (25.2 (21.3 (10.66 (1.86) * 2.37 (1.38 (3.3 (10.

190 (.840) .990) . 128 Fourth National Report on Human Exposure to Environmental Chemicals .090 (<LOD-.60) 1.140) .310) < LOD < LOD < LOD < LOD .099-.580) 471 576 310 664 822 717 814 1118 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .10) .610 (.650 (.30) .620 (.130) .42) .330-.680 (.162) * * * * * .470 (.130-.460 (.110-.290) < LOD < LOD < LOD < LOD 90th . and 0.610-1.10 (.410-.42) .300-.S.870 (.560 (.850 (.290 (<LOD-.190 (.410-.10) .680) .130) .320-.40) .870 (.400-.490 (.100 (. 01-02.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.180) .830) < LOD .120 (<LOD-. 0.270 (.130 (.690-1.170-.870) < LOD .540) .350) < LOD < LOD < LOD < LOD .220 (.700) 952 1187 946 997 1329 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .160) .830) .780) < LOD 1.720-1.1.120-.12 (.410-1. which may vary for some chemicals by year and by individual sample.36) .30) .720) .090 (<LOD-.1.640 (.190 (.700-1.160-.290) < LOD < LOD < LOD < LOD .370-.280) < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.450 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .730) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.210 (.230) .610 (.530-.570) .130-.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethyldithiophosphate (DEDTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.390) < LOD < LOD .540 (<LOD-.120-.350) .450 (.540) Sample size 1949 2516 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .850) < LOD .080 (<LOD-.200) < LOD < LOD .940 (.00) .440-1.650) .680-1.760) < LOD .05.380-.650-1.930 (.117 (.860) .310 (.700-1.090 (<LOD-.420-.390 (.870 (.540) .380-.430 (.32) .640) .140-.730-.840) .090 (<LOD-.460-.310) < LOD < LOD < LOD < LOD .230-.090 (<LOD-.430-.240 (<LOD-.150 (<LOD-.600 (.220 (<LOD-.320 (.680-1.660 (.20) .140-.360-.830 (.310-.700-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .650) .640-1.770) < LOD 95th .160) .360-.300-1.900 (.150) .410) < LOD < LOD < LOD < LOD .10) .630 (.510-1.820 (.470-1.740) < LOD .850 (. and 03-04 are 0.080 (<LOD-.210 (.050-.830 (.140-.630 (.610-.640) .870 (.860-1. respectively.260 (.990) .130-.450 (.084-.15) . see Data Analysis section) for Survey years 99-00.990 (.380-.310 (.550) .30) .090 (<LOD-.650-1.13) .820 (.560 (.171) * * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.03) .58) .700-1.370-.720 (.870 (.770 (.

750) < LOD 95th .67) .940) .66) 1.140-.660-1.19 (.140-.740 (.057-.370 (<LOD-.270) < LOD < LOD < LOD < LOD .860 (.110) .510-.740) < LOD 1.860 (.380-.390-.640) 952 1187 945 997 1328 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .29 (.600) .150-.810 (.170 (.870) .330-.12) < LOD .390-.360 (.360) < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.260-.090 (<LOD-.330 (.070 (<LOD-.290) < LOD < LOD < LOD < LOD 90th .380 (.380-1.310) < LOD < LOD < LOD < LOD .140) .330-.070 (<LOD-.610-1.800-1.230-.110) .700-1.880-1.500-1.540 (.110) .36 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.780 (.210 (.100 (<LOD-.410) .570-.400 (<LOD-.710-1.180-.720 (.780) < LOD 1.080 (<LOD-.60) .540) 471 576 310 664 821 715 814 1118 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .580 (.670-1.110-.300-.080 (.970) .120) .116 (.940) .111) * * * * * .240-.060-.220) < LOD < LOD < LOD < LOD .730) .Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethyldithiophosphate (DEDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.03 (.410-.230 (<LOD-.070 (<LOD-.580-1.00) < LOD .860-2. Fourth National Report on Human Exposure to Environmental Chemicals 129 .440 (.170) < LOD < LOD .03 (.14) 1.190 (.02-1.700) .460 (.190-.990) .450) .090 (.250-.380-.260) .570 (.410) < LOD < LOD .300 (.58) 1.140-.400) .510) Sample size 1949 2515 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .43) .24 (.580 (.230) < LOD < LOD < LOD < LOD .01 (.670 (.330 (.890 (.170 (.190 (.200 (.220 (.140-.161) * * .990) .38) 1.080) .78) .960) .580) < LOD .62) 1.86) .730 (.360-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.410 (.580) .540) .650) < LOD .540 (.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .09) .20) 1.050 (<LOD-.520-.850 (.490-1.320 (<LOD-.03) .084-.550 (.560 (.380-.670 (.300-.340-.03 (.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.280) < LOD < LOD < LOD < LOD .880 (.720 (.640-1.600-1.86) .730) .110) .270 (.140-.410 (.650-1.330-.360-.700 (.500 (<LOD-.730) .500) .02) .450 (.550 (.700 (.24) .570-1.S. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .410-.200 (.120) .100-.070 (<LOD-.470 (<LOD-.760) .440-1.

59-5.691 (.0) 2.770 (<LOD-1.48 (2.370-.800) 90th 13.65) 1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70-50.53) 20.0-38.00 (.30 (1.750-1.40 (1. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00.33 (4.63) 32.800) 17.50) .0 (17.0 (5.90) .99) 19.40-8.82-4.80 (4.87) 5.99) 11.94 (1.32-9.0-38.90 (2.840 (.0) 3.1.94-8.52) 5.30 (1.0) 2. < LOD means less than the limit of detection.840-3.170-1.40-4.330 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.690 (.52 (1.90-20.39) .49 (1.51-8.03 (.0 (7.07 (1.360-1.0 (16.0) 5.15) 19.10 (.39 (2.880) 5.0 (17.40-7.36-3.0 (5.21-3.97) 20.0-44.00) .720) 2.51 (2.0 (5.830 (.0) 4.960 (.40 (1.12) * * * * * * * * .080-1.07) 1.01) 5.11) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10-3. 0.210-1.730 (.800-4.S.10-3.740 (.05-3.425-1.38-3.15) 14.07-3.40-20.0-38.0) 2.0) 5.0-40.0) 7.590 (.00) .61 (1.0) 2.480-.14-5.0 (5.35) 11.42) . and 0.55-4.48) 13.20-17.3) 952 1187 935 997 1331 995 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .94-3.840 (<LOD-1.30 (1.67 (2.20) < LOD < LOD < LOD < LOD < LOD 1.750-2. 130 Fourth National Report on Human Exposure to Environmental Chemicals .88-3.31-10.30) 95th 19.62) 471 575 306 664 821 699 814 1122 925 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .30-3.45 (2.640 (.60) 1.00-17.49) 17.30) .66) 4.97) 20.07 (3.0 (17.70) 2.250 (<LOD-.70-3.11 (1.12-1.29-10.0) 2.0) 2.90) .400-1.14) .30-6.53-7.260-.07 (3.1.110 (<LOD-.21) 3.32 (1.23-6.52 (1.0 (5.610) < LOD < LOD < LOD < LOD < LOD 2.350-.28) 1.90) .0) 2.26 (2.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.0-39.36-3.190-1.85-3.13 (3.14) 2.0) 5.53 (2.05 (3.05 (2.0 (17.67 (1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.610 (.30 (2. respectively.76 (1.600 (.900 (.42) 2.0) 4.0-40.60) .11) 13.28-9.83-3.10 (3.30-7.00-17.620-1.0 (4.47 (3.87) 12.0) 4.40) 2.96 (1.63 (3.70-7.90-9.74 (3.0 (3.40) 1.0) 5.0 (13.870) < LOD < LOD .10 (3.0 (6.28) .31) .20-4.16) Sample size 1949 2518 1930 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .50) 2.510-.910) 2.62-8.00 (1.850) 16.20 (1.20 (1.6) 5. and 03-04 are 0.580 (.0) 4.08.07-3.960 (<LOD-1.83-3.74) 5.770) 2.890 (.70-17.18) 1.68) 2.30 (.37) .350-.49 (1.00) 1.90-28.83) 2.35-10.43-4.90-37.640 (.380-.46 (1.67) .70-30.86) 4.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20-4.0 (17.99 (1.10-9.90 (1.35) 5.55-8. 01-02.0 (4.24-7. population from the National Health and Nutrition Examination Survey.

60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.S.650 (.850-3.260-.60 (1.50 (2.64-4.33-3.29-4.580 (.29 (4.860-2.7) 4.17 (1.82-11.02 (.12 (4.190-1.64) 30.5) 7.69-7.9 (11.47) 5.10-3.470 (.79 (.970-3.88) 17.56) .360 (.80 (.370 (.25 (1.48-42.01 (1.38 (2.740-1.21-3.0 (4.474-1.2-38. Fourth National Report on Human Exposure to Environmental Chemicals 131 .90-6.49-2.1) 471 575 306 664 820 697 814 1122 924 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .97) .32) 9.7) 6.250 (<LOD-.18) 95th 21.00-19.9) 6.62 (1.75) 5.4) 2.590) 2.53) .14-6.44-11.8) 2.340-.39) 20.48-7.23-7.580) 1.57) 1.4-34.8) 2.02) .50 (4.5 (9.06 (.960 (. population from the National Health and Nutrition Examination Survey.98 (4.81-17.22-27.748 (.28-6.47-10.47-10.840-3.07 (2.790) 11.820) .8) 7.35 (.96) 2.57-40.33 (1.27 (2.540 (.40-12.31-7.03) 2.56 (1.10 (2.89 (2.700) < LOD < LOD < LOD < LOD < LOD 1.96-8.22) 2.45 (1.91) 2.630-1.25-9.5-40.0 (9.690-5.940-4.5) 2.8) 7.800-2.09-3.430 (<LOD-.31-18.67 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.340-.270 (<LOD-.07-21.51-44.930) .0) 4.50) .33 (3.2 (8.600 (<LOD-1.340 (.40-2.11) .1) 672 678 497 509 694 551 595 947 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.790 (.85-3.14 (1.390-.17) 5.85 (1.6) 952 1187 934 997 1330 993 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .92 (2.660) < LOD < LOD .890 (.08) .04 (1.650) 90th 10.4 (4.02 (1.88-3.8) 4.540-1.57 (.9) 5.5 (8.91-4.320-1.32-6.330-1.40 (.56) 2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.88 (.13 (2.74 (2.77 (.8) 1.43) .55) 21. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3) 2.3) 3.450 (.370) < LOD < LOD < LOD < LOD < LOD 1.560 (.61) Sample size 1949 2517 1927 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .88 (2.770) .67) 2.150 (<LOD-.1 (7.59 (1.18) 1.69) 2.55) 21.7) 3.11-5.71 (2.96-25.830-3.47) .710 (<LOD-1.31) .260-.86) .580) 16.73 (4.830 (.86 (3.5 (11.7) 5.18) * * * * * * * * .67-6.00) .50) 11.670 (.62-17.310-.41 (4.52 (.270-.1 (5.8 (20.7 (12.240-.57) 8.1) 2.8-33.04-16.05) .33-4.10) 2.430) 1.55 (3.44) .5) 2.67) 1.83-11.15) 9.36 (.40) 1.84) 9.53) 27.41) 18.700) 6.580-1.51-4.820 (.37) 4.340-.71 (.7 (6.33-5.66-47.620-3.31) .780-4.25-38.03) 16.12-4.80) 3.48 (4.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.24) 3.730-3.30 (4.500 (.65 (2.370-1.02-4.83 (4.

Organophosphorus pesticide urinary metabolite levels of children in farmworker households in eastern North Carolina. J Expo Sci Environ Epidemiol 2006. Organophosphate urinary metabolite levels during pregnancy and after delivery in women living in an agricultural community. Garrison RP. Chen W. Elgethun K.38(1):91-97. Environmental and biological monitoring of exposure to organophosphorus pesticides: application to occupationally and non-occupationally exposed adult populations. Kelly-McNeil K. McKone TE. Boccalon P. Jolley L. Griffith W. Lunghini L. Fenske RA. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Arch Environ Health 1998. Robinson LR. Giordani B. et al. J Occup Environ Med 2004. Correlation of urinary pesticide metabolite excretion with estimated dermal contact in the course of occupational exposure to Guthion. Angerer J. Environ Health Perspect 2002. Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets. Richardson RJ. Sciarra G.111(13):1640-1648. Neurobehavioural effects among workers occupationally exposed to organophosphorous pesticides. Bradman A. Quandt SA. Abdel-Azis M.15(2):164-171.12(6):619-645. Charnley G.37(3):382-395. Young AD. Amr MM. Occup Environ Med 2002. Environ Res 1992. Eskenazi B. Fiedler N. Bradman A. Eigenberg DA. Barr DB. Castorina R.60(4):279-286. Urinary excretion of alkylphosphates in the general population (Italy). Reprod Toxicol 1998a. Astroff AB. Eaton DL. Leffingwell JT. Heudorf U.7(5):715-731. Duggan A. Surveillance of occupational. Environ Res 2001. Curl CL. Chukwudebe A. and incidental exposure to organophosphate pesticides using urine alkyl phosphate and phenolic metabolite measurements. Shebl MM. Regul Toxicol Pharmacol 2003. Toxicol Ind Health 1998b.14(6):869-889. Biologic monitoring of exposure to organophosphorus pesticides in 195 Italian children. Peterson JC. Buchanan D. Bozzi N.16(5):417-426.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites References Albers JW.53(1):714. Berent S. Garabrant DH. Atlanta (GA). Kissel JC. Neurophysiological function in farm workers exposed to organophosphate pesticides. Regul Toxicol Pharmacol 2003. Neuropsychological performance among agricultural pesticide applicators.113(12):1802-1807. Temporal association of children’s pesticide exposure and agricultural spraying: report of a longitudinal biological monitoring study. Pilkington A. Environ Health Perspect 2000. Curl CL. Di-alkyl phosphate biomonitoring data: assessing cumulative exposure to organophosphate pesticides. Cumulative organophosphate pesticide exposure and risk assessment among pregnant women living in an agricultural community: a case study from the CHAMACOS cohort. J Expo Anal Environ Epidemiol 2005. Barr DB. Krieger RI. Curl CL. neurophysiological. Freshwater KJ.111(3):377382. The effect of the 14-day agricultural restricted entry interval on azinphosmethyl exposures in a group of apple thinners in Washington State. Fisker-Andersen J. Koch D. Fenske RA. Environ Health Perspect 2003. Kedan G. Momas I. Am J Ind Med 2006. Harnly ME. Lu C. Fenske RA. Centers for Disease Control and Prevention (CDC). Schweitzer SJ.32(5):487-496. Denley HV. Environ Health Perspect 2005. Ann NY Acad Sci 1997. Hansen S. Costa LG. et al. Hawk R.108:521-525. Checkoway H. Anger WK. Sartorelli P. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies.59(7):434-441. Barr DB. Davies JE. Farahat TM.49(9):751-760. Blanchard O. and neuropsychological study of sheep farmers and dippers exposed to organophosphate pesticides. Gillham RA. J Toxicol Environ Health 1981. Mathieu L. Long-term use of organophosphates and neuropsychological performance. Lu C. et al. Eskenazi B. Keifer MC. Sartorelli E. Bouvier G. The relationship between maternal and fetal effects following maternal organophosphate exposure during gestation in the rat. Kissel JC. 86:80-87. Castorina R. Davis SW.59(1):217-228. Environ Health Perspect 2003. Demers P. Grzywacz JG. Vaughan TL. Engel LS. Barnhart S. Metabolites of organophosphorous insecticides in urine specimens from inhabitants of a residential area. Chevrier J. Fenske RA. Jamal GA. Sci Total Environ 1996. A clinical neurological.837:257-268. Franklin CA. Bravo R. Daniell W. Seta N. Abdelrasoul GM. Arcury TA. 2005. Occup Environ Med 2003. Fenske R. Third National Report on Human Exposure to Environmental Chemicals. Greenhalgh R. The effects of occupational exposure to chlorpyrifos on the neurologic examination of central nervous system function: a prospective cohort study. 132 Fourth National Report on Human Exposure to Environmental Chemicals .177:37-41. et al. Novelli MT. Strambi M. Orsi D. et al. et al.110(8):829-833. Aprea C. Astroff AB. Farahat FM. Aprea C. accidental. Kipen H. Barr DB. Am J Ind Med 1997.46(4):367-378. Miller M.

Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Gillham R. Keifer M.2000 and 2001 market estimates. Smit LA. Tumino R. Myers JE. 1991. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Bradman A. Samuels S. et al. Stokes L. Weisskopf C. The Pesticide Health Effects Study Group. Russo J. Salvini S.58(11):702710. Beach J. et al.20(2):115-22. Pesticide industry sales and usage .338(8761):223-227. Narang A. Environmental Protection Agency (U. Int J Occup Environ Health 2006. Jamal GA. Lewis JA. London L. Bull Environ Contam Toxicol 1994. vibration sense and tremor among South African farm workers.52(2):190-195. Caltabiano LM. Washington (DC): U. Eskenazi B. Bravo R. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. low-level exposure to the organophosphate diazinon. Vitayavirasak B. Available at URL: http://www. 2004. Stark A. J Toxicol Environ Health A 2005. 1993 [online]. Barr DB. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Chrislip D. Stephens R. and spatial learning in monkeys and rats. Steenland K. Marshall E.12(2):134-141. Chronic central nervous system effects of acute organophosphate pesticide intoxication.43(1):38-45. Arch Environ Contam Toxicol 2000. metabolite clearance. Johnson C. Berry H. Santana J. Occup Environ Med 2001. Petchuay C.epa. Nell V. Ruberu DK.24(1):18-29.30(2):98-103. Available at URL: http://books. Dinoff TM. May. EPA). Occup Environ Med 1995. Neurotoxicology 2005. and cholinesterase status of date dusters and harvesters in California. McCauley L. Buchanan D. Muniz J. Lasarev M. Office of Prevention Pesticides and Toxic Substances. An epidemiological study of the relations between exposure to organophosphate pesticides and indices of chronic peripheral neuropathy and neuropsychological abnormalities in sheep farmers and dippers. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates.38(4):546-563. Gladstone EA. Spurgeon A.332(1-3):71-80. Pilkington A.pdf. Scand J Work Environ Health 1998. J Occup Environ Med 2002.26(2):199-209. Weerasekera G. Pedersen L. Thompson ML. 4/7/09 Young JG. National Academy of Sciences. National Research Council (NRC).nap. U. Effects of chronic. Hore P. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. et al. Saieva C. Heaton RK. Calvert IA. Masala G. Robson MG. Rothlein J. et al. gov/oppbead1/pestsales/01pestsales/market_estimates2001.52(10):648-653. Claypoole K. Rodnitzky RL. Hansen S. Lu C.edu/ openbook. Lancet. Am J Ind Med 1987. Arch Environ Health 1975. Rosenstock L. Keefe TJ.S. Sci Total Environ 2004.php?record_id=2126&page=1. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Lambert WE. Effects of long-term organophosphate exposures on neurological symptoms. Environ Health Perspect 2005. O’Malley M. et al. S.114(5):691-696. Am J Public Health 1994.113(4):504-508. 1/12/09 Peiris-John RJ. Savage EP. Lasarev M. Buccafusco JJ. Visuthismajarn P. Burcar PJ. discrimination.345(8958):11351139. Environ Health Perspect 2006. Takamiya K. Schenker M. Scherer J. Seiber J. McConnell R. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Wickremasinghe AR. Washington (DC). Occupational exposure to organophosphate pesticides: a neurobehavioral study. Rohlman D. Lancet 1995. Pesticides in the Diets of Infants and Children.44(4):352-357. Levy LS. Jenkins B. Rothlein J. low-level organophosphate exposure on delayed recall. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Mounce LM. Prendergast MA. Chronic neurological sequelae to organophosphate pesticide poisoning. van der Hoek W. Irish RM. Malathion deposition. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Aprea C. Daniell WE. Phillips J. Kidd M. A behavioral evaluation of pest control workers with short-term. Terry AV Jr. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Neurotoxicity among pesticide applicators exposed to organophosphates.84(5):731-736. EPA. Muniz J. Arch Environ Health 1988.12(2):153-172. Frasca G. Neurotoxicol Teratol 1998. Ames RG.68(3):209-227 Maizlish N.S.

malathion is metabolized to malathion dicarboxylic acid. the level may reflect exposure to the environmental degradation products of these pesticides. For example. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides.Organophosphorus Insecticides: Specific Metabolites Organophosphorus Insecticides: Specific Metabolites General Information The specific metabolites of the organophosphorus insecticides discussed in this section are those that are often measured in biomonitoring studies.6-Trichloro-2-pyridinol (6515-38-4) 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol 2-Isopropyl-4-methyl-6-hydroxypyrimidine (2814-20-2) Malathion dicarboxylic acid (1190-28-9) para-Nitrophenol (100-02-7) 2-(Diethylamino)-6-methylpyrimidin-4-ol/one 134 Fourth National Report on Human Exposure to Environmental Chemicals .” Organophosphorus insecticide (CAS number) Chlorpyrifos (2921-88-2) Chlorpyrifos-methyl (5598-13-0) Coumaphos (56-72-4) Diazinon (333-41-5) Malathion (121-75-5) Ethyl parathion (56-38-2) Methyl parathion (298-00-0) Pirimiphos-methyl (29232-93-7) Primary urinary metabolite (CAS number) 3. In addition to reflecting exposure to the parent insecticide. For general information about the organophosphorus class of insecticides.5. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. parathion and methyl parathion are metabolized to para-nitrophenol.

90-4.80) 2.4 (9.3) 8.S.4-15.20-3.7) 9.38 (3.20) 2.02) 1.16) 2.4 (8.25) 3.5.20-16.9 (10.94 (4.90 (3. population from the National Health and Nutrition Examination Survey..0) 10. For instance.0) 8.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.97) 4.78 (7.88 (1.00-24.0 (7.and post-construction structural applications for termite control were to be phased out by 2005 (U. 2002).22) 2.64) 3.97-7.37 (4.60) 5.39-2.80) 1. and is infrequently detected in ground water (IPCS.10 (4.0 (13.40-10.3 (8.0) 8.70-16.43-2. but can be detected in streams receiving runoff from application sites. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.50-2.50-5.44-5.24-1.5) 7.15 (1.0 (7.3 (10.97) 2.80) 4.0 (7.87-6. and on plants for days to several weeks. It also has been applied directly on animals to kill mites.0 (7.81-2.30-1.63 (8.77-6.09 (2. chlorpyrifos was no longer registered for indoor residential uses in the United States.0) 15.24-3.60 (4.90) 7.30) 4.70-11.0 (7.77) 1.40) 2.30) 4. 5598-13-0 General Information The chemical 3.20 (4. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.03) 1.89 (2.71 (2.0) 11.90-8.40-2. pre.0) 18.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.50-4.97) 7.20-4.80-8.67 (2.63 (2.10 (1.0) 10. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.66-4.9 (7.0) 12.83) 1.36 (4.20-2.4 and 0.76 (1. in 142 urban homes and preschools in North Carolina.44-2.EPA.0) 12.47 (4.1) 5.05) 1.20) 10.40-13.80 (7.00) 3.9) 697 660 521 701 602 947 Limit of detection (LOD.71 (1.76 (1.95) 7.3 (11.35) 2.00) 1.10) 2.32) 2.17 (1. and dust.92 (1.50 (2.10 (5.28-3.70-15.6) 7.51-2.25) 1.EPA. interval) 1.62-2.29) 90th 7. USGS.90 (2.61 (1.90 (1.32-1. 1999.4 (10.40 (6.0) 7.55-5.8-15.20-11.37) 5.52-12.9) 11.50 (1.50 (2.1-16.86) 4.52-2.30-9.0) 14.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.50 (2.9 (9.0) 6.5 (8. Fourth National Report on Human Exposure to Environmental Chemicals 135 . The general population may be exposed to chlorpyrifos via oral.8) 9. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.51 (1.31-2.60 (5.44 (3.51) 1.67 (1.27 (7.59-2.68-2.47-11.90-2.09 (3.20 (2.8) 10.30-12.43-2.30 (4.84) 1.50-2.7) 8.50-14.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.31-2.70-17.70 (1.61) 75th 3.29-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.60-3.5-24.72) 2.40 (5.9-18.77 (1.5. Approximately 80.19-3.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.0) 12.10) 6.74 (1.7-23.80) 12.34) 1.53 (1. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al. 2007).70-5. although some tolerances for specific food crops have been reduced in the past to avoid exceeding recommended intake limits for total dietary intake in special groups (U.0 (10.66-15.61-7.21) 3.02 (7.91) 16.19 (1.74-9.00) 2.80 (1.60 (2. dermal.30-11. 2921-88-2 Chlorpyrifos-methyl CAS No.90-7. air.35) 1.0 (9. Exposure can also result from contact with contaminated surfaces.60-2.26) 7.13 (1.0) 12.80-10.46-2. Approximately 21-24 million pounds per year were used domestically from 1987-1998. 2005).05-5.0) 12. applied to structures to kill termites.50 (1. Estimated intakes from diet and water have not exceeded recommended intake limits.60-4. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.90) 3. staying bound to soil particles.63 (1.20) 2. Chlorpyrifos is Urinary 3.68 (7.77-15.7) 13.39) 4.13-3.72-4.59) 2.0) 9.S.60-3.95 (4. Survey Geometric mean (95% conf.04-10.0-28.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.04-10. and sprayed to kill mosquitoes.30) 5.99-4.71 (6. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.57 (2.47) 1.45 (1. and inhalation routes.01) 1.30 (2.47-9.70) 1.02 (1.30 (2.22 (1.000 pounds are used per year.50-8.67 (2.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30-2.28) 2.10-17.2 (10. 2002).90 (6.30-5. It has low leachability.47-13.10 (3.20) 4.S.40) 9.37 (1.79-2.89-2.97) 2.90 (1.20-14.40 (5.96) 3.4.40-26.70 (1.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.98-15. After 2001.00-8.91 (1.0) 10.50-4.

63 (5.55) 1.89) 4.41 (1.19) 6.49-2. Two observational studies of pregnant women and their offspring exposed to chlorpyrifos at environmental levels have found inconsistent relationships with birth outcomes of weight and length (Eskenazi et al.43 (4. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.92 (1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.75 (1.60-3.28) 2. TCPy can also occur in the environment from the breakdown of the parent compounds.93 (2.72) 2.00-8.47 (1.86 (1.59) 3.62) 1. Once absorbed.42 (5.99-8.5.43-10. 2002).73 (1. 2006a.59-2.50 (4.1-21.03) 1.88-9. 2006.30-1.49-2..30-4.07) 1.22 (6.3) 8.29 (3.49-2.56-2.84-6.88 (1.06 (1.33 (5.71 (1. Howard et al.88-8.1 (7.19-1.16) 6.24 (1.24-1.42 (6.97) 3.54) 5.05) 3.05-4. and other metabolites.93 (4. Survey Geometric mean (95% conf.91) 2. Metabolic hydrolysis leads to the formation of TCPy.58-5.65-11..97) 3.4) 4.71) 3.81) 2.05-8. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).06 (5.5) 5.00-13.54 (2.02) 7.1-38. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.31) 1.91 (4..98 (6..19-2.68) 6..48 (1.EPA. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.22 (4.24) 75th 2.36) 1.87-3. and seizures.74) 1.28) 2.05-1. 2006b).3) 9.39-1. vomiting.51 (1.95 (3. 2005.66-11. and producing acute symptoms such as nausea.33) 2.44 (1.76 (2.09 (1.83) 1..3) 8.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals . Based on animal data and human cholinesterase monitoring during occupational exposure. Thus.31-4.62) 90th 5.44 (5.64-7. 1984).17-4.39) 6.66 (1.82-4.86 (3.56 (1.95 (1.85) 1.20-1.2) 6.93) 5.24-24.14-8.94-14.53 (2.82) 8.21-1.33 (1. 2006.72-2.22-6. 2005.57) 9.47 (1.33 (.44 (6.64 (1.2 (7.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.57) 2.11-9. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.01) 3.86 (1.80-6.65-15.31-1.21-6.35) 1.14) 1.91) 1.40) 1. Roy et al.85-4. cholinergic effects.93 (1.39 (2.12-1.9 (12.32) 1.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.35) 2.63-2.49 (1.82 (2. Betancourt et al. 2005.27-1.63 (4.24-4..6-Trichloro-2-pyridinol (creatinine corrected) Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.940-1.57-2. interval) 1..33-7.24) 5. In pesticide applicators.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.77) 1.44 (1.91-13.11 (2.5 (6.46 (2.80-4.09-3.53-5.58) 5.94-12.23) 14.09-2.42-2.8) 9.00 (7.75) 6.39 (4.0) 10.83-11.58) 1. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.70-4.69 (1.56) 2.96) 3.56) 5.88) 6.91-4.35-1.17-4.85 (3.58 (1.0) 6. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.46 (1.25-12.S.6) 10.55 (4. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.05-3.25-1.11 (2.02 (5..01) 1.25-11.52 (5.91) 10.88 (1.45-1.88-8.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1. Urinary 3.47 (5.12-3.20 (2.60 (1. TCPy is more persistent in the environment than chlorpyrifos itself (U. population from the National Health and Nutrition Examination Survey. Ricceri et al.56 (4.92-2.06-4. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.58 (1.15 (4.48 (2.26-14.85) 4.72) 1. Slotkin et al.64-2.97-3.6) 9.00) 1.82 (3.90-9.01) 3.07) 5.3 (7.16 (4. 2000).80) 3. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.99) 1. weakness.97 (3.91) 1.80-11.92) 3.79-13.38) 3.08) 6.93) 2.S.1 (10.66) 1. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.11) 7.88-10. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.47-2.97 (2.37 (1.57-2.12) 1.24-5.19) 3.44 (5.23-1.09-1.98 (7. resulting in excess acetylcholine at nerve terminals.3) size 1994 2508 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.76 (3.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.81 (3.0) 16.68) 1.55 (1.22) 1.85 (2.0) 12.91 (3.62-7.45 (1.78 (1.83-2.44-6. neurotransmission.27-7. paralysis.7) 7.58 (4.34-1.

urinary TCPy levels in children were reported not to have increased (Hore et al. Aldridge JE. J AOAC Int 1999.Reference values of urinary 3. Clayton CA. Albers JW.5. 2005. representative subsample of NHANES 19992000 (CDC..gov/pesticides/.S. 2002). et al. Freeman NC. subsamples of NHANES 1999-2000 and 2001-2002 (CDC.gov/toxpro2.Organophosphorus Insecticides: Specific Metabolites 2004. Fourth National Report on Human Exposure to Environmental Chemicals 137 . Barisano A. 2001) and Italy (Aprea et al. 2005). Koch et al. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. CDC. Lotti A.S.. 1992. et al.S. but not chlorpyrifos. Haidar S. the weighted population mean of TCPy measurements was approximately three times higher (Adgate.EPA. 2005. 2007).epa. environmental levels) and health effects is available from ATSDR at: http://www. Curwin et al. 2005).. Burgess SC. Eberly LE. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC.109(6):583-590. 2001).e. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Occup Environ Med 2006. Meyer A. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. EPA at: http://www.S. Magnaghi S. Whyatt et al. Burns CJ. but levels were roughly four to six times higher than the geometric means in the U. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Betta A. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al.S. Slotkin TA. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. Biomonitoring studies of TCPy provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of chlorpyrifos or chlorpyrifos-methyl than are found in the general population. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP.. Catenacci G. Lioy PJ. 2003. Environ Health Perspect 2005. In Iowa farm families using several different pesticides. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. In Minnesota and South Carolina farmers who used chlorpyrifos.. the geometric mean urinary TCPy levels were similar in parents and children. 2004). et al. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Betancourt AM. Carr RL.. Seidler FJ. U. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). In a probability-based sample of 102 Minnesota children aged 3-13 years. 2000).. Giordani B. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.html and from U.. 1999).atsdr.. population (CDC. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. Following crack-and-crevice application of chlorpyrifos in their homes. Of 482 pregnant women living in an agricultural community. 2005. 2005). Barr DB. Aprea C. Perera et al.. 2006). Berent S.113(8):1027-1031..82(2):305-312.. References Adgate JL. MacIntosh et al. Garabrant D. 2004). Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. 2005).cdc. Environ Health Perspect 2001. Chlorpyrifos exposure and biological monitoring among manufacturing workers. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy... Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. Toxicol Sci 2006.92(2):500-506. 2005). 2005)..63(3):218220. Levels of TCPy in the U. Additional information about external exposure (i. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect..

Toxicol Appl Pharmacol 2005. Biomonitoring for farm families in the farm family exposure study. Lorenzini P. Brain Res Dev Brain Res 2005. Int J Hyg Environ Health 2001. Weltzien E. Curwin BD. Sanderson WT.5. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . et al. Slotkin TA. Pesticide residues in urine of adults living in the United States: reference range concentrations. Cometa MF. Dick RB. et al. Chlorpyrifos: pharmacokinetics in human volunteers. Ozkaynak H. Striley C. Environ Res 1995.nih. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. U. Rick DL. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. et al.114(10):1542-1546. Seidler FJ.S. Honeycutt R. Fenske RA. Jewell NP. Ricceri L. Scand J Work Environ Health 2005. Levin ED.5.6-trichloro-2-pyridinol.15(4):297-309. Venerosi A. Bucelli R.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC).cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Robson M. 4/7/09 Perera FP. Available at URL: http://www.51(1):53-65. Wartenberg D.111(2):201-205. Gurunathan S. J Expo Anal Environ Epidemiol 2005. Yang D. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Gregg M. chlorpyrifos. Seidler FJ. Barr D. Hines CJ.niehs. Toepel K. 4/7/09 Koch HM.114(5):746-751. Environ Health Perspect 2004.73:8-15. Head SL. Zhang J.inchem. Bradman A. Exposures of preschool children to chlorpyrifos and its degradation product 3. Tsai WY. Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition. Mandel JS. A longitudinal investigation of selected pesticide metabolites in urine. et al. Ann Occup Hyg 2007. 1999. Steenland K. Environ Health Perspect 2006. International Programme on Chemical Safety-INCHEM (IPCS). Atlanta (GA). Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Hill RH Jr. Meeker JD. Bravo R. Roy TS.org/documents/jmpr/jmpmono/ v99pr03.155(1):71-80.31 Suppl 1:98-104. Harley K. February 5. Sheldon LS. Chlorpyrifos. Sharma V. Toxicol Appl Pharmacol 1984. 1992. et al.207(2):112-124. Bravo R. Freeman N. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Shealy DB. Morgan MK.112(10):1116-1124. Robertson GL. et al. Baker S. Environmental Protection Agency (U. gov/ntpweb/index. Seidler FJ. Toxicol Sci 2006. Environ Health Perspect 2006a. Eskenazi B. Kromhout H. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. et al. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Jones PA. Capone F. Fortuna S. Chuang JC. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Lu C. Bruun D. Hardt J. Edwards RD. Freeman N. MacIntosh DL. Bennett DH. J Expo Anal Environ Epidemiol 1999. Nolan RJ. Levin ED. Hein MJ. Croghan CW. Available at URL: http://ntp. Jett DA. Acquavella JF.114(2):260-263. J Expo Anal Environ Epidemiol 2005. 2005.108(4):293-300. 2921-882.10(4):327-340. Herrick RF. Camann D.113(2):211-219.71:99108.93(1):105-113.htm. Barr DB. Barr DB. Third National Report on Human Exposure to Environmental Chemicals. Heederik D. Environmental Health Criteria 198. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. et al. Interim registration eligibility decision for chlorpyrifos. Ryan L. Irish R. Freshour NL. Environ Health Perspect 2006b. Ryde IT. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Pellizzari E. Tate CA. Executive summary of safety and toxicity information. Slotkin TA. et al. Kinney P. Bailey SL.15(3):271-281. Neurologic function among termiticide applicators exposed to chlorpyrifos. Needham LL. Lioy PJ. Reid TM. Hore P. et al. Chapman P. Chrislip DW. Baker BA. Environ Health Perspect 2000. Angerer J. Lein PJ. Ryan PB. Howard AS. Hammerstrom KA. Environ Health Perspect 2003.204(2-3):175-180.9(5):494-501. mothers and fathers living in farm and non-farm households in Iowa. Adgate JL.6-trichloro 2-pyridinol in their everyday environments.S. Barr DB. Howell RJ. Environ Health Perspect 2005. Saunders JH. Slotkin TA. Rauh V. Alexander BH. Urinary pesticide concentrations among children. J Expo Anal Environ Epidemiol 2000. National Toxicology Program (NTP). EPA).

The Quality of Our Nation’s Waters. 1992-2001. Geological Survey (USGS). Pesticides in the Nation’s Streams and Ground Water.gov/ oppsrrd1/REDs/chlorpyrifos_ired.pdf. Barr DB. Fourth National Report on Human Exposure to Environmental Chemicals 139 . Barr JR. Available at URL: http://www. March 2006. 2007 [online]. revised February 15. Kinney PL. Environ Health Perspect 2003.111(5):749-56. February 2002. Camann DE. 1/14/09 U.S.gov/circ/2005/1291/. Andrews HF. Available at URL: http://pubs.Organophosphorus Insecticides: Specific Metabolites 01-007. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. et al. 6/1/09 Whyatt RM.epa.usgs.

Olsson et al.S. and other metabolites. 140 Fourth National Report on Human Exposure to Environmental Chemicals . 2000). mites..S. At high doses. 2000). 2005).EPA.S. In the NHANES 2001-2002 subsample. Coumaphos is not considered mutagenic and rated by the U. coumaphos and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. though exposure through dietary meat and milk intake is possible. General population exposure to coumaphos is unlikely. Biomonitoring studies of 3-chloro-7-hydroxy-4-methyl-2H-chromen-2one/ol provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of coumaphos than are found in the general population. Finding a measurable amount of 3-chloro-7-hydroxy-4methyl-2H-chromen-2-one/ol in urine does not mean that the level will result in an adverse health effect. ornamentals. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). Coumaphos is generally immobile in soils and can persist for up to a year in some types of soils.Organophosphorus Insecticides: Specific Metabolites Coumaphos CAS No. (2003) found that urinary levels of 3-chloro-7-hydroxy-4-methyl2H-chromen-2-one/ol were below the limit of detection. swine. and certain other farm animals. Coumaphos may enter the environment from spillage of animal dipping and spraying solutions (U. dairy cows. Once absorbed. In a nonrandom study of 140 adults and children in the United States.epa. and seizures. e. Biomonitoring Information Urinary levels of 3-chloro-7-hydroxy-4-methyl-2Hchromen-2-one/ol reflect recent exposure. and alkyl phosphates.g.S. 56-72-4 General Information The chemical 3-chloro-7-hydroxy-4-methyl-2H-chromen2-one/ol is a metabolite of coumaphos.EPA. Coumaphos is highly toxic to birds and aquatic invertebrates and moderately toxic to fish. Estimated intakes from diet and water have not exceeded recommended intake limits (U..gov/pesticides/. It degrades to chlorferon.EPA. Animal studies indicate elimination in the urine over a period of a week. or for residential use. Additional information about pesticides is available from U. resulting in excess acetylcholine at nerve terminals.S. Toxic effects below doses that cause inhibition of acetylcholinesterase are unknown. though the 95th percentile was 0. coumaphos is an organophosphorus insecticide that is used to control ticks. and producing acute symptoms such as nausea. 6-hydroxyl3-methylbenzofuran. Human health effects from coumaphos at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2000). it has limited use in controlling mites in honeybee hives. reproductive effects such as decrease litter size are unlikely at doses that do not inhibit acetylcholinesterase (Astroff et al. Also. Farm and animal workers may have higher exposures as a result of absorption through dermal and inhalational routes. paralysis. Coumaphos is considered to be an organophosphorus insecticide of moderate-to-high acute toxicity in animal studies. vomiting. and arthropod pests on beef cattle. weakness. lice. It is not registered for uses on food crops. phosphorothioates such as coumaphos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide. most of the measurements of 3-chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol in urine were below the limit of detection. First registered in 1958. cholinergic effects. 1998).200 μg/L for the non-Hispanic black subsample (CDC. EPA at: http://www. Metabolic hydrolysis leads to the formation of 3-chloro-7-hydroxy-4-methyl2H-chromen-2-one/ol.EPA as not likely to be carcinogenic in humans (U.

2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey.S. < LOD means less than the limit of detection.27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.S. population from the National Health and Nutrition Examination Survey.270) < LOD 659 701 920 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 141 .380 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (<LOD-. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample. Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.200 (<LOD-.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 01-02 is 0.210) < LOD < LOD 567 815 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1312 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .670 (<LOD-1.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

Anal Bioanal Chem 2003. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. Eigenberg DA. EPA). 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals .gov/oppsrrd1/ REDs/0018tred.12(6):619-645.376(6):808-815. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Nguyen JV. Third National Report on Human Exposure to Environmental Chemicals.S.S. Environmental Protection Agency (U. Atlanta (GA). Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. Freshwater KJ. U. September 2000. Reprod Toxicol 1998. EPA 738-R-00-010. Sadowski MA. 2005. Barr DB. Centers for Disease Control and Prevention (CDC).epa. Olsson AO. Available at URL: http://www.pdf.

It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. Prior to 2000. but is rapidly absorbed orally (IPCS.S. diazinon cannot be sold for residential use. seed and foliar applications are planned to be phased out (U.2 and 0.49 (<LOD-2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). an organophosphorus insecticide that is used to control insects on nuts. Most granular formulations. but these uses have been phased out. in some pest strips. < LOD means less than the limit of detection. 2004).05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. diazinon was widely used in residential and garden application. Fourth National Report on Human Exposure to Environmental Chemicals 143 . fruits. and forage crops. It is toxic to birds. It is also used for cattle ear tag applications to control flies and ticks and. as inferred Urinary 2-Isopropyl-4-methyl-6-hydroxypyrimidine Metabolite of Diazinon Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7. Diazinon is not well-absorbed through the skin. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. and particularly when it was ingested in granular form. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. Inhalational and dermal routes of exposure can be significant for pesticide applicators.S. Human exposure to diazinon from dietary sources is expected to be low due to its limited applications to food crops and due to its rapid degradation. population from the National Health and Nutrition Examination Survey. aerial. Before these restrictions. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. diazinon produced wild bird kills before use restrictions were in place. USGS.45 (<LOD-3. in the past. 1998).S. 1998.EPA. 2004). Once absorbed. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. since 2004. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. Estimated intakes from diet and water do not exceed recommended intake limits (U.11) < LOD < LOD < LOD < LOD 454 580 632 829 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No.EPA. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and other metabolites. which may vary for some chemicals by year and by individual sample. vegetable. Survey Geometric mean (95% conf. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. 2007). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1842 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.

1992). 1998).45) < LOD < LOD < LOD < LOD 454 580 632 828 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. EPA at: http://www. respectively.epa.. resulting in excess acetylcholine at nerve terminals. weakness.S.S. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. 1998). In animals.e. diazinon does not accumulate in tissues (IPCS. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. 2002).S. environmental levels) and health effects is available from ATSDR at: http://www. paralysis. agricultural. At high doses. Survey Geometric mean (95% conf. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound.48) < LOD < LOD 644 678 484 699 554 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. population from the National Health and Nutrition Examination Survey. The U. 2003). 1986.cdc.gov/pesticides/.45 and 1. respectively (Baker et al. and producing acute symptoms such as nausea. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants.html and from U. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate.gov/toxpro2.49 μg/L.EPA considers diazinon unlikely to be carcinogenic in humans. subsamples of NHANES 1999-2000 and 20012002. cholinergic effects. In addition to being a human metabolite of diazinon. Diazinon has moderate acute toxicity in animal studies. teratogen. 144 Fourth National Report on Human Exposure to Environmental Chemicals . and seizures. or reproductive toxicant (IPCS. in the 2001-2002 subsample (CDC. In two nonrandom samples of United States adults and children. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1842 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Thus.76 (<LOD-3.. animal carcinogen. vomiting. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.. In the U. Olsson et al. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1.S.atsdr.72 (<LOD-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Seifert and Pewnim.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. Intoxications in humans from intentional overdose... Diazinon is not considered to be a mutagen. Urinary 2-Isopropyl-4-methyl-6-hydroxypyrimidine (creatinine corrected) Metabolite of Diazinon Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2000. Additional information about external exposure (i. 1986 Rajendra et al. and indoor applications have been documented..

Swan SH. Kruse RL. In 23 children. 2006). Bouchard M. Irish R. Barr DB.pdf. Centers for Disease Control and Prevention (CDC). Pewnim T. Semen quality in relation to biomarkers of pesticide exposure.htm. Baker SE. Carrier G. Barr DB.9(2):117-131.111(12):1478-1484. Bravo R. Drug Chem Toxicol 1986. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Redmon JB.S.114(2):260-263. Oloffs PC.134(1-3):105-113. Environmental Health Criteria 198. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers.. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. EPA 738-R-04-006. Diazinon.50(5):505-515. March 2006. Toepel K.44(11):2243-2250. Pesticides in the Nation’s Streams and Ground Water.org/documents/ehc/ehc/ehc198. Jones K. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http://www.inchem. Swan et al.gov/circ/2005/1291/. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Effect of sublethal levels of diazinon: histopathology of liver. 1992-2001.S.10(6 Pt 2):789-798. Available at URL: http://www. Sadowski MA. Oloffs PC. Anal Bioanal Chem 2003. Driskell WJ. 2007 [online]. Cocker J.376(6):808-815. Toxicol Lett 2002. 4/7/09 Lu C. Rajendra W. Atlanta (GA). Interim reregistration eligibility decision (IRED. Biomonitoring studies of 2-isopropyl-4-methyl-6-hydroxypyrimidine provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of diazinon than are found in the general population. Geological Survey (USGS). International Programme on Chemical Safety-INCHEM (IPCS). Biochem Pharmacol 1992.. Third National Report on Human Exposure to Environmental Chemicals. J Expo Anal Environ Epidemiol 2000. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Environ Health Perspect 2006. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. EPA). Liu F. May 2004. Nguyen JV. Available at URL: http://pubs.37(4):501-507. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Fenske RA. U. 2005. Environ Health Perspect 2003. Bull Environ Contam Toxicol 1986.usgs. et al. Noisel N. Drobnis EZ. Beeson MD. Banister EW.epa. Dumas P. References Anthony J. Barr DB. In 54 Canadian greenhouse workers. Garfitt SJ. Mason HJ. Finding a measurable amount of 2-isopropyl-4-methyl-6hydroxypyrimidine in urine does not mean that the level will result in an adverse health effect. 1/14/09 U.S. 2006). Study for Future Families Research Group. 1998. Needham LL. Barr DB. Olsson AO. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. In a small number of men visiting fertility clinics in Missouri and Minnesota. Environmental Protection Agency (U. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. revised February 15. The Quality of Our Nation’s Waters. Seifert J. Banister E. Ann Occup Hyg 2006. Brunet RC.Organophosphorus Insecticides: Specific Metabolites 2005).gov/ oppsrrd1/REDs/diazinon_ired. Diazinon.

2000). < LOD means less than the limit of detection. Survey Geometric mean (95% conf. which is an organophosphorus insecticide that is used on a wide variety of agricultural crops. Once they are absorbed.S. vomiting. phosphorothioates such as malathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticide. Malathion is rapidly eliminated from the body within 12-24 hours (Bouchard et al. At high doses. Malathion is infrequently detected in groundwater sampling (USGS. but is more rapidly and efficiently absorbed via ingestion. and plants. Malathion is slowly absorbed through the skin. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1920 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Most of the estimated 15 million pounds used annually are applied to cotton (U. 2007).EPA. malathion dicarboxylic acid.. and seizures. Pesticide applicators and agricultural workers can have higher exposures via dermal. see Data Analysis section) for Survey year 99-00 is 2. 146 Fourth National Report on Human Exposure to Environmental Chemicals . Thus. malathion has low acute toxicity. malathion and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. inhalational. Compared with other organophosphorus insecticides. usually only a small fraction of the crop is treated. weakness. ornamental trees. It is registered for use in public health mosquito control. the detection of malathion dicarboxylic acid in a person’s urine may also reflect exposure to the environmental degradate.5%) to kill body lice. About 31-35% of oral doses of malathion are excreted in the urine as malathion monocarboxylic acid (Krieger and Dinoff.EPA. 2003). which may vary for some chemicals by year and by individual sample. Limited general population exposure occurs through the diet. resulting in excess acetylcholine at nerve terminals. and other metabolites.S. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). 121-75-5 General Information Malathion dicarboxylic acid is a metabolite of malathion. shrubs. Estimated intakes for the general population have not exceeded recommended intake limits. population from the National Health and Nutrition Examination Survey. 2006). When malathion is used on food or feed crops. cholinergic effects. in fruit fly control.Organophosphorus Insecticides: Specific Metabolites Malathion CAS No. depending on the species.50) < LOD < LOD 453 660 807 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 937 983 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 680 498 580 Limit of detection (LOD. gardens. In addition to being a metabolite of malathion. malathion dicarboxylic acid can also occur in the environment from the breakdown of the parent compound. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Severe toxicity or deaths have been reported from Urinary Malathion dicarboxylic acid Metabolite of Malathion Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Human health effects from malathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Malathion is also used medically in lotion form (0. It is highly toxic to aquatic invertebrates and rare fish kills have been reported from wide area applications onto surface waters and runoff into waters. It is moderately to highly toxic to fish. Metabolism of malathion leads to the formation of malathion monocarboxylic acid. and in government programs such as the USDA’s Boll Weevil Eradication Program.80 (<LOD-5.S.64. and producing acute symptoms such as nausea. paralysis. 2006). as well as lawns. It has a short halflife in soils and water and is not considered persistent in the environment. or oral routes (U.

a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. Survey Geometric mean (95% conf.. 2005. representative subsample from NHANES 19992000 (Adgate.S. 2006). Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. 2001.5 and 5.. 2003).. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid.50) < LOD < LOD 453 660 807 99-00 99-00 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 937 983 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 680 498 580 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. but isomalathion.atsdr. Lu et al.e. Urinary Malathion dicarboxylic acid (creatinine corrected) Metabolite of Malathion Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. Malathion itself has not been considered genotoxic (U. Fourth National Report on Human Exposure to Environmental Chemicals 147 .S. but cholinesterase activity was not affected. 2000).. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1920 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3..74 (<LOD-5. 30% had detectable levels of malathion dicarboxylic acid at a detection limit about tenfold lower than the detection limit in the NHANES 1999-2000 analyses (Eskenazi et al.. 1996. 2002. Human studies of single oral doses between 0.EPA. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample.. and it is not considered an animal teratogen or a reproductive toxicant.S. 2004). median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. 1990). 2005). Biomonitoring studies of malathion dicarboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of malathion than are found in the general population.gov/pesticides/. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. The 95th percentile urinary levels of malathion dicarboxylic acid in both urban and nonurban Minnesota children aged 3-13 years (adjusted for sociodemographic variables) in 1997 were several-fold higher than the analytical detection limits reported for children aged 6-11 years in the U.. Thomas et al.epa. A study of 13 children from an agricultural region of Washington State reported median levels that were below the detection limit in the NHANES 1999-2000 subsample (Kissel et al.. 1993. A study of agricultural workers reported preshift urinary levels of malathion dicarboxylic acid that were twofold to eightfold higher than detection limits in the NHANES 1999-2000 subsample (Krieger and Dinoff. 2006). Additional information about external exposure (i. 1999). Giri et al. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. 1987. environmental levels) and health effects is available from ATSDR at: http://www.cdc.EPA.gov/toxpro2. EPA at: http://www. Flessel et al.html and from U.S. 2005). IARC considers malathion not classifiable as a human carcinogen. Pluth et al.S. 1999. 2006). Toxicity from unprotected bystander exposure during applications is rare (U.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. Of 382 pregnant women living in an agricultural community.. CDC..

J Expo Anal Environ Epidemiol 1999.S. Giri A. International Programme on Chemical Safety-INCHEM (IPCS). Am J Public Health 1987.inchem. 2007 [online]. 1992-2001. Pesticides in the Nation’s Streams and Ground Water. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Grether JK. Nicklas JA. metabolite clearance. Dumoulin MJ. Sharma GD. O’Neill JP. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Centers for Disease Control and Prevention (CDC). Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Giri S. revised February 15. Eberly LE. Environ Health Perspect 2004. Reregistration eligibility decision (RED) Malathion. Hertz-Picciotto I. Rappaport E. A longitudinal investigation of selected pesticide metabolites in urine. Available at URL: http://www. EPA). Neutra R. 6/1/09 U. March 2006. Flessel P. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Atlanta (GA). Griffith W.514(1-2):223231. Environ Mol Mutagen 1993. Barr DB. Environ Health Perspect 2006. Am J Epidemiol 1990. 2005.109(6):583-590. July 2006. Cancer Res 1996. Toepel K.74(2):following table of contents.9(5):494-501. Dinoff TM. Kedan G.56(10):2393-2399.epa. Irish R. Jewell NP. Krieger RI. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Genetic toxicity of malathion: a review. Weltzien E. Freeman NC. Pluth JM. Clayton CA. Needham LL. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Hammerstrom KA. Malathion deposition. Samuel O. Geological Survey (USGS).22(1):7-17.73(1):182-94. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo.S. Ryan PB. Lu C.114(2):260-263. Lu C. Harley K. Toxicol Sci 2003 May. Environmental Protection Agency (U. Fenske RA. Hooper K. Trzeciak A. Third National Report on Human Exposure to Environmental Chemicals. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues.112(10):1116-1124. Petitti D. Reproductive outcome in women exposed to malathion.38(4):546-553. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Thomas D. The Quality of Our Nation’s Waters. et al. Jaloszynski P.gov/circ/2005/1291/.gov/oppsrrd1/REDs/ malathion_red. et al. Barr DB. Brunet RC. Barr DB. and cholinesterase status of date dusters and harvesters in California. Arch Environ Contam Toxicol 2000. Environ Health Perspect 2001. Goldhaber M.usgs. MacIntosh DL. Curl CL.org/documents/jmpr/jmpmono/v2003pr06.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Harris JA.445(2):275-283. Bravo R. Lioy PJ. Blasiak J. Gosselin NH. J Expo Anal Environ Epidemiol 2005.S. Erratum in: Toxicol Sci 2003 Aug. Prasad SB. Swan SH.pdf. Albertini RJ. Available at URL: http://www. U.132(4):794-795. Malathion (addendum). Bouchard M. et al. Carrier G. Szyfter K.15(2):164-171. Available at URL: http://pubs. Eskenazi B. EPA 738-R06-030.77:1009-1010. Bradman A. Mutat Res 1999. Quintana PJ. htm. Barr DB. 4/7/09 Kissel JC. Mutat Res 2002.

28 (1. which may vary for some chemicals by year and by individual sample.70 (3.850) < LOD .61) < LOD 1.01) 4.15-3.0) 3.45) 5. 1977).910) < LOD < LOD < LOD 1.18-3.30 (1.70) 2. 2006).24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .58) 3.60-19. Methyl parathion use is highly restricted. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.37-2. 2000).48) 90th 2.70-3.70 (<LOD-3.40-4.32-1.790 (<LOD-.92) 5.70-6. Given its limited use.90 (1.74) 5. pulmonary.EPA. was once a restricted-use insecticide with limited applications on certain agricultural crops.67) < LOD 1.910) < LOD < LOD .47) 2.00) 3.60-5. all registered uses were voluntarily cancelled (U. Methyl parathion has low water solubility. more slowly absorbed through the skin..30-5.10) 22. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. and oral routes can occur in pesticide and agricultural workers (Muttray et al.32-3. and of the chemical nitrobenzene.20) 5.49 (1.80 (2.12) < LOD < LOD 1.44) 2. on cereal grains. binds tightly to soils resulting in low leachability.21-1.02-6.45 (1.28-4.11-4.S.90-9.60-24.71 (3.770 (.62 (1.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.37-4. fish. 2002. In the 1990s. Many previous registered agricultural uses of methyl parathion have been cancelled (U.37) 2.0) 4.50 (1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.71 (2.46 (3.40) 1.50) 1.05) 4.27) 2.50) 3.10 (3. Methyl parathion is not registered for residential use in the United States. Both are toxic to birds.910) < LOD . < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30 (2.0) 3.20 (2.860 (<LOD-1. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.01) 695 660 518 679 603 941 Limit of detection (LOD.60) 1.700 (<LOD-.37-4.30-3. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS. Morgan et al.79) 4. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.0) 3.40-4.91-3. methyl parathion was rapidly absorbed after ingestion.60-36.61) < LOD 1. and to a lesser extent. 2007). It had been applied to cotton.69) 4..01-4.70-3.80) 2.69 (2.34 (3. first registered in 1948.22-3.730 (<LOD-.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .EPA.11) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.30-16.09-1.80 (2. Methyl Parathion.0 (3. Fourth National Report on Human Exposure to Environmental Chemicals 149 .57) 1.92-2.89 (2.10 (3.21 (2. Survey Geometric mean (95% conf.10) 4.1. Once absorbed.50) 3..33) 2.00) size 1989 2477 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1. and aquatic invertebrates.0) 3.13-1.990-1.80 (1.00 (2.33 (1.19 (.70-6. and has a short half-life in soils and on plants.28 (1. Estimated intakes from diet and drinking water have been below recommended limits. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50-14.S. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.298-00-0 Ethyl Parathion CAS No. and eliminated rapidly from the body after absorption (Kramer et al.66 (2.300-.40) 2.10-11.32-1.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .50 (2.72 (3. ethyl parathion.00 (2.40-3.0) 2.16) < LOD 1.70) 2. peak domestic use was as high as 5-6 million pounds per year.50 (1.S. Increased risk of exposure via dermal.70 (2.40 (1. 2003).20 (<LOD-2.70) 2.41-4.70 (2.10-1.90-11.50) 2.36-1.8 and 0.70-6.20-5. In animal studies. with limited applications in agriculture.67 (1. Ethyl parathion.0) 3.85 (2.940 (<LOD-2.70 (2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50-9.60 (4.50 (2.26 (1. but by 2003.57-4.40) 4.50 (1.50 (1. population from the National Health and Nutrition Examination Survey.32 (1.10 (<LOD-6.

retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.20) 3.05) 4. Slotkin et al. 1990.2) 2.56-2. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. population from the National Health and Nutrition Examination Survey.97 (<LOD-4.00) 2.13-12.94-47.11-4. 2006.30-1. 1995. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.atsdr.59 (1.30) 3. Recent in vitro and in vivo animal studies suggest that parathion may have additional neuronal and glial cell effects at lower doses (Guizzetti et al.17) . environmental levels) and health effects is available from ATSDR at: http://www.04 (2.S.33-3.95) 1.730-1.72-2.77-7.10) 90th 2. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.73 (1. paralysis.400 (<LOD-.20 (3. 1991).90 (1. accidental exposure. 2003. but lists ethyl parathion as a possible human carcinogen.71 (1.S.60 (1.07) 2.38-3..60-2.930 (.21) 1.310-.7) 3. Lores et al. and other metabolites.970 (.04) 1..06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . Methyl Parathion. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. and seizures. does not inhibit acetylcholinesterase enzymes.09) 2.530) < LOD < LOD < LOD .720 (<LOD-.21-21.11) 1.89 (2.33-3.430 (.850-1.20) . vomiting.78) 2.Organophosphorus Insecticides: Specific Metabolites Metabolites”).55 (<LOD-3.17-4.57-7.840 (.EPA considers methyl parathion unlikely to be carcinogenic to humans.44-3.2) 2.26 (1.33-6.440 (<LOD-. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.37-1. Survey Geometric mean (95% conf.82 (2. Orsorio et al.cdc. paranitrophenol. The metabolite..71) 1. 2004).78-2. Zurich et al.94-4. 1978.3) 2.55) 2.23) 1.980 (.87 (1. Additional information about external exposure (i. Karanth and Pope et al. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.10 (1.08 (1.29) 2.97 (2.950) < LOD ..78-2.76-14.870) < LOD .67-2.640) < LOD < LOD 1.940 (<LOD-1.60) 2. 150 Fourth National Report on Human Exposure to Environmental Chemicals .08) < LOD .43) 4.39 (1. and producing acute symptoms such as nausea. teratogenic.1) 2.29 (2.16-4. cholinergic effects.57) 6..70) 3.86 (2.96 (1.44-3.01-3.93 (2.00 (1.4 (3.84) 3.880 (.29) 1.html and from U.48-4.39) 1.00 (1.79) 1.98-7.e.930 (. Thus.80 (1.epa..97-10.91 (1.78 (2. ethyl parathion.790-.92 (2. WHO.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .91) 1..96 (1.80 (1.500) < LOD < LOD .690-1. EPA at: http://www.08-3. resulting in excess acetylcholine at nerve terminals.61) 4.31) < LOD . In large doses.9) 1.88) 1.25) 1. weakness.79 (1.25 (2..07 (1.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. U.89 (2.680 (<LOD-1.800-1. methyl parathion.790-1.540) < LOD . and unintentional acute or chronic high-level occupational exposure (Hill et al. 2006. Parathion and methyl parathion have high acute toxicity in animal testing.26) 17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Jaga and Dharmani.41-2. 1995). At high animal doses of methyl parathion.67 (3.88 (1. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.15) 3.970 (.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . gov/toxpro2.31-3.35-3. 2004).57-2. gov/pesticides/.82) < LOD .13) 4. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.370 (<LOD-.01 (2.S. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.720-1. 2005.830-1.01 (.14-3.15-10.23) size 1989 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th . interval) Selected percentiles ( 95% confidence interval) Sample 95th 4. Methyl parathion is not considered genotoxic. In addition to being a metabolite of methyl and ethyl parathion.35-3.83 (1.

.71:99108. References Barr DB. Levels of para-nitrophenol in the NHANES 1999-2000 and 2001-2002 subsamples were similar or slightly lower than those in a nonrandom subsample of NHANES III (19881994) participants (CDC. Head SL. Barr DB. Alley CC. Hill et al. Arch Environ Health 1978. oral or dermal administration. Barr DB. Chicago area methyl parathion response. Pope C. Dharmani C.. 2004). Wellman SE. Children and adults living in residences where methyl parathion was applied indoors had urinary levels of para-nitrophenol which were several hundred times higher than those in the NHANES 19992000 subsample. 1995. Lu C. Gregg M. 2005). Environ Res 1995. Pharmacokinetics of methyl parathion: a comparison following single intravenous. McCann et al. CDC. Lores EM.110 Suppl 6:1075-1078. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Shealy DB.org/documents/jmpr/jmpmono/v95pr14. Cline RE. 4/7/09 Jaga K. Available at URL: http:// www.htm. Slach EF. Barr DB. and levels were similar or slightly lower that those in a small convenience sample of the U.S. Laboratory investigation of a poisoning epidemic in Sierra Leone. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al.. Arch Environ Contam Toxicol 1977. Ashley DL.215(3):182-190. Moseman RF.. et al. Bradway DE.21(1):5767. Guizzetti M. Weltzien E. Hryhorczuk DO. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. 2005. Baker RC. Rev Environ Health 2006. 2005. 2002). Hill RH Jr. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Kramer RE. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Environ Health Perspect 2002. Parathion-Methyl (addendum).110 Suppl 6:1085-1091. Rockhold RW. Environ Health Perspect 2002. Clark JM.5 mg (500 µg)/g creatinine for workers at the end of shift. J Biomed Sci 2002. Methyl parathion: an organophosphate insecticide not quite forgotten. Atlanta (GA). Kedan G. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Hill RH Jr. 2005. Occup Environ Med 1999. general population (CDC. 2002. 1999). DiPietro E. Pathak S. McClure PC.9:311-320. population (Olsson et al. Needham LL. Neurotoxicol Teratol 2003. Eskenazi B. Baker S. Hetzler HL. 1995). Role of individual susceptibility in risk assessment of pesticides. J Expo Anal Environ Epidemiol 2005.. J Anal Toxicol 1990. Rubin et al. Morgan DP. 2005). Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. McCann KG..14(4):213-216. Pesticide residues in urine of adults living in the United States: reference range concentrations. Bradman A. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In a study of workers who handle parathion.inchem.112(10):1116-1124. Costa LG. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Curl CL. Kissel JC. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Biomonitoring studies of para-nitrophenol can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of parathion than are found in the general population. Jewell NP. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. et al. A study of 13 children from an agricultural region of Washington State reported median levels that were more than threefold higher than median levels in the NHANES 1999-2000 subsample (Kissel et al. et al. Runkle KD.S. Moomey CM.15(2):164-171. Toxicology 2005.33(5):270-276. Lin LI.25(5):599-606. Leng G. Centers for Disease Control and Prevention (CDC). Head SL. and many residents were symptomatic (Barr et al. Third National Report on Human Exposure to Environmental Chemicals.. Baker SE. et al. Giordano G. Bailey SL. Pesticide workers may have much higher levels following pesticide applications.6(2-3):159-173. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. International Programme on Chemical Safety-INCHEM (IPCS). Lewalter J. Turner WE. ACGIH recommends a BEI of 0. a range of values several hundred times higher than levels found in the U. Griffith W. et al. Harley K. Barr JR. Environ Health Perspect 2004. Karanth S.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure.56(7):449553. 2002.

S.110 Suppl 6:1047-1051. 5/19/09 Zurich MG. Available at URL: http://www. Interim reregistration eligibility decision (IRED) for Methyl Parathion. 0153.04/106.E. EPA). 2004. Available at URL: http://www. Mengle DC. Rosenberg J. Investigation of a fatality among parathion applicators in California. gov/oppsrrd1/REDs/methylparathion_ired.gov/circ/2005/1291/. Kieszak S.usgs. Pesticides in the Nation’s Streams and Ground Water. U. revised February 15. Sadowski MA. Rubin C. Costa LG. Dunlop B. Available at URL: http://www. Yacovac R. Geological Survey (USGS). Ethyl parathion.114(10):1542-1546. Seidler FJ. Esteban E. May 2003.162(2-3):219-224. pdf. 1/12/07 U. Nguyen JV.20(4):533-546. et al. Toxicol Appl Pharmacol 2004. Facts.epa.S. Ryde IT.S. EPA-738-FOO-009. Ames RG. Case No. Barr DB. Letzel S. Tate CA.S. Schilter B.Organophosphorus Insecticides: Specific Metabolites Muttray A. Olsson AO. Anal Bioanal Chem 2003. WHO/SDE/WSH/03. Environmental Protection Agency (U. Environmental Protection Agency (U. Am J Ind Med 1991.376(6):808-815. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Jung D. September 2000. 6/1/09 World Health Organization (WHO). Backer G. Slotkin TA. R.pdf. Hill RH Jr. External and internal exposure of wine growers spraying methyl parathion. Environ Health Perspect 2006. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Levin ED. Osorio AM.gov/oppsrrd1/REDs/factsheets/0155fct. Environ Health Perspect 2002. The Quality of Our Nation’s Waters. 1995-1996.who. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Available at URL: http://pubs. 2007 [online].pdf. Honegger P.S. Hill G. Toxicol Lett 2006.epa. Ohio. Monnet-Tschudi F. Methyl parathion in drinking water. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. 1/14/09 U. Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition. 1992-2001. March 2006.int/water_sanitation_health/dwq/chemicals/ methylparathion.D. EPA).201(2):97-104.

U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Pirimiphosmethyl has low acute toxicity in animal studies. pirimiphos-methyl and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. 29232-93-7 General Information The chemical 2-(diethylamino)-6-methylpyrimidin-4-ol/ one is a metabolite of the organophosphorus insecticide pirimiphos-methyl. or known to cause delayed neurotoxicity. Biomonitoring studies of 2-(diethylamino)-6-methylpyrimidin-4-ol/ one provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pirimiphos-methyl than are found in the general population. 2005). 1992). Fourth National Report on Human Exposure to Environmental Chemicals 153 . weakness. infrequent dietary exposure to pirimiphos-methyl residues may occur from ingestion of food products containing stored corn or other treated grain (FDA. or reproductive toxicity (IPCS.gov/pesticides/. Once absorbed. occurrence of such toxicity is mitigated by its rapid degradation and its use in closed storage systems.S. 2003). teratogenic. Metabolic hydrolysis leads to the formation of 2-(diethylamino)-6methylpyrimidin-4-ol/one. The metabolite 2-(diethylamino)-6-methylpyrimidin-4-ol/one does not inhibit acetylcholinesterase enzymes. In addition to being a human metabolite of pirimiphos-methyl in the body. 2-(diethylamino)-6-methylpyrimidin-4-ol/one can also occur in the environment.epa. 1992. Pirimiphos-methyl is not registered for residential use in the United States. subsample of NHANES 2001-2002.EPA. although the 95th percentile was characterized at 0. and it is not considered persistent. weevils. (2003) detected 2-(diethylamino)6-methylpyrimidin-4-ol/one in 7. Human health effects from pirimiphos-methyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown. which has limited applications for control of beetles. Thus. Additional information about pesticides is available from U. Biomonitoring Information Urinary levels of 2-(diethylamino)-6-methylpyrimidin-4ol/one reflect recent exposure. In animal studies. Estimated intakes from diet and water have not exceeded recommended intake limits (U. Toxic effects below doses that cause inhibition of acetylcholinesterase are unknown. In a nonrandom sample of 140 urine specimens obtained from adults and children in the United States.47 μg/L for the total population (CDC. Though considered moderately-to-highly toxic in birds.S. In the general population. and producing acute symptoms such as nausea. At high doses. and seed. most of the urinary measurements of 2-(diethylamino)-6-methylpyrimidin-4-ol/one were below the limit of detection. It has a lesser use as a cattle ear tag application to control flies. Pirimiphos-methyl is not considered mutagenic. the detection of 2-(diethylamino)-6-methylpyrimidin-4-ol/one may also reflect exposure to the environmental degradate. and seizures. fish.1% of the sampled population.EPA. which are mainly excreted in the urine (IPCS.Organophosphorus Insecticides: Specific Metabolites Pirimiphos-methyl CAS No. sorghum. phosphorothioates such as pirimiphos-methyl are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide. and aquatic invertebrates. EPA at: http://www.S. cholinergic effects. and other metabolites. In the U. pirimiphos-methyl is rapidly absorbed and metabolized to 12 metabolites. and moths on stored grain products such as corn. Olsson et al. Finding a measurable amount of 2-(diethylamino)-6methylpyrimidin-4-ol/one in urine does not mean that the level will result in an adverse health effect. vomiting.S. It easily hydrolyzes in the environment to 2-(diethylamino)-6-methylpyrimidine and other breakdown products. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). paralysis. resulting in excess acetylcholine at nerve terminals. 2006). 2006).

Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.470 (. 154 Fourth National Report on Human Exposure to Environmental Chemicals .94) . Survey Geometric mean (95% conf.580-1.840) 669 687 929 Limit of detection (LOD.55) . which may vary for some chemicals by year and by individual sample.670 (<LOD-1. Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one (creatinine corrected) Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.430 (<LOD-.200-.210-1.770) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300-1.17 (.210 (<LOD-.740 (.27) .00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. interval) Selected percentiles ( 95% confidence interval) Sample 95th .740-1.680 (<LOD-.15) < LOD . < LOD means less than the limit of detection.850 (.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .760 (<LOD-.21) < LOD .2.840 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.610 (<LOD-1.700-1.780 (.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.950) < LOD < LOD 1.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .410 (<LOD-1.250 (<LOD-.820) < LOD < LOD .780 (<LOD-1.210-.31) .64) .780 (<LOD-1.S.07) .930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .700-.780 (.

EPA). July 2006. Environmental Protection Agency (U. 2005. Available at URL: http://www. Pesticides residues in food: 1992 evaluations Part II Toxicology.S. Third National Report on Human Exposure to Environmental Chemicals. 850. Available at URL: http://www. Atlanta (GA). Total Diet Study: Summary of Residues Found Ordered by Pesticide. Anal Bioanal Chem 2003. Sadowski MA. 2535.fda.epa. 1/14/09 Fourth National Report on Human Exposure to Environmental Chemicals 155 . gov/oppsrrd1/REDs/pirimiphos-methyl_ired.Organophosphorus Insecticides: Specific Metabolites References Centers for Disease Control and Prevention (CDC).pdf. cfsan. Barr DB. 4/7/09 International Programme on Chemical Safety-INCHEM (IPCS). A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.inchem.S. Pirimiphos-methyl. Nguyen JV.pdf. Available at URL: http://www. Market Baskets 91-3-01-4. 4/7/09 Olsson AO.376(6):808-815. Food and Drug Administration (FDA). org/documents/jmpr/jmpmono/v92pr16. June 2003. Finalization of interim registration eligibility decision for pirimiphos-methyl. U. Case No.htm.gov/~acrobat/tds1byps.

Pyrethroids are not well absorbed through the skin (ATSDR. and deltamethrin have been used frequently on cotton.2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. resmethrin.. In agriculture. About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U. Leng et al. 1999. Compared with other classes of insecticides such as organochlorines. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers. solvent oils. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides. 2007). Estimated intakes from diet and drinking water are below recommended limits. cypermethrin. and then eliminated over several days in urine and bile (Kuhn et al.. 2003.EPA.Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins. 2003. they are not persistent in the environment due to their rapid degradation within days to several months.. Woollen et al. deltamethrin has been used for indoor protection against mosquitoes that carry malaria.. or carbamate pesticides. Possible other additional actions on neuroreceptors Pyrethroid Insecticides Metabolites in this Report Pyrethroid (CAS number) Cyfluthrin (68359-37-5) Cypermethrin (52315-07-8) Cyfluthrin (68359-37-5) and Permethrin (52645-53-1) Deltamethrin (52918-63-5) Cyhalothrin (68359-37-5) Cypermethrin (52315-07-8) Deltamethrin (52918-63-5) Fenpropathrin (39515-41-8) Permethrin (52645-53-1) Tralomethrin (66841-25-6) Urinary metabolite (CAS number) 4-Fluoro-3-phenoxybenzoic acid (77279-89-1) cis-3-(2. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations. This class of pesticides has low toxicity in birds and mammals. agricultural fields. Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. Woollen et al.2-Dichlorovinyl)-2. 1992).S. Soderlund et al. Adverse effects from large doses are related to the action of pyrethroids on the nervous system.2-Dichlorovinyl)-2. 2005).. such as piperonyl butoxide. Certain pyrethroid insecticides (such as permethrin. 1997. WHO. by either ester hydrolysis or hydroxylation. Soderlund et al.S.2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. in some situations replacing the use of DDT. warehouses. and synergists.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals . and are rarely detected in ground waters (USGS.. where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. Outside the U. and greenhouses.. 2002.2-Dibromovinyl)-2. The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. followed by conjugation. but may be poorly transferred across the placenta (ATSDR. pyrethroid pesticides have less acute toxicity in animals and people. EPA. and sumithrin) are also registered for use in mosquito-control programs in the United States. but pyrethroids are highly toxic to fish and some aquatic invertebrates. They are also applied on livestock to control insects. They are ranked as having moderate acute oral toxicity. bind to soils. 1992).. cyfluthrin. There are about 30 different pyrethroid pesticides in use. animal facilities. 2006b). organophosphorus. which are natural chemicals found in chrysanthemum flowers. Pyrethroid pesticides have low volatility. 2002). so usage is restricted near water (U. 2006a. The table shows the urinary pyrethroid metabolites measured in this Report. 2002). pyrethroids are rapidly metabolized. After absorption from inhalation or ingestion. 2005. Generally.S. Unmetabolized pyrethroids have been measured in breast milk.

2006). choreoathetosis. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Bernardi MM. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Cruz-Casallas PE. Ose K.23(6):665-673. et al. Regul Toxicol Pharmacol 2002..html. Levsen K. Sugiri D..gov/toxpro2.50(2):245-255. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Soderlund et al. et al.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Lemonica IP.1/15/09 Aziz MH. Leng G. Kim et al. Caudle WM. Shaw IC. Kim IY. Shukla Y. Kunimatsu et al.. Wieseler B.205(6):459-472. fenvalerate. and seizures (ATSDR. Berger-Preiss E. Wolff MS. Ray et al..62:101-108. Spinosa HS. and striatal dopamine levels in male and female rats. et al. Biochem Biophys Res Commun 1998.27(12):1273-1283. cdc. Zhao RC. Kamita Y. Song L. Go V.atsdr. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. et al. 2005). 2003. Sunami O. EPA at: http://www. Hu et al. Shafer. 2003. Available from URL: http://www.. WHO. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. 1991. Kang IH.251(3):855-859. Leng G. Okuno Y.gov/pesticides/ and from ATSDR at: http://www. Pyrethroid pesticide-induced alterations in dopamine transporter function. Seth PK. Florio JC. Yang J. Chen JH. Lazarini CA. J Reprod Dev 2004. 2003.. salivation. J Environ Monit 2006.. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Neurotoxicol Teratol 2001. Environ Health Perspect 1999..atsdr. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Idel H.. Salzgeber SA. Adhami VM. Fourth National Report on Human Exposure to Environmental Chemicals 157 . IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Additional information about pesticides is available from U. Abell AD. Yamada T. Leng G. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. 1998. 2006.27(4):609-614. Garey J. In developing rodents.cdc. McCarthy AR. Eriksson and Fredriksson. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides.107(3):173-177. Neurotoxic effects of two different pyrethroids. Kim TS. on immature and adult mice: changes in behavioral and muscarinic receptor variables. 2001.211(3):188-197. Lee SJ. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation.. Toxicological profile for pyrethrins and pyrethroids.gov/toxprofiles/ tp155. Garey and Wolff. 2002. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Wolff MS. References Agency for Toxic Substances and Disease Registry (ATSDR). Elwan MA. dopaminergic.html. McCarthy et al. Kunimatsu T. Go et al. Agrawal AK. Pogo BG. Shin JH. Pauluhn J. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Neurotoxicol Teratol 2005. Bull Environ Contam Toxicol 1999. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Toxicol Appl Pharmacol 1991. No relationship of indoor air or housedust concentrations of permethrin and irritant symptoms was found in a study of urban residents in 80 private homes (Berger-Preiss et al. 2000. Wang SL. 2002).300(3):161-165.35(2 Pt 1):227-237. Fredriksson A. Varoli FM.. Leng A. motor activity. Estrogenicity of pyrethroid insecticide metabolites.S. Kuhn K. Lazarini et al. epa. 2005). 2003. Int J Hyg Environ Health 2002. Idel H. Neurosci Lett 2001. Bernardi MM.. 2006. In California.108(1):78-85. Eriksson P. Miller GW. Kim HS. neurochemical changes in cholinergic. Garey J. 2002). Richardson JR. Guillot TS.. bioallethrin and deltamethrin. Moniz et al. Lewalter J. 1999. 2001. Ranft U. hypersensitivity. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Generally. Elwan et al. Kuhn KH. tremor. Toxicol Appl Pharmacol 2006. Thomson BM. Moniz AC. and permethrin) in the Hershberger and uterotrophic assays.8(1):197-202. 2004. 2005). Xenobiotica 1997.8(1):18-21. 2005). the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. September 2003. Hu JY. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation.

epa.usgs. Mullin LS. and therapy.38:95-101.htm.Pyrethroid Pesticides Ray DE. Piccirillo VJ. Soderlund DM. Pesticide and Evaluation Scheme. Meyer DA. Pesticides in the Nation’s Streams and Ground Water. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. April 2002. et al.S. March 2006. Available at URL: http://www. EPA). Environ Health Perspect 2005. Revised February 25. Pyrethroid insecticides: poisoning syndromes.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Shafer TJ. Available at URL: http://www. Geological Survey (USGS). 5/26/09 Woollen BH.S.22(8):983-991. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . Laird WJ. Sheets LP.186:57-72. Forshaw PJ.S. Environmental Protection Agency (U. Xenobiotica 1992. Available at URL: http://whqlibdoc. Rev Environ Contam Toxicol 2006.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. 5/26/09 U.gov/oppsrrd1/REDs/cypermethrin_red.gov/ circ/2005/1291/. O’Malley M. 2005.S.epa. synergies.who. Safety of pyrethroids for public health use. Marsh JR. World Health Organization (WHO). U. resmethrin.S. Environmental Protection Agency (U. EPA). Reregistration Eligibility Decision for Cypermethrin. 2007.htm. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. 19962002. Pyrethroid illnesses in California. Lesser JE.epa.pdf. 1992–2001. sumithrin synthetic pyrethroids for mosquito control.171:3-59. Available at URL: http://www. Toxicology 2002. June 2006b. Permethrin. Clark JM. Sargent D. June 2006a. Crofton KM. Available at URL: http://pubs. J Toxicol Clin Toxicol 2000. 5/26/09 U. Environmental Protection Agency (U. EPA). Spencer J.113(2):123-136.S. 5/26/09 U. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).10.S. pdf.

median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC.. 2005). 2001.68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin.. Cyfluthrin is rapidly metabolized and eliminated from the body.95 µg/L. 2005. Biomonitoring studies of 4-fluoro3-phenoxybenzoic acid in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of cyfluthrin than levels found in the general population. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount of 4-fluoro-3-phenoxybenzoic acid in urine does not mean that the level will result in an adverse health effect. Thus. 2003).S.Pyrethroid Pesticides Cyfluthrin CAS No. most of which were dermal and respiratory irritations (Spencer and O’Malley... Studies in Germany of 396 children and adolescents (Becker et al. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2 μg/L) in the U.. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. representative 2001-2002 NHANES subsample (CDC. 2003). 2004). Baker et al. Urinary levels for adults and children in these studies were similar (Heudorf et al.. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0. Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. 2005). representative subsample in NHANES 2001-2002 (CDC. Fourth National Report on Human Exposure to Environmental Chemicals 159 . Seven individuals participating in floor exercises on cyfluthrin treated carpet demonstrated a rise in the urinary excretion of 4-fluoro-3-phenoxybenzoic acid in the 72 hours following the activity (Williams et al. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. Following an indoor application exposure. but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. 2003).. Leng et al. 2001) showed that urinary levels of 4-fluoro-3-phenoxybenzoic acid at the 95th percentile ranged from either slightly higher or lower than the detection limit in the U. 2006). In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). 2006) and 1177 urban adults and children (Heudorf et al.S.

population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.S.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2. 160 Fourth National Report on Human Exposure to Environmental Chemicals . < LOD means less than the limit of detection.2 and 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 831 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 701 594 957 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 830 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 700 594 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid (creatinine corrected) Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 161 .

209(3):221-233. Atlanta (GA).109(3):213-217. Heudorf U. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Int J Hyg Environ Health 2006. Butte W. Angerer J. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int J Hyg Environ Health 2003. Third National Report on Human Exposure to Environmental Chemicals. Pyrethroid illnesses in California.209(3):293-299.46(3):281-288. 162 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. Int J Hyg Environ Health 2006. J Expo Anal Environ Epidemiol 2003. Angerer J. Krieger RI. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Williams RL. Schulz C. Hadnagy W.Pyrethroid Pesticides References Baker SE. Rev Environ Contam Toxicol 2006.77(1):67-72. Heudorf U. Becker K. Sugiri D. Ranft U. Olsson AO. Bernard CE. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Berger-Preiss E. Centers for Disease Control and Prevention (CDC). Arch Environ Contam Toxicol 2004.186:57-72. Heudorf U. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Angerer J. Kolossa-Gehring M. Angerer J. Environ Health Perspect 2001. Seiwert M. Int Arch Occup Environ Health 2004. Spencer J. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. 19962002. Barr DB. Drexler H. et al. Hoppe HW. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Idel H.206(2):85-92. Ball M. Leng G.13(2):112-119. O’Malley M.

350) .15) .740 (.07 (.630-. Similarly.68) .670 (.490-1.790 (.21) .200) < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample.880 (.670-2.670-1. Fourth National Report on Human Exposure to Environmental Chemicals 163 .120-.300-.12 (.110 (<LOD-.740-2.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.790-1.and trans-isomers.200 (.890 (.53) .490-. 1985. In the body.10) size 1951 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .2dichlorovinyl)-2.490-1.240) .870) 1.68359-37-5 Cypermethrin Permethrin CAS No.510 (.340-.850 (.460 (.310) .700) .910-5.47 (.44 (.220-.240) .140 (.262) * * * < LOD < LOD .1.80) . Generally. cis-3-(2.68 (.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .or trans-3-(2.24) 1.140 (<LOD-.570 (.920) 1.200-.35) .400-.340) .2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.2dichlorovinyl)-2.380 (.600-1.790-1.68) .2-dichlorovinyl)- CAS No.2-Dichlorovinyl)-2.110-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.2-dichlorovinyl)2.410) . trans-permethrin.202 (. but it can also reflect exposure to cis-3-(2. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.630) . more of the trans-metabolite than Urinary cis-3-(2.890 (.570-.470 (.550) . 1999).490-.960 (.S.180 (.650-1.500 (.610) .460-1.200) .110-. ciscypermethrin and cis-cyfluthrin.380-.170 (.2-dichlorovinyl)-2.710) .280 (. The presence of cis-3-(2..2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.330 (.680 (.54) .220-.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.770) . 52315-07-8 CAS No. and trans-cyfluthrin. cis-cypermethrin.510 (.770-1.900 (.210) 90th .330) .380-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.13 (.200) .600 (.580) 1.680-3.630 (.730 (. population from the National Health and Nutrition Examination Survey. cis-permethrin.690) .220-.260 (.300 (.470-1.670-1..680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .430-.250-.740) 1.820 (.710-1.460-.300-.1 and 0.120-.32) . and ciscyfluthrin. Cyfluthrin.600) .950-2.280-.230) . Kuhn et al.200-.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .630) .150 (.640 (.520) .2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.370 (.08) .500 (.780) .220-.270-.410) .270 (. 1985. Kuhn et al. trans-cypermethrin.50) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.270 (. transcypermethrin and trans-cyfluthrin.160 (<LOD-.340) .790) .370-.155-.300 (. but can also reflect exposure to trans-3(2.610) .Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.110-.250 (. 1999).210) .380-.580-1.43) .420-.2-dichlorovinyl)-2.35) 1.200-.510 (.210-.180) . The chemical trans-3(2.530 (.11) .52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.730 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. < LOD means less than the limit of detection.730 (.740-1.220) .160 (. Biomonitoring Information Urinary levels of cis.120-. the presence of trans-3-(2.160 (.28) 671 680 518 701 591 957 Limit of detection (LOD.120-.440 (.380) .2-dichlorovinyl)-2.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.77 (.270 (.

Pyrethroid Pesticides 2.59) .300) .840 (.11) .280 (.550-1.220) .430-. Studies in Germany of 396 children and adolescents (Becker et al.130-.750 (.830) .430 (.840 (.11) 1.12-2.380-.29 (.200-.370-.440 (.260 (.250 (<LOD-.300) .550 (.290-.590) .640-1. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.190) . 2004.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U. urinary levels of cis-3-(2.540 (.250) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.250) 90th . Schettgen et al.290) ..2-dimethylcyclopropane carboxylic acid did not increase.370-.430-1.59) .890 (.440 (.190) .390 (. 2001) showed urinary levels of cis.250-.240 (<LOD-. 2006. Survey Geometric mean (95% conf.67 (.270 (..2dichlorovinyl)-2..270-.11 (.37) . 2005).182) * * * < LOD < LOD .680 (.180 (..410) .21) . 2006.300 (.320-.49) . In a study of urban residents in Germany (Berger-Preiss et al..230-.290) .S. In the same residents. Cyfluthrin.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.03) 1.440-.280-.250) .640-..33) .250-.800 (. In these volunteers.270) .580-1.. 2005).370-.138 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.530 (.400 (. 2002).530 (.450-1. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al. representative NHANES 2001-2002 subsample (CDC.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.550) .2-dichlorovinyl)-2. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.350 (.150-. 2001.170) < LOD < LOD < LOD .640) 1.260 (.350) .200) .570) .750-1. post- Urinary cis-3-(2.170 (.160 (<LOD-. 2005) In a small group of indoor pest-control operators.150-. Lu et al.400-1.500 (.260 (.680-1. 2002).230 (..390-.150-. median urinary levels of trans-3-(2.690-1.03) size 1951 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .550-1. population from the National Health and Nutrition Examination Survey...510-1.450-. 2006) and 1177 urban adults and children (Heudorf et al. 2004). 2005).and trans-3(2.890) . Other studies have provided evidence that urinary levels of cis.300-. 164 Fourth National Report on Human Exposure to Environmental Chemicals . Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.230-.24) .31) .170 (.810 (. 2003). the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.67) .190 (.440-.S.340) .450 (.11) .580) .640 (.380 (.2dichlorovinyl)-2.640-1.390-.2-dichlorovinyl)-2. the median and 95th percentile of urinary levels of cis-3-(2.420 (.210-. 2006).2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.120 (.230-.2-Dichlorovinyl)-2.290 (.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.680-1.560) .and trans-3-(2.59 (1.080-.380) .33 (.260) .2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC..710-3. 2003). and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.220 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.560) 1.104-.470-1. 2006).250-. In a study of volunteers.880) . 2005).550) .600 (.540) .220 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.360-1. urinary trans-3-(2.700-2.590 (.920 (.540 (.320) .700) .200-.900 (.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .140-.340-.710 (.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.2-dichlorovinyl)-2.780 (.340) .80) .780) 1.260-.700) .270) .300 (.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .200 (.180-.12 (.

77) 1.400-.500 (.11-1. Biomonitoring studies on urinary levels of cisor trans-3-(2.4.19 (3.560 (. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.54) 4.76-4.520-.77 (1.28 (2.60) .2-Dichlorovinyl)-2.670) .54 (1.39 (1.560 (.90) 1.970 (. < LOD means less than the limit of detection.42 (2.66) . Fourth National Report on Human Exposure to Environmental Chemicals 165 .760) .03-1.43) 2.55-5.500-.500) .620) < LOD 2.520) .77) 2.41-14.08-6.Pyrethroid Pesticides application median urinary levels of summed cis.03-1.2-dichlorovinyl)-2. 2005).490 (<LOD-.400 (<LOD-.63) 1.810-1.55-4. 2005).62 (1.19) 1.12-6.910-1.49-3. which may vary for some chemicals by year and by individual sample.55-3.68) 2. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.59 (1.680-1.01) 4.60) 1. Urinary trans-3-(2.68) 1.26 (.42) 1.50 (1.700) .49-3.97-11.550 (. population from the National Health and Nutrition Examination Survey.48) 4.23) 2.41 (1.68) 1.01 (1.63) 1.S.and trans-3-(2.09 (. trans-Cypermethrin.66) 691 680 518 690 595 954 Limit of detection (LOD.08) 1.4 and 0.480-.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .840-1.56 (1.84 (1.28 (1.860) .14-2.14) 1.68-3. Finding a measurable amount of cis.16) 1.660) 1.25-3.410-.56) 2.35) 1.920-1.08-4.49-5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.64-4.560 (.20 (.850-1. Survey Geometric mean (95% conf.07 (1.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.25 (1.76-3.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.85) 4.60-4.95) 3.470 (.56) 2.19 (2.94 (1.780 (.800-1.470 (<LOD-. The maximum post-application urinary levels.87 (1.40 (1.830-1.530) .730) .2-dimethylcyclopropane carboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pyrethroid pesticides than are found in the general population.820) .460-.07-3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.420 (<LOD-.39-5. however.17 (.70) size 1976 2525 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .17 (.710 (.81) 2.910-1.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .10) 2.700-1.95) 2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.670) .14-6.69 (1.89 (2.2-dichlorovinyl)-2.20 (.56 (1.13) .27 (1.7) 2.410 (<LOD-.460-.410 (<LOD-.22 (1.570) 90th 1.410-.23 (.940 (.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .610) 1.or trans-3-(2.20 (.440 (<LOD-.2dichlorovinyl)-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.17-1.91 (1.69) 1.750) .5) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.490-1.580 (.11-2.37 (1.68-2.

13) 1.15-3.900 (<LOD-1.00) 5.00) 1.48 (1.560 (.480-.34-3.750) .74) 2.15) 2.41) 1.780) .880-1.56-2.02-1.720 (<LOD-.47 (1.27-2.87) 1.47-2.87) 1.640) .36) 2.56-5.07) 2.19 (1.08 (.470 (.68) 3.60) 2.730) .07-3.57) 3.60) 2.15) 3.570 (<LOD-.00-5.00 (1.11) .39 (1.500-.70 (.31) 1.91-11.15-3.55 (2.28) 2.770) < LOD 2.760 (.13) .57 (1.91 (1.720-1. Survey Geometric mean (95% conf.22) 1.470-.850) .31 (. 166 Fourth National Report on Human Exposure to Environmental Chemicals .530 (<LOD-.970 (.87-8. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.33 (1.39) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.45 (1.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .850) 1.33-1.Pyrethroid Pesticides Urinary trans-3-(2.07-2.55 (2.22-1.700 (.3) 2.98 (1.610-.30-3.74) .67 (2.850-3.800-1.800-1.00) 1.64 (1.880 (<LOD-1.44) 2.12 (.60 (1.34-4.40-2.580) .520 (<LOD-.42) 1.820-2.37 (1.35) 1.33-2.660) .88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.55 (2.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .540) .720-1.65) 1.47-2.700 (.410-.65 (2. population from the National Health and Nutrition Examination Survey.26 (1.75 (1.35 (1.86 (2.930-1.30-6.87-3. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.15-3.07) 2.20 (1.22-2.36 (1.48-2. trans-Cypermethrin.81 (2.580 (.2-Dichlorovinyl)-2.61) 1.880 (.740) .700-.56 (1.16 (1.42 (.27-2.440-.670) .45-2.570 (.29) 1.S.570-.780 (<LOD-.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.87 (1.31 (2.12-1.08 (.91) 1.07-1.530 (.20-2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.780) 90th 1.80) 1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .89) 2.19) .15 (1.

Sugiri D. Ranft U. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.109(3):213-217. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Bravo R. Int J Hyg Environ Health 2006. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.62:101-108. Bartell S. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Wieseler B. Idel H.209(3):293-299. Int Arch Occup Environ Health 2003. Environ Health Perspect 2006. Berger-Preiss E.68(6):1160-1163. Barr DB.114(9):14191423. Int J Hyg Environ Health 2003. Heudorf U. Idel H. George DA. Int J Hyg Environ Health 2002. Third National Report on Human Exposure to Environmental Chemicals. Bull Environ Contam Toxicol 1999. Angerer J. Schettgen T.205(6):459-472. Drexler H. Leng G. et al. Leng G. Heudorf U. Angerer J.206(2):85-92. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Angerer J. Int J Hyg Environ Health 2006. Ball M. Angerer J. Kuhn K. Schulz C. Levsen K. Lu C. 2005. Ranft U. Leng G.209(3):221-233. Angerer J.134(1-3):141-145. Kolossa-Gehring M. Butte W. Environ Health Perspect 2001. J AOAC 1985. Heudorf U. Hardt J.77(1):67-72.76(7):492-498. Angerer J. Idel H. Seiwert M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Biological monitoring of workers after the application of insecticidal pyrethroids. Sugiri D. Atlanta (GA). Int Arch Occup Environ Health 2004. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Drexler H. Centers for Disease Control and Prevention (CDC). Heudorf U. Permethrin and its two metabolite residues in seven agricultural crops. Hoppe HW.Pyrethroid Pesticides References Becker K. Pearson M. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Hadnagy W. Berger-Preiss E.

Deltamethrin can degrade to cis-3(2..2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid of 0. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population. Finding a measurable amount of cis-3-(2. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample. 168 Fourth National Report on Human Exposure to Environmental Chemicals . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Pyrethroid Pesticides Deltamethrin CAS No. 2006) and 1177 urban adults and children (Heudorf et al. 2001. mean peak urinary levels of cis-3-(2. 2005).2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2-dibromovinyl)-2..2-dibromovinyl)-2.5 μg/L) than the detection limit (0. (2004) reported a geometric mean concentration of cis-3(2. 2005). Following residential spraying with deltamethrin for malaria protection in Mexico. 52918-63-5 General Information Cis-3-(2. Outside the U. Biomonitoring Information Urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. 1990).3-0.2-dibromovinyl)-2. Baker et al. deltamethrin has been used against mosquitoes that carry malaria. in some situations replacing the use of DDT. Urinary levels for adults and children in these studies were similar (Heudorf et al. Studies in Germany of 396 children and adolescents (Becker et al. 2001) showed that urinary levels of cis-3-(2. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.2dimethylcyclopropane carboxylic acid formed in the environment.. in detection of cis-3-(2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. 2004).1 μg/L) for the NHANES 2001-2002 subsample (CDC..2-dibromovinyl)-2.. 2005).2-dibromovinyl)-2.2-dibromovinyl)-2.39 µg/L. In the NHANES 2001-2002 subsample. urinary levels of cis-3-(2..S.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.2-dibromovinyl)2. Thus.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.

1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Fourth National Report on Human Exposure to Environmental Chemicals 169 .1 and 0.2-Dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD.S. which may vary for some chemicals by year and by individual sample.Pyrethroid Pesticides Urinary cis-3-(2. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey.

population from the National Health and Nutrition Examination Survey.Pyrethroid Pesticides Urinary cis-3-(2.2-Dibromovinyl)-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 830 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 700 527 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S. Survey Geometric mean (95% conf. 170 Fourth National Report on Human Exposure to Environmental Chemicals . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

[online] 1990. Deltamethrin. et al. Angerer J. Angerer J. Environ Health Perspect 2001. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Centers for Disease Control and Prevention (CDC). Int J Hyg Environ Health 2006.209(3):293-299. 5/26/09 Ortiz-Perez MD. Atlanta (GA). Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Available at URL: http://www. et al. Grimaldo M. Ball M.109(3):213-217.org/documents/ehc/ehc/ ehc97. Int Arch Occup Environ Health 2004.77(1):67-72. International Programme On Chemical Safety (IPCS). Hoppe HW. Environ Health Perspect 2005. Heudorf U. Third National Report on Human Exposure to Environmental Chemicals. Int J Hyg Environ Health 2006. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Schulz C.inchem. Angerer J.209(3):221-233. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Heudorf U. Butte W. and genotoxicity in exposed children. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Torres-Dosal A. Carranza C. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Kolossa-Gehring M. Heudorf U. 2005. Drexler H. Environmental Health Criteria 97. toxicokinetics. Batres LE.113(6):782-786.htm. Seiwert M. Angerer J.Pyrethroid Pesticides References Becker K. Lopez-Guzman OD.

representative NHANES 2001-2002 subsample (CDC. 2005). 39515-41-8 CAS No. 2005). 2005).. A small sample of occupationally unexposed Italian residents had median levels of urinary 3-phenoxybenzoic acid that were about fourfold higher than for adults in the NHANES 2001-2002 subsample (CDC.. 2005). Becker et al.. 2004). Saieva et al.Pyrethroid Pesticides Cyhalothrin CAS No. Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al. 2006) showed that urinary levels of 3-phenoxybenzoic acid at the 95th percentile were similar to levels at the 95th percentile for children in the U. 2006. 2005). a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. 2005). 68359-37-5 Cypermethrin Deltamethrin CAS No. mean peak urinary levels of 3-phenoxybenzoic acid in children increased at least sixtyfold over non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (OrtizPerez et al. 2003. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. CDC. 2005). 2006). 2003). median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. (2004) reported geometric mean levels of 3-phenoxybenzoic acid that were approximately sixfold higher than levels for adults in the NHANES 2001-2002 subsample (CDC.. Fenpropathrin Permethrin CAS No. In a small group of indoor pest-control operators. CDC. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. In the New York City study. Biomonitoring studies of 3-phenoxybenzoic acid provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of pyrethroids than levels found in the general population.. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. Baker et al. CDC. A study of 396 German children (Becker et al. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. In one study of 145 urban residents in 80 private homes in Germany. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. 2005. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.S.. Following residential spraying with deltamethrin for malaria protection in Mexico.52315-07-8 CAS No. urinary 3-phenoxybenzoic acid levels at the 95th percentile were about threefold lower than the levels at the 95th percentile in the 2001-2002 NHANES subsample (Berger-Preiss et al.. 2003. Hardt and Angerer. 2005. Urinary levels of 3-phenoxybenzoic acid in children were found to be related to residential pesticide 172 Fourth National Report on Human Exposure to Environmental Chemicals . Thus. 52645-53-1 Tralomethrin CAS No. 2002.. 52918-63-5 use and house dust levels (Lu et al.

interval) .1) 3.336 (.730 (.25 (2.49-2.320) .35 (1.43) 3.83-11.330) .620-1.76 (1.298 (.1) 3.41-2.454 (.430-.238-.226-.990) .51-3.370) .35 (2.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .345) Selected percentiles ( 95% confidence interval) Sample 95th 4.630) .450 (.38 (2.210-.434) .16-1.560-. Survey Geometric mean (95% conf.430-.266-.04-5.670 (.330) .590 (.560-.27-2.89-71.300 (.54) 1.16) 1.680 (.41-3.200-.25-7.45-5.14-6.75 (1.292-.1) 3.44) 5.340) .26) 2.23 (2.850) .270) .90) 1.52-5.750) .530-.30 (.190-. Deltamethrin.520 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.271-.03 (3.34) 8.810) 1.81 (1.39) 2.55 (1.32 (1.21 (2.86 (1.280 (.490-.12 (.51-6.384) .230 (.93 (1.265-.64) 697 680 524 701 603 957 Limit of detection (LOD.05) .374) 99-00 01-02 99-00 01-02 99-00 01-02 .320) .13) .820) .260-.04) .48-2.550-.13 (.27-11.960 (.230 (.780) 4.34-6.610) .45 (2.362) .428-.62) 5.570-1.05) 1.601) .12) 4.340) 1.25) size 1998 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .700-1.18 (2.35) 2.60) .160-.62-6.65 (1.314) .295) .340) 75th .364) .49-2.640 (.78) 6.33) .48-2.52-4.73) 1.490) . Fourth National Report on Human Exposure to Environmental Chemicals 173 .350-.250 (.427) .420) .16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .240 (.53-3.940) 1.267 (.160-.253-.233-.328 (.740 (.297 (.740 (.750-1.18 (1.230-.650 (.200-.273 (.227-.180-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.353 (.840-1.230-.65-2.30 (1.320 (.220-.26-2.32-21.69) 3.8) 3.29-1.26) 2.50 (2.46) 2.35) 2.25 (2.02-6.69 (1.260 (.315 (.352-.01 (1.260 (.92-3.830-2.36) 1.246-.800 (.507 (.250 (.325 (.369) .49 (1.27-2.33 (2.63-3.276-.360) .33 (1.288-.200-.270 (.260 (.49 (1.440) .1 and 0.373) .250 (.750) .300 (.510-.760 (.210-.53) 1.78) 1.25-4.46) .71 (1.850) .560-1.30) 3. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.25-1.35) 1.230-.590-.247-.406) .32 (2.300) .72 (1.586) .417 (.300 (.311 (.820) .190-.41) 3.870 (.290 (.42-2.240 (.830) 90th 1.387) .56-5.288 (.800) 1.470-.41 (1.595) .62-8.510-.28) 1.190-.390) .34 (2.78) 1.79) 3.314 (. population from the National Health and Nutrition Examination Survey.78 (1.600 (.570-.700 (.S.320) .710 (.320) .12) .710 (.530-.63 (3.277-.38 (2.190-.321 (.1.292 (.355) .250-.

480-.750-1.200-.580 (.310) .48 (1.09 (.210 (.91-4.17 (.280 (.590-1.440-.278) .640 (.173-.67 (1.490 (.357) .387) .400) .84 (1.330) 1.670) 3. population from the National Health and Nutrition Examination Survey.35) .253) .19 (2.370 (.02-1.61-2.380-.95) 1.67) 1.410) .200-. Survey Geometric mean (95% conf.400-.49) 1.330) .86 (1.299-.230) .740) .270 (.27) 1.44) 2.810) 1.40 (1.272) .37 (1.15-2.21-4.440-.S.530-.229-.240-.460-.60-4.91) 9.510 (.401) .378 (.224-.230-.446) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.423 (.41-4.420-.25-2.35) 1.94 (1.272 (.04 (.13-1.240-.51-7.270-.309 (.290-.49 (1.19-6.09-2.650) .49-2.410-.32 (2.490-.240 (.43) 1.400-.261 (.264 (.83) 1.55) 3.49) 3.540 (.11 (.930) .280 (.25) 2.80) 4.760) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .274-.35-3.05-3.240-.590) .362 (.335-.240-.09-2.81 (1.590) .860-1.280) .03-1.62) 1.534) .328) .83 (1.230-.19) 2.372) .39) 1. Deltamethrin.250 (.150-.200-.88-5.316 (.220-.490 (.271-.290) .329) .41) 1.02 (2.280 (.370-.240 (.440-.730) .06-3.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .220 (.190-.275 (.270 (.216-.300-.246 (.720 (.330) 75th .330 (.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .390-.07-5.460-.96 (1.60) 1.550 (.200-.960-1.329) .240 (.311 (.840-1.190 (.91) .860-1.13 (.04 (3.300-.40) 2.36 (1.10 (2.160-.270) .52) 2.510 (.62) .500) .64-5.261-.677) .350 (.321-.72 (1.730) .13-1.510 (.280) .210-.53 (1.570) .210 (.670) .91 (2.480 (.238-.234 (.225-.280-.350) .560 (.530-.190-.16-4.00) 5.63-3.274 (. interval) .37) 1.07) 2.11 (.550 (.860 (.09) 3.330) .63) 1.720) 90th 1.43 (2.43 (1.309) .450 (.88) size 1998 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .930) 1.640 (.178-.437) .320) .73-4.312 (.580) .55 (1.35 (1.52 (1.630) .0) 3.365) 99-00 01-02 99-00 01-02 99-00 01-02 .250 (.00) 1.610 (.227 (.75-8.03 (.323 (.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.290) .21 (1.00) 1.380 (.202-.17-1.25-5.43-64.74) 3.226-.73) 1.36-6.590) .700-1.44 (1.730-1.240 (.90) 3.250) .270) .54 (1.22 (1.550 (.67 (1.

urban cohort. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Obel J. Arch Environ Contam Toxicol 2004. Third National Report on Human Exposure to Environmental Chemicals.209(3):221-233.113(6):782-786. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Deych E. Batres LE. Idel H. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Sugiri D. Ranft U.205(6):459-472. Ranft U. et al. Bravo R. Torres-Dosal A.46(3):281-288. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Ball M. toxicokinetics.206(2):85-92. Lu C. Ortiz-Perez MD. Becker K. Bartell S. Centers for Disease Control and Prevention (CDC). Exposure to indoor pesticides during pregnancy in a multiethnic. Pearson M. et al. Biological monitoring of workers after the application of insecticidal pyrethroids. Environ Health Perspect 2005. Leng G. Barr DB.Pyrethroid Pesticides References Baker SE. Environ Health Perspect 2006. Hardt J.111(1):79-84. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Idel H. Barr DB. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Berger-Preiss E. Int J Hyg Environ Health 2002. Lapinski R. Leng G. Int J Hyg Environ Health 2006. Berkowitz GS. Olsson AO. Godbold J. et al. and genotoxicity in exposed children. Int Arch Occup Environ Health 2003. Carranza C.114(9):14191423. Int J Hyg Environ Health 2003. Seiwert M. Lopez-Guzman OD. Grimaldo M.76(7):492-498. Environ Health Perspect 2003. Liu Z. Angerer J. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Angerer J. Sugiri D. Levsen K. Berger-Preiss E. 2005. Hoppe HW. Hadnagy W. Kolossa-Gehring M. Atlanta (GA).

260 (.119) .330) .300) .088-.140 (.320 (.190) .145 (.100 (.126 (.110-.320-. coal-fired plants.300 (.250 (.Metals Antimony CAS No.120-.141-.134-.200-.160 (.145) Selected percentiles ( 95% confidence interval) 50th .510) .280-.200-.460 (.150) .160) .120) .460) .197) .150-.120-.144) .370) . and +5.220-.280 (.156-.280-.400) .137) .200-.270) .180 (.154) .360 (.330) .330) . water.131-.160) .190 (.120-.070 (<LOD-.410) .220) .S.270 (.330) 1132 1335 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .150) .420) .260-.240 (.154-. 176 Fourth National Report on Human Exposure to Environmental Chemicals .170-.230) .190 (.220) .130) .080) .04.207) .112-.350 (.130 (.142) * Sample size 2276 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .120 (. distribution.230-.270 (.360) .210 (. and refuse incinerators that process or release antimony.160-.130-.110) .170 (.400 (.460 (.310 (.140) .320) Total .150 (. The absorption. 01-02.184) .350-.130 (.240 (.460 (.200) .130-.143 (.140) .230 (.440) .390-.150-.090) 75th .190-.160-.390 (.120 (.530) .140) . People are exposed to antimony primarily through food and. to a lesser extent.470 (.07.137) .400) .210) . Antimony can exist in one of four valences in its various chemical and physical forms: -3.100-.350-.330 (.180-.210) .134 (.240 (.250-.310) .090 (.330-.350-.200 (.200 (.190-.070 (<LOD-.136-.130 (. Urinary excretion appears to be greater for pentavalent antimony Urinary Antimony Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.270-. 7440-36-0 General Information Antimony is found in ores or other minerals.430 (.280) .079-.140-. solder.210) .080-.180-.120) .180 (.230-.280-.220-.130-.200 (.490 (.470) .150-.300) .120 (.300 (.154) .390) .320) 316 368 290 663 762 725 1297 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .178) .230 (.330) .260) .109-.260 (.270 (.110-.340) .310 (.115-.120 (.190) .410-.150) .470) .230-.250-.115) .130 (.161) .160-.090 (<LOD-.140 (. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.350) .160-.430 (.350) .320-.04.180) .310 (.130) .350 (.340 (.157) .100 (.180 (.123 (.080 (<LOD-.093 (.310) .150-.240 (. and glass.710) .210) .300-.117-.190 (.330 (.160) .330-.400 (.210-.099 (.220 (.140 (.220-. 0.130-.169 (.360) .350 (.280-.190) .160 (.142 (.170-.120) . or other substances containing antimony is another means of exposure.110-. metal bearings.390) .240 (.128 (.270) .140) .280-.148-.280) .176 (.320) .320-.560) .390-.160) .100-.320 (. and excretion of antimony vary depending on its oxidation state.103) .146 (.180 (.140) .240-.570) .170-.164-.200 (.130-.175 (.130-.120-.130) < LOD .280 (.260) .320-.400 (.230) .330 (.170) .180) .180-.440 (. storage batteries.126-.120-.130 (. Antimony enters the environment from natural sources and from its use in industry.220-.160) .090-.500) . and 0.200) .350 (.200) . ceramics.210-. Workplace exposures can occur at smelters. Dermal contact with soil.260 (.170 (.130 (.390-. see Data Analysis section) for Survey years 99-00.250 (.110 (.100) .170-.120) .290 (.105 (. Stibine is a metal hydride form of antimony used in the semiconductor industry.125 (.190) .120 (.135) * .220-.400-. respectively.220) 95th .150 (.260) .350) . 0.350 (.300-.280) .140) .220) .200) . fireworks.250-.180-.280) .120-.410) .150) 90th .200-.122 (. It is used in metal alloys.087-.300-.190-.120-. from air and drinking water.290-. It is also used in paints. which may vary for some chemicals by year and by individual sample. sheet and pipe metal. interval) .128 (.500) .490) .190) .190 (.150-.230 (. and pewter.130 (. < LOD means less than the limit of detection.230) .250) . castings.120-.190-.200 (.210) .095-.108-. enamels.080) . population from the National Health and Nutrition Examination Survey.310-.260-.190-.200 (.160) .180-.240-.210 (.230-. ammunition.098-.350) .136) * .340 (.250-.600) .119-.108 (.310-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. and 03-04 are 0.110-.132 (.120-.360-.180 (.130) .270 (.170-.310 (.300) .400) .220 (.095 (.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.070-.140 (.220-.130-.230-.250 (.114) . and as a fire-retardant in textiles and plastics.290-.090-.160 (.390) . +3.133) * .117-.180 (.430 (.130 (. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.158 (.150 (.132 (.390) .440) .190 (.240) .370-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.360 (.

130) .193) . Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.238) .130) .103-.119 (. and ulcers (Werrin.167 (.209 (.086) 75th .138 (.140) < LOD .098) .113-.127) .194-.277 (.135 (.095-.315) . 1953).128-.173 (. 1958) and occupational exposures (Briegner et al.143) .074 (.152) .151) .430) .263 (.107-.129 (.300) .112 (.741 (.134) .211) .108 (.320-.136) .391) .250-.114 (.127) .103-.120 (.320 (.209) . and eyes..146-.163 (.333-1.241-.125 (.333 (.061-. 1986).226 (.156 (.078 (.127) .112-.124-.181) .085) .131 (.147-.115 (.385 (.149-.271-.124 (.126 (.429 (.132 (. Histopathologic inflammatory and degenerative changes in the lung.077) .228-.333) .308-.300) .107-.125-.267 (.203) .294) 316 368 290 663 762 725 1297 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .500) .102-.200-.146-.256 (.253-.222 (.318-.266 (.267-.320-.127 (.082 (<LOD-.338 (.200-.245) .338 (.109-.425) .173) .098-.071-. myocardium.146) . and route of exposure (Elinder and Friberg.127) .333-.318-.139 (.741) .265-.333 (.205-.109 (.192 (.235-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.154-.124) .075 (.115 (.317) .259 (.137 (.133) .131) .181) .100 (. 1988.173 (.321) .272) .229-.095-.143 (.170 (.200) .080 (. and gastrointestinal symptoms such as vomiting.084) .069-.108-.255-.192-.112 (.114 (. diarrhea.417) .156-.255) . Workplace standards and recommendations for air exposure Urinary Antimony (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.250-.115) .187) .373) . liver.206-.414) .308) .333) 1132 1334 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .278 (.320) .S.119-.310 (.171) .480) .143) Selected percentiles ( 95% confidence interval) 50th .108-.106-.164) .333 (.313-.200-.111-.126-.081 (<LOD-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.248-.213 (.122 (.131-.204-. skin..140) .144-.400 (.193 (.265 (.145) .118 (. abdominal pain.444) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.119-.421) .176 (.225 (.106-.115-.108-.203) .117-.185-.167 (.209) .115-.195-.178-.143) .257) .116 (.120 (.114 (.121) .447 (.310) .278) .429) . resulting in hemolysis with abdominal and back pain (Dernehl et al.159-.391) .135) .333-.076-.118 (. interval) .129 (.148-.132) .104-.109 (.380 (.268) .317) .220) .320 (.250 (.364 (.129) .092) .228 (.173-.188) . The toxicity of stibine after acute inhalational exposure is similar to that of arsine. species.727) .111 (.098-.172-.150-.444) .081) .241-.086 (.134) * Sample size 2276 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .280 (.181) .250) .242-.176 (.122 (.123 (.135) .087) .138) * ..138-.176-.102-.139 (.371 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.150-.364 (.227-.160 (.175 (.159-.159-.107-.207) .153 (.092-.153-.185 (.233-.117-.097-.263-.099-.146-.230-.352 (.Metals than for trivalent compounds (Elinder and Friberg.164-.182 (..120 (. and kidney have been demonstrated in high dose animal studies depending on the dose.152) .317) .209-.30) .224 (.167-.178 (.357) .105-.198) .250-. 1944).161) .280-.192) . Inorganic antimony salts irritate the mucous membranes.281-. 1954).247) . 1995).238) .300 (. Fourth National Report on Human Exposure to Environmental Chemicals 177 .121 (.298 (.199-.196 (. Acute antimony poisoning may cause a metallic taste.147) .068 (.099-.163 (.233 (.343 (.286 (.104-.068-.217 (.208-.117-.253 (.230) 95th . 1962). Ming-Hsin et al.135 (.338) .129) * .261) .239-.233) .236 (.250-.276 (.123) .096-.082) .079 (<LOD-.186) .115 (.228 (.333-.143) 90th .183) . 1986). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.195 (..130) .225) .357-.069-.438) .244-.352) .405) .148) * . 1973).417) .135) .195-.189 (.161) .288 (.076-.250 (.130 (.294) Total .149) .164 (.116-.208 (.162-.214) . population from the National Health and Nutrition Examination Survey.185 (.138-.124-.485) .269 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.310) .080 (<LOD-.121 (.191 (.075 (.113) .267) .333) 787 682 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.089) .179-.238 (.082) .148-.295 (.126) .248) .188-.471 (.167 (.471) .113-.120 (.

Semisch CW.13:361-362. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Nordberg GF. Gallorini M. or exposure differences.html. EPA. Ming-Hsin H.46:931-936. Bolten C. Pozzoli L.. Minoia C. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Weltle D. stibine. 2005. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Luedersdorf R.59:469-474. Kentner M. Industrial Medicine 1944. VI. Br J Ind Med 1991. Pietra R. et al. Arch Dis Child 1997. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Industrial antimony poisoning. 1997). Elinder CG. Kiberd B. Arsine. which may be due to methodologic. Dernehl CU. Yu H-S. Chemotherapy for leishmaniasis: Biochemical mechanisms. Briegner H. Liao Y-H. Antimony trioxide is rated by IARC as a possible human carcinogen. Stocks J. Iavicoli et al. J Trace Elem Med Biol 2002. gov/toxpro2. Leinemann M.48:93-97.. Delves HT. Konings J. Stead FM.)1954. 20012002. HH. 1991. 1998. Review of elements in blood. Ludersdorf et al. Environ Health Perspect 1998. indium. Iavicoli I. Int Arch Occup Environ Health 1995. and hydrogen sulfide. Buchet JP. Antimony in blood and urine of infants. Dezateux C. Cheng-Wei L. Trace element reference values in tissues from inhabitants of the European community I. Earlier measurements in general populations (Minoia et al. 1998) or compiled reference ranges (Hamilton et al. Liao Y-H et al. Stasney J. Piatnek DA. Biomonitoring of a worker population exposed to low antimony trioxide levels. Kuo-Juie Y.. J Clin Pathol 1998. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . eds. Vouk VB. and antimony in optoelectronic industry workers. arsenic. and 2003-2004. 1987). Int Arch Occup Environ Health 1987. Ju-Sun P. Chin Med J 1958.. Schaller KH.16: 33-39.10(3):560-586. clinical efficacy. Caroli S. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Mahieu P. Mayne P. Lenert G.cdc. Cordasco EM. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Costeloe K.e. 1990. Alimonti A.. Matthews T. Skulsukai G. Chest 1973. 2002.521-523.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Roland H. Apostoli P.106:33-39. Stone FD. Mayer P.158:165-190. pp. Friberg L. Schacke G. environmental levels) and health effects is available from ATSDR at: http://www. Wade A. External and internal antimony exposure in starter battery production.. References Berman JD. Urinary antimony in infancy. Industrial Medicine and Surgery (Dec.64(2):182-185. 1998). population. O’Regan M. Nau CA. Kentner et al. respectively.. Antimony. 1994) have reported values slightly higher than those in this Report. 2004. Wu M-T. Biological assessment of exposure to antimony and lead in the glass-producing industry. Lauwerys R.. gallium. 1995. even when exposure levels were below workplace air standards (Bailly et al.51:238-240. Chen J-R. Carelli G. Biomonitoring Information Levels of urinary antimony reflect recent exposure. and future strategies. et al. Dunkelberg. Rev Infect Dis 1988. Atlanta (GA). J Occup Environ Med 2004. Information about external exposure (i. Handbook on the toxicology of metals.. Delves HT. Sabbioni E.67:119-123. and a drinking water standard has been established by the U. Element reference values in tissues from inhabitants of the European community. New York: Elsevier. Suchenwirth R. Bailly R.atsdr. Yang C-Y.. Petrucci F. Dezateux et al.S.76(2):103-115. Centers for Disease Control and Prevention (CDC). Shao-Chi C.. Biological monitoring of exposures to aluminum. Third National Report on Human Exposure to Environmental Chemicals. Cullen A. Paschal et al. Sci Total Environ 1994. Ho C-K. 26-42. 1986.76:432436. Hamilton EI. Chia-Yu H. Sabbioni E. Van der Venne MT. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Pulmonary edema of environmental origin.Metals to antimony have been established by OSHA and ACGIH. Gebel TW. et al. Biomonitoring studies on levels of urinary antimony can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of antimony than are found in the general population. Fuchs A. Pilgrim L. 2nd ed. In: Friberg L.

et al.76(1):53-59. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Renes LE. Sci Total Environ 1990. Werrin M.99-108. Sampson EJ. Jackson RJ. Trace metals in urine of United States residents: reference range concentrations. 27:38-45. Paschal DC. and serum of Italian subjects. Pirkle JL. Antimony poisoning in industry. Morrow JC. Ting BG.Metals in urine. Industrial Hygiene and Occupational Medicine 1953.95:89-105. blood. Chemical food poisoning. Environ Res 1998. Fourth National Report on Human Exposure to Environmental Chemicals 179 .

8) 7.5 (36.25-9.34-10.7) 90th 37.2-20.55 (7. cancers.90 (5.12-10.10-10.9-34. population from the National Health and Nutrition Examination Survey.6 (9.7-83. +3 and +5).30 (6.8-61.10 (6. Arsine (AsH3) is a reactive.1-18.6-35.8) 34. referred to as inorganic arsenic compounds.6-43.0-60. and. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.00 (6. The United States no longer produces arsenic from mining but imports about 22.4-65. though in some locations arsenite may be prevalent (WHO. and arsenosugars.7-95. Also.3) 10. Arsenic is measurable in most soils.3-19.2 (12. or rarely as elemental metalloids (yellow. mostly for use in wood preservation (ATSDR.4) 40. to a lesser extent. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.90-7. Survey years 03-04 Geometric mean (95% conf.70-9.5) 41.0 (15.90-14.1) 7. Gallium.3-111) 78.8-77.5-52.1) 15.2 (51.9 (17.41 (7.84) 8. trimethylarsine oxide.4 (24.5) 95th 65.08 (5.70) 8. aluminum. the smelting of copper.0 (22.9 (8. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. lead.7) 24.0 (11. 2005).0 (43. cacodylic acid.1) 290 725 1542 03-04 03-04 9.2) 46.19-9.8) 30.8 (48. Various arsenic compounds were used in paint pigments and for tanning animal hides.6 (15.27) 9. arsenic compounds. 2001).34-9.10-7. arsenites.10) 10.4 (31.Metals Arsenic CAS No.13-8.S.30 (7.57) Selected percentiles ( 95% confidence interval) 50th 7. In the last century.0-19. Before the 20th century. and indium arsenides are used in the semiconductor industry. interval) 8. see Data Analysis section) for Survey year 03-04 is 0. grain.4 (48.77) 6.1 (38.9-46.9) 21.6) 618 722 1074 Limit of detection (LOD. Arsenic and its compounds have had many uses in the past and present as medicines. black.97) 8.1-40. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.90 (7. 180 Fourth National Report on Human Exposure to Environmental Chemicals .4) 60.5 (14.2-17. and other metals.40) 7. Arsenic trioxide (As2O3.3) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2557 03-04 03-04 03-04 7.74.7) 65. and as a cosmetic to lighten complexion.20 (8.5-41. from coal burning. were used as treatments for syphilis.9-62.84) 8.8) 29. and in lead-acid storage battery grids.5-178) 46. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.30) 17. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. General population exposure to inorganic arsenic can occur through consumption of drinking water and.0 (14. lead hydrogen arsenate.6 (32.80-9. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.90-8.3-15. and gray forms).1) 1281 1276 03-04 03-04 03-04 9. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.90) 16.66-8. arsenic as elemental metalloids may be used in some ammunition.2-61.80 (5.1 (32.29 (8. arsenocholine.6 (13. ocean and fresh waters.5 (34. particularly arsenic trioxide.7 (11.4) 13. retaining walls.000 metric tons annually. and play sets.2-93. Since the 1940s. and produce. such as arsenopyrite (FeAsS) and realgar (As4S4). pesticides.02-8.2) 15. In nature. gaseous hydride manufactured in small quantities for use in the semiconductor industry.6-141) 53. sodium arsenite. copper arsenates. Although it is still widely used in the United States. alloys.90-11.8) 17. as alloy in metal bearings.6) 11.90 (7. psoriasis.90-8.2 (13.5-19. it is found in over 200 crystalline or mineral forms.5) 66.70 (6.5 (23. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. mental disorders. and as homicidal poisons. Water sources contain mostly inorganic arsenate.50-14. solders.4 (7.8) 33.00-9.8) 7. meats. and foods.5) 43.80) 6.2 (41.12 (6. and arsenates (oxidation states of -3.90) 75th 16.9) 68.5 (40. Arsenic trioxide is approved to treat acute promyelocytic leukemia.50 (8. to a lesser extent. semiconductors.4 (26.

93-9. population from the National Health and Nutrition Examination Survey. and contact with CCA-preserved wood structures.44) 6. mine tailings).0) 26.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .5-17.2 (12. The semiconductor dopants. 2007.25-9.4 (40.6 (10. 2001).32 (5. 2001.45) 5.0-26.0-38.3 (24. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. 2006.07-9.0-18.12-10. inorganic arsenic is widely distributed within the body.96) 12.81-9. U.0) 12. and arsenosugars.4 (12. WHO.93-8.13) 8. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established. 2001).4) 32.0) 42.8 (11. Chowdhury et al.1) 6.S.8) 22. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.6 (17.0) 1281 1276 03-04 03-04 03-04 8.7 (9.4 (11.33 (6.64 (7.3-64.88 (5. Gamble et al. 2007.7) 95th 50.S. 2001).66-8. Extremely high groundwater arsenic levels.01) 11.5) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2557 03-04 03-04 03-04 8. selenium. 2001.7) 28. shellfish. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. Survey years 03-04 Geometric mean (95% conf.0 (31. organic arsenic can be converted back to methylated and inorganic arsenic.25 (6.1 (14.35) 7. Arsenate is reduced in the body to arsenite (oxidation state +3).38-10..0-69.9 (45.76 (6. gallium arsenide and indium arsenide. though some reduction may occur in the gut prior to absorption. dust.75 (5.11 (5.3-53.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U. arsenocholine.0) 14.99-9..1-36. and folate status (Chen et al.23-7. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.1 (11.1) 58. EPA.88) 7.4 (24.31 (6. 2001). 2006.4 (42.9) 53.59) Selected percentiles ( 95% confidence interval) 50th 7. Children may have additional exposures from ingestion of contaminated soils (e.7 (11. Smoking tobacco is also a source of inorganic arsenic.9-56. Some studies suggest that variation in the degree of methylation among persons is related to the susceptibility of arsenicinduced disease and may involve consideration of genetic polymorphisms. 1988).30-9.44-11.8-75..2-46..58-10. 2003.8-32.g.10-8. Fish. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.0 (17.01) 7.3) 9.1) 8. kelp.7 (25.1) 7. EPA’s maximum contaminant level (Hughes.8 (20..66 (7. 2001). Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.2-15.18 (5. After absorption. interval) 8. and some other seafood can contain organic forms of arsenic including arsenobetaine. are used in enclosed ultraclean operations within the semiconductor industry. WHO.51) 75th 14.47 (7.24 (7.61 (7. Steinmaus et al.. but is poorly absorbed dermally (WHO.28-7. cacodylic acid and monosodium methyl arsenate. trimethylarsine oxide (TMAO).7-35.20-9.10-16. so exposure to the general population is extremely limited.4) 54.8 (21. dose level.41) 6.7-18. NRC. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. In aquatic sediments.5) 290 725 1542 03-04 03-04 8. 2001).75) 13.5) 17.04) 7.1) 24.04 (5. 2007.50 (6.7-34.66-8. Inorganic forms of arsenic demonstrate high acute toxicity. Direct exposure to DMA and MMA may result from use of the two pesticides. Though modest bioconcentration occurs in some aquatic life. 2001).0) 33.8 (27.6 (35. Tseng.4-64. arsenic does not show biomagnification in the food chain (WHO.2) 90th 30.9) 13.86-17.2) 15.2) 40. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.3) 6.3-41.5-120) 40.47-6.7-188) 27.5 (9.S. 2001).8-62. In aquatic organisms.6-17.4 (26. age.06 (4.3 (27.33-10. have caused clinical arsenic poisoning.7-17.3-62.8 (12. as observed in Bangladesh where millions of people have been exposed.40) 8.00 (6. The reduced form of MMA (oxidation state Urinary Total Arsenic (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6) 45.47 (6.8) 27.

2006. Chronic human intake of arsenic at less than acutely toxic doses. Survey years 03-04 Geometric mean (95% conf. Arsenic has many actions demonstrated in cellular studies.60) 1. hyperkeratosis.g. leading to a decrease in adenosine triphosphate energy production. WHO. < LOD means less than the limit of detection. Cohen et al. food residue. Bredfeldt et al. Acutely.20 (<LOD-1. interference in signal transduction pathways. 2006. and endothelial injury (Kumagai and Sumi. 2007. Such actions may lead to decreased energy production. and diarrhea.. hematocytopenias.. vomiting.. and altered gene expression. hypertension. some of these effects may take years to develop. population from the National Health and Nutrition Examination Survey.50) 621 725 1078 Limit of detection (LOD. 2006) or when exposure occurs in smokers (Chen et al. and production of glutathione may be affected as well.. 2006. 182 Fourth National Report on Human Exposure to Environmental Chemicals .S. but additional or confirmatory research is needed (Kapaj et al. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells.10 (<LOD-1.80) 1. 2001). 2004. which can lead to dehydration and shock.S.20 (<LOD-1. Although arsenate is reduced in the body to arsenite. renal failure. Cardiac arrhythmias. and it also will inhibit succinate dehydrogenase. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose.. and DNA repair inhibition (Cohen et al. The U.10 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 1. Taiwan. including drinking water sources with elevated arsenic levels (e.. and hyperpigmentation of the skin (NRC. can cause peripheral sensorimotor neuropathies. U. WHO. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 1.0. peripheral vascular disease.. Chronic elevated arsenic intakes have been associated with diabetes.S. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e.10 (<LOD-1. The organic forms of arsenic occurring in seafood have little known toxicity. gluconeogenesis. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring.60) 1. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. 2007). Chronic arsenic exposure in humans is considered to be a cause of skin. which may vary for some chemicals by year and by individual sample. apoptosis. 2004). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 2001). fatty acid oxidation.. 2001. noncirrhotic portal hypertension. WHO. hepatotoxicity. Studies of arsenic at levels typical of U. Cellular glucose uptake. substitution in phosphate metabolism. 2000.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. and by uncoupling oxidative phosphorylation (NRC.EPA has established drinking water. 2001).10 (<LOD-1. cytotoxicity.. Raml et al. 2004).. drinking water have not been associated with increased cancer rates (Schoen et al.EPA.. 2001.20 (<LOD-1. and childhood neurodevelopmental effects in observational human studies. respectively. increased oxidative stress. and environmental standards for arsenic and arsenic Urinary Arsenic (V) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. NRC. 2001). 2007. 1998. Chile). cell transformations. 2001).20 (<LOD-1. and bladder cancer (IARC.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al.10 (<LOD-1. 2001).g.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. NRC. including inhibition of numerous enzymes. Bangladesh. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. arsenic trioxide) includes hemorrhagic gastritis with nausea. With chronic exposure.30) 1.S. lung. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. WHO.50) 1.

Though CCA-treated wood contains several thousand times more arsenic than untreated wood. median urinary total arsenic levels in 4052 adults varied with seafood intake.18) 3.. population in NHANES 2003–2004 (Schulz et al. In the German Environmental Survey III of 1998. 2006)..S.. 2000). higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al.. In animal studies. 2007. 1998. arsenic has been fetotoxic and teratogenic. urinary arsenic levels have been accepted as a good biomarker of dose (WHO..33 (<LOD-3.e.. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.61 (<LOD-3.. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 2007. Survey years 03-04 Geometric mean (95% conf. Vahter et al. and were about two-fold lower than those for the U.. Meza et al. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3. hand washings from children playing on CCA-treated wood compared to children playing on non-CCA-treated wood playground equipment were slightly to fivefold higher (Kwon et al.. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.80 (<LOD-4. Compared with this Report. Josyula et al. Pellizzari and Clayton 2006). 2003. had decreased since the prior 1990– 1992 survey. 2008). Pellizzari and Clayton. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. 2006. 1999). 2008). DMA produced bladder cancer in some chronic rat studies (Cohen et al.. Valenzuela et al. Shalat et al.. but generally only at maternally toxic doses (WHO... In a Nevada town where groundwater levels were naturally elevated. Offergelt et al.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2001). Additional information about external exposure (i..75 (<LOD-2. 1999. Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al.. 2004. population in the National Health and Nutrition Examination Survey (NHANES) 2003–2004 were similar to levels reported in the National Human Exposure Assessment Survey (NHEXAS) 1995–1996 for about 80 children residing in the Great Lakes region (Caldwell et al.41) 3.html. although urinary arsenic levels were not associated with CCA contact (Shalat et al. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Caldwell et al.. 2006). population (Rubin et al. Several studies have shown that urinary arsenic levels are not correlated with low levels of arsenic measured in house dust or in washings taken from hands (Hysong et al.04 (<LOD-3. 2006)...S. 1986).69 (<LOD-3. 2000.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 2008.50) 1. and the FDA has established a bottled drinking water standard. Urinary arsenic levels were a better predictor for risk of arsenical skin lesions than were arsenic levels in drinking water in Bangladesh (Ahsan et al. Calderon et al..18 (<LOD-3. 2001). 2001).S. 2006. 2006).cdc. gov/toxpro2.. Levels of total urinary arsenic in the U.75 (<LOD-2. Caldwell et al.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. population from the National Health and Nutrition Examination Survey. environmental levels) and health effects is available from ATSDR at: http://www. 2004.. Consequently.Metals compounds.19) 3.. 1999. Pellizzari and Clayton..33 (<LOD-3. 1992. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. 2006.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Shalat et al. WHO.atsdr.S.00) 1.

see Data Analysis section) for Survey year 03-04 is 0. After recent seafood ingestion.30) 10.37 (1.700-1. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al. vasospasm. when seafood organic arsenic is subtracted).80-5.2-35. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.50) .800-4.17-1.3 (9.50-6. 2008)..4) 23.8 (17.05) < LOD .0) 4. In the late 1980s.3) 35.6. 2007) with higher levels of arsenic in the drinking water. 2008). 2006)..2-38. and 0. Median and mean total urinary arsenic levels for residents in some districts in Bangladesh were reported to be about 50-fold higher than respective levels in the U.00-6.7) 15.. 184 Fourth National Report on Human Exposure to Environmental Chemicals .6 (11..70 (3. arsenobetaine. 2005.5 (14.20 (2.30) 2.3 (21.8-40.3) 1284 1284 03-04 03-04 03-04 1.900-1. 1996. interval) 1.9-23.9) 13. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. Survey years 03-04 Geometric mean (95% conf.80) 1. Also. arsenite. Caldwell et al.19 (. and two methylated metabolic products.0-23. 2001. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.4) 31.00 (. geometric mean levels were about 70-fold higher than for the U.1-94.50) 90th 16. 1985.8.00-4. < LOD means less than the limit of detection.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.11-1.90-29.1) 45.30 (2.5 (26. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.40-7.20-3.1-51. 1990. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.70) 6. Measurable organic arsenic species in this Report are three biologically generated environmental forms.55 (1.00-1.5) 621 725 1078 Limit of detection (LOD..700-1. 2005. 2008). DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.00 (1. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.600 (. WHO. 2008.48-2..5) 32..20 (4.9 (7.. which may vary for some chemicals by year and by individual sample. arsenocholine. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. 4.4.4 (16.500-1.6 (13. respectively.80 (3. 2005.74 (1.28) 1.1) 18. For residents of Inner Mongolia.800-1.70 (5.20) 18. with DMA..10) 4.20) 3. in NHEXAS 1995–1996. and duration of exposure are also considered important.29 (1. population (Ahsan et al. Valenzuela et al.00-12.6 (25. Blom et al.10 (4.90-7.4-35. DMA and MMA. When seafood intake is avoided. arsenite. Arsenate. 2001).70-21. 2008. 2000.6-44.70-21.45 (1.40) 75th 5.871-1.3% of a representative sample of the U.20-25.40) 5. MMA.8 (12..g. Aposhian et al. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. 2000.S. population in the NHANES 2003–2004 subsample.3) 95th 35. methylation capacity.30 (1. Caceres et al.5) 29.31-1.S. Pellizzari and Clayton.43-1.. The higher percentiles of total urinary arsenic levels in the U. and other factors such as nutrition.S.68) . These associations are stronger at higher urinary levels.62) 2.9 (6. 2008). as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.10) 8.8) 35. and TMAO were detected in only 7.7-22.800 (.800 (.0 (26.. Some noncancer effects of arsenic (e. 2003). dermal keratosis.80 (.20) 7. In the residents of a Chilean town who consumed water with high levels of arsenic.5) 292 728 1548 03-04 03-04 1. and TMAO.6.83) Selected percentiles ( 95% confidence interval) 50th 1. Individually measurable species resulting from inorganic arsenic exposure are arsenate. Caldwell et al..00) 3.40-6. Total arsenic measured in the urine includes all species of inorganic and organic arsenic. population showed a higher contribution of arsenobetaine (Caldwell et al. Caldwell et al..e.7) 13.3-39. 1.80 (4.7 (21.Metals other areas of the world (Ahsan et al. China.1-25. Tseng et al. 2007).20-190) 31. In most human studies.8-50.66 (1. arsenocholine.93) 1.400-.20 (.6) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1. population (Sun et al.50) .800) 1.S. population from the National Health and Nutrition Examination Survey.. Sun et al.2 (6.60) 1..60-3... and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.0) 29.900 (.20 (1. 2000. Chowdhury et al.0 (27..7 (13..

.5 (18. population for the sum of inorganic related species was 18.32-7.29 (4.S.16 (.55) 1.47 (1.05) 1.612-1. 2001).9 (25.83) 8.58 (3.21) 5.4) 13.3-24.. not to imply a safety level for general population exposure.7) 30.50-15.54 (1. occupational monitoring and research studies have focused on the sum of inorganic-related species (arsenate + arsenite + DMA + MMA) as a measure of inorganic arsenic intake.28) 1. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.13-39.4) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1.7) 17.0-36.8) 29.51-2.9 (13.9-18. Offergelt et al.53 (.1-36.4-28.30) 1.. 2006. Fourth National Report on Human Exposure to Environmental Chemicals 185 . 2003.65 (1.44 (1.5-20.88 (5.6-46.833-1.4) 292 728 1548 03-04 03-04 1.78 (3.2 (12.6 (6.70) 5.3) 95th 29. Studies of small groups of metal and sulfuric acid smelter workers with varying industrial hygiene conditions have reported urinary inorganic arsenic levels (arsenate + arsenite + DMA + MMA) ranging as high as several hundreds of μg/L during or after work exposure (Jakubowski et al.50-7.959-1.. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.4) 32. The American Conference of Governmental Industrial Hygienists (ACGIH) provides an occupational biologic effect index (BEI) for urinary inorganic arsenic plus metabolites equal to 35 μg/L (ACGIH. 1986. WHO.15-1.1 (26.81 (4.2 (13.05 (.1) 26.15-1.00 (1.67) 4.6) 19.25-7.43) 75th 5.61-6.14 (1.91 (4.1-18. 2001).36) 2. Caldwell et al.79 (1.9) 14.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.3 (10..11 (. The 95th percentile of the U. 2007).18-1.5 (18.400-.43) 14.29-14. 1992. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.37-2.83) 2. In recent years.3 (10.91) 90th 16.88) 2.47 (2.19-2.45) 1. 1998. Sun et al.73-6.82) 4.4 (24.40) 1.. 2008).72) 12. which is below the ACGIH BEI (Caldwell et al.12) < LOD . Vahter et al..909-1..877 (.0 (9.51) 5.9) 32.39-3.00 (3.5) 26. 2008).9 μg/L.80) .64-29.901-2. Information about the biological exposure indices is provided here for comparison.15-4.25 (.5) 17.10 (.6 (9. Biomonitoring studies of urinary arsenic can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of arsenic than are found in the general population.76-27.78-5.80-153) 17.938-1.6-29.4-21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.531 (. population from the National Health and Nutrition Examination Survey. Timber treatment workers had median urinary DMA levels that were about 15-fold higher than the general adult median levels reported in NHANES 2003–2004 (Morton et al.S.7) 9.2 (12.82) Selected percentiles ( 95% confidence interval) 50th 1.638) 1.2 (4.62-6.3) 1284 1284 03-04 03-04 03-04 1.93 (1. Survey years 03-04 Geometric mean (95% conf.68 (1.Metals as with DMA.786-1.6-32.30-1.40 (1.67) 1.4-82.4 (11. interval) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample.S. see Data Analysis section) for Survey year 03-04 is 0. Survey years 03-04 Geometric mean (95% conf. Survey years 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.Metals Urinary Arsenocholine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 186 Fourth National Report on Human Exposure to Environmental Chemicals .6. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 621 725 1078 Limit of detection (LOD. Urinary Arsenocholine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

80) < LOD 621 725 1078 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.08 (<LOD-4.00) 1.20 (<LOD-1. < LOD means less than the limit of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (<LOD-2.95 (<LOD-2.2.44) 2.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Fourth National Report on Human Exposure to Environmental Chemicals 187 . Survey years 03-04 Geometric mean (95% conf.40 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 1. Survey years 03-04 Geometric mean (95% conf.S.S. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. population from the National Health and Nutrition Examination Survey.00 (<LOD-3. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

5) 95th 13.0) 11.82) 3.5 (11.14) Selected percentiles ( 95% confidence interval) 50th 3.4 (7.0 (11. Survey years 03-04 Geometric mean (95% conf.34 (3.82-9.0-16.0) 292 728 1548 03-04 03-04 4. population from the National Health and Nutrition Examination Survey.61-11.24-4.80) 7.00 (5.92-12.77 (3.60-4.48 (2.27-2.65-8.9) 12.29-4.57-5.38 (3.20-4.00) 9.00 (5.34-4.31-4.90 (3.00) 6.11 (3.50 (4.2) 10.00 (3.00-8.0 (10.00) 4.70-3.00 (6.46 (4.84-18.69-3.59 (6.44 (2.0 (10.00-4.69 (3.0 (8.9) 5.3 (8.18 (6.80 (4.00-13.62) 4.00-11.17-6.05) 5.90) 5.42) 3.0-25.00 (7.88 (4.7-16.49) 10.32 (8.00-4.0 (12.85 (3.44) 5.97-3.98) 4.86 (2.00-15.00-3.0) 13.0) 17.00) 6.11) 4.0 (9.5) 12.24) 3.80-6.34 (3.13-4.7) 1284 1284 03-04 03-04 03-04 4.32-10.0 (9.80-3.9) 11.84-8.95-4.00-5.0) 12.28) 2.00) 12.67) 8.94-3.00 (3.49-4.00-7.30 (7.80) 2.0-19.16-11.00) 90th 11.9 (11.00-3.S.0) 9.0 (14.00-4.78 (4.27-5.00 (3.89 (3.7) 13.1-18.74) 90th 9.37 (3.05) 10.17-4.03 (3.71-4.32 (4.37 (2.0 (10.00-11.3 (8.8) 7.08 (2.33) 3.6) 1284 1284 03-04 03-04 03-04 4.00-12.0 (9.33-4.90) 2.57 (3.20-12.0) 9.50-5. interval) 3.25 (4.0) 14.19) Selected percentiles ( 95% confidence interval) 50th 3.00-15.81 (5.95 (4.1 (8.05) 3.8) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 3.69-6.03-6.86-7.00) 7.45) 3.00) 6.45) 8.39-3.00) 3.0 (13.0) 16.00 (3.48 (3.6-18.09 (7.00-4.60-7.0) 13.1-22.10) 3.00-4.0 (8.71 (3.95-6.6) 292 728 1548 03-04 03-04 3.00-4.0) 10.8) 7.00 (7.3 (7.0 (10.69 (3.12 (3.0 (12.00-22.73 (3.00 (3.71) 3.70-4.61-16.0-18.1-15.94) 3.73) 6.6 (9.00 (6.00) 6. see Data Analysis section) for Survey year 03-04 is 1.20) 11.00 (6.82-5.65-6.0) 17.70) 5.10) 6.9) 13.17 (2.00) 75th 6.14) 3.00 (3. interval) 3.95-3.78) 4.0) 621 725 1078 Limit of detection (LOD.70-12.9 (7.55 (2.00-7.86-21.50-15.00 (5.00 (5.91) 75th 5.00-15.00) 3.0-17.45 (8.74 (2.S.60-3.16 (4.70 (3. Survey years 03-04 Geometric mean (95% conf.0-16.12-4.0) 95th 16.52) 3.0-17.80-5.34-4.0 (13.7) 12.00-11.60-6.34) 3.7 (10.7.00) 5.00-7.00-9.00 (4.15) 4.06) 5.00 (5.79 (3.0) 9.71 (4.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .00) 4. population from the National Health and Nutrition Examination Survey.27 (3.27 (2.00-12.16 (2.92) 3.31) 4.72 (4.0) 16.22) 4.00-10.0-12.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.67) 9.0) 11. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.30) 3.00-7.

60 (1.23) 1.85) 1.84-3.54) 90th 2.60) 2.30 (1.52 (2.28 (1.00 (1.90 (1.10 (.9.10-3.15-1.30) 2.00) 1.816 (<LOD-.11-1. which may vary for some chemicals by year and by individual sample.50) 1.10 (. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00-2.50) 621 725 1077 Limit of detection (LOD.61) 2.79) 2.61-3.00-1.80 (2. Survey years 03-04 Geometric mean (95% conf.00) 1.31 (1.30 (1.37 (1. population from the National Health and Nutrition Examination Survey.40-2.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.77) 1.20 (1.50 (<LOD-1.40-3.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.07) 2.40 (2.10 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50 (2.20-1.00 (2.80-2.40-3.43-3.20 (1.00-2.40-2.96-2.17) 2.70) 2.10 (1.36 (1.853-1.20 (1.22 (1.90) 2.93) .53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.10) 95th 2.900-1.10-1.05-1.73-2.985) 1.70-2.18-1.86) 2.70-2.40) 1.70-2.60-2. Survey years 03-04 Geometric mean (95% conf.35-3.71-2.50 (1.80-2.90) 2.40) 2.80) 1. population from the National Health and Nutrition Examination Survey.30 (1.30-1.82-2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.S.62) 2.31-3.80) 1.07-3.00 (2.10 (1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.00 (<LOD-1.14-1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.88 (1.86) 3.50-2.00-4.28 (1.53 (1.82-2.70-3.20) 2.58) 2.00-1.00 (<LOD-1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < LOD means less than the limit of detection.20 (1.34) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70-2.80 (1.30-2.30) 1.88-2.20 (1.46-2.18-1.85) 2.80 (1.30) 90th 1.63 (<LOD-1.00) 1.22) 3.S.90) 1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .46 (1.88 (1.81) 1.10-1.60) 2.40 (1.33 (1.45) 3.53-2.07 (1.60) 1.30) 1.30-1.90 (2.00) 2.10) 2.86 (2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.36) 1.00) 2.33 (1.20 (1. see Data Analysis section) for Survey year 03-04 is 0.60 (2.30 (2.16 (2.50 (1.86 (2.80 (1.80 (1.57) 95th 2.20-3.40) 1.

S.S. < LOD means less than the limit of detection. Survey years 03-04 Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Urinary Trimethylarsine oxide (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. population from the National Health and Nutrition Examination Survey. 190 Fourth National Report on Human Exposure to Environmental Chemicals . interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 621 725 1078 Limit of detection (LOD.Metals Urinary Trimethylarsine oxide Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 1. which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

J Occup Environ Med 2000. Aposhian HV. Le XC. Lewis AS. Peterson H. Hysong TA. J Appl Toxicol 1988.iarc. J Environ Sci Health A Tox Hazard Subst Environ Eng 2003. Perrin M. Liu X. Cincinnati (OH): ACGIH Worldwide. Hall M. Poplin GS. Roy S. Chen CL. Ahsan H.47:243-262. Sengupta MK. Sandstrom M. Matczak W. Hudgens E. Environ Res 2005. Cebrian Garcia ME.71 Suppl:S29-32. Ye X. including Arsenic. et al. 7th edition. Arsenic: signal transduction. et al. Schreinemachers D. International Agency for Research on Cancer (IARC). Linderholm H. Hopenhayn-Rich C. Coble K.gov/toxpro2. Methylated arsenicals: the implications of metabolism and carcinogenicity studies in rodents to human risk assessment.84(5):1093-1101. Lagerkvist B. J Expo Anal Environ Epidemiol 2003. arsenate. Eldan M.11(4):265-269. 8/7/08 Ahsan H. Documentation of biological exposure indices. et al. Moore LE. Beck BD. Concentrations of the sunscreen agent benzophenone-3 in residents of the United States: National Health and Nutrition Examination Survey 2003-2004. Environ Health Perspect 1999. Chem Res Toxicol 2000. and biotransformation involved in cellular response and toxicity. Trzcinka-Ochocka M.98(2):151-159. Kurzius-Spencer M. van Geen A. Reduction in urinary arsenic with bottled-water intervention. Graziano JH.cdc. Arsenic methylation patterns before and after changing from high to lower concentrations of arsenic in drinking water. Environ Health Perspect 2006. House dust and inorganic urinary arsenic in two Arizona mining towns. Wu MM.41(10):2399-2428. Razniewska G. 2001. Needham LL.13(3):211-218. J Environ Sci Health A Tox Hazard Subst Environ Eng 2006. Chen Y. Thomas DJ. Some Drinking-water Disinfectants and Contaminants. Kalman DA. Slavkovich V. et al. Moldeus P. JAMA 2004. Jakubowski M.pdf. Pilsner JR. Biomarkers of exposure: a case study with inorganic arsenic. Exposure to inorganic arsenic in drinking water and total urinary arsenic concentration in a Chilean population. Lu X. Zheng Y. Montesinos N. Burbacher T. Calderon RL. Reidy JA. Pino P. Hughes J. Associations between drinking water and urinary arsenic levels and skin lesions in Bangladesh. Mash EA. Ryhage R. Hysong TA. Kalman DA. van Belle G. Chowdhury UK.8(2):119-127. A prospective study of blood selenium levels and the risk of arsenic-related premalignant skin lesions. 8/7/07.42(12):1195-1201. Pattern of excretion of arsenic compounds [arsenite. Crit Rev Toxicol 2006. Stute M. Toxicological profile for arsenic. Burgess JL. Ilievski V. Environ Health Perspect 1990.html. Bolgiano D. Arnold LL. transcription factor. placebocontrolled folic acid-supplementation trial in Bangladesh. Gurzau A. Amigo H. Scand J Work Environ Health 1985. et al. McClellen H. Loomis D.36(2):99-133. Ingested arsenic. Blom S. Bredfeldt TG. Chen SY. Josyula AB. cigarette smoking. American Conference of Government Industrial Hygienists (ACGIH). Liber K. Calafat AM. Volume 84.104(11):1200-1207. Hughes MF. Thor H. Gamble MV.292(24):2984-2990. Updated September 2004 [online]. Am J Clin Nutr 2006.116(7):893-897. Toxicol Appl Pharmacol 2006.13(8):693697. Kumagai Y. Monomethylarsonous acid induces transformation of human bladder cells. Kapaj S. Environ Health Perspect 2008. Caceres DD.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Chanda CR. et al. Cancer Epidemiol Biomarkers Prev 2007. Cohen SM.atsdr. Le XC. et al. and lung cancer risk: a follow-up study in arseniasis-endemic areas in Taiwan. Hsueh YM. Bhattacharya P.89:145-151. Cellular metabolism of arsenocholine.216(1):69-79. Slavkovich V. Int Arch Occup Environ Health 1998. Gandolfi AJ. Norin H. Human health effects from chronic arsenic poisoning--a review. Biggs ML. Smith AH. O’Rourke MK. September 2005 [online].fr/ENG/Monographs/vol84/ volume84.24(3):298304. Sumi D. Excretion of arsenic in urine as a function of exposure to arsenic in drinking water. Eblin KE.38(1):87-113. Hsu LI. Occurrence of monomethylarsonous acid in urine of humans exposed to inorganic arsenic. Available at: http://www. Fourth National Report on Human Exposure to Environmental Chemicals 191 .16(2):207-213. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Clinical and neurophysiological studies. Annu Rev Pharmacol Toxicol 2007. The effect of variable environmental arsenic contamination on urinary concentrations of arsenic species. DMA(V)] in urine of children compared to adults from an arsenic exposed area in Bangladesh. Wong LY. Atalah E.114(11):1790-1796. Christakopoulos A. Folate and arsenic metabolism: a double-blind. Biological monitoring of occupational exposure to arsenic by determining urinary content of inorganic arsenic and its methylated metabolites. Summary of Data Reported and Evaluation. Gurzau ES. et al. Parvez F. Chiou HY. Healy SM.107(8):663-667. Lodh D. Rahman MM. Jagadish B. J Health Popul Nutr 2006. MMA(V). Sturup S. Parvez F. Environ Health Perspect 1996. Available at URL: http://monographs. Arsenic exposure to smelter workers. Rahman A.

EPA 815-F-00-015. Arsenic in drinking water-2001 update. CruzGonzalez MB. using a routine LC-ICP-MS method. Mason H. Rumpler A. Li L. Holmes AK. Arsenic.inchem. Arsenic drinking water exposure and urinary excretion among adults in the Yaqui Valley. EPA).115(1):151-157. Morton J. 3rd Ed. 1998 [online]. html. Jimenez M. Fok N. Environ Health Perspect 2007. In:Industrial Chemical Exposure. Biggs ML. Mexico.S. Increased mortality from lung cancer and bronchiectasis in young adults after exposure to arsenic in utero and in early childhood. 2nd ed. Jin Y. Twenty years of the German Environmental Survey (GerES): human biomonitoring--temporal and spatial (West Germany/East Germany) differences in population exposure. A pilot study of children’s exposure to CCAtreated wood from playground equipment. Available at URL: http://www. Wang Z. Seiwert M. Ferreccio C. Environ Health Perspect 2006. 2001. Ibata K. Black K. Roels H. Nolinder P.20(8):1120-1125. Thio-dimethylarsinate is a common metabolite in urine samples from arsenic-exposed women in Bangladesh. Fleming LE. Goessler W. et al. Buchet JP. Integrated Risk Information System. Liaw J. Nygren A. Guidelines for Biological Monitoring. Environ Health Perspect 2007. Environ Health Perspect 2005. Vahter M. 8/8/07 192 Fourth National Report on Human Exposure to Environmental Chemicals . J Toxicol Environ Health A 2007. J Anal Toxicol 2006. Huang YL. EPA).htm.S.367(1):80-88. Toxicity of dimethylmonothioarsinic acid toward human epidermoid carcinoma A431 cells.70(2):159-170. World Health Organization (WHO). Tseng CH. Lauwerys RR. Huang YK. Speciation of arsenic compounds in urine from occupationally unexposed and exposed persons in the U. 2001. and metabolism of arsenic. Lauwerys R. von Ehrenstein O.115(4):648-652. Available at URL: http://www. pp.114(8):1293-1296. Sun G. Geneva 2001. Urinary arsenic metabolites in children and adults exposed to arsenic in drinking water in Inner Mongolia. Clayton CA. Boca Raton (FL). Nevada. Environmental Health Criteria 224.25(1):1-22. Environmental Protection Agency (U. urinary arsenic metabolites and human diseases: current perspective.Metals Kwon E. Kolossa-Gehring M. Suzuki KT. et al. Kieszak SM.36-37. Urinary trivalent methylated arsenic species in a population chronically exposed to inorganic arsenic. Becker K. China. Offergelt JA.113(3):250-254. 8/7/07. Sun X. Rey OA. Li B. Marshall G. et al. Toxicol Appl Pharmacol 2007. Belson MG. Seifert B. Solo-Gabriele HM. January 2001 [online].49(6):387-393. et al. Pellizzari ED. Lewis Publishers. Burgess JL. inorganic.112(14):1375-1380.gov/iris/subst/0278. Conrad A. Friberg L. Borja-Aburto VH. Jhangri GS.206(3):299-308. Xu Y. Environ Res 2004. Arsenic in Drinking Water. Environ Health Perspect 2004. Rubin CS. Shipp M. Boeckx M. Meza MM. Erratum in: Toxicol Appl Pharmacol 2006. Available at URL: http://www. Toxicol Appl Pharmacol 2005.211(2):175. Flanders WD. Yuan Y.gov/safewater/arsenic/regulations_factsheet. Smith AH.S.epa. Arsenic exposure.222(3):374-380. Yang MH. Int J Hyg Environ Health 2007.K. 8/7/07 U. Garcia-Vargas GG.htm.114(2):220-227. GSTM1 and T1. Francesconi KA. Investigating childhood leukemia in Churchill County. Schulz C. Zhang H. Raml R. National Research Council (NRC). and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. Hoet P. Ochi T.30(5):293-301.57(2):79-91. Chung CJ. urinary arsenic speciation. et al. Gandolfi AJ. Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites. Arsenic on the hands of children after playing in playgrounds. Garcia-Montalvo EA. Tseng CH.epa.96(2):119126. Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers. Valenzuela OL. Chen CJ. Washington (DC) National Academy Press.S. Kopplin MJ. Naranmandura H. Moore LE. et al. Steinmaus C. Li X. Lu X. Fact Sheet: Drinking Water Standard for Arsenic. Kalman D. Assessing the measurement precision of various arsenic forms and arsenic exposure in the National Human Exposure Assessment Survey (NHEXAS). Arsenic and Arsenic Compounds. Chem Res Toxicol 2007. Rahnster B. Calderon-Aranda ES. Vahter M. Jones RL.org/documents/ehc/ ehc/ehc224. Int Arch Occup Environ Health 1986. et al. Br J Ind Med 1992. Genetic polymorphisms in MTHFR 677 and 1298. Environ Health Perspect 2006. Environmental Protection Agency (U. Sci Total Environ 2006.210(3-4):271-297. Arsenic. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 2007. Sonora. Shalat SL. Buckley BT. U. Arsenic methylation.

38) 2.30) 8.20-6.52 (4.12 (2.30-2.34 (2.40 (5.90 (6.41) 1.01 (4.42 (1.05-2.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.76-7.70) 3.60 (1.90-9.90) 4.46) 1.02 (7.06-1.30 (5.87 (6. such as brazil nuts.69 (1.8 (6.90) 2.65-5.86-5.15-1.18) 3.16) 5.30) 5.55-7.57) 3.20 (4.30 (2.93 (4.32-1.86 (4.70-5.50) 2.20-5.50 (1.56) 1.53) 1.29-5. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.4) 7. 0.80 (1.43 (1.97 (1.34 (1.73-5.30-1.47) 4.06-2.39) 4.40) 7.49-1.18-1.01-7.93-2.63 (1.84) 5.39-1.90) 2.30-5.65) 1.8) 9.71 (2.56) 4.37-8. are high in barium (Genter.20 (3.36 (4.80 (2.41-3. Small amounts of barium can be released into the air during mining and other industrial processes.60) 1.08-8.19-1.03 (1.87-3. 2001).44-2.30) 3.19) 2.00-3.88 (5. Certain foods.81-2.24-1.20-1.g.82) 1.40 (5.60) 3.50 (5.32) 8.53) 2.50 (3.44-5.51) 2.70) 1. tiles. and 0. population from the National Health and Nutrition Examination Survey.20-8.76-3.54 (6. 01-02.99-5.93-8.54 (2.62) 1.16 (1.40) 7.66 (4.70 (5.77-3.90-2.51) 1.25-1.72) 75th 3. barium sulfate and barium carbonate).20) 2.78-2.57 (5.70) 5.76 (3.90 (4.30) 5.85 (2.64 (1.53-5.50 (4.80 (5.48-4.56 (1. soluble forms of barium.64-3.63) Total 1.12-1.94-6.75) 2.39 (1.40 (5.64) Sample size 2180 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.30 (1.87) 7.30-1.95-6.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.9) 5.39) 1.26-1. Barium compounds are used by the oil and gas industries to make drilling muds.21 (1.26-7. In nature. Workers employed by industries that make or use barium compounds can be exposed to barium dust.73 (5. In single dose animal studies.49) 8.71) 2.91) 2.40 (1.35 (3.30) 2.63) 1.40 (1.61 (2.71) 95th 6.59) 3.51 (1.77 (3.99 (4.47-1.11 (3.40 (4.38) 8.59-11.10) 1083 1335 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.20-1.72) 1.22) 6.80) 1.80 (1.70 (1.12. and food.87-9.36-1.63 (2.50 (4. whereas others are practically insoluble (e.49 (1.46) 1.65) 3.50 (1.54) 1.33 (1.35-4.98) 1.12 (2.80 (1.21 (1.54-8.71) 1.10 (2.61 (5.14 (6.40) 3.12.61-8.00-8.00) 1.88) 4.47-1.31 (2.50-1.20-8.49) 11.07 (2.20 (1.37) 5. Barium compounds are also used commercially in paint.4) 9.10 (4.21-8.62 (1.80-7.20-1.56 (1.60-10.78-3.43 (1.80) 7.86) 6.70) 1. such as barium chloride.40-13.32-7.87 (5.08 (6.88) 7.65-8.10 (3.45) 7.92) 2..70-8.15-1. it combines with other chemicals such as sulfur or carbon and oxygen.11-1.78) 1.61 (1.43 (5. depilatories.00 (2.80-3.1) 9.37 (4.31-2.4) 6.30) 4.50 (6.62 (1.80-5.15) 5.68 (1.50-6.28-1. The general population can be exposed to low amounts of barium in air.43) 2.49-9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.22-1.62) 1.31.50 (1.38 (1.34 (1.50 (1.70-6.37-1.61 (3.80) 6.15 (6.46-1.35) 5.25 (1.20-8.24-1.10) 5.22-1.51) 7.67) 6.90) 1.70-3.56 (6.49) 2.10-5.48) 1.41-1.8) 5.60-3. Some barium salts are freely soluble in water.00-76.75-3.82) 2.12) 6.63 (5.60-2.86 (4. fireworks.76) 1.29-1.50) 2.65) 1.30) 5.81-2.91 (2.14-1.35 (2.80 (2.44 (1.30 (5. interval) 1.26) 5. rubber.49) 4.10) 3.26) 2.54-1.39 (1.25-11.35-1.50) 1.50-1.63) 1.15-11.29) 5.20-1.45 (1.73) 3.38 (1.87-14. and 03-04 are 0.50) 4.21-2. bricks.56 (2.28) 90th 5.05% of the earth’s crust.60) 1.11 (2.60-6.70) 4.36) 5.14-6.30 (3.65 (5.2) 6.24 (4.00 (1. respectively.88) 1.78) 1.50-6.48 (6.81-3.12) 7.77) 1.37) 1.52 (1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.00) 4.15 (1.54-1. and ceramics.95 (4.17-1.04-6.71-9.36 (1.27 (1.43) 6.76-2.82-6.55-3. see Data Analysis section) for Survey years 99-00.72) 4.70) 7.73) 1.74-2. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.11 (3.48-4.35 (1. glass. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).40 (1.54) 2.96-2.60) 4.10-4.30-3.63 (8.50 (2.60 (2.00) 6.65-1.54) 1.09 (1.30-2.85) 1. 7440-39-3 Medically.66) Selected percentiles ( 95% confidence interval) 50th 1.60-6.61 (1.Metals Barium CAS No.70-2.74-3.57-7.73 (6.27 (1.87-7.09 (2.04-2.91) 6.15 (2.36-1.80-2.27) 2.48) 1. Fourth National Report on Human Exposure to Environmental Chemicals 193 .35-1.50 (4.90 (1. water.S.90-13.00) 1.34) 2. Barium salts have also been available as rodenticides.18 (6.86-4.85) 1.70-2.74) 3.50 (1.

67-6.15-4.88 (2. hypertension.10-1.02 (3.29-3.31-1.09) 6.85-5.73-2.28) 5.87) 1.01 (5.76 (2.04) 5.99 (2.19-1.23-5.10-2.06) .40 (1.38) 1. vomiting. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40 (1.33 (1.56-3.33-4.60 (2.77) 1.20-1.55 (4.61) 2.40-1.905 (.13-2.28-11.59 (1.35-1.12) 2.48-1.21 (1.42 (4.2) 5.10) 3.61 (4.55 (1.37-1.69-9. interval) 1.33-1. Perry et al. and cardiac dysrhythmias.3 (6.59) 1. Symptoms following acute high dose include perioral paresthesias.81-6.53-21.33) 6.55-6.36 (3.60 (1.39 (2.64 (1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.58 (4.44 (1.97 (4.46 (2.62 (1.44-2.57-5.47-8.26-1.59-7.56) Selected percentiles ( 95% confidence interval) 50th 1.47) 1.77) 5.25) 4.54) 2.27-1.41) 5.54 (1.50 (4.97-4.83) 3.29 (3.01 (4.59 (1.S. Following intravenous injection in animals. diarrhea. Barium is not rated for human carcinogenicity.00) 1.38-7..80) 3.46) 1.45 (1.49-1. Toxicity from soluble barium salts is rare.38 (1.50) 2. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.82) 1.60 (2.64 (1.14-2.77-5.915 (.44-2.34-1.58) 1.81-7.08-1.54 (2. 1994.963 (.57-7.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .39) 4. in urine.47 (5.0) 5.05-1.68-3.30) 2. 1984.65 (2.49-1.83) 2.11) .22-4.46) 3.47 (2.42) 1. such as those used in medical radiographic procedures.50) 1.00-7.41 (1.91) 2.64 (1.20-2.27-3.86-7. water solubility.96-6.29-7.11) .92 (4.84 (3.34-5.34) 1.2) 6.55 (1.73) 2..49-1.46) 2.25 (1.26-1.73-4.34 (1. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.62) 2.65 (5.33 (1.710-1.19-1.91 (3.38 (1.8) 4.38-1.92) 2.16 (1.29-4.02) .68 (3.36-1.51 (1.56 (1.921 (.56) 4.33) 1.18 (1.26-4.29-1.39-1.45) 95th 6.77) Total 1.24-1.24-3. chemical form.52) 1.38 (4.53 (2.76) 1.45 (3.00) 4.45-6.24 (3.51) 4.880-1.84) 2.89) 90th 4.00-1.30 (1.43-6.891 (.78 (2.70) 4.36 (5. Wones et al.4) 5.29) 1.28 (1.32 (1.68-3.29-4.52) 2.22-2.42) 1.76 (3.80) 4. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.63-4.52-4.91-2.49 (1.27) 7.35-1.00) 6.62 (2. Chronic high doses in animals resulted in kidney damage (McCauley et al.36 (1.79-5.31 (4.70) 1.31) 5.51) 4.27 (2.24-1.25-11.37-2.97) 1.72) 6.70) 10.80-6.31-1.77) 1. 1985.52-10.72 (2.19-2.49 (1.24) 3.64) 7.Metals was eliminated primarily in feces and to a lesser extent.86 (2.3) 6.20) 4.58) 75th 2.832-1.37) 2.75-22.20 (1.20-8.86) 5.96) 4.51 (3.75) 2.84-5.22-1.47) 1.03) 3.00 (3.76 (4.55-5.38) 1.97-3.50) 1.47) 4.22-1.74 (5.24-6.06) 2.00 (5.64 (1.56 (1. 2001). 1986).48-3.60 (1.39 (2.36-1.90-2.24-11.04 (2.2 (3. 1990).99) 1.38) 4.38-5.76) 2.66 (1. Insoluble barium salts.45-1.57 (6.59) 1.60) Sample size 2180 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.57) 2.02-5.68) 1.48) 2.84-2.00 (3.52) 7.33 (5.36-2..36 (3.00 (2.48-5.4 (5.39-10.34-3.703-1. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.99 (4.74) 1.59) 2. weakness.02) 4.32 (2.96 (4.57-10.23-2.69 (5.51 (1.04) 1. a benign condition that may occur among barite ore miners.37 (1.16-1.32 (1.64) 7.28-6. 1989).79) 1. population from the National Health and Nutrition Examination Survey.82) 1.39-1.10 (6.18 (1.55) .74) 1.96) 7.29 (1.62 (4.63) 1.11-2.10) 6.45-1.48 (1.39 (2. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. and route of exposure.24-6.48 (1.88 (6.47) 10.32) 2.77) 1.96 (4.03-1.71 (5.35-3.00) 4.777-1.75-3.52 (3.36 (1.38 (4.39-5.754-1.28-1.24 (5.48 (1.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0) 7.60 (5.45-8.16) 11.37 (1.76-3.55 (5.31-1.75) 1.23-1.881 (.08-2.26) 4.41 (1.89 (2.41) 4.03) 1. The health effects of exposure to barium compounds depend on the dose.40 (1.01) 1.28-7.68) 3.58 (2. Chronic exposures to natural low levels of barium in drinking water have not produced general health effects or evidence of cardiovascular risk (Brenniman and Levy.58) 4.76) 2.41 (2.98 (2.58-6.43) 1.0) 6.96) 4. NTP.96) 4.72) 4.81-6.54) 1.53) .68 (2.51) 6.46-22.97 (5.32) 2.26-1.26-1.30 (1.68 (3.75) 1.51-3.39 (3.31 (1.19-1. paralysis.03) 2.75) 2.91 (3.45) 1.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.13-3. are not absorbed when administered.03-1.

html?charset=iso-88591&url=http%3A//ntp. Gallorini M. Int Arch Occup Environ Health 1992. patient population and literature reference intervals for urinary trace elements.197210.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. In: Inorganics in drinking water and cardiovascular disease. Exposure to soluble barium compounds: an interventional study in arc welders. p.S. eds. environmental levels) and health effects is available from ATSDR at: http://www. 1984. In Friberg L. Environ Health Perspect 1990. Centers for Disease Control and Prevention (CDC). Patty’s toxicology. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. Douglas BH.cdc. Handbook on the Toxicology of Metals.. pp. 1985. In: Calabrese EJ.76(1):53-59. Minoia C. p. Ting BG. et al. Epidemiological study of barium in Illinois drinking water supplies. McCauley PT. Stadler BL. EPA. Biomonitoring Information Levels of urinary barium reflect recent exposure. Lack of effect of drinking water barium on cardiovascular risk factor.html. New York: John Wiley & Sons. 84-94.nih. Pozzoli L. p. 2nd Ed. and a drinking water standard has been established by U. Jr.gov/toxpro2. Wones RG.gov/ntp/htdocs/LT_rpts/tr432.85:355-359. Cohressen B. PS. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Magnesium. 2005. Information about external exposure (i. Princeton NJ: Princeton Scientific Publications.e. Vouk VB. A study of 46 elements in urine. New York: Elsevier. Reeves AL. Genter MB. Laurie RD. LA. ed. blood.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en.. Perry HM. eds. Pirkle JL. barium. 5th ed. 1994. calcium.64(1):13-23.. Comparison of representative ranges based on U.. Howerton K. Inc.. Third National Report on Human Exposure to Environmental Chemicals. References Brenniman GR.S. 2005. J Toxicol Environ Health. National Toxicology Program (NTP). Frohman. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. 221-252 Komaromy-Hiller G.. Trace element reference values in tissues from inhabitants of the European community I. 1998). strontium. 2001. Schaller KH. Morrow JC. Princeton (NJ): Princeton Scientific Publications. 4/8/09 Paschal DC. Kopp SJ. Paschal et al.. 1992).95:89-105. Trace metals in urine of United States residents: reference range concentrations.28(3):373-388. Biomonitoring studies of levels of barium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of barium than are found in the general population. Fourth National Report on Human Exposure to Environmental Chemicals 195 . 1989. Advances in modern toxicology. Nordberg GF. Powell C.nih.296(1-2):71-90. Vol 2: Specific Metals. and 2003-2004 (CDC. Atlanta (GA). and radium In: Bingham A. et al.gov:8080/cs. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. 1990. Minoia et al. Perry EF.niehs. Jackson RJ. et al. 1986. Pietra R. Sabbioni E. Zschiesche W. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al.niehs. ed. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. 231-249. Levy. [online]. Weltle D. the welders had no obvious adverse clinical effects (Zschiesche et al. and serum of Italian subjects. Environ Res 1998. Sampson EJ. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Clin Chim Acta 2000. Available at URL: http://ntp.atsdr. Sci Total Environ 1990. Costa R. Barium. 2001-2002. 2000) to levels in NHANES 1999-2000 and 2001-2002. Ash KO. et al. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies).. Investigations into the effect of drinking water barium on rats.. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. Apostoli P. NTP. Calabrese EJ.

and refined beryllium is used in mirrors and special metal alloys for the automobile. the lightest of all metals. Exposure to beryllium occurs mostly in the workplace. see Data Analysis section) for Survey years 99-00.13. population from the National Health and Nutrition Examination Survey. aircraft.130 (<LOD-. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames.160) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.Metals Beryllium CAS No. nuclear. 0. x-ray machines. and 03-04 are 0. and 0. Beryllium compounds are commercially mined. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. and volcanic dust. are mined for commercial recovery of beryllium. and machine-parts industries. and can be found in mineral rocks. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . coal. electrical. or drinking water containing the metal. which may vary for some chemicals by year and by individual sample.13. beryllium is used in instruments. and from breathing tobacco smoke.S.150) < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and dental bridges. soil. 7440-41-7 General Information Pure beryllium is a hard gray metal. eating food. near some hazardous waste sites. computer. 01-02. In medicine.130 (<LOD-. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. Low-level beryllium exposure in the general population can occur through breathing air.13. respectively. In studies of laboratory animals. 196 Fourth National Report on Human Exposure to Environmental Chemicals . Two types of minerals.140 (<LOD-. bertrandite and beryl.

based upon excess lung and central nervous system cancers in studies of workers.333) < LOD < LOD < LOD < LOD 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . S. Chronic beryllium disease. or berylliosis. population from the National Health and Nutrition Examination Survey. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. and drinking water and environmental standards have been established by U. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. respectively. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. More information about external exposure Urinary Beryllium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 1990). IARC has classified beryllium as a human carcinogen. which produces pneumonitis.. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .391) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine. including contact dermatitis and subcutaneous nodules. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS.231 (<LOD-. Skin exposure can result in delayed hypersensitivity reactions. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH.281 (<LOD-. NTP considers beryllium to be a known human carcinogen.S.346 (<LOD-.273) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Maier. EPA. 2003. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. Fourth National Report on Human Exposure to Environmental Chemicals 197 . 2002).

Maier L. Sampson EJ. References Apostoli P. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. 2001).html. Hamilton et al.12 to 0. They reported urinary beryllium levels ranging from 0. 106.. Clin Chim Acta 2000.atsdr. Kriess K.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. 2000. Available at URL: http://www. Apostoli P. 20012002.74:162-166. et al. Jackson RJ. patient population and literature reference intervals for urinary trace elements.. 1990.inchem. Beryllium [online].13 μg/L. Element reference values in tissues from inhabitants of the European community.htm. Third National Report on Human Exposure to Environmental Chemicals.S. In other studies. 0. and serum of Italian subjects.e.1 μg/L). Hamilton EI. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Environ Res 1998. blood. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Pirkle JL. Howerton K.157:388-398. 1998). A study of 46 elements in urine.76(1):53-59. Schaller KH. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Sabbioni E. Gallorini M. Minoia C. et al. Sabbioni E. Ting BG. population are lower than levels in workers. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Pietra R. Biomonitoring studies on levels of beryllium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of beryllium than are found in the general population. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Costa R. Sci Total Environ 1994.Metals (i. 1990. Given these results. Weston A. Clin Chest Med 2002. Genetic and exposure risks for chronic beryllium disease. International Programme on Chemical Safety (IPCS).. Morrow JC. less than 0. Levels of beryllium in urine for the U. Atlanta (GA) 2005. HLA-DPB1 and chronic beryllium disease: a HuGE review. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Comparison of representative ranges based on U. Centers for Disease Control and Prevention (CDC).296(1-2):71-90. Review of elements in blood. McCanlies EC. Am J Epidemiol 2003.. Paschal et al..e.gov/toxpro2. plasma and urine and a critical evaluation of reference values for the United Kingdom population.org/documents/ehc/ehc/ ehc106. and 2003-2004. 3/27/08 Komaromy-Hiller G.cdc.23:827-839.S.158:165-190. and the fact that most NHANES participant levels were undetectable. Trace element reference values in tissues from inhabitants of the European community I. which approximate this Report’s limit of detection. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Pozzoli L. environmental levels) and health effects is available from ATSDR at: http://www. it is likely that urinary beryllium levels in the U. Sci Total Environ 1990. Ash KO.S. Trace metals in urine of United States residents: reference range concentrations.95:89-105. Andrew M. population were generally undetectable in NHANES 1999-2000. VI. Int Arch Occup Environ Health 2001. Environmental Health Criteria. Van der Venne MT. and the 95th percentile for males in NHANES 2001-2002. Minoia et al. Paschal DC.

400 (. and nonferrous alloys.400) < LOD .20) 1.300-.500-.3. 7440-43-9 General Information Cadmium is a soft.50 (1.30-1.00 (.393 (.300 (.10 (1.500) .400 (. and 03-04 are 0.300 (.300 (<LOD-.300) .700) .30-1.900-1.382 (.900-1.300-.300 (.400-.20-1.20-1.00-1. and 0.30) 1.500) .500 (.403 (.60 (1. plastic stabilizers.235 (.600) .700) . Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.10 (1.200-.00-1.900-1.20) 1.500 (.00 (.10) 1.60 (1.470) * .300 (.400) < LOD < LOD < LOD .700) . cadmium use has declined in response to environmental concerns (http:// minerals.376-.300-.452) .500-.200 (<LOD-.412 (.500-.300 (.500-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.300 (.900 (.20) 1.20-1.90) 1.300 (. as zinc sulfide) and to a lesser extent.300) .309-.500) .700 (.300) .70) 1.500) .50) 1.500 (.70) 1.00 (.333 (.200 (.300-.70) 1.10) 1.200-.378-.40) 1.500-.10 (1.600 (.50 (1.50-1.800-1.900-1.300) .255) .425 (.400 (.400-. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.449) Selected percentiles ( 95% confidence interval) 50th .900-1.400-.40-1.460) .216-.500-.275-.400 (.400) .00-1.50-1.304-.80 (1. Other uses include pigment production.Metals Cadmium CAS No.300) .400) .362-. which may vary for some chemicals by year and by individual sample.500-.00-1.40 (1.300-.500) .10) 1.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .00 (.500-.60) 1.304 (.283 (.300-.600 (.20) 1.40 (1.400 (.368-.300 (.400 (.300-.20-1.10) 1.300 (.500-.900 (.20) .10 (1.800 (. Cadmium also may be emitted into the air from zinc.S.10) 1.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .00 (.424) * . lead.300 (.80) 1.200 (<LOD-.600-.50 (1.313 (.600 (. 0.00-1.600) .700) .700-1.500 (.296-.20-1.700) .468 (.600 (.300) . < LOD means less than the limit of detection.600 (.30 (1.300 (<LOD-.500 (.00-1.60 (1.20) 1.S.300-.300 (.400) .400 (.20) 1.600 (.395 (.266-.300 (.386-.700) .300-.400 (.421 (.20) 95th 1.500) .40 (1.400) .3.40 (1.378 (. or copper smelters (U.361-.400) .60) 1.800) 1.600) . U.289-.60-1. coatings and plating.20) 1.00-1.70) 1.30) 1.40 (1.500-.600) .50-1.600) 90th 1.800) .427) * .800-1.00 (.326 (. EPA.00-1.500-. and incineration of municipal waste materials.900-1.20-1.300) .300-.400) .400 (.400-.700) 1.900-1.300) .600-.400) .00) .300 (<LOD-.20) .00) .200) .300) .00 (.20 (1.300-.300) . see Data Analysis section) for Survey years 99-00.40 (1.300-.500-.300) 1.200-.367-.600) .300-.500 (.10 (1.600 (.600 (.700-1. malleable.10 (1.600) .30) .500-.300-.600 (.400) .40-1.900-1. respectively.500 (.513) .00 (1.500 (.200) .70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400 (.600 (.600-1.400 (.300) .500-.30) 1.441) * .00-1.344) .400) .300-.70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 . 01-02.600 (.500) .30-1.400) < LOD . Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.10 (1.40 (1.S.usgs. The predominant commercial use of cadmium is in battery manufacturing.400) .400) < LOD .400 (.200 (.20) 1.400 (.400 (.420 (.400 (.300-.400-.600 (.400-.00 (.366) * * .00 (.900-1.60 (1.700) .900-1.gov/minerals/pubs/commodity/cadmium).400-.14.400-.331) .10) 1.600 (.200 (.400) .300) .500-.300 (<LOD-.10) 1.60) Total * .60 (1.00 (.400) . Fourth National Report on Human Exposure to Environmental Chemicals 199 .426-.10) 1.20-1. Since 2001.300-.400) .600) .400-.60) 1.400 (. during refining of lead and copper from sulfide ore. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) 1.400) .600) 1.359-.600) .600 (.50) 1.80) 1.30-1.300-.400 (.50-1.600-.800 (.300-.300) .300 (. interval) .300-.50) 1.30-1.500-.398) < LOD < LOD < LOD < LOD < LOD < LOD .500-.200-.300 (.403) .500-.700-1.50 (1.00 (1.337) .500 (. population from the National Health and Nutrition Examination Survey.700) .200-.300-.304 (.300-.20 (.400-.600) .400-.10 (.800) .300) 75th .

zinc.238) .190-. wheat.308) .41 (.067-.972 (. 1994).229-.200-.01-1. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.436-.388-.200 (.240) .240-.22 (1.260-.065-.17 (.295) .610) .433-. ingestion through food is the largest source of exposure.061-. potatoes.330-.136) .216 (.46) 310 368 287 648 762 724 1299 1560 1532 12-19 years 20 years and older 99-00 01-02 03-04 Gender Males 99-00 01-02 03-04 .412) .167-.456-.37) 1121 1335 1277 1136 1355 1266 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 . 2003). 1999.510-. see Data Analysis section) for Survey years 99-00.** Survey Geometric mean (95% conf.169-.220) .214-.426 (.160) .607) .589 (.209 (.199 (.249-.492 (. 0.38) 1.253-.191-.500) 90th .101) .148) .191-.230) 75th . interval) .455 (.148-. and 0. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.705-.28 (1.193-.210) .466 (.30-1.875 (.210 (.400-. Cadmium absorption may be increased with iron deficiency (Berglund et al.S.211 (.980) .Metals 2000).360) .249) .351-.135 (.316 (.160 (.177-.173) .257-.080 (.836-1.580) . respectively.067-.25 (1.112-.260-.870) .206) .220) Selected percentiles ( 95% confidence interval) Sample 95th 1.476-.20 (1.302 (.229) .22 (.366-.230 (.452 (.01) .51 (1.717-.700-.507) .060-.700-.270 (.310) .12 (.170-.192-.843-1.989-1.283 (.233) .892-1.320) .559 (.191 (. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.481) .300) .15) .210 (.281 (.263) .313) .381-.890 (.440 (.107-. however.892 (.087-.24) 1.234 (.475 (.120 (. Horiguchi et al.551 (.235) .700-.387) . 01-02.450 (.061 (<LOD-.251) .326) .246) .12-1.17) .327 (.350 (.445 (. population from the National Health and Nutrition Examination Survey..229) .07-1.171-.980-1.440-.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .01 (.390 (.83) 1.203) .090) .43) 1.633-1.551) . For nonsmokers who are not exposed to cadmium in the workplace.480) .219 (.336) .366) . Kikuchi et al.72) 1.179-.545 (.289-.192-.482) .763-.272-.187 (.479) .519) .855-1.126) .540) .300 (.220 (.243-. copper) and protein.260 (.848 (.423-.790 (.310 (.208-.157) .48 (1.13 (. 200 Fourth National Report on Human Exposure to Environmental Chemicals .078 (.790 (.06-1..733-.860) 1.196-.520-.233) .170-.03) .875) .165-. 2004a.279 (.810-1.713) .150) .189-.820 (.06) .134) .184-.077 (.919) .150-.081) .109-.990) . Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.539) .26) 780 683 614 546 667 717 760 1132 1070 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.237-.462 (. Cadmium in soil is absorbed by plants.977) .04 (.109 (.210 (.748-1.140 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.839 (.090) .34) 1.241) . With chronic exposure.640) .284) .277 (.100-.115-.210 (.141 (.963-1.270 (.306 (. 2001).210 (.077 (.110-.980 (.17 (. 2003).450 (.28-1.285-.239 (. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..204 (.151-.206 (.230) .231) .201 (.20 (1.430) .800 (.135-.817 (.714-1.550 (.25) 1.20) 1.52 (1.510) ..160) .633 (.817 (.153-.440 (.339) .493-. including many food crops such as cereal grains.200-. calcium.372) .220-.189) .09-1.20 (1.299) .741-1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.198) .13) .232 (.390-.733) ..20-1.686-.06.282 (.181 (.255) .178-.47) 1.36) 1. rice. and various seeds.190-.06-1. Renal tubular and glomerular damage.820) 1.220-.680 (. 2003.10 (1.366-. Cadmium is absorbed via inhalation and ingestion.255) .257) . Diamond et al.19) 1.13-1.130 (.265) .813 (.596) .175 (.261-. whose body burdens of cadmium can be approximately twice that of nonsmokers.390-.980-1.800-.06.730-.430-.202-. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.940-1.128 (.232) .818 (.886) .092) .753-.500) .890-1.114-..490) 1.255) .15 (.04 (.394-.219 (. 2003). an inducible metal binding protein.322 (.17 (.175 (.265 (.190-.74) 1.32 (1.470-.170 (.157-.180 (.886-1.189-.458 (.222) .329 (.498-.28) 1. To a lesser extent.160-.445 (.980) .06.447 (.211-.530 (.806) . Inhalation of cigarette smoke is a predominant source of exposure in smokers.918-1.238-.530) .121 (.880) .262) .223 (.38) 1.766 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.960) 1.362) .354) .221 (.393-.820-1.82) 1.219 (.273 (. and 03-04 are 0.183-.193 (.221) .247) .226) .207-.194-.227 (.57) 1.02-1.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .261-.400-.202 (.195-.38) .490) .623) .200 (.290-.15) 1.210) . drinking water is a source for cadmium intake.280 (.203 (.38) .858 (.960 (.519) .092 (.

184-.876-1.404) .617 (.113-.137 (.170-.382-...449) .198) .622 (.209) Selected percentiles ( 95% confidence interval) Sample 95th . most often a result of occupational exposure (Roels et al.175 (.813-1.207-.10) 1. 1999).541) .221 (.630-..02 (.256-.123-.722-.176 (.757 (.418-.487 (.296 (.09 (.100 (.431) .688-.174-.833-1. 2004b).220 (.281) .441-.263-.197-.226) 75th .205 (.388-.686 (.440) .253) .123-.091 (.533) .289) .316) .252 (.500-. 2003.146-.210) .281) .177) .00 (.097) .308 (..199 (.159 (.727-.418) . older adults and postmenopausal women with Urinary Cadmium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.303) .929) .196 (.175 (.560-.199-.856) .094) .208-.865 (.210 (.343-.173 (.941 (.412 (.690 (. Horiguchi et al.189-.156 (.398-.414 (.17) .143-.783 (.381-.472) .687 (.545) .415) .716-.183 (.718 (.091 (.491-. 2004).192) .690-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.666-.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .856 (.433-.219 (.690-.147-. 2002.181 (.318 (.426-.874-1.712 (. population from the National Health and Nutrition Examination Survey. 2002.136-.07) .562-.311) .221-.147 (.607) .404 (.219 (.185) ..678 (.S.091) .266) .917) .873 (.270 (.795) 1.282 (.201-.222-.253 (.135) .085 (.096) . During the 1950’s and 1960’s.650-.719 (.725-1.170 (.917 (..178) .484 (.143) .767 (.653) .255-. interval) .247-.940-1.083-.998) .236-.090 (.693 (.168-.813-.792 (.16) 1. Noonan et al.16) .00 (.187) .940 (.438-.767) .516-.176 (.729 (.331 (.818) .084-.663 (.191-.667) . At lower environmental exposures.136-.335 (. Olsson et al.204-.184-.112) . 1996.071 (.387-. Whether the markers of renal tubular effects found in populations with low environmental exposure are likely to progress or predict an increased risk for developing clinically evident renal dysfunction is unknown (Hotz et al.631) .828) .316 (.308) .181) .247-.769 (.156-.423-.321) ..122 (.234-.278) .274) 1.184) .241) .181-.645-.229) .292) .225) .267 (.085-.075-.156) .08) .240) .696-.078 (.175-.479 (.093 (.470) .300-.182) .826-1.051-.075 (<LOD-.168-.143-.293-.501 (.239-.839) .350) .716) .157-.211 (.228-.14) 310 368 287 648 762 724 1299 1559 1532 12-19 years 20 years and older 99-00 01-02 03-04 Gender Males 99-00 01-02 03-04 .181 (.336-.223) .063-.340) .084 (.329 (.227-..473 (.234) .162 (.283 (.234 (.421 (.387 (.235) .224 (.446) .754) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.647-.438) 90th .261) .185 (.38) .250) .687-.104) .700 (.225) . 2002.107) . However.325 (. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.158-.159 (.126 (.21) 1121 1334 1277 1136 1355 1266 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 . This condition of painful osteomalacia or osteoporosis was associated with advanced renal tubular damage that led to increased urinary excretion of calcium and phosphorus and decreased hydroxylation of vitamin D metabolites.245 (.783) .850) .985 (..434 (.074-.538) .708-1.200 (.098) .148 (.140-. Jarup et al.261-.826-1.147-.242) .304-.700) .078-. Staessen et al.551) .423 (.067-.779 (.884) .280 (.906) .077-.154 (.518) .268 (.144-.757) .212 (.559-.104) .802 (.13) .927-1. 2000.208 (.06 (.263 (.218) .266-.740 (.161-.691-.668-. Fourth National Report on Human Exposure to Environmental Chemicals 201 .137-.507-.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .130-.182) .432 (.297) .470) .111-.919 (.288) .183) .352) .232) .173-.614) .247-.150-.806-1.101) .537-.304) .140-.166 (.233 (.238-.238) .481 (.154-.444-.182) .171-.163) . 1999).216-.** Survey Geometric mean (95% conf.391-.206-.830-1.909-1.08) 780 682 614 546 667 717 760 1132 1070 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 * Not calculated: proportion of results below limit of detection was too high to provide a valid result.678-.168 (.202 (.207) . 1999).178-.531 (..377-.273 (.382) .950) .288-.850) .131-.931 (.190 (.827) .240) .261 (. Kidney dysfunction that led to osteoporosis was associated with very high urine cadmium levels in residents of an area of China where extensive environmental cadmium pollution occurred (Jin et al.07 (.414-.962) .210 (. Most studies of relatively low level environmental exposure to cadmium have demonstrated associations between higher urine or blood cadmium levels and an increased prevalence of various biomarkers of renal tubular effects (Alfven et al.106) .190 (.784) .490 (.086 (.830) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.674-1.440) .789 (.12) 1.267 (. can result from high dose chronic exposure.05) 1.163 (.338 (.289) .288 (.191) .187-.232) .157-.476) .536 (.364) .591 (.215 (.818) .194-.979 (.191 (.209) .

2003.1 mg/L (Alfven et al.. approached these values associated with subclinical changes in renal function and bone mineral density. Women had higher blood and urine cadmium levels compared to men of similar ages.. Mannino et al. 2003).. not to imply a safety level for general population exposure. Staessen et al.. Becker et al. 2003. 2004b).S. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. respectively. 2002.26 and 3.. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH.. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney. 2006).cdc. In the typical environmental exposure.. However. 2006). Wilhelm et al.S. CDC. EPA.e. Several studies of populations residing in areas with higher cadmium soil concentrations or with frank cadmium pollution have reported mean blood and urine cadmium levels considerably higher (as much as 10 times higher) than control groups or representative U. Horiguchi et al. 2004b. 2002). Becker et al... Noonan et al. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals .. Creatinine-corrected urine cadmium values in U. 2003. with peak values observed in the fifth to sixth decades (CDC. Staessen et al. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity.. data (CDC. Salpietro et al.. 1999). 2005. 1996). 2005). Jarup et al. intermediate in former smokers and lower in never-smokers (Becker et al. Olsson et al.. study subjects living near a former zinc smelter were similar to those from an unexposed community and to those in this Report (Noonan et al. 2002). 2000.... 2006.. 2002. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. Komaromy-Hiller et al.46 mg/gram of creatinine) (Ezaki et al. 2003. 2000. 2002). 2000). 2006. Both IARC and NTP consider cadmium a human carcinogen.. Becker et al. potentially fatal pneumonitis (Fernandez et al. Acute and heavy exposure to airborne dusts and fumes. 1996. maternal blood or maternal urine and birth weight (Nishijo et al. Moriguchi et al. 2000. 2004.. 2002)... 2004. 2004... Further research is needed to address the public health consequences of such exposure in the United States. Horiguchi et al. Olsson et al. 2002) and length at birth (Nishijo et al. Olsson et al..html.. Zhang et al.. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al.atsdr. has resulted in severe. Wennberg et al..Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. Staessen et al. Information about external exposure (i.. 1999. Friedman et al. Cadmium can produce lung. In adults aged 60 years and older. 2003.. Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 mg/gram of creatinine (Akesson et al.S. Jarup et al.. 2005. 2005.gov/ toxpro2. The 95th percentiles for cadmium levels in this Report were less than the OSHA standards for both blood cadmium (5 mg/L) and urine cadmium (3 mg/gram of creatinine). Ezaki et al. 2005. respectively. 2002. 2004.. 2002. 1999). Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. 2002. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. environmental levels) and health effects is available from ATSDR at: http://www.. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. as may occur from welding cadmium-alloyed metals. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC.. two studies of women in Japan with lower exposures found no correlation between renal tubular effect markers and blood or urine cadmium levels (geometric means were 1. 2002. and drinking water and environmental standards have been established by U.. Wennberg et al. 2002).. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. Suwazono et al. Ezaki et al.. 2003. Occupational standards are provided here for comparison only. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. In postmenopausal women.. Animal studies have demonstrated reproductive and teratogenic effects. For NHANES 19992000. Jin et al. 2004).. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. 1988)... the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1... In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles.

Occup Med 1996. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Jones RL. et al. Alfven T. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Persson B. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Lundh T. Horiguchi H. Comparison of representative ranges based on U. Moriguchi J. Oguma E. Akesson A. et al. Lidfeldt J. Oguma E.96:353-359. Centers for Disease Control and Prevention (CDC). Fayers PM. Miyamoto K. Mucha A. population. Friedman LS. Komaromy-Hiller G. Kaus S. et al. Atlanta (GA). Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Buchet JP. et al. Bellerup P.Metals with reference values so they can determine whether people have been exposed to higher levels of cadmium than are found in the general population. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Machida M. Ikeda Y. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Anthropometric. 1999 [online]. Carlsson MD. Bregante G. Fukui Y. Ezaki T. environmental. Kumagai N. Kikuchi Y. Environ Health Perspect 2005. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. 2005.45:43-52. Lancet 1999. et al. Toffoletto F. Greves HM. Environ Res 2004b. Seiwert M.57:668-672. Holguin F.76:186-196. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake.46:372-374. Machida M.cdc. Elinder CG.gov/toxprofiles/tp5. Krause C. Environ Res 2004. Tsukahara T. Fukui Y. et al.354:1508– 1513. Vahter M. Kundiev YT. Fourth National Report on Human Exposure to Environmental Chemicals 203 .000 women in the Japanese general population: a nationwide large-scale survey. Seiwert M. Lison D.95:20–31.148(1-2):11-20. Jin T. Sanz P.110:699-702. Moriguchi J. Ezaki T. Third National Report on Human Exposure to Environmental Chemicals. Schulz C. Nordberg G.59:497]. possibly better than b2microglobulin. Ye T. et al. Int J Hyg Environ Health 2002. Venables KM.296(1-2):71-90.13(11):1627-1631. Comprehensive study of the effects of age. Int J Hyg Environ Health 2003. Becker K. Thayer WC.S. References Akesson A. Mannino DM.24:717-724. Bernard A. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers.S. J Occup Health 2003. Consonni D. Savage-Brown A. Toxicological profile for cadmium update. Fernandez MA. Fatal chemical pneumonitis due to cadmium fumes. Howerton K. Lepom P. Dekio F. Kaus S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Palomar M. Miyamoto K. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Takebayashi T. Ukai H. Environ Health Perspect 2002. Zhu G. Costa R. Cadmium fume inhalation and emphysema. Lukyanova EM. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Neurotoxicology 2003. Olfactory function in workers exposed to moderate airborne cadmium levels. Nerbrand C. ShkiryakNizhnyk AZ. Schulz C. Occup Environ Med 2000. 196:114-123. et al. Nermell B.atsdr. Int Arch Occup Environ Health 2003. Lancet 1988. Seifert B. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Vahter M. iron deficiency. Toxicol Lett 2004. Taylor AJ.59:194-8. Uemura T. Furuki K. et al.66(Pt A):2141-2164. Clin Chim Acta 2000. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Mascagni P.205:297-308.html. Pickering CA. Sasaki S. Ikeda Y. Berglund M. Bo M. diabetes mellitus. Grubb A. J Toxicol Environ Health 2003.1(8587):663-667. Chislovska NV. Serra J. Becker K. et al. Jarup L. et al. Okamoto S. Agency for Toxic Substances and Disease Registry (ATSDR). Environ Health Perspect 1994. patient population and literature reference intervals for urinary trace elements. Stock AL. Environ Res 2006. Thorax 2004. Hellstrom L. Nomiyama T. Jarup L. Lauwerys R. Hotz P. Diamond GL. Wang H. Furuki K. Tsukahara T. Ash KO. Gadea E. 206:15-24. Horiguchi H. Sasaki S. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Choudhury H. 102:10581066. Darbyshire J. 4/8/09 Alfven T. Toxicol Appl Pharmacol 2004a.102:83-89. Davison AG. Chiappino G. Available at URL: http://www.

209:301305.epa. Vangronsveld J. et al. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. Mueller PW. New York: Plenum Press.353:1140-1144. Nordberg GF. lead. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Arch Environ Health. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women.533(12):107-120. 4/8/09 Waalkes MP. Suwazono Y. J Environ Sci Health B 2004. Ginucchio G. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Lybarger JA. Stegmayr B. Staessen J. Int J Hyg Environ Health 2006. Environ Health Perspect 2002. Honda R.Metals Nishijo M. eds. Zhu HD. et al.gov/ttn/atw/ hlthef/cadmium.84 (Section A):4455. iron status.21(3-4):251-262. Kuznetsova T.html. Schultz C. Lijnen P. Revised and new reference values for arsenic. Skerfving S. Usefulness of biomarkers of exposure to inorganic mercury. Zhao YC.59(1):22-25. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Sager PR. Merlino MV. Revised 2000 [online]. Staessen JA. Nogawa K. 2000. Environ Res 2006. Liu QF. Wennberg M. Nishijo M. Biological monitoring of cadmium. Fan YG. Oskarsson A. Ottosson H. EPA). Wang JX. 151-168. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Zhang YL. et al. forearm bone density. age. Nordberg GF. Sarasua SM. Available at URL: www. Environ Res 2000. Lison D. J Perinat Med 2002. Biological monitoring of toxic metals.110:1185-1190. Hazard Summary. lead. Ren Fail 1999. Friberg L. In: Clarkson TW. created 1992. Stelitano A. Nakagawa H.30(5):395-399. Kido T. cadmium. Salpietro CD. Campagna D. Cadmium in blood and urine – impact of sex. Thijs L.39:2507-2515. Mutat Res 2003. Cadmium carcinogenesis. Honda R. Gallmans G. Kathman SJ. J Cardiovasc Risk 1996. 2004. Hoet P. Lauwerys R. Toyama. pp. Nakagawa H. Lundh T. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Gangemi S. United States Environmental Protection Agency (U. Japan. Relationship between newborn size and mother’s blood cadmium levels. et al. Lundh T. Environ Health Perspect 2002. Cadmium compounds. Bruiglia S. Schwenk M. Roels HA. Occup Environ Med 2002. 2001. Okubo Y. Tawara K. Lancet 1999. Time trends in burdens of cadmium.110:151-155. and former smoking – association of renal effects. Bergdahl IA. lead.3:26-41. Saito S. et al.59:394-397. Nakagawa H. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Nordberg M. Wilhelm M.S. Kobayashi E. and mercury in the population of northern Sweden. Roels HA. dietary intake. Noonan CW. et al. Environmental exposure to cadmium. Bensryd I. Buchet JP. Olsson IM. Jansson J-H. Minciullo PL. Tanebe K. and risk of fractures: prospective population study. Emelianov D. Tanebe K.100:330-338. Roels H.

4 (9.62) 4.59) 7.08 (6. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.14.50-7.71-8.8) 9.8) 9.10 (8.60-7.22-4.07) 4.25-5.1) 9.33-5. and cardiac arrhythmia (ATSDR.60-7.2-13.35 (4.03 (4.54-11. and 0.0) 12.4) 95th 11.80-6.29 (4.60 (7.80-13.8) 12.94 (4.3) 9.17 (6.90) 7.5-13.20) 7. 0.82) 5. Little is known about the health effects of this metal.77 (9.4) 10.80) 7.40-11.81) 9.60-12.42-7. scintillation counters.7 (10.56-11.13-8.90-12.7 (10.67 (4. Radioactive 137Cs has been used medically to treat cancer. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.40-5.32-5.71 (8.7) 11.70 (8.93 (4.8) 11.56) 5.14.45-8.99-6.40) 5. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.84) 5.30-10.2-13.07-11.98 (7.39) 7.81-14.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.90) 5.37) 5.72) 4.91 (7.79 (4.12-11.35-5.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4. 2004).64 (4.2-12.74) Selected percentiles ( 95% confidence interval) 50th 4.8-13.90-10. respectively.09) 5.50) 9.20 (4.89) 5. and as polymerization catalysts. and high-power gas-ion devices.04 (4.53 (6.7-14.3) 10.4) 11.89-5.10-9.3) 12.94-4.05-5. For absorbed cesium salts.80 (4.99-11.17) 4.20-5.0-15. nausea.9 (11.73-5.29) 4.3 (8.05) 5.32 (3.1) 10.40-5.7) 10.76-6.31-8.3) 10.70 (5. Fourth National Report on Human Exposure to Environmental Chemicals 205 .2-13.60) 7.84 (4.0) 12.6) 10.49) 75th 7.60-6.4) 9.0) 12.27) 4.8) 11.69-6.3-13.39-4.1-13.96 (6.77-8.95) 5.84) 8.08 (7.00) 6.64) 5.7 (10.1-12.00-4.70 (6.63-4. semiconductors. photographic emulsions.47-4.88 (8.3) 10.00) 4.2) 11.4-13.74 (4.64-5.53-11. Whether cesium compounds are carcinogenic is unknown.70 (8.73-11.40) 5.91-8. 01-02.80 (8.36 (3.3) 10.40-5.80-10. and 03-04 are 0.2) 12.70) 7.12 (4.40-11.9) 12.2.90-10.20) 4.7) 10.60-6.49 (4.36) 3.01-6. Most human exposure to cesium occurs through the diet.7 (9. the body half-life is estimated to be 70-109 days based on 137Cs exposures.14 (4.9) 11.59 (5.3-13.08-5.80-10.71 (4.7 (9.8 (11.30 (6.13 (7.8 (10.90) 5.30) 7.50 (4.97-7.1) 9.61) 7.5-16.56 (4.68) 9.52-9.7 (8.50 (6.03 (4.1 (10.6) 11.26) 4.8 (10.32) 4.34 (4.47-8.50 (4.71-9.0) 11.80-10.87-7.87) 5.10-7.90-12.10-5.22 (4.5-14.81) 4.03-4. although cesium was generally of low toxicity when given to animals.71-5.70-8.4) 10.82-4.13 (5.35 (4.00-9.15-8.05-5.8) 12.97 (7.10 (6. soil.26-11. cesium hydroxide is corrosive and irritating at high concentrations.55 (7.6 (9.61-6.6 (9.70 (4.21) 90th 9.0 (10.5) 10.33 (6.50) 5.24) 4.1 (11.60 (8.71) 4.30-5.6 (11.5 (8.86-12.50 (4.20-7.95-4.98 (7.62 (5. However. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60) 5.Metals Cesium CAS No.05) 5.27 (7.90-10.20) 8.38) 5. and clay.60) 7.64) 5.43 (5.S.5 (10. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.68 (7. see Data Analysis section) for Survey years 99-00.80-11.99-11.80 (4.84-9.77 (4.10 (6.0) 10.70) 5.5-14.49) 4.77 (9.5) 12.9) 8. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.4) 12.56 (4.54) 4.66 (7.9 (11.30 (6.10-8.34) 9.87 (4.94) 4.04) 7.7) 11.8) 12.52) 7.00) 7.26 (3.9 (10.40-7.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.16-6.50 (7.42) 7.40-5.43-8.86 (7.62 (5.02 (4. interval) 4.20) 5.7 (9.20 (6.2 (9.23-4.90 (4.86-11.0) 11.40 (4.09-5.83-4.70-5.45-5.3 (8.13 (8.55-11.99) 7.4 (9.17-6.44 (8.1) 11.90-8.0-13.0 (9.99) 9.83) 6.3-15.12) 5.90) 9.9 (11.59-5.0) 9.40) 7.5) 9.81 (4.00 (7.37) 7.70) 5.49 (5.6 (11.20-4.95 (3.2 (9.12-5.64-10.80 (8.90 (6.9) Total 4.97) 4.1) 11.01) 7.1-12.21 (4.08-5.59-5. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.2-14.89) 4.63 (4.84-5.60-5.01-8. infrared lamps.7 (11.74-5.42) 6.4 (10.08) 7.26) 7.10 (8.59-5.9 (11.4) 12. population from the National Health and Nutrition Examination Survey.72-7.87 (4.16-6.00-10.00-8.90) 4.30) 5.25) 4.33 (5.27-5.94 (4.80 (4. diarrhea.80 (8.20-8.81) 4.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.9 (10.6 (9.23) 9.87 (4.64) 4.70 (9.25 (3.63) 6.55 (4.1 (9.92-13.00-8.46) 7.6 (9.57-5.70 (6.36 (6.

66 (5.3) 11.08 (3.48) 90th 7.64) 5.05 (4.10-4. Two small studies of European populations reported urinary cesium levels similar to U.20-4.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .16-8.5) 7.62) 5. population.81 (4.31-4.33 (5.10) 7.20-4.45 (4.91) 5.56) 3.6 (9.84-9.46-4.26 (4. Minoia et al.7) 10.35 (3.47) 4.18-6.44 (8.46) 6.30-4.01-8.53 (6.23 (7.73 (3.42 (5.63 (7.21-4.87) 5.74-11.60-20.43 (4.41-4.90-8.96) 4.05) 3.16-8.09 (4.65 (6.19-3.17-4.85) 5.67 (6.91) 4.77) 4.71 (7.44 (4.31 (4.33-3. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.5 (9.25) 4.43 (3.67 (5.62-8. interval) 4.38 (3.95 (5.20-8.50-5.58 (4.43-11.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.38 (3.91 (5.34 (5.65-3.35) 3.60-10.99-9.49) 3.26-6.08 (5.67) 5. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.40-5.3) 9.64-6.82-4.12) 3.50) 4.08-3. Biomonitoring studies on levels of cesium can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cesium than are found in the general population.08 (6.97) 8.78) 4.75 (6.42-6.92) 3.58) 3.27-4.03) 5.15-4.51) 4.03) 6.41) 9.93-7.35-7.3 (10. Using clinically submitted specimens.77 (4.68) 6.43 (8.07) 8.S.54 (4.00-4.30-4.10 (5.44-5.57) 3.66-6.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.36-10.18 (7.16-5.14) 4.54 (3.79 (5.70 (7.14-7.07) 8.74) 75th 5.7-12.36-3.41 (5.55-5.18-7.41 (4.08) 4.46 (7.17) 9.00) 6.72-5.29) 5.2) 11.7) 10.09) 4..85-4.11 (5.28) 7.2 (8.03-5.9) 10.99-4.60 (3.47) 6.88-10. and were also roughly similar to those in this Report.78) 4.66 (6.43-6.53) 3.05) 6.63 (6.84-7.51 (4.90-8.97-4.84-9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.12-6.06 (5.04) 6.38-7.74) 3.47) 7. (2000) found urinary cesium levels that were slightly lower than those reported for the U.47 (4.64 (4.14-6.28 (5.16) 5.3 (9.99) 4.48) 7.72 (4.96) 4.70) 6.42-4..27-6.41-7.10 (3.27 (8.47 (7.56-10.59) 4.44-9.8) 5.58-5.68 (4.43) 8.95) 10.42-4.61 (7.98 (6.89-4.95-12.82) 7.14 (6.21-5.64) 9.53) 6.05-3.30 (3.63 (4.50 (6.25) Selected percentiles ( 95% confidence interval) 50th 4.94 (5.52-5.09) 8.40) 7.3-15.17) 4.14-4.53 (4.72) 4. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.41 (8.65-4.78 (3.68) 3.50 (7.04) 5.91-9.77 (6.5) 9.29-3.8) 6.56) 4.00-10.75 (7. Komaromy-Hiller et al.0 (7.43 (4.79) 9.99 (3.19-6.8) 10.26 (3.74 (4.96-4.S.83-7.13 (3.30 (7.54 (4.38-12.99-9.13-9.12 (3.15 (7.0) 7.85) 4.88-4.90-3.84-7.30 (4.83) 8.30) 10.63-6.24-4.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.59-8.87-4.68) 4.79) 4.21 (2.28 (4. 2004).42 (4.48-6.64 (8.20) 5.6 (9.46-8.06 (3.51 (7.55) 4.22) 6.22 (3..13-9.15-11.54 (5.83-6.5) 9. 2005.05-3.03-6.08) 3.10 (3.30) 10.98 (7.35 (4.9 (9.29) 4.18) 8.27 (6.60) 3.91 (5.8 (9.63) 6.00-5.00-9.90 (7.S.2 (8.00-5.31-6.50 (5.14) 4.77-5.20-4.73-4.05-4.07-4.91-7.35-11.76-6.91-6. 1990).04-11.66 (5.56 (4.41) 4.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.93-9.64) 4.74 (5.91) 5.29-3.77 (7.45-6.94) 7.15) 95th 8.95 (3.84-11.39) 5.78 (3.17 (6.51 (4.13) 7.37-3.58) 8.4) 10.38) 10.76-9.27 (6.00-8.00 (8.92 (5.31 (4.39 (5.44) 3.96 (4.33-8.70) 7.6) 6.9 (10.81 (4.02-4.24-10.97-5.58 (6.79-5.63-6.29) 4. population results shown in this Report (Alimonti et al.95) 4.60 (5.55 (3.61-3.71) 6.27) 4.36-6.04-5.02 (5. population from the National Health and Nutrition Examination Survey.47) 6.1) 11.06) 5.51 (3.50) 8.0) Total 4.3 (8.87 (5.95-6.40) 6.08) 4.68-11.79) 6.11 (5.56) 4.98) 5.46 (8.08-7.95) 8.22-11.37) 4. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.80) 6.21-3.51 (3.50) 4.86 (4.96-4.06) 4.98) 5.24 (3.33 (5.50) 4.39) 8.28) 8.75-11.07 (5.

Forte G. cesium.14:120-128. Sci Total Environ 1990. Rapid Commun Mass Spectrom 2005. Voorhees RE. Clin Chim Acta 2000. Paschal D.Metals References Agency for Toxic Substances and Disease Registry (ATSDR).19:3131-3138. J Expo Anal Environ Epidemiol 2004. Sewell CM. Trace element reference values in tissues from inhabitants of the European community I. Wood CM. Pietra R. Wolfe MI. et al. Sabbioni E. Komaromy-Hiller G. Howerton K. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA) 2005.gov/toxprofiles/tp157. Minoia C. Spezia S. Ash KO. Gallorini M.html. Toxicological profile for cesium. blood. Ronchi P. Available at URL: http://www.atsdr. Fourth National Report on Human Exposure to Environmental Chemicals 207 .cdc. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium.2004 [online]. New Mexico. Mott JA. patient population and literature reference intervals for urinary trace elements. antimony and tungsten.S. Gatti A.95:89-105. et al. 2000. A study of 46 elements in urine. et al. Costa R. Comparison of representative ranges based on U. 4/8/09 Alimonti A.296(1-2):71-90. Centers for Disease Control and Prevention (CDC). Pozzoli L. Apostoli P. Mincione G. Assessment of urinary metals following exposure to a large vegetative fire. and serum of Italian subjects.

39) 1.270-.530-.310 (.04) 1.660) .750 (.500) .367 (.17 (1.450) .620-.600-.22 (1.338-.60 (1.690 (.08.550 (.350-.420) .53) 1.460 (.890-1.334) . Cobalt compounds are used as catalysts in producing oil and gas. Cobalt is used as a drying agent in paints.26) 1.980-1.24 (1.340) .350 (.350-.26) Total .291-. and soil.340) . large appliances.570 (. automobile airbags.65) 1.355-.398) .380 (.42) 1.810-. and in synthesizing polyester and other materials.400-.620) .480 (.270-.460-.520) .46 (1.350) 75th .305-.890-1.680 (.336-.08-1.S.06 (.03) 1.930) .420 (.02-1.32-2.52 (1.523) .05 (.660) . The cobalt used in U.03) .710 (.610 (.316-.650 (.610-.300 (.900) .64) 1.480 (. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.388-.490-.68 (1. diamond-polishing wheels.410) .520-.870 (.450) .15 (1.690-.16 (1.07.04-1.910-1.13) 1.670 (.670 (.47 (1.950-1.540-.480-.800-.581) .590 (.760 (.610) .510) 1.24 (.348-.47) 1.33-1.800) .59 (1.900) .430 (. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.23-2.319) .590-.640) .09 (.410 (.515 (.435 (. blue-colored pigments.940 (.380 (.14) .32 (1.810) .430-.350-. hard metal (alloys of cobalt and tungsten carbide).417) . and kitchenware.29 (1.564) .790 (.580 (.440-.270-.450-.340 (.377-.580 (.950) .379 (.340-.550-.790) .620-.330 (.380-.750-.700) .01-1.12) 1.331-.03 (.640) .570) .880 (.14) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .28 (1.461 (.460) .460) .890) 95th 1. steel-belted radial tires. Usual human exposure is from food sources.75 (1.370) .48) 1.47 (1.600 (. and magnetic recording media.460 (.540-.680) .04 (.393-.640) .543) .660-.424) . 01-02. industry is imported or obtained by recycling scrap metal that contains cobalt.930 (.450) .01 (.890-1.900-1.620-.419) Selected percentiles ( 95% confidence interval) 50th .610) .320 (.08) .01-2.496) .370 (.431) .670-.410 (.333-.00) .460) .980) .900-1.820 (.48) 1.370-.398 (.530) .740-.17 (.310-.364-.09) .330) .44) 1.16 (1.Metals Cobalt CAS No.580 (.17 (1.05 (.740-.386) .28-2.20 (1.360-.374 (.47) 1.380 (.520) .03 (. see Data Analysis section) for Survey years 99-00.371 (.308-. varnishes.430) .370-.570-.313) .390-.416) .410-.499 (.630-.06-1.950-1.418 (.520-.410 (.19) .469-.940-1.81) 1.930-1.56) 1.710) .280-.960-1.05) 1.470) .04-1.373-.373) .410 (.399) .570) .600) .28 (1.22) 1.99) 1.07-1.67) 1.840) .570-.820 (.16) 1.450-.940-1. It is also a component of porcelain enamel applied to steel bathroom fixtures.290-.540) 1.770) .22-1.410) .730) 1.850) .50 (1.454 (.810) . and fertilizers. and 0.650 (.434 (.372) .285 (.850-1.294 (.650-.16) 1.07-1.431) .26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.03) 1.740 (.820 (.73) 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .379 (.50) 1.630 (.375 (.850-1.316 (.520-. Cobalt occurs naturally in airborne dust.920) 1.37-1.07.405-.850) 1. and 03-04 are 0. interval) .348-.463-.359 (.26-2.870-1.36) 1.380-.23) .12) 1.670-.470 (. hard metal or in combination with other elements.530 (.680) .33 (1.870 (.04-1. Cobalt may be released into the systemic circulation of patients who receive joint prostheses that are Urinary Cobalt Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.670 (.520 (.710) 1.519 (.343 (.630 (.465) .32) 1.327-. shiny.550) 90th .390) .410-.333-.21) 1.45 (1.800-.390 (.950 (.520-.750 (.01 (.300-.900) .520 (. seawater.28 (1.32) 1.360-.690-.680 (. population from the National Health and Nutrition Examination Survey.540-. 0.830-1.950 (.500 (. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.16 (.330-.14-1.369 (.520 (.430 (.394) .17-1. and inks.583) .32 (1.301 (.92) 1.81) 1.414) .760) .490-.450) .370-. 208 Fourth National Report on Human Exposure to Environmental Chemicals .25-1.339 (.920-1.26-1.590) .520 (.352 (.340-.15-1.390 (.590-.360-. respectively.790-.259-.700) .16-1.07 (.410-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.430 (.427-.390 (.430) .540-.420) .560 (.73) 1.452 (.487) .410 (.404) . Cobalt compounds are also used in manufacturing battery electrodes.06 (.890) .343) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 . It is emitted into the environment from burning coal and oil and car and truck exhaust.428-.860 (.16-1.880-1.750 (.03-1.09 (.502) .S.

or using diamond-polishing wheels that contain cobalt metal.537 (.550-.777-.407) .500 (.33) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .328) .976 (.334) .15) 1.35) .781-1.740-1.349) .386 (.667-1.326-.35) 1.313-.378-.03 (.294-.609) .396) . and to a lesser extent. respectively.324) .353 (.17) .327-.Metals fabricated from cobalt alloys (Lhotka et al.547 (.00) .317 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.469-.439) .234 (.378-.911-1.360) .278 (.616-.314 (.563-.626-.29 (1.361 (.00 (.667-1.851 (.365-.407 (. 1972). Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.392 (.542 (.215-.704-.257 (.50 (1.304) .585) .393-.327 (.449) .16 (1.296) .04 (.838 (. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.442-.457) .728 (.402 (. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.457 (.917) .335 (.289) .337 (. A portion of cobalt retained for long periods is concentrated in the liver.15 (.417 (.297) .346 (.352 (.848 (.829) .280-.329 (.495 (.983-1. Exposure in the workplace may come from electroplating.850 (.275-.239-.33) .900-1.708) .488) .378-.12-1.599) .562) .23 (1.503-.286) .328 (.60) 1.28) 1.13) 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 209 .574-.990-1.348) . cobalt is excreted predominantly in the urine.634-.02 (.523 (.281) .707) .247 (.733-1.27) 1.561) .581) .256-.898 (.727 (.369 (.S.274-.804) 1.723 (.372) .679-.434-.429) 1.606 (.821-3.384) .462) .391 (.500-.963) .598 (.248-.615) .554 (.325) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .660-.343 (.750-.10) 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .608 (.279 (.54) 1.990) .353-.949) .300) .435-. 1979). interval) .10) Total .475 (.786-.428-. with pulmonary clearance half-lives of from one to two years (Hedge et al.638-1.257-.824 (.533 (.387) .00) .728) . Cobalt is absorbed by oral and pulmonary routes.513) .534 (.303-.435 (.368 (.479-.461) . 1994).471-.49) 1.593) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.19) . population from the National Health and Nutrition Examination Survey.471-.529 (.513 (.983) .313-.381) .09) 1.29) 1.268 (.600-..313 (.278-.744) 1. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.361-..296-.297-. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.394) . refining or processing alloys.673-.00-1. Once absorbed and distributed in the body.396) .879-1.273 (.290 (.29) .393 (.259 (.872 (.792-1.343-.419) .352) .29 (1.391) Selected percentiles ( 95% confidence interval) 50th .964 (.750) .774 (.30 (1.523 (.857-1.895-1.313-.10-1.647) .00 (.975 (.36) 1.689 (.895-1..368) .409) .438) .342-.324-.339-.830 (.821 (.237-.560-.452-.272-.842) .467-.476-.16 (.844 (.444 (.833-1.738 (. an essential human nutrient.33) 1.361-.963-1.271 (.960 (.57) 1.408 (.591 (.753) 1.03-1.362 (.955) .352 (.00 (.358 (.309) .468) .513-.937 (.487-.595) .471 (.505) .955) .293 (.337) .552 (.781) 95th 1.457-.433) .277-.756 (.290 (..333-.12 (.543) .515 (.463-.700 (.500-.479) .400 (.55) .259) .640) . 2003).316 (.669) .792 (.829-1.694) .425-.548 (.10) .00 (.534-.27) 1.963) .785) .10 (.611) .582-.683-.44 (.298 (.404-.421) .522) .301) .313-.11-1.388 (..259-.487-.630-.963-1.306 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).282 (.508-. using hard metal cutting tools.279) .04-1.630-.50) 1.382-.378 (.25 (.365) .760-1.310) .363) . Smith et al.36) 1.632-.329-.635 (.24) .481) 90th .426 (.449-.355) .313-. 1972).826-1. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.333-.594) .275-.952 (.16 (.83) 1.323) .737 (.16) .736-.306) 75th .644 (.251-.06 (.611) .60) 1.700 (.861-1.333 (.344-..290 (.417) .328 (.757-1.73) 1.554 (.662) .380-.25 (.847) .425) .248-.291 (.850-1.319-.11-1.562) .243-.29 (1.861 (.376 (.301-.905) .691 (.362) .250) . 1994.938) .362-.282-. in the feces.302-.333-.50) 1.455 (.331-.738 (.929) .703-.361 (.938-1.388 (.753-.304-.14 (.368) .932-1.

A 1982-1992 surveillance programme on Danish pottery painters. 1998). usually in combination with tungsten carbide (Cugell et al. 2003. Poulsen OM.S. population (CDC.. Alexandersson R. Toxicol Sci 1999. 1998). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Krause et al.. Cobalt-beer cardiomyopathy. 1988). Lison et al.. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. 1988).. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al. Iavicoli et al.. 1985.. 1993).. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. Biomonitoring studies on levels of cobalt provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cobalt than are found in the general population.... Hailey JR.43(4):299-303. 1999).. has been associated with exposure to dusts that contain cobalt. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L. Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. 2005 [online]. Rubin A. 2006.html. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . A clinical and pathological study of twenty-eight cases.. 1992). Am J Med 1972.e. Grumbein SL.50(13):95-104. Information about the BEI is provided here for comparison. Dunstan et al. Haseman JK. Swennen et al. 1989). A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al.53:395417.atsdr. Lisi.. Cobalt was once added as a foaming agent to beer. Lauwerys and Hoet. Urinary measurements mainly reflect recent exposure.. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect.. 210 2006. Information about external exposure (i. Centers for Disease Control and Prevention (CDC). 1994. For workers exposed to cobalt in the air. 2001.S.. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. 2005..Metals Toxic effects of cobalt have been encountered in workplace settings. 4/3/08 Christensen JM. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. 2005. Shirakawa et al. 1997). Sci Total Environ 1994. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis. 2001). not to imply that the BEI is a safe level for general population exposure. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. Blood and urinary concentrations as estimators of cobalt exposure. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. 1990). Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. 1994. Thomassen et al.gov/toxpro2.cdc. Third National Report on Human Exposure to Environmental Chemicals. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. 1997. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. Arch Environ Health 1988. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al. 1972). Linnainmaa and Kiilunen. with mean levels that were about 15-20 times higher than in the general U. Morgan WKC.gov/ exposurereport/. 1955). population results in this Report (Kristiansen et al. White and Sabbioni... 1994). 2001. although substantial occupational exposures have produced elevated urinary levels for many weeks.49:56-67.. References Alexander CS... et al. Atlanta (GA). Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. 2003. environmental levels) and health effects is available from ATSDR at: http://www. 1993). Roycroft JR. Sills RC. Daniel et al. Cugell DW. Perkins DG. Bucher JR. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. “Hard metal” disease... Available at URL: http://www. 2001. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. 2003). MacDonald et al..cdc. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al.

Steffan I.533:135-152. Lisi P. Lison D. Lauwerys RB. Bacis M.48:172-173. Falcone G. Edmonds CJ. Sci Total Environ 1998. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Hoet P. Bozec C. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Christensen JM. salt. J Rheumatol 2001. Long-term clearance of inhaled 60Co. Sci Total Environ 1997. Int Arch Occup Environ Health. Molders J. Alessandrelli M. Kristiansen J.150(1-3):167-171. Lauwerys R. Dunstan E. Health Phys 1979. Zhuber K. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors.22:359367. Lison D. et al. Pradhan C. Moulin JJ. et al. Palmroos P.55(4):269-276. Meyer zum Buschenfelde K-H. Pisati G.58(10):631-634. Contact Dermatitis 2003. Hammon E. 3rd ed. Co-sensitivity between cobalt and other transition metals. Cannon SR.204:147-160.406:282-296. Biological monitoring of workers exposed to cobalt metal. Dickel H. Sci Total Environ 1994. Oksa P. Unwin P. Hoher T. Swennen B. 2001. Kiilunen M. Romazini S. Br J Ind Med 1993. Leghissa P. et al. J Occup Med 1992. Kirsch-Volders M. Tilley S. Hedge AG. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein.150:177-183. Diepgen TL. Kato M. Science 1988. Absorption and retention of cobalt in man by whole-body counting. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium.Metals effects of cobalt.36:732-734. Occup Environ Med 2001.21(2):189-195. Rorabeck CH.88(4):443448. oxides. Ichikawa Y. Lung cancer risk in hard-metal workers. Zobelein P.51(7):447450. Chest 1989. J Bone Joint Surg Br 2005. Cobalt and antimony: genotoxicity and carcinogenicity. Meier R. a study of 13 elements in blood and urine of a United Kingdom population. Sabbioni E. Kuska Y. Laippala P. Respiratory health of cobalt production workers. Peltier A. Health Phys 1972. MacDonald SJ. Bunn HF. Barnaby CF. Kriss JP. Buchet JP. Swennen B. Chess DG.44:124-132.242:1412-1415. Occupationallyinduced “isolated cobalt sensitization. X. Fourth National Report on Human Exposure to Environmental Chemicals 211 .157:117121. Cresti R. Linnainmaa M. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Iversen BS. Dunning SP. Gross RT. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial.216:253-270. and hard metal dust. Sci Total Environ 1994.87(5):628-631. Ghat IS. cobalt salts. White MA. Occup Environ Med 1994. Cleland D. et al.95:29-37. Cobalt cardiomyopathy. Am J Ind Med 2003. Stanescu D. and cobalt metals.148:241-248. et al. Lauwerys R. Shirakawa T. Am J Epidemiol 1998. J Orthop Res 2003. Goto S. Vitali MT. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Schramel P. Jarvis JQ. A report of two cases from mineral assay laboratories and a review of the literature. Sanghrajka AP. Daniel J. Kusaka Y. Angerer J. DeSantis V. Outcome of occupational asthma due to cobalt hypersensitivity.” Contact Dermatitis 2001.28(5):1121-1128. Ziaee H. Smith T. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Lhotka C. Carnes WH. Thabe H. Goto S. Roto P. Thakker DM. Weber A. Mosconi G. Blunn G. Weyher I. J Bone Joint Surg Br 2006. Sabbioni E. Zedda S. Radulescu M. HoffmannB. McCalden RW. Szekeres T. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Sabbioni E. Uitti J. Goldberg MA. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Int Arch Occup Environ Health 1997.150.69(3):193-200. Zweymuller K. Bourne RB. Thomassen H. Mutat Res 2003. Salama A. Lasfargues G. Salvatori S. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Fujimura N. Clin Orthop Relat Res 2003. et al.34:620-626. Arch Intern Med 1990. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Boca Raton (FL): Lewis Publishers. Lison D. The release of metals from metal-onmetal surface arthroplasty of the hip. Epidemiological survey of workers exposed to cobalt oxides.20(1):25-31. Buchet JP. Wild P.45:246-247. Iavicoli I. Schaller KH. Linna A.(1-3):133-139.50(9):835-842. Trace element reference values in tissues from inhabitants of the European Union. Schank M. De Boeck M. 1985. Heki S. McMinn DJ. Robinson C. Kraus T. J Trace Elem Med Biol 2006.

09) 1.34-1.g.50) 5.60-1.50-6.70-6.69) 1.50 (4.30 (2.60 (3.70) 1.50-1.50 (3.30 (2.60) 2. ammunition.30-5.00) 1. 7439-92-1 General Information Elemental lead is a soft.3.50 (2.00) 4.60-3.60 (3.22 (1.40-1.48) 1. blue-gray metal that occurs naturally in soils and rocks.77 (1.00) 2.900 (. malleable.80 (1.20-4.20 (3.20) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.70-4.20 (1.20-3.80) 2.60) 5.50-2.00-1.50-1.50) 5. interval) 1.60) 3.90) 3.20-1.30 (4.90 (3.65 (1.20) 3.50) 7.50) 3.20 (3.20 (1.50) 2.20) 1.10) 1. such as lead phosphate and tetraethyl lead.50) 2.36) 1.36-1.90) 3.80) 2.30) 5.60-4.00) 5.80) 1.50) 1.62 (1.60) 2.00-6.49-1.10) 3.70) 4.40 (2.70-2.30 (3.43 (1.10 (1.50 (3.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.40) 1.19 (1.90) 2. brass.70) 1. Lead was used in plumbing for centuries and may still be present.01 (1. bronze). Lead is most often mined from ores or recycled from scrap metal or batteries.00) 6.80 (1.40-6.70) 1.S.12-1.87 (1.30-2.70) 1.70-2.40) 4.89) 1.10-3.32-1.20 (1.40-1.71-1.43) 1.39) 1.00-5.20) 3.40) 2.36-1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.00 (5.52-1.90-2.80 (1.90-4.50) 4.50) 4.80-3.20) .60 (3.10-2.00 (6.51) 1.40-2.90) 2. and 0.62-1.14-1.60) 1.50-5.50-5.23 (1.80 (1. and for radiation shielding.31) 1.900-1.55-1.20-2.10-1.90) 1.90-2.80 (1.90 (4.60) 1.10-3.43) 1.40) 2.90-4.90) 2.00) 2.50-3.60 (1. dense.70 (3.00-4.80 (5.60 (1.55-1.60 (1. solders.02) 1.70 (5.37-1.80) 1.53) 1.60) 4.60-4.70) 2.00) 3.942 (.50) 1. and 03-04 are 0.80-3.00-1.70 (1. Before the 1980’s.80) 1.00) 3.00) 1.70) 4.10) 2.30-1.90-3. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.50-4.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.60) 5.60-1.40-2.00) 2.00 (2.80 (3.60) 2.30 (1.90 (3.90 (3.10-2.40 (1.30) 2.60 (2.00) 4.30-4.10-4.40 (1.14-1.70 (2.10-8.45-1.10-2.30-2.51 (1.70-1.40) Total 1.70) 3.60 (1.10) 2.87) 1.50 (2.75 (1.20 (2.10-3.50-2. antique-molded or cast ornaments.Metals Lead CAS No.78 (1.32-1.45 (1.90 (1.40) 3.30-1.40 (2.20 (3.30 (1.40-2.80 (5.00 (1.40) 1.40 (4.80 (1.30-2.70 (1.20 (1.40 (1.80 (4.50-1.66 (1.986) .S. metal alloys (e.30-6.10-2.20 (3.40 (1.70 (1.17) .60 (4.40-3.95) 1.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.90-4.00) 2.00-4.50-4.80-3.80-2.90-2.66) 1.50) 1.30 (1.00) 1.30 (1.80) 3.50) 75th 2.40-4.30-1.60 (2.60) 2.72) Selected percentiles ( 95% confidence interval) 50th 1.60-2.60) 4.00) 1.00) .10 (2.86) 1.70) 4.10-4.10 (3.90 (2.70) 3.10-2.60 (1.30 (4.10) 1.3.50-1.69 (1.90-6.14-1.90 (2.10-6.40-1.62) 1.800-1. leaded glass.30 (2.75) 1.60 (2.20) 5.40-3.80-4.50 (1.83 (1. 0.10 (2.70-3.40-1.28.30) 95th 5. see Data Analysis section) for Survey years 99-00.50-1.70-5.20-6.40-3.00 (3.899-.81) 1.60) 2.20 (3.80) 2.00 (4.60 (2.20) 3. respectively.52 (1.90) 1.40-1.20) 2.60) 1.00 (1.60) 3.55 (1.70) 4.00 (4.80) 1.40-6.50-2.30 (2.10) 1. population from the National Health and Nutrition Examination Survey.70-2.20 (3.40) 1.10) 5.10) 4.20-1.20 (3.50) 1.10) 3.30) 1.90-4.70) 1.20) 3.80-5.70-1.20 (2. Elemental lead can be combined with other elements to form inorganic and organic compounds.04-1.40 (3.60) 1.20-3.60 (2.60-1.80 (2.43 (1.90) 2. 212 Fourth National Report on Human Exposure to Environmental Chemicals .70 (1.20) 4.10-2.946 (.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.20 (1.60) 3. In the past.90) 2.90-2. lead was added to gasoline and residential paints and used in soldering the seams of food cans.60 (1.50 (2.25) 1.50 (4.00-2.60-1.10-1.40) 5.68-1.30 (2.00-4.20-2.91) 1. Lead has a variety of uses in manufacturing: storage batteries.10 (2.56 (1.90 (3.80-3.10-6.60) 3.70 (2.60) 4.80-4.46 (1.30-1.80) 1.90) 5.40-1.20-3.69) 1.30) 2.50-3.30) 2.40) 2.20) 90th 3.60 (2.00) 1.90) 1.10-3. plastics.70) 3.90 (3.20-3. ceramic glazes.10 (1.30 (4.50 (1.75-1.878-1.10) 3.20 (4.60) 4. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.80) 2.25 (1.50 (2.50 (1.80 (2.43-1.50-2.69 (1.30-2.10 (4.10 (1.70-1.30-1.39-1.80-4.52-1.80 (2.60 (1.37 (1.30 (2. the main source of lead exposure for the general U.30-1.70 (2.50 (2.60-2.50 (1.60-6.80 (4.40-5.60) 1.90 (1.900 (.40) 2.93-2.96-2.37 (1.75-2. 01-02.25 (1.30 (2. Since lead has been eliminated from gasoline.60 (3.70 (3.40 (5.10-1.

90 (2.680-.960-1.60-2.800 (.600-.40 (2.900-1.10 (1.00-2.90 (1. Fourth National Report on Human Exposure to Environmental Chemicals 213 .50 (2.900) .540-.480-.579-.840 (.20) . lead-based painted surfaces undergoing renovation or demolition.97) 4.753 (.29 (2.80) 3.935) 1.691-.20 (1.19 (1.1.970-1.10 (.30) 1.900) .50-2.20) .941) .50 (2.40) 2.955-1.749) .50 (2. lead-containing folk remedies and cosmetics.13-3.59) 1.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .553-.564 (.44-2.75) 4.616) .60-3.674) 1.818) . Lead is absorbed into the body after fine lead particulates or fumes are inhaled. 2007.82 (1. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.920 (.70) 3. battery and radiator manufacturing) and recreational sources.80-3.10) 2.78-2.20 (1.810-1.70 (2.30-5.40) 2.642 (. stained glass framing.710-.40) 2.02 (.40 (1.795 (. older plumbing systems with leaded pipes or lead soldered connections.40-1.910-.900) .20 (3.70) 3.00) 2.00-1.40-5.00-2.573 (.800-1.613) .90 (1.600-.800) .20-1.03 (1.00 (1.556-.78-2.790 (.651) .00 (1. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.915-1.50 (1.80 (1.808 (.00) 1.800) .900-1.20 (2.572-.40) 1.30-1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.700 (.00) .900) .80) 2.800) .27) 1.33-2.30) 2. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.78-2.800-1.990) 2.800) .20) 1.20 (2.579-.49 (1.30) 1.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.50-3.833-1.700 (.815 (.10) .700-.752 (.80-2.661-. or after soluble lead compounds are ingested.833 (.g.90-4.35 (.10 (.10) 2. population from the National Health and Nutrition Examination Survey.33 (2. and contact with soil.10-3.640 (.800 (.10-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) 2.920 (.931) .40-1.20) 1.18-1.40 (1.862) .900 (.30-1.40 (1.07-1.610 (.52-1.70-3.10-3.800) .30) 2.660) .700-.70 (2..580-.86 (1.680-.31 (1.30) 1.10-1.923 (.40 (1.10 (.22) 1.20-1.04-2.822-1.80) 2.02) 1.506-.729-.14-1.21 (2.900 (.80 (1.690) 75th 1.10 (1.526-.80-2.80 (2. CDC.60 (1.Metals occupational (e..80) 1.60-3.595-.636 (.31-3.10-1.620 (.90-3.14 (1.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.62) Total .07 (.70-2.20) .32 (1.730 (.40 (2.00 (.560-.09) 1.80) 3.10-5.620) 1. Approximately half of the absorbed lead may be incorporated into bone.70) 1.718) .600 (.90 (2.40-2.40) 1.773) .695 (.41) 2. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient.80) 1.900-1.589-.641-.700-.708-.30 (1.60-2.00 (2.848 (.700) .03-2.20) 1.30-2.857) .52 (1.10) 1.20 (1.757-.00-2. 0.600 (.50 (1.900 (. see Data Analysis section) for Survey years 99-00.90 (2.90-2.960 (.986) .625 (.60 (2.650) 1.60 (1.700 (.900) .700) 1.60 (1. lead-contaminated dust in indoor firing ranges.80) 2.10-1.700-.40) 1.60) 2.20 (1.20 (2.20-1.20-2.50) 3.535-. 2000).91) 2.625-. respectively.701) .590 (.820-1.82 (2.900) .605) .10-3.23-4.00) 2.23) .50) 2. pewter utensils and drinking vessels. and 03-04 are 0.70) 1. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead. or water contaminated by mining or smelting operations. dust.828) Selected percentiles ( 95% confidence interval) 50th .20) .17 (1.637-.33.70 (2.90-2.591 (.90) 2.540 (.766 (.50) 1.40-1.800 (.11) 2.90 (1.60-1.680) .30) 2.10) .90-3.S.75) 3.850 (.800-.70 (1.30) 1.73 (1. 01-02.710-1.86) 1. In the blood.70 (2. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00) .80) 1.52-1. interval) .90) 2.20 (1.700-1.90) 2.59-2.990) 1.50) 2.12) 90th 2.13) .24-1.90-2.659 (.50-2.62-4.30) . bullet fragments retained in human tissue.671-.630 (.700 (.40 (2.700 (.29) 2.30) 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.04) 2.600-.558 (.40) 3.89) 2. However.00 (1.731 (.940 (.00) .30-1. and 0.50-1.600-.30) 1.960-1.600) .700 (.70) 2.00 (1.04 (.80) 2.900-1.50) 1.86-2.800 (.06) .66 (2.66 (2.11 (1.30 (2.72) 1.60 (1.04) .00) .1.40 (2.04 (.40) 1.10 (1.50-2.80) 2.700-.640-.20 (1.27 (1.90-2. imported children’s trinkets and toys.628) 1.40) 1.14 (1.10-1.40-3.20-2.30 (3.570-. 1991).30-1.30-3.600-.90) 1.800-.00-1.600) .500-.785) .00-1.745-.40 (1.64) 2.86) 95th 2.10 (1.688 (.677 (.50) 1.70) 1.40-1.604 (.738) .

535) .940 (.667-.79) 1.77) 2.50 (1.708 (.681-.Metals 90% of the body lead burden in most adults.11 (1.639 (.20) .09-1.67-4.461) .92) 2.853-1.97) 1.15) 1.603-.436) .828-1. 1996).61) 3.97 (1. Staessen et al.63) 4.59-3.758) .55 (1.03 (.03 (1.44 (1.53-1.38 (2.862-.622 (.25-1. The skeleton acts as a storage depot. Nash et al.882-1.00 (1.900 (.710) .43 (2.98-2.15-2.11) ..72-2.981-1.06 (1.645-.977) 1. and through binding to ion channels and regulatory proteins.41) .49 (1.28-1. 1991.31 (1.73-2.88) 1.65 (1.66 (1.592-.23 (1.03 (.876-1.698) .655) 75th 1.02) 1.82) 1.09-1. CDC.22-1.14 (1. Large amounts of lead in the body can cause anemia.979 (.679) 1. and paralysis.31 (2.33) 2.583-.17-1.588-.933-1.607-.753) .44) 1.918 (.765) .551-.696 (.03) 1.00 (.914 (.718) 1.S.725) .66) 2.492-.61) 1.625 (.56 (1.78-4.31 (1.380-.12-1.992-1.496 (.06) 1. For instance.997-1.988 (.43) 1.800-.898) .52) 1.633 (.73) 2. Approximately 70% of lead excretion occurs via the urine.47) 1.33 (1.946-1.739) .18) .53) 1. 2003.28) 2.98 (1.35) 2.01 (.529-.652 (.56-2.43-1.645-.677 (.85 (1.702) .20) .64) 2.579-.702-.586-.679-.774 (.667-.701) .838) .79 (1.02-1.673) .94 (1.31) 1.962 (. population from the National Health and Nutrition Examination Survey.594-.56-3.88) 2.938 (.98) 2.96 (1.15-3. Lead can cross the placenta and enter the developing fetal brain.50-2.594-.10) 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites 214 Fourth National Report on Human Exposure to Environmental Chemicals ..38 (2.621 (.746) .688) .18) 1.701 (.725) . hair.342-.04-3.432 (.20-3.469 (.612-.618 (.33-1.62-3.20) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .920-1.31) 1.730) 1.79) 2.617-.623 (. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger. 1993.05-1.404 (.26) Total . In 1991.404-.10) 1.914 (.593 (.408-. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.83 (2.587-. seizures.681-.588-.69 (1.698) .971 (.61) 1.638 (.00 (1.655) .604-.03) 1.75-2. BLLs and associated toxic effects differ in children and adults.742) Selected percentiles ( 95% confidence interval) 50th .677) . based on prospective population studies.428) .03) 2.11) 1.742) .571-.639 (.22) 1. 1995).64) 95th 2.52 (1. 2004.50-2.734) .975-1.01) . and nails (Leggett..88 (1.06 (.793-1.05 (.50-2.676) .668-.89-5.08) .09) 1.720 (.541-.03) .508) .988-1.639 (.383-.64-2.43) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.19) 1.46 (1.460-.375 (.559-.75 (2.71-2.51) 1.790) .22) 1.569 (.38 (2.671 (.56) 3.763) .03) 90th 1.74 (1.00) .33) 1.781-1.41 (1.11-1.27 (1.644) .721 (.34-1.718) .64 (1.29 (1. O’Flaherty.933) .720 (. and iron.870 (. kidney injury.70 (1.649 (.87) 1.639) .683-.03) . through the inhibition of certain enzymes.893) .85) 1.662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.654) .686) . encephalopathy.05 (1.644 (.11 (.655-.50) 1.46 (2.917-1.700-.667) .07-1. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.658 (.812-1.571-.615 (.22) .15) 1.608-.55 (1.62-1.19-5.632 (.702) .641 (.08-2.03) 2.10 (.510-. The toxic effects of lead result from its interference with the physiologic actions of calcium.841-1. scant amounts are lost through sweat.68 (1.755 (. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.05-1.992-1.47 (2.914-1.707 (.17 (.66 (1.48 (1.04) 2. the Centers for Disease Control and Prevention (CDC) established a BLL of 10 Urinary Lead (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.61) 1.609 (.94-2.40-1.722 (.62) 2.58) 1.601-.712 (.00 (1.887 (. with a half-life of years to decades.51 (1.605-.62-2.963-1.44 (1.45 (1.07 (.07) .828) .03-2.71 (1.635 (.50-1.86 (1.97) 1.63) 1.37-1.24 (1. abdominal pain.18 (1.83) 1.796-1.648 (.14) 1.36-2.731-.670) 1.85-2.918-1.28) .12) 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .703) .88) 2.06) .88-2.11 (.72-2.15-2.561-.957-1.43 (1.938-1. interval) .810 (.26) 2. 2007).11 (1.659-.693 (.851) .47 (1.0) 3. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.615 (.709 (.608 (.400) .603 (.10 (1.65-2.25-1.37-1.03 (.72) . 1995.623 (.09-1.97-18. with lesser amounts eliminated via the feces.926 (.606-.08) .39-1.85-2.41-1.18) 1. Schwartz.78 (2.22-2.603-.677-.722 (.990 (.404 (.61) 1.682) . zinc.657) 1. 1993).89-2.18) 2.

lead in women may be associated with hypertension during pregnancy. 2003. For example. IARC considers inorganic lead compounds probable human carcinogens. approximately 11. Bellinger 2005. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. adults in the 1999-2000 NHANES sample.xls). Pirkle et al.07 µg/dL (Becker et al. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3.. and organic lead compounds not classifiable with respect to human carcinogenicity. Muntner et al.. 2005b). and spontaneous abortion (Baghurst et al.Metals µg/dL or higher as the level of concern in children. The U. Korrick et al. Fourth National Report on Human Exposure to Environmental Chemicals 215 .. both the geometric mean (1. 2002a). particularly in the skeleton. Borja-Aburto et al. though there is greater individual variation in urine lead than in blood and greater potential for contamination. 1996. 1998).75 µg/dL in U. 1999). residing in housing built before the 1950’s. when the geometric mean BLL was 2. Data submitted through state public health programs from 2006 showed that 1. 2000). Overall.. Urine levels may reflect recently absorbed lead. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U..4% in NHANES 1999-2004. EPA..cdc.S.S... 2003. and decrease fertility (Alexander et al.7 µg/dL and 4. Schwartz et al. almost double the geometric mean of 1. 1984. 2003. However. Staessen et al. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. 2009). adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. 2000). Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. Payton et al. 1995. Schwartz. 1996...e. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. usually with BLLs greater than 40 mg/dL.S.. 2002).cdc. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. In NHANES 1999-2002 in children 1-5 years old. 2006).. 1996.. the geometric mean BLL was 3. Jones et al.5 per 100.atsdr. 2001). Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. Information about external exposure (i.html.. with overt encephalopathy. BLLs higher than 40 mg/dL can result in proximal tubular dysfunction and decreased glomerular filtration rate leading to interstitial and peritubular fibrosis when high body burdens persist. adult residents.S. state childhood lead programs also show a decline in the percentage of children younger than 6 years of age who had BLLs of 10 mg/dL or higher..4% of children had BLLs of 10µg/dL or higher (CDC.S.. higher than 100-200 µg/dL). 2003). Lanphear et al. premature delivery. BLLs reflect both recent intake and equilibration with stored lead in other tissues.S. which is an 84% decline. 1994). urban residence. The Adult Blood Lead Epidemiology and Surveillance program has tracked BLLs reported by states for mostly for occupational but also for non-occupational exposure in U.. 1991. Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al. More recently. CDC.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006.0 µg/dL in females (Soldin et al.. 2007). 1987. the prevalence rate has declined annually since 1994 (CDC.21% of approximately 3. may alter sperm morphology. 2005b. 1999). subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. 2006).000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample.. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. In occupationally exposed adults. including minority race or ethnicity. seizures. 2005a). adults in the 19992000 NHANES sample (Apostoli et al. Both drinking water and ambient air standards for lead have been established by the U. High dose occupational lead exposure. Surveillance data reported by U.6% in NHANES 1988-1991 to 1. NTP considers lead and its compounds reasonably anticipated to be human carcinogens.. At low environmental exposures. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.3 million children tested had BLLs of 10 mg/dL or higher (http://www..gov/toxpro2. respectively.2 µg/dL in males and 3. 2002..g. environmental levels) and health effects is available from ATSDR at: http://www. and peripheral neuropathy generally occurring at much higher levels (e. reduce sperm count.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. and low family income (CDC. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors.000 adults. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. Telisman et al..6%) were lower than those from NHANES 1991-1994.

Farias P. Adult blood lead epidemiology and surveillance—United States. Kaufman JD. Manton WI. Homa DM. Atlanta (GA). Seiwert M. Sci Total Environ 2002. Bellinger D. Acquisition and retention of lead by young children. 4/14/09 Centers for Disease Control and Prevention (CDC).8(3):395-401.287:1-11. Apostoli P.54(20):513-516. Hänninen H. Jusko TA. Robertson EF.atsdr. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Luukkonen R. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Bellinger D. Checkoway H. Becker K. Roberts RR. Am J Epidemiol 1999. Public Health Rep 2000. A prospective follow-up study on psychological effects in workers exposed to low levels of lead.cdc. Ga. Jacobson SW. Pirkle JL. Pediatrics 2004. Vupputyuri S. Birth Defects Research (Part A). The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Wigg NR. Blanco J.55(32):876-879. Weiss ST. Blood lead levels—United States. Speizer FE. Rojas LM. Rios C.cdc. Batuman V.87:1-471.89:330-335. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Borja-Aburto VH. Angle CR.53:411-416. Muntner P. Lead.gov/mmwr/preview/mmwrhtml/ mm5532a2. Neurotoxicol 1987. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention.Metals Biomonitoring studies on levels of lead provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of lead than are found in the general population. 1999-2002. Rotnitzky A. Kaus S.cdc. van Netten C.113(4):1016-1022. et al.10:43-50. Am J Public Health 1999. Neurodevelopmental effects of postnatal lead exposure at very low levels. Jones RL.cdc. 2005. Blood lead reference values: the results of an Italian polycentric study. References Agency for Toxic Substances and Disease Registry (ATSDR). Brody DJ. Kuehnemann TJ. Bavazzano P. Neurotoxicol Teratol 2004. Hu H.htm. Hernberg S. Available at URL: http://www. Blood lead levels measured prospectively and risk of spontaneous abortion. Caldwell KL. doi:10.html.275:1177-1181. Wager C. Scand J Work Environ Health 1984. Available from URL: http://www. Semen quality of men employed at a lead smelter. Krause C. Meyer PA. Hu H. Available at URL: http://www. JAMA 1996. Third National Report on Human Exposure to Environmental Chemicals. MMWR Morb Mortal Wkly Rep 2005a. Inorganic and Organic Lead Compounds.htm. Lepom P. Weiss ST. Lead and hypertension in a sample of middle-aged women. MMWR Morb Mortal Wkly Rep 2006. et al. Sparrow D. Cox C. Occup Environ Med 1996. Korrick S. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. 2002 [online]. Reese YR. Hertz-Picciotto I. N Engl J Med 2003. Available at URL: http://www. Atlanta (GA). 4/14/09 Centers for Disease Control and Prevention (CDC). Jacobson JL. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . The relationship of bone and blood lead to hypertension. Preventing Lead Poisoning in Young Children. Aug 2007 [online]. Baghurst PA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Vimpani FB. Payton M. 4/14/09 Centers for Disease Control and Prevention (CDC). Environ Health Perspect 1993. Cory-Slechta DA. Sparrow D.1542/peds:2007-3608. Centers for Disease Control and Prevention (CDC). et al.26:359-371. 1991 [online]. Environ Res 2000.205:297-308. Int J Hyg Environ Health 2002. Atlanta. Managing Elevated Blood Lead Levels Among Young Children. Lanphear BP. 4/14/09 Centers for Disease Control and Prevention (CDC).htm. Teratogen update: lead and pregnancy. Korrick SA. McMichael AJ. Hunter DJ. Ronchi L. Muller CH.150(6):590-597. Ewers TG. 2005b.123:e376-e385. Hu H. 4/14/09 Alexander BH.101(7):598-616. Age-specific kinetic model of lead metal in humans. Mantere P.gov/nceh/lead/ CaseManagement/caseManage_main. Baj A.cdc. Canfield RL. CDC. Available at URL: http://www. Lanphear BP. JAMA 1996. gov/mmwr/preview/mmwrhtml/mm5420a5. et al. Leggett RW. Toxicological profile for lead.73:409-420. Pediatrics 2009. Neri A. Chiodo LM. et al.htm. Dietrich K. Kim R.gov/nceh/lead/publications/ books/plpyc/contents. 2003-2004.275(15):1171-1176. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Henderson CR. Cox C. 1988-2004.82:60-80. Auinger P. Ganzi A. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Schulz C.348:15171526. IARC Monogr Eval Carcinog Risks Hum 2006. Rotnitzky A. Stanek KL.115:521-529.gov/toxprofiles/tp13. Coresh J. Aro A.

Environ Health Perspect 1998. Schwartz J. Environ Health Perspect 2000. Blood lead concentrations in children: new ranges. Payton M. O’Flaherty EJ. cadmium. Amery A. Toxicol Appl Pharmacol 1993. Lauwerys RR. and hypertension in perimenopausal and postmenopausal women. and copper in men. Schulz D.9:303-327. and tibia lead with neurobehavioral test scores in South Korean lead workers. Fourth National Report on Human Exposure to Environmental Chemicals 217 . stable lead isotopes to determine release of lead from the skeleton. Hwang KY. J Hum Hypertens 1995.118:16-29. Stewar WF. Physiologically based models for bone-seeking elements.104(1):60-66. cadmium. Semen quality and reproductive endocrine function in relation to biomarkers of lead. blood pressure and cardiovascular disease in men.209:301305.153(5):453464. Schwenk M. Hickman T. Gavella M. Association of blood lead. Low-level lead exposure and renal function in the Normative Aging Study. Revised and new reference values for arsenic. Pirkle JL. Lustberg M. Schwartz BS. Arch Environ Health 1995. Soldin OP. population to lead: 1991-1994. Flegal AR. dimercaptosuccinic acidchelatable lead. Magder L.140:821-829.S. Wilhelm M. Kinetics of lead disposition in humans. Hanak B. JAMA 2003. Low-level lead exposure and blood pressure. Kaufmann RB. Sparrow D. Gunter EW. Am J Epidemiol 1994. Lee SS. Soldin SJ.Metals results from NHANES III. Jurasovic J.63:1044-1050. IV. blood pressure. Use of endogenous. Nash D. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Brody DJ. Paschal DC.108(1):45-53. Lee BK. Telisman S. Clin Chim Acta 2003. Lee GS. Kidney Int 2003. Pizent A. Weiss ST. et al. Sherwin R. Osterloh JD. Int J Hyg Environ Health 2006. Exposure of the U.327:109-113. Lead. Hu H. Roels H. Rocic B. Cvitkovic P. Am J Epidemiol 2001. Smith DR. Rubin R. Staessen JA. 50:31-37.106:745-750. Kaufmann R. et al.289(12):1523-1531. Environ Health Perspect 1996. lead. zinc. Blood lead.

700-.672) ..800 (..50) 1.800-1.90 (1.300) .30) 3.20-4. predominantly from fish and other seafood.600) 1. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).. which create an episodic potential for volatization and inhalation of mercury vapor.g.90) 3.919) . Some cosmetic skin creams from countries other than the U. 1998. and mercury compounds are still used as preservatives (e. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.60-6.30) 1.90 (4. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. sphygmomanometers and barometers.800-1.300 (. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.. Woods et al.60) 1. Poorly absorbed from the gastrointestinal tract.800 (. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal). such as chlorine (e. Apart from methyl mercury.80 (1.655-.979 (.2.490 (.00 (2.60) 2085 2293 3478 Limit of detection (LOD. 1993).S.g. see Data Analysis section) for Survey year 03-04 is 0. Kingman et al.90 (1. with the highest concentrations occurring in the kidneys (Barregard et al. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.900) 1. elemental mercury is absorbed mainly by inhaling volatilized vapor.12) . an organic form of mercury. and organic forms.500-. merbromin). thermostats and switches). Elemental mercury is a shiny.70 (3.500 (.900 (.419 (.700-. and mining and smelting. Hursh et al.600 (.903) Selected percentiles ( 95% confidence interval) 50th ..00-5.860-1.800-1.927) . 2002).30-6.00) 3.60-2.472-.40 (4. thimerosal.900) 1. 1994. Survey years 03-04 Geometric mean (95% conf. The kinetics of the different forms of mercury vary considerably.797 (.02) .400-.40-2.20-4.90-3.40-1.40-3.574) .30-4.900) .70 (1.80) 3.00-1.g.900) 1.50) Total Age group 1-5 years 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 8373 03-04 03-04 03-04 03-04 .60-6. Also. constitutes the main source of dietary mercury exposure in the general population.20-3.776 (.30 (1.484) .800 (. 2007).363-.00 (.70) 911 856 2081 4525 03-04 03-04 .285-.800-1.400 (.00 (.700-..10) . mercuric chloride).50-3..500) .60-3. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.80 (1. and dental amalgam.S.372) .80 (3. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.00 (. The ingestion of methyl mercury.700 (.90) 95th 4.30) 3. solid-waste incineration.40) 1. Atmospheric elemental mercury can be deposited on land and water.700-.00 (2. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.Metals Mercury CAS No.703-.40 (3.40-1. and is distributed to most tissues. have often required public health intervention (Zeitz et al.50) 4.70-2. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.10-3.80) 1. thermometers.30) 5.70 (1. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.714-. interval) .40-2.80) 4..800-1.60-5.20 (2.60 (2.50-2.90) 90th 3.400-.500 (.50) 5.700) .753-1.40 (4. Accidental spills of elemental mercury.886) . After elemental mercury is absorbed. In addition. 1999 .80 (1.800 (.700-.300-.g. which can bioaccumulate in aquatic and terrestrial food chains. may contain inorganic mercury.00 (.30 (2. sulfur.30-5.00) 1.700) . Other major uses include electrical equipment (e.500-.60 (1. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.00 (1.40 (3.00) 4. 218 Fourth National Report on Human Exposure to Environmental Chemicals .50-1.30-2..689-. IARC.00 (2.418-.70 (4. synthetic organomercury compounds were once used in pharmaceutical applications. population from the National Health and Nutrition Examination Survey.20) 2. or oxygen.814 (.30) 1.877 (.50) 2.60 (1. to form inorganic mercury compounds or salts. inorganic.326 (. electrical lamps.60) 1.40) 3. 1980.30) 4132 4241 03-04 03-04 03-04 .781 (.563 (. phenylmercuric acetate) or topical antiseptics (e.00) .900) 75th 1.00) 1.

50-2.475) . interval) Selected percentiles (95% confidence interval) 50th . the transfer Total Blood Mercury−1999-2002 Geometric mean and selected percentiles of blood concentrations (in µg/L) for males and females aged 1 to 5 years and females aged 16 to 49 years in the U. Geometric mean Survey years (95% conf.90) 2.407) . 1971)..10) 1..500-. and a useful marker of exposure in epidemiologic studies (Grandjean et al.300) .Metals the tissues to mercurous and mercuric inorganic forms.00) .10 (5.600 (. 1973).400-.700 (..825-1. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.10 (1.80 (3.300 (..900 (..10) .824) 1.. 1999-2002.80-3.800) 75th .667 (.27) . Sandborgh-Englund et al.50 (2. 1999).395) ..300) .726-1.329 (.00) 7.90 (3.20) 1.70-3.664-1.820 (.90 (4.300) . Methyl mercury enters the brain and other tissues (Vahter et al.738-..900-1.20-3.30-4..10 (1.297-.700 (.541-.20-3.90 (1. Myers et al...70-5. 1984.10-3.10) .00-2.50-3.90 (4.00 (2. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.700-.269-.800) 1.70-5. 1994). 1990). Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola. thereafter.50) 1.377 (.200-.30) 1. 1975.30) 1. 1996.60 (1.70 (1.20 (.14.01) .30-11. Methyl mercury is incorporated into growing hair.. 1993).50) 95th 2.30-2.60) 1..800-1. Smith and Farris. with most elimination occurring through in the feces (Sherlock et al.500-.800) .90) 2. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al. population.10 (.60) 3.256-.300) . 1991.200-.300) .40-2. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . Vahter et al. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.00) 4.200-.800 (.265-.40) 2. Miettinen et al.50) 3.70-6. 2003).268-.06-1.50-12.30 (1. 1998).20-3.30-6.7) 4.40 (1.900 (.300 (.800) 1.90) 5.200-.30 (.80 (1.00-6.00 (2.500 (.30-4. 1969. 1993). and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al..60 (3.. 1992)..800) ..0) 4. Jonsson et al. 1992 and 1999.40 (1.500-.60) 1.80) 1.00-2.200 (.500 (.700-.60 (1.30) 3..600) . Excretion occurs by renal and fecal routes.20 (2. 1995..30-6.800 (.307 (.299-.833 (.944 (.10-1.00 (2.40-2.377) . 2005).90) 3.10 (3. 1992.40) 5.70 (1.500-.300 (.14 and 0.200-..90 (1.00 (1.70) 1.90) 90th 1.50 (1.500-1.50) 1. National Health and Nutrition Examination Survey.80) 579 527 370 436 588 806 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 219 .70) 4. After exposure to elemental mercury.919) .369) 1.871-1.35 (1.00) 1.70 (1.60) 2.50) 2. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.700 (.800-1.10 (1. 1994.S.374) .60 (1. 2004. a measure of accumulated dose (Cernichiari et al.10 (.29) .90) Sample size 705 872 318 432 387 440 1709 1928 Age Group 1-5 years (females and males) Females Males 16-49 years (females only) 99-00 01-02 99-00 01-02 99-00 01-02 99-00 01-02 .30 (1. Smith et al.900 (.800-1. 1994) and then undergoes slow dealkylation to inorganic mercury. 1998).700-1.697-.300 (. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.60 (3. Suzuki et al. for both acute and chronic exposures.60 (2.73) 1.3) 4.600) .700) 2. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.343 (.20-2.200 (. 2003).800 (.20) .00-1. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.30 (1.02 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.20) .900-1.00-2..317 (.300) . The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.500-. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.940) Race/ethnicity (females.00-3.30-3..06 (.30-5.318 (.00) 1.700-1. 1996). Vimy et al.23) .40-1.40) 1.70-3.00) 6.00) 2. Blood concentrations decline initially with a rapid halflife of approximately 1-3 days followed by a slower half-life of approximately 1-3 weeks (Barregard et al.20-11. McDowell et al.00 (3. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.200-.700 (.30-6.70) 4.

600) .600-.S. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.. population from the National Health and Nutrition Examination Survey. gingivitis.600) .. 1963). 2006. At levels below those that cause acute lung injury...500) . 2005. sensory impairments. insomnia. Smith et al. The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure. DeRouen et al.500-. 2004.600-. 220 Fourth National Report on Human Exposure to Environmental Chemicals . pain in the extremities.600-. and neurocognitive and behavioral disturbances. Bellinger et al. Survey Geometric mean (95% conf.500 (<LOD-.. depression.600 (. In recent epidemiologic studies.700-.. altered physical growth. anorexia.600 (..600-. the existence of a causal relation is unresolved (Chan and Egeland. 1987).. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. hearing impairment. 1998. 2000. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. 1993)..600) .600 (.Metals may be more efficient for inorganic mercury (Grandjean et al. 2005).700-. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. cerebellar ataxia. 2000). Sakamoto et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Smith et al.500-.500 (. 2004). Overt poisoning from methyl mercury primarily affects the central nervous system.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. short-term memory loss. Stern 2005. lower levels of prenatal exposure due to maternal seafood consumption have been associated with an increased risk for abnormal neurocognitive test results in children (NRC... fatigue. and progressive constriction of the visual fields. particularly irritability. and pinkish discoloration of the hands and feet (Tunnessen et al.600 (.600 (.700) 2007 2240 3406 Limit of detection (LOD. 2000.700 (.500 (<LOD-.600 (.500-. which may vary for some chemicals by year and by individual sample.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD ...700-. Drexler and Schaller. and cerebral palsy (NRC. 1995.700 (.600 (. 2004). Factor-Litvak et al.600) . dysarthria.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD ...800) . causing parasthesias.700) size 8147 Total Age group 1-5 years 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .500-. 2002.500 (. Oskarsson et al. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.800) . 1995. hypertension. Once absorbed.700 (. and sleep disturbance (Bidstrup et al. Sakamoto et al. typically after a latent period of weeks to months.500-.700 (. overt signs and symptoms of chronic inhalation may include tremor. < LOD means less than the limit of detection. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.700 (. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. Vupputuri et al. 2003). limb deformities.600) .700 (.. 1996).600) .. irritability. ataxia.500-.600 (.500-. dysarthria. 1983). Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. Inorganic mercury exposure usually occurs by ingestion..500-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1970. Rice. Rissanen et al. The constellation of findings may include anorexia.700) . see Data Analysis section) for Survey year 03-04 is 0. 1951. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. Acute. 2006. 2004. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.42. maculopapular rash.600) . Salonen et al.500-.600) .600) .

960 (.20 (1. 2002).atsdr.05) 1.520) .413-. In Germany the geometric mean for blood mercury was 0.46) 3.930-1.42) 95th 3.00 (.370) .34-3.88) 287 722 1529 03-04 03-04 ..60 (1.68 (2.67-2.530) .416 (.24) 1. 758 children.00) 1.480 (..24 (2. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U..90) 2.33 (2. see Data Analysis section) for Survey year 03-04 is 0. who participated in a 1998 representative population survey (Becker et al.280-.31) 2. 2001.46 µg/L for children.23) 2. average age 9..530-..433 (. Grandjean et al. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.88 (1.430 (.8 years. aged 18 to 69 years.420 (. EPA at: http://www.97) 2.60-2. Benes et al.396-. Among the three racial/ethnic groups.441 (. particularly methyl mercury. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.840-1. These distinctions can help interpret mercury blood levels in people. et al.330-.07 (. 1995.31) 1266 1272 03-04 03-04 03-04 .66) 3. the total blood mercury concentration is due mostly to the dietary intake of organic forms. During the same survey periods.S. range 40 years to 78 years) had an average total blood mercury concentration of 2.330-.14) 90th 2. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.530) .16 (.400 (.509) . and the age-related changes differed across the groups (Caldwell et al.890 (. the median concentration of blood mercury was 0.405-. Fourth National Report on Human Exposure to Environmental Chemicals 221 .epa.254 (.19 (2. 1998)..60) 619 713 1066 Limit of detection (LOD.03-4.360-.555) .340-.14-2.S.580) .19 (1.700 (.05) 3. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.840) 1. slightly higher total blood mercury levels were found in U.200 (. Total blood mercury levels increase with greater fish consumption (Dewailly et al. 2006).30) 3. EPA. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.96 (1.gov/toxprofiles. Kingman et al. 2003).290-.460 (. Over the NHANES 1999-2006 survey periods.28) 1. military veterans (mean age 52.430) . environmental levels) and health effects is available from the U.700-1.440 (. Mahaffey et al.358 (.76-3..78-2. 1998).S. average age 33 years.480) 75th 1.476 (.08 (1. Biomonitoring Information In the general population.09 (2. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.. and increased slightly in non-Hispanic white children (Caldwell.304) ..406-. 2004.250) .463) .89) 3.23) . Urinary mercury consists mostly of inorganic mercury (Cianciola et al.410-.534) .76-4.96 (1.509) .313-.12 (. However.85-2.08 (1. 2000).430 (.870-1.63-2.940 (.78 µg/L for adults and 0.93 (1.58 µg/L for 4645 adults.460) .gov/mercury and from ATSDR at: http:// www.01 (. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning. total blood mercury geometric mean levels in females aged 16-49 years did not change.55 µg/L.840-1.29) 1.360 (.330 (.442-..61) 1. interval) .570) . Information about external exposure (i.88-3.408) .870-1. In NHANES 19992002. adult women in several ethnic subgroups (Hightower et al.492) Selected percentiles ( 95% confidence interval) 50th . total blood mercury increased with age. Schober et al.420 (.770-1.610-1..26 (1. 2009).S.350-.55) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2538 03-04 03-04 03-04 . A cord blood mercury level of 85 µg/L (lower 95% confidence bound = 58 µg/L) is associated with a 5% increase in the prevalence of an abnormal Boston Naming Test (NRC..77-2.382-.S.16 (1. population from the National Health and Nutrition Examination Survey.330-.65) 1..447 (.39-3. 2009).213-.9 years). 2003).160-.Metals standard for inorganic mercury has been established by U.. A cohort of 1127 U.52) 2.13-2. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.18) 2.14.cdc.67-3. Sanzo et al.549) .99-6.360-.e. Survey years 03-04 Geometric mean (95% conf. 2001. 1997.54 (2. From 1996 through 1998.495 (.76-3.

599) .297 (.S.362 (..246-.365 (.696 (.51-2.. Recent studies in children with dental amalgams and urinary levels less than 5 µg/g of creatinine did not have changes in cognitive-behavioral testing when followed for 5-7 years (Bellinger et al. interval) . In the study of U.687) .532 (.289) .485 (.616) .522-.61) 1. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.768 (.23-2.. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine. 2006).619-.S.06 (.667-1.714-1.333-.77 (2. 1998).88 (1.566) .79) 1.32 (1. DeRouen et al.11) 1.11) 2.652) .376-.255 (.358) .64-2.476 (.56) 1266 1271 03-04 03-04 03-04 . 1992).525 (. 2003).39) 1.875-1.67 (1. military veterans with dental amalgams.196-. 1988.620-.301-.400-.1 µg/L for each surface with a dental amalgam (Kingman et al.535) 1.276 (.85) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2537 03-04 03-04 03-04 . the urine mercury increased by approximately 0.969-1.343 (.217 (.00 (.28 (.67 (1.09) 1. 2002).587 (.455-.417) .13 (1.588) . ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.275) .784) 1. reversible increase in urinary N-acetyl-glucosaminidase.455) .65 (1.S..508 (. et al.12-3.384 (.537) .498) 75th . Survey years 03-04 Geometric mean (95% conf.13-2.63) 1.392-.347) ..964-1.447-.07) 1. Levels in U. 2005). et al.30) 2.970 (.464 (. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Department of Health and Human Services noted that several studies have observed a modest.447 (.41-2.46-2. and Italian (Apostoli et al.87 (1.368) . 2009). and on average. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell. a biomarker of perturbation in renal tubular function.35 (1.309-.54 (2.455-.44) 1..31 (1. An expert-panel report recently prepared for the U.385-. 2002) adult population surveys were similar to those in a U.32-2.11-2.365 (. 2009).208-. 2006.909 (.18-1. population from the National Health and Nutrition Examination Survey. Czech (Benes et al. Information about the biological exposure indices is provided here for comparison. women of childbearing age have generally been much lower than these levels (CDC.S.88-2.62 (1. mean urinary mercury was 3.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .30) 1.225-. Biomonitoring studies provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of mercury than are found in the general population.76 (1.463 (.800-1.400) . Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.25 (.545 (.443 (.1 µg/L. Urine mercury and the number of dental amalgams were correlated.265-.40-1.86) 95th 2.280-.480) ..Metals 2000).88-2.630) .06 (.785-1. Urinary mercury levels in recent German (Becker et al. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.404-.391) ...16) 1.40 (1.486) Selected percentiles ( 95% confidence interval) 50th . Langworth et al..S.78-4.01) 2. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.306 (.87) 2.472-.391-. not to imply a safety level for general population exposure.79 (1.00) 90th 1.03) 2.00) 286 722 1529 03-04 03-04 .04-3.990) .21) 1.307-.

S.00 (3.97 (1.17) 95th 5.46 (1.43-1.710) 1.05 (3.03 (.772 (.22-3.526-.S.72) 1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.45) 95th 3.560-.657 (.832-1.632 (.05 (2.833) .30 (1.45 (1. interval) Selected percentiles (95% confidence interval) Survey years 50th .806) .410-. 1999-2002.810) .79) 1.61-6.560 (.606 (.37 (1.32 (1.07-2.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .07-5.16) 5.540-.45-2.565 (.846) .27-1.44) 3.624-.665) .24-1.65) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.706 (.92) 3.21-3.03 (.21 (1.723 (.99 (2.14-2. interval) Selected percentiles (95% confidence interval) 50th .51 (3.615 (.719 (.69-3.664) .32-3.09-1.09-1.25) 2.03) 1.35 (1.97) 2.16-5.909-1.53-3.799) .656-.77) 2. Geometric mean Survey years (95% conf.76 (1.00 (2.70 (2.47) 1.91 (2.500-.56) 4.04-10.580 (.650) 1.637) .55-3.658 (.68-3.850-1.18) 3.30-2. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.65-4.28 (1.84 (2.Metals Urinary Mercury−Females Aged 16-49 Years Old.61) 1.76-5.62 (4.97) 2.553-.605-.46) 3.50 (2.742-1.76) 2.655 (.42) 2.650 (.930) .38) 4. population.831) .87-4.831) .41 (1.520-.540 (.596 (.50 (1.79) 3.69 (1.622-.686) . 16-49 years) 99-00 01-02 .824) .42) 90th 2.870) .51) .63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.07) 1.24) 6.650 (.89 (2.04-1.600 (.699) 1.450-.502-.06 (.32) 2.31-1.582-.724 (. 16-49 years) 99-00 01-02 .13 (2.501-.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .62 (1.13-4.35) .56 (1.83-3. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for females aged 16 to 49 years in the U.22 (. Geometric mean (95% conf.21 (2.774) .27 (2.516 (.31 (1. 1999-2002.45) 2.30 (2.760 (.426-.892) .14.23-1.94) 1.54) 595 531 381 442 594 826 Limit of detection (LOD.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .710 (.685 (.27 (1.81-6.30 (2.740 (.610-.557-.92) 4.47) 1.62 (3.569-.14 and 0.744) 1.23-1.709) 75th 1. population.68 (3.59-5.15-1.387-.639 (.37) 1.84 (2.55) 90th 3.620 (.92) 2.592 (.522 (.636-.14) 3.631-.3) 5.50-4.77) 1. National Health and Nutrition Examination Survey.809) .670) 75th 1.52) 3.99-2.710 (.790) .42-3.41 (2.97) 2.14-1.691) .39-3.616-.81 (3.56) 3.95 (2.57-4.46-4.48 (2.475-.98 (5.68) 3.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.18 (3.966) .99 (3.580-.10-4.41 (1.15 (2.721 (.520-.45) 2.91-7.10-2.910) .00) 2.03-2.420-.41-6.85) 4.85-3.578-.508-.709) .45-3.99) 1. National Health and Nutrition Examination Survey.579-.

Levallois P. Tissue levels of mercury determined in a deceased worker after occupational exposure. Weihe P. Third National Report on Human Exposure to Environmental Chemicals. Drago I. Barbon R. and Se in blood of the population in the Czech Republic. Sci Total Environ 2002. Jones RL. Bernard AM. Locket S. Weihe P. et al. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. and heart diseases. Martin MD. Garrett N. Zn. Bellinger DC. Luis H. Dewailly E. Barregard L. Debes F. Cianciola ME. Barregard L. Brewer R. and lead. Kline J. Centers for Disease Control and Prevention (CDC). Martin MD. Biennow M.72:169-173.2:856-861. Arch Environ Health 1992.61:65-69. Bidstrup PL.62(2):68-72. Leroux BG. Sallsten G. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure. et al. Sallsten G. Seifert B. Grandjean P. Neurotoxicology 1995. Environ Health Perspect 2003. Assessment of reference values for mercury in urine: the results of an Italian polycentric study.111:719-723. Br J Ind Med 1993. Barregard L. Gagliardi T. Arch Environ Health 2001. Lebel G. Seiwert M. Bonnell JA. Environ Health Perspect 2005.16(4):705-710. Caudill SP.50:17-27. Mercury derived from dental amalgams and neuropsychologic function. Bruneau S. et al. Subrt P.19:478-484. Persson G. Sandborgh-englund B. Vahter M. Fish consumption. Trachtenberg F. 2007 TLVs and BEIs. Cox C. McKinlay S. Castro-Caldas A. Woods JS. Markers of early renal changes induced by industrial pollutants. population: 19992006. Becker K. Schulz C. Townes BD. Sallsten G. Schaller KH. Kaus S. et al. Videro T. Cerna M. Attewell R.56(4):350-357.149:301-305. Cent Eur J Public Health 2000. Conradi N. Skerfving S. Snihs JO. 224 Fourth National Report on Human Exposure to Environmental Chemicals . Ayotte P. Clarkson T. Cutress T. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Osterloh JD. Lapham LW.47(3):185-195. Aposian HV.S. ACGIH. Int JHyg Environ Health 2002. Int Arch Occup Environ Health 1988.212:588-598.205:297-308. The concentration levels of Cd. Cincinnati (OH): Signature Publications.289:1324. Seiwert M. et al. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Roels H. Jarvholm B. Mortensen ME. Kaus S. Arch Environ Health 1992. 206:15-24. Lancet 1951. Benes B. Int J Hyg Environ Health 2003. Cernichiari E.113(10):1381-1385. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. mercury exposure. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Bates MN. Arch Environ Health 1969. Cu. Lepom P. Int Arch Occup Environ Health 1999. Berglund B. Greitz U. Environ Res 1998. Daniel D. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.. Chronic mercury poisoning in men repairing direct-current meters. Cernichiari E.77(2):124-129. Lauwerys RR. Geier J. Factor-Litvak P. Bjornberg KA. Weber JP. Jacobs D. Jorgensen PJ. Int J Epidemiol 2004.8(2):117-119. Cortesi I. Tavares M. Int J Hyg Environ Health 2009. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Nutr Rev 2004. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo). Cernichiari E. JAMA 2006. Myers GJ. Jorgensen PJ. Chan JM.295(15):17841792. et al. Enzymuria in workers exposed to inorganic mercury. Atlanta (GA). Buchet JP. Fawcett J. DeRouen TA. Cardenas A. Elia G. White RF. Caldwell KL. Hasselgren G. I.7(3):176-184. Kinetics of mercury in blood and urine after brief occupational exposure. Echeverria D. Spevackova V.Metals References Aberg B. Egeland FM. Niklasson B. Pb. Harvey DG. Budtz-Jorgensen E. Hg. et al. Begg M. Martins IP. Ekman L. Total blood mercury concentrations in the U.33:1-9. Hultberg B. Bernardo M. Barregard L. selenium. Application to workers exposed to mercury vapour. Am J Epidemiol 1999. Rosenbaum G. J Toxicol Environ Health 1997. Falk R. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. Grandjean P. Drexler H.295(15):1775-1783. Metabolism of methyl mercury (203Hg) compounds in man. Health effects of dental amalgam exposure: a retrospective cohort study. Woods JS. Schutz A. Krause C. JAMA 2006. Schulz C. Cejchanova M. 2005. Apostoli P. Impact of maternal seafood diet on fetal exposure to mercury. Kjellstrom T. Becker K. 52:19-33. Schuzt A. Marsh DO. Mangili A. Leitão J. Smid J.

Metals Grandjean P. and Exposures in the Glass Manufacturing industry. Circulation 2000. Hair mercury levels in U. Kolff WJ. Hum Exp Toxicol 1994. Renal and immunological effects of occupational exposure to inorganic mercury.3dimercaptosuccinic acid (DMSA). Lakka TA. Amalgam tooth fillings and man’s mercury burden.S. National Academy Press. Cadmium. Hernandez GT. Voutilainen S. Rice DC. Hightower JM. and polychlorinated biphenyl and other organochlorine concentrations in human milk. methylmercury transport across the placenta via neutral amino acid carrier. National Research Council (NRC).48:247-53. Nyyssonen K. Miettinen JK.112(5):562-570. Boeckx M. Sallsten G. Patterson DG Jr. Bodurow CC. Johanson G. and the risk of myocardial infarction and coronary. Hattula T. Arch Environ Health 1996. Beryllium. Kauhanen J. Greenwood MR.91:645655. Albertini T. Kubota M.77(3):461-467.59(5):692-706.iarc. Available at URL: http:// monographs. Elimination of free and protein-bound ionic mercury (203Hg2+) in man. Kingman A. Lagerkvist BJ. Sandborgh-Englund G. Urinary excretion of mercury after occupational exposure to mercury vapor and influence of the chelating agent meso-2. Mercury.114(2):173-175.90:185-189.95:406-13.13:496-501. Environ Sci Technol 2004. Cox C. Vesterberg O. Mehaffey KR. Sakamoto M. Murata K. Pellizzari E. Hattula T. Hursh JB. Ekstrand J. Sundquist KG. children and women of childbearing age: reference range data from NHANES 1999-2000.38:3860-3863. Clickner RP. and any death in eastern Finnish men. Environ Physiol Biochem 1975.php. Declining risk of methylmercury exposure to infants during lactation. Langworth S. Environ Res 2002. Liu XJ. Elinder CG. Osterloh J.77(4):615-624. Environ Health Perspect 2004. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study. Br J Ind Med 1992. Ann Intern Med 1963. Rissanen T.361:1686-1692. Tillander M. Korolainen A. J Dent Res 1998. Seppanen K.5:214-219. Fish oil-derived fatty acids. Davidson PW. 7/15/09 Jonsson F.70(5):310-314. Ann Clin Res 1973. O’Hare A. selenium. Sakamoto M. Environ Res 1995. and the risk of acute coronary events— The Kuopio Ischaemic Heart Disease Risk Factor Study. Ann Clin Res 1971. Blood mercury reporting in NHANES: Identifying Asian. Native American. Rahola T. Hirayama K. IARC Monographs on the Evaluation of Risks to Humans. Elinder CG. Rahola T.5:252-257. Br J Ind Med 1991. 1999 and 2000. Weihe P.103:2766-2679. et al. Hallen IP. Rahola T. Environ Health Perspect 2004. Schutz A. Allen J. McDowell MA. Toxicol Appl Pharmacol 1999. KajiwaraY. Volume 58. Sampson EJ. Toxicological effects of methylmercury. arsenic. Kubota M. Lancet 2003. lipid peroxidation.112(11):1165-1171. The distribution and biological half-time of 203 Hg in the human body according to a modified whole-body counting technique. 2000. Clarkson TW. Elimination of 203Hg-methyl mercury in man. J Pharmacol Exp Ther 1980.49(6):394-401. Demuth S. Lauwerys RR. Hattula T. Circulation 1995. Relation of a seafood diet to mercury. Mercury in biological fluids after amalgam removal.fr/ENG/Monographs/vol58/index. Schutz A. Cernichari. 1993. Satoh H. Oskarsson A. Palumbo D. Fernando R. Ohlin B. Nakamoto S. Environ Res 2004. Needham LL. International Agency for Research on Cancer (IARC). and multiracial groups. Blood organic mercury and dietary intake: National Health and Nutrition Examination Survey. Nyyssonen K. Environ Health Perspect 2006. Seto DS. et al. Langworth S. Dillon CF. A compartmental model for the kinetics of mercury vapor in humans. Decrease in mercury concentration in blood after long term exposure: a kinetic study of chloralkali workers. cardiovascular. Br J Ind Med 1993. Maternal and fetal mercury and n-3 polyunsaturated fatty acids as a risk and benefit of fish consumption to fetus. Sanchez-Sicilia L. Sandborgh-Englund G. Mercury concentrations in urine and whole blood associated with amalgam exposure in a US military population. Halbach S. Shamlaye CF. Salonen JT. Burse VW. Roels HA. Yasutake A. Washington (DC). Fourth National Report on Human Exposure to Environmental Chemicals 225 . Bolger PM. Arch Toxicol 1996. Skerfving S. The effect of ethanol on the fate of mercury vapor inhaled by man. Pacific Islander. J Dent Res 1998. docosahexenoic acid and docosapentaenoic acid. Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillings in lactating women. The US EPA reference dose for methyl mercury: sources of uncertainty. Ceulemans E.51(3):234-241. Miettinen JK. Nakai K. Kantola M.50(9):814-821. Myers GJ. Akagi H. et al.3(2):116-122. Schultz A. Korpela H.71(1):29-38.155(2):161-168. Adachi T. Acute mercurial intoxication treated by hemodialysis. Brown LJ.214(3):520-527. Rissanen K. Nakano A. Matsumoto S. Salonen JT. et al. Intake of mercury from fish. Barregard L.

Takahashi Y. Amiano P. 1999-2000.40:413-419. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish.79:786789. Farris FF. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. JAMA 2003. Environ Health Perspect 2002. et al.111(12):1465-1470. Sherlock J. Stern AH. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Leroux BG. Blood mercury levels in US children and women of childbearing age. The kinetics of intravenously administered methyl mercury in man. Am J Physiol 1990. Kaye WE. DeRouen TA. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Sandler DP. Smith JC. 226 Fourth National Report on Human Exposure to Environmental Chemicals . et al. Imai H. Zeitz P.Metals Sanzo JM. Goldberg J. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Mooney TF. Bernardo MF. Effects of occupational exposure to elemental mercury on short term memory. Toxicol Appl Pharmacol 1994.37:245-252. Arch Environ Health 1993. Public Health Nutr 2001. Dorronsoro M. Amurrio A.97(2):195-200. Azpiri MA.128(2):25125-25126. Vupputuri S. Environ Health Perspect 2003. Mottet NK. The contribution of dental amalgam to urinary mercury excretion in children. McMahon KJ. et al.98(1):133-142. Toxicol Appl Pharmacol 1996. Vahter M. Martin MD. Suzuki T. Burbacher T. Friberg L. Newton G. Allen PV. Turner MD. Smith RG. Jones RL. Sinks TH. Osterloh J.31:687-700. Woods JS. Bolger PM. The hair-organ relationship in mercury concentration in contemporary Japanese. 1993-1998.124:221-229. Baser M. Leitao JG. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Fisher HL. Lorscheider FL. Orr MF. Environ Res 2005. Stern AH. Daniels JL. Aguinagalde FX. Topping G.2:117-131. Toxicol Appl Pharmacol 1994. Schober SE.4(5):981-988. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Effects of exposure to mercury in the manufacture of chlorine. Nakazawa M. Longnecker MP. Smith JC.48(4):221229. Environ Health Perspect 2007.115(10):1527-1531. Smith PJ. Pediatrics 1987. Langolf GD. McDowell M. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Hislop D. Whittle K. Smith AE. Guo S. Shen DD. Am Ind Hyg Assoc J 1970. Vimy MJ.110:129-132. Environ Res 2005. Most B. Acrodynia: exposure to mercury from fluorescent light bulbs.289(13):1667-1674. Br J Ind Med 1983. Matsuo N. Yoshinaga J. Hongo T. Tunnessen WW. Lind B. Methyl mercury pharmacokinetics in man: a reevaluation. Vorwald AJ.258(4 Pt 2):R939-945. Hum Toxicol 1984. Hall LL. Patil LS.

aldehyde dehydrogenase.7 (45.1-88.5) 80.4) 56.5 (67.8 (82. which exert homeostatic regulation over molybdenum balance.6) Selected percentiles ( 95% confidence interval) 50th 50.6-55.5-41.6-42.4) 42.4) 49.0-110) 90.7-105) 69. 01-02. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.2-70.7-39. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.1 (71.7) 78.3) 85.0) 39.6) 71.7 (58. and 1. In humans.2-37.3 (46.7 (44.5) 47.1-48. 2001. respectively.7) Sample size 2257 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 78.0 (48.5) 80. chemical reagents in hospital laboratories.9) 62.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52.2 (61.0-65.2) 48.1) 46.7 (51. lubricants.1) 126 (106-147) 109 (94. WHO.2 (40.6-46.0-77.7-68. 0.1-63.0) 54.0) 60.4) 41.5 (49.2) 53.5-52.6 (55.6-82.1) 35. More recently.2 (49.7-96.0-85.7) 46. 7439-98-7 General Information Elemental molybdenum is a silver-white.8-90.0-62.2-91.3) 65.8-108) 87.2) 37.3 (47.3 (55.7-122) 93.8.7-50.2) 40.6) 93.3 (37.0-100) 63.Metals Molybdenum or ore deposits. At a daily oral molybdenum dose of 24 µg.7) 86.9 (37.7-84.9 (40.2 (55. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.7 (71.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.4 (34.1-59. interval) 45.6-96.1) 57.8) 75.3 (55.1) 82.8.3) 41.7 (50.5-91.2) 79.9 (34. population from the National Health and Nutrition Examination survey.9-85.1 (91. hydrogenation catalysts.3-44.6 (40.3) 47. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0-71.6 (40.3 (73.5-66. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.3) 83.9) 67.7) 78.8) 46.4) 52. urinary excretion over six days CAS No.9 (33.6 (55.9 (78.2-53.9-55.3 (71.2) 41.4 (48.5 (81.3 (64.2-59.1-52.8 (42.2 (83.4) 45.9 (52.0) 55. see Data Analysis section) for survey years 99-00.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.6) 53. semiconductor and battery industries have begun to use molybdenum.7 (73.0 (41.0) 84.3 (79.9-83.5-124) 108 (92. Fourth National Report on Human Exposure to Environmental Chemicals 227 .3-75. 2001).5) 44. Excretion occurs predominantly via the kidneys.4-82. Compounds of molybdenum are also used as corrosion inhibitors.9) 34.5) 85.6) 121 (103-139) 133 (113-155) 121 (106-143) 153 (126-188) 132 (121-147) 117 (109-129) 135 (119-154) 117 (108-129) 107 (99.8) 40.6 (73.7-41. and xanthine oxidase (Kisker et al.8 (85.9 (32.2) 178 (147-259) 169 (138-197) 138 (127-152) 146 (112-171) 145 (129-159) 118 (105-125) 126 (114-134) 114 (103-124) 105 (98.1-44.7) 77.5-46.2) 52.0 (81.8) 39.3-115) 152 (120-217) 177 (142-207) 152 (141-169) 206 (150-274) 166 (147-170) 156 (135-175) 187 (146-223) 152 (134-180) 130 (119-142) 780 683 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD. and 03-04 are 0.5 (48.9-56.7 (36.3-108) 215 (161-278) 169 (145-194) 148 (136-163) 154 (132-180) 158 (130-177) 127 (114-139) 1121 1335 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 47.0) 62.2 (56.4 (80.5.4) 76. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.2-79.8-46.3-47.1) 59.5 (41.7) 75th 84.4 (72.3 (53.9-82.1-55.2 (63.5 (37.9 (73. and paints.0 (43.7-60.7) 57.5-65.6 (43.6-62.9-109) 97.2 (69.7-92.1-52.0-53.8-106) 88.5-68.7-91.4 (48.1) 60.7 (37.8-94.1 (38.5 (43.5 (41.4-52.7-51.4-61.2 (49..1 (34.0) 97.6) 71.5) 60.2 (38.6-72.8-49.8) 48.7-73. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.0-56.0) 45.9-55. 1997).0-101) 82.3) 37.0 (42.2-59.3) 54.4 (79.0 (42.4-75.7) 45.2-42. inks.0-38. 1996).5-52.7) 51.3-91.6 (52. and in pigments for ceramics.3 (84. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.8 (67.S.0 (76.6) 51.9 (44.1-51.0 (46.5 (74.8) 44.7-47.6-58.3 (38.

5 (39.1-45.6-76.5 (41.9-41.8 (90.1 (33.9-87.7-137) 129 (109-155) 112 (97.2-96.9 (40.3-141) 109 (81.2-80.5 (37.5-62.9-71.7) 112 (95.3-56.8) 39.1-39.5 (40.0) 53.9 (35.6-41.5-46. U.2 (37. EPA. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.4) 48.4 (56.1 (37.0-133) 119 (88.1-81..0) 33.Metals was 18% of the ingested dose.7-40.0) 39.6-61.5-50. 1997).0-120) 85.6 (71.5 (38.3) 37.5 (35.5) 60.5-45.9-45.2 (40.7-44.1 (82.S. 1993).1-109) 89.5-60.2) 58.9-68.3 (37. and urinary levels reflect intake from all sources.8-46.1-100) 86.8) 71.9) 41.7 (75.4-107) 85.8-52.0) 39.9-61.2 (43.0 (58.9 (49.8) 38. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.9 (36.4 (53.3-52.7) 42.3) 40.4 (59.4-120) 101 (84.2) 42.2-40.5 (80.5) 73.3 (37.4 (40.5 (65.7-52.9) 44.5 (83.2-49.5 (54.2-121) 107 (92.2) 43.0-56. Based on studies finding adverse reproductive effects in rats and mice.9) 40.3 (36. Biomonitoring Information Molybdenum is an essential element for health. population from the National Health and Nutrition Examination survey.7) 53.0) 72.6) 43.2 (50.3) 64.4-76.2 (52.3-43.1) 37.9 mg/kg/day and established a tolerable upper intake level of 0.2) 37.2 (40.5 (78.1-39.5-48.9) 92.2 (36.2) 37.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42. and clinical or epidemiologic evidence of adverse effects is limited.2) 42.5-44.8-84.2) 55.8) 38.0 (74.6-88.9) 31.1) 40.4 (67.3) 41.3) 56.5-119) 90.S. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.1-67.4) 77.9-96..2-46.5 (35.3 (36.8-42.1-34.9-117) 57.1-38.5 (79.3-44.6 (42.8 (36.7-120) 87.2 (73.1-43.7 (30.0-38.4) 58. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3 (83.8 (37.9 (64.8) 61.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.7) 75th 63.0) 62.2 (57. 1995).3 (58. Molybdenum is generally considered to be of low human toxicity.5-35.0-46.6) 36.4-39.4-41.6-45.3-46.4) 116 (101-126) 104 (88.3-102) 122 (116-147) 123 (109-139) 118 (101-134) 310 368 290 648 762 725 1299 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 40.4-106) 85.6-63.3-59.8) 45.6 (36.7) 45.2 (33.4 (78.1) 37.8-66.5 (39.5-99.9) 79.1 (30. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.03 mg/kg/day in humans (IOM.0 (80.7-93. at daily oral doses of 95 µg and 428 µg.9-118) 91.3) 61.4) 47.1-79.9-40.1-41.5 (36.9 (64.1) 56. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.1-127) 90.2-41.5) 63.7 (77.6) Selected percentiles ( 95% confidence interval) 50th 41. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7 (66.0) 36.4) 40.6) 48. but available epidemiologic data are scant.0) 38.7-62.4) 44.2) 39.6-61.4) 60.2) 38. In industry.1 (42.8) 79.3 (71.8-118) 81.1 (39.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.8-65.4 (44.7-43.6) 39.4) 61.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.6-63.5 (34.1 (40.4) 89.5 (65..7) 41.0) 88.3) 44.6-78.4-66.5 (59.5-97.1) 101 (83.1 (44.5) 90th 108 (97.4-42.9-42.2-47.8 (57.4-185) 106 (94.0) 44.1 (54.0-46.9 (73.2 (69. interval) 43. 1999).1-112) 78.3-115) 98.5 (37. 2001).3-68.3) 57.7) 62.3) 43.7) 115 (93.8-67.2-96.1) 65.5) 72.5 (41.1-40.4 (37.5 (40.6 (38.8 (56.9 (79.5-69.6) 39.3 (71.9-45.4 (55.1 (38.9 (39.6 (36.9 (39.2-65.2 (40.8) 37.8) 62.3 (55.3-45.1-43.8-47.1) 43.0 (35.1 (38.5) 71. urinary excretion over six days rose to 50% and 67%. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.5-70.8 (75.6 (59.7) 57.4) 122 (107-133) 109 (99.5 (50.4-118) 172 (131-195) 138 (120-163) 118 (106-134) 780 682 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites 228 Fourth National Report on Human Exposure to Environmental Chemicals .6 (57.3 (53.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.0-41. 1961.8-47. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.2) 39. of the ingested dose (Turnlund et al.5-92.3 (51.0-103) 103 (90.7-100) 77.1 (49.7-38. respectively.

56:322-327. In: Trace elements in human nutrition and health. Molybdenum 1993 [online]. vitamin K. 420-441. 2005). Peiffer GL. iron.nap. 1996. Kisker C. 4/14/09 White MA. Sciarra G. vanadium. Washington. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC.Metals in urine for the U. molybdenum.nih. Fourth National Report on Human Exposure to Environmental Chemicals 229 .epa. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Koval’skiy GA. 1998. 4/14/09 Iversen BS. Occupational risk factors of lung cancer: a hospital based case-control study. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Analyst 1998.66:233-267. copper.22(3):179-191. Available at URL: http://www. Environmental Protection Agency (U. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Yarovaya GA. (DC): National Academy Press. Keyes WR. nickel.gov/index. boron.216:253-270. Ronchi A.123(1):81-85. Turci R.niehs. excretion. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1998). White and Sabbioni. silicon. 2001. EPA). pp. van Sprundel MP.. chromium. Zhurnal Obshchey Biologii 1961. 2001). Schleyerbach U. Molybdenum absorption.15(2-3):149-154. edu/openbook. Ann Rev Biochem 1997. Food and Nutrition Board. 144-154. 16:1313-1319.htm. Christensen JM. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Aprea C. National Toxicology Program (NTP). TR-462. A study of 13 elements in blood and urine of a United Kingdom population. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. arsenic. Available at URL: http://books. et al. iodine. X. Kristiansen J. Weyler JJ. Available at URL: http://ntp..S. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Institute of Medicine (IOM). World Health Organization (WHO).62(4):790-796. Trace element reference values in tissues from inhabitants of the European Union. Gatti A. Sci Total Environ 1998.S. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Minoia C. Dietary reference intakes for vitamin A. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Molybdenum. Geneva: WHO. Minoia et al.gov/iris/ subst/0425. Occup Environ Med 1999. Sabbioni E.S. Sabbioni E. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Schaub J. 2005. Am J Clin Nutr 1995. White MA. Menne C. Rapid Comm Mass Spectrom 2002.. Shmavonyan DM. J Trace Elem Med Biol 2001. Rees DC. pp. 4/14/09 Sievers E. Third National Report on Human Exposure to Environmental Chemicals. Turnlund JR. U. Atlanta (GA). and zinc: a report of the Panel on Micronutrients. 2002. Droste JHJ. References Centers for Disease Control and Prevention (CDC). Molybdenum in infancy: methodical investigation of urinary excretion. Van Meerbeeck JP. Vermeire PA. Schindelin H. manganese.php?record_id=10026&page=420. Biomonitoring studies on levels of molybdenum can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of molybdenum than are found in the general population.

g. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.04.04. respectively. 01-02. dental alloys. carboplatin) in the treatment of cancer. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. 230 Fourth National Report on Human Exposure to Environmental Chemicals . Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. and iron. population from the National Health and Nutrition Examination Survey. Platinum compounds are used in electrodes. and high catalytic activity. and as drugs (e. and 0. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. see Data Analysis section) for Survey years 99-00. 7440-06-4 General Information Platinum is a silver-gray. however. as oxidation catalysts in chemical manufacturing. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. strength at high temperatures.Metals Platinum CAS No. thick-film circuits printed on ceramic substrates. cisplatin. Important properties of platinum are resistance to corrosion. and 03-04 are 0. 0. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. < LOD means less than the limit of detection.07. copper. which may vary for some chemicals by year and by individual sample..S. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. the ambient air concentrations of platinum associated with its use in automotive engine catalytic converters are estimated to be thousands of times lower than occupational exposure limits.. jewelry. 1998).

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.. intravenous medicinal use. or organometallic). When ingested or inhaled. 1975b).Metals doses or at biomonitored levels from low environmental exposures are unknown.g. Fourth National Report on Human Exposure to Environmental Chemicals 231 . whereas soluble platinum compounds (e. The pharmaceutical cisplatin is an animal carcinogen and reasonably anticipated to be a human carcinogen as determined by NTP.. Information about external exposure (i. Most absorbed platinum accumulates in the kidneys and is excreted in urine (Moore et al. Platinum metal is biologically inert. 1975a. population from the National Health and Nutrition Examination Survey.. Toxicity is determined by the type of compound (e.g. metallic.e. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. oral). platinum metal and insoluble salts are very poorly absorbed (<1% of a dose) and cleared from the body within a week after a single dose. Animals exposed to cholorplatinate salts used in industry have demonstrated severe hypersensitivity with asthma-like symptoms and anaphylactic shock (Parrot et al.S. route of exposure (e. or recommended for the metal form by NIOSH (Czerczak and Gromiec.. 1969. The carcinogenicity of other platinum compounds remains uncertain.. Workplace air standards for external exposure are established for soluble salts of platinum by OSHA and ACGIH. Saindelle et al. inhalational. 2000). environmental levels) and health effects is available from Urinary Platinum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 1969). cutaneous.g. and duration of exposure. inorganic salt.. halogenated salts) encountered in occupational settings can cause platinum salt hypersensitivity with symptoms that include bronchitis and asthma after inhalational exposure and contact dermatitis after skin exposure. Platinum metal and insoluble salts can produce eye irritation.

References Becker K. Stilianakis NI. 2003). Fruhmann G. Herr CE. Biomarkers 1999..005 µg/L (Iavicoli et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kulka U.. Hysell D. Raab W. Urinary excretion of platinum from platinum-industry workers. Several studies have shown that background concentrations in general populations were usually less than 0. J Expo Anal Environ Epidemiol 2003. Turfeld M. Ruff F: Platinum and platinosis.inchem. Arch Environ Health 2001. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. 3/31/08 Moore W Jr. Allergy and histamine release due to some platinum salts. Analyst 1998. eds. et al. and gold excretion of patients after insertion of noble-metal dental alloys. Platinum. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Iavicoli I. Seiwert M. Saindelle A. Fries HG. Gieler U. and in blood and urine in the United Kingdom. Cohrssen B. Petrucci F.13(1):24-30. New York: John Wiley & Sons. Saindelle A. Levels of platinum in urine for the U. 1999. Duneman L:Long-term urinary platinum. Influences on human internal exposure to environmental platinum. 2004). 5th ed. Herr et al. palladium. pp. Gromiec JP. In: Bingham E. Nowak D. Senofonte O. Begerow J. Carelli G.org/documents/ehc/ehc/ehc125. Crocker W.04 µg/L) in this Report. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Environ Health Perspect 1975b. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al.. Schierl R. Pethran A. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Nickel. Pethran A.35:313-321. Ewers U. Uptake of antineoplastic agents in pharmacy and hospital personnel. 1998). Blanks R.123(3):451-454. Boos KS. population were below the limit of detection (0. Br J Pharmacol 1969. 2001). Hysell D. Occup Environ Med 2004. which elevate urinary platinum by five to twelve-fold (Begerow et al. Herr et al. Hebert R. Schulz C.. Biomonitoring of traffic police officers exposed to airborne platinum. Kuster W. Kazantzis G. Jankofsky M.56(3):283-286. osmium.4(1):27-36. 2004) or less than 0. Schierl R. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect..Metals the International Programme on Chemical Safety at http:// www. Pethran et al.01 µg/L (Becker et al. 289-380. Angerer J.207(1):69-73. International Programme on Chemical Safety (IPCS). Czerczak S. Ensslin AS. Modest (ten-fold or less) elevations in urinary platinum concentrations were associated with handling of cisplatin and carboplatin by pharmacy and other hospital personnel (Ensslin et al. Int Arch Occup Environ Health 2003.55(2):138-140. 2003. Patty’s Toxicology.76(1):5-10. Hall L.. 1991 [online]. Hauff K. Moore W Jr. 206:15-24. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Environmental Health Criteria 125. Ruff F: Histamine release by sodium cholorplatinate. Urinary platinum levels associated with dental gold alloys. Int Arch Occup Environ Health 1997. rhodium.S.9:152-158.61(7):636-9. van de Weyer C. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine... Available at URL: http://www.htm. 2003. ruthenium. International Journal of Hygiene and Environmental Health 2003. Schierl. Campbell K... palladium.70(3):205-208. Schulz C. Schierl et al. Arch Environ Health:1969. Int J Hyg Environ Health 2004.inchem. Schierl R. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Biomonitoring studies on levels of platinum provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of platinum than are found in the general population. Grimm CH. Schierl R. Powell CH. Rommelt H.19:685-691. 1997. Thornton I. Platinum concentrations in urban road dust and soil. 2004. Parrot JL. Part 1: monitoring of urinary concentrations. Kavanagh P. Seifert B. Environ Res 1975a. Biomonitoring Information Urinary platinum levels reflect recent exposure. Wilhelm M. Wilhelm et al. et al. Huber R. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.htm.org/documents/ehc/ehc/ ehc125. Farago ME. 1998). Bocca B. 2000. Alimonti A.10:63-71.. et al. and platinum. et al. Kelly J. 2003. Kaus S. Occup Environ Med 1998. Neuendorf J.

172) .290 (.190 (. the latter being the current major industrial consumer of thallium in this country.201 (.380-.300-.181-.210) .173) .290) 90th .410-.490) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.420) .300 (.202 (.270) .430) .147-.410-.270 (.260 (.340-.239) .Metals Thallium depilatory cosmetics.500) .156) .182-.260 (. Thallium disappears from the blood with a half-life of several days.156-.200 (.400) 95th .490) .400) .250-.240) .144 (.218) .180-.400 (.150-.490) Total .217 (.177) .290) .160-.150-.440-.470 (.280-.202 (.280) .165) Sample size 2413 2653 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .340-.250-.270 (.183) .147-.450 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.510 (.420 (.260-.160-. see Data Analysis section) for Survey years 99-00.260) . it has not been specifically mined or refined in the United States since 1984.360 (.180-.250-.170) .180-.200-.180-.450) .225) .320) .200) .300) .170 (.350-.250 (.550 (.156) .300) .163) .340-.185 (. 0.178) .350 (.220) .250-.460-.270-.520 (. thallium readily crosses the placenta and also distributes into breast milk.380 (.190-.340) . From these and other sources.400 (.187-. and 0.250-.370 (.520) .450 (.460) .185-.380 (.170-.360 (.160-.380-.460 (.147-.160 (.230) .360-.370 (.260-.206) .196) .140-.290 (.145-.170 (.02.220 (.150-.310 (.218) .159 (.420) .480) .430 (.190 (.170-.400-.450 (. 01-02.220 (.240-.160-.160 (.350-.250 (.430-.330-. and 03-04 are 0.640) .160 (.330-.240) .400 (.410-.440 (.390) .280 (.370-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.230 (.190 (. thallium was obtained as a by-product of smelting other metals.450 (.320-.200-.202) .280-.370 (.210 (.320) .400) .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.430) .400-.250-.340-.330-.02. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.370-.200) .300 (.270-.179-.220 (.350) .196) .230-.330) .410 (.240-.190 (.155 (.480) .430 (.290 (.370 (.290 (.158) .410-.410) .370 (.410 (.170-.500) .400) .197 (.250) .260-.280) .420) .390) .400-.171 (.145-.290 (.148-.450 (.270 (.145 (.200) .167-.300 (.410-.230) .380) .330-.191 (.330) .146 (.172 (.360 (.490) .420-.290-.320 (.149 (.520) .480) .350 (.290) ..470 (.200) .220) .S.190 (.390-.170) .390) .360 (.250-.450 (.200-.370-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.310-.440 (.270) .170-.154-.180 (.260-.450 (.360-.520) .270 (.160-. however.370 (.300) .320) .450 (.135-.160 (.260-.340) .280 (.420-.410 (.440) .230) .390-.300) .172 (.410-.310 (.330-.210-.460) 336 362 290 697 746 725 1380 1545 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .330) .160 (.560) .220) .220 (.220) .220) .180 (. Human health effects from thallium at low environmental CAS No.188) .370) .480) .370) .350-.150-.243) .180) .215) .470) .500 (.420-.350-.240) .184 (.410 (. In the United States.360-. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.280 (. respectively.200 (.430-.400-.165 (.310 (.420) .167-.470) .250-.200) .510) .410 (.490 (. 2005). interval) .290 (.170) .170-.170-.280) .240-.290) .510) 1200 1313 1281 1213 1340 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .176 (.330-.370-.350) .150-.201 (.480) .137-.197-.360) .340 (.350-.390-.175) .133-.420-.400 (.170 (.630) .400 (.390 (.153-.150-.200-.330-. In addition.134-.430 (.390 (.02.430-.420) . thallium has been restricted from use in rodenticides and Urinary Thallium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.360-.500) .200 (.217) .230-.159 (.350-.270 (.200 (.167 (.260 (.330) .200 (.590) .200) .420) .220-.390-.590) .230) .210 (.290) .360-.400-. In the past. representing distribution into other tissues.192) Selected percentiles ( 95% confidence interval) 50th .159 (.170-.410 (.180 (. population from the National Health and Nutrition Examination Survey.183) .430 (.162-.470) .180) 75th .290-.230-.173) .420) .440 (.370 (.450 (.190 (.270-.440) .220) .200 (.157-.440) .400) .690) .440 (.220 (. Fourth National Report on Human Exposure to Environmental Chemicals 233 .390) .310) .173-.

and a drinking water standard has been established by U.229-.198-.218 (.148-.297 (.333 (.267-.364 (.278-.189) .151-.328 (.456) .377) .142 (.160-.350) .280) .300) .241) .176) . neurologic injury. Biomonitoring Information Urinary thallium levels reflect recent exposure.153 (.424 (.146 (.238-.362) .304) .306-.167 (.153 (.156 (.160 (.412) 1200 1312 1281 1213 1340 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .atsdr.214 (.238) .150) .321 (. population have been well characterized in NHANES 1999-2000 and 2001-2002 Urinary Thallium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.215) .191-. interval) . 1992) Workplace air standards and guidelines for external exposure are established by OSHA and ACGIH.273 (.143-.328-.233) . Levels of thallium in urine for the U.254-.152) .293) .255 (.304) .162) .169 (.155 (.184-.194 (.138 (.317 (.164) .217-.400-.147-.203-.208-.171-.208-.215 (.212) .250) .161) .182 (.254 (.338-.346) .380 (.179) .313-.169) .370 (.300-.207-.184-.172) .333 (.369) Total .326-.369 (.383 (.153-.155-.333-.235 (.173) .158 (.271-.198-.149-.286 (.207 (.229) .159) .185 (.271-.135-.153 (.343 (.158) Sample size 2413 2652 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .211 (.166 (.363) 861 674 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites 234 Fourth National Report on Human Exposure to Environmental Chemicals .156) .237) .329) .149 (.389) .274-.200-.151) .317 (.156 (.286-.246-.161 (.286 (.264 (.318-.282 (.224 (.312 (.402) .137-.214) .208) .317) .160) .200-.171) .286) .278-.338 (.Metals doses or at biomonitored levels from low environmental exposures are unknown.e.160) .205 (.S.221 (.198-.167 (.278) .158-. population from the National Health and Nutrition Examination Survey.353) 336 362 290 697 746 725 1380 1544 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .300) .135-.221) .146-.176) .140 (.291-.162) .146-.154 (.217-.184-. arthralgias.286-.412 (.356) .269 (.266-.258 (.319) .244-.248) .148-.200-.222) 90th .244 (.306 (.260 (.325-.333-. and polyneuropathy.187-.204 (.188 (.307 (.297 (.143) .306-.304) .147-.286 (.143 (.211 (.125-.198) .297) .300 (.364 (.169-.149) .293 (.168 (.152) .250-.155) .141-.153-.S.161) .289) . environmental levels) and health effects is available from ATSDR at: http://www.154 (.196 (.350 (.153) .202 (.226) .282-.149-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.173 (.278) .231) .216 (.197-.146 (.389-.271-.356-.458) .217) .259) .234-.207) .146-.226-.180-.html.263-.532) . and death.237-.283 (.258-.200 (.161 (.162-.340-.222) .600) .167 (.142 (.365) .424) .170) .157 (.214) .119-.170-.167 (.194 (.301-.134-.148-.148 (.287-.337-.375 (.292 (.142-.286 (.272 (.170) .162) .348 (.324) .154 (.327) .145 (.133-.200) .181) .206 (.140-.144-.213 (.164) .197) .222 (.153 (.148-.250-.214 (. Peripheral neuropathy and alopecia are well-documented effects of acute and chronic exposures.191-.180) .133 (.377) .412 (.231-.342) .140 (.192-.146) .177) .156 (.389) .152) .402) .167-.364) .146) .273-.192 (.364) .348) .167) .159 (.273-.162 (.148 (.281-.230) .153-.333) .145) .462) .269) .313 (.128 (. Information about external exposure (i.313-.166 (.321) .156 (.167) .299-. respectively.136 (.214-.204) .304 (.gov/toxpro2.167-.144-. EPA.236) .346-.210 (.223 (.233 (.160) 75th . Relatively high-dose intentional or accidental ingestion can result in gastrointestinal symptoms followed by multiorgan failure.366 (.333-.143 (.272-.171) . although additional mechanisms of action are possible.128-.278) .192-.176) .196-.366) .147-.150) .383) .235-.178 (.304) 95th . (ATSDR.243) .462) .145-.173) Selected percentiles ( 95% confidence interval) 50th .289) .153) .378 (.387) .278 (.240) .154 (.S.159-.157-.260-.cdc.280-.145-.349 (.153 (. IARC and NTP consider the evidence for the carcinogenicity of thallium as inadequate or unclassifiable.143-..361 (.458 (.287 (.330-.122-. Chronic high-level exposures have been associated with weight loss.271-.323 (. Thallium produces toxicity by replacing intracellular potassium in the body.387) .219) .222-.179-.265-.135-.215-.176) .222 (.157) .348-.129-.422) .162-.221) .469) .223) .333) .368 (.155-.227 (.131-.343 (.313 (.256 (. Severe accidental thallium poisonings from ingesting of rat poisons that contained water-soluble thallium salt have occurred.278 (.307) .

Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Dolger R.47(3):223-231. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U.atsdr. A study of 13 elements in blood and urine of a United Kingdom population. 1980. Trace metals in urine of United States residents: reference range concentrations.. Third National Report on Human Exposure to Environmental Chemicals.gov/toxprofiles/tp54. Int Arch Occup Environ Health 1980.1 mg/m3 (Marcus. Minoia C. Sci Total Environ 1990. 2005. Toxicological profile for thallium.113(1):47-53. 1981. White MA. Valentin H. There was no increase in the prevalence of symptoms at levels less than 20 μg/L and only a slight increase in nonspecific symptoms greater than 20 μg/L. Ting BG. Brockhaus A.95:89-105. 1998). Gallorini M. Available at URL: http://www. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Schaller KH. Ewers U. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Paschal et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Sci Total Environ 1998. et al. Pietra R. Challeton-de Vathaire C. 1985). A study of 46 elements in urine. Morrow JC. X. Buhlmeyer G. 2005) and are shown with results from NHANES 2003-2004 in this Report.76(1):53-59. 1992 [online].S. 1990. Kramer U. Biomonitoring studies on levels of thallium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of thallium than are found in the general population. Centers for Disease Control and Prevention.. Manke G.Metals (CDC.216:253-270. Radiat Prot Dosim. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Investigations of thallium-exposed workers in cement factories. Trace element reference values in tissues from inhabitants of the European Union. References Agency for Toxic Substances and Disease Registry (ATSDR). Cassot G. Boisson P. Investigation of a working population exposed to thallium. Minoia et al. Trace element reference values in tissues from inhabitants of the European community I. et al. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. et al. Martin J-C. Pirkle JL. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Celier D. Sabbioni E. Pozzoli L. 1998. 7/15/09 Blanchardon E.48(4):375-389. J Soc Occup Med 1985. 2005. Environ Res 1998. (1981) studied 1.html. Apostoli P.5 μg/L. Raithel HJ. Wiegand H. White and Sabbioni. Schmidt M. Atlanta (GA).cdc. Fourth National Report on Human Exposure to Environmental Chemicals 235 .. Brockhaus et al. Paschal DC. Sampson EJ. Marcus RL. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Soddemann H.35(1):4-9.265 people living near a thallium-emitting cement plant in Germany. with concentrations ranging up to 76.. Int Arch Occup Environ Health 1981. blood. and serum of Italian subjects. Jackson RJ. Schaller et al. Sabbioni E.

Occupational exposure is from dusts released during grinding or drilling of hard metals.500 (.380 (.260 (.330) .120-.060 (.090-.380-.450-. respectively.570 (.120) .090-.080-.330-.160 (.092) .200) .110 (.130) .080) 75th .140-.180-.100 (.150-.104) .088 (.065-.430-.090 (.060-.320-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.570 (.080 (.270-.130-.090 (.350 (.460) .130) .090) .04.360) .204) .107 (.080 (.390 (.460 (.113 (.082 (.074-.00) . Evidence is lacking for the carcinogenicity of tungsten.350-1.560) .400 (.111-.116) .830) .04. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.062 (.110 (.060-.090) .53) .380-.270-.160 (.080) .290-.070-.095-.510-1.260 (.290-.300 (.420-.113 (.250) .151) .090-.060-.120-.210 (.490 (.084) .050-.530 (.069-.300 (.080 (.066-. and 0.290 (.190 (.310-.060-.370-.430 (.240 (.380-.400) .430-.130) .800) .270-.330) .132) . Tungsten compounds are used as lubricating agents.550) .070 (.160-.620) .470) .190-.105 (.300) .630) .137 (.530 (.090-. Little information is available on the toxicity of tungsten.250-.210 (.050-.370 (.096 (.370 (.120) .068) .550) .110-.160 (.140 (.320-.350) .069) .090-.130 (.130-.120-.170 (.230-.310 (.360-.170-.070) .310-.330 (.050-.110-.064-.400-.130) .058-.060 (.126) .110 (.270-.160-.110-.Metals Tungsten CAS No.370) .470 (.078) Sample size 2338 2652 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .070 (.070) .180 (.370-.590) . Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.180 (.410-.170) .071-.123-.077-.160) . filaments for incandescent lamps.100 (.070-.240-.100) .135) .160 (.080 (.580) .120) .190) .450 (.460 (.073 (. mainly as scheelite (CaWO4).950) .280 (.560) .260-. and as catalysts in the petroleum industry.090 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.101 (.380) .310-. and 03-04 are 0.160-.440) .140 (.270 (.200 (.460) .300) 95th .370 (.160) .100 (.101-.093-.470-.810) .250) .360 (.290) .770 (.380 (.097-.150 (.158 (.060 (.220) .150 (.340-. which is used in the steel industry.220) .230-.350) .095-.120-.170 (.086 (.530 (.250) .410 (.380-.220-. bronzes in pigments.180) .073) .080-.340) .250) .520) .130 (.100) .460) 1160 1307 1281 1178 1345 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .080) .056-.084-.090-.04. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.096-. which are used in rock drills and metal-cutting tools.100-.105) .230-. population from the National Health and Nutrition Examination Survey.490) .060-.110) .113 (.120-.430) .340-.093 (.290) .340-.073-.091) .350) .130) .090-. 0. 236 Fourth National Report on Human Exposure to Environmental Chemicals .080-.560) .109) .360 (.400 (.250) .620) .060-.560 (.310) .060 (.100-.190-.050-.230) .210 (. 01-02.190-.210-.550) .140-.210) .120 (.220) .090) .092 (.460 (.120) .150 (.160-.133) .100-.080) .140) 90th .300-.550 (.110 (.070) .230-.320 (.270 (.420-.210 (.130-.093) .082) .070-.180-.180) .230) .520) .087) .090-.180) .790) .510-. interval) .220 (.400 (.430) 320 363 290 679 744 725 1339 1545 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .120-.320 (.310-.100) .290-.300 (.640 (.100) .470 (.087-.076 (.084 (.088) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).070) .330-.170) .090) .250-.500 (.690) .110 (.071 (.160 (.056-.082 (.076 (.180) .260) .430 (.140 (.082-.170) .200-.150) .120) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.390) .100) Selected percentiles ( 95% confidence interval) 50th .320) .100 (.073-. see Data Analysis section) for Survey years 99-00.190-. and for producing ferrotungsten.310-.081 (.190 (.230 (.500) .430 (.070-.122) .360 (.670) .250) .260-.070 (.180-.140 (.800) .280 (.065 (.080 (.062 (.060 (.S.210 (.260-. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.510 (.078-.270 (.100) .180-.113 (.070-.170) .130-.620 (.650) . Tungsten is used mainly for producing hard metals.092 (.060 (.480) Total .120) .470) .560) .400 (.280-.110) .360-.520) .

167) .075) .057-.153) .084) .120) .315-.186 (..167) .(Kraus et al.431) .071) .158) .090-.073 (.146) .095) Selected percentiles ( 95% confidence interval) 50th . Nicolaou et al.121 (.091) .106 (.353 (.333 (.074-.091) .375) .071-.138 (.370) 320 363 290 679 744 725 1339 1544 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .071 (.179-.170-.071) .354) .439 (.063-.088) .208-.109-.056-.301) .089 (.197) .136 (.452-. Using neutron activation analysis to 2000. 2003.157) .069 (.086) .064-.188-.133) 90th .667) . (1987) found possibly due to methodologic.077) .072-.308) .098) .331-.200-.084 (.063 (.085-.439) 790 679 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 237 .091) .120) .426) .066 (.119 (.083 (.077-.555 (.143-.125 (.138) .078) .279 (.392) .121-.152-.275 (.093-.153-.105 (.093) .459) .083) .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.209-.222) .326) . population (CDC.272-.497 (.381) .098-.095-.109 (.180-.285) .339 (.199 (. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.317) .085) . and 2003-2004 (Paschal et al.131-.154) .078-.214) .060-. 1997).158) .217-.059-.124-.465) .136-.105 (.056-.126-.414) .069 (.216-.060-. similar to those in this Report (Schramel et al.431) .358) .060 (.079 (.554) .190) .103-.071) .293 (.359 (.426) .062 (.176-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.057-.201) .130 (.117 (.300) .739) .197 (.154) .250-.333) . 2005).092) .218 (.133) .075 (.061-.301) .079) .200-.133) .410-.086-.065-.329-.067-.300 (.S.077) .082) .265 (.302-.054-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.217-.155-.059-.383 (.130-.074) .136-.436) .267-.064-..258-.174 (.116) .117) .158) .081) .073 (..094) .231-.080 (.344-.333 (.151 (.582) .084 (.116 (.245-.144 (.083 (.087 (. or exposure that a control group of non-metal workers had mean levels differences.061-.484) . population from the National Health and Nutrition Examination Survey. 1998).605) .080-.339 (.068 (.237) .199 (.075) .083) .107-.116-.111 (.284) .067 (.439) Total .482 (.074) 75th .270 (.086) .439 (.078 (.286-.436-1.053-.081 (.079) .294 (.065-.216-.215 (.068-.144-.341 (.797) .077-.203-.059-.124 (.347 (.139-.333 (.078 (.215) .634 (.080 (.727) .333-.098-.139) .084) .161) .074 (.250 (.100) .119-.359 (.198-.329 (.300-. 2001-2002.070 (.108-.823) .094-.S.071 (.439) 1160 1306 1281 1178 1345 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .098-. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.184 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.216 (.138 (.072 (.255-.090-.211 (.055-.231 (.214-.187) .145 (.100 (.061-.088) .360 (.098 (.079) .S.317-.136-.333-. interval) .150-.168 (.067 (.122 (.224) .100) .164 (.167-.073 (.255 (.083-.306) .086) .073 (.205-.216 (.059 (.087) .385 (.279 (.094) .049-.412 (.197) .279 (.072-.179-.075 (.108) .462) .379 (.150-.091 (.071 (.169) .075-.174) .139 (.880) .063-.500) .222-.104-.386) .146 (.143 (.453) .364 (.299 (.176-.283) .538) .078) Sample size 2338 2651 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .181 (.267) .096) .237) .081 (.258 (.148 (.080-.484 (. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.089) .250 (.136-.28) .169 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.069-.233-.148) .063-. 2001).197-.340 (.058-.122-.253) 95th .091 (.091) .216-.198) .125) .146 (.063-.278-.085 (. population. measure urinary tungsten. the residents’ embolization coils showed elevated tungsten levels in Urinary Tungsten (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.201 (.465) .300-.065 (.075-.431) .158 (.301) .287) .308) .079 (.237-.065-.255 (. Patients with medically-inserted tungsten found at increased levels in drinking water.065) .150 (.074-.206-.054-.253 (.122-.333) .167-.253-.065 (.333 (.082) .317 (.261-.353 (.354-.063 (.302-.667 (.240-.081-.165) .079) .078) .082 (.066 (.070 (.099-.

Angerer J.cdc. Third National Report on Human Exposure to Environmental Chemicals. Nevada Exposure Asssessment. 238 Fourth National Report on Human Exposure to Environmental Chemicals .gov/nceh/clusters/Fallon/study. The determination of metals (antimony. and hair (Bachthaler et al. Paschal DC. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Morrow JC. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Angerer J. Atlanta (GA).69(3):219-223. Kraus T.(2):73-77. Occup Environ Med 2001. Link J. 2004). Nicolaou G. 2005. bismuth. References Bachthaler M. palladium. cadmium.62:380-384. Cassina G. Biomonitoring studies on levels of tungsten provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of tungsten than are found in the general population. [online] 2003. Schramel P. Weber A. Centers for Disease Control and Prevention. Jackson RJ. Sampson EJ. tellurium. urine. lead.58(10):631-634. Churchill County (Fallon). et al. mercury. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. J Trace Elem Electrolytes Health Dis 1987. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.76(1):53-59. Paetzel C. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Schramel P. Feuerbach S. Mosconi G.htm. platinum. Environ Res 1998. Catheter Cardiovasc Interv 2004. Cancer Clusters. Available at URL: http://www. Ting BG. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. Schaller KH. National Center for Environmental Health. Manke C.Metals blood. Int Arch Occup Environ Health 1997. Wendler I. Pietra R. Lenhart M. Sabioni E. 4/15/09 Centers for Disease Control and Prevention. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. thallium. Zobelein P. Seghizzi P. Pirkle JL. Trace metals in urine of United States residents: reference range concentrations..

069) .065) .049) . 0.012) .045) .022-.010) .024-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.007 (.007-.008-.017-. and as an aid in electron microscopy and photography.012 (.027 (.039-.008 (.010-.008-.044 (.011) .008 (.008) .022 (.054) .017) .030 (.019-.009 (.023) .040) .023 (.009-.007-.011-.015) .005-.033 (.006 (.010-.020-.027-.006-.009-.052 (.013 (.048) .036 (.018 (.024 (.045) .004.062) .017 (.026) .035) .010) .019-.008 (.010 (.017-.033 (.017) .008 (.011-.013 (.008-.036 (.020-.007-.007-.027-.046 (.009-.021 (.040-.007 (.020) .027) .010 (.006-.014 (.018) .007-.020-.039) .008 (.006-.038) .006 (.008 (.008 (.009) * .013 (.009-.006-.046) .046 (.012 (.021-.050) .011-.037-.038 (.027 (.046-.009 (.009 (.014 (.017) .030-.011 (.008 (.007 (.006 (.009) .025-.011) . interval) .012) .014 (.056) .009) .039) 1227 1335 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .009) .043 (.008 (.011) .040 (.010-.009 (.040-.009) . including nuclear weapons.027) .011 (.005-.005-.007 (.008 (.013-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.023-. and 234U.050) .040 (.006-.026) .029-.034-.007-.017) .007) .026-.010-.010) .008) .007-.054-.009) .009) .016-.051) .009) .026-.021 (.006-.042) .015) .007) .021) .007-.010 (.037) .012 (.016) .018-.022-.013 (.012-.031 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.010) * .014 (.017 (.064 (.012-.014 (.008-.020 (.021) .008 (.022-.023) .009) .067) .007) .016) . in some ceramics.017-.009-.055 (.023-.073) .088) .037) Total .009 (.011-.007-.047 (.016-.008) .011-.010 (.279) .010) .006-.028 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.010-.009-. 235U (about 0.017-. and 03-04 are 0.010) .008) Sample size 2464 2690 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .015 (.009) .006-.035-. nuclear fuel.023 (.026 (.S.029 (. population from the National Health and Nutrition Examination Survey. or processing.028 (.022) .007) .036) .127) .011) .007 (.027 (. Uranium has many commercial uses.031-.005.013-. respectively.009 (.007 (.017-.012 (.008 (.007-.011) .013) .012-.007-. Fourth National Report on Human Exposure to Environmental Chemicals 239 .008-.046 (.027) .042 (.028 (.72%).053 (.016) .009 (.034) .019-.021 (.011) .039) .007-.015 (.009) .020-.006-.012 (.024-.011) .007-.030 (.021) .008 (.041 (.031 (.013 (.037 (.009) Selected percentiles ( 95% confidence interval) 50th .028-. Depleted uranium (DU) refers to uranium in which the proportions of 235U and 234U isotopes have been reduced compared with the proportion in natural uranium.006 (.013 (.009) .018 (.007-.013-.007-.010) .027 (.158) .009-.009) .067) .031 (.009 (.038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .010-.010) .023) .035) .018) .007 (.007 (.031 (.023-.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.065) .015-.018) .016 (.041 (.019 (.018) .008-.007-.046 (.007) 75th . milling. Variable concentrations of uranium occur naturally in drinking water sources.048 (.008) .020) .006-.037) . human exposure occurs primarily by inhaling dust and other small particles.021-.006-.009 (.060 (.026) 95th .007) .011-.023 (.009) .010 (.012-.049) .008-.004. see Data Analysis section) for Survey years 99-00.017-. Exposure to DU may occur in military personnel from retention internal shrapnel that contains DU or exposure to dust generated from ammunition Urinary Uranium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.024-.012 (. 01-02.016-.006-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).033-.036) .027) .017) .006-.031 (.015 (.013) 90th .026 (.029-. Since the 1990’s.005-.013 (.027-. Thus.008 (.015 (.005-.030 (.030) .032 (.036-. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.026 (.009-.007-. In workplaces that involve uranium mining.010) * .054) .007 (.008-.008 (.016) .020-.053) .072) .009-.056) .009-.023-.028-.014 (.019-.Metals Uranium CAS No.016) .010) .063) .012-.036-.007-.007 (.016) . and 0.007 (.034-.114 (.008) .012) .012) .008 (.012-.011-.033) .043) .040) .066) .037) .008 (.009 (.

010-.018-.006-.021 (.008-.009-. After exposure to soluble uranium salts. 240 Fourth National Report on Human Exposure to Environmental Chemicals .014-.009) .013 (.013 (.011) .048) .019) .019 (.017 (.016) .006-.Metals impact.007-.009 (.010-.006-.034-.026 (.053) .015-.009) .022 (.010-.034) .013) .022 (.018) .006-. interval) .050) . After long term or repeated exposure.012) .032) .039) .035 (.010 (.024) .042) .053) .009-.010-.018-.009-.016) .028) .013 (. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.007-. Inhaled uranium-containing particles are retained in the lungs. liver.009 (.024) .006-.005 (.024 (.027 (.007 (.025-.007) .010-.029) .017-.017) .019-.022-.077) .007 (.022) .S.024-.016-.008 (.007-.011-.042-..016 (.023-.019-.008 (.030) .005-.016-.013 (.008 (.027-.021) .019-.028 (.009) . 1992).006-.007 (.037 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.033 (.028 (.006-.025) 95th .010) .012 (.051) .021-.027) .010-.022 (.011-.080) .009 (.100 (.010 (.010 (.026-.041) .010) .007-.074) .006-.030 (.044) .005 (.007-. Uranium is eliminated in feces and urine.020-.012 (.017-.010) . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.012 (.022-.014-.029) .034 (.006-.012-.008) 75th .006-.012 (.017-.058) .006-.024) .006) .007 (.012-..067) .015 (.008 (.019 (.050 (.005-.025 (.043 (.014) .007 (.010-.034-.007-.020-.007 (.028) .010) * .011) .039) .039) .039) Total .030-.034 (.010) .013) .013) .040 (.045 (.014) 90th .047) .006-. where limited absorption occurs (less than 5%).033 (. After inhalation.009) .015-.008-. the initial half-life of uranium is about 15 days (Bhattacharyya et al.027) .030 (.006 (.032) .012) .007-.013 (. Health effects from uranium exposure result from chemical toxicity to the kidney.015-.016) .010 (. which can occur occasionally from high occupational exposure.048) .007 (.024-.007 (.029 (.014 (.009-.008 (.030 (.051) .016) .038) 340 368 289 719 762 725 1405 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .011-.008) .020 (.006-.009) .007 (.007 (.006) .006) .016) .051) .005 (.033) .009) Selected percentiles ( 95% confidence interval) 50th .005-.011-.008-.006-.051 (.020-.006) .014) . which represents distribution and excretion.004-.006 (.021 (.024 (.022-.006 (.025-.063) .012 (.008-.007 (.024-.016-. population from the National Health and Nutrition Examination Survey.017) .059 (.009) .025-.017-.013 (.015 (.011) .056) .010-.018-.006-.042) .270) .013 (.007) .010-.019 (.020 (.008-.006 (.034 (. 2005).006-.009) .007 (.035 (.011 (.011-. Radiation risks from exposure to natural uranium are very low.008) .015-.029 (.029) .010-.050) .006-.014) .034 (.015-.007) .020 (.007-.004-.017 (.020) . In cases of retained DU shrapnel.031 (. low level exposure.034 (. 0.025-.005 (.007 (.009-.028-.009) * .021 (.008 (.008) .024) .033 (.007 (.018-.026) .018-.031-.030-.028) .007 (.019-. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.041) 1227 1334 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .010-.016) .013 (.007-.027-.029) .005-.024) .005-.006-.011-.011-.009 (.006 (.019) .015) . Depending upon the specific compound and solubility.008 (.008) .012 (.008) .008) .033 (.017) .008 (.007-.006) .012) .008) .024 (.007 (.007 (.028) .006-.009) .006-.007 (.008-.010) .029 (.054) .006-.015) .009) .015 (.015) .011-.018 (.013 (.009) .058) .006-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract..1%-6% of an ingested dose may be absorbed.008) Sample size 2464 2689 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .027 (.014 (.005-.012 (.020-.027 (.026 (.010 (.011 (.010) .061) .006 (.009) .030) .016-.027-.014-. 2003).026 (.009-.021 (.006-. kidneys.027-.013 (.016) .007 (.146) .040) 883 682 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites * Not calculated: proportion of results below limit of detection was too high to provide a valid result.008) .008) .009 (.008 (.011) * .015 (.007 (.005-.025 (.006-.019-. Studies of persons with chronic exposure to soluble uranium salts in drinking water have not shown kidney Urinary Uranium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.007 (.008) . the shrapnel acts as a source of chronic.013-. with much slower elimination from bone.016) .015) .008) . about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.008 (.011-.

the geometric mean urinary uranium concentration was 0. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. Six workers in a depleted uranium program showed concentrations of 0. 2004). Metivier H. or wound contamination. Pillai KC. Breitenstein BD.. Dietz LA. Karpas et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Pullat VR.. Squibb K.. 2002). urinary levels of uranium were as high as 9. Health Phys 2000. et al. Atlanta (GA). Benedik L. eds.. Muggenburg BA. Hamilton MM. References Bhattacharyya MH. environmental levels) and health effects is available from ATSDR at: http://www.62:562-566. In two studies of a Finnish population with high natural uranium concentrations in their drinking water..S. 2006. but in whom no shrapnel was embedded. Radiation protection dosimetry. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population.html. (Kurttio et al. Centers for Disease Control and Prevention (CDC). Carmichael AJ.1996.atsdr. Thomas RG. Volf V. Estimate of the time zero lung burden of depleted uranium in Persian Gulf War veterans by the 24-hour urinary excretion and exponential decay analysis.. EPA... 2000).78:143-146. 28 soldiers who may have been exposed to DU by inhalation. and no consistent effects on multiple endpoints of kidney function were found. In: Gerber GB. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Tolmachev et al. The U. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. 2000). pp. and after deployment had geometric mean urinary uranium concentrations that were less than the NHANES 1999-2000 and 2001-2002 geometric means at all three time periods. Health Phys 1992.110 to 45 μg/L (Ejnik et al.078 μg/L (ranging up to 5. 1-49.. 1978).cdc. McDiarmid M.162 μg/L) (Orloff et al.e. Hamilton et al. NRC. Galletti.107:143-157. 2003. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure.. although slightly increased during and after deployment. Drinking water and other environmental standards have been established by U. the median urinary concentration was 0. soldiers who had been injured and had embedded DU shrapnel for as long as eight years.1992.. ingestion. Durakovic A. Zimmerman I. McDiarmid et al..55 μg/L (median 0. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al.S. Information about external exposure (i. Ejnik JW. Stradling GN. In 17 U.. Uranium content of blood.S. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. soldiers evaluated before. and 2003-2004 (Dang et al. Third National Report on Human Exposure to Environmental Chemicals. 1992. 2004). Sci Total Environ 1991. 2004).gov/ toxpro2. Mil Med 2003. respectively. 41 (1). Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. 2006). 2006). 2004). during. Komaromy-Hiller et al. Vol. Boyd P. Fourth National Report on Human Exposure to Environmental Chemicals 241 . with emphasis on quality control.. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Kent (England): Nuclear Technology Publishing. Biomonitoring studies on levels of uranium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of uranium than are found in the general population. 1994. had a mean urinary uranium concentration of 0. population. (May et al.61 μg/g creatinine. the median urinary uranium concentration was 2. In a study of 105 persons exposed to natural uranium in well water.65 μg/L). Determining the normal concentration of uranium in urine and application of the data to its biokinetics. 2002. In the same study.S. 2006).. 2006). Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. Horan P. Dang HS.066 μg/g creatinine (Gwiazda et al. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.S.168(8):600-605.. in that the levels were below their respective detection limits (Byrne et al.S. A cohort of 46 U. IARC and NTP have no ratings for uranium human carcinogenicity. Byrne AR.. 1991. Follow up of 32 veterans with embedded shrapnel showed that increased urinary uranium levels persisted more than 12 years after the first exposure (McDiarmid et al. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. 2005.011 μg/L (McDiarmid et al.Metals injury associated with elevated urinary uranium levels (Kurttio et al. 2001-2002.

Nuclear Regulatory Commission (U. Shelly T.91(2):144-153. Lorber A. Cordero S. Sabbioni E. Inductively coupled plasma mass spectrometry as a simple. Engelhardt SM. Health Phys 2002.82(4): 527-532.S. Lewis BM. Halicz L. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Heller J. Gucer P. Hamilton EI. et al. U. Makelainen I. Wilson PD. Li WB.71(6):879-85. Health Phys 2003.S. Biologic monitoring for urinary uranium in Gulf War I veterans. Health Phys 1996. Van der Venne MT. July 1978. Cremisini C. Health Phys 2006. Oeh U. Kalinsky V. Sci Total Environ 1994. Englehardt SA. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Ash KO.158:165-190. Marko R. et al. Human exposure to uranium in groundwater. McDiarmid MA.S.86:12-18. Marino R. Saha H. et al. Charp P. Karpas Z. Jarrett JM. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Uranium daily intake and urinary excretion: a preliminary study in Italy. Salonen L.22–Bioassay at uranium mills. Bennett LG. Biokinetic modeling of uranium in man after injection and ingestion. Int Arch Occup Environ Health 2006. Hancock RG. Roiz J. Orloff KG. Health Phys 2004. Jackson RJ.85:228-235. J Toxicol Environ Health A 2004. concentration and daily excretion of uranium in urine of Japanese. Sampson EJ. Radiat Environ Biophys 2005. et al. Kurttio P. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Oliver M. Noguchi H. Salonen L. D’Annibale L. Kidney toxicity of ingested uranium from drinking water. VI. McDiarmid M. NRC).67(8-10):697-714. Squibb K. Review of elements in blood. Pinto V. Pekkanen J. Kurttio P. Nuclear Regulatory Commission (NRC) Guide 8.81:45-51. Environ Health Perspect 2002. McDiarmid MA. Pirkle JL. Kuwabara J. Uranium and thorium in urine of United States residents: reference range concentrations. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Ough EA. Health Phys 2004. et al. Oberbroekling KJ. Roth P. Environ Res 2004. Andrews WS. Wahl W. Renal effects of uranium in drinking water. rapid.296(1-2):71-90. Metcalf S.110(4):337-342. Ejnik J. Paschal DC.S.44:29-40. Auvinen A. Washington (DC): NRC. Paretzke HG. Environ Res 1999. Kane R.47(6):972-982. Costa R. Mistry K.Metals Galletti M. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Howerton K. Komaromy-Hiller G. Element reference values in tissues from inhabitants of the European community. Karpas Z. Am J Kidney Dis 2006. Smith D. Katorza E. patient population and literature reference intervals for urinary trace elements. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. U. Ting BG.94:319-326. May LM. et al. Komulainen H.79(1):11-21. Scott K. Hollriegl V. Clin Chim Acta 2000. Squibb K. Tolmachev S. Comparison of representative ranges based on U. Harmionen A. Saha H. Gwiazda RH.87:51-56. Auvinen A.

0-19.49-3. 2007).0) 13.32 (3.30 (2. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.12) 3.26 (2.03) 3.0) 9.40 (3.10 (6.40-4.89-3.90 (5.0-15.0) 10.0) 10.0 (11.22-5.5 hours and has a small estimated volume of distribution (Crump and Gibbs.10 (6. 1998).55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.0-15.40-7.0 (8.10) 12.96 (3.75-3.0) 13.20) 4.0) 13.68) 4.80-12.90-11.70 (3.10 (7.80-4.40) 4. Perchlorate was added to the U.30-17.80) 7.80 (3.20-4.50) 3.0-17.0-29.90-10.0) 13.50-4.90 (4.S.0) 14.90 (5.0 (11.0) 9. 2005).0) 9.30 (5. population from the National Health and Nutrition Examination Survey.10 (5. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.20 (8.70-11.0 (11.20) 7.0 (13.0 (9.90-12.0 (9.40 (8.40 (5.10 (2. and electroplating.0 (8. Survey years 01-02 03-04 Geometric mean (95% conf.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.51 (3.0) 10.05.50-7.80-6.60) 3.0 (12.S. 2005).40) 3.40 (4.54 (3.00-5. In addition.16) 3.79 (2.93-4.30 (2.65) 3.20 (5.44-4.0 (8.40) 2.47-4.60) 5.Perchlorate Perchlorate (Urbansky.0) 14.00) 5.40-13.40) 3.90 (5..90-3.0) 15.20-11. and limited applications in pharmaceutics.70-3. and certain plants with high water content (e.80-15.60 (4.0 (8. fabric dyeing.19-4.0) 11.38) 5.0-18.0 (11.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.60 (4.50-3.0) 8. Drinking water.10-12.20 (2.0) 12. 2002).50 (5.20-12.66) 3.0-17.90-3.0) 708 617 681 652 1228 1092 Limit of detection (LOD.20 (7.10) 5.10) 3.70 (3. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.70) 3.0-17.07-4.05 and 0.00-6.20) 3.30-6.0-18.40) 3. lettuce) can be the main sources of intake for humans (FDA.50) 11.80-4.76 (3.90) 6.93 (4.0 (11. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.50) 6.80) 3. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.05 (2.30) 6. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 ..50) 5.40 (4.0 (12.75 (3.0 (8.0 (11.20 (4.80) 75th 6. leather tanning. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS. and reducing agents.90-11.29-3.0 (11.0 (9.18-3.40-6. certain catalytic metals.70-12.70 (3.09) 3.0-17.87-3.90 (3.10-11.20 (2.50 (8. or ammonium salt.0) 95th 14.90-6.0) 9.81-16.70-3.40-4.01 (2.56) 3.0) 13.00) 3.80 (3. Other manufactured uses include fireworks.40-5.20-4.0-18.70-7.76) 4.88) 3.90-9.50) 5.0 (12.40 (5.0-20. interval) 3.81) Selected percentiles ( 95% confidence interval) 50th 3.90) 5.0-17.0 (9. laboratory analysis.0) 13.40 (3.0 (12.50-4.0) 13.10) 5.40) 90th 10.02 (3. Inhibition of iodine uptake by competition for the sodium/iodide symporter in the thyroid can be estimated in humans by measuring radioiodine uptake CAS No.0) 8.90 (2.74-3. It is normally found and produced as the anion of a sodium. milk.S.50 (3.35 (3.00-6.60-7. matches.EPA.g.67-5.84) 14.39-4.30-19.60 (7.0 (10.46) 3.0 (9.0) 16.20 (4.30-7.0-14.0-17.40 (5.0) 9.08-3.0) 11.10-7.70-9.50-11.21 (2.11) 4.0 (11.10-4.70-5. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.30-7.51 (3.0 (11.00) 7.45-4.70-6.60) 8.20-3.00) 4.0) 13.22 (2.30 (5.0-23.0) 14. potassium.60-6.90-9. Perchlorate is stable under most environmental and physiological conditions.31) 2.20 (6.00) 3.80 (7.80 (6.10-11.0) 15.80-8.80) 12.93-3.0) 19.10) 3.0 (11.0) 11. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.40) 6.19 (3. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.0 (9.40-11.0) 9. 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. but has strong oxidant properties in the presence of concentrated acids.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.30) 6.0 (9.11) 3.62 (3.

60-3.20) 8.45) 3. NAS.30) 90th 9.37 (4.20 (7.50-3. However..10) 4.0 (10.70-3.89-3.98) 3.80) Selected percentiles ( 95% confidence interval) 50th 3.21 (2.S.20-10.90) 5.40) 3.40) 5.66) 3.12 (6.4 (8.8 (11.87 (5.40 (4.20-9.Perchlorate inhibition (RUI).S.18-3.26 (3.70 (2.58) 2. levels. menopausal status.0) 9.87) 2.30) 75th 5.86) 4. 2005).3) 8.10 (4. U.72 (3. In the U.46-13.0-17.1 (11.10-7.0 (8. 2006.60) 8.80 (4.73) 3.7 (11.70-4.50) 5.2) 8.0 (9.00) 4.00-2.70-5.50 (3.93-5. Steinmaus et al. Survey years 01-02 03-04 Geometric mean (95% conf.25) 5.20) 3.54 (3.00) 9.44) 3.08 (3.30 (3.60-11.20-3.47) 2.3) 11. chronicity of exposure.29-6.50-5. Follicular cell thyroid tumors would Urinary Perchlorate (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.40-10.99 (5.00 (4.30-10.0) 12.50 (6.60-8.37-13.80-3.. medications)..87) 7.51 (3.50) 6.22-6.80 (7.0-14.3-14.4) 13.80 (7. levels and sufficient in most participants (Tellez et al.60-5.00) 3.50) 9.59) 3.00 (6.90-3.87-3. Li et al.4) 8.89 (2.10) 13.10) 6. women with urinary levels of iodine less than 100 micrograms per day.0-19.91) 4.25 (3. 2005.5) 8.50) 95th 12.35 (4. 2002).0) 12.6) 12.03 (2.20 (3.60-15.10 (4.70 (2.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.3 (10.29) 2.00-11.2) 8.0-14.0) 10.0) 6.08) 3. and the presence of other substances known to affect thyroid function (e.50-9.52 (8.90 (4.0 (8.24-2.93-8. perchlorate is negative in most genotoxic assays (U.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.0) 9.20 (4.4 (11.76 (3.74) 7.04-3.77 (3.12-2.60 (3.00-3.24 (4.02) 3.70-15.67) 5.93) 3.. Also.81-3.50) 2.60) 3. Many factors may be important in consideration of perchlorate action on the thyroid: dose. Lawrence et al.20-4.10-3.0 (9.05 (4.50) 2.70) 10.S.93-7.45-2.60) 10.96) 2.33-12. 2005).39 (3.64-3.30) 3.. up to 68% RUI has been demonstrated.04-3.6-17.09) 3.60-5.19-10.19-6.44-6. 1999. 2005).0 (11.6) 20.30 (6. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses. in a representative sample of U.0) 12.35) 3.S.1-16.EPA.70) 2.95 (2.40 (7.20 (6.90 (7. In these small short-term experimental studies on males and studies of male perchlorate workers with doses or estimated exposures thousands-fold higher than known environmental exposures.20-3.41-9. dietary iodine intake. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.90-2.33-6.S. 2003. Greer et al. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.0) 13.97-5.0) 12.40 (3.30-5.53 (2.30-5..0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3..1-14.54 (2..1) 8. interval) 3.46-4.84) 2.10 (6.83 (5.1 (8.20 (2.80-3.90-20. 2001. 2002.22-4.4 (11.52-9. thiocyanate..90-15.4 (10.22 (2.10 (1.26) 4.61-5.46 (3.40) 17.0 (11.30) 5.33 (7.1-22.64) 5.22-4.32) 5.00 (2.39) 2.43) 6.93-5.10 (2.35 (2.30 (5. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.71 (5. During gestation and infancy.0) 11.90 (2.09 (7.5 (13.56-3.0-44.25) 5.82 (5..51-4.99-3.0) 14. 2002.14 (2. gender. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al. although iodine intake was higher than U.0 (11.S. nitrate.60-11.10) 3.56 (3.0) 708 616 680 648 1227 1080 2001-2002 performed on surplus samples (variable unavailable of NHANES website) 244 Fourth National Report on Human Exposure to Environmental Chemicals .60-6. altered thyroid function was not found in Chilean pregnant women or their newborns with mean urinary perchlorate levels about 40-fold higher than average U.90-9.75) 3. Ecologic studies from screening programs with elevated perchlorate in the regional drinking water have indicated no increased prevalence of abnormal neonatal screening tests for this disorder in these regions (Kelsh et al.EPA.0) 7. 2005.39-4.0 (9.25) 5.90 (2.61-10. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.87 (7. Lamm and Doemland.16-3.61 (5.60-8.76-3.15-12.07 (2. 2000). 2007).40 (3.34-3.4-16. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.0) 13.0) 4.02-4.70 (4.36 (8.90-11. population from the National Health and Nutrition Examination Survey.g.1-13.42 (3.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.S. age.3) 12.

Page Last Updated: 05/28/2009. et al. Blount BC. Lawrence J.gov/toxpro2. Deyhle GM. Pino S.41(5):409-411. (2007) analyzed a subsample of NHANES 2001-2002 which demonstrated detectable perchlorate in all urinary samples and showed slightly higher levels in children as compared to adults. He X. Greer SE. Magnani B. Goodman G. Food and Drug Administration (FDA). Primary congenital hypothyroidism. Kelsh MA. Pino S. Rutherford GW.115(9):1333-1338. Sesser DE. Crump KS. J Occup Environ Med 2003. Pleus RC.gov/safewater/ccl/perchlorate/perchlorate. Mauldin JP. Erratum in: J Occup Environ Med 2004. Available at URL: http://www.17(4):400-407.42(2):200-205.S. 2007). Pirkle JL. Li Z. Daaboul JJ. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Abarca CR.fda. and nitrate on thyroid function in workers exposed to perchlorate long-term. Crump KS.40(21):6608-6614. National Academy of Sciences (NAS). Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U.S. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999.htm. Additional information about exposure and health effects is available from the U.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Lau EC. Perchlorate in the United States. 2005.113(8):10011008. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. J Occup Environ Med 2000. Blount BC. Environ Health Perspect 2007. Perchlorate Exposure of the US Population. Neonatal thyroxine level and perchlorate in drinking water. epa. Lamm SH. Environ Health Perspect 2002. the women in the community with the highest drinking water levels had mean urinary perchlorate levels about 40 times greater than the geometric mean for participants in NHANES 2001-2002 aged 20 years and older (Tellez et al. Caldwell KL. Lawrence JE. Benchmark calculations for perchlorate from three human cohorts. Li FX. Tellez RT. Thyroid 2001. Thyroid 2000. References Blount BC. Pirkle JL. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. The effect of short-term low-dose perchlorate on various aspects of thyroid function.45(10):1116-1127. J Expo Sci Environ Epidemiol 2007. Erratum in: Environ Health Perspect 2005. the 95th percentile of NHANES 2001-2002 participants aged 20 years and older have urinary perchlorate levels that are several thousand times less than urinary levels measured during occupational exposure of perchlorate workers (Braverman et al. Barnard JC.110(9):927-937.10(8):659-663. Dyke JV. 2005). Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Environ Health Perspect 2006.90(2):700-706. Chacon PM. Steinmaus C. Analysis of relative source contributions to the food chain. et al. Gibbs JP. CFSAN/Office of Plant & Dairy Foods. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Low dose perchlorate (3 mg daily) and thyroid function. The effect of perchlorate. Biomonitoring studies of urinary perchlorate provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of perchlorate than levels found in the general population.cdc. Lamm S.atsdr. 6/2/09 Greer MA. Valentin-Blasini L.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653.. Blount et al. Also.46(5):509. Osterloh JD. Braverman LE. Doemland M. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Braverman LE.html and from ATSDR at: http://www.113(11):A732. J Clin Endocrinol Metab 2005. Health Implications of Perchlorate Ingestion. Buffler PA. most of the population is considered to be below the U. Byrd D. Lamm SH.. 2005). Braverman LE. Howd R. Environ Health Perspect 2005. et al. Cross M. Valentin-Blasini L. and environmental perchlorate exposure among residents of a Southern California community. et al. Osterloh JD. National Research Council of the National Academies.html. Washington (DC): National Academy Press. Landingham CB. EPA reference dose (Blount et al. Miller MD. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Richman K.. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Kirk AB. Skeels MR. newborn thyroid function.11(3):295. May 2007.EPA at: http://www. Lamm SH. population. Dasgupta PK. Jackson WA. 2001-2002.114(12):1865-1871. thiocyanate. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Environ Sci Technol 2006.

S. No.S.S. Doc. Perchlorate. EPA/600/F-98/002 Washington (DC). 1988. Urbansky TF. Integrated Risk Information System (IRIS). Environmental Protection Agency (U. Available from URL: http://cfpub. 246 Fourth National Report on Human Exposure to Environmental Chemicals . EPA). U.1/15/06 U.epa. Perchlorate as an environmental contaminant. Environmental Protection Agency (U. Revised 2/11/05. Drinking Water Contaminant Candidate List. EPA). cfm?substance_nmbr=1007.gov/iris/quickview.Perchlorate pregnancy and the neonatal period.S. Environ Sci Pollut Res Int 2002. Thyroid 2005.9(3):187-192.15(9):963-975.

or form in the final product (e. U. Perfluorooctanoic acid (PFOA) has been manufactured since the 1950s. However. fluoropolymer products are used in a wide range of industries including aerospace. 2006). textiles. Because of their properties. POSF-based polymers have been used in a wide variety of products such as waterproofing.. such as perfluorochemical telomers. fire retardant foam. Perfluorooctanesulfonyl fluoride (POSF) was synthesized as a polymerization starting material.Perfluorochemicals Perfluorochemicals General Information The perfluorochemicals (PFCs) are molecules in which all bonds of the alkyl chain are carbon-fluorine bonds except for the terminal functional group. automotive. PFOS) (Hekster et al. PFOA is usually not a residual contaminant in non-stick surfaces made of polytetrafluoroethylene. Fluoropolymers have applications in waterproofing and protective coatings of clothes. perfluorooctane sulfonate. primarily as its ammonium salt. low volatility (as salts or ionized) and can remain in the environment and bioconcentrate in animals (e. semiconductor. adhesives. and alcohols which are by-products. polytetrafluoroethylene. several pathways (during manufacturing) can lead to formation of PFOS or other sulfonyl-containing PFCs as residual contaminants in the final polymer products.. furniture. There are many other fluorocarbon type chemicals which are not addressed here. and textiles. or form as degradation products during its reaction to create the intermediate reacting monomers. some fish bioconcentrate Perfluorinated Compounds Serum Perfluorobutane Sulfonic Acid Serum Perfluorodecanoic Acid Serum Perfluorododecanoic Acid Serum Perfluoroheptanoic Acid Serum Perfluorohexane Sulfonic Acid Serum Perfluorononanoic Acid Serum Perfluorooctanoic Acid Serum Perfluorooctane Sulfonic Acid Serum Perfluorooctane Sulfonamide Serum 2-(N -Ethyl-Perfluorooctane sulfonamido) Acetic Acid Serum 2-(N -Methyl-perfluorooctane sulfonamido) Acetic Acid Serum Perfluoroundecanoic Acid CAS number 335-76-2 307-55-1 375-85-9 355-46-4 375-95-1 335-67-1 1763-23-1 754-91-6 2058-94-8 Abbreviation PFBuS PFDeA PFDoA PFHpA PFHxS PFNA PFOA PFOS PFOSA Et-PFOSA-AcOH Me-PFOSA-AcOH PFUA Fourth National Report on Human Exposure to Environmental Chemicals 247 . as a solubilization aid in the synthesis of polytetrafluoroethylene. 2006). current manufacturing Perfluorinated Chemicals in this Report practices reduce the formation of these by exclusively using fluorotelomers (Prevedouros et al.g. 2003). perfluorooctane sulfonamide. Discussed here are perfluoroalkyl acids. end products. The PFCs have limited water solubility. Worldwide annual production of PFOA was estimated to be 260 metric tons in 1999 (Prevedouros et al. N-methylperfluorooctanesulfonamidoethanol (MeFOSE) and N-ethylperfluorooctanesulfonamidoethanol (EtFOSE).g. Perfluorohexane sulfonate (PFHxS) has also been used to synthesize the fluoropolymers used in firefighting foams and some carpet treatments.. A major application of one important fluoropolymer. electrical and electronics. Other PFCs (including small amounts of PFOA) can also form as side-reaction by-products in the synthesis of POSF (e.S. amides. 2003. and also as constituents of floor polish. Production rates and emission rates have fallen since 2002 after conversion to a new synthesis process. Perfluorononanoic acid (PFNA) was an impurity in the process that produces PFOS. building/construction. Global production that year for POSF materials was 3700 metric tons (Prevedouros et al. has been the heat-resistant non-stick coatings used on cooking ware and other protected surfaces.S. MeFOSE and EtFOSE have been used in food packaging and textile treatments. and fire protection. and their oxidation products.. or processing aids used in the synthesis of fluoropolymers. and insulation of electrical wire. manufacture of POSF-based products began ending in about 2000. may be markers of food or consumer exposures. and other products. In addition. U. chlorofluorocarbons and investigational blood substitutes. 2006). finalized perfluorochemical polymer products. Other perfluoroalkyl carboxylates of various chain lengths were also formed in the process used prior to 2002. N-methylperfluorooctanesulfonamidoacetic acid (Me-PFOSA-AcOH) and N-ethylperfluorooctanesulfonamidoacetic acid (EtPFOSA-AcOH).. chemical processing. PFOSA). 2005.g... EPA. respectively.. Olsen et al.

may metabolize or degrade to PFOA (Dinglasan et al. Tittlemier et al.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). the 8-2 telomer. but still can have long residence times in the body.S.. Keller et al. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins. In some cases. The elimination half-life of PFOA in humans is roughly estimated to be 3. It is unclear if environmentally degraded telomer products are a major source of other PFCs. Olsen et al. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. human toxicokinetics... including immunologic effects and tumor induction. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver... 2005).. 2005). approximately 4. Prevedouros et al. Kannan et al. environmental breakdown products of the telomers used to make fluoropolymers or the metabolic products of fluorochemicals in the body can produce PFCs that are measured human blood. Lau et al. 2004. C7). 2005. All sources of human exposure are uncertain.. environmental fate. 1995. pancreas. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al.. 1990). Guruge et al.. 1993). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.. PFCs have been identified in surface coastal and ocean waters (Yamashita et al. 2004. Excepting PFOS and PFOA. heptadecafluoro-1-decanol. 2003).8 years (Olsen et al. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. thymus and spleen... For instance. 2003.. 2004). 248 Fourth National Report on Human Exposure to Environmental Chemicals . but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al.. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. 2007a).. and in human blood and semen (Calafat et al. 2002. there is limited information on the sources. Taniyasu et al. 2006. endocrine and immune effects. Unlike many organohalogen contaminant chemicals.. 2006a. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. U.... Vanden Heuvel et al. in part. 2005.e. C5. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al.. 2004). 2004. growth retardation and delayed sexual maturation (Kennedy et al. C6. and in offspring. population from the National Health and Nutrition Examination Survey. EPA. 2005). 2003a and 2004a). PFOA has been reported to cause liver. Survey Geometric mean (95% conf. 2003).5 years and for PFOS. or effects of other PFCs.S. Bookstaff et al. in a wide variety of marine and land animals (Kannan et al. Lau et al. but probably include dietary sources (Kannan et al. Some of the effects in animals may be mediated through peroxisomal proliferation. 2004. see Data Analysis section) for Survey year 03-04 is 0.4. PFOA is mostly excreted in the urine in animal studies. < LOD means less than the limit of detection. 2000. 2005. peroxisomal proliferation. and β-oxidation of lipids (Kudo et al... hepatotoxicity... kidney. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. The PFCs often measured in human serum are listed in the table. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue.. 2007). by high protein binding in plasma and other proteins. which may vary for some chemicals by year and by individual sample.

500) .400 (<LOD-.500) .800) 1. 2005). Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.00) . possibly related to lung immaturity (Lau et al.00) ..S. 2004).800 (.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0.600 (.400-1.. PFOA..S.600 (.400) . 2003a. 2004.400-1. Harada et al.400 (<LOD-.300 (<LOD-. Kennedy et al. 2007b)...500 (<LOD-1. Olsen et al. reproductive. EPA. 2007. and perfluorononanoic acid (PFNA) are detectable in a high percentage of the participants and PFOS levels are generally 3-10 times higher than PFOA levels (Calafat et al. < LOD means less than the limit of detection.80) 640 1454 03-04 03-04 * * < LOD < LOD . 2003. Fei et al.400-1.500-.80) 485 538 962 Limit of detection (LOD. and there was no clear evidence of excess all-cause or diseasespecific mortality. However. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. In such studies. Thibodeaux et al.900 (.00) . In comparing three separate reports on adults. Serum PFOS levels associated with toxicity in test animals were 310-1550 fold higher than 95 percent of the levels found in a study of adults (Olsen et al. development in offspring was stunted and hypothyroxinemia was observed. 2004). the potential to estimate risks to humans from animal doses is uncertain.800 (.. At doses causing maternal toxicity. which may vary for some chemicals by year and by individual sample.900 (. EPA.500) . Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants..600-2. 2003).900 (. 2007a. population.10) .800 (. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. the median PFCs values tend to be roughly similar in these age categories (Olsen et al.. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. PFOS. 2003).50) . 2003a).500-1.00 (.400-1. 2007).400 (<LOD-..600 (.3.300 (<LOD-..500) 90th . 2005)..10 (.800 (. Survey Geometric mean (95% conf.500-1. U. 2001. At high but non-toxic maternal doses of PFOS. Animal studies of PFOS have demonstrated weight loss. interval) Selected percentiles ( 95% confidence interval) Sample 95th . hepatotoxicity. 1999. population from the National Health and Nutrition Examination Survey.500 (. and humans. Olsen et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. PFOA.800) 1.. Lau et al..700) .. 2003a).. Olsen et al. 2007a. 2004b). 2003. PFOS.300-1.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. or increased cancer rates (Alexander et al. developmental and teratogenic effects were demonstrated in offspring.S. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.40) .20) . Analysis of the NHANES 20032004 subsample demonstrated higher levels of PFOA and PFOS in males and a slight increase in levels of PFOS with age (Calafat et al. and changes in thyroid hormone concentrations (Grasty et al. U.. 2004.300 (<LOD-. 2007b. elderly and children.10) * 03-04 03-04 * * < LOD < LOD < LOD . 1992.500-1.. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.400-. 2003a.700 (. thyroidal). 2003). 2003. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al..500-1. 2003a.500) . Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 249 . perfluorohexanesulfonate (PFHxS).10) . and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.500-3.S.108 times higher than background serum levels in humans (Butenoff et al. 2004a.500 (. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .. monkeys..400-.400-1. Cook et al.

S. PFC levels for the U. population. Poland. (2003a) were similar to those of pooled samples (1990 through 2002) of the U. 2007b). possibly due to PFOA being a by-product in POSF-related production. Belgium. Finding a measurable amount of PFCs in serum does not mean that the levels of PFCs cause an adverse health effect. 162% for PFOA. Notably.. and more than thirtyfold higher than in Peru (Calafat et al. population (Calafat et al. median levels to about fivefold lower levels (Harada et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Recently. 2004). respectively (Olsen et al. 2006b). appear to be higher in the U. 2004). 2006a).. Malaysia. are much lower than those reported for occupational exposure. 2003b). Brazil.S... Olsen et al. PFOS and PFOA were shown to be highly correlated in that study and also in NHANES 2003-2004 (Calafat et al.S.. Korea and Japan. The median levels of various PFCs in Olsen et al. Olsen et al (2005) also showed that PFCs serum concentrations increased from 1974 to 1989 in 58 paired samples: 25% for PFOS. In Japan.. Biomonitoring studies of serum PFCs can provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of PFCs than are found in the general population. 2003a). Serum levels of PFCs. and 204% for Et-PFOSA-AcOH. surprisingly little variance in across five widelydispersed U.S. In monitored workers employed at a POSF production facility with no biochemical or clinically observable effects. PFOS levels tended to vary within regions of the country ranging from U. particularly PFOS. representing environmental exposures. cities was seen in median PFC levels. median levels of PFOS and PFOA were over 40 to 300-fold higher. and about eight to sixteenfold higher than in Italy and India (Kannan et al..Perfluorochemicals In a study of 598 blood donors aged 20-69 (Olsen et al. 250 Fourth National Report on Human Exposure to Environmental Chemicals .S. the sample sizes were small in these studies. (2007b) reported reductions in PFOS and PFOA concentrations for a group of Red Cross blood donors in the United States from 2000 to 2005. than in some other countries: about two to threefold higher than in Columbia.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.400 (<LOD-.400) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .600 (.S. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 251 .300 (<LOD-. which may vary for some chemicals by year and by individual sample.300-.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD . Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD.600) < LOD .900) < LOD . see Data Analysis section) for Survey year 03-04 is 0.500-.500 (<LOD-.S.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection. see Data Analysis section) for Survey year 03-04 is 1. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.0.500) 485 538 962 Limit of detection (LOD.400 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (<LOD-.300 (<LOD-.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.3.

60 (6.08) 2.10 (.60 (1.20-2.00 (5.40 (1.40) 1.60-4.40) 4.00 (.60 (1.20) 03-04 03-04 2.26) 2.72) 1.80) 90th 2.826-1.50 (2.00 (1.60) 1.80) 4.5) 5.809) 1.03) 1.70) 1.835-1.20) 1.70-5.30-9.90 (4.17 (1.50 (1.30 (7. see Data Analysis section) for Survey year 03-04 is 0.852 (.20 (1.30) 3.10) 4.30 (2.90-2.834-1.20) 1.30 (2.60-3.50 (4.0) 1053 1041 03-04 03-04 03-04 1.80-4.721-1.00) 1.67-2.900-1.S.90 (1.20) .70) 1.10-5.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.30) 03-04 03-04 .27) 1.40 (1.00 (1.60-2.77-2.900 (.01 (1.40) 2.80 (4. interval) 1.44 (2.50) 2.40-1.00) 1.87-2.80-7.80-4.10) 75th 1.80) 5.20-1.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.30-12.80-3.50 (4.900 (.40-3.56-1.40) 1.00 (1.30-6.00 (.40) .60) 9.80-2.30 (1.12) .20-1.10) 1053 1041 03-04 03-04 03-04 .800-1.90) 1. Survey Geometric mean (95% conf.70-7.00-1.20-3.50 (1.16) .91) 2.60-3.60-4.92 (1.60-7.14 (.816-1.50 (1.10 (1.10-9.700-1.30 (6.30 (1.700 (. interval) .900-1.90-10.900-1.10 (.90) 1.30 (1.00-6. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.70-6.05-2.86 (1.40 (1.42 (1.70 (2.10 (4.80-7.800 (.73-2.00-1.70) 2.04) .00-7.80-3.60) 2. see Data Analysis section) for Survey year 03-04 is 0.00) 2.90) 90th 5.70-2.30 (1.20) 2.90) 3.60-8. 252 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.90 (1.40 (1.20-1.20 (1.912-1.10) 6.50) 6.10) 75th 3.60 (1.54) .50 (6.984 (.40 (2.10) 6.600-.30) .20 (1.90 (2.50) 2.50-3.1) 485 538 962 Limit of detection (LOD.80-6.60-2.40) 640 1454 03-04 03-04 2.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.900-1.90 (4.966 (.S.80-8.80 (1.40) 640 1454 03-04 03-04 1.861 (.50-6.70) 13.3 (9.50-6.80 (1.50 (1.80) 1.6) 7.30 (3.689 (.20-1.60) 3.1.0) 8.80-8.20) 485 538 962 Limit of detection (LOD.00 (1.50 (6.80) 3.51) 1.00-8.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.00) 3.10) 8.40-1.90 (1.5) 8.80-4.10) 4.72 (1.70-2.50-10.10) 1.00 (2.90) 1.20 (1.900-1.60-2.30) 3.3.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.10) 1.90 (1.30-2.90-19.900-1. population from the National Health and Nutrition Examination Survey.70 (1.10 (.70) 3. Survey Geometric mean (95% conf.10 (4.20 (6.30) 3.20 (6.93 (1.586-.963 (.70-10.80-12.70) 2.10) 5.17-1.697-1.10-9.90) 8.09 (.900) 1.62-2.

3 (35.40-6.0-70.1-24.9-19.91) 3.50-6.40) 75th 5.40-14.0-20.5) 8.8-35.50-4.00 (5.5 (28.70 (5.0) 21.40) 3.9-23.8) 46.10) 5.40-10.80-4.79) 4.8-22.7 (7.2-22.47-4.3-22. interval) 3.30 (3.5) 32.0) 485 538 962 Limit of detection (LOD.5) 9.60-6. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.7-33.96 (3.37 (2.6) 35.7-30.70-5.70) 4.00 (3.1) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 4.2 (18.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.7-49.4 (19.4) 640 1454 03-04 03-04 23.S.2) 30.6 (19.50) 7.5 (28.00) 3.90) 6.7 (19.8-30.6-24.8-81.40) 5.8-22.2) 45.4-42.2) 640 1454 03-04 03-04 4.00 (5.60) 8.2 (28.65-4.40 (4.60 (5.8) 27.4 (28.6) 62.6-50. population from the National Health and Nutrition Examination Survey.47 (4.2 (21.10-3.85-4.6) 9.6-45.3) 41.0) 23.1 (24.40) 90th 7.8) 32.21-3.30) 7.0-16.30 (5.60) 03-04 03-04 3.8-22.8 (45.1-52.3) 42.70-9.80) 8.0) 36.70) 3.1.7 (35.4) 20.0) 21.3-61.60 (7.70-7.50 (4. interval) 20.10 (3.80 (5.2-57.1) 57.60-9.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.40-6.6) 1053 1041 03-04 03-04 03-04 3.20) 5.9 (19.20) 7.84-3.4 (17.90 (7.0 (20.60 (4. see Data Analysis section) for Survey year 03-04 is 0.5-21.70) 6.9 (13.90-4.3) 28.7-69.6 (42.95 (3.30-11. Survey Geometric mean (95% conf.9) 22.60 (6.7 (43.4-25.90 (7.7 (13.30-3.4 (19.40-17.1-33.5-62.60-13.8-78.50) 4. population from the National Health and Nutrition Examination Survey.67-4.20) 7.9 (22.30 (3.30) 6.4 (23.1-36.10 (6.5-33.6 (44.90-4.60-14.20) 5.20-5.1-35.35) 3.9) 9.80 (7.3 (17.89 (3. see Data Analysis section) for Survey year 03-04 is 0.60 (6.0-66.1 (23.70 (5.4) 56.7 (43.99-3.11 (2.0) 03-04 03-04 19.2 (27.2 (19.30-6.6) 21.80 (6.5-23.30-5.4) 75th 30.6) 18.7-53.70 (3.5) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 21.3 (35.5) 57.0 (27.4) 21.9) 27.40 (6.9 (17.20-9.60 (3.6 (35.27) 4.0) 90th 41.20) 10.18 (3.5) 1053 1041 03-04 03-04 03-04 14.8 (34.20) 4.50-13.90 (5.53) 3.80 (6.3 (44.20 (4.6) 7.5) 7.70-10.7 (35.80-12.4.6) 42.30-8.0) 43.3 (28.07-4.1-25.4-17. Fourth National Report on Human Exposure to Environmental Chemicals 253 .7) 39.90 (7.9) 22.9-38.80-9.3) 485 538 962 Limit of detection (LOD.5) 18.2 (16. Survey Geometric mean (95% conf.S.90-12.50 (3.20 (4.5) 19.8 (37.2) 30.70-7.20-4.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.1 (19.82) 4.7-23.10 (3.1) 15.

which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 0.4.300 (.300) .300 (.300 (.200-.300-. population from the National Health and Nutrition Examination Survey.200-.300 (.300 (.200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) . Survey Geometric mean (95% conf.S.300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (.200-.200-.300 (.300) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2. < LOD means less than the limit of detection.300 (.200 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .200-.300 (.500) < LOD 485 538 962 Limit of detection (LOD.300) .200-.300-.200-.300 (.400 (<LOD-.300) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0.300 (.500) .300) .300-.200-.S.300 (.200-.500) . 254 Fourth National Report on Human Exposure to Environmental Chemicals .400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.500) 485 538 962 Limit of detection (LOD. Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300) .500) .300 (.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th . which may vary for some chemicals by year and by individual sample.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .

70) 1. population from the National Health and Nutrition Examination Survey.S.30 (1. which may vary for some chemicals by year and by individual sample. which may vary for some chemicals by year and by individual sample.600 (<LOD-1.900-1.600) .30) 1.300 (<LOD-.900-1.10) .10-1.00 (.90) .80) 1.00 (.10) 1.10 (1.900) .700) .700 (<LOD-.900-1.900-1.30) 1.20 (1.900) 485 538 962 Limit of detection (LOD.S.00) < LOD . < LOD means less than the limit of detection.600 (<LOD-.800) .900 (<LOD-1.10) * 03-04 03-04 * * < LOD < LOD .600 (<LOD-1.400 (<LOD-1.800 (<LOD-.10 (.700) 1.800) .Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.700 (<LOD-2.60) 485 538 962 Limit of detection (LOD.10) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.700 (<LOD-.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey.300-2.00-1.10 (. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400 (<LOD-.700) 90th 1.80) 1. Survey Geometric mean (95% conf.00 (.30 (1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .00 (.900-1.900 (.20-1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .700 (<LOD-.700) 1.20) 1.30) .500 (<LOD-.900) 1. Survey Geometric mean (95% conf.700 (<LOD-.10-1.10) .900-1.10 (.700 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .40) 1.50 (1. < LOD means less than the limit of detection.6.30 (1.60) 640 1454 03-04 03-04 * * < LOD < LOD .10-1.50 (1.600 (<LOD-1.3. see Data Analysis section) for Survey year 03-04 is 0.300 (<LOD-1.700 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.900-1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .10-1.10-1.40) < LOD < LOD .

et al. Biegel LB. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. The influence of time. Apelberg BJ. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Calafat AM.38(10):2857-2864. Tarone RE. Mohotti KM. Olsen J. Caudill SP. Hurtt ME. Katakura M. Mandel JH.Koizumi A. Crit Rev Toxicol 2004. Calafat AM. Fei C.41:2237-2242.39(1):80-84. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. et al. Olsen GW. and perfluorinated contaminants in livers of polar bears from Alaska. Wijeratna S.S. The toxicology of perfluorooctanoate. Mandel JS. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Moore RW.39(23):9101-9108. Birth Defects Res B Dev Reprod Toxicol 2003. Kuklenyik Z. 256 Fourth National Report on Human Exposure to Environmental Chemicals .40:21282134. Ye Y.115(11):1677-1682. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Environ Sci Technol 2005. Suzuki E. Environ Health Perspect. Dinglasan MJ. Saito N. Loganathan BG. Burris JM. Calafat AM. Hekster FM. de Voogt P. 2007b. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. O’Connor JC.99(2):253-261. Needham LL. Harada K. Environ Health Perspect 2007. Kennedy GL Jr. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Hurtt ME. Olsen GW. Reidy JA. Calafat AM.60(1):44-55. Murray SM. Environ Sci Technol 2005. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. et al. Cook JC. Koizumi A. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Harada K.S.115(11):1596-1602. Environ Sci Technol 2004. Cook JC. Rodricks J. Toxicol Appl Pharmacol 1990. Butenhoff JL. Kamiyama S. et al. Environ Health Perspect 2007. Keller JM. Yamashita N.38(17):4489-4495. J Environ Monit 2005. Gaylor DW. Olsen GW. Environ Res 2005. Rogers JM. Ingall GB. Bignert A. brominated. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Witter FR. Kumar KS.134(1):18-25. Seacat AM. McLaughlin JK.1968--2003. Chem Biol Interact 2000. Tully JS. Polyfluoroalkyl chemicals in the U. Kannan K. Reidy JA. Yoshinaga T. Grasty RC. Taniyasu S. et al. O’Connor JC. Day RD.Perfluorochemicals References Alexander BH. Chlorinated. Sasaki S. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Needham LL. Grey BE. Bookstaff RC. Cook JC. Corsolini S.113(2):209-217.34(4):351-384.179:99-121. Lau CS.60(10):722729. Tully JS. Calafat AM. Regul Toxicol Pharmacol 2004. Needham LL. Kuklenyik Z. Hurtt ME.7(4):371-377. Aguilar-Villalobos M. Kannan K. Peterson RE. Kannan K. Inoue K. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Environmental and toxicity effects of perfluoroalkylated substances.68(6):465-471. Rev Environ Contam Toxicol 2003. Mabury SA. Fillmann G.39(23):9057-9063. Kuklenyik Z. Jarnberg U. Moore JA. Environ Sci Technol 2004. Kawashima Y. Morikawa A. Arendt MD. Toxicol Appl Pharmacol 1995. Inoue K. Environ Sci Technol 2006a. Saito N. Environ Sci Technol 2007a. Toxicol Appl Pharmacol 1992. Androgenic deficiency in male rats treated with perfluorodecanoic acid. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Characterization of risk for general population exposure to perfluorooctanoate.63:490496. Watanabe T. and ex vivo studies. Edwards EA. et al. Falandysz J. Butenhoff JL. Frame SR. Needham LL.46(2):141-147.124(2):119-132. Halden RU. Perfluorinated chemicals in selected residents of the American continent. Environ Sci Technol 2005. Kuklenyik Z. in vivo. Guruge KS. Mandel JH. Reidy JA. Herbstman JB. Yamashita N. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Liu RC. Bandai N. Holmstrom KE.and perfluorinated acids.39(3):363-380. J Occup Health 2004. Perkins RG. Fluorotelomer alcohol biodegradation yields poly. Reidy JA.104(2):322-333. Biegel LB. Toxicol Sci 2001. Taniyasu S. Evans TJ. et al. Kudo N. Laane RW. Occup Environ Med 2003. Wong LY. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Seneviratne HR. Yun SH. Chemosphere 2006b. Yoshinaga T. Caudill SP.115(11):1670-1676. Frame SR.

htm. and perfluorooctanoate in retired fluorochemical production workers. Environ Sci Technol 2003. I: maternal and prenatal evaluations.2(1):53-76. Olsen GW. fast foods. Chemosphere 2004a. Ehresman DJ. Burlew MM. Fourth National Report on Human Exposure to Environmental Chemicals 257 .26(1):47-51. Mandel JH. Mar Pollut Bull 2005. Environ Health Perspect. Hansen KJ. Taniyasu S. et al. Yamashita N. Hanari N. J Children’s Health 2004b. Butenhoff JL. Hansen KJ. Olsen GW. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Bronson R. Seymour C. Lau C.82(1):359.115(9):1298-1305.) Tittlemier SA. Olsen GW. Thibodeaux JR.S. Half-life of serum elimination of perfluoroo ctanesulfonate. Coordinate induction of acyl-CoA binding protein. et al. (Erratum in: Environ Health Perspect.74(2):369-381. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Olsen GW.51(8-12):658-668. Cao XL et al. Cousins IT.198(2):231-241. Toxicol Sci 2003. Kannan K. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Butenhoff JL. and humans from Japan. Ehresman DJ. EPA). Burris JM. Toxicol Sci 2003. Olsen GW. Burris JM.45(3):260-270.74(2):382-392. J Occup Environ Med 1999. 1/15/06 Vanden Heuvel JP. Froehlich JW.113(5):539-545. Thomford PJ. Lundberg JK. Biochim Biophys Acta 1993. Helzlsouer KJ. Butenhoff JL.Perfluorochemicals Kudo N. Horii Y. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse.gov/opptintr/pfoa/pfoara. Hanson RG. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Gamo T. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Environ Sci Technol 2006.1177(2):183-190. Ellefson ME. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Lundberg JK. II: postnatal evaluation. Zobel LR. Seacat AM. Environ Health Perspect 2005. Peterson RE. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Burris JM. Kawashima Y. Butenhoff JL. Hanson RG. Reagen WK. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. A global survey of perfluorinated acids in oceans. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Hansen KJ. J Ag Food Chem 2007. Butenhoff JL. Toxicol Sci 2002. J Occup Environ Med 2003b. Mair DC. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. fate and transport of perfluorocarboxylates. Taniyasu S. Grey BE. Chemosphere 2007b.68:105–111. Olsen GW. van Belle G. Hansen KJ. Larson EB. Seacat AM. Sterchele PF.37(12):2634-2639. Horii Y.68(1):249-264.111(16):1900) Olsen GW. Hansen KJ.111(16):1892-1901. Available from URL: http://www. Olsen GW. Case MT. Church TR. et al.40(1):32-44. Stanton ME. Biol Pharm Bull 2003.55:3203-3210.perfluorohexanesulfonate. Olsen GW. Rogers JM. Kannan K.41(9):799-806. and food items prepared in their packaging.. Nesbit DJ. Church TR.54(11):1599-1611. Grey BE. (Erratum in: Toxicol Sci 2004. Moisey J. fish. Huang HY. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Richards JH. Historical comparison of perfluorooctanesulfonate. U.epa. Mandel JH. Petrick G. et al. birds. Toxicol Appl Pharmacol 2004. Miller JP. fish. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. et al. 2003a. perfluorooctanoate andother fluorochemicals in human blood. 2007a. Yamashita N. Sources. Rogers JM. Thibodeaux JR. Mandel JH. Korzeniowski SH. Buck RC. Environ Health Perspect 2003a. The developmental toxicity of perfluoroalkyl acids and their derivatives. Prevedouros K. Pepper K. et al. Lau C. Burris JM. Rogers JM.S. Butenhoff JL. Washington. Church TR. 2003. Environmental Protection Agency (U. Mandel JH. Barbee BD. Burris JM.

Phthalates Phthalates General Information Phthalates are industrial chemicals that are added to plastics to impart flexibility and resilience and are often referred to as plasticizers. Human health effects from phthalates at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. 1998). Parks et al. 1989).. garden hoses. and personal-care products. Infants may have relatively greater exposures from ingesting indoor dust containing some phthalates (Clark et al. and teratogenicity. 2004. Ingested phthalate diesters are initially hydrolyzed in the intestine to the corresponding monoesters. 1982. Phthalates are metabolized and excreted quickly and do not accumulate in the body (Anderson et al. shampoo... lotions. deodorants. The intravenous or parenteral exposure route can be important in patients undergoing medical procedures involving devices or materials containing phthalates. 1997. Albro and Lavenhar.. Nielsen et al. 1985.. Zacharewski et al. People are exposed through ingestion. some medical devices and pharmaceuticals. however. blood product storage bags. detergents. 2002).. phthalates can be released into the environment during use or disposal of the product. solvents. In chronic rodent studies. 2006). such as soap. and. In vitro studies showed that certain phthalates can bind to estrogen receptors and may have weak estrogenic or anti-estrogenic activity (Coldham et al. urinary metabolite and air phthalate concentrations are roughly correlated (Liss et al. indoor and ambient air. Dirven et al.. Phthalates have low acute animal toxicity.. 1985. For the general population.. and nail polish. inflatable recreational toys. followed by inhaling indoor air.. indoor dust. not all phthalates Phthalates and Urinary Metabolites in this Report Phthalate name (CAS number) Benzylbutyl phthalate (85-68-7) Dibutyl phthalates (84-74-2) Dicyclohexyl phthalate (84-61-7) Diethyl phthalate (84-66-2) Di-2-ethylhexyl phthalate (117-81-7) Abbreviation BzBP DBP DCHP DEP DEHP Urinary metabolite (CAS number) Mono-benzyl phthalate (2528-16-7) (some mono-n-butyl phthalate) Mono-isobutyl phthalate Mono-n-butyl phthalate (131-70-4) Mono-cyclohexyl phthalate (7517-36-4) Mono-ethyl phthalate (2306-33-4) Mono-2-ethylhexyl phthalate (4376-20-9) Mono-(2-ethyl-5-hydroxyhexyl) phthalate Mono-(2-ethyl-5-oxohexyl) phthalate Mono-(2-ethyl-5-carboxypentyl) phthalate (40809-41-4) Mono-isononyl phthalate Mono-methyl phthalate (4376-18-5) Mono-(3-carboxypropyl) phthalate Mono-n-octyl phthalate (5393-19-1) Abbreviation MBzP MiBP MnBP MCHP MEP MEHP MEHHP MEOHP MECPP MiNP MMP MCPP MOP Di-isononyl phthalate (28553-12-0) Dimethyl phthalate (131-11-3) Di-n-octyl phthalate (117-84-0) DiNP DMP DOP 258 Fourth National Report on Human Exposure to Environmental Chemicals . 2001. 2003). lubricating oils. 1997.. in humans. and other oxidized metabolites included in this Report. 2003. 1982. There are numerous products that contain phthalates: adhesives. 2001).. 1995). 2000. dietary sources have been considered as the major exposure route. 1993). Mortensen et al. Absorbed monoester metabolites are usually oxidized in the body and. but these effects either have not been demonstrated when tested in non-human primates or are yet to be studied. corresponding monoester metabolites. Human milk can be a source of phthalate exposure for nursing infants (Calafat et al. inhalation. liver injury. fragrances. vinyl tiles and flooring... Various phthalate esters have been measured in specific foods.. Harris et al.. 2005). liver cancer. Phthalates are also used as solubilizing and stabilizing agents in other applications. dermal contact with products that contain phthalates. Phthalates are often used in polyvinyl chloride type plastics. and toys (ATSDR. such as plastic bags. automotive plastics. and sediments (Clark et al. several of the phthalates produced testicular injury. hair spray.. The table shows the phthalate diesters. Okubo et al. excreted in urine largely as glucuronide conjugates (Albro et al. but in vivo studies did not support phthalates having estrogenic effects (Milligan et al. plastic raincoats. Pan et al. 1998. water sources. Jobling et al. 2003). In settings where workers may be exposed to higher air phthalate concentrations than the general population. Because they are not chemically bound to the plastics to which they are added. to a lesser extent. which are then absorbed (Albro et al. intravenous medical tubing.

reducing estrogen production. Environ Health Perspect 1982. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels.New York.gov/toxpro2. Springer. These differences may contribute to species-specific differences in toxicity (ATSDR. Also.. The National Toxicology Program’s Center for the Evaluation of Risks to Human Reproduction (NTPCERHR) has reviewed the developmental and reproductive effects of specific phthalates (http://cerhr. Evaluation of a recombinant yeast cell estrogen screening assay. Food Addit Contam 2001. at very high levels.cdc. In animals. Anderson WA.e.. Albro PW and Lavenhar SR. Massey RC. Available at URL: http://www. 2005.805:49-56. Scotter MJ. 2003. Castle L. Lovekamp-Swan and Davis. Rhodes et al. 2004. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). van der Broek PH. Springall C. Population estimates of concentrations of specific phthalate metabolites may differ by age. Calafat AM..niehs.cdc. Mackay D. 2003. Needham LL. Drug Metab Rev 1989.45:19-25. Silva MJ. 2004). Hoppin et al. and race/ethnicity (Silva et al. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . NTP-CERHR.. Sauer MJ. In Staples CA (ed). McDonnell DP.21:13-34. at higher doses. 2005). Cousins IT. Hauser et al. Biomonitoring studies on levels of phthalate metabolites provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of phthalates than are found in the general population.18(12):10681074. McKee et al. interactions with macromolecules and species differences in metabolism of DEHP. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. Jongeneelen FJ.. Peck and Albro.atsdr.3. 2002. Clark K. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. Herbert AR. which may be a pathway to the development of liver toxicity and cancers in these animals. Finding a measurable amount of one or more phthalate metabolites in urine does not mean that the levels of the metabolites or the parent phthalate cause an adverse health effect. 1985.cdc.. Slakman AR.. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. 2002). A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Available at URL: http://www. 2002). Coldham NG. Silvapathasundaram S.atsdr. 2004.. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. J Chromatogr B 2004. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. Environ Health Perspect 1997.. Schroeder JL. 2001. 4/20/09 Albro PW. 1986).. phthalates produced anti-androgenic effects by reducing testosterone production and.. and extent of metabolite conjugation to glucuronide (Albro et al. 1982. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites.. Pharmacokinetics. Hauser et al. Kessler et al.gov/toxprofiles/ tp135. 2006). 105:734-742.. 2000b. pp.. phthalates have been shown to induce peroxisomal proliferation in rodents. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. Toxicological profile for di-n-butyl phthalate update [online].Phthalates and metabolites have been tested. and Sertoli cell abnormalities in the male animals and. 1982). Information about external exposure (i.. gender. Part Q: Phthalate Esters.. but there are known species-related differences in the hydrolysis of diester phthalates. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. 2001). Vol. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2006). environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. efficiency of intestinal absorption. High doses of di2-ethylhexyl phthalate (DEHP). 2000c. dibutyl phthalate (DBP). 2004.html). Connor C.gov/ reports/index. Dave M. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. atsdr. ovarian abnormalities in the female animals (Jarfelt et al. 2001. 2007.html. testicular atrophy. Assessment of critical exposure pathways. 2000a.html. Corbett JT. Matthews HB. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. The Handbook of Environmental Chemistry. variation also occurs in the same person during repetitive monitoring (Fromme et al. Dirven HA.html.gov/ toxprofiles/tp9. 227-262.nih. 2007). Metabolism of di(2-ethylhexyl) phthalate. 2004. References Agency for Toxic Substances and Disease Registry (ATSDR). However. Jordan S.

Research Triangle Park (NC).niehs. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic.105:802-811.gov/chemicals/ phthalates/dbp/dbp-eval. Parker MG. Hauser R. 6/2/09 NTP-CERHR. Koch HM. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Park S. Skakkebaek NE. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Silva MJ.html.niehs. Epidemiol 2005. 6/2/09 NTP-CERHR. Zhang S. Fromme H. Baird DD. 6/2/09 NTP-CERHR.18(1):122. Csanády G. Kano I. Available at URL: http://cerhr. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Yokoyama Y.nih. Leffers H. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Anal Bioanal Chem 2005. Sumpter JP. Park MG. Ryan L.46(11):643-647. Jacobsen H. Jarfelt K.html. Hass U. Kalita JC. Mechanisms of phthalate ester toxicity in the female reproductive system. Environ Health Perspect 2003. Decreased serum free testosterone in workers exposed to high levels of di-n-butyl phthalate (DBP) and di-2-ethylhexyl 260 Fourth National Report on Human Exposure to Environmental Chemicals . Grote K. Ladefoged O.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Chahoud I. 2000c [online]. Meeker JD. White R. Tsukino H.nih. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Environ Health Perspect 1997. Reynolds T. Duty SM. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Sumpter JP. Brock JW.195:142-153. Numtip W. J Androl 2004. et al. Drexler H. Liss GM. Brock JW. Harris CA. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].11(5):381-387. Kano K. Determination of phthalate monoesters in human milk. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Dalgaard M. Yoshimura M. Hoppin JA.103:582-587.html. Nielsen J. Gans G. Reproducibility of urinary phthalate metabolites in first morning urine samples. Andersson A-M. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Duty S.19(4):505-515. 6/2/09 Okubo T. et al. NTP-CERHR. 2000b [online].Phthalates in human urine samples. Int J Hyg Environ Health 2007. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.64(8):555-560. Angerer J. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride.26(8):1219-24. Jonsson BAG. Biol Pharm Bull 2003. Richthoff J. Hartle RW. et al. Meeker JD. Environ Health Perspect 1995.html. 2006 [online]. Boehmer S. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Stringer WT. Albro PW. Environ Health Perspect 1998. Calafat AM. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Filser J. Hanaoka T.nih.210:21-33. gov/chemicals/dehp/dehp-eval. The estrogenic activity of phthalate esters in vitro. Milligan SR. Chen Z. Skerfving S. McKee RH. Suzuki T. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Int Arch Occup Environ Health 1993. Hauser R. Kessler W. Jobling S.niehs. Balasubramanian AV. Research Triangle Park (NC).gov/chemicals/dehp/dehp-eval. Main KM. Lovekamp-Swan T. et al. Davis BJ. Environ Health Perspect 2002.110(5):515-518. Available at URL: http://cerhr. Henttu P. Toxicol Appl Pharmacol 2004. Giwercman A. Pan G. Mortensen GK. Hum Reprod 2007. Silva MJ. Akesson B. Calafat AM. Rylander L. Ryan L. Available at URL: http://cerhr.22(3):688-695.25(2):293-302.nih.niehs. Davis BJ. and infant formula by tandem mass spectrometry (LC-MS-MS). Borch J. Research Triangle Park (NC). Silva MJ. Butala JH.106(1):23-26. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004.112(17):1734-1740. 2000a [online]. Reprod Toxicol 2005. Environ Health Perspect 2004. Singh NP. Scand J Work Environ Health 1985. David RM. Wang P. Available at URL: http://cerhr. Bolte G. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. consumer milk. Am Ind Hyg Assoc J 1985.16(4):487-493.112(17):1740].382:10841092. Hagmar L. Research Triangle Park (NC). Reprod Toxicol 2004.111(2):139-145.

Urinary levels of seven phthalate metabolites in the U. Jackson SJ. Albro PW. Reidy JA. Orton TC.45:11-17. Klinefelter GR. Parks LG. et al. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.58:339349. Fourth National Report on Human Exposure to Environmental Chemicals 261 .65:299-308. Barr DB.S. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Crit Rev Toxicol 2006.46:282-293. Silva MJ. Meek MD. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Toxicol Sci 2000. Abbott BD. Zacharewski TR. Lambright CR. Rusyn I. Peters JM. 112(5):A270]. Environ Health Perspect 1982. Wu ZF. Environ Health Perspect 1986. Barlow NJ. Pratt IA. Bratt H. et al. Peck CC. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. et al. Matthews JB. Clemons JH. Rhodes C. Fielden MR. Environ Health Perspect 2004.112(3):331-338. Malek NA. Cunningham ML. Toxicol Sci 1998.114(11):1643-1648.36:459-479. Batten PL. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Ostby JS. Caudill SP. Environ Health Perspect 2006. Hodge CC. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man.Phthalates phthalate (DEHP): a cross-sectional study in China.

9-87.4) 129 (98. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.9-16.3-21.2-38.8 (50.7-15. because it is not bound to products in which it is incorporated.2 (43.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16.3 (29.4) 98.6-92.1 (32.5 (55.8-48.3 (12.7-172) 103 (74.4) 14.3-74.4) 71.1.8 (21.6) 13.5-94.3 (13.2 (19.0-55.4) 35.0 (55.5-35.9) 49.4-15.3-18.6 (21.3 (30.7-82. 2000).7 (53.4 (13.4-25.1) 29.4) 65.4 (29.5 (26.8) 63.1) 76.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5-25.0 (23.6 (41.8-133) 89.0) 23.0 (27.6) 95th 103 (94.S.0) 24.5 (66.2-19.8-121) 79.4) 12. and 03-04 are 0.7 (13.5) 15.0) 16. High dose BzBP and its monoester metabolites.6) 13.5-97.7-119) 99.4-24.1 (55.9) 12.9) 11.8 (71.6) 35. sealants. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.8 (30.2-40.4-62.6) 24.2-33.5 (47. and diet is the major source for general population exposure.1 (10.5) 30.8) 14.3-75.2 (14. can produce developmental and reproductive toxicity in rodents.1) 67.8-35.6-43.5) 16. 2004.4-92.8.3-34.3) 63.0 (11.2) 15.8 (71.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.1-18.1-16.2-183) 101 (78.0 (20.3-161) 99. residents (Blount et al.7 (15.1-15.9) 18.7-14.3) 13.1-16.1) Selected percentiles ( 95% confidence interval) 50th 17.2) 32.3-27.3 (54.0 (30.6) 16. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8 (53.9 (28.4 (27.3 (29.3-12.9 (13.7) 38.8 (14. and to a lesser extent.9-62.4) 49.7) 23.0) 32.3-125) Total 15.9-30.6 (12.5-145) 138 (106-241) 143 (127-179) 120 (99.4 (31.4) 38.8-14.5) 23.0-85.1 (19.1 (14. it can be released into the ambient air during use or disposal of the products.4 (10.6-39.5-84.1) 13.1-120) 52.6) 35.7-13. including MBzP.8-17.1 (14.6-38.9 (11.1 (58.0-106) 58.6-150) 94.2) 12.8-64.0 (12.2) 14.8 (80.8-76.0 (30.9-47.4-127) 80.1-214) 166 (116-191) 145 (110-213) 88.2-31.8-98.1) 31.0) 70.2 (47.8 (12. IARC considers BzBP not classifiable with respect to human carcinogenicity.1-15.3 (22.5-41..4) 33.5 (67.7 (82.6-79. and 0.0 (14. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1-43.6 (13.0 (15.4 (48.6-116) 122 (102-142) 101 (85.0 (43.3) 23.5-18.3) 94.3 (12. NTPCERHR.9-14.8 (86.Phthalates Benzylbutyl Phthalate CAS No. 262 Fourth National Report on Human Exposure to Environmental Chemicals .6) 25.9) 14.5) 27.4) 35.1) 32.8-72.5 (13.1 (13.6-92.1-61.0) 34.8 (28.2) 13.1 (13.8-13.4 (68.3) 15.7 (11.8) 33. 01-02.5) 15.6-18..1) 68. respectively.9) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 39.2-20.0 (26.1-35.9 (16.6-132) 103 (84.9 (39.9-28.8-41.2) 78. some personal care products.3) 54.2) 22.5-40.6) 63.7-16. vinyl tile.0-130) 101 (86.4) 80.7-58.9 (12.5-14.8 (38.8-18.9-49.2-115) 113 (91.6) 67.0 (33.5 (76.4-120) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 13. 0.9 (22.8-17.2 (25.3 (44.3) 37.2) 33.6 (13.8) 24.2) 66.8) 28.3-88.S.3-43. see Data Analysis section) for Survey years 99-00.1) 12.1-38.9 (12.7-16. interval) 15.9) 43.4 (63.6) 14.6-29.5-36.6 (13.9) 15.5-33.3-130) 122 (88.0) 90th 67.4 (53.6) 29.5-62.6 (32.7) 40.0) 20.5) 55.5 (57. and 2003-2004 were generally similar those reported in U.7-170) 169 (134-198) 152 (99.6) 50.2 (11.1-39.4) 51.8-16.9-190) 86. 2001-2002.5-36.6 (53.6) 37.9) 14.6-72.8-14.4 (32.1 (20.3-18.5) 82.4 (53.4 (10.3-91.7-35.6-17.4) 75th 35. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.0-26.9) 13.7 (51.0) 33.5 (27.5) 65.9 (70.2 (10. population from the National Health and Nutrition Examination Survey.7-16. car care products.1-90.2) 14.2) 69.4 (59.2-39.7 (80.2-16.0 (34.7 (70.2-17.4-16.1) 14. Food crops take up BzBP.3.3 (12.2-116) 122 (102-143) 101 (84.0 (15.9-27.9 (21.7 (12.2) 17. 2000).3-82.6) 15.6 (13. BzBP can be released into the environment during its production and.4) 108 (96.2-16.1-116) 122 (93.2-155) 91.8 (10.7-25.7-17.4 (32.3 (33.3) 13.5 (61.4) 81.6 (66. particularly male animals (McKee et al.6) 14.2 (19.8-16.

8) 13.3-11.7-14.6-20.0) 24. 2003).0-51.9) 11.1 (21.3-34. 2005).7 (11.3) 14.8) 33.9 (15. Urinary Mono-benzyl phthalate (MBzP) (creatinine corrected) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6-26.9) 12.7) 25.6-12.8) 16.4) 90th 50.6) 13.7 (13. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.9 (51.6 (34.9 (12.9 (24. In an annual sample of German university students.0 (41.8 (50.3-73.1) 142 (99. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect. 2004).7-69.3) 37.6) 38.2-78.7-14.5-99.7-15.2) 26.4) 60.1 (14.8-13.4-27.4-60.5) 23.4-14.2-57.8-16.4-19.0-15. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.5 (11.7 (14.7-15.2-12.1) 17.2-117) 95. 2006).3-64.3) 18.4 (26.2-13. 2007). 2004.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .8-14.2 (56.2) 11.5-42.4 (74.8 (69.3 (35.5) 41.5) 16.9 (9. in young Swedish men (Jonsson et al. and in a small sample of German residents (Koch et al.6 (24.3) 55.7) 38.0 (10. 2007).9-13.1 (21.4-15.1 (13.Phthalates York City (Adibi et al.4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.1 (21.8) 11.6-99.4 (11.6 (51. population from the National Health and Nutrition Examination Survey.8-13.8) 33.8-15.8-48.6 (11.5) 78.7 (54.4-18.1-35.6 (19.9 (39.4-93.3 (60.7 (23..3) 16.1 (15.0) 60.6) 73.7-123) 77.6-86.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.4) 13.1) 35.0) Selected percentiles ( 95% confidence interval) 50th 13.4) 12.4) 21.1 (43.2) 15.9) 52.1 (13.5) 10.3) 36.0-48. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.1-27.9-23.5) 20.0-53. Weuve et al.0 (67.7 (11.3 (38.0) 12.8) 46.4) 14.5-38.9) Total 14. in men attending a Boston infertility clinic (Duty et al.1-14.2 (69.4) 25.9-104) 62.2 (27.8) 54.4 (69.9) 64.9 (24.7-12.4-23.4 (11.4) 50.0 (41.6 (30.8-39. Hauser et al.4-90. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2 (40.5) 14.6 (22.9 (12.8-64..4) 28.1-120) 77.8 (49.4-116) 73.6 (15.9-40.3) 13.2-15.6-15.5 (10..2) 32.1-12.1 (9.3-38.1) 27.6) 58.4) 15.5-31.8-14.S.7 (38.5-58.7-20.7-29.1 (18.7 (19.0 (12..2-49.8 (11.3) 12.4-79.2) 12.9-16.5-29.0 (49.7 (55.5 (49.7 (11.4) 17.7) 11.0-26.9-14.3 (23.95-14.8 (46.4-142) 134 (116-176) 136 (85.2) 67.0) 13.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.73-12.2 (41.3) 89.1 (46.6) 75th 25.9) 42.8 (10.1) 24.9-69.2-13.8 (12.3 (15.8-173) 195 (121-305) 229 (99.8) 71.4 (21.3) 90.8) 108 (75.6) 12.7) 46.9 (55.0) 11..0 (33.4 (25.6 (11.8) 26.1-29.9) 11.2) 11.5 (42.7-20.8-85.1-125) 86.4) 51.5 (48.6 (30.1 (25.1 (34.9) 24.3 (24..4 (33.6-81.5 (9.7 (12.2-15.0 (13.1) 12.8-15.4 (34.9 (10.6 (11.3-16.2-21.5-13.6) 25.4) 44.5-26.0 (62.6-116) 74.4 (60.1) 24.8 (64.8-42.8-60.5-58.5-79.0) 15.1-58.1 (41.1-12.9) 12.3) 29.7-61.1-79. A small study of African-American women in Washington.4-17.8) 53.6) 30.4 (10.8-69.4 (63.8-34.7 (21.1 (23.6-40.5 (35.9) 100 (80.1 (19.2-51.7-56..9 (54.0) 49.5-26.5-213) 49.5 (10. interval) 14.4-14.0-109) 65.7) 56.8-27.0 (12.8 (30.6 (36.0 (11.7 (18. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.4 (11. Hoppin et al.3) 14.6-47.5-76.5-23.3) 67.5) 46.4 (12.9 (43.9-13.8) 68.5-16.5 (12.8-80.2-17.9 (29.. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.2-26.4 (13.9 (22.8 (13.4 (46.3) 13.7-90..3 (39.7 (59.8) 53.9 (10.7) 19.8) 15.5) 13.6 (57. and females compared to males (Silva et al.0-90.6) 12.7 (13.9-115) 57.1) 39.1 (11. adolescents compared with adults.1 (21.7-19. 2003).3 (13. 2005.9-83.1) 80.1 (53.9) 12.9-28.5 (56. 2002).8) 34.9-62.7-397) 70.3) 73.69-11.9 (15. In NHANES 1999-2000.4) 13.4) 104 (89.4-102) 70.8 (57.0) 24.5-57.4-42.2) 11. 2002.5) 17.6) 53.3) 21.8) 24.7-19.1) 23.4-99.5) 95th 77.3) 13.3 (12. Limited studies in children younger than 2 years old have found median and geometric mean urine MBzP that were similar to children aged 6-11 years in the NHANES subsamples (Brock et al.8) 56.0 (38.5-61..0-27.8-13.6 (14.7-31.6-13.8) 80.

Giwercman A. Caudill SP. Wittassek M. Camann DE.110(5):515-518. Butala JH. Weuve J. Wiesmuller GA. Hum Reprod 2007.210(3-4):319-333. Baird DD. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Ryan L. Environ Health Perspect 2004. et al.93:177-185. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Calafat AM. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.18(1):122. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Hodge CC. Atlanta (GA). Silva MJ. et al. et al. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Davis BJ.nih. 2000 [online]. Silva MJ. Needham LL. Sanchez GN. Reidy JA. Sampson EJ. Environ Health Perspect 2000. Meeker JD. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Phthalate monoesters levels in the urine of young children. Brock JW. Barr D. et al. Environ Res 2003. Needham LL. Bull Environ Contam Toxicol 2002. Levels of seven urinary phthalate metabolites in a human reference population.Phthalates References Adibi JJ.22(3):688-695. Environ Health Perspect 2006. Reprod Toxicol 2004. Int J Hyg Environ Health 2007. Schettler T. Urinary levels of seven phthalate metabolites in the U. Third National Report on Human Exposure to Environmental Chemicals. Caudill SP. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Caudill SP. 2005. Silva MJ. 4/20/09 Silva MJ. Epidemiol 2005. Hu H. Green RA. Chen Z. Duty SM. Angerer J. NTP-CERHR. Hauser R.108(10):979-982. Poland. Rossbach B.S. Richthoff J. Perera FP. Hilborn ED. Available at URL: http://cerhr. Jonsson BAG. Dobler L. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Gans G.68:309-314.111(14):1719-1722. Calafat AM. Pirkle JL. Rylander L. Koch HM. Barr DB. Reproducibility of urinary phthalate metabolites in first morning urine samples. Research Triangle Park (NC). Environ Health Perspect 2002. Jacek R.16(4):487-493.niehs. Hagmar L. McKee RH. Drexler H. Environ Health Perspect 2003. et al. Helm D.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Koch HM. Malek NA. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Jedrychowski W. David RM. Ryan L. Singh NP. Brock JW.25(2):293-302. Prenatal exposures to phthalates among women in New York City and Krakow. Duty S. J Androl 2004. Centers for Disease Control and Prevention (CDC). DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Eckard R. 112(5):A270]. Hoppin JA. Silva MJ.112(3):331-338. et al. Blount BC. et al.html.114(9):1424-1431. Brock JW.

00) 4.1 (8.60) 3. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.0) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2. Survey Geometric mean (95% conf.9 (16.5) 14.0) 12. NTP-CERHR. 2003)..30-3. 2000.20-12. 2001).2 (8. Biomonitoring Information Median concentrations reported in the NHANES 19992000.20 (3.00-11.40-4.55 (3.7 (16.8) 677 652 703 699 1216 1088 Limit of detection (LOD. 2004. pharmaceutical coatings.56 (3. interval) 2. about 65% to 80% of a dose is eliminated in urine within 24 hours.3.10-9. population from the National Health and Nutrition Examination Survey.50 (6.90 (4.6 (13.0 (11.5) 19.7 (17.5) 23.30) 6.70-4.2 (12.91) 4.4) 12.46 (3.5 (27.30 (1. in men attending a Boston infertility clinic (Duty et al.30 (4.6-18.7 (7. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.3 (13.3) 33.40-17.90 (4.80 (2.9-23.0-38.8) 40.6 (14.5 (11.4 (20..00-4.6-14.9) 10.37) 6.00 (7.4-12.1) 16.40-5. in a small sample of pregnant women in New York City (Adibi et al.6 (10.90 (3.3-24.67 (5.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.20-6.0 and 0.10) 8.63) 3.97-7. 2007).94) Selected percentiles ( 95% confidence interval) Sample 95th 17.S.49-2.90-2.2 (11.40-3.46) 2. and in a small sample of Japanese adults (Itoh et al. 2003).6 (11.5-16.46-5. Following oral administration of DBP to humans. 2000).40 (3.44-2.50) 18.80 (3. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.60 (2.90-4.71 (2.50-6.59) 3. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.10 (4.30-6. and insecticides.55) 2.9) 15.5) 22.9 (16. the median Urinary Mono-isobutyl phthalate (MiBP) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5) 25.5 (10.90-4.20-12.5) 12. 2005.00) 4.20-2.0-14.90) 12.3 (19.3 (11.7) 15.30 (3.2-33.8 (9.90-7.1 (13.73 (2.50) 8. 84-74-2 Di-isobutyl Phthalate CAS No.1-25.6 (10.00-6.7) 18.07 (3.48 (2.22 (3.7-31.70 (5.80-5. 2004.70 (2.10) 3.56 (5.10) 9.60 (5.50) 2.6) 16. residents (Blount et al.11-3..3-30.17 (2.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.66) 2..80-5.28-5.0) 13.20-9..30-6.80 (2.22) 3.10 (3.00) 7.80) 75th 5.82-3.40 (6. Fourth National Report on Human Exposure to Environmental Chemicals 265 .40 (2.7) 4. 2005).8) 21.9-14. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine. In addition. and also in some printing inks. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.5-16.00-6.50) 5.40 (2.1-12. Koch et al. CDC.30) 10..60 (8.50-2.1) 25.72-3.70) 5.60 (4.5-29.50 (3..90 (6.00 (5.30-2. 2005).68 (2.30) 2. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.6-34.40) 5.3 (18.4) 22.4) 5. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.17) 4.3) 18.0) 20.97) 2.0) 9.19-3.73-5.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.Phthalates Di-n-butyl Phthalate CAS No.10) 11.2-22. When total DBP metabolites have been measured.02) 4.20 (7.0-25.10-2.30-13.70-8.50) 90th 12.20) 7.30) 5.5 (17.96) 3.6-20.6 (9.43) 6.7 (18. they have been referred to as monobutyl phthalate (MBP).30) 10..3-20.10) 2.00) 6.6) 16..1) 22. Hauser et al. see Data Analysis section) for Survey years 01-02 and 03-04 are 1. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.00-9.2) 5.24-8.60-6.56) 3.40-12.3-19.20) 4.46 (2.6) 12.97) 4.00) 10.7-20.5) 18.5 (20.40 (7.56-4.40-9.0-18. 2005).6 (13.30-11.81 (3.40-3.80 (5.7-18.6) 17.0 (13.6 (14.7 (9.0 (19.50-10.26 (2.33 (2.6) 10.7) 7.10 (4.30-7.80 (5.50) 7.2-14.3-48.85-6.S.40-4.20 (6. OSHA has established a workplace air standard for external exposure to DBP.6) 26.7-31.3-18.7 (17.0 (13.84) 4.3-43.1-20. Studies of children found age-related differences in urine MBP levels.3 (16.6-26.4-27.3 (16.70) 3.5) 18.6) 17.0) 24.5-24. mostly as MnBP (Anderson et al.1-17.7) 14. DBP can produce reproductive toxicity in male rodents (McKee et al.70-4.3 (13.10-9.50-4. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.4 (14.6 (29.3) 3.

00 (3.4) 7.62-12.18 (4.76 (3.02 (7.31) 2. 2004).8-18.56-4.33 (2.72) 5.0-18. Biomonitoring studies on levels of MnBP and MiBP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of dibutyl phthalates than are found in the general population.3) 28.31) 2.6 (9.89-5.8 (8.6) 11.2 (11.1) 4.1 (10.36-7.4-16.31 (2.2) 24.39) 5. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.32 (7.26-2. population from the National Health and Nutrition Examination Survey.24) 3.04-5.6-19.69) 4. up to four and 13 fold.81) 9.7) 11. ranging from more than one-tenth the NHANES median (Itoh et al.20-3.8-36.21 (5.7) 19.5-19.33) 3.1) 7.and gender..4) 23.2 (10.84 (8.56-15.17 (2.43) 3. Over this time.0 (10. Weuve et al.27-12.02-10.5 (9.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.1-15.3 (17.98 (2.3) 13. 2005).79-6. 2004).18) 4.38 (6.54) 2.32) 7. An analysis of NHANES 2001-2002 showed similar age.99) 7.47-12. Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.53-4.45) 3.14 (4. Survey Geometric mean (95% conf. 2006). to about two to fourfold higher (Fromme et al.88 (2.30) 2.1-24.13-6.2) 9.3) 16.34 (3.04) 3.18-4.81) 4.44 (3.19 (2.51) 2.29-8.93-6.73 (5.05) 2.03-11.83 (2.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.20-4.64-7.32 (3.8) 10. the students’ median values for MiBP levels remained relatively unchanged.22 (2.7 (11.08) 75th 4.68) 3.75 (4.1) 15.41 (2.57 (3.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.86) 6.78-8.52 (2.65-11.9 (15.18-10.42) 2.1-25.94) 6.5) 13.76-15.20-2. 2007).52-3.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.5 (11.96 (3.11) 5.00-3.9) 12.25) 5.20 (7.6) 13.0 (12.53-5.8 (10.1 (11.0) 3. Between 1998 and 2003.36-2. 2002.76-3.57 (3.15) 3.53-3.07 (2.38-10.30 (6.11-2.43) 3.51) 5.54 (2.58-4.35) 3.00-3. respectively.74-3.31 (7. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al.33 (3.3) 18.6 (10.1) 11.9-16. 2005).4) 15.67-5.6 (8.00-7. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.6 (15.0 (8.62 (6.03 (5.7-28.68) 5.09-2.52-20.39-3.01-2.0) 7.69) 6.9 (11.54 (4.04) 7. samples from German university students had consistently higher median urine levels of MnBP and MiBP.68 (2.3) 13.10-5.55-6.59 (4. while MnBP declined (Wittassek et al.66) 2..18 (1.46) 3.82) 4.2-13.95) 10.61-3.00) 01-02 03-04 01-02 03-04 01-02 03-04 4..8 (9. In an analysis of NHANES 1999-2000.8-13.86-4.0) 11.07-5.11 (5.1-12.17) 90th 8.9 (9.56) 2.08-2.6 (8.3 (13.7 (21.84 (4.80 (3.72-7..85 (2.66) 10.95-3.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .S.78) 8.95) 2.6 (12.21) 10.4 (12.7 (9.29-3.99-4.66 (8. than adults in NHANES subsamples during the same time period.7) 10.6) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2.56) 5.2) 8.69-7.82 (4.58-3.5) 15.9-40.7) 3.37) 3.15-4.81 (6.28 (4.89 (3.91-6.64-10.97-2.81 (3. 2007).33-9.8-18.13 (2.64-7.66) 4..20 (2.76-3.79-8.7 (13.74 (4.75 (6.. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.18) 3.65-4.78) 9.69 (2.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.80-3.26 (2.47-5.79 (4.51) 15.1) 13.80) 7.57-4.17-12.47 (3.43) 3.92 (7. Finding a measurable amount of MnBP or MiBP in urine does not mean that these levels or the parent compound cause an adverse health effect.1) 10.65 (4.52) 3.46 (2.94-12.20 (2.03-7.46-11.28-13.94 (5.6-19.9-26.89) 6..0) 15.2-15. interval) 2.

7 (18.0-32.0 (36.5 (59.2-87.7 (19.3 (17.4 (84.3) 24.4-44.7 (24.2 (18.3-96.8) 62.8 (19.4) 20.4-20.4-31.3 (42.7 (64.6) 21.2 (59.0-24.7) 92.5) 19.2-159) 92.0-21.9-79.0) 38.6-20.5) 65.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.5 (28.5) 17.8) 43. and 0.7 (18.6-37.5) 78.2-93.6-143) 127 (99.7 (38.6 (32.5-27.6 (26.1) 36.5-43.9.4 (36. population from the National Health and Nutrition Examination Survey.5 (30.5-121) 106 (94.2 (21.0 (45.7) 52.5-53.5-47.6-36.4 (21.8-42.0-26.9 (20.2) 90th 98.4 (35.1 (28.5) 31.6) 38.0) 120 (98.3 (23.6 (61.0-73.9) 71.7) 42.1 (26.4-18.4) 64.6 (44. and 03-04 are 0.7 (22.5) 36.0-19.4 (38.6) 39.0 (78.8-29.7) 74.7-111) 64.6 (90.9) 18.3 (36.1 (21.1) 46.0 (30.4-26.3 (23.0 (15.6) 20.8) 23.0 (25.7-42.1 (17.1-92.2) 68.7-106) 69.1 (51.1 (18.9) 21.7) 124 (98.3 (56.3 (51.8) 19.7-92.1 (41.0 (18.1) 17.4-42.4-25.3-136) 137 (107-162) 119 (90.3-76.5) 40.7-42.2 (25.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.1-51.7-34.2 (58.6) 46. referred to as monobutyl phthalate (MBP).9 (17.1 (36.6-40.3-85. see Data Analysis section) for survey years 99-00.3 (30.3-79.3) 21.1-24.6-29.6-69.7 (43.5) 20.3-60.2-23.4.4 (25.6 (65.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.1-80.9 (17.S.6) 35.3-67.6) 17.4 (23.1-27.6) 80.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.6 (19.2) 38. 1.4-159) 107 (84.5) 47.1 (19.5) 34.7-116) 95.2-49.0) 117 (104-131) 112 (84.4) 59.1 (31.2 (74.8-123) 101 (90.2 (21.9-42.0) 84.5) 95. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.3 (30.3 (37.0 (23.1.6-31.9-28.8 (57.1) 30.6 (22.9) 36.6-24.8) 58.5-60.5) 85.2 (17.1) 23.2-56.0 (72.3) 36.6-44.1) 23.2) 42.4) 22. Survey Geometric mean (95% conf.7-26.6 (16.8-22.2) 62.1 (16.7 (33.4 (35.5) 24.9 (79.8-25.6-29.1) 19.0) 20.9) 26.1) 23. 01-02.9-53.3-24.7-127) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 22.1) 20. Fourth National Report on Human Exposure to Environmental Chemicals 267 .4 (35. interval) 24.4 (72.3 (60.6-113) 108 (90.5) 21.4 (35.2) 32.1 (54.7 (51.9-114) 116 (97.5-44.5) 26.2 (78.2 (19.9-87.9-22.7) 28.8-119) 90.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.7-53.4) 52.6 (55.5 (59.0-19.5) 36.1 (19.4-60.5-42.0) 30.0) 21.0 (20.3-40.9 (79.9) 75.9-33.9) 29.3) 19.1-20.4 (71.1 (62.0-24.2-21.7-117) 118 (108-143) 93.1) 25.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.1-75.6-48.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8-132) 95.2-114) 73.0) 27.2-63.2 (79.9-22.5 (74.2-32.3-21.1-29.2 (20.1 (19.7-91.5-117) 95.7-24.3) 40.3-145) 85.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.5 (29.1) 47.3) 26.2) 26.7 (28.7-20.7-34.2-33.6) 71.2-24.3) 23.1) 31.1 (34.9) 46. *In the 1999-2000 survey period.3) 18.0 (31.6-49.7 (16.8) 75th 51.7-121) 97.6 (48.6-33.1 (58.0) 31.2-22. respectively.9-101) 77.0 (17.8) 48.4 (19.2) 20.1-22.7 (70.9-92.0-58.2 (75.1 (19.5-47.5) 37.0-51.1-82.

6-44.9 (19.1) 22.1-23.2-22.4 (50.7 (60.2-21.5 (30.7-19.5) 84.0 (71.3 (52.9) 28.8) 30.5) 90th 68.2-16.8) 34.7 (81.2 (38.0-92.2 (16.9-100) 86.3-20.2-22.6) 18.3) 52.6 (61.3 (17.9) 52.5 (18.6-27.6) 24.3-38.6-53.9 (56.0 (70.8 (33.S.8-43.3 (21.3 (46.2) 21.4-76.1) 44.5-76.8) 17.1) 53.8) 23.2-28.1-32.6) 24.9 (37.9-49.2-106) 64.7-21.1 (61.8) 34. Survey Geometric mean (95% conf.3) 20.0) 19.4) 16.8) 20.1) 42.3 (17.7-39.9 (20.1-83.9-68.0 (26.3 (76.9 (30.4-34.6 (57.6-50.6-128) 96.4 (17.5) 21.4-164) 96.4) 53.3 (24.3) 59.0 (50.8-24.4 (31.0) 53.3-114) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older 99-00* 01-02 03-04 Gender Males 99-00* 01-02 03-04 99-00* 01-02 03-04 17.6-119) 63.4) 51.7) 20.3) 18.8) 75th 38.1 (29.3 (60.3-78. interval) 22.9 (16.5 (15.0) 55.0) 41.0-75.8 (13.2) 159 (102-263) 147 (93.6 (74.7-23.5-142) 89.9-26.3 (42.2 (19.9 (35.7-26.3-81.0-19.1-128) 97.3-39.9-56.6) 83.1 (46.0 (16.9-38.8) 35.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.4 (56.4 (45.8) 22.5) 17.3) 19.5-22.7-80.3-49.6) 39.5-70.3) 33.9) 39.6-24.9-14.2-27.9 (30.9-70.8) 20.6-19.8 (16.2-85.9 (39.1) 61.7 (73.6-32.3-32.7 (20.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4 (16.4-131) 81.2) 59.8) 28.5-142) 81.7-78.6) 25.7) 42. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.2) 65.7-28.5) 91.3 (52.2) 16.1 (34.7-51.8-235) 137 (108-198) 88.9-68.0 (20.8) 13.3-71.4-72.0) 28.2) 31.2-22.3 (28.5) 39.6-28.8) 19.0-17.6-26.6) 64.4 (16.6 (29.9 (30.8 (17.3-26.0-113) 104 (83.6-155) 91.2-18.7 (16.0) 25.1-18.3) 35.8-23.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.4 (19.0) 26.5-21.7 (43.3-18.1) 35.6-24.6-92.4 (13.7-42.6 (25.2) 74.6 (25.8-32.1) 37.1) 21.4) 62.5-18.7 (12.6) 34.9) 30.8 (18.4 (33.4 (68.8 (22.2 (19.4-65.0 (34.6 (31.0-38.9 (58.9) 20.4 (31.6 (41.0 (61.1 (32.3-17.9) 14.4 (20.6-42.9 (35.3-21.6 (19.9) 24.5 (64.9-36.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.6) 37.9 (64.3) 33.4) 15.3 (48.4-47.3) 21.0-47. population from the National Health and Nutrition Examination Survey.8) 17.8 (50.4) 20.6 (17.4-103) 117 (83.0) 35.3 (17.4-24.2 (83.7 (54.8 (65.1 (15.6 (27.5-16.7) 36.6-43.8-24. 268 Fourth National Report on Human Exposure to Environmental Chemicals .1 (56.3-23.9) 19.0) 75.0 (43.3 (55.3 (69.6-23.7-20.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.7) 19.9-84.1) 20.4-135) 71.0-60.1 (21.0 (18.4 (31.3-106) 74.5-23.3 (16.2 (35.3-21.8) 17.5-30.4 (53.4 (17.5) 134 (93.9 (21.0 (18.0 (15.8) 40.6 (72.0) 94.2-61.0) 59.5-64.3) 19.9) 91.3 (19.1-21.2-48.0) 70.8 (25.1-62.6-74.4 (23.4 (50.6-23.4 (47.8 (18.5-37.5 (14.6) 23.9-105) 85.0) 29.1-99.5) 82.7 (27.1) 17.6) 31.3 (71.4) 19.7-37.0 (19.4 (37.6-22.0) 81.1) 50.8) 63.2-179) 84.7 (60.2-73.9 (73.1) 20.9-34.7 (28.6-44.8 (18.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.0 (27.5) 60.3) 17.7-19.5-15.0 (52.9) 62.6) 38.3-40.4-61.1-99.6-16.3) 67.5 (18.4) 21.7 (19.0-90.5-41.5 (81.0-41.4) 15.2-86.0) 108 (71.0 (69.9) 49.7 (57.7 (14.4 (18.6) 14.6) 65.

Environ Res 2003. et al. et al. 2000 [online].18(1):122. Giwercman A.25(2):293-302. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.nih. 112(5):A270]. Phthalate monoesters levels in the urine of young children. Butala JH. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Third National Report on Human Exposure to Environmental Chemicals. Jedrychowski W.93:177-185.114(9):1424-1431. Yoshida K. Schettler T. Duty SM. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. 2005. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Environ Health Perspect 2003. Masunaga S.22(3):688-695. Brock JW. Koch HM. David RM. Sampson EJ. Boehmer S. Barr DB. Jacek R. Koch HM.210(3-4):319-33. Hum Reprod 2007. Int J Hyg Environ Health 2005.112(3):331-338. Epidemiol 2005. Itoh H. Reidy JA. Environ Health Perspect 2000. Available at URL: http://cerhr. Poland. Singh NP. Koch HM.108(10)979-982.niehs. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Eckard R. Int J Hyg Environ Health 2007. Rossbach B.16(4):487-493. Caudill SP. Pirkle JL. Meeker JD. Silva MJ. Weuve J. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Wittassek M. Green RA. Hauser R. Wiesmuller GA. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Duty S. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Food Addit Contam 2001. Castle L. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.html. Ryan L. Angerer J.gov/chemicals/ phthalates/dbp/dbp-eval. Atlanta (GA). Needham LL. Hodge CC. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Perera FP. Urinary levels of seven phthalate metabolites in the U. Dobler L. Calafat AM. Silva MJ. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Silva MJ.18(12):10681074. Springall C. et al. Anderson WA. Centers for Disease Control and Prevention (CDC).Phthalates References Adibi JJ. Caudill SP. Levels of seven urinary phthalate metabolites in a human reference population. Ryan L. Drexler H. Hu H. et al. Scotter MJ. Chen Z. Silva MJ. Drexler H. Blount BC. Barr D. et al. Sanchez GN. Fromme H. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Environ Health Perspect 2004. Brock JW. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. et al. Hagmar L. Hilborn ED. Gans G. J Androl 2004. Jonsson BAG. 4/20/09 Silva MJ. Malek NA. McKee RH. Reprod Toxicol 2004.111(14):1719-1722. Bolte G. Angerer J. et al. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Richthoff J. Camann DE. Needham LL. Bull Environ Contam Toxicol 2002. Calafat AM. Prenatal exposures to phthalates among women in New York City and Krakow.S. Massey RC. et al. Int J Hyg Environ Health 2007. NTP-CERHR. Environ Health Perspect 2006. Rylander L.208:237-245. Helm D. Research Triangle Park (NC). Caudill SP.68:309-314.210:21-33.

only levels at or above the 90th percentile could be characterized.400 (.400-.400 (<LOD-.500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500) .400) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.500 (. < LOD means less than the limit of detection.10) .600) < LOD .20) .400 (.400-.S. polyvinyl acetate.00 (<LOD-1. which may vary for some chemicals by year and by individual sample.9.10 (. 01-02.300 (.300) < LOD .900-1.600) .500) 1.70) .500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. including nitrocellulose.300-.300 (.300-.300-.700) .300 (.500 (. see Data Analysis section) for Survey years 99-00. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.3.500) < LOD < LOD .400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .500) 1.500 (.500 (.50) .300) < LOD . 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.00-3.700) .500) .00 (<LOD-1. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.600) .200-. In this Report. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400) < LOD < LOD .500 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.70) .400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400) < LOD 1.300-.400 (.300 (.600) .500) .400-.500 (.400 (.600) .400-.200-.400 (<LOD-.300-.400-.00 (<LOD-1. respectively. and 0.500 (.700) .500) .600) .200-. and 03-04 are 0.500) < LOD 1.200-.200 (<LOD-.90) .300-.400-.400-.Phthalates Dicyclohexyl Phthalate CAS No.00-2.400) 1. resins. 0. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.300 (. Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population.300-.200-. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.500-.400 (.10 (<LOD-1.500) 1. 270 Fourth National Report on Human Exposure to Environmental Chemicals . and polymers.2.300 (.400 (<LOD-.300-.300-.400 (. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.00) .50) .300 (<LOD-. and polyvinyl chloride.400 (<LOD-.300) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .10 (<LOD-1.500) < LOD < LOD . Survey Geometric mean (95% conf.500 (.70 (1.10 (<LOD-2.80) .300-.70 (1.600 (.400 (. population from the National Health and Nutrition Examination Survey.200-.300 (.500 (.

590 (<LOD-.400-.54-6.170-.250 (.390 (.910 (.770 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.82 (1.420-.490) .510-.44) .16) .360-.500) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .450 (.530 (.450 (. population from the National Health and Nutrition Examination Survey.630 (<LOD-.690 (.500-.54) .43 (1.830) 1.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.260-.350-.74) .22 (<LOD-1.82) .33 (<LOD-3.54 (<LOD-2.36-1.410 (.510 (.660) < LOD < LOD .12-1.310) < LOD .710) .240-.690-1.910 (.330 (.630 (<LOD-.00 (<LOD-3.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .06) .380 (.770-1.770-1.790-1.530-.560) 1.10) .480 (.420-.34) .53) .950 (.690) < LOD < LOD .530) 1.530) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.670-1.33) . Survey Geometric mean (95% conf.11) .16 (<LOD-3.05) .690) < LOD 2.940 (.53) .380-.270) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 271 .290-.470 (.670 (<LOD-.420-.660) .740) .530-1.770-1.620) < LOD .880 (.500 (.14 (<LOD-3.590 (.910 (.310-.770) < LOD 2.500) 3.740) < LOD < LOD .370 (<LOD-.910 (.400-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .06) .690) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.330 (.220 (<LOD-.17) .00) .Phthalates Urinary Mono-cyclohexyl phthalate (MCHP) (creatinine corrected) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.67 (1.470) 3.610 (.800-1.18) .

1 (71. soaps.3-103) 193 (141-256) 184 (148-227) 221 (165-294) 180 (140-221) 181 (152-212) 188 (158-219) 197 (129-249) 183 (142-217) 196 (170-241) 564 (419-818) 479 (387-651) 557 (432-695) 482 (390-590) 498 (441-567) 533 (471-629) 378 (290-730) 451 (315-636) 521 (295-571) 1510 (1050-2150) 1260 (983-1480) 1250 (973-1560) 1340 (1010-1660) 1350 (1060-1660) 1590 (1220-2070) 756 (379-1070) 808 (572-1090) 827 (542-1440) 3260 (1550-4420) 2070 (1470-3050) 2310 (1360-3310) 3480 (2230-4640) 2720 (2160-3670) 2980 (2250-3800) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 179 (149-215) 182 (157-211) 197 (173-224) 178 (154-206) 174 (153-198) 189 (160-225) 154 (119-197) 171 (139-199) 171 (148-201) 174 (138-210) 167 (139-194) 182 (138-219) 523 (372-650) 502 (419-603) 536 (449-654) 425 (350-508) 427 (387-498) 478 (392-564) 1440 (1020-2280) 1450 (1060-2110) 1520 (1210-2070) 988 (880-1230) 1050 (879-1310) 1260 (969-1640) 3500 (2130-4560) 3100 (2110-4390) 2910 (2210-3480) 2230 (1370-3880) 1860 (1490-2500) 2590 (1800-3420) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 181 (157-209) 226 (195-262) 267 (239-298) 322 (275-377) 352 (324-384) 357 (310-412) 152 (133-175) 158 (141-178) 167 (145-193) 174 (146-210) 220 (190-264) 249 (212-307) 306 (256-350) 357 (290-407) 306 (253-414) 134 (108-157) 147 (119-177) 148 (125-175) 441 (390-541) 530 (444-660) 597 (523-688) 789 (635-949) 853 (709-1090) 948 (769-1150) 367 (287-482) 413 (366-451) 418 (366-477) 1280 (851-1510) 1490 (1050-2110) 1640 (1320-2180) 1890 (1410-2270) 2160 (1620-2470) 2500 (1840-2980) 986 (798-1340) 1020 (905-1230) 1210 (954-1480) 1720 (1460-2130) 2630 (1540-4460) 3050 (2230-4300) 3610 (2130-4640) 3540 (2810-5070) 4370 (2780-5910) 2470 (1590-3880) 2320 (1560-2720) 2250 (1590-3290) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 2003) and African-American women in Washington.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. particularly those containing fragrances.9-92. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. Products that may contain DEP include perfumes. 2001-2002.3 (74. shampoos.. 2002). colognes. respectively. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.8-111) 85. 272 Fourth National Report on Human Exposure to Environmental Chemicals .2-102) 95. Biomonitoring Information MEP levels in the NHANES 1999-2000.S.Phthalates Diethyl Phthalate CAS No. and 03-04 are 1. population from the National Health and Nutrition Examination Survey.. In contrast. A small study of children less than 2 years old reported mean urine MEP levels that were about twice as high as levels in children (aged 6-11 years) in NHANES 2001- Urinary Mono-ethyl phthalate (MEP) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7) 71. and hand lotions. and also in men attending a Boston infertility clinic (Hauser et al. interval) 179 (156-204) Selected percentiles ( 95% confidence interval) 50th 164 (136-201) 169 (141-194) 174 (151-208) 75th 454 (370-538) 465 (415-527) 502 (457-555) 90th 1260 (1010-1480) 1230 (1040-1440) 1380 (1170-1750) Total 178 (159-199) 193 (169-220) Sample size 2840 (2150-3770) 2536 2500 (1860-3220) 2782 2700 (2160-3310) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 91. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.7 (70. 2007).1-93.5) 81.2.4. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. and 2003-2004 subsamples were similar to median or geometric mean levels in small samples of pregnant women in New York City (Adibi et al. deodorants..3 (82. and 0. 0. see Data Analysis section) for Survey years 99-00.9 (61.4 (62. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 01-02.9. DC (Hoppin et al.

2002).7-110) 81. Other population estimates also differed by sex and race ethnicity (Silva et al.. In an analysis of NHANES 1999-2000.2 (66. interval) 163 (149-178) Selected percentiles ( 95% confidence interval) 50th 141 (129-157) 148 (133-162) 153 (137-177) 75th 360 (307-422) 388 (330-435) 452 (386-504) 90th 905 (753-1180) 969 (805-1180) 1110 (889-1290) Total 167 (150-185) 181 (163-202) Sample size 1950 (1670-2310) 2536 1840 (1450-2200) 2782 2040 (1640-2540) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 92. Finding a measurable amount of MEP in urine does not mean that the levels of MEP or the parent compound cause an adverse health effect.S.9-110) 96. population from the National Health and Nutrition Examination Survey..Phthalates 2002 (Brock et al. Analysis of NHANES 2001-2002 showed similar findings. 2004).9 (82.3-105) 87. Median MEP levels found in a small sample of German residents (Koch et al. the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups. 2003) were slightly lower than levels found in NHANES 2001-2002. This age-related trend is opposite the direction seen for other phthalates..6 (77.5-113) 122 (93.5-114) 101 (87.0-156) 140 (111-180) 150 (123-184) 154 (136-177) 160 (146-182) 177 (147-202) 165 (127-208) 177 (135-224) 180 (145-203) 364 (275-495) 330 (249-409) 363 (292-485) 390 (336-452) 419 (363-486) 512 (423-632) 341 (219-554) 512 (290-802) 470 (310-596) 879 (676-1260) 808 (590-1100) 791 (589-1080) 1010 (803-1460) 1060 (884-1320) 1230 (989-1610) 625 (400-784) 843 (512-1320) 719 (470-1330) 1760 (1000-2000) 1330 (868-1840) 1470 (987-2220) 2170 (1790-3350) 2120 (1520-2790) 2290 (1770-3200) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 141 (124-159) 148 (130-168) 154 (139-171) 187 (165-211) 187 (166-210) 211 (180-248) 120 (107-134) 126 (110-147) 127 (108-150) 158 (142-179) 171 (148-188) 181 (148-217) 324 (249-415) 352 (282-425) 390 (341-465) 377 (307-495) 407 (355-473) 508 (379-634) 1000 (693-1480) 1100 (839-1480) 1070 (852-1360) 822 (697-1170) 860 (712-1100) 1120 (889-1400) 1950 (1460-2900) 2120 (1490-3030) 2000 (1610-2410) 1930 (1170-3410) 1430 (1190-2010) 2250 (1440-3330) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 164 (142-190) 213 (182-249) 241 (213-271) 208 (183-236) 247 (226-271) 254 (225-287) 149 (135-165) 157 (142-173) 165 (144-189) 154 (136-174) 199 (164-242) 233 (202-270) 196 (166-228) 227 (185-270) 212 (188-246) 128 (111-142) 136 (124-150) 135 (120-158) 382 (314-472) 461 (396-572) 533 (417-665) 443 (390-505) 557 (478-618) 619 (476-791) 313 (239-387) 338 (288-402) 386 (338-485) 814 (673-974) 1080 (860-1650) 1230 (956-1610) 1030 (762-1700) 1240 (961-1480) 1530 (1200-1970) 856 (655-1390) 919 (712-1160) 989 (831-1330) 1330 (974-1920) 1940 (1410-2630) 2270 (1810-3140) 1920 (1230-2590) 2090 (1550-2800) 2590 (2160-3500) 1950 (1480-2740) 1590 (1320-2170) 1920 (1400-2780) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 273 . 2005). with adjusted geometric mean levels of urinary MEP that increased with age (CDC.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.6 (65. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biomonitoring studies on levels of MEP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEP than are found in the general population. Urinary Mono-ethyl phthalate (MEP) (creatinine corrected) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0 (66. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.

Centers for Disease Control and Prevention (CDC). Koch HM. Barr D. Silva MJ. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Silva MJ. Angerer J. Poland. Prenatal exposures to phthalates among women in New York City and Krakow. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Bull Environ Contam Toxicol 2002. Brock JW. Caudill SP. Brock JW. Davis BJ. Jedrychowski W. Silva MJ. Reproducibility of urinary phthalate metabolites in first morning urine samples. et al. Third National Report on Human Exposure to Environmental Chemicals. et al. Barr DB. Environ Health Perspect 2003. Baird DD. Environ Res 2003. Hilborn ED. 112(5):A270].110(5):515-518. Camann DE. Jacek R. Urinary levels of seven phthalate metabolites in the U. Atlanta (GA).S. Caudill SP. Hauser R. Duty S. 2005. Hoppin JA.111(14):1719-1722. Perera FP. Drexler H.112(3):331-338.22(3):688-695.93:177-185. Hodge CC. Reidy JA.Phthalates References Adibi JJ. Needham LL. Hum Reprod 2007.68:309-314. Ryan L. Environ Health Perspect 2002. et al. Meeker JD. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Singh NP. Environ Health Perspect 2004. Malek NA. Rossbach B. Phthalate monoesters levels in the urine of young children.

82) 3. Albro and Lavenhar.50-6.10 (3.50-3.60) 90th 14.40-1.2) 6.27) 2.34 (2.1 (10.90) 4.5 (12.84) 3.50-8.90 (3.40-8.30 (3.90 (4.. as glucuronide conjugates (Albro et al.4) 20.54) 4.62) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5. Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4-40.9) 13.5-17. Fourth National Report on Human Exposure to Environmental Chemicals 275 .85) 4.70 (2.10 (2.70) 2.30-8.50-5.3) 28.40 (4.6-23.S.43 (3. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.4-20.0 (9.30-6.23) 3.8 (19.2) 42.4-42.93) 6.0) 11.9 (15. mainly polyvinyl chloride.7 (17.40) 4.40) 75th 7.70) 16.7-58.00) 19. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.20 (3.37-4.50-14.6-130) 31.7) 37.10) 3.1) 22.0 (14. Concentrations in plastic materials may reach 40% by weight.3 (24.3-49.9-48.9 (17.5 (12.6 (16.26-2.7-18.1-17.9) 18.50-2.10-5.4 (16.90) 1.9-57.92-2.9 (29.6-60.50-20.0 (13.9-26.5-36.10-5.90) 7.9) 5.24-4.96-5.9 (29.20 (4.20 (1.9) 27.7) 35.00 (5.0) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.9-49.0 (19.10 (4.40-11.00) 11.6 (10.50-6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6) 5.4-27. 1989.90) 3.50 (7.80-3.7) 27.80) 9.5) 43.4) 13.00) 1.30 (4.5 (25.50) 4. and 03-04 are 1.50) 9. 1.92) 4.80 (8.9) 13.80-4.10-11.40-9.7) 8.68 (3.5) 40.32 (3.27 (3.8) 17.67-4.90-11.91-3.50-2.92-2.50 (3.5-28.70 (3.8-47.40 (2.10-11.90) 4. packaging film.6 (11.3-26.9-29.1-48.2) 23.94-3.40) 9.3) 13.5-41.6 (20.39) 3.50 (7.50-16.0) 23.46) 3.60) 7.60) 4.4-20.35) 4.0-29.3-57.56 (2.8 (17. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).6) 95th 23.70 (8.16-3.2 (7. interval) 3.10 (3.9-55.7) 19.5 (24.2) 4.75 (3.4) 23.6-25.4) 22.9 (17.4 (13.0-19.00) 1.5) 32. see Data Analysis section) for Survey years 99-00.4-53.0 (16.80) 6.90-4.7) 6.6) 39.0 (21.9 (7.70-5.2 (29.40) 1.4) 15.4) 7.80 (4.41) 3.9-28. 1982.20 (3.40-8.80 (1.10) 3.50 (2.69) Selected percentiles ( 95% confidence interval) 50th 3.00-5.2 (11.5-40.07-4.5-28. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.86) 2. ATSDR.10 (5.6-28.4 (21.87-2.80-5.21 (2.40-12.5) 37.3 (15.96) 4.70-2.98) 2.75-4.60) 4.5) 21.40 (6.42) 3. DEHP has been removed from or replaced in most toys and food packaging in the United States.70-2.92-5. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).21 (2.2-39.10) 4.5 (31.1 (8.6) 14.31 (3.1-17.89-3.70) 7.80 (8.2-17.10 (4.3) 52.70 (3.30 (7.0. Following ingestion.3 (19.51) 4.80 (2.3 (10.50 (8.00-3.2 (10. and 0.16 (2.1-27.1) 19.0-18.1) 29.5 (30.10-2.86) 2.00) 2.9.50-3.40) 8.42-5.50 (3.80-4. and in humans. 2002.19-3.4) 5. 01-02.00) 9.7-32.0) 23.9) 15.5 (18.4) 33. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP). population from the National Health and Nutrition Examination