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

2-Dichloropropane 2.3-Tetramethylbutyl] phenol) Triclosan (2.1.4. The process for selection is described at http://www.4.2-Dichlorobenzene (o-Dichlorobenzene) 1.2’.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .4.4’.4'.2'.4.2'.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 2.5.1.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.4.4.What’s New in this Report What’s New in this Report In this Fourth Report.4'-Tribromodiphenyl ether (BDE 28) 2.5'-Tetrachlorobiphenyl (PCB 49) 2.4'.2-Dichloroethene trans-1.4'-Tetrabromodiphenyl ether (BDE 66) 2.1-Dichloroethene (Vinylidene chloride) cis-1.4.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.3’.5.2-Dichloroethene Dichloromethane (Methylene chloride) 1.5.4.3'.4-Dichlorobenzene (p-Dichlorobenzene.3.2'.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.1-Dichloroethane 1.2'.4-Tribromodiphenyl ether (BDE 17) 2.5'.1.2'3.5'-Tetrachlorobiphenyl (PCB 44) 2.2'.1-Trichloroethane (Methyl chloroform) 1.4.1. 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 (2.2-Dichloroethane (Ethylene dichloride) 1.3. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.6'-Hexabromodiphenyl ether (BDE 154) 2.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.2'.2'.4'-Tetrabromodiphenyl ether (BDE 47) 2.2.4'. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.3.4.4'.3-Dichlorobenzene (m-Dichlorobenzene) 1.2'4.2'.cdc.4’.6.5.5-Pentabromodiphenyl ether (BDE 99) 2.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.4.5'-Hexabromodiphenyl ether (BDE 153) 2.5’.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.2-Trichloroethane Trichloroethene (Trichloroethylene) m. Paradichlorobenzene) 1. Table 1.4'.6-Heptabromodiphenyl ether (BDE 183) 2. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.6-Pentabromodiphenyl ether (BDE 100) 2.4'-Pentabromodiphenyl ether (BDE 85) 2.3.gov/exposurereport/chemical_selection.html.2'.

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

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

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

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

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

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

serum. One exception is the American Conference of Governmental Industrial Hygienists (ACGIH). disposition within the body.gov/niosh/rtecs) Agency for Toxic Substances and Disease Registry (ATSDR) • Toxicological Profiles and ToxFAQs (http://www. This organization notes that these values are for workers and that it is not appropriate to apply them to the general population.htm) • National Institute for Occupational Safety and Health (NIOSH) o Databases and Information Resources (http://www. the U. 2007 TLVs and BEIs.htm) U. Cincinnati (OH). and pathways of human exposure. sources. BEIs can be the blood or urine levels of a chemical that correspond to air-exposure limits for workers set by ACGIH. and comparative blood or urine levels from other studies.cdc.gov/nchs) o National Health and Nutrition Examination Survey (NHANES) (http://www. 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. generally recognized guidelines for blood or urine levels are presented in the text. Where can I find more information? For more information about environmental chemicals.epa. and urine levels result in disease or adverse effects.gov/toxpro2. Some guidelines are from federal agencies. the information was compiled from many publicly available sources. Separate studies of varying exposure levels and health effects associated with these levels are required to determine whether blood.gov/iris) • Office of Prevention.cdc. Statements are based on common general information.S.cdc. and it is not intended as a comprehensive review of each chemical.S. consensus agreement among experts. population to environmental chemicals. not to imply that the BEI is a safety level for general population exposure. and Toxic Substances (OPPTS) (http://www.cdc.Chemical and Toxicological Information Chemical and Toxicological Information The Fourth Report presents biomonitoring data on the exposure of the U. If available. The Fourth Report provides descriptive information about each chemical or chemical group including uses. peer-reviewed scientific papers obtained from electronic searches.S. The information in the text is provided as an overview.asp) U.S. Pesticides.gov/niosh/database.gov) • National Center for Toxicological Research (http://www. For most chemicals in this Report. Governmental Sources Centers for Disease Control and Prevention (CDC) Resources: • National Center for Health Statistics (NCHS) (http://www.html) • Toxic Substances Portal (http://www.cdc. Food and Drug Administration (FDA) • Center for Food Safety and Applied Nutrition (http://www.atsdr. Environmental Protection Agency (EPA) • Integrated Risk-Information System (IRIS) (http://www. including documents from national and international agencies and organizations. Information about the BEI level is provided here for comparison. The data and information in the Fourth Report do not establish health effects.gov/nchs/nhanes. CDC is not responsible for the content of an individual organization’s Web pages found at these links. and the agencies of the World Health Organization. and public government documents. Advances in analytical methods allow us to measure increasingly lower levels of environmental chemicals in people. nor do they create guidelines.atsdr.gov/nctr) U.fda. 2007. or concordance among multiple scientific papers and sources. Examples of common institutional sources of information include the Agency for Toxic Substances and Disease Registry. American Conference of Government Industrial Hygienists (ACGIH). These links do not constitute an endorsement of these organizations or their programs by CDC or the federal government.S. 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. Generally. refer to the list of web links below and the references given in the text.fda.cfsan. Environmental Protection Agency.gov/substances/index. 2007).cdc. such guidelines are not available. effects in animals or humans. U. Links to nonfederal organizations are provided solely as a service to our readers.gov/opptsmnt/index.epa. Geological Survey (USGS) • (http://www/usgs. Signature Publications.gov) 9 Fourth National Report on Human Exposure to Environmental Chemicals .html) o Registry of Toxic Effects of Chemical Substances (RTECS) (http://www.S.

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

Animal studies indicate that acrylamide is well absorbed.0 (57.4) 57. FDA. and cosmetics (NTP-CERHR.5) 58.0-58.2-114) 163 (147-191) 96.2-91.4-60.4 (54.2-67.7 (58. EPA. gels.0-108) 152 (139-175) 126 (111-142) 108 (86.6 (56.S. People may be exposed to acrylamide from foods. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.8 (91.3 (53.4) 57.8-57. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.1 (73.1-64. Fennell et al.7-64.7 (63.4) 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. Tareke et al. and in some cosmetics.6-108) 61. 2002).0 (69. pulp and paper production. and is either metabolized to the reactive epoxide.1) 46.5 (44.9) 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.0. FAO/WHO.6-65.3 (55. 2006).7) 54. These estimated intakes are hundreds of times lower than occupational exposures.9-61.2-70.2 μg/kg/day (U.1) 62. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. but can covalently bind to form adducts with proteins. as an absorbent in disposable diapers. such as potatoes and some grains.4-89.4-83.1) 53.7) 96.7-64.S. and well below doses known to cause nerve damage or carcinogenicity in animals.3) 86. Elimination occurs mainly in the urine as mercapturic acid conjugates. widely distributed in tissues.3) 70.1 (83.9 (69. 2005).6-75.5) 66. Polyacrylamides are useful water-compatible polymers used in water treatment.Acrylamide Acrylamide CAS No. Acrylamide is not thought to accumulate in the body at environmental doses.0) 57.0 μg/kg for adults (FAO/ WHO. are heated at temperatures used for frying and baking. 2005).8 (52. the main source of exposure is from the diet. soil conditioners.2-93.. Recently.S. but are generally above the U. 1990. acrylamide is synthesized and used in the production of polyacrylamide polymer.9 (54.1-61.0-66.8 (81.0 (67.1-64. EPA reference dose of 0.7) 73. it was discovered that acrylamide is formed when starch-rich foods.4-76.9 (60.S. and binding agents. Estimated intakes in children are about twice that of adults (DiNovi and Howard. drinking water.3-2. acrylamide has produced upper airway irritation following inhalation of high levels. mineral processing.2) 57.0-104) 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 61.4 (53. 1994).6) 73.5-85.7-60.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.6-61. and an average daily intake is estimated as 0. in some sealing grouts. population from the National Health and Nutrition Examination Survey.5 (74.5 (52.6 (81..2 (75.5-80. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.2) 57.2 (58. 2005.6-66.0) 85. Since acrylamide has limited volatility and high water solubility. Survey Geometric mean (95% conf.3) 63. In the general population. smoking.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.7) 75th 79. EPA. ocular and dermal irritation from direct contact with acrylamide containing materials. 2005).2-59.1 (52. or to glutathione conjugates (Calleman et al.6-104) 82.2-118) 98. In 1997.5 (79.S.9) 75.1) 55.. 2004).6 (51.4 (54. see Data Analysis section) for Survey year 03-04 is 3.1) 101 (95. 217 million pounds of acrylamide were produced commercially in the U. Fourth National Report on Human Exposure to Environmental Chemicals 11 .1 (88.2-77.0 (53. 2005).4-60. In humans. interval) 61.7 (65. glycidamide.7 (55.2 (62.9) 63.9-105) 86. Commercially.4 (51. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U. in permanent press fabrics.6) 71.9-52.6) 90.6) 50. and from dermal contact with products that contain residual acrylamide.1 (47. Natural substances in the food are converted to acrylamide. 2006.4) 100 (89.1-57. 2005).9) 58.0-49. and in the synthesis or compounding of dye materials.3-71. (NTP-CERHR.8-55. 2004.7) 58.8 (57.4 (59.

2005.pdf.2 (63.8) 60.2) 65.1-62. population from the National Health and Nutrition Examination Survey. 2005) have been demonstrated in animals. reproductive effects (reduced litter size.4 (61.2) 87.7) 90.5) 75th 85. Hagmar et al. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.8-49. 2006) have been demonstrated after acrylamide dosing.. 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.3 (56. 2005. AHA levels have been shown to increase with dietary intake (Hagmar et al. Klaunig et al.9 (57.. 2005) and sperm DNA adducts (Xie et al.6 (90.0-62. and other sites) (FAO/WHO. altered gene expression in testicular tissues (Yang et al.9-76.4 (56..8 (51.. EPA. Puppel et al. and cancer (mammary.9-62.5) 71.3) 85.1-60. Animal studies have shown that acrylamide can cause nerve damage (neuropathy). glycidamide (NTP-CERHR.. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al. male germinal cell injury.1-70.8) 45. 2005.9 (58.9) 87. 2005. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. respectively) are markers of integrated acrylamide exposure over the preceding few months.9-138) 143 (130-159) 96.6-90..S.5) 87.9) 59. 2005. Glycidamide has been shown to react with DNA (Doerge et al.7 (87. EPA.7 (84. Puppel et al.0 (70.5 (42.3-101) 95.8 (44. 2001). 1997. 2005.3) 59.7) 61.5-66.7-64. 2005. adrenal.6-64.5-92. 2005).9) 75.4 (51. 2008). 2005. Vesper et al. and neuronal DNA reactivity (Doerge et al.int/ ipcs/food/jecfa/summaries/summary_report_64_final.. 2006).5 (59.3) 59.9-64. 2005. 2003.1) 56. Survey Geometric mean (95% conf..4) 53..1 (82.S.2-68.9 (81.2-90. scrotal. 2006. Schettgen et al. Rice..4-103) 79. 2002.. In addition.7-86.0 (80.5 (56.2) 55. 2004). thyroid.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.8-48.7) 74..1 (66. fetal death.5-64. After exposure ceases. probably through its epoxide metabolite.1 (57.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71. dominant lethality).3-78.0) 94.4 (90. uterine.0 (75. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood..1) 62.9-78.1 (70.0-103) 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. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. although different analytic methods can affect results.2 (72.5-94.7 (57. NTP-CERHR..2-91. interval) 59.3) 59. 2004.0) 118 (103-126) 121 (112-134) 113 (94.S.9-77. most non-smokers had levels less than about 100 pmol/gram hemoglobin. 2009).4) 46. Acrylamide is clastogenic and can produce dominant lethal mutations. U. U..4-98.7-62. 12 Fourth National Report on Human Exposure to Environmental Chemicals .9) 65. Vesper 2005) and smoking (Bergmark. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.epa. IARC classifies acrylamide as probably carcinogenic to humans. 2005. 2002..1 (56.4) 83.4-65.who.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 59.1) 60. 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. 2005).6-62.Acrylamide occupational exposures. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al...6 (66.0 (52.8-61.7 (61. 2005). presynaptic nerve terminal binding (LoPachin. EPA at: http://www.7) 60. 2005). Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. 1997. see Data Analysis section) for Survey year 03-04 is 4.0..4 (81. Additional information is available from U.. 2006). 2005. Maniere et al.4 (57.2 (56.1-56. Axonal degeneration.S. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.5 (83.0-93. Mucci et al. 2008). Schettgen et al.4-59.

56. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al.fda.niehs. July. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Joint FAO/WHO Expert Committee on Food Additives. 6013-6019. Burgess J. Spicer R. 2009 Jan 8. Bergmark E. Churchwell MI.cfsan. Laurentie M. Becher G.580(1-2):131-141. Chicago. In another study. Kautiainen A. Available at URL: http://www. Fennell TR.pdf. 2006. Tornqvist M. April 13-15.561:21-37.Acrylamide In occupational settings. Metabolism and hemoglobin adduct formation of acrylamide in humans. Alexander J. Guffroy M. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Yang JS. Hagmar et al. Chem Res Toxicol 1997 Jan.27(4):219-226. smoking habits and gender. Toxicol Sci. Costa LG. et al.126(2):361-371.Toxicol Appl Pharmacol 1994. Adv Exp Med Biol 2005. Bergmark E. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Wirfalt E. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). [Epub ahead of print] Dybing E. et al. Scand J Work Environ Health 2001. 2001. He F. Toxicol 2005. Bjellaas T. References Bergmark E.580(1-2):157-165. 2004. McDaniel LP.. Doerge DR. et al.43:365–410. Aprea P. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Mechanisms of acrylamide induced rodent carcinogenesis.3:406-412.. Available at URL: http://cerhr. Kamendulis LM. J Agric Food Chem 2008.. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Bruze M. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Axmon A.120(1):45-54. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. morphological and molecular endpoints in animal models. Mucci LA. 1994). Wilson KM.html#u1004. 1999). 2/3/09 Klaunig JE. Snyder RW. Churchwell MI. Rome.pdf. Adv Exp Med Biol 2005. 2004 Acrylamide in Food Workshop: Update Scientific Issues. 2/3/09 Hagmar L. NIH Publication No.85:447-459. and Research Strategies. Food Chem. gov/~dms/acrydata. National Toxicology Program. Bridson WE. Calleman CJ.. Nordander C. 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. Beland FA. Rosen I. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Malmberg B. Italy. 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. Bergmark E. Chem Res Toxicol 1990.. Available at URL: http://www. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Mutat Res 2005. 2/3/09 Perez HL. Summer SCJ. DiNovi M and Howard D. CFSAN/Office of Plant and Dairy Foods. Tian G. Wu Y. LoPachin RM. Osterman-Golkar S. Acrylamide neurotoxicity: neurological. Andersen M. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Fennell TR. Calleman CJ. Mutat Res 2005. 054472. da Costa GG. Hagmar L. Twaddle NC. Doerge DR. He F. et al.561:49-62. 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. Perez et al. Survey data on acrylamide in food: individual food products. Toxicol Sci 2005. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Acrylamide intake through diet and human cancer risk. 8-17 February 2005. Paulsson B. Paulsen JE. 2001). Costa LG.who. Uncertainties. February. Food and Drug Administration (FDA). Human exposure and internal dose assessments of acrylamide in food.int/ipcs/ food/jecfa/summaries/summary_report_64_final.nih. Mutat Res 2005. Duale N.580(1-2):119-129. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. Calleman CJ. The Updated Exposure Assessment for Acrylamide. Illinois. Magnusson AL. Zhang S. Cheong HK. Maniere I.gov/chemicals/ acrylamide/Acrylamide_Monograph. Toxicol Appl Pharmacol 1993. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Farmer PB. 64th Meeting: Summary and Conclusions (FAO/WHO). Granath F. Tornqvist M. 2005. Haugen M. Godard T.10(1):78-84. smokers and nonsmokers. 1993.

Adv Exp Med Biol 2005.gov/chemfact/s_acryla. Smith A.206(1):9-14. Myers GL. Liu Y. Han DU. Ingham L. Weiss T. Schettgen T. Integrated Risk Information System (IRIS).S. EPA). Office of Pollution Prevention and Toxics. Tareke E. Environmental Protection Agency (U. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. U.Acrylamide glycidamide by gas chromatography-mass spectrometry. U.epa. Fueller F. Yang HJ. Hemoglobin adducts of ethylene oxide.134(1-3):65-70. Han CH. Tjaden Z.txt. J Agric Food Chem 2008. et al. September. Available at URL: http://www. Agudo A. Toxicol Lett 2002. J Agric Food Chem 2002. 2/3/09 Vesper HW. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Rossbach B. Ospina M. Drexler H. Int J Hyg Environ Health 2003. Ding X. Tjønneland A. Lee MH.S. Tornqvist M.50(17):4998-5006. Ospina M.561:89-96.56(15):6046-53. Lee SH. Drexler H. Anal Biochem 1999. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Fu D.epa. Letzel S. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Angerer J. Meyers T. Schettgen T.580(1-2):71-80. Licea-Perez H. Rapid Commun Mass Spectrom 2006. Toxicol Lett 2006. Angerer J. Mutat Res 2005. Analysis of acrylamide. Schettgen T. Eriksson S. Choi JH. Acrylamide. Xie Q.274(1):59-68. Washington (DC). Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. 14 Fourth National Report on Human Exposure to Environmental Chemicals . a carcinogen formed in heated foodstuffs. Reprod Toxicol 2005.S. Jin Y.19(4):527-34. Puppel N. 1994. Vesper HW. Kutting B. Gray JG. Slimani N.htm. propylene oxide. Available at URL: http://www. Meyers T. Drexler H.20(6):959-64. Environmental Protection Agency (U. Hallmans G.S. 2/3/09. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Liu K. Int J Hyg Environ Health 2004. Mutat Res 2005 Feb 7. revised 1/3/06.gov/iris/subst/0286. Angerer J.207(6):531-9. Rice JM. Vesper HW. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany.163(2):101-8.580(1-2):3-20. et al. EPA). Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Marko D. Chemical Summary for Acrylamide. Sun H. Benetou V. Toxicological effects of acrylamide on rat testicular gene expression profile. Karlsson P. The carcinogenicity of acrylamide. Chae C. Broding HC. Rydberg P.

990) .50) 3. maternal exposure during pregnancy can result in lower birth weight. Fourth National Report on Human Exposure to Environmental Chemicals 15 .071 (.19-2.120 (.130) .920 (.S.062 (.087 (.090-.66 (1.5% nicotine by weight (Kozlowski et al.059-.20) 1.44 (1.076-. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.054 (.35 (2.308 (.140 (.860 (.047-.077) .310-1.190-.124 (.070 (<LOD-.44 (2.120-.540 (.480-.12) 1.57) 2.55-2.99) 2.144 (.16) .42-4.213) .120 (.150) . ** In the 2001-2002 survey period.063) .163 (.950-1.600-1.740-1.500 (.060-.55 (1.20-2.87-3.660) .030-.350-.04 (1.137-.730 (.230 (.180) .950 (.15 (2.190-.180) .280 (.188) .21-1.32-2.050) .910-1.040 (.220) .00) 1. 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.580 (.580-1.740-1.104-.02 (.060 (<LOD-.210 (.198) * .450-.75) 1.96-4. cardiovascular disease.100-.02) 1.066) .621-1.68) .44) 2.060 (<LOD-.164 (. DHHS.01) 3.230) .050-.790) .580) .428-.106-.110 (.48-2.130 (.88 (1.050 (<LOD-.39 (1.630 (.059-.020-.040-.187) .080) < LOD .26-1.047-.140-.77 (1.110 (.53 (1.28-1.930 (.160 (.070) 75th .32-2.153-.20) .066 (.015.S.62 (2.040-.44) 2.197) .23-2. emphysema.086 (.030-.21-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.160) .142-.20 (1.115-.110) .30) 2.20 (.320) .12 (1.066-.201) . and 03-04 are 0.820) .260-1.190-.070) .800 (.052 (<LOD-.81-2.094) .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 .139) * .200) 1. and 17% had an LOD of 0.32) 1.19) 1.50 (1.110-.70-2.12 (2.193) .080 (.22) 2.17) .45) 1.430-1.62) 2.220-..180) .49) 1.148-.53-4.089) Age group 3-11 years 99-00 01-02** 03-04 .070) . and various other disorders (U.17 (1.050 (<LOD-.23 (1.470-.312) .060-.110 (.060 (.015 ng/mL.66-3.080-.54) 1.506 (. and 0.770) .68) 2.01 (1.077) .154-. 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. respectively.160 (.110-.110 (.090-.49) 1.14) . Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.12-4.410) .080-.080-.620 (.620-1.770) .43 (1.310) .94) 1.302) .28) .95) 1.18-3. DHHS.120 (.050 (<LOD-. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.960-1.21 (.131 (.39) 3.120 (.088-.997-3.150) .510 (. which may vary for some chemicals by year and by individual sample.108) * .63 (2.09-3.30) * . acute respiratory illness. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.48-3.85 (1.180) .180) .160-.180 (.090-.350 (.060) .11) .050 (<LOD-.175 (.70) 2.850 (.120 (.061) < LOD .053 (<LOD-.23 (.96) 2.89) 1.05.670) .42 (1.126) .30) 2.370-. stroke.990 (.47-3.570 (.040 (.084) .54 (1.310) 90th 1.052 (<LOD-.180 (.50-1.690 (.068) .043-.520 (. 2004). Survey Geometric mean (95% conf.38-2.260) 1.19) .060 (.058 (.111-.65 (1.710 (.02) 1.137 (.040 (.120-.78) 2.240 (. acute respiratory infections.05 ng/mL.030-.66) 1.23 (2.310-1.09-2.505 (.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.080 (.15) 2.Cotinine Cotinine CAS No.120) .073) < LOD .625) .057-.79) 3.145) .060-.480-1.164 (. < LOD means less than the limit of detection.50-4.570-1.00) . The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.14-1.83-2.76 (1.160) . ear problems.360) .840) 3.77 (2.071) .300) .630 (.92 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.163) . population from the National Health and Nutrition Examination Survey.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .34 (1.050) .070-.140 (.68 (1.93) .216 (. Children exposed to ETS are at increased risk for sudden infant death syndrome. Cigarettes contain about 1.14) .080) < LOD < LOD .110 (.050-.60-2.533-.087) < LOD < LOD .167 (.99) 2. see Data Analysis section) for Survey years 99-00.84-3. 83% of measurements had an LOD of 0.140-.40) .087-.400-.77 (1.050 (. 2006).63-2.S.110) . and exacerbated asthma (U.770-1.160 (. 2004).726) . 1998).110-.080-.33-2.88 (.900-1.09-3.96 (1.17 (.54 (1.05) 1.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .234) .068) .075 (.030 (.350-.220) .630 (.

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

Int Arch Occup Environ Health 1991. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Vol 83. Department of Heath and Human Services. Jacob P III. 1999. Benowitz NL. Available at URL: http://monographs.S.15:302-307.280:152-156. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Pharmacol Rev 2005.nih. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. cigarette smokers: the Third National Health and Nutrition Examination Survey. 2004. Modin G. Pechacek TF. Kira S. Benowitz NL. Exposure of the U. Fong I. Houseman TH. Jacob P. National Institute for Occupational Safety and Hygiene (NIOSH). Vogler GP. Tob Control 1998. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children.gov/tcrb/monographs/10/. Giovino GA.S. Brody DJ. Warner K. Bernert JT. Coordinating Center for Health Promotion. Tobacco Smoke and Involuntary Smoking. Tobacco Smoke. Clin Pharmacol Ther 1994. Etzel RA. Summary of Data Reported and Evaluation [online] 1986. Benowitz NL. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.niosh.S Department of Health and Human Services (U. 4/13/09 Iwase A. Tobacco related exposures. National Center for Chronic Disease Prevention and Health Promotion. 4/13/09 Centers for Disease Control and Prevention (CDC). Centers for Disease Control and Prevention. Herrera B.iarc. 1991. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace.php. Pechacek TF. Respiratory nicotine absorption in non-smoking females during passive smoking. Available at URL: http://ntp.pdf. Third National Report on Human Exposure to Environmental Chemicals. JAMA 1998. 4/13/09 Perez-Stable EJ. In Report on Carcinogens. Strauss WJ. et al.gov/eid/rmca/critdocs/ criteriadoc/33. Epidemiol Rev 1996. Jacob P III. Racial/ethnic differences in serum cotinine levels among adult U. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Centers for Disease Control. and the United States. 1988-1991. Turner DM.291(3):1196-1203. Schober SE. U.pdf. Office on Smoking and Health [online] 2006. Benowitz NL. Maurer KR.94(2):314-320.gov/library/ secondhandsmoke/. Summary of Data Reported and Evaluation [online] 2004.surgeongeneral. IARC Monogr Eval Carcinog Risks Hum. Giovino G. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.114(6):853-858.fr/ENG/Monographs/ allmonos90. et al. [online]. Soliman S. Bernert JT. 4/13/09 International Agency for Research on Cancer.S. George CF. Nicotine metabolism and intake in black and white smokers. Herrera B. available at URL: http://mtn. Atlanta (GA): 2005. U. Kozlowski LT.7:369-375. DHHS). Ethnic differences in N-glucuronidation of nicotine and cotinine. BMJ 1975.63:139-43. U.57(1):79115. Mehta NY. Pirkle JL.S. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Benowitz NL. Coordinating Center for Health Promotion.S. Am J Public Health 2004. population to secondhand smoke: 1988-2002. Smoking and Tobacco Control Monograph 10 [online]. Absorption and metabolism of nicotine from cigarettes. Pickett MA.4:313-316. National Toxicology Program (NTP). Pollack HA. 1988-1991.cancer. Lewis PJ. J Pharmacol Exp Ther 1999. Perez-Stable EJ. Tob Control 2006. Curtin LR. Aiba M. IARC Monogr Eval Carcinog Risks Hum. 4/13/09 National Cancer Institute (NCI). JAMA 1996. Caraballo R. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Vol 38. Brody DJ. Jacob III P. Centers for Disease Control and Prevention. JAMA 1998.275:1233-1240.gov/ntp/roc/eleventh/profiles/ s176toba. Cotinine as a biomarker of environmental tobacco smoke exposure.S Department of Health and Human Services (U. Sosnoff CS.php. 11th ed. Pirkle JL. Available at URL: http://monographs.cdc.18:188-204. Richter PA. Caudill SP.280:135-140. Dollery CT. Trends in the exposure of nonsmokers in the U. iarc. June. Metabolism and disposition kinetics of nicotine. DHHS). Environ Health Perspect 2006. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.56:483-493. Sweeney CT.S. Mowery PD.fr/ENG/Monographs/allmonos90. Flegal KM. the United Kingdom.S.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. 1999-2002. International Agency for Research on Cancer. 4/13/09 U. Jarvis MJ. Available at URL: http://www. Department of Heath and Human Services. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency.niehs. Hukkanen J. References Armitage AK. Schwartz SS. Available at URL: http:// cancercontrol.

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

population from the National Health and Nutrition Examination Survey.140-. < LOD means less than the limit of detection.140) < LOD . Additional information is available from U.110-. Survey Geometric mean (95% conf.130 (.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.150) < LOD .240) < LOD . 1998).110 (.N-Diethyl-meta-toluamide (DEET) N.140 (.130) < LOD .270) 688 678 518 700 598 956 Limit of detection (LOD.130-. One survey detected DEET in 74% of sampled streams in the U. and they range in concentration from 4% to 100%. 2002). including seizures and encephalopathy.S. 2003).110 (<LOD-.EPA at: http://www. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.110 (.120-.180) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.S.160) < LOD . and it has not been rated by IARC or NTP with respect to human carcinogenicity.130) < LOD .110 (.140) < LOD . Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. Sudakin and Trevathan. which may vary for some chemicals by year and by individual sample. 2005).180 (. DEET is not genotoxic.EPA.N. 1998).250) < LOD .epa.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 .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 .220 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .130 (.130 (..N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.140) < LOD .190) < LOD . EPA.110-. After absorption.120-.110 (. Fourth National Report on Human Exposure to Environmental Chemicals 19 .S.S.180 (.170 (. Neurological effects in humans. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.520) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.100-.130-.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .100-.S. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. DEET is not registered for use on agricultural commodities.. 2002). DEET is not a developmental or reproductive toxicant in animals (U.100 (<LOD-.560) < LOD . DEET is also used in combination with dermal sun screens (U.S. DEET can be applied to clothing and the skin to repel biting insects.130-.180 (.100-.1.449 and 0. Urinary N.110 (<LOD-. Its use is recommended for prevention of several vector-borne diseases..N-Diethyl-meta-toluamide (DEET) CAS No.210 (. 1995. DEET has low acute toxicity.170 (.130-.EPA.100-.100-. 2003). have been reported as result of self-poisoning by ingestion or excessive dermal application.gov/pesticides/.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 . DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. About 3-8% of dermally applied DEET is absorbed.100-. (U. (Kolpin et al. 134-62-3 General Information N. There are over 225 insect repellents brands containing DEET.

93) < LOD . 20 Fourth National Report on Human Exposure to Environmental Chemicals .320) < LOD .330 (.250-.410 (. In this survey period.390-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1992).500 (.250 (.290-.230-.190 (.N.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.350-.S.270) < LOD .170-.410 (.150) < LOD . population from the National Health and Nutrition Examination Survey.370) < 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 .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 .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 . 2005). 2007). the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC. Urinary DEET levels as high as 5. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.300 (. representative subsamples from NHANES 2001-2002.230) < LOD .330 (.440) < LOD .140-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .370-.270 (<LOD-. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.250) < LOD .240) < LOD .640 (. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.S.410-. 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.200 (.130 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .280 (.240-.480 (.270-.190 (.270 (. Survey Geometric mean (95% conf.320 (.230-..190-.350) < LOD ..550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Urinary N. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.630) < LOD .280-1.350) < LOD .490) < LOD .150-.190 (<LOD-.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.

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

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

Marr MC. Cunha G. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.113(4):391-395. Rubin C. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. and Hardy MP. Watanabe C.gov/chemicals/bisphenol/bisphenol. Hara K. Kiguchi M.35(2 Pt 1):238-254.149:988-994.pdf. Fujii S.145:592-603. vom Saal FS. 2007. Environ Health Perspect 2008. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Reidy JA. Available at URL: http://ecb.S. Szigeti-Buck. NC. with estrogen receptors alpha and beta. Hanaoka T.Environmental Phenols References Akingbemi BT. Exposure of the U. 2003. Barr DB. Ema M.jrc. 2/4/09 Fujimaki K.14(2):149-157. Department of Health and Human Services.pdf . J Am Dent Assoc 2006. Kim YH. niehs. Yoshinaga J. Bisphenol A. Barr JR.780(2):365-370. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Richter CA. Brussels.nih.Scientific Committee on Toxicity. et al.. Ecotoxicity and the Environment (CSTEE). Available at URL: http://ntp. 5: 505-523.S. Kroes R.10:875-921. Bradley S. T. Caudill SP.68(1):121-146. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Chung MK. 1999-2000: a national reconnaissance. Koh WS. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). and Hajszan. 2/4/09 Ouchi K. Endocrinology 2004. 2008. streams. Matthews JB. Munro IC. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents.S. Sottas CM. September.59(4):403-408. Lynch BS. Chem Res Toxicol 2001. McConnell EE. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. MacLusky. N.pdf. Myers CB. Proc Natl Acad Sci USA 2005.36(6):1202-1211. Cohen JT. Italy. Available at URL: http://cerhr. In vitro and in vivo interactions of bisphenol A and its metabolite. Zacharewski TR. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). An evaluation of the possible carcinogenicity of bisphenol A to humans. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Haighton LA. Occup Environ Med 2002. Ye X. Tyl RW. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). November 26. Serizawa S. Gender differences in the levels of bisphenol A metabolites in urine. Calafat AM.137(3):353-362. Kuklenyik Z. Imai H. 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. Keimowitz AR.J. Zaugg SD.102(19):7014-7019. Calafat AM. et al. Arakawa C. Wong LY. Human Health. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Needham LL. Hughes C.pdf . Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. Joskow R.europa. Hum Ecol Risk Assess 2004. Barber LB. Reidy JA. Available at URL: http://cerhr.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Calafat AM. Furukawa M. European Commission. Yang M. Furlong ET.eu/ health/ph_risk/committees/sct/documents/out156_en. Toxicol Sci 2002. Environ Sci Technol 2002. Gray GM. May 22. 2/4/09 European Commission. Kolpin DW. Meyer MT. Park S. Timms BG. Reprod Toxicol 2001. Ekong J.69(22):2611-2625.nih. Life Sci 2001. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Thurman EM. Rat two-generation reproductive toxicity study of bisphenol A.niehs. Research Triangle Park. 4. Barton L. National Toxicology Program. Brine DR. Hlywka JJ. U.. Biochem Biophys Res Commun 2003.pdf. Koulova AI. Belgium. Klinefelter GR.gov/chemicals/bisphenol/BPAFinalEPVF112607. Available at URL: http://ec. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Joint Research Centre Institute of Health and Consumer Protection.59(9):625-628. Ispra. Tsugane S. Nippon Eiseigaku Zasshi 2004. Leranth. August 2001. Cha SW. DirectorateGeneral Health and Consumer Protection. Rhomberg et al. Needham LL.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Kawamura N. Watanabe S. Regul Toxicol Pharmacol 2002. 2002. Kim JC. Harazono A. Twomey K. Howdeshell KL. National Institute of Environmental Health Sciences. K.nih. Han SS. bisphenol A glucuronide. Needham LL. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Doull J. Ikka T. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Thomas BF. et al. National Institutes of Health.116(1):39-44. Kim CS.. Endocrinology 2008.312(2):441-448. Shin HC. C.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Pharmaceuticals. Pyo MY. niehs. Han SY. hormones. and other organic wastewater contaminants in U. Environ Health Perspect 2005. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats.

Kawamoto T. vom Saal FS. Chang SS. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure.147(6 Suppl):S56-69. Dekant W.Environmental Phenols Volkel W. Colnot T.44(4):546-51. and nonylphenol at home and daycare.15:12811287. Sheldon LS. Chem Res Toxicol 2002. III. bisphenol-A. et al.113(8):926-33. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. An observational study of the potential exposures of preschool children to pentachlorophenol. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Chuang JC. Csanady GA. Filser JG. Vom Saal FS. Lee SM. Morgan MK. Yang M. Endocrinology 2006. Environ Res 2007. Large effects from small exposures. Kim SY. Wilson NK. Hughes C. Welshons WV. Food Chem Toxicol 2002. Nagel SC. Jang JY.40(7):905-12.103(1):9-20. Biological monitoring of bisphenol a in a Korean population. Lordo RA. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Environ Health Perspect 2005. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Arch Environ Contam Toxicol 2003. Witorsch RJ.

orally administered 4-tert-octylphenol was well absorbed. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.70 (1. altered neonatal sexual development.10 (.50) 1.80 (1.600) . Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.30 (. 2002).Environmental Phenols 4-tert-Octylphenol CAS No.50) .60-3. Several alkylphenols.500) .600-1. altered estrus cycles and reproductive outcomes.20-2. In rats. Disposition in humans has not been studied sufficiently.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 .200-. through sewage.477) .. 140-66-9 General Information 4-tert-Octyphenol.000 tons of alkylphenol ethoxylates were produced annually worldwide.20-2..800-1.20-2.600-1.299-.20-2.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. leading to inhalation as another potential exposure route (Rudel et al.600) .600-1.60) 1. 2000. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.70 (1. streams in 30 states (Kolpin et al. and some personal care products. 4-octylphenol monoethoxylate was detected in 43.400) 1.600) 1. 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.30) 1. and the polyethoxy chain may consist of up to 50 ethoxy units.20-2.90) 2.1.500-1. 2002).30 (1.497) * .60-3. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. and some of their degradation products are toxic to aquatic life. Katsuda et al.80) 2. which are anionic surfactants used in detergents.30) 90th 1. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. industrial cleaners. and from contact with some personal care products and detergents. Survey Geometric mean (95% conf.30-2.300 (<LOD-.200-. and through manufacturing waste streams (Warhurst.. 2006.500 (. and to alkylphenoxycarboxylates. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers..3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Bian et al.600-1.. 2004).274-. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).60) 613 652 1092 Limit of detection (LOD.00 (1. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.50 (1.300-. is used to manufacture alkylphenol ethoxylates.10-2.300 (<LOD-. 1997. to shorter chain alkylphenol ethoxylates.60-3.369 (.389 (.00 (.. impaired steroidogenesis. fish) and drinking water.30 (1.700-1. 1996).g.00 (.507) * < LOD .268-.300 (<LOD-. have demonstrated estrogenic effects particularly when injected at high doses in animals.357 (.3. The alkylphenols can bioaccumulate in some fish. the various alkylphenols have also been used as emulsifiers and modifiers in paints.400 (.20) 2.20-2.30 (1.60) . Ying et al.60-3.40) 2.300 (<LOD-. and emulsifiers. see Data Analysis section) for Survey year 03-04 is 0.900 (.20) 314 715 1488 03-04 03-04 * * .10 (1.900 (.400 (.5% of 139 U. Urinary 4-tert-Octylphenol (4-[1.50-3. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.900 (. pesticides.40 (1.30 (1. and impaired spermatogenesis (e.50) 1.40) 1.2.20) 1. 2000..300 (<LOD-.10) 2.10 (.60-3. 34 Fourth National Report on Human Exposure to Environmental Chemicals . During the 1980s and 1990s.70 (1. In 1999-2000.70 (1. Blake and Boockfor.g. including 4-tert-octylphenol.500-1.50-2.30) 2.50) . 1995. 2003.40) 2. over 500.90) 2.S. testicular atrophy..400 (. Laws et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In the 1990s.600-1. The alkylphenol ethoxylates enter the environment through human use of products containing them.300-.600-1. did not bioaccumulate..500) 75th .10) 1. and was quickly eliminated from the blood (Certa et al. textiles.50) 1. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. Saito et al.00) 1229 1288 03-04 03-04 03-04 * .20 (1.80 (1.900 (. Less frequently. Indoor and to a lesser extent.600) .40) * 03-04 03-04 03-04 .40) 1.80 (1. an alkylphenol.60-3.S.500) .500) . < LOD means less than the limit of detection.900 (.

78 (1.14) 314 713 1487 03-04 03-04 * * . Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.31 (1.400) . 2005..40 (1.17 (.54) * 03-04 03-04 03-04 . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..420) .33) 3. at lower or environmentally relevant doses (Blake et al.470-1.160-.337-.860 (.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.550-1.740 (.207-..43) 1.11-2. or their corresponding ethoxylates with respect to human carcinogenicity.380 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 35 . 2001.05-2. representative subsample of NHANES 2003-2004. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.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 .00 (.15) 1.560) .24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.68-2. 2004.410 (.S. 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.00) 2.03 (1.270-.S.199-.320 (<LOD-.65-3.59 (1. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.78) 3.270 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.06 (2.740 (.20 (1.850 (.470) 75th . 2004).11) 1.450) .630-1.68) 2.1. 4-tert-Octylphenol is not considered directly genotoxic. population from the National Health and Nutrition Examination Survey. 1999).730-1.300 (<LOD-.25) 2. Sweeney et al.890-2.08) 1.620) .270 (.260 (<LOD-.. 2001).00) 2.00) 1. Yoshida et al.. 2000. 2003.770 (.18-4.540-1.60 (1.50 (2.470-1.640-1.40-4. Tyl et al.22) .530) .170-.85 (1.64 (.370 (<LOD-.349) * < LOD . Kawaguchi et al. Nagao et al..460 (.03 (1.435 (. In a small number of adult Japanese volunteers.25-2.269 (.96-4.78) 1228 1286 03-04 03-04 03-04 * . 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.11) 2.610) . Survey Geometric mean (95% conf.73) 2.29) 2. It is unclear if estrogenic or other effects occur in animals through oral dosing.3.67-2. nonylphenol.25) 90th 1.00 (.36-3.02-4.910 (.384) * . Calafat et al.03-6.76 (2.59) 1.Environmental Phenols Myllymaki et al.41) .62 (1.10-2.62) .620-1.33 (2.53-3.276 (.81 (1.62 (1.31-2. IARC and NTP have not rated octylphenol. Urinary 4-tert-Octylphenol (4-[1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.570) .450) 1.71) 2.43) 1.43-3.500-1.280-.

Toxicol Lett 2001. Biol Reprod 1997. Myers CB. Nakagomi M. Xu L. Karjalainen M.57(2):255-266. Inoue K. Toxicol Appl Pharmacol 2000. Food Chem Toxicol 2006.pdf. Exposure of the U. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.28(3):215-226.121(1):21-33. Environ Sci Technol 2003. pesticides. Endocrinology 2000. Makino T. Usumi K. et al.Environmental Phenols References Bian Q. Kookana R. et al. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Phthalates. hormones. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Rudel RA. Carey SA. Reprod Toxicol 2004. Nicol L. Raychoudhury SS. Warhurst AM. Toppari J. Bolt HM. testis size.15(6):683-692. Inoue K.165(3):217-226. Nagao T.S. Regul Toxicol Pharmacol 1999. Yoshimura Y.30(2 Pt 1):81-95. Boockfor FR. Toxicokinetics of p-tert-octylphenol in male Wistar rats.folliclestimulating hormone. Anal Chim Acta 486:41-50. Ito R. Blake CA.18(1):43-51. Fedtke N. Boockfor FR. Millette CF. Environ Health Perspect 2008. Korn LR. Saito Y. Indoor air pollution by alkylphenols in Tokyo. Marr MC. Nair-Menon JU. Brine DR.S. Fail PA. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Furlong ET. and other endocrine-disrupting compounds in indoor air and dust. polybrominated diphenyl ethers. Saito I. McCoy GL. Yoshida M. Ye X. Wang X. Kawaguchi M. et al. Ono H. Arch Toxicol 1996. nonylphenol.54(1):154-167. Toxicol Sci 2000. Katsuda S. Watanabe G. Pharmaceuticals. Estrogenic activity of octylphenol. Barber LB. Wiegand HJ.207(1):59-68.37(20):4543-53. Calafat AM. streams. Zaugg SD.uk/resource/reports/ethoxylates_alkylphenols. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Bodman GJ. Meyer MT. Okada F.36(6):1202-1211. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Maekawa A. Reprod Toxicol 2001. Yoshida M.44(8):1355-1361. bisphenol A and methoxychlor in rats. Brody JG. Spengler JD. Ferrell JM. Tyl RW. Reidy JA. 1999-2000: a national reconnaissance. Yoshimura S. Watanabe G. 2/4/09 Ying GG. Onuki A. 1995. Thurman EM.foe.co. Myllymaki SA. et al. Indoor Air 2004. Taya K. Environ Int 2002. Horie M.14(5):325-332. Wong LY. and sertoli cell number. Takai N. Maekawa A. Laws SC. Chen J. Needham LL. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Katsuda S. Sweeney T. Brooks AN. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Muller AM. Sakui N.799(1):119-125. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Roche JF. Toxicol Appl Pharmacol 2005. Song L. alkylphenols. Haavisto TE. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Williams B. Kawaguchi M. Certa H.71(1-2):112-122.116(1):39-44. Two-generation reproduction study with para-tert-octylphenol in rats.141(7):2667-2673. Seto H. 2003. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. and testosterone. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. prolactin. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Qian J. Blake CA. Paranko J. Available at URL: http:// www. Seely JC. Taya K. Takenaka A. Cooper RL. and other organic wastewater contaminants in U. Camann DE. Environ Sci Technol 2002. 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. Izumi S. Kolpin DW.

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

6) 90th 212 (172-241) 03-04 03-04 03-04 9.00 (4.0-15.1 (45.70-16.92-12.3 (8.0 (8.0-73.48-10.S. population from the National Health and Nutrition Examination Survey.4) 90th 249 (188-304) 03-04 03-04 03-04 8.9) 8.4) 357 (225-456) 203 (87.20 (7.2) 9.3) 47.0 (11.0) 49.8-127) 37.6) 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 9.40-17.74 (5.3-35. Urinary Triclosan (2.3) 6.90-10.50-10.4-19.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-58.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0 (26.6 (10.9) 32.1) 9.1) 9.20 (7.3 (11.1) 14.94 (7.6-37.7) 123 (36.20-10.7) 10.48 (8.45-13.82 (8.5-14.50) 10.1 (8.10-9.6-65.6-111) 33.Environmental Phenols Urinary Triclosan (2.5 (11.2 (27.4 (38. population from the National Health and Nutrition Examination Survey.7 (39.21 (6.4) 7.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.7 (28.11-11.45-10.4) 73.5) 13.7 (14.4 (12.6) 10.1) 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 9.80 (5.3-31.8-85.0 (34.5) 20.1) 9.0 (36.2 (37.3 (9.1) 9.6) 39.7 (9.3-15.4) 317 (231-433) 144 (96.32-14. interval) 12.43-13.5-86.7 (11.10) 84.0-19.60 (8.2 (25.6-14.2-46.29-12.4 (32.6-20.6) 31.8-63.4.4) 75th 43.89-11.9 (8.1) 13. see Data Analysis section) for Survey year 03-04 is 2.1) 50.8 (21.S.6-14.2) 13.72-13. Survey Geometric mean (95% conf.8) 14.0) 65.60 (6.1-39.18 (5.6 (9.9) 7.3 (26.55 (4.2 (11.1) 11.4) 51.3.9-61.3-67.16 (6.20-13.8-60.2-14.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.9 (33.93 (7.45 (5.2) 12.6 (30.2 (13.9) 75th 47.6-15.86-12.4 (11.9 (11.22-10.00-8.5) 11.4) 25.54 (8.1) 7.2 (10.3) 10.20-11.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.30-14.2-58.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.4-18.4.9 (50.1 (15. Survey Geometric mean (95% conf.5) 66.40-11.7) 292 (151-432) 132 (78.0) 9.8-112) 30.8) 7.6 (12.0-15. interval) 13.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.8) 9.6) 12.9-236) 193 (90.0-213) 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 .8) 116 (39.38-18.

. Pharmacokinetics of triclosan following oral ingestion in humans. Calafat AM. Ishibashi H.38(2):64-71.S. Teitelbaum SL.66:1052-1056. streams.28(9):1748-1751.23(5):579-583. Bennett ER. Photolytic degradation of triclosan in freshwater and seawater. Chemosphere 2007. Benson WH. Kaneshima H. Watanabe N.115:116-121. Wigmore H. Environ Sci Technol 2002. Zaugg SD. Odham G. Gunderson MP. Arch Environ Contam Toxicol 1988. Thurman EM. et al. Anal Chim Acta 1004. Shiratsuchi H. Howes D. Kanetoshi A. Triclosan: applications and safety. 1999-2000: a national reconnaissance. Gomez MJ. Pilot study of urinary biomarkers of phytoestrogens. Hong HC. Aquat Toxicol 2006. Osachoff H. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis).36(6):1202-1211. Hirano M. Matsumura N. Bhargava HN. Bodey GP.4.116(3):303-307. Leonard PA. Moss T. Clapson DJ.83(1):84. Pinney SM.7/2. Needham LL. Readman JW. Pharmaceuticals. The oral retention and antiplaque efficacy of triclosan in human volunteers. Erratum in: Aquat Toxicol 2007. Developmental evaluation of a potential non-steroidal estrogen: triclosan. hormones. Evidence of 2.67(4):532-537. Okui T. 4’-trichloro-2’-hydroxydiphenyl ether.524:241-247. Reidy JA. Barber LB. Biol Pharm Bull 2005. Urinary concentrations of triclosan in the U. Larson EL. Mar Environ Res 2000. Foran CM. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. and other organic wastewater contaminants in U. Ye X. Ferrer I. et al. Toxicology of 2. Ebersole R.4’-trichloro-2’hydroxydiphenyl ether). Mezcua M. Wolff MS.69(20):1861-1873. Environ Health Perspect 2008. Fernandez-Alba AR. Aranami K.24(3):209-218. Ogawa H.80(3):217-227. Lyman FL. Furlong ET. Britton JA. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Aguera A. Nagao Y. Windham G. Environ Health Perspect 2007. J Invest Dermatol 1976. population: 2003-2004. Williams FM. Wong LY. Adolfsson-Erici M.50(1-5):153-156. Hernando MD. Chelimo C. Meyer MT.17(5):637-644. IMS Ind Med Surg 1969.38(4):361370. Gilbert RJ.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. and phenols in girls.S. phthalates. Ekstrand J. Am J Infect Control 1996. et al.45 Suppl 2:S137-S147. Levy SB. Veldhoen N. Fourth National Report on Human Exposure to Environmental Chemicals 39 . et al. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Sandborgh-Englund G. Williams PE. Food Chem Toxicol 2000. Furia T. Katsura E. 4. Percutaneous penetration and dermal metabolism of triclosan (2. Br J Clin Pharmacol 1987. Skirrow RC. Kolpin DW.Environmental Phenols References Aiello AE. J Toxicol Environ Health A 2006. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps.

350-2. herbicide.960) 1. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.30) 1.350 (.350-.08-3.00 (.630 (.10) 1.80) .350 (. mollusicide.98 (1. After a single dose.10 (. are eliminated in the urine.70) .30 (. algaecide and insecticide.350 (.510-5. Since 1984.65 (.62 (.00) 1.75) 2.660 (.350 (.350-1.650) 1.350-.980 (. PCP is absorbed rapidly and well by all exposure routes.350 (. and dermal contact with PCP-treated products. and possibly of lindane (IPCS.94 (1.350-.S.350-.350) < LOD .350) < LOD .990 (<LOD-2. population from the National Health and Nutrition Examination Survey.23 (.350-.350 (.350-.350 (.350-. General population exposure to PCP may occur by inhalation of contaminated air..00) 1.350 (.76) . 1979).18 (<LOD-1. and animals.00) 2.390 (. the elimination half-life may be a week or more (Uhl et al.350) < LOD .47-3.48-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.350-.54-2.37) . 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.510-3.350) < LOD .530) 1.76) 1.S.990-2.860-2.350-. 1986).890 (.350 (.30 (1. 1997).94 (1.01 (<LOD-1.67) 1. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350-.10) 1.350) < LOD .350-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.58-2..590-1.350 (. To-Figueras et al.78) 1.90) 1.350) 90th .890-1.350) < LOD .350 (.350-.350-.650 (. Acute.350) .350) < LOD < LOD 75th .70) 2. The parent compound and conjugates.350-. PCP is eliminated over a few days (Braun et al. < LOD means less than the limit of detection. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.42) 696 680 521 696 603 951 Limit of detection (LOD.10 (1.33) ..350-1.53) 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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.58-2.32 (. air.850-2.480-2.37 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .09) .350) < LOD . 1976. PCP use in the U. PCP cannot be used on wood in residential or agricultural buildings.350) < LOD .83 (2. Kohli et al.350 (.90 (1.350-1.350-. Survey Geometric mean (95% conf.350) < LOD ..680-1.30 (.350 (.350) < LOD . 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. ingestion of contaminated food or water.350) < LOD . 2002.350 (. which may vary for some chemicals by year and by individual sample.350 (.350 (.350-. has been restricted.350 (.350 (.04) 1.350-.73 (1.10 (<LOD-1.350-2. Human exposure to PCP has become less common. bactericide. along with small amounts of tetrachlorohydroquinone and conjugates.770 (. water and sediments because of the large amounts that were produced and used historically.60) 1.40 (.45-2. plants. utility poles and fence posts).90) 2. with repeated or chronic exposure. hypertension.64) 1.30) 1.30) .350-2. so it is relatively non-persistent.350-2. In the environment.350-1.350) < LOD .350-.350-.65 (. 40 Fourth National Report on Human Exposure to Environmental Chemicals .350-.350) < LOD .350 (.g.48 (.350-2.91 (1.500-2.350) < LOD .42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .50) 1.350) < LOD .25 and 0. Effects including hyperthermia. PCP is degraded by sunlight and metabolized rapidly by microorganisms.33-2. PCP is distributed to most tissues and is not extensively metabolized. and metabolic acidosis were observed in CAS No.350 (.390 (. and it is used primarily as a preservative for wood to be used outdoors (e.51) 1.5.47-5. other polychlorinated benzenes.60) 1.350-.350-.350) < LOD . After absorption.350 (..Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. PCP has been detected in soils.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .

40) 1.400 (.360-.650 (. 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 (4.67-3.430) < LOD . the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.25-2. OSHA has established an occupational standard.56) 1.95) 3.10 (1.06 (.290-.21-2.94 (1.380-.920 (.30) 1.73 (1. respectively) (Seifert et al.48-2.30 (.830) < LOD .760 (.78) 1.290-.500-.630 (.800-1.730) < LOD .09 (<LOD-2.94 (1. 2003).html.0 mg/L.10-2.25-2.590-1.40) 1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.55) 1.84-4.34 (.epa.320) < LOD < LOD 75th .950-1.330-.310) < LOD .510-.52 (<LOD-1.30) 1.82) 1.570 (.S.780-1. 1991). 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. and the FDA has established a standard for bottled water.6 and 14.S.290) < LOD .. population from the National Health and Nutrition Examination Survey. 1989). More information about external exposure (i.25-1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .300 (. environmental levels) and health effects is available from the U.370 (.69 (1.67 (1.84 (1.40-2.500-1.52) 1.09) 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 .35-2.19) 2. 1995). van Raaij et al.19) 2.16 (.270-.950-1. Among adults in the NHANES 1999-2000 subsample. In animals. respectively) (Becker et al.850 (.650) 90th 1..25 (1.67 (1.cdc.18 (1.S.35-2. and adversely affected thyroid function (U.320) < LOD . inhalation.gov/ pesticides/ and from ATSDR at: http://www.67 (1.26 (1.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .35) 1. Pentachlorophenol is not mutagenic or teratogenic.560) < LOD ..26 (1.910-1..360 (.650 (.580-.310-.52 (1.57 (1.67-3. In a small sample of U. 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.240-.09-1. 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.67-2.94-3.950-1.250 (.780) < LOD .75 (<LOD-2. EPA at: http://www.40) 1.19 (1.atsdr.83 (1.25 (1.16-1.35) 1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine..40) 1. 2000).82 (1.500 (.11) 2.06-3.29-3.280) < LOD .900-1.320 (. 2004. 2003).350) < LOD .S.79) 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.270-.9 mg/L.. chronically administered high doses of PCP were hepatotoxic.52 (<LOD-1. The U.57 (. carcinogenic.13 (.21 (.560-.800) < LOD 1.06) 1.220-. or skin absorption.340-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300 (.78) 1.84) 1.00-1.700-2.440 (.560) < LOD .990 (.250 (.490) < LOD .36) .420) < LOD .90) 1..430-.40) 1.67 (1.00) 1.e.S.67 (1.320) < LOD .18) .610 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 41 . In NHANES 2001-2002 subsamples.220-.510-.470 (.51) 1. 1989).710-1.19) 2.92) 1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * . EPA has developed standards for PCP in drinking water and the environment..590) < LOD .gov/ toxpro2.08 and 5.25) 1.30-2.260 (.EPA.Fungicides adults and children severely exposed to PCP through ingestion. Death can result from seizures and cardiovascular collapse.00-1. children in the 1980’s.75) 1. 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.

Environmental Protection Agency (U.inchem. Pesticide residues in urine of adults living in the United States: reference range concentrations. htm. Helm D. Safe A.10:552-65. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. To T. Blau GE. house dust.S. van den Berg KJ. Can J Biochem 1976. Dev Toxicol Environ Sci 1979.54(3):203-208. 11/30/2004. Notten WR. 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 . Jones D. Environ Res 1995. Hill RH Jr. EPA). 206:15-24. Cline RE.4:289296. Otero R. Pharmacokinetics of pentachlorophenol in man. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Gregg M. Needham LL. Baker S. urine.105(1):78-83. Environ Health Perspect 1997.18(4):469-474. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. 2002. available at URL: http://www.18:475-481. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Available at URL: h t t p : / / w w w.org/documents/jmpr/jmpmono/2002pr08.S. 4/21/09 Kohli J. International Programme on Chemical Safety (IPCS). German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.71:99108. Bailey SL. Hill RH. To-Figueras J. Arch Toxicol 1986. drinking water and indoor air. Hill RH Jr. 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. Kaus S. Shealy DB. J Expo Anal Environ Epidemiol 2000. Phillips DL. Santiago-Silva M. Lindane. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Toxicology 1991: 67(1):107-16. Schulz C. et al. Braun WH. Krause C. hair. Schmid P. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. et al. References Becker K. Seiwert M. Bragt PC. Chenoweth MB. PCP: Human Risk Characterization [online]. Engel R. Rodamilans 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. The metabolism of higher chlorinated benzene isomers. Head SL. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Barrot C. Sala M. Uhl S. Arch Environ Contam Toxicol 1989. Needham LL. 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. Int J Hyg Environ Health 2003. Holler JS. Arch Environ Contam Toxicol 1989. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. et al. 4/21/09 van Raaij JA. Schlatter C.58:182-186. Seiwert M. Becker K. Seifert B. U. Fast DM. Seifert B. Schulz C.

540-2.389-. Fourth National Report on Human Exposure to Environmental Chemicals 43 . on ornamental plants and turfs.410-.10) 2.88) 1. Both chemicals degrade within hours to weeks in the environment (U.Fungicides ortho-Phenylphenol CAS No.40-5.03) 1.580-1.50-2.00 (1.20) < LOD 1.00-2.10) .20 (. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.800-3.600-1.10-1. are antimicrobial agents used as bacteriostats.550-1.60 (1.600) < LOD .90) .10) .3 and 0.497 (. OPP is volatile..840-1. population from the National Health and Nutrition Examination Survey. OPP is considered to be moderately toxic after acute oral doses in animal studies.3.490 (<LOD-.349-. 2002. 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. fungicides.610 (.50) .860 (.90 (1.480-1.80-3.500-2.50) 1.710-2.386-.570-2.23) 695 680 520 695 603 953 Limit of detection (LOD.390-.930 (. and it has limited water solubility.630) < LOD .20-2. Most agricultural food applications have been revoked.50 (1.850 (.27 (. 1998.970 (.10) 1.470 (<LOD-. and as a wood preservative.40-5. Timchalk et al. 1989).830 (.950) < LOD .50) < LOD . whereas SOPP is not volatile and is more water soluble.600-1.20 (1.30) < LOD .670) 2.433-.820 (. inhalational. formulate.17 (.90 (1.90) .50 (1.85) 2.50-3.30) 1.10) .450 (<LOD-. SOPP is applied topically to the crop and then rinsed off.61) 2.76) 1.22) 2. 2006).19 (.450 (<LOD-. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.750-2.364-.30 (1. and sanitizers.50) < LOD . OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.10) 1. < LOD means less than the limit of detection.490 (<LOD-.80) 1. Available evidence suggests that OPP does not accumulate in the body.00) < LOD .466 (.00 (1.600) < LOD .640) < LOD .28 (.836) * .624) * .10 (1.90) 1.60-2.80) 1.80 (2.60 (1.09) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.570-1.30-7.890) 1.890 (.552 (.493 (.610-1.570-.450 (<LOD-.770 (.690) < LOD .509 (. or 2-phenylphenol) and its water-soluble salt.742) * .20-3.14 (<LOD-3.590-2.621) * .00) . which may vary for some chemicals by year and by individual sample.570 (.S. in paints.560-8. such as fruits and vegetables.880-2.696) * .636) * .34) 1.370-. EPA.370-.490 (<LOD-. General population exposure can occur via dermal.60-3.790) 2.07 (.496 (.508 (. however.20) < LOD 2.10-2.389-.710) 3.780) < LOD .770 (. sodium ortho-phenylphenate (SOPP).50) < LOD . 2006).23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .50-4. but OPP and SOPP are still used on pears and citrus (U.. interval) .632) Selected percentiles ( 95% confidence interval) Sample 95th 2. In the past.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .20 (1. leaving the chemical residue OPP.20) 2.S.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 . or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.10 (1. 2006). Cnubben et al. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.690-1.520 (.370-. Estimated human intakes have been below recommended intake limits (U. OPP is still used as a disinfectant fungicide for industrial applications. 2006).22 (.600-1.S. Survey Geometric mean (95% conf.30) < LOD 1.638) * .420 (<LOD-. Workers who manufacture.40-2.40-7.00) ..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 .60 (1.402-.00 (1. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.600) < LOD 1.28-3.350-1. 90-43-7 General Information Ortho-phenylphenol (OPP.890 (.EPA.30) < LOD 90th 1.498 (. Both have been used in agriculture to control fungal and bacterial growth on stored crops.740 (.567 (.S. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.02) 1. 1998).00 (1.90) 2.600) < LOD 75th . or apply these chemicals may be more highly exposed than the general population.92 (.30-2.645) * .490 (<LOD-.EPA.490 (<LOD-.40 (. it was used in home sanitizers for surfaces.33 (.760-2.50 (1.570 (.

13) 1.550) < LOD .08-1. reproductive. by possible genotoxic mechanisms (Hagiwara et al.74 (1.248-.47) .380 (.21) 1.640-1.09 (1.910 (. Additional information is available from U. leading to production of two metabolites.4) 3.01) 1.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 . In high dose animal studies.620-1. IARC has classified SOPP as a possible human carcinogen. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.11 (.. U.444 (.650-1.24-2.473) * . or developmental toxicity was observed (Bomhard et al.21-2. 2002.11 (.403-.301-. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.670 (.02 (. OPP was not found to be mutagenic. Ito et al.61 (.43) 3.600-1.410 (<LOD-. Bomhard et al.420 (<LOD-.00 (1.860 (.455-.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. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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.666) * .780 (.670 (.361-.93) 1. Kwok et al.epa.51-3.590) * . U.. or.910-1.810-1. 2002).410 (<LOD-.0) 1. Zhao et al.43-2.382 (.78 (2.470) < LOD . 1984.97 (2.568) * .44 (1.17) 2.33) 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 .Fungicides anemia.910 (<LOD-1.940-2.28 (2.470 (<LOD-.75 (1.07) 2. interval) . 1999.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .59) 1. 1999. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.508) * .860 (.64 (2.900) < LOD .EPA at: http:// www. 2005).93 (1.453 (.06-5.320 (<LOD-.93) .360 (<LOD-. population from the National Health and Nutrition Examination Survey.58) 2.18) 2.62) .26) 1. Biomonitoring Information Urinary OPP levels reflect recent exposure.11-1.75 (1.385 (.560-2.12-2.500) < LOD .580) < LOD .12) < LOD 1.750 (. 1984.96 (1..329-.06-4.91 (1.25-6..53) 1.11) < LOD 90th 1.20) < LOD 3.04-4.620-1.510 (<LOD-.61 (1.52 (..17 (.43 (1. Murata et al.311-.46) < LOD 1. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.EPA 2006).690 (.17 (.86 (1. Pathak and Roy.480-.61 (2.800-1. CDC.24-2.484) * .460-.900-1.656) * .440 (.770-2.496 (. Brusick.05-2.EPA 2006).59) .32) 1.96-4.09-6.08) 1.610) < LOD 1. Volunteers exposed to 0.84 (1. 2000.353-.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.810) < LOD .28 (<LOD-4.510-.93) .33) .514 (.06 (1.840 (.38) 2.08-2. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.09-3.29) 1. 2002. 1986).gov/pesticides/.40-13.550 (.31) < LOD .560) < LOD 75th .81) 1. 1992.970) 1. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.291-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .950) < LOD .980 (.33-2. and it has classified OPP as not classifiable with respect to human carcinogenicity.420 (<LOD-..980 (<LOD-1. Survey Geometric mean (95% conf.11) 4.32) 3.38-3.29) 1.750 (.550-. 1998..S.21 (.69 (1. Nakagawa et al.880-1.43-2.89 (1. less likely. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC..88-4. Detectable levels were seen in over half the U. 44 Fourth National Report on Human Exposure to Environmental Chemicals . 1997.791) * .S.270-.990) < LOD .580-1. Smith et al.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine..38) 1..343 (. 2005).96) 1.780-14.S.570) < LOD 1. 1993.750-2. but no neurologic.00 (. 2005.27) < LOD .S.96 (1.670) < LOD .

St John MK. Vogel JS. J Chromatogr B Biomed Sci Appl 1997. Sangha GK. The carcinogenicity of the biocide ortho-phenylphenol. Toxicol Appl Pharmacol 1999.nih. rat and man.S. Tayama S. Buchholz BA. Available at URL: http://ntp. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Fukushima S.S. Glas K. 90-43-7) in Swiss CD-1 mice (dermal studies). Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. 4/13/09 Onstot JD. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Mutat Res 1993. July 28. Bartels MJ.150(2):402-413.28(6):579594.286(2):309-319. 4/9/09. Fukushima S. Richter M. Drugs. Ito N.epa. Ito N. Coelhan M. Regul Toxicol Pharmacol 2002. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Roberts AL. Kawanishi S. Murata M. Hagiwara A. Centers for Disease Control and Prevention (CDC). Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries.703(12):97-104.S. Bartels MJ. 2006. food additives and natural products as promoters in rat urinary bladder carcinogenesis.32(6):551-625. Biochem Pharmacol 1992. Moldeus P.Fungicides References Appel KE. Moriya K. Arnold LL. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Timchalk C. Selim S. Roy D. Inoue S. Identification of SARA compounds in adipose tissue. 2005. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Hagiwara A.159(1):18-24. Brzak KA.22(10):809-814. J Agric Food Chem 2002. Bormett GA. et al.gov/oppsrrd1/REDs/ phenylphenol_red. Imaida K.(56):399-407. Atlanta (GA).17(8):411-417.20(5):851-857. Smith RA.54(16):5731-5735. Environ Mol Mutagen 2005. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Kwok ES.EPA). Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol.50(11):3351-3358. Brendler-Schwaab SY. Brusick D. McNett DA. Eadon G.pdf. Shibata M. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Crit Rev Toxicol 2002.gov/ntp/htdocs/LT_ rpts/tr301. Hum Exp Toxicol 1998. Third National Report on Human Exposure to Environmental Chemicals.. Environmental Protection Agency (U. Christenson WR. et al. Sangha G. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. IARC Sci Publ 1984. Turteltaub KW. Bomhard EM. Herbold BA. Environmental Protection Agency (U. EPA-560/5-89-003. van de Sandt JJ. Comparative metabolism of orthophenylphenol in mouse. Bartels MJ.S. Christenson WR.35(2 Pt 1):198-208. Pathak DN. Carcinogenesis 1999. Leser KH. Shirai T. EPA 739 R-06004. National Toxicology Program (NTP). J Agric Food Chem 2006. Elliott GR. Freyberger A. Office of Toxic Substances. Available at URL: http://www. Zhao S. 1989. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP).pdf. Xenobiotica 1998. Stanley JS. Bartels MJ. Narang A. Arch Toxicol 2000. U. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Bromig KH. U. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats.45(5):460-481. Nakagawa Y. Timchalk C.74(2):61-71. Meuling WJ. Gierthy J. Toxicol Appl Pharmacol 1998. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. EPA).43(7):14311437. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Cnubben NH. Eastmond DA. Moore GA. Mendrala AL. Food Chem Toxicol 1984. Hirose M. March 1986. Cano M.niehs. Hakkert BC.

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

2000.epa.S. environmental levels) is available from U. EPA at: http://www..EPA. renal injury. Hladik et al.. In animals. Plants can degrade acetochlor to 2-ethyl-6-methylaniline. However.EPA 2000. Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Acetochlor is moderately toxic to fish and honey bees. 2-hydroxyethyl-6-methylaniline. a major pathway for acetochlor metabolism involves mercapturate conjugation. It is absorbed by plants and inhibits plant protein synthesis. Urinary acetochlor mercapturate levels of 0. 2007). but other pathways occur. Additional information about external exposure (i. 2005).5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al. Kolpin et al..S. which are often more prevalent in the environment. General population exposure to acetochlor may occur through diet or drinking water. 2005. animals have demonstrated tumors of the lung. but it has produced testicular atrophy.EPA considers acetochlor likely to be carcinogenic in humans. 2000. and hydroxymethyl ethyl aniline (U. including one that produces 2-methyl-6ethylaniline and its reactive metabolite. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies.Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure.S.S... 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. Davison et al.S.. and neurologic movement abnormalities (U.e. and has been detected in watersheds of agricultural lands (Battaglin et al. remains in soils for up to 3 months. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8. 2006). Estimated human intakes of acetochlor have been below recommended limits (U.. 1989. Acetochlor is microbiologically degraded. CAS No. the latter which may account for some observed effects (Coleman et al. 2006). and thyroid (U. mainly corn.. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid.. 2006). nasal epithelia. Feng and Wratten. and it is unlikely to be genotoxic at relevant doses (Ashby et al. 1998). U. 1994. Jefferies et al. People exposed to acetochlor will excrete acetochlor mercapturate in their urine. 2005).gov/ pesticides/. in some species and at doses above maximum tolerated doses. 1996). this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. however.0 μg/L (Curwin et al. Acetochlor has low acute toxicity.EPA. Fourth National Report on Human Exposure to Environmental Chemicals 47 . 2000. 2000). Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown..S. 2006). NTP and IARC do not have ratings regarding human carcinogenicity.EPA. Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect. 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. Acetochlor is not mutagenic.

Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.S. Survey Geometric mean (95% conf. 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. Survey Geometric mean (95% conf. 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. see Data Analysis section) for Survey year 01-02 is 0. population from the National Health and Nutrition Examination Survey. 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. 48 Fourth National Report on Human Exposure to Environmental Chemicals .

J Agri Food Chem 1989. Linhart SM. Linderman R. EPA). Xenobiotica 1994. Environmental Protection Agency (U.17(6):559-566.248(2-3):115-122. and metolachlor herbicides in rats.39(17):6561-6574. Quistad GB. Chem Res Toxicol 1998. Thurman EM.html. Number 15. 2000. Camann DE. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Comparative metabolism and elimination of acetanilide compounds by rat. J Expo Anal Environ Epidemiol 2005. pages 3682-3690. U. Deddens JA. et al. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Feng PCC. Centers for Disease Control and Prevention (CDC). Kinney PL. Sci Total Environ 2000.15(9):702-735. Coleman S. Tinwell H. Environ Health Perspect 2003. Davison KL.111(5):749-756. Ward EM. Striley CA. Wratten SJ. Curwin BD. et al. Peter CJ. Kolpin DW. Lefevre PA. Feil VJ. Barr DB. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Sci Total Environ 2000.37(4):10881093. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Acetochlor (Harness) Pesticide Petition Filing 1/00. Atlanta (GA). Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. 5/30/06.EPA): http://pmep. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Rose RL. Environ Sci Technol 2005. Fourth National Report on Human Exposure to Environmental Chemicals 49 . and other herbicides in rivers. 2005. et al. Available at URL(non U. Kier L. Battaglin WA.S. Wilson AG. Whyatt RM.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100.24(10):1003-1012. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. acetochlor. Hines CJ. Furlong ET.S.cce. Available at URL: http://www. Burkhardt MR. Barr DB.248(2-3):123-133. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Sanderson WT. reservoirs and ground water in the Midwestern United States. Heederik D.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Barr DB. Roberts AL. Andrews HF. Hein MJ. imidazolinone. Green T. sulfonamide. Volume 65.pdf. Olsson AO. Federal Register: January 24. Dialkylquinonimines validated as in vivo metabolites of alachlor. J Expo Sci Environ Epidemiol 2007. Hsiao JJ.Herbicides References Ashby J.15(6):500-508. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Environ Health Perspect 2000. 1998.108(12):1151-1157. Hladik ML. 5/30/06 U. Alavanja MC. Occurrence of sulfonylurea. Reynolds SJ.cornell. Environmental Protection Agency (U. EPA 738-R-00-009.S. Hodgson E. epa. Jefferies PR.S.11(4):353359. Third National Report on Human Exposure to Environmental Chemicals. Barr JR. Hum Exp Toxicol 1996. Casida JE. Bravo R. EPA). March 2006. Larsen GL.S.

2000. 2003). Because it can be absorbed through skin. USGS. and uveal degeneration. 1995. soybeans. U. Alachlor has a soil half-life of a few weeks. 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.. whereas 60% of applicators had detectable amounts. peanuts and other crops. the dermal exposure route is potentially significant for applicators. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. 1999 and 2007. In a study of applicators and workers exposed to alachlor. 1998..S. U. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC.EPA. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. but not likely at low doses.EPA.. 2003). Jefferies et al.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. U.Herbicides Alachlor CAS No. including corn. WHO.S. 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. about 20-25% of the U. 1997.1 mg/L at various collection times (Sanderson et al. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. Since the late 1980s alachlor use has been declining. (2003) showed that 2.S.epa. formulators.. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. Feng and Wratten. U..EPA. mean values of urinary concentrations of alachlor metabolites. IPCS.S. 1996. 1989. hemosiderosis. but another metabolic pathway can produce 2. 1999. 2000. Alachlor has low potential for acute toxicity.6-diethylaniline and its reactive metabolite. corn cropland was treated with alachlor. 1996). Additional information about is available from U. mercapturate conjugates were predominant metabolites. and field workers. 2005). WHO. 50 Fourth National Report on Human Exposure to Environmental Chemicals . stomach.S.S.EPA considers alachlor to be a probable human carcinogen at high doses.. In animal studies.. 2003). It is absorbed by plants and inhibits plant protein synthesis. as measured through conversion to deethylamine. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. Alachlor itself is not considered mutagenic. In 1993-1995.. WHO. Hladik et al. In chronic animal testing. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.EPA.gov/pesticides/. 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. 2003)..S. 1998. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. 1998). the latter may account for some observed effects (Davison et al.EPA.1 to 1. ranged from 0. WHO. and on non-crop land for general weed control. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Hines et al. but shows little bioaccumulation. 1998). alachlor has demonstrated hepatotoxicity. 1996. Hill et al. Estimated human intakes have been below recommended limits (U. 1995). Kolpin et al. 1998. Tessier and Clark.. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. NTP and IARC do not have ratings regarding human carcinogenicity. 1998). 1988. EPA at: http://www. In animals. General population exposure to alachlor may occur through consumption of contaminated food or drinking water.S. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. but has not shown developmental or reproductive toxicity in mammalian systems (U. 1994.

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. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.18. population from the National Health and Nutrition Examination Survey.S. < LOD means less than the limit of detection.Herbicides Urinary Alachlor mercapturate Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Urinary Alachlor mercapturate (creatinine corrected) Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf.S. 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. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. * 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 51 .

EPA 738R-98-020. J Agri Food Chem 1989.S. Martens MA. Reregistration Eligibility Decision (RED) Alachlor.php. Whyatt RM. Alachlor in Drinking-water. 1999. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Roberts AL. who.gov/oppsrrd1/ REDs/0063. Brown KK. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals .56(9):883-889. California. and other herbicides in rivers. International Programme on Chemical Safety (IPCS). Casida JE. 2/27/09 Jefferies PR. Thelin GP.S. Andrews HF.inchem. Biagini RE. World Health Organization (WHO). Environmental Protection Agency (U. Available at URL: http://www. Striley CA. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.Herbicides References Battaglin WA. Wilson AG. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.24(10):1003-1012. Supplemental Technical Information (available on-line only). Atlanta (GA). EPA). Kinney PL. Brown MA. Quistad GB. 86. Wratten SJ.47(6):503-517. Heydens WF. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Environ Sci Technol 2005.org/documents/pds/pds/pest86_e. Gilliom RJ). Barr JR. Xenobiotica 1994. sulfonamide. Sci Total Environ 2000.248(2-3):115-122. Life Sci 1988. Biagini R. Ann Occup Hyg 2003. J Ag Food Chem 1995. WHO/ FAO Data Sheets on Pesticides. Third National Report on Human Exposure to Environmental Chemicals. Quistad GB. Thake DC. Burkhardt MR. Available at URL: http://water. Linhart SM.S. ALACHLOR. 2007. Occurrence of sulfonylurea. Available at URL: http://www.S. Tolos W. Deddens JA. An evaluation of the carcinogenic potential of the herbicide alachlor to man. DNA adduct formation by alachlor metabolites.18(6):363-391. Sanderson WT. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Hsiao JJ.39(17):6561-6574. Sacramento. Hines CJ. 1999.37(4):10881093. Jefferies PR. 2005.epa. December 1998. Feng PCC. Davison KL. Circular 1291.usgs. Clark JM. Hladik ML.43(9):2504-2512. Casida JE. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Geological Survey (USGS). Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.56(6):853-859. Am Ind Hyg Assoc J 1995. Centers for Disease Control and Prevention (CDC).44(18):1325. and metolachlor herbicides in rats. Shoemaker DA. 1996. Background document for development of WHO Guidelines for Drinking-water Quality. Comparative metabolism and elimination of acetanilide compounds by rat. et al. revised February 15. 2003. Shealy DB. Hill AB. Kolpin DW. Tessier DM.248(2-3):123-133. Kimmel EC. Dialkylquinonimines validated as in vivo metabolites of alachlor.43(25):2087-94. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. MacKenzie B. Thurman EM. Geneva. No.111(5):749-756.11(4):353359. 1992-2001.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Bull Environ Contam Toxicol 1996. Casida JE.htm. Kier LD.pdf. Peter CJ. Lau H. 2/27/09 U. Erratum in: Life Sci 1989. 1998. Hill RH Jr. acetochlor. Furlong ET. Feil VJ. Available at URL: http:// www. Henningsen G. Barr DB. Larsen GL. Sci Total Environ 2000. Driskell WJ. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Camann DE.pdf. Hull RD. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor.int/water_sanitation_health/dwq/chemicals/en/alachlor. U. reservoirs and ground water in the Midwestern United States. Mutat Res. et al. Kolpin DW.395(2-3):159-171. imidazolinone. 4/2/09 U. 1997. March 2006. Chem Res Toxicol 1998. World Health Organization. Environ Health Perspect 2003. 98-4245 (by Barbash JE. Hum Exp Toxicol. Geological Survey (USGS). Hines CJ.

1993.791 and 0. atrazine is slowly degraded to dealkylated products. It is also used as a non-selective herbicide. 2003b). As a result. Fourth National Report on Human Exposure to Environmental Chemicals 53 . It has little toxicity in birds and moderate toxicity in some fish and aquatic invertebrates. and then eliminated in the urine over a few days (Bradway et al. 2002. 2003b). Atrazine has limited water solubility and is not tightly bound to soil. Timchalk et al. with about 75% of corn cropland receiving treatment. 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. which have half-lives of several months. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 1982. Survey Geometric mean (95% conf. For the general population. Related chlorotriazine herbicides include simazine. < LOD means less than the limit of detection. Atrazine may alter the sexual development of frogs at environmental levels (Gammon et al. Applicators of atrazine may be exposed dermally and by inhalation. U.. Catenacci et al. it is one of the more commonly detected pesticides in surface and ground waters (USGS. Urinary Atrazine mercapturate Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. but it is leachable into ground and surface waters. all of which act by inhibiting plant photosynthesis...EPA.. 2003a). but estimates of seasonal intakes from drinking water in a small number of communities have exceeded the recommended limits (U..Herbicides Atrazine CAS No. 1912-24-9 General Information Atrazine is a widely used chlorotriazine herbicide that acts against broadleaf and grassy weeds. The dealkylated chloroatrazine metabolites. More than 70 million pounds have been applied annually in recent years. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.. and cyanazine. Atrazine is well absorbed orally.EPA. drinking water is an infrequent source of atrazine exposure.S.S.S. In soils.3. 1990). Atrazine is applied pre. U.and post-emergence to agricultural land for crops such as corn and sorghum. 1996. Atrazine was first registered as an herbicide in 1958. atrazine use has progressively been restricted in an effort to reduce surface and ground water contamination. 2005.S. Bacteria and plants can metabolize atrazine to hydroxyatrazine. glutathione conjugation appeared to be the major route of biotransformation. propazine. 1993). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. resulting in atrazine mercapturate and N-dealkylation products (IPCS. Atrazine does not bioaccumulate.EPA. In animals and humans. In regions where atrazine is used. Hayes et al. metabolized. 2007). Atrazine mercapturate products accounted for a major proportion of human urinary metabolites (Lucas et al.

.atsdr. Eldridge et al.html. developmental ossification defects. population from the National Health and Nutrition Examination Survey.. U. detection of these dealkylated metabolites in a person’s urine may also reflect exposure to these degradates in the environment.cdc.. Gammon et al. EPA at: http://www. 2003). Estimated human exposures are thousands of times lower than doses that caused effects in animals (Gammon et al.gov/pesticides/ and from ATSDR at: http://www. 2000. 2002. 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. propazine. Thus. Atrazine and the dealkylated chlorinated metabolites did not have estrogen receptor activity. Sathiakumar and Delzell. Gammon et al. 2005.. Dealkylated metabolites from atrazine can also result from metabolism of other chlorotriazine pesticides. may mediate some effects of atrazine (Laws et al. 1999). 2003.S. prolactin. 2000 and 2003. and reduced levels of luteinizing hormone. 2000 and 2002. 2005). atrazine is rated as having low acute toxicity. and testosterone (Gillis et al.. IARC considers atrazine not classifiable with respect to human carcinogenicity... 1994.S.S. altered estrus cycles. the dealkylated atrazine metabolites and hydroxyatrazine can occur in the environment from the breakdown of the parent chemical.EPA.gov/toxpro2. Sanderson et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Laws et al. 2003b). impaired fertility. Atrazine is not considered genotoxic.epa. Human health effects of atrazine at environmental doses or at biomonitored levels from environmental exposure are unknown. Atrazine product formulations can be mild skin sensitizers and irritants.S. liver toxicity. 1997). 2005. myocardial muscle degeneration.. but the effects are difficult to attribute due to lack of exposure markers or due to mixed chemical or pesticide exposures (ATSDR. Chronic high dose toxicity observed in animals includes decreased body weight. In addition to being human metabolites of atrazine.Herbicides particularly diaminochloroatrazine (the main dealkylated product). increased pituitary weight. Urinary Atrazine mercapturate (creatinine corrected) Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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. Additional information is available from U.. 1994 and 1999. Rayner et al. In mammalian studies. Stevens et al.. and cyanazine. Survey Geometric mean (95% conf. 54 Fourth National Report on Human Exposure to Environmental Chemicals . Some human ecologic and epidemiologic studies of reproductive and cancer outcomes have shown either positive or no associations. Stoker et al..EPA considers atrazine unlikely to be a human carcinogen. delayed onset of puberty. and U. 2004.. including simazine.

Bradway DE. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. 3/11/09 Arcury TA. Environ Health Perspect 2001. Wetzel LT. In a small number of field workers. Moseman RF. Barbieri F.76(1):190-200. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. levels of atrazine mercapturate were generally not detectable (CDC. Lioy PJ. Gammon DW. Pest Manag Sci 2005. Eberly LE. Collins A. 2001). Lucas AD.cdc. Gillis JH. Noriega N. ATRAZINE. diamino-S-chlorotriazine and hydroxyatrazine.43(2):155-167. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1993).115(8):1254-1260.69(2):217-222. Barr DB. Biagini RE. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure.61(4):331-355. Lee M. Catenacci G. Tyrey L. Brown KK. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. In the NHANES 2001-2002 subsample. Carr WC Jr. Toxicol Sci 2000. 2001 [online].30(2):244-247.. atrazine was detected in only four children (Arcury et al.. Seiber JN.53(2):297-307. et al. J Agric Food Chem 1982. 82. WHO/ FAO Data Sheets on Pesticides. 2007). Stoker TE. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Cooper RL. Goldman JM. Atlanta (GA). Chen H. 2005.. Perry et al. Hines CJ. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.org/documents/pds/pds/pest82_e. Extrom PC. Shoemaker DA. Ferrell JM. Geneva. Hein MJ. Proc Natl Acad Sci USA 2002. Reynolds SJ. Centers for Disease Control and Prevention (CDC). Heederik D.64(9):672-678. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Gillis JH.58(2):366-376. Grzywacz JG. et al. Fleenor-Heyser DG. Stevens JT. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Saiz SG. Maroni M. Simpkins JW. Sanborn JR. Toxicological profile for atrazine. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 .inchem. Ferrell JM. Stuart AA. Ferioli A. Mendoza M. References Adgate JL. Barr DB. Vonk A.109(6):583-590. et al. et al. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Available at URL: http://www. 2005). Cooper RL. Bersani M. Hermaphroditic. Biological monitoring of human exposure to atrazine.15(6):500-508. Toxicol Sci 2003. Ann Occup Hyg 2003. Toxicol Lett 1993. The geometric mean of urinary atrazine mercapturate was 1. Schmid J. Agency for Toxic Substances and Disease Registry (ATSDR). Stoker TE. Freeman NC. Cottica D. Third National Report on Human Exposure to Environmental Chemicals. et al. 3/11/09 Laws SC.atsdr. Cooper RL.html. Steroids 1999. Breckenridge CB. Environ Health Perspect 2007. In small studies of Maryland residents in 19951996 (MacIntosh et al.43(2):155-167. J Expo Anal Environ Epidemiol 2005. Clayton CA. Sanderson WT. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Eldridge JC.. 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. No.99(8):5476-5480. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Aldous CN.47(6):503-517. Striley CA. McElroy WK. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Tapia J. World Health Organization.gov/toxprofiles/tp153.htm. 1996. et al. Curwin BD. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Pfeifer KF. International Programme on Chemical Safety (IPCS). 2000). 2005).2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. A risk assessment of atrazine use in California: human health and ecological aspects. J Toxicol Environ Health 1994. Eldridge JC. 2003. Blewett C. Jones AD. Stoker TE. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.. In a study of 60 farm worker children. Barr DB. Hayes TB. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Wetzel LT. Quandt SA. Goodrow MH. Laws SC. J Toxicol Environ Health 1994. Available at URL: http:// www. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Toxicol Sci 2000.. Deddens JA.

EPA). Geological Survey (USGS). May 2003a.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. J Expo Anal Environ Epidemiol 1999. Sathiakumar N.usgs. Pesticides in the Nation’s Streams and Ground Water. Dryzga MD. Environmental Fate and Effects Division.9(5):494-501.epa. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Rayner JL. Sanderson JT. Hammerstrom KA. Laws SC. J Toxicol Environ Health A 1999. 3/11/09 U.195(1):23-34. Available at URL: http://www. 6/1/09 U. Toxicol Appl Pharmacol 2004. The Quality of Our Nation’s Waters. Available at URL: http://www. Perry M. Ryan PB.pdf.Herbicides development of a biomarker of exposure. Stoker TE. Available at URL: http://water. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats.S. MacIntosh DL. van den Berg M. Fenton SE. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function.pdf. Osborne DW. Circular 1291. Chem Res Toxicol 1993.27(6):599612. Lansbergen GW. 1992-2001. Dagenhart D. Toxicology 1990. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Needham LL. Supplemental Technical Information (available on-line only). Wood C. Stevens JT. Cooper RL.S.61(1):27-40. EPA).gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Tortorelli J. 0062.epa. Delzell E. A longitudinal investigation of selected pesticide metabolites in urine. Laws SC. revised February 15. Environmental Protection Agency (U. Christiani D. White paper on potential developmental effects of atrazine on amphibians.56(2):69-109. Environmental Protection Agency (U. 2007. Guidici DL. A review of epidemiologic studies of triazine herbicides and cancer. 2003b. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine.67(2):198-206. Wetzel L.6(1):107-116. March 2006. Singzoni B. Case No. Toxicol Sci 2000.10(7):479. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Washington (DC).S.php.S. Cooper RL. Stoker TE. Langvardt PW. Ann Epidemiol 2000. Boerma J. Office of Prevention. Pesticides and Toxic Substances. A risk characterization for atrazine: oncogenicity profile. Kastl PE. Guidici DL. Interim Reregistration Eligibility Decision For Atrazine. Timchalk C. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. U.58(1):50-59. EPA Office of Pesticide Programs.182(1):44-54. Toxicol Appl Pharmacol 2002.S. Crit Rev Toxicol 1997. Breckenridge CB.gov/oppsrrd1/REDs/ atrazine_ired. Toxicol Sci 2002.

and delayed Urinary 2. 2004).08) < LOD . It is not well absorbed through the skin.952 and 0. headache. and by consuming food or drinking water contaminated with 2.. myotonia.610-.4-D) controls broadleaf weeds in residential.250 (<LOD-. It is poorly bound in soils. < LOD means less than the limit of detection. 2.20 (.440-1.4-D has low acute toxicity.260 (<LOD-. but at higher levels they are herbicidal.EPA.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2.70) 1. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. renal and hepatic injury.490) < LOD < LOD < LOD .550-1.310) < LOD .2. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.560-.51 (1.4-Dichlorophenoxyacetic Acid CAS No.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.230-.890) < LOD .40) 1. 1977). Kohli et al.27 (.420) < LOD .16) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and aquatic environments.27 (1. General population exposure to 2. by direct contact with agricultural and residential areas after applications.22) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0..Herbicides 2.4-D can be applied either as an aqueous salt or as oil-soluble esters.S.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al. As much as 62 million pounds of 2. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.310 (. 94-75-7 General Information Widely used throughout the United States. hypotension.370-.660) 1.4-D or exposed for prolonged periods. it acts as a plant growth hormone.320) 90th .S. At low levels. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 1.27-2.930-1. 1974.350) < LOD < LOD < LOD . MCPA.930 (. abdominal pain.07 (. the chlorophenoxy herbicide 2.670-1. Similar to other chlorophenoxy herbicides. which may vary for some chemicals by year and by individual sample.EPA in 1948. 2.690 (.S.02-1.540-.910) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 57 .420-. It is rarely detected in ground waters (USGS.230 (<LOD-.250 (<LOD-.740 (.210 (<LOD-.690 (.4-dichlorophenoxyacetic acid (2.10 (<LOD-1.490 (.20 (<LOD-1.S. Once absorbed.05-2.4-D may occur during residential applications. dizziness.210-.410) < LOD .400) < LOD .330 (.910) 1. Human health effects from 2.24 (.760 (. Survey Geometric mean (95% conf.4-D have been below recommended intake limits (U. 2. 2005). 2007).690 (. and mecoprop).560-1.21) 1.4-D is rapidly absorbed via oral and inhalation routes. nausea.60) 1. 1989.S. Sauerhoff et al. population from the National Health and Nutrition Examination Survey.30 (<LOD-2. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .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 . 4-D.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .48) < LOD 1.43) 1.55 (1.00-2.810-1. in 2001 (U.680-1.32 (1. It was first registered with U.10) < LOD 1.03) 695 659 520 668 589 892 Limit of detection (LOD.610 (.4-D were used in the U. with a half-life of several days to several weeks. these herbicides can enhance plant growth.890 (.13) < LOD . Recent estimates of chronic intakes of 2.730 (.10 (<LOD-1.. agricultural.EPA.960-1.66) < LOD 1.690-1.

340 (.4-D levels were detectable in less than a quarter of the individuals studied. population from the National Health and Nutrition Examination Survey.780 (.S..590 (<LOD-1.16) 1.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.08 (.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.24) 1.4-D reflect recent exposure. U.19) .. U. 1996. thyroid.590 (<LOD-1.580-.EPA at: http://www. IPCS.380-.350 (<LOD-. 2003.920) < LOD 1.S. 2. U. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. 2000).560-.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. Epidemiological studies have reported associations of several types of cancer. other exposures.340-. urinary 2. Frank et al. U.17 (. Hill et al. 2005). 1996. 2002.. 1989).40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.epa. and evidence of histological injury to the kidneys.640 (.56) ..410) < LOD 1.S..520-.32 (<LOD-2..930-1.570) < LOD .890) < LOD 1. 2004). Additional information is available from U. Biomonitoring Information Urinary levels of 2.3.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .13 (.S.610-.4-D production plant workers and a few forestry workers spraying 2. 1995).990-1. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 1995.05) . 2005).410) 90th . 2. 2005.39) < LOD 1.890-1.13 (. 2002.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.390) < LOD < LOD < LOD . Pearce and McLean. population (Hill et al.EPA. IOM. 2006.610-. myotonia.EPA.EPA 2005).410) < LOD < LOD < LOD . or to contaminants in the herbicide formulations (specifically 2.780) .790) 1. Knopp et al.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and of adults and children (Baker et al.EPA.14 (.27-1. Survey Geometric mean (95% conf. IPCS.08 (. In previous samples of the U. 58 Fourth National Report on Human Exposure to Environmental Chemicals .270-.Herbicides neuropathy (Bradberry et al.720 (.7.410 (<LOD-.810-1. in small samples of children (Hill et al.gov/pesticides/. 2005.620-. It is unclear whether these associations are related to the chlorophenoxy herbicides.790) < LOD . 2001.850) < LOD .490 (.. 1994).08 (.4-D does not have significant reproductive. 1992).470) < LOD ..670 (<LOD-1.560-.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .73) . or teratogenic effects in chronic rodent studies (Charles et al.670 (.670 (.740 (. Average post-application urinary levels of 2.680) < LOD .550-. adrenals and gonads (NTP. Kolmodin-Hedman and Erne.S.S.330-.440 (.380 (<LOD-.41 (1.270 (<LOD-.700 (. 2005.26) 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 . Kutz et al. CDC.4-D are eye irritants.660) < LOD .S. 1985.660 (. developmental..780-1. 1996. 2. 2005).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.480 (. eyes. The acid and salt forms of 2.980) < LOD 1. 2005. Post-application levels in farmers and home gardeners were dependent on Urinary 2. 1980. liver.380 (<LOD-. IPCS.35) < LOD .380) < LOD . Acute high doses administered to laboratory animals produced ataxia.810-1.. 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.820-1. 2005).

4-D than levels found in the general population.71(2):99-108. TOX-63: TOXICITY REPORT CURVES. Sircar KP. Holler JS. Biomonitoring of herbicides in Ontario farm applicators. Scand J Work Environ Health 2005. Exposure of homeowners and bystanders to 2.4-D). Campbell RA. Smith SJ. Brody D. Hanley TR Jr. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.4-. van Ravenzwaay B. Dichlorophenoxyacetic acid.edu/catalog. Available at URL: http://ntp.. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Arch Toxicol Suppl 1980. Kutz FW. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Driskell WJ.15(6):500-508. Baker S. Ritter L. J Environ Sci Health B 1992. Forestry workers involved in aerial application of 2.27(1):23-38. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.4. 2005. Selected pesticide residues and metabolites in urine from a survey of the U. Centers for Disease Control and Prevention (CDC).4-dichlorophenoxyacetic acid in man. Fast DM. Harris et al. Review of 2. Pesticides residues in food: 1996 evaluations Part II Toxicology. Honeycutt R. Baker SE. Gupta BN.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Mandel et al. J Toxicol Environ Health 1992. Ripley BD. Murphy RS. Occup Environ Med 1994.31 Suppl 1:90-97.4-D): exposure and urinary excretion. Barr DB. Available at URL: http:// www. Bailey SL. 2003. and the use of protective clothing or equipment (Arbuckle et al.5-T). Frank R. Developmental toxicity studies in rats and rabbits on 2. In farm families. Shealy DB. Needham LL. Acquavella JF.niehs. Bus JS. geometric mean urinary levels of 2. Kolmodin-Hedman B. Hill RH Jr. Arnold EK.4:427-435. Absorption and excretion of 2.S. 2006. Beeson MD. Erne K.php?record_id=10603. Cole DC. 914.31(2):121-125.. Veterans and Agent Orange: update 2002.org/documents/jmpr/jmpmono/v96pr04.60(1):121-131.4-D. Third National Report on Human Exposure to Environmental Chemicals.4-dichlorophenoxyacetic acid (2. Chapman P. Arch Environ Contam Toxicol 1989. Sirons G J. et al. J Expo Anal Environ Epidemiol 2000. Washington (DC): National Academies Press. National Toxicology Program (NTP). 2. Kohli JD.4-dichlorophenoxyacetic acid and its forms. References Arbuckle TE. Board on Health Promotion and Disease Prevention. Wilson RD. Tandon JS. To T. Scand J Work Environ Health 2005.gov/index. Head SL. Toxicol Sci 2001. International Programme on Chemical Safety-INCHEM (IPCS). general population. the amount of pesticide applied.4-D in urine does not mean that the level of the 2. Philbert MA.4-D will result in an adverse health effect. Biomonitoring for farm families in the farm family exposure study. Assessment of exposure to 2. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4:318-321.4-dichlorophenoxyacetic acid (2. Solomon KR. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Vet Hum Toxicol 1989. Pesticide residues in urine of adults living in the United States: reference range concentrations. Gregg M.4 dichlorophenoxyacetic acid (2. Heederik D. Dhar MM. the number of acres to which it was applied (Curwin et al. Stephenson GR. Baker BA. Cook BT.4-Dichlorophenoxyacetic Acid). Reynolds SJ.htm. Curwin BD. Beasley VR.4-D) epidemiology and toxicology.37(2):277-291. Xenobiotica 1974.32(4):233-257.4:97-100. Barr DB. Survival and Growth Curves from NTP Toxicity Studies.31 Suppl 1:98-104. Needham LL. Garabrant DH. Khanna RN. 2005. Crit Rev Toxicol 2002. et al. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Atlanta (GA). Mandel JS. Environ Res 1995. Updated March 7. Available at URL: http:// www.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. Carter-Pokras OD. Estimation of occupational exposure to phenoxy acids (2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 3/17/09 Institute of Medicine (IOM).inchem. Biomonitoring studies of 2.4-D and 2.nap. 2005 Charles JM. 2005).nih. Tables.Herbicides the time since application. 1992). 2005). Sanderson WT. Harris SA. Finding a measurable amount of 2. TOX-63 Peroxisone Project (2.10(6 Pt 2):789-798. J Expo Anal Environ Epidemiol 2005 Nov. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Hill RH Jr. Arch Environ Contam Toxicol 1985.51(3):152-159. Alexander BH. et al. 3/17/09 Knopp D..4-D were highest in the farmers who applied the 2.18(4):469-474. Hein MJ.

Toxicology 1977. Available at URL: http://www. 4/2/09 U. Pesticide industry sales and usage . S. June 2005. The fate of 2.php. March 2006.4-D RED Facts. The Quality of Our Nation’s Waters.EPA. Available at URL: http://www.epa.epa. 2. Circular 1291. Environmental Protection Agency (U.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.S. Environmental Protection Agency (U. EPA 738 F-05-002.4-D) following oral administration to man.usgs. Pesticides in the Nation’s Streams and Ground Water.htm.Herbicides Sauerhoff MW. 1992-2001.4-dichlorophenoxyacetic acid (2. Supplemental Technical Information (available on-line only). Braun WH.S. 3/17/09 U. Geological Survey (USGS).S. Blau GE. Office of Prevention Pesticides and Toxic Substances.8:3-1U. Available at URL: http://water.pdf. Washington (DC): U. May.gov/oppsrrd1/ REDs/factsheets/24d_fs.EPA). gov/oppbead1/pestsales/01pestsales/market_estimates2001. 3/17/09. Gehring PJ. revised February 15.S.2000 and 2001 market estimates.S. 2004. 2007. 60 Fourth National Report on Human Exposure to Environmental Chemicals .EPA).

but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. Hladik et al. Kolpin et al. In animals. lacrimation. and it was not mutagenic in mammalian cells (U.S. The geometric mean metolachlor mercapturate was 4. Biomonitoring Information CAS No. (2003) showed that 2. Metolachlor is well absorbed dermally. and field workers may have significant exposures via this route.. General population exposure may occur through the consumption of contaminated food or drinking water. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1999.epa.S.EPA. 1995). in both ground and surface waters (Battaglin et al.S.S. 2007. Gilliom. Metolachlor did not show developmental or reproductive toxicity in chronic animal studies. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. 2003). including corn.. metolachlor levels in water have exceeded lifetime human health advisory levels (U. This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment. Fourth National Report on Human Exposure to Environmental Chemicals 61 . Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown..EPA. and on non-crop land for general weed control.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al.Herbicides Metolachlor available from U. 2005). Occasionally in the past. 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. sorghum and other crops.S.gov/pesticides/. It is absorbed by plants and inhibits plant protein synthesis. formulators. Salivation. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. People exposed to metolachlor will excrete metolachlor mercapturate in their urine. 1994. 2003). Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. though the 95th percentile for males was 0. and eliminated in urine and feces over two to three days (WHO. Metolachlor has low potential for acute toxicity (U.EPA considers metolachlor to be a possible human carcinogen. 1995).EPA. 1995.200 μg/L (CDC... 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..2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine.S. Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect. 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. 1998). USGS. EPA at: http://www. In animal studies. and convulsions were observed at lethal doses in animal studies. Feng and Wratten. Jefferies et al. Estimated human intakes have been below recommended limits (U. U. 2000. 2007. 2005. Hines et al. Davison et al. so applicators. metolachlor was quickly absorbed after dermal or oral doses. WHO. WHO. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample. soybeans. 2003). 2005). 1989. 1995). mercapturate conjugates were the predominant metabolites.. NTP and IARC do not have ratings regarding human carcinogenicity. whereas 60% of applicators had detectable amounts. 2000. EPA.

S. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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 . 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 .740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 62 Fourth National Report on Human Exposure to Environmental Chemicals .2. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.S. see Data Analysis section) for Survey year 01-02 is 0.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .240) 679 701 957 Limit of detection (LOD.670 (<LOD-.200 (<LOD-. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.440 (<LOD-.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Brown KK. 2003.15(6):500-508. Atlanta (GA). Jefferies PR. Heederik D. Linderman R. Peter CJ. Gilliom RJ). Shoemaker DA. Reynolds SJ. et al. March 2006. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Supplemental Technical Information (available on-line only).S.pdf. Circular 1291. revised February 15. Hodgson E.S. Background document for development of WHO Guidelines for Drinking-water Quality. Wratten SJ. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Biagini RE. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Davison KL.usgs. R. reservoirs and ground water in the Midwestern United States. Striley CA. California. Available at URL: http://www. Third National Report on Human Exposure to Environmental Chemicals. EPA 738R-95-006. usgs.html. Environ Health Perspect 2003. 1998. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Roberts AL. 1992-2001. Thurman EM.php.who. 2005.gov/oppsrrd1/ REDs/0001.248(2-3):115-122. Burkhardt MR. 1999. Feil VJ. Comparative metabolism and elimination of acetanilide compounds by rat. 3/26/09 U. Pesticides in U. Reregistration Eligibility Decision (RED) Metolachlor. and other herbicides in rivers. EPA).S. J Expo Anal Environ Epidemiol 2005.47(6):503-517. Hsiao JJ. Deddens JA.ESTfeature_gilliom.248(2-3):123-133. 98-4245 (by Barbash JE.gov/nawqa/ pnsp/pubs/wrir984245/text. Feng PCC.int/water_sanitation_health/dwq/chemicals/ metolachlor. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Metolachlor in Drinkingwater. Centers for Disease Control and Prevention (CDC). Sanderson WT. Sci Total Environ 2000. Ann Occup Hyg 2003. Linhart SM. Environ Sci Technol 2007. Curwin BD. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Kolpin DW. Available at URL: http://water. Environ Health Perspect 2000. Coleman S. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes.24(10):1003-1012. Available at URL: http://water.39(17):6561-6574. Larsen GL.S. and metolachlor herbicides in rats. Gillion.pdf. Available at URL: http://www. Kolpin DW. Environ Sci Technol 2005. J Agri Food Chem 1989. Hladik ML.usgs. Hein MJ.11(4):353359. Dialkylquinonimines validated as in vivo metabolites of alachlor. Thelin GP. Sci Total Environ 2000. Camann DE. acetochlor. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. U. Xenobiotica 1994. April 1995. Casida JE. Environmental Protection Agency (U. sulfonamide. Geological Survey (USGS). Andrews HF. Furlong ET. Ward EM. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Quistad GB.gov/nawqa/pnsp/pubs/files/051507.Herbicides References Battaglin WA. Available at URL: http://water.41:3409-3414. Barr DB. World Health Organization (WHO). Barr JR. Sacramento. Barr DB.37(4):10881093. Rose RL. Kinney PL.S. Chem Res Toxicol 1998. imidazolinone. Alavanja MC. 2007.pdf 3/30/09 Hines CJ. Occurrence of sulfonylurea.epa.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.111(5):749-756. 4/2/09 U. Geological Survey (USGS). et al.108(12):1151-1157. streams and groundwater. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. 6/1/09 Whyatt RM.

Once absorbed into the body. myotonia.3. nausea. 2. 2004). Epidemiological studies have reported associations of several types of cancer. Ester forms of 2. hypotension.4. Although 2.5-T was once applied as either an aqueous salt or as an oil-soluble ester. abdominal pain.5-T has been rarely detected in ground waters (USGS. 1974).4. Omer. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. but higher levels are herbicidal.4.. 1989.5-Trichlorophenoxyacetic acid (2. it is not well absorbed through the skin.4. < LOD means less than the limit of detection. 1986. Kohli et al. and concern about contamination with 2. the general population is unlikely to be exposed to it. Given the commercial unavailability of 2.5-Trichlorophenoxyacetic Acid CAS No.4.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.1.4. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. 1992).4.5-T use as a herbicide in 1985. 2007). 2. headache.4-D were used as defoliants in the Vietnam War (e. 93-76-5 General Information 2. population from the National Health and Nutrition Examination Survey.2 and 0..4.5-T and 2. Human health effects from 2.5-T is eliminated mostly unchanged in the urine. Agent Orange). 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.5-T degrades to 2.Herbicides 2. with an elimination half-life of approximately 19 hours (Arnold et al..5-T.4. 64 Fourth National Report on Human Exposure to Environmental Chemicals . Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.g.5-trichlorophenol and other degradates.. 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.S. which may vary for some chemicals by year and by individual sample. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.5-T (Holson et al. At low levels. renal and hepatic injury. dizziness.4.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5-T in soil varies with conditions.4. Chlorophenoxy herbicides act as plant growth hormones. ranging from several weeks to many months.4..5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7. Nelson et al. and delayed neuropathy (Bradberry et al.4. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. The half-life of 2. these herbicides can enhance plant growth.4. Mohammad and St. 2. 1992.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.4.5T is rapidly absorbed via oral and inhalation routes.4. Survey Geometric mean (95% conf.

2003. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.S.4. 2004).4.gov/pesticides/.epa. similar to results of NHANES II (19761980).EPA at: http://www.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.5-T reflect recent exposure. Additional information is available from U.4. Fourth National Report on Human Exposure to Environmental Chemicals 65 .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. 1992). U.5-T were generally below the limit of detection.4.5-T does not mean that the level will result in an adverse health effect. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. It is unclear whether these associations are related to the chlorophenoxy herbicides.S. 2005. Pearce and McLean.4.EPA.5-T than levels found in the general population. Finding a measurable amount of 2. Biomonitoring Information 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. other exposures.5-T also were below the limit of detection (Kutz et al.S. 2005). Biomonitoring studies on 2.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.7. in which urinary levels of 2.4..4. Urinary 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. Survey Geometric mean (95% conf. 1996. 2002.Herbicides or contaminated herbicides. IOM.5-T itself is not mutagenic.4.3. Mean urinary levels of 2. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. or to contaminants in the herbicide formulations (specifically 2. population from the National Health and Nutrition Examination Survey. IPCS. 2. urinary levels of 2.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. 1980).

Estimation of occupational exposure to phenoxy acids (2. J Toxicol Environ Health 1992. Arch Toxicol Suppl 1980. Pesticides residues in food: 1996 evaluations Part II Toxicology. Environmental Protection Agency (U. Washington (DC): National Academies Press.4. 2004. Dichlorophenoxyacetic acid. Vale JA.edu/catalog. Fundam Appl Toxicol 1992. Scand J Work Environ Health 2005. Garabrant DH. Centers for Disease Control and Prevention (CDC). Beasley VR.19(2):298-306. International Programme on Chemical Safety-INCHEM (IPCS). Toxicol Rev 2004. McLean D.pdf. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Absorption and excretion of 2. 2005.5-t mixture.S. Gaines TB.inchem.19(2):286-297.5-T).5-trichlorophenoxyacetic acid (2. I. Office of Prevention Pesticides and Toxic Substances.S.4-D/2. Crit Rev Toxicol 2002. et al.htm. Poisoning due to chlorophenoxy herbicides. Third National Report on Human Exposure to Environmental Chemicals. 2. II. Selected pesticide residues and metabolites in urine from a survey of the U.23(2):65-73.nap.4. Sheehan DM.4.EPA).4.4. et al.org/documents/jmpr/jmpmono/v96pr04. 2003. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Kolmodin-Hedman B.4-D and 2. general population. Fundam Appl Toxicol 1992.5-T in four-way outcross mice. Cook BT. Agricultural exposures and non-Hodgkin’s lymphoma.5-trichlorophenoxyacetic acid (2. Erne K.32(4):233-257. Available at URL: http:// www.Herbicides References Arnold EK. May. Proudfoot AT. Developmental toxicity of 2. Holson JF. Gaines TB. Tandon JS. Bradberry SM. Review of 2.php?record_id=10603. LaBorde JB.2000 and 2001 market estimates. Mohammad FK. Philbert MA. Arch Int Pharmacodyn Ther 1974. Available at URL: http://www.S. Holson JF. Gupta BN. Board on Health Promotion and Disease Prevention. LaBorde JB. 3/17/09 Institute of Medicine (IOM). Kutz FW. discussion 5-7. Neurobehav Toxicol Teratol 1986.4. Behavioral and developmental effects in rats following in utero exposure to 2. Pesticide industry sales and usage . Developmental toxicity of 2.4-dichlorophenoxyacetic acid (2. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.8(5):551-60. Atlanta (GA).31 Suppl 1:1825. Multireplicated dose-response studies with technical and analytical grades of 2. Nelson CJ. 3/17/09 Kohli JD.4-D) epidemiology and toxicology.31(2):121-125. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Gaylor DW. Wolff GL. Nelson CJ. Dhar MM. Washington (DC): U. St Omer VE. Available at URL: http:// www. Pearce N.EPA. Veterans and Agent Orange: update 2002.5-T). Brody D. Khanna RN.4. 210:250-255. Sircar KP. Vet Hum Toxicol 1989. S. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .4:318-21.5-trichlorophenoxy acetic acid in man. 914. Murphy RS.epa.5-T).4. U.4-. McCallum WF. Carter-Pokras OD.37(2):277-91.

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

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

. the median serum dieldrin level was generally similar to the 90th percentile for females in this Report (Ward et al. 1995). and the FDA monitors foods for pesticide residues.gov/toxpro2. IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity. the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al.html. 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). Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. 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. Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al.... When dieldrin was fed to pregnant rodents. 1991). 1987). The U.. 2000). 1998).. environmental levels) and health effects is available from ATSDR at: http://www..6% of the subsample had dieldrin levels above the limit of detection (Stehr-Green 1989). seizures (Smith. EPA has established environmental standards for aldrin and dieldrin. When fed to experimental animals. 78 Fourth National Report on Human Exposure to Environmental Chemicals . Li et al. 2004).S. population from the National Health and Nutrition Examination Survey.e. similar to results in a subsample of NHANES II (19761980) (Stehr-Green. in which only 10.S. but no estrogenic effect was noted in a study that used cultured cells (Tully et al. Information about external exposure (i. 2005. 1998) and behavioral changes (Carlson and Rosellini. serum aldrin levels were below the limit of detection. 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. both aldrin and dieldrin caused liver enlargement and liver tumors. 2000). In a study of pesticide applicators with occupational exposure to aldrin. and seizures. tremors. OSHA has established workplace exposure standards for aldrin and dieldrin. In samples obtained between 1973 and 1991 from Norwegian women.atsdr. and occasionally. Epidemiologic and animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al. Kanthasamy et al. vomiting. 2004). nausea.Organochlorine Pesticides twitching. dieldrin at higher doses caused irritability. 1989). 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.. which may vary for some chemicals by year and by individual sample..cdc. Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al.. 2000. 2005). 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.. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

see Data Analysis section) for survey years 01-02 and 03-04 are 10.160 (.064 (.110 (.0 (15.S.069) < LOD < LOD .6-24.9 (13. 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.6) 19.1) 14.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.124) .4) < LOD < LOD 16.160) .50) 15.109-.090-.8 (11.058) < LOD .5 (<LOD-11.120 (.1-19.4) 19.8. which may vary for some chemicals by year and by individual sample.130) .054-.140 (.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 8.0) 19.1) < LOD 9.130-.100-.9 (13.0 (10.080 (.9 (12.7 (<LOD-15.158) .084-.4) 539 456 484 487 980 885 Limits of detection (LOD.060) .1-16.190) .1) 20.4-17.8-17.40-9.049-.9-38.070 (<LOD-. Survey years 01-02 03-04 Geometric mean (95% conf.062 (.130-.120 (.1) 15. population from the National Health and Nutrition Examination Survey.130) .139 (.6-24.0 (10.180) . Fourth National Report on Human Exposure to Environmental Chemicals 79 .048 (<LOD-.8) 14.0) < LOD 9. 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) .0-25.7-22.3 (19.147 (.090-.130) .170) .077 (.098 (.110) .2) 15.1-18.242) .7 (14.90) 90th 15.1-24.100-.117) < LOD .1) 15.4-18.190) .086-.80-9.116) .110 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.089 (.080) .0 (11.2) 14.8 (9.090 (<LOD-.080-.100-.6 (14.110 (.090 (.00 (8.160 (.130-.093) .100) .2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.101) .1 (18.8-24.7-19.180) .149) .7) 15.109-.10 (<LOD-16.110-.3 (14.1 (13.5-15.00-14.055 (.6 (15.062-.2-15. population from the National Health and Nutrition Examination Survey.103 (.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .110) .083-.6) 16.130 (.140-.139 (.7 (15.100) .054-.4) 95th 20.1) 10.053 (<LOD-.077-.3 (13.80-10.112) 95th .5 (16.5-17.140) .80 (<LOD-10.6 (15. < LOD means less than the limit of detection.4 (12.088-.120-.4) 14.1) 13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.073-.8-19.102 (.064) 90th .40-10.30 (8.109 (.056-.2) 11.3 (18. Survey years 01-02 03-04 Geometric mean (95% conf.070-.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 (18.054-.9 (14.090-.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 .108-.60-10.5 and 7.112-.096-.S.062 (.6-33.8) < LOD 8.8) 15.120 (.113 (.138 (.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.3-21.100 (.30 (8.50 (8.059 (.4) 20.6) 9.103 (.150 (.9 (12.5) 21.9-23.8 (18.0-21.120) .138) .8-25.150 (.9-22.5) 19. 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 .5-17.8-17.4) 21.2) 12.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .5) 15.4 (12.0) 21.70 (7.063-.075) < LOD . which may vary for some chemicals by year and by individual sample.

Chemosphere 2004. pp. 1992-2001. toxicology. 4/21/09 Hoyer AP.9:1357-1367. Tully DB. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Edwards JW. Neurotoxicol 2005. Sanchez-Ramos J.gov/~dms/ pesrpts. Academic Press. Cancer Epidemiol Biomarkers Prev 2000. Mink PJ. Smith AG. Andersen A. Finley B. Daniel SE. Part A 2000. 731-915. Mumtaz MM.atsdr. VT. Organochlorine exposure and risk of breast cancer. Handbook of Pesticide Toxicology.cdc. 1989. David VL.14:95-102. are nonestrogenic in transfected HeLa cells.54:1431-1443. Vol. Turner W. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Cox. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis.109(Supp1):113-139. Sonnenschein C. Carlson JN.64-65 Spec. PA. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.html. McIntosh LJ. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures.htm. and epidemiology in the United States.fda. Needham LL. Olea N. Int Arch Occup Environ Health 1994. References Agency for Toxic Substances and Disease Registry (ATSDR). Exp Neurol 1998. Available at URL: http://www. Chapin RE. 1991. and lymphocyte sister chromatid exchange. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Lancet 1998. Available at URL: http://pubs. Toxicol Lett 1992. Rosellini RA. Patterson DG Jr. Hartvig HB. Schulte P. 4/21/09 Bates MN.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). et al. 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. Narahashi T.27:405-421. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Chung KL. Pesticides in the Nation’s Stream and Ground Water. September 2002. Jorgensen T.gov/ circ/2005/1291/. In Hayes WJ. United States Geological Survey (USGS). Aldrin and Dieldrin [online]. Priestly BG. Anantharam V. Stehr-Green. bioaccumulation. 2 Classes of Pesticides. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Six high-priority organochlorine pesticides. Available at URL: http://www. Soto AM. Environ Health Perspect 2001. Jr. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Buckland SJ. No:429-436. Chlorinated Hydrocarbon Insecticides. Environ Health Perspect 1995. Garrett N.103(Suppl 7):113-122. Jr and Laws ER. Kitzazwa M. 4/21/09 Jorgenson JL. Eds. Song S.47:1059-1087. Reprod Toxicol 2000. Available at URL: http://www. Basit A. plasma dieldrin. 2007 [online]. Psychopharmacology (Berl) 1987. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.59:229-234. Shore RF. Inc. 15. Wienburg CL. Grajewski B. Teta MJ. Roy ML. Aldrin and dieldrin: A review of research on their production environmental deposition and fate.150:263-271. Environmental Health Criteria 91. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants.html. either singly or in combination. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Frey JM. 6/1/09 Ward EM.352:1816-1820. Revised Feb. Serrano FO. Mann D. J Toxicol Environ Health 1989. J Toxicol Environ Health. Ginsburg KS. Li AA.cfsan.66(4):229-234.26:701-719.91(1):122-126. Facca A.org/documents/ehc/ ehc/ehc91. Kanthasamy AG. et al. Patterson DG Jr. Grandjean P. Toxicological profile for aldrin/dieldrin [online]. Brock JW.gov/toxprofiles/ tp1. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Corrigan FM. Food and Drug Administration (FDA). New York. Demographic and seasonal influences on human serum pesticide residue levels. Kanthasamy A. International Programme on Chemical Safety (IPCS). August 2008. Fernandez MG.usgs.inchem. Ellis H. J Occup Environ Med 2005.

9 (15.1 (15.6) 8.9 (11.0) 31.3) 18.9) 23.Organochlorine Pesticides Chlordane CAS No.5-65. 2007).3-45.5-13.9) 11. 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.6) 39.S.0 (37.8 (17.10 (8. and in soil.4) < LOD 11.7 (34.7) 19.2 (39.8 (42.6 (16.8..8 (18.8-20. and 7. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.9) 11.82-11.3 (9.6-24.6) 20.4 (<LOD-12.0-33.2) 36.6 (43.5-43.1 (<LOD-12.9 (21.1 (25.2) 46.5) 9.3-43.7-12.5 (41.5) 56.5) 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 * * * * 11.4-51.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.7 (34.5 (<LOD-12.0 (16.9) 23.6-18.4) 39.7 (32. 10. < LOD means less than the limit of detection.5 (34.89-10.4 (10. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.0 (26. and 03-04 are 14.6-53. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2) < LOD 11.1) * 11. 01-02.3 (28.3 (27. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.1 (<LOD-12.37 (8.9 (18.7 (10.8-31.6) 36.7) 42. 2007).1-15.8-23.3) 18.7) 19.2-49.0) 41.4-14.9 (26. 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.4 (35.3-24.6 (25.8 (17.1 (44.5) < LOD < LOD < LOD < LOD 13.0) 20.7-70.7 (17.5-47.2 (9.3) 41.6) 49.9 (36.0) 75th 20.4-21.2) < LOD 11.8-42.3) 37.9-40.S.9) 10.6-12.4) 37.1 (40.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.7) 31.6) 9.5) 10.3 (11.1 (17.9 (26.8-43. respectively.63 (8.9) 36.5 (31.2-49.S.9-38. Fourth National Report on Human Exposure to Environmental Chemicals 81 .9) 39.4 (30. 1994. Survey Geometric mean (95% conf.2) 37. in addition to trace amounts of numerous other related compounds (ATSDR.4) 12. buildings.4 (30.69-10.5-38.70 (<LOD-10.6) < LOD 11.1 (16. heptachlor use has been limited to treatment of fire ants near power transformers. Chlordane is not currently produced or used in the U. Since 1992. which may vary for some chemicals by year and by individual sample. from the early 1950’s until the mid-1980’s.0-25.9 (17.8-61.7-56. fish.5 (8.9 (15.3) 10.9-21.6-45.6) 9.1 (11.3 (<LOD-19.8) 52.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (<LOD-12.5-41.5) 21.30-11.8) 53.1) 30.8) 44.7 (<LOD-32.8-73. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.9) 13.4 (22.8 (40. 1994).8-33.0-12.0 (32.4-40.7-39.2-28.9) 17.9) 47.0) 21.2 (21.8) 27.9 (11.1 (20.36-11.7 (19.1-50.7 (42.1 (27. Consequently.0) 37.2 (28.1) < LOD < LOD < LOD < LOD < LOD 8.2 (37.0-13.9) 37.5) 38.1) 30.2-56. the technical grade product of each chemical contains 10%-20% of the other chemical.6) 23. 57-74-9 Heptachlor CAS No.7) 9. population from the National Health and Nutrition Examination Survey. foods high in fat such as meat. As a result of the manufacturing process.5) < LOD < LOD 9.9 (31.8-33.7) 28.6 (9.3-49.4) 29.0) 27.5-32.5) 44.1) 16.2) 22. see Data Analysis section) for Survey years 99-00.9-42.2 (36.3-32. Technical grade chlordane had contained 7% trans-nonachlor.9-21.8 (10.3 (25. chlordane was used to kill termites and other insects on agricultural crops. 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. and dairy products are the usual sources of exposure to these chemicals in the general population.4-45.1-19.1-25.2 (10.1-51.20-11.1 (<LOD-12.3 (21.7 (<LOD-13.1) * 11.1-65.4) < LOD < LOD < LOD 23.1) 22.6 (9.0-61.2) 34.5.2) * 12.0 (20.8-32.6) 48. lawns.5-40.7 (43.2-26.3 (26.10-18.1) 90th 34.3 (20.4) 18.2) 33.74 (<LOD-10.0-18.2-21. Until 1988.9 (29.7) 35.1-25.2 (41.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.8) 52.6-24.3-45.90 (8.8 (10.8) 18.4) 22.5-44.4 (31.7-25.20-10.7-14.20 (<LOD-11.5) 37. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.0-67.3) 10.9) 31.5 (33.6) 48.5-42.5.6) 11.10-11.

077) .208 (.260 (.130 (.370 (.100 (<LOD-.063) . which is also persistent in the body (ATSDR.189 (. neonatal mortality.290-.080) . Smith.290) . 1986).230 (..230-.S.150 (. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility. and heptachlor epoxide in foods and bottled water.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * . Rogan.077) .140-.053-. dermal.280 (.240 (.049 (<LOD-.240) .063 (.200-.258 (.S.112 (.074-.300 (. and inhalation exposure.450) .140 (. IARC.070 (.128 (.148-.225 (.140) .058 (. 2001.180) .077) .073) < LOD < LOD < LOD < LOD . OSHA has established occupational exposure criteria.080 (.090-.240-.056 (.180-.190-.220-.061-. chronic doses of heptachlor have produced liver enlargement and injury.160) .242-.440) .150) .340) .057 (.280) .160) . and breast milk is a major excretion route in lactating women. 2006).190-.108-.146) .400) .180-.350 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.070 (<LOD-.133) 90th . Chlordane is metabolized primarily to oxychlordane and to a lesser extent.110-.104) .450) .100-.150 (.080) . FDA established allowable residues of chlordane.120-.370 (.104-.S.320 (.330 (.410) .300) .048-.075 (.130-.170) .246-.130-.380) .170) .160) .062) < LOD .360) .110 (<LOD-. which may vary for some chemicals by year and by individual sample.213) * . Le Marchand et al.126 (.064) < LOD .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 * * * * .083) .057-.070-.070-.130 (.271 (.150 (.510) ..189-.290-. 2007).057) * .120-.140 (.087-.230-.350 (.290 (.280 (.106-.310) .070) .320 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.320) . heptachlor. In laboratory animal studies.070 (<LOD-.430) .290) .149 (.170) .207 (.269 (.090) .120 (.170-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.310-.066-.250-.280-. EPA has established environmental criteria for chlordane and heptachlor. 1977b.430) . and the U. Takahashi et al.220 (.260-.300) .063 (.300-.090) .130) .130 (.160 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.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.066 (. Elimination of all these chemicals from the body occurs over months to years.080 (. characterized by seizures and paralysis.220-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.253-.210-.080) .170) . 1986).270 (.230 (.250 (.207) .136) .120-.180) .073 (.270 (. population from the National Health and Nutrition Examination Survey.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .250 (.190-.231) .258-.168-.092) .210 (.058-.315 (.560) .070 (<LOD-.066-.083 (.150-. Shindell and Ulrich.065-.204 (. Acute.270 (.079) < LOD < LOD < LOD .130-.100 (.340) .067 (. 2007.320 (.050-.310 (.071 (. 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.063 (.320 (.058-.290-.260 (.100-.047 (<LOD-.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .200-.348) .260 (.050 (<LOD-.146) < LOD < LOD .200-. 1991).223) .130) .286 (.063) * .140 (.140-.240-.Organochlorine Pesticides (Dallaire et al.170) .280-.373) .126) .203-.370 (.320) .070 (<LOD-.115 (.287) .165-.068) .066 (<LOD-.068) 75th .216-.300) . Chlordane and heptachlor are absorbed after oral.119 (.400) .130-.115-. and alterations in immune function of offspring.. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.199-.070) < LOD < LOD < LOD < LOD < LOD . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.148) . 2002.310) .230-.210 (. 1996.082 (. 1977a.070-.091) . IARC considers chlordane and heptachlor as possibly carcinogenic to humans.350) .200 (.068-.130-.063-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.063 (. 1991.060 (<LOD-. Survey Geometric mean (95% conf.140 (.227) < LOD .053-.286 (..300) .245-.302) . The major metabolite of heptachlor is heptachlor epoxide. The U.310) .076) < LOD .055-. to heptachlor.280-. 1981). interval) Selected percentiles ( 95% confidence interval) Sample 95th .230) .069 (<LOD-.077) .079) . 82 Fourth National Report on Human Exposure to Environmental Chemicals .

cdc.. 2004). Biomonitoring data can also help Fourth National Report on Human Exposure to Environmental Chemicals 83 .. 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. than the 90th percentile values of NHANES 1999-2000 (Baker. 2006). A recent assessment of heptachlor is available at: http://www. 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. trans-nonachlor. 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. respectively..Organochlorine Pesticides about external exposure (i. 1993).e.gov/toxpro2. Biomonitoring Information Serum oxychlordane and trans-nonachlor levels in NHANES 1999-2000. from ATSDR at: http://www. For the exposed persons drinking milk in the Arkansas episode. the mean serum heptachlor epoxide and oxychlordane levels were more than twice as high. 2000). 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. Two episodes (one each in Arkansas and Hawaii) of inadvertent heptachlor contamination of dairy cattle feed occurred in the early-to-mid 1980’s. resulting in human exposure to heptachlor epoxide that was excreted into the milk. than the 90th percentile values of NHANES 1999-2000 (Stehr-Green et al. 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.html.org/documents/cicads/cicads/cicad70. respectively. 1988).. transnonachlor. transnonachlor.htm#ref. or heptachlor epoxide causes an adverse health effect. mean serum heptachlor epoxide and oxychlordane levels were about sevenfold and threefold higher. 2001-2002. Finding a measurable amount of oxychlordane.. 2002). In serum samples obtained in between 1994 and1997 from Inuit women in different Arctic countries. Biomonitoring studies on levels of oxychlordane. or heptachlor epoxide in serum does not mean that the level of oxychlordane.. inchem. 2003).atsdr. environmental levels) and scientists plan and conduct research on exposure and health health effects of chlordane and heptachlor is available effects. In the Hawaii episode. and 2003-2004 subsamples were comparable to levels measured in Swedish women from 1996-1997 (Glynn et al..

1-38.4 (<LOD-54.8) 13. respectively.3) 18.20 (<LOD-9.0 (15.1-16.2 (<LOD-16.1) 20.8.90 (<LOD-9.4) 18.5 (<LOD-32. which may vary for some chemicals by year and by individual sample.3) 18.1) 13.1) 23.5 (<LOD-21.4 (<LOD-19.0 (11.2) 15.2 (18.6 (14.9) * * * 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 8.0-17.6) 13. see Data Analysis section) for Survey years 99-00.3) 16.6 (16.2-17.7-25.0-17.8) 19.0-19.3 (<LOD-25.7-18.8 (18.8) 13.8) 14.8 (13.0-16.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.5) 19.8-46.5 (10.6.8) 21.6) 14.6-21.2 (<LOD-62. 84 Fourth National Report on Human Exposure to Environmental Chemicals .10-13.9-29.0-54.9 (15.5) < LOD 14.4 (11.3) 18.S.9) 15.9-29.6 (11.2) 26. and 03-04 are 14.6) 22.8 (<LOD-23.0) 13.3) 27.1-29.4 (11.1 (16.9-16.7 (16.2-27.7-19.4 (15.8-24.2-16.5 (11.9 (12.2-27.4) 21.5 (18.8-24.1 (19.8 (13.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6) < LOD < LOD < LOD 27.3) 10.8 (15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.5 (11.2) 20.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.7 (13.5) 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 7.40) 15.8-24.3) 23. < LOD means less than the limit of detection. and 7.8) 16. Survey Geometric mean (95% conf.9-23.6 (16.6 (12.8-23. 01-02.6 (13.8) 15. population from the National Health and Nutrition Examination Survey.8) 20.2 (<LOD-25.5.50) < LOD < LOD < LOD 17.0) 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) 22.6-17.6 (8.6 (<LOD-27.8 (18.3 (13. 10.8) 14.1-15.9-25.8) 19.7 (10.2) 13.3-18.

069 (.180) .098 (.310) .067-.117) .077-.110) .096 (.055 (<LOD-.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 .090 (.094 (.180 (<LOD-.170 (<LOD-.190) .110 (<LOD-.170 (.100-. population from the National Health and Nutrition Examination Survey.104) . Survey Geometric mean (95% conf.110) .101 (.190 (.120 (<LOD-.100 (.200 (.170 (.140) .097) < LOD .110 (<LOD-.100 (<LOD-.087 (.090 (<LOD-.063) < LOD < LOD < LOD .070-.128 (.100 (.180) .116) < LOD < LOD < LOD .130-.120 (.100 (.094 (.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.133 (.111) .170) .149) .200) .150 (.110-.100 (.077-.170) .161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .090-.057 (<LOD-.110 (.113) .107-.180) .110-.130 (.082-.076-.053-.180 (.111-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.135 (.130) .380) .090-. which may vary for some chemicals by year and by individual sample.170) .130-.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 .120) .108-.130 (<LOD-.090-.140) .200) .106-.074-.157) .110 (.190) .170 (. Fourth National Report on Human Exposure to Environmental Chemicals 85 .220) .190) .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.150 (<LOD-.108) .120 (<LOD-.180) .135 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .071-.140-.240) .120-.126 (.270) .150 (.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 .101 (.113-.130) .S.130-.310) .063) .090-.090-.130-.090-.100-.120) .

9 (28.5.86-13.1) 18.3 (16.8 (26.4) 19.1) 62.1) 17.1) 18.8 (28.2) 34.3 (17.7) 78.0) 33.7 (30.5) 36.5 (45.1-20.1) 17.1 (41.2 (14.5-19.2) 19.8) 51.6) 54.0 (62.7-23.8-21.0-23.6 (12.6) 56.3) 32.6 (56.2 (25.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.2 (19.5) 90th 55.9 (<LOD-14.5 (44.2 (26.9-64.8 (19.6 (16.9-65.0) 49.2-23.8-79.5) 19.2-18.7-113) 68. and 7.2-16.0-37.8 (16.9-45.9 (29.3 (14.4) 107 (84.2 (59.8 (71.3) 25.2 (7.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.1-126) 67.7-77.5) 14.S. which may vary for some chemicals by year and by individual sample.4 (11.5) 22.7 (74. respectively.3) 18.3) 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.5-87.6 (15.9-89.7) 28.1) 16.1-34.8 (13.4-36.8 (17.9 (66.0) 75th 31.5) 78.8 (<LOD-20.4-67. population from the National Health and Nutrition Examination Survey.1 (10.7-160) 86.1-51.0-68.8) 19.9-36.7-17.3 (45.7) 14.2-18.7) 15.8 (49.0-93.4-18.9 (19.8 (30.7-21.3-32.1) 30.8-129) 74.3-58.5 (13.7) 56.6) 60.9-40.1-22.5-69.8-16.2-21.6 (57.1-28.2 (27.5-36.6-82.7) 73.3 (56.4) 48.0 (13.0 (19.5 (25.9) 51.6-22.3 (14.1 (65.4-22.0) 18.7-35.1) 17.1 (48.4) 55.0) 13.6-54.0-59.1) 14.2-88.4-23.8.3) 30.6) 56.4) 16.2 (64.5 (15.5.7 (59.0 (15.3) 18.7 (16.8 (12.7-34.1-55. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 17.9 (51.5) 26.5) 14.0-24.7 (35.0) 19.8-41.7 (11.10 (<LOD-11.8) 80.1-16.7-20.0-38.6) 10.4) 59.1 (22.6 (50.1-16.9 (47.8 (42.3-30.3-86.3 (49.2 (15.7-18.6) 25.0-93.7 (59.8-110) 59.5) 30.0 (60.3 (58.1) 17.8-19.8-77.4 (45.0 (16. 01-02.4 (12.8 (26. 10.6 (32.6) 34.2 (60.6-19.1-34.8-67.5-20.5-95.0 (14.8-16.5-111) 68.2) 39.3) 15.7 (18.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.2) 17.1) 32.7) 59.8 (26.5) 48.9 (36.2 (36.4-35.0 (15.0-113) 68.8 (13.3-57.6) 82.1) 78.0-123) 74.7 (28. and 03-04 are 14.5) 20. 86 Fourth National Report on Human Exposure to Environmental Chemicals .9 (16.2-37.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.8 (28.5) 77.1) 78.9 (51.1 (17.5 (15.6-88.0-20.8) 47.1) 17.3) 30. Survey Geometric mean (95% conf.2) < LOD 10.7-38.3-50.8-90.1) 31.6 (52.4) 20.0 (42.3) 32.5) 35.6 (56.0 (13.0 (42.9-20.6-66.7) 35.9) 14.4-52.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.8 (11.8-19.9) 51.0 (29.0 (48.9-65.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.9) < LOD < LOD < LOD 20. interval) 18.7) 17.6-20.1) 17.0 (16.0-143) 112 (68.7-32.9-58.7) 52.9 (15.7) 78.70 (<LOD-12.9 (15.7 (13.0-23.2 (14.3) 36.9-22.1-18.5) 9.4 (30.3) 19.3-74.1 (47.8 (28.0) < LOD < LOD 8.9-35.5-17.4 (28.3-21.3-39.3) 16.4-62.7-22.0-22.2) 20.7-29.9) 14. < LOD means less than the limit of detection.2) 30.0) 40.6) 13.8 (45.8-90.2-17.6 (<LOD-14.9-69.8 (15.2) 59.6) 84.4 (67.4 (16. see Data Analysis section) for Survey years 99-00.

084-.099-.390-.069-.093-.288-.310-.110 (.580 (.440-.279-.110-.458 (.096-.180-.055 (<LOD-.960) .930) .092 (.108 (.240) .395) .090 (<LOD-.250) .130 (.240-.090-.116) .237) .106 (.310 (.041 (<LOD-.690) .190-.330 (.310-.S.430-.205 (.510 (.580 (.327 (.371) .100-.085-.140) .684) .680) .103 (.400-.098-.450) .470 (.080-.134) .330-.089 (.097) .420) .060 (<LOD-.090-.078-.087 (.210 (.651) . Survey Geometric mean (95% conf.104 (.120-.559) .190-.286-.220 (.120) .100-.109 (.380 (.290-.440) .232) .320-.470-.490) .180-.410-.130 (.085-.160 (.125 (.119) Selected percentiles ( 95% confidence interval) Sample 95th .300-.355 (.171-.390 (.397-.405) .400 (.270-.410-1.099-.126) .110 (.100 (.340-.400-.220 (.145-.580 (.141) .091) .047-.510-.111-.130) .112 (.120 (.280) .460-.470 (.430-.300) .161-.130) .113) .112 (.079-.301-.110 (.095-.640 (.150) .340) .260) .470 (.760 (.120-.210) .106 (.114) .120) .090-.360-.490 (.091-.190-.350 (.098 (.186-.177-.079-.565) .080 (.130) .470-.130) .124) .202 (.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.094 (.130) .120) .100-.113) < LOD .420 (.080-. which may vary for some chemicals by year and by individual sample.090 (.120-.230 (.210-.210) .116 (.540) .117) .417 (.480) .680 (.108) 75th .092 (.150) .220 (.111 (.630) .069) .122) .090-.310-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.129) .461 (.080-.520 (.106 (.430-.490-.160-.220 (.594) .060) .141) .105 (.060-.190-.497-.110 (.081-.240 (.082) .288 (.520) .830) .310) .390 (.690) .630) .350-.210) .20) .400) .103 (.550 (. interval) .210 (.100-.520 (.390) .573 (.234) .119) < LOD < LOD < LOD .170 (.460) .116-.186 (.135 (.093) .460) .370 (.068-.600 (.130) .210 (.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .320-.093-.250) .062 (.490 (.180-.400 (.127) < LOD < LOD .130) .390 (.110) .310-.120 (.340-.840) .108) .260) .414 (.090-. population from the National Health and Nutrition Examination Survey.054-.173-.183 (.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 .122) .600) .098 (.220 (.210-.211) 90th .110 (.131) .800) .080) .590 (.096) .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .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.630) .190-.370 (.367) .240) .161) .240) .285-.360-.090) .191 (.078 (.590 (.120) .104-.324 (.343 (. Fourth National Report on Human Exposure to Environmental Chemicals 87 .158-.250) .100 (.830) .110 (.080-.070 (.220 (.090-.390) .242) .272-.330-.125) .500) .128 (.390 (.317 (.220 (.061-.085-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .120 (.098) .071 (<LOD-.220) .590) .081 (.190-.093-.109 (.237) .096-.395-.409-.220 (.

International Agency for Research on Cancer (IARC). Available at URL: http://www. Wolff MS. 1986. 2001. Gilman A. Available at URL: http://www.inchem. Concise International Chemical Assessment Document 70 Heptachlor [online]. Laliberte C.nih. Chashchin V. Glynn AW. Jaraczewska K.cdc. et al.inchem.niehs. Chlorinated Hydrocarbon Insecticides. Voorspoels S. Environ Health Perspect 2002. 4/21/09 Dallaire F. Darnerud PO. 2 Classes of Pesticides.atsdr. Loo S. Bjerselius R. Canada). Saidein D. JAMA 1988. Environ Health Perspect 2002. Available at URL: http://www.Summaries & Evaluations. 88 Fourth National Report on Human Exposure to Environmental Chemicals . KalubaSkotarczak A. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Jr. Vol. Takahashi W. Inc. Lawrence River (Quebec. Bioassay of heptachlor for possible carcinogenicity. 4/21/09 Baker DB. In Hayes WJ. Kolonel LN. Available at URL: http://www. 731-915. Smith AG. Toxicological profile for heptachlor and heptachlor epoxide [online]. Eds. Odland JO. Chlordane and heptachlor [online]. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Handbook of Pesticide Toxicology.heptachlor. Poland.150:981-990. Hansen JC. Available at URL: http://ntp. Baker DB. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort.htm. Bleiweiss IJ.372:20-31.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).pdf. Arch Pediatr Adolesc Med 1996. Shindell S and Ulrich S. Willman E.110:617-624. Stehr-Green P. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. LeMarchand L.28:497501. Atuma S.330:55-70. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Available at URL: http://www.gov/toxprofiles/tp31. A Report to the Hawaii Heptachlor Research and Education Foundation. Brower S. Pollutants in breast milk. Lulek J. et al.110(8):835-838. 2006. Hertz-Picciotto I. Covaci A.111:349355. Dewailly E.org/documents/iarc/ vol79/79-12. maternal serum and milk from Wielkopolska region. gov/toxprofiles/tp12. National Toxicology Program (NTP).org/site/foundation/ research/projects2. Arch Environ Health.html. Granath F. Available at URL: http://ntp. Ayotte P. Aune M. Vol. Hawaii Med J 1991.gov/ntp/ htdocs/LT_rpts/tr008. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Royce W.html. Drews K. Keller JA. Sci Tot Environ 2006. 6/1/09 Rogan WJ. Senie R. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Mortality of workers employed in the manufacture of chlordane: an update. J Occup Med 1986. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. 1993.html. et al. Academic Press. Wohlleb JC. August 2007. Bull Environ Contam Toxicol 1981:27:506-511.htm.9:1-109. Barker J. Wong L. Organochlorines in Swedish women: determinants of serum concentrations.nih. Distribution of polychlorinated biphenyls.pdf.org/ documents/cicads/cicads/cicad70. Van Oostdam JC. Environ Health Perspect 2003. Tartter P. Jr and Laws ER. Head SL.gov/ntp/ htdocs/LT_rpts/tr009. Charles MJ.41:145–148. 1979-1980. Siegel BZ. Dewailly E.niehs. 4/21/09 James RA. Takei G. 9/25/07 International Programme in Chemical Safety (IPCS). 1991 pp.84:151-161.8:1-123. Sci Total Environ 2004. Circumpolar maternal blood contaminant survey. Berkowitz GS. Organochlorine exposures and breast cancer risk in New York City women. Organochloride pesticide residues in human milk in Hawaii. Muckle G. Toxicological profile for chlordane [online].50(3):108-118. Environ Res 2000. Dendle WH. International Agency for Research on Cancer (IARC) .atsdr. May 1994. 1963-1967. New York. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Bioassay of chlordane for possible carcinogenicity. 79. 6/1/09 National Toxicology Program (NTP). et al.259(3):374-377. 1994-1997 organochlorine compounds.cdc.

0-37.3-236) 24.3) 22.1) 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 12.0 (21.0 (10.3 (<LOD-31.7-16.S.1 (<LOD-39.8. and 03-04 are 20.5) 25.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.7. Smith.1’-(2. < LOD means less than the limit of detection.6 (22. after World War II until 1972.8-26. DDT is converted to DDE and several other metabolites.9) 17.2-bis(p-chlorophenyl) ethane (DDD).00 (<LOD-10.8-17. fish.8) 15.8-39.5 (23. DDT was used at one time as a treatment for head and body lice.4) < LOD < LOD < LOD 61.0-27.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. Food imported from countries that still use DDT may contain the chemical or its residues. respectively. 17.1-71.0 (18.7) 12.50-11.6 (31.9 (10. and water. 1991). It was produced and used in the U.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.9 (21. particularly for endemic vector and malaria control. Only a small proportion of DDT is metabolized and excreted (Smith.S. 1988). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In the general U.0) 26.7) < LOD 18. o. The biodegradation half-life of DDT in soil varies from 2 to 15 years.2 (11.2-95. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.3-590) 293 (104-541) 48.8) 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 8.4 (23.2) 155 (59. p. although DDT and DDE intakes have decreased over time (FDA.6 (9.0-35.p’-DDT (15%-21%).8) 36. which may vary for some chemicals by year and by individual sample. Both Serum p.0 (18.6 (25. Fourth National Report on Human Exposure to Environmental Chemicals 89 .10-13. 1991).3) 21. including 1. 01-02.5) < LOD < LOD 9.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. particularly meat.1 (23. It is still used in some countries. and dairy products.5-54. sediments.0) 20.5) 23.9 (10.1 (33. population. or dermal exposure.3 (27. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.90 (<LOD-12. DDT usually refers to the technical product.9) < LOD < LOD 9. which is a mixture containing p.2-65. food. 2008. population from the National Health and Nutrition Examination Survey.2) < LOD < LOD 9. continues to be the primary source of DDT exposure. resulting in fetal exposure.9) 14. DDT is converted in the environment to other more stable chemical forms. In the body.S.5-36.3 (<LOD-21. DDT can be absorbed after ingestion. see Data Analysis section) for Survey years 99-00.8-23.6 (<LOD-25. inhalation.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.10 (<LOD-12. 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.2) 30.6-33.1) 31. 2002.9) 29.0) 40. Survey Geometric mean (95% conf.p’-DDT (65%-80%).9-34.9 (<LOD-20.3) 28.5 (14.0-53.9 (10.3-16.4. and 7.0-15.7 (15.1-27. when virtually all use of it was banned.3) 21.0-155) 83. air. as well as in plant and animal tissues. and trace amounts of several related compounds.70 (8.p’-DDD (4% or less).8) 30.2 (<LOD-40. These chemicals are highly persistent in soil.0) 19. Gunderson.4) < LOD 17.1’-dichloro-(2.5 (23.7) 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. DDT and DDE can cross the placenta. depending on conditions.7 (19.9-28.5 (15.

080-. In high dose.p’-DDE can produce anti-androgenic effects (Gray et al. resulting in exposure to nursing infants (Rogan.530) .084 (.106) < LOD < LOD .150-.250-1.071 (.059-.220) .180) . dioxins and furans)..g.146 (. lung cancer. 1996).106) .26) 1. and o. and leukemia have also been inconclusive (ADSDR.201 (. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.343) < LOD .130 (<LOD-. Studies of DDT exposure and pancreatic cancer.62 (.170 (. Animal studies reported reduced fertility.095) < LOD .190 (.01) .150-.054-. population from the National Health and Nutrition Examination Survey..130 (<LOD-.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 .190 (. Longnecker et al.240) .. Jusko et al.150) . Survey Geometric mean (95% conf. 2006.064 (.180 (. Jusko et al. 2004.Organochlorine Pesticides chemicals are excreted in breast milk. other organochlorines. 2002.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. In laboratory animals.230) ..160-. 2000.107) 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.140) .240 (.530 (.400 (. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.200 (. 1956).330-4.078 (.120-.105-. Gladen and Rogan.180) . reproductive organ abnormalities.170-. 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.203) .250 (. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. 2006).170) . 2001). Snedeker. 2001).069) .180 (..00 (.190-1.207) 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 .086 (.260) . 2002. 2006.189-.. Calle et al. 2006..051 (<LOD-.132-. 90 Fourth National Report on Human Exposure to Environmental Chemicals .112 (.108 (. which may vary for some chemicals by year and by individual sample.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .p’-DDD and p.130-.220) . accidental exposures.075) 1..S. 1998). Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown. fertility.142 (.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 .140-.150 (<LOD-.313 (.128 (.063 (<LOD-.230) . premature delivery. Mariussen and Fonnum. 2001).570-4. 2002.00) .143) < LOD < LOD .071-. tremor.180-. A workplace standard for DDT has been established by Serum p. and altered behavior after neonatal exposure (Eriksson and Talts.074-.114-. Gray et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130 (<LOD-. and duration of lactation. Reproductive effects in humans affecting birth weight. 2001).146 (.150 (<LOD-.106-.120 (<LOD-.. DDT may bind to estrogen receptors (Chen et al. and seizures. Hayes et al.079) < LOD < LOD . both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.400) .061) < LOD < LOD < LOD ..068-..290) . Beard.34) . 2006). 1997).420) . 2002.065-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . have not been consistently demonstrated (Beard.098-.087 (.. 2006). 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.078-. polychlorinated biphenyls.048 (<LOD-.627) . 1995.

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. environmental levels) and health effects is available from the U. 2004).. 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. 2002. 1989). compared to levels observed in this Report (Anderson et al. population from the National Health and Nutrition Examination Survey. 2005). mean serum levels of DDT and DDE in the U. see Data Analysis section) for Survey years 99-00. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. Survey Geometric mean (95% conf.p’-DDT) as a possible human carcinogen.Organochlorine Pesticides OSHA and a guidance established by ACGIH. IARC classifies DDT (p.html. 1991).7-119) 113 (100-140) 93. Declining DDE levels over time have also been observed in the German population. 2002. population declined by about fivefold to tenfold.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.. In general. Heudorf et al.S.. 1998..cdc. Fourth National Report on Human Exposure to Environmental Chemicals 91 .3.. respectively. EPA at: http://www. Link et al. Compared to females in the NHANES 1999-2000 subsample. for males and females in the NHANES 19992000 subsample (Pavuk et al.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. 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. respectively. and 7... Biomonitoring Information DDE persists in the body longer than DDT. 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.. Smith.8.S. Stehr-Green. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.e. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al.epa. 2004).6. More information about external exposure (i. Since the 1970’s.6 (81.gov/ pestcides/ and from ATSDR at: http://www. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.gov/ toxpro2. 8.atsdr. 2003. and 03-04 are 18. 2003). 01-02. In a population-based sample of men and women from eastern Slovakia. NTP considers DDT as being reasonably anticipated to be a human carcinogen.S. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.

Finding a measurable amount of p.05 (3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.25) 8.01) 1.04-1.8 (14.39) 1.40 (3.646) .6) 9.5) 7.02 (2.635) 1.2-32.13) 4. Survey Geometric mean (95% conf.36 (3.14-1.81 (7.25-14.6) 13.5) 22.59) 3. 2004).6) 8.46-2.41-12.9-38.456 (.10-5.31-12.8) 15.2 (9.2 (6.30-1.82) 1.52-6.90-8.0) 2.40-4.66) 4.80) 1.49 (1.6) 9.7) 13.26 (1.27-1.38 (1.1) 12.54) 8.520 (..88 (2.85-10.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.69 (.61-2.66-17.53 (2.01-5.34) 6.02-8.15-4. Serum p. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L. 309 versus 268 ng/g lipid.18-3.75 (8.92) 1. population from the National Health and Nutrition Examination Survey.60-13.01-15.81) 11.50-17.79) 4.430-.53) 7.97 (3.6 (8.870 (.23 (7..01) 1.9 (15.00) 7.34 (7.69 (2.4) 13.81 (1.24) 1.0 (12.8 (9.9-17.63 (1.730) .18-1.57) 2.28) 1.51-8.5) 16.419-.820-1.76-3.6 (9.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .81-18.994-2.Organochlorine Pesticides nearby agriculture (Botella et al.11-1.17-3.600) .48 (6.6) 9.30 (1.3) 10.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.10-1.41 (1.22) .43 (5. interval) 1.30 (1.84 (3.32) 1.01-1.59 (4.57 (1.01-11. High mean levels of whole blood DDT (about 3.32-1.00 (.12-1.77 (1.62-6.49 (6.69) 8.9) 7.84-3.385-.63 (1. In a subsample of NHANES II (19761980) participants.534-.07 (5.20 (.4 (12.57 (3.30-1.47 (1.56-2.69 (1. 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.26) 3.57 (1.19-14.04 (6.75 (4.34) 2.7 (8.76 (2.63-15.03-4.18-4.34-11.53-15.22 (7. o.890-1.71) 32.6) 11.37-16.3) 13.10) 2.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.26-2.18-1.13 (1.796 (.5) 5.39 (3.40-8.2 (19.27) 3.66) 1.14 (1.75) 6.4) 9.91-2.91) 3.68-4.64) 3.0 (9. In the NHANES 1999-2000. 1991).80) 3.01-1.p’-DDT.53) 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.6) 12.2) 19.61 (1.85 (1.33-1.44) 1.557) 1.22-1.36) 3.93 (7.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.46 (1.7) 16.71 (6.59 (1.57-13.8-90.25-16.05) 1.37 (1.51-15.92 (3.48-4.49) 8.59) 6.51 (1.36-2.31 (1.58) 75th 3.16-1.7-19.10) .3 (9.45 (1.9 (26.36-11.77 (1.52 (3.1 (8.9) 5.38 (1.70) 1.40-4.623 (.07) 1.59 (1.51-49.516 (.25 (.8 (13.47) 3.81-5.66-2.860 ng/L) and DDE (about 14.06) 3.14) 2.07) 1.2) 26.50 (2.14) 2.39-2.03-1.32 (1.3-43.12 (6.26-10.75) 2.91-3.64-2.75) 1. 1971).25) 1.96) 1. 2004).4) 14.58) 1.29 (1.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.51) 3.68 (2.69) 4.21) 3.68) 2.36-1.39-1.16 (2.0) 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 .6 (17.58) 1.96) .43-4.18 (6.70-3.1) 40.35) 1.52 (1.76) 1.51) 1.963-1.80 (2.7) 9.90) 22..590 (. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.4-19.24 (1.00 (6.55 (2.56-3.09-1. 2001-2002 and 2003-2004 subsamples.1 (9.80) 1.76) 1.4 (8.71) 12.37-10. 1989).56-6.02) 1.72) 1.14-9.55-9. 2005).488-.726) . or p.1) 7.00-1.31-2.56) 2.82 (1.500-.49 (1. serum levels of o.88-35.7-20.5) 10.57-3.965-1.63 (6.66) 3.99) 1.37-1.8 (13.32 (1.06) 1.6) 9.43-8.66) 1.561 (.17 (3.7-48.p’-DDT (Stehr-Green.611-1.25 (1.85-4.46 (1.32-9.54 (1.91 (6.6 (7.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1. considerably higher than levels in this Report (Smith.21) 90th 7.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.13-2.12 (.54-7.87 (5.83 (1.11 (2.p’-DDT. less than one percent had detectable serum levels of o.3) 16.p’-DDT were below the limits of detection.2 (9.92 (3.45 (1.71 (5.S. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.18) 1.19) 4.32-1.87-16.37-4.72) 1.43-4..680-1.66-4.24-17.65 (1.78 (4.3 (8.65) 1.57-2.01-11.97-4.34-3.

which may vary for some chemicals by year and by individual sample.7.4.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 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey. and 7. < LOD means less than the limit of detection. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 93 .Organochlorine Pesticides Serum o. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and 03-04 are 20. 01-02. 17. see Data Analysis section) for Survey years 99-00. respectively.8.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.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.p'-Dichlorodiphenyltrichloroethane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. 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. 94 Fourth National Report on Human Exposure to Environmental Chemicals .S. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf.Organochlorine Pesticides Serum o.

Jr. Angerer J. et al. et al. HCH.97(2):178192. and DDD [online]. Biochem Pharmacol 1997. Patterson DG Jr. Becker K. Kashyap R. Zaidi SS.54:1431-1443. Chemosphere 2004. J Assoc Off Anal Chem 1988. September 2002. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Profiles of ortho-polychlorinated biphenyl congeners.gov/~dms/ pesrpts. Vorojeikina DP. Krause C. Buckland SJ. DDE and shortened duration of lactation in a northern Mexican town. Link B. Bates MN. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. et al.cdc. Vena JE. Available at URL: http://www. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Brock JW.52:301-309.206:485-491. Exposure of women to organochlorine pesticides in Southern Spain. Olea N. Bhatnagar VK. Falk C. Int J Hyg Environ Health 2002. Garrett N.atsdr.155(4):313-322.72:261265. Hediger ML. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Eriksson P. dietary intakes of pesticides. Beard J. Saiyed HN. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP).58:1185-1201. Ostby J.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Swanson MK. Sci Tot Environ 2006. Moysich KB.112(17):1761-1767. and dichloro(diphenyl)ethylene (DDE). Effects of environmental antiandrogens on reproductive development in experimental animals. hexachlorobenzene.71(6):1200-1209.358:110-114. Botella B. Talts U. Seiwert M.7(3):248-264. Davis MD. Crespo J. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Kulkarni PK. Environ Health Perspect 2004. Chen CW. India. Gray LE Jr. selected elements. Koepsell TD. Atuma S. Klebanoff MA. Organochlorines in Swedish women: determinants of serum concentrations. Bull Environ Contam Toxicol 2004. Klebanoff MA.html. Olson JR.. Available at URL: http://www. Hanrahan L. Parks L. Levels of DDT. Bloom MS. Gladen BC. Rogan WJ. Klebanoff MA. CA Cancer J Clin 2002. et al. Aune M. Herrman T. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Epidemiology 2006. Needham LL.1-dichloro2. Jusko TA.cfsan. DDT and human health. Rivas A.gov/ toxprofiles/tp35. Gunderson EL. Kaus S. Brock JW. Heudorf U. dichlorodiphenyldichloroethylene. Lancet 2001. Longnecker MP.106(5):279-289. Katz SH. Toxicological profile for DDT. et al. Willman EJ. Environ Res 2005. Biomonitoring of persistent organochlorine pesticides.53(8):1161-1172.17(6):692-700. Henley SJ. lindane (g-HCH). Granath F. Bjerselius R. Am J Public Health 1995. Int J Hyg Environ Health 2003. Ellis H. Maternal DDT exposures in relation to fetal and 5-year growth. Lambright C.111:349355. FDA total diet study.fda. Drexler H. Longnecker MP. Darnerud PO. Burse VW. Zhou H. Environ Res 2004. Environ Health Perspect 2003. April 1982 to 1984. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Greenfield TA. Paepke O. Hum Reprod Updat 2001. Lepom P. Barr DB. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.21(1-2)37-48. et al.html. Notides AC. Neurotoxicol 2000. Organochlorines and breast cancer risk. and other chemicals. 4/21/09 Gladen BC. Needham LL. and polythelia among male offspring. Wolf CJ.85:504508. The Great Lakes Consortium. Schulz C. Jr. Hayes WJ. Glynn AW. et al. Cueto C. et al. Hurd C. Savitz DA. Gray KA. Maternal serum level of 1. and HCB residues in human blood in Ahmedabad. Calle EE. Gabrio T. DDE. Baker RJ. Charles MJ.96:34-40. hypospadias. JAMA 1956. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Zoellner I. Food and Drug Administration (FDA). Zhou H. Durham WF. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Cerrillo I. Thun MJ.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Chemosphere 2005. et al. Arnold SF. Piechotowski I. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Needham LL. Am J Epidemiol 2002. August 2008. Environ Health Perspect 1998.355:7889.205:297-308. Olson J. Frumkin H. Furr J. Fourth National Report on Human Exposure to Environmental Chemicals 95 .162:890-897. Olea-Serrano MF. 4/21/09 Anderson HA.

1991 pp. Schecter A.Organochlorine Pesticides Mariussen E. Reddy AB.27:405-421. Chovancova J. Inc.109:35-47. Chlorinated Hydrocarbon Insecticides. Chemosphere 2004. Crit Rev Toxicol 2006. Rogan WJ. Handbook of Pesticide Toxicology. PA. children and newborn infants. Lynch CF. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Neurochemical targets and behavioral effects of organohalogen compounds: an update. and DDD in male rat liver and cultured rat hepatocytes. Petrik J. Pollutants in breast milk. Deichmann WB. Nims R. Arch Pediatr Adolesc Med 1996. Jr. Lubet R. In Hayes WJ.53:455-477. Eds. Jones CR. Environ Health Perspect 2001. Vol. Stehr-Green. et al.54:1509-520. Pesticides and breast cancer risk: a review of DDT. J Toxicol Environ Health Part A 1998. Academic Press. Toxicol Appl Pharmacol 1971. et al. DDE. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Snedeker SM. Cerhan JR. Smith AG. 731-915. Fox S. New York. Fonnum F. Rey AA.36:253-589. Radomski JL.20(2):186-193. Pavuk M. J Toxicol Environ Health 1989. 2 Classes of Pesticides. Comparative pharmacodynamics of CYP2B induction by DDT. DDE.150:981-990. Jr and Laws ER. Astolfi E. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. and dieldrin. Demographic and seasonal influences on human serum pesticide residue levels. Thomas PE.

S.. which may vary for some chemicals by year and by individual sample. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. 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. endrin is converted rapidly to its major metabolite. anti-12hydroxyendrin. 1992). 1987).60 (5. 72-20-8 General Information Endrin.. Endrin was used as an insecticide. EPA. Endrin was not widely used as a termiticide.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 5.8. 1992).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. manufactured. Because it is metabolized so rapidly.40 (<LOD-6. 1992. 1991).40-5.S. and occasionally at low levels in sediment and surface waters. Over time. * 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. 1979.S. or from contact with contaminated soils and sediments in areas where endrin was applied.50) < LOD 5. Ketoendrin is a major photodegradation product (IPCS. Survey Geometric mean (95% conf. 2008). Endrin does not accumulate in body tissues (IPCS.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. a stereoisomer of dieldrin. rodenticide and avicide. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. have been cancelled by the U. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. All uses of the pesticide in the U. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. 1991). Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown.20 (<LOD-5. unlike aldrin and dieldrin.. In the body. At high doses. endrin can persist for years. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used.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. IPCS. 1992). Endrin is absorbed rapidly after ingestion. inhalation or dermal exposure routes.S.Organochlorine Pesticides Endrin CAS No. and inflammation (Smith.10 (<LOD-5. Endrin has been detected in soils. total diet surveys (FDA. An epidemic of acute endrin poisoning. or discarded.10 (<LOD-5.S. Smith.50) < LOD < LOD < LOD 5. Fourth National Report on Human Exposure to Environmental Chemicals 97 . largely the result of historical agricultural application or run off from contaminated soils (ATSDR.30 (<LOD-6. < LOD means less than the limit of detection. Hepatic effects of endrin exposure have included necrosis. see Data Analysis section) for Survey years 01-02 and 03-04 are 5.20 (<LOD-5. Depending on soil conditions. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. 1981).09 and 7. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. Kavlock et al.. endrin usually is not detected in serum of exposed individuals. is no longer manufactured in the U. 1996. unless the dose is high and the exposure is very recent.30) < LOD 5. fatty infiltration. endrin has been detected with declining frequency in U.

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 . Ward et al.24 ng/mL (about 6.020) < LOD . which may vary for some chemicals by year and by individual sample.. with the highest value 6. serum levels of endrin were below the limit of detection.020) < LOD .020 (<LOD-. and the FDA monitors foods for pesticide residues.atsdr. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.020 (<LOD-.e. endrin was detected in 9% of serum samples. In a small study of Spanish women hospitalized for elective surgery. environmental levels) and health effects of endrin is available from ATSDR at: http://www. Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect..S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.020 (<LOD-. 2000).24 ng/g of serum) (Botella et al.html.020 (<LOD-.020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level.Organochlorine Pesticides The U.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 . Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.S.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 .gov/toxpro2.020 (.020) < LOD < LOD < LOD .020 (<LOD-. Survey Geometric mean (95% conf.020-. Workplace exposure standards for endrin have been established by OSHA.cdc. This finding is consistent with other general population studies (Bates et al. EPA has established environmental standards for endrin. 2004. Information about external exposure (i. 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 98 Fourth National Report on Human Exposure to Environmental Chemicals . IARC has determined that endrin is not classifiable with regard to human carcinogenicity..020 (<LOD-.. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. 2004). population from the National Health and Nutrition Examination Survey.

August 1996. Chernoff H. In Hayes WJ. Olea-Serrano MF. Hardjotanojo W. New York. Fetotoxic effects of prenatal exposure in rats and mice. 4/21/09 Bates MN. Ward EM. Exposure of women to organochlorine pesticides in Southern Spain. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Perinatal toxicity of endrin in rodents. Rab MA.htm.html. Jr. Jr and Laws ER. Toxicology 1979.org/documents/ehc/ehc/ ehc130. Chemosphere 2004. Saleem M. et al. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Olea N. Convulsions caused by endrin poisoning in Pakistan. Gray JA. Ellis H. Patterson DG Jr.13:155-165. Eds. Turner W.atsdr. Fourth National Report on Human Exposure to Environmental Chemicals 99 . Chlorinated Hydrocarbon Insecticides. Rogers E. Garrett N. No:429-436.fda. Cerrillo I. Rowley DL. Liddle J. August 2008. 2 Classes of Pesticides.cdc.9:1357-136. Hanisch RC.gov/~dms/ pesrpts.cfsan. Smith AG. Vol. Inc. et al. II. Gray LE. Patterson DG Jr. Whitehouse DA. Environ Res 2004.54:1431-1443. Needham LL. Academic Press. 4/21/09 International Programme on Chemical Safety (IPCS). Ginsburg KS. 1992. Pediatrics 1987. Available at URL: http://www. Buckland SJ. Fetotoxic effects of prenatal exposure in hamsters. I. 1991. Cancer Epidemiol Biomarkers Prev 2000.inchem.21:141-150. Toxicological profile for endrin [online]. Frey JM. Perinatal toxicity of endrin in rodents. Grajewski B. Gray LE. Andersen A. et al. Hanisch RC. Narahashi T. Environmental Health Criteria 130. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. et al.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 4/21/09 Kavlock RJ. Toxicology 1981. Sokal D. pp. Botella B.96:34-40.html. Crespo J. Available at URL: http://www. Gray J. Handbook of Pesticide Toxicology. Rivas A.64-65 Spec.79(6):928-934. Roy ML. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. 731-915. Kavlock RJ. Toxicol Lett 1992. Food and Drug Administration (FDA).gov/toxprofiles/tp89. Schulte P. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Available at URL: http://www. Burse VW. Chernoff N. Endrin [online].

100 Fourth National Report on Human Exposure to Environmental Chemicals .2 (14.3 (22.S.4) < LOD < LOD 22.4 (22.2 (24. population from the National Health and Nutrition Examination Survey.5-15. particularly by consuming fish.4.9 (25..6) < LOD < LOD 14. 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.4-16.5-TCP) and 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.6) < LOD < LOD 26.1 (13.0) * * 15.3-22.9-32.1-16. and 7.6-19.7-22.5-15.0) < LOD < LOD 24.2-15. HCB is well absorbed after oral administration.9-30.0) < LOD < LOD 15. HCB has been detected in fewer foods since the 1980s (FDA.5 (13. and sediment (Barber et al.1) < LOD < LOD 15.7-15.3) < LOD < LOD 20.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. EPA cancelled its use in 1984.0-16. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.7) < LOD < LOD 24.3) 24.7 (27.9-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) < LOD < LOD 14.9) < LOD < LOD 16. Urinary metabolites include pentachlorophenol (PCP). 1976).5-18.2-15.1 (14.9-15. Gunderson.4) < LOD < LOD 19.0 (25..6-32.6-trichlorophenol (2.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.7-26.4. and accumulates in fatty tissues where it persists for years.6-33.6 (23.4 (18.0 (14. primarily as a fungicide and seed treatment until the U. The FDA dietary surveys have shown that over time.9-20.8 (22. and foods with a high fat content.8. < LOD means less than the limit of detection. The general population may be exposed to HCB through diet.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 * * 14.4 (18. air.8 (26.8 (15.3 (22.1) * * 15.7-29. 31.0-25. or game taken from areas with HCB contamination. 01-02.0-28.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.2 (17.3-20.4 (11.S.7-21. water. 2008. 1988).9) < LOD < LOD 19.1-20.7 (15.9 (23. respectively.4. Therefore.4.2) < LOD < LOD 29.9 (14.9) < LOD < LOD 15. HCB is slowly metabolized.0 (18.5-33.9-24. Survey Geometric mean (95% conf.2-31.0-19. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.2) < LOD < LOD 13. and 03-04 are 118.9) < LOD < LOD 20.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.S. breast milk is an additional route of elimination in nursing women.Organochlorine Pesticides Hexachlorobenzene CAS No.4-15.0 (18.6) < LOD < LOD 25.7 (19.1 (17. Although it is not manufactured as an end-product in the U.3) < LOD < LOD 29.3-26.2 (14.4) < LOD < LOD 18.4) < LOD < LOD 33.6) < LOD < LOD 24.6-TCP) (To-Figueras et al.7 (15..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 (21. and has been detected in soil.3 (20.5-14.5 (13.5-trichlorophenol (2..1 (14. and elimination occurs by renal and fecal routes.9) < LOD < LOD 20. see Data Analysis section) for Survey years 99-00.6-44. distributes widely throughout the body.S. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.6 (24.5) < LOD < LOD 18. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.9 (25.5-14. 2002).0.8-15.8) < LOD < LOD 27.6-26.2 (13.3 (14.7-30. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.3) * * 15.6) < LOD < LOD 26.7-16.9) < LOD < LOD 28.7-16.3 (16.9) 19. wildfowl. 2005). 2.5 (14.0) < LOD < LOD 15.4) < LOD < LOD 23.7) * * 14.3 (12.4. 1997). which may vary for some chemicals by year and by individual sample.

html.094) < LOD < LOD .S.097 (.095 (.225 (.099) < LOD < LOD .212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .145-.102) < LOD < LOD .203) < LOD < LOD . Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.069) * * . 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.152) < LOD < LOD .atsdr.135-.147-.gov/pesticides/ and from ATSDR at: http://www.089-.091-.085-.118) < LOD < LOD .121 (. and the FDA has established a bottled water standard for HCB.111) < LOD < LOD . IARC classifies hexachlorobenzene as possibly carcinogenic to humans.082-.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.090 (.182 (. anorexia.081 (.097) .097) < LOD < LOD . arthritis.089-.cdc.102 (.140 (.Organochlorine Pesticides chemical.191 (.epa. HCB interferes with normal heme synthesis.157-. Schmid.120 (.073-. population from the National Health and Nutrition Examination Survey.092 (.130) < LOD < LOD . EPA has established a drinking water standard.190 (. This condition.e. Biomonitoring Information Serum concentrations reflect the body burden of HCB.176) < LOD < LOD .060-.258) < LOD < LOD . With chronic exposure.104 (..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 * * .167 (.094 (.109) * * . Infants were exposed transplacentally and through breast milk.107) < LOD < LOD .113-.169-.163) < LOD < LOD .118-.gov/toxpro2.078 (.147 (.072-.099) < LOD < LOD . 1960).087 (.174-. 2002).077-.S. 1982.122) < LOD < LOD . environmental levels) and health effects is available from the U.126) . Chronic feeding studies in animals have demonstrated kidney injury.099) < LOD < LOD . EPA at: http://www.090 (.S. reproductive and developmental toxicities.098 (.163 (.092 (.088-.090-.065 (. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.090 (.186 (.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 * * .. and many died before 2 years of age (Peters et al.175) < LOD < LOD .111-.114-.115 (. acute doses produce central nervous system depression and seizures.118-.159-. and liver and thyroid cancers (ATSDR. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda. thyromegaly.086-.129) < LOD < LOD .092-.143-.127-.196) < LOD < LOD .178-. which may vary for some chemicals by year and by individual sample.163-.095) * * . In humans.069) < LOD < LOD .095-. and weakness.095 (.086-.123 (.176-.083) < LOD < LOD .085) * * . ACGIH has developed workplace exposure limits for HCB. Fourth National Report on Human Exposure to Environmental Chemicals 101 . 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.141) < LOD < LOD . very high.064 (.173) < LOD < LOD .081-.123 (.086) < LOD < LOD .179 (. immunologic abnormalities. as well as hypertrichosis. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.157 (.062-.107-.123 (.079 (.203) < LOD < LOD . More information about external exposure (i.125 (.100) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.156 (.088-.132) < LOD < LOD .167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .088-.155) < LOD < LOD .095) < LOD < LOD 75th < LOD < LOD 90th * * . Survey Geometric mean (95% conf.171 (. The U.160 (.114-.145-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .092 (.148-.

.fda. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al.135(4):400404.. 4/21/09 Glynn AW. Environ Health Perspect 2002. The metabolism of higher chlorinated benzene isomers. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.205:297-308. Sala M. Schwartz JM. 102 Fourth National Report on Human Exposure to Environmental Chemicals . IARC Sci Publ 1986. 2002).81(2):82-85. 2002) and among children (Link et al. 2005). declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Seiwert M.cfsan. 2006). and other chemicals. Arch Dermatol 1999. selected elements.. Lawrence River (Quebec.58:1185-1201.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. only 4. 2005. Holland NT. 2002. trends and processes. Paepke O.cdc. Kemper FH.gov/ toxprofiles/tp90. 1986. Muller C. distribution. 1999). Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.77:173182. Canada). Granath F. Muckle G. 2002. 1989).. Available at URL: http://www. Fenster L.9% of participants had quantifiable levels (Stehr-Green. Toxicological profile for hexachlorobenzene update [online]. References Agency for Toxic Substances and Disease Registry (ATSDR). J Assoc Off Anal Chem 1988.71(6):1200-1209. 2003). Dewailly E..110(8):835-838. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Int J Hyg Environ Health 2002. Ozalla D. 4/21/09 Barber JL. et al. Bjerselius R. however. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. HCB detection in serum also was proportional to age. Herrero C. Cripps DJ. Organochlorines in Swedish women: determinants of serum concentrations. Jones KC. Dogramaci I. Arch Neurol 1982. Schulz C. Krause C. et al. van Wijk D. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Bryan GT. Bradman et al. Aune M.. Jones D. Environ Health Perspect 2003.39(12):744-749. Hexachlorobenzene in the global environment: emissions. Lepom P.349:144. Darnerud PO. Becker K. 2002. levels. Kohli J. Over the past two decades. et al. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Santiago-Silva M.44 mg/L. Bertram et al. Otero R. et al.. Kaus S. Gabrio T. more HCB levels were quantified. Bertram HP. Barr DB.. Atuma S. As a result of the lower limit of detection in NHANES 2003-2004. Lackman. Sweetman AJ. 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. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al.111:349355. Safe A. 2002. Link et al. HCB levels were directly related to age. In a representative sample of the 1998 German adult population. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. 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. Zoellner I. Food and Drug Administration (FDA). Glynn et al. but overall. Can J Biochem 1976. Piechotowski I. Chemosphere 2005. Available at URL: http://www. September 2002. Lecha M. Peters HA.17:388–399. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In Spain. Gunderson EL.. In the 1976-1980 NHANES subsample. J Exp Sci Environ Epidemiol 2007. Bradman A. Lackmann.gov/~dms/ pesrpts. respectively. Ayotte P.html. FDA total diet study. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Sci Tot Environ 2005.54(3):203-208.. Link B. Gocmen A. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Laliberte C. and the geometric mean concentration of HCB in whole blood was 0.atsdr. dietary intakes of pesticides. Biomonitoring of persistent organochlorine pesticides. Lackmann GM. 2005). August 2008. Eskenazi B.. Reference values updated. Herrman T.html. April 1982 to 1984. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Biol Neonate 2002. Dallaire F. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.

263:397-398. Santiago-Silva M.Organochlorine Pesticides Schmid R. N Engl J Med 1960.105(1):78-83. et al. Stehr-Green. J Toxicol Environ Health 1989. PA. Fourth National Report on Human Exposure to Environmental Chemicals 103 . Cutaneous porphyria in Turkey. Environ Health Perspect 1997. Otero R. Barrot C. Sala M. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population.27:405-421. Rodamilans M. Demographic and seasonal influences on human serum pesticide residue levels. To-Figueras J.

each result has been multiplied by 1.7) 56.9-14.70 (6. environmental levels declined.8 (33.8 (17. The gamma isomer. the U.8-16.8 (10.0 (<LOD-12.3-56.4) 27.3-85.4) 21. It is no longer produced or sold in the U.4) < LOD 9.5 (24. As pesticide applications of HCH were increasingly restricted or eliminated.5) 11.9-178) 48.61-12.8) 39.7) 23. beta.6 (33.1-32.7-166) 70. 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) 653 758 589 1240 1533 1370 20 years and older 10.7-96.90-8.6-20.8. 608-73-1 beta-Hexachlorocyclohexane CAS No.4 (52.80 (6.2 (31. commonly known as lindane. and delta.7 (62.80 (<LOD-14.9 (26.36.7 (13.1) 13.8 (32.1 (9.5) 90th 42.2) 36. 58-89-9 General Information Hexachlorocyclohexane (HCH).0 (35. exists in several isomeric forms.1 (18.2-87. particularly alpha and gamma have been detected widely in air.3) 14.6) 16.3 (62.0) 35.1-16. EPA cancelled agricultural uses of lindane (ATSDR.2-22.5 (43.6 (22.1-37.9 (32.2 (34.2-46. which may vary for some chemicals by year and by individual sample.9) 15.43 (<LOD-9.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.6) 50.6 (10.6-47.8-68.7-69.50) 8.7) 10.3) 51.1-36.30-11.3 (42.89 (<LOD-9.3) 25.8 (23.1-15. and have been used either as fungicides or to synthesize other chemicals.70 (8.9) 81. formerly referred to as benzene hexachloride.6-62.1 (30.1 (21.7) 32.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.9-81.9 (11.9-51.0 (14.5) 16. < LOD means less than the limit of detection.6 (40.46-11. containing about 64% alpha and 10%-15% gamma isomers.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.7 (53.5) 14.4) 10.7 (30. HCH isomers.68 (<LOD-10.1-49.7-20.4) 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 21.5) 29.2 (50.0 (19.5 (14.0 (33.20-16.8-19. gamma.7-96.2-98.8) 12. **In survey period 2001-2002.2 (29.4) 11.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14. Technical grade HCH is a mixture of all four isomers.2 (9. 6.6-89.70-12. respectively.60-13. and 7. However. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.76.3) 37.0-21.1 (27.S.1 (9.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16. and 03-04 are 9.2-52. water.8) 95th 68.7 (<LOD-16.0) 17.1 (16.2) 9.4) 51.5528.1) 31.0) 8.56-12.4-73.0-20. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.1 (12.7) 97.4) 44.5 (8.2) 142 (99.6) 47.6-37.7) 10.Organochlorine Pesticides Hexachlorocyclohexane CAS No.3-38.5) 40.9 (50.6) 36. so they can accumulate in fatty tissues of animals.3) 34.7 (35.0 (8.8) 27.7) 18. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects. soil.8) * * * * * * 15.0-111) 70.2-55.7 (29.8) 52.9 (30.6-135) 69. and sediment as a result of historic production and use.3 (26.2 (18.4 (11. Lindane has a half-life of about two weeks in soils and water.2-67. interval) 9.04-10.66-12.0) 7.5) 67.6) 35.0-34.8) 7.2 (48.9 (62.9-56. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90-8.4 (50.1 (11.0) 71. In 2006.87 (9.8-87.1-32.9 (40.4) 901 1067 952 992 1224 1007 Females 11.5) 22. HCH isomers are lipophilic.8 (9.6-14.1) 71.4) < LOD < LOD < LOD 46.4 (8.0-70.7-26.8) < LOD 10. 2005).2) 62.2-17.2-42.0-70.9) 45.9-21.8 (64.4-111) 84.7) 73.9) 17.3 (42.9 (9.0 (37.5-123) 49.7-69.7 (25. The other isomers can be formed during the synthesis of lindane.7) 27.8-199) 134 (85.2-20. 2005). 104 Fourth National Report on Human Exposure to Environmental Chemicals .90) 7. 01-02.1-27.4 (12.4-45.S. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.1) 12.5 (11.6-42.8 (21.5 (16.6) 18.0-23.1) 12. See the section “What’s New” at the beginning of this Report for details. including alpha.4 (16.70-19. 319-85-7 gamma-Hexachlorocyclohexane CAS No.3 (13.5 (37.6-18.6 (16. see Data Analysis section) for survey years 99-00.5-29.4-50.9-24.0) 41. population from the National Health and Nutrition Examination Survey.6 (17.S.8-54.2) 13.

enlarged livers.150 (. population from the National Health and Nutrition Examination Survey.297-.191-.S. and memory loss (Nigam et al.340-.098 (.260) .510) .090 (.244-. and nephropathy developed (IPCS.214) .110) .200-.072 (.092 (.100) .580-1.250-.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .. 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.620) .331 (.710) .210) .Organochlorine Pesticides exposure to HCH is through the diet.294-.140) .190) .130 (.380 (.250 (.390-. Rogan. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.150-.360-.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .370-.470 (.080-. 1971.01 (.069) .120-.700) . the serum half-life was about 20 hours among children (Ginsburg et al. hepatic enzyme induction.350) .100-.340) .119) .S.120) .372 (.442 (.083 (.240-.310) .308-.070-.290 (.240 (.090 (.460) .220-. 1983).690) . 2002). **In survey period 2001-2002.270 (.254) 95th .480 (.290) .580 (.062 (.073-.120) .250) .320 (.080 (. for lindane.501) .350 (.661) 901 1067 952 992 1224 1007 Females . HCH isomers are absorbed after inhalation.221-.144 (.360) .167 (.050-.080-.470) .174) . Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.047-.050) ..250-.070 (.290 (.070) .150) .600) .110) .056-.096) .091) .070-.103-.360 (.125) < LOD < LOD < LOD . 1981).048 (<LOD-.120-.260) .090 (.050 (<LOD-.064 (.080-.160 (. tremors. After dermal application of lindane 1% lotion.170-.216 (.190) .057-.086) < LOD < LOD < LOD < LOD < LOD < LOD .110) .059-.222 (. Distribution is mainly to fatty tissues.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.146-. or dermal exposure.05) . Fourth National Report on Human Exposure to Environmental Chemicals 105 .103) 90th . each result has been multiplied by 1. which may vary for some chemicals by year and by individual sample.118-.200 (.057 (<LOD-. See the section “What’s New” at the beginning of this Report for details.280-.120 (.330 (.330-.250 (.131-.300-.070-.281 (.382-.120 (.400) .680) .260-. Gunderson 1988).404) .067) .100) .210-..124-.083) .450 (.050 (.080) * * * * * * .210 (.220 (. ingestion. 1996. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.078 (.150) .140) . 1986).290 (.521 (.S.420-.058 (<LOD-.077) < LOD . respectively.410-.050 (<LOD-.120-.220-. The U.290) .089-.040-.077) < LOD .220) .090-.37) 1.050-.480 (.180-.100 (.280-.210 (.056-.200-.110-.120 (. and FDA has established a bottled water standard and food residue tolerances for lindane.5528. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.480) . Saxena et al.234 (.390 (.173-.410) .587) 653 758 589 1240 1533 1370 20 years and older .160) .065 (. 1977).570 (. ataxia. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.100-.305) .062 (.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .130) . paresthesias.070 (.410) .130-.560 (.460 (.560) .910 (.051-. When animals were chronically fed lindane at high doses.410 (.412 (.100 (. and seizures. OSHA and ACGIH have established workplace standards and guidelines.081-. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.100-. interval) . from 6% of samples in 1982-1984 to 2% in 1994 (FDA.140 (.32) .060) .118 (..057-.319) .250 (. EPA has established a drinking water standard.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 .190-.080 (.103 (.230-.450) .310 (.050 (.287 (. 2008.400) . The beta isomer accumulates in fatty tissues and is metabolized more slowly.051 (<LOD-. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.140) .050-..160-.840) .139 (.170-. resulting in a half-life of about seven years.067 (.089) .310) .175 (.191-. U.814) .065 (.190-1.080) . probably by blocking inhibitory neurotransmitters in the central nervous system. Workers who directly handled HCH have complained of headache.050-.620-1.064) .450-. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.068-.

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.. population from the National Health and Nutrition Examination Survey. 2002.. respectively.. Stehr-Green. 1998). 2001-2002.e. which may vary for some chemicals by year and by individual sample..S. 1971.. 1989). 2005. Link et al. In NHANES 1999-2000. 1991. Becker et al. Kutz et al. 2004.. male sex.gov/toxpro2. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. aged 9-11 years. the maximum and 95th percentile beta-HCH values.cdc. In populationbased studies of New Zealand adults and German adults and children. were similar to the 95th percentiles in this Report.5.S. 2005.. Kutz et al. see Data Analysis section) for Survey years 99-00.html. older age... More information about external exposure (i. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers.. and 2003-2004. and 03-04 are 14. In an earlier (1996-1997) sample of German children. Survey Geometric mean (95% conf. and a diet that includes meat (Becker et al.5. Stehr-Green. serum levels of lindane were generally below the limits of detection.atsdr. Radomski et al. respectively. and 7. 2004).gov/pesticides/ and from ATSDR at: http:// www. In recent years. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. 1991.. Additional factors associated with higher beta-HCH levels include rural residence. 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. 2004) and India (Bhatnagar et al.8. 1989.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2002). Biomonitoring Information Because of its longer half-life. < LOD means less than the limit of detection. 01-02. EPA at: http://www. Sturgeon et al. 1998. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al.. 10. environmental levels) and health effects is available from the U. 106 Fourth National Report on Human Exposure to Environmental Chemicals .epa. Bates et al.

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. Fourth National Report on Human Exposure to Environmental Chemicals 107 .Organochlorine Pesticides 2001-2002 survey period (Link et al. Survey Geometric mean (95% conf. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al. respectively.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In a small study of adults who consumed sport fish from the Great Lakes. Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. 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... which may vary for some chemicals by year and by individual sample. 1971). 2003).S. 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. 1986. 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). 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.. in this Report (Nigam et al. 1998). 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..

Biomonitoring of persistent organochlorine pesticides.20(2):186-193. Glynn AW. Rev Environ Contam Toxicol 1991. Lowry W.91:998-1000. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Link B. Rothman N. children and newborn infants.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).fda. Bai KM. Arch Pediatr Adolesc Med 1996. Needham LL.120:1-82. Rivas A. Patterson DG Jr. India. Bull Environ Contam Toxicol 2004. Olson J. Chemosphere 2004. Brinton LA. Exposure of women to organochlorine pesticides in Southern Spain.71(6):1200-1209. 4/21/09 Ginsburg CM. Radomski JL.150:981-990. Becker K. et al. Olea-Serrano MF. Astolfi E. Bhatnagar VK. Stehr-Green. Paepke O. Deichmann WB. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Int J Hyg Environ Health 2002. Metabolism of gammahexachlorocyclohexane in man. et al. Siddiqui MKJ. Seiwert M. J Toxicol Environ Health 1989. Heinrich R.htm.72:261265. Darnerud PO. Chemosphere 2005.106(5):279-289. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Kulkarni PK. Brock JW. April 1982 to 1984. and other chemicals. Potischman N. Piechotowski I. Bhargava AK. J Pediatr 1977. Environ Health Perspect 2003. Cerrillo I. Environ Res 2004. Occupational exposure to hexachlorocyclohexane. et al. HCH. selected elements. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.gov/~dms/pesrpts. Reisch JS. 4/21/09 Kutz FW. Placental transfer of pesticides in humans. Available at URL: http://www. Raju GS. The Great Lakes Consortium. August 2008. Int Arch Occup Environ Health 1986. dietary intakes of pesticides. Toxicological profile for hexachlorocyclohexanes update [online].html.58:1185-1201.9(4):417-424. Falk C. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Int Arch Occup Environ Health 1983. Hanrahan L. Ellis H. August 2005. Gabrio T. available at URL: http://www. Lindane.atsdr. Zaidi SS. Zoellner I.48:127-134. Kutty D. Bates MN. J Assoc Off Anal Chem 1988. Garrett N. et al. 4/21/09 Anderson HA. FDA total diet study. Environ Health Perspect 1998. Bjerselius R. Kashyap R. International Programme on Chemical Safety (IPCS). Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Buckland SJ. Nigam SK.52(1):59-67.cdc. Pollutants in breast milk. Crespo J. Wood PH. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.html. Needham LL. Demographic and seasonal influences on human serum pesticide residue levels. et al. Bottimore DP. Available at URL: http://www. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. PA. Aune M. and HCB residues in human blood in Ahmedabad. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. et al. Krause C.54:1431-1443. Angerer J. Burse VW.57(4):315-320. gov/toxprofiles/tp43. Sturgeon SR. Karnik AB. Olea N. Gunderson EL. Visweswariah K. Organochlorines in Swedish women: determinants of serum concentrations.inchem. Needham LL.27:405-421. Arch Toxicol 1981. Absorption of lindane (g benzene hexachloride) in infants and children. Schulz C.111:349355. Krishna Murti CR. VI.205:297-308. et al. Levels of DDT. Herrman T. Majumder SK. Saxena MC. Botella B. Lepom P. Rogan WJ. Atuma S. 2002. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). org/documents/jmpr/jmpmono/2002pr08.96:34-4Food and Drug Administration (FDA). FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Cancer Causes and Control 1998.cfsan. Toxicol Appl Pharmacol 1971. Maass R. Rey AA. Granath F. Saiyed HN. Kaus S.

sediments. or pesticide application.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.8 (<LOD-73. (Kutz et al.5-82. resulting in exposure to newborns and nursing infants. Some states and the U.3 (15. < LOD means less than the limit of detection.0-374) 11. and 7. population from the National Health and Nutrition Examination Survey..8) < LOD 15.6-305) 15.4-230) 18.2) 51.S. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.5 (9.0 (<LOD-108) < LOD < LOD 50.5.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.5-291) 11. mirex was detected in human adipose samples.7 (<LOD-47.6 (<LOD-31.70-24. soil. animals. Mirex has been detected in air.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.6) < LOD < LOD < LOD < LOD 71.1 (13.0 (12.5 (<LOD-115) 153 (30..7 (12. Mirex is not metabolized in the body. which may vary for some chemicals by year and by individual sample.6 (<LOD-108) 9.3) 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. water.Organochlorine Pesticides Mirex CAS No. 1991). where it has a half-life of 12 years.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 19.70-40.10-37. Formerly.S.3 (15.S.8. 1995). see Data Analysis section) for Survey years 99-00. 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. Occupational exposure is limited to workers at sites where mirex contamination is present. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.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. 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. where it was applied directly to soil and by aerial spraying. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. after which it is widely distributed in the body and stored in fat.S.6) 9.S.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. disposal. 2385-85-5 General Information Mirex has not been produced or used in the U. and 03-04 are 14.70 (<LOD-15.4) < LOD 63.1 (<LOD-65.4 (8.1 (8. In studies conducted in the 1970’s and 1980’s.8 (12.5 (<LOD-42. Mirex binds strongly to soil.6 (<LOD-23.6.5-425) 40.90-29.0 (14.2-230) 13. 01-02.3-225) 15. and foods.7) < LOD 66. Fourth National Report on Human Exposure to Environmental Chemicals 109 .2 (7. it is a highly persistent chemical in the environment.7) 8. since 1977. Survey Geometric mean (95% conf. Mirex is absorbed through the skin and from the gastrointestinal tract. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. 10.4) < LOD 15. respectively. Mirex can cross the placenta and be excreted in breast milk.10 (<LOD-15. especially those from persons living in the southeastern U. aquatic organisms. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.40 (<LOD-13. 1985.

and NTP classifies mirex as reasonably anticipated to be a human carcinogen.256 (.090-1. and 2003-2004 subsamples.170-3.215) 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 .170) < LOD . EPA has established environmental standards for mirex. 2004).02) . 1991). In samples obtained between 1994 and 1997..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 .S. 2005).108 (.Organochlorine Pesticides exposures are unknown.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . and 4.8. More information about external exposure (i. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.093 (.080-1.7 ng/g of lipid.106) < LOD . reproductive toxicity included decreased fertility and testicular damage. 1989).100 (<LOD-.089-.052-.S. Biomonitoring Information In the NHANES 1999-2000.090 (<LOD-.690) .220) .635) < LOD .470) .79) .atsdr. environmental levels) and health effects is available from the ATSDR at: http://www.41) .100 (<LOD-.370 (.079 (<LOD-. Laboratory animals fed high doses developed liver enlargement and liver tumors.106 (.054 (<LOD-.79) .053-.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. 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.080-1.430 (.090 (<LOD-.112 (.73) . as well as in a subsample of NHANES II (1976-1980) participants.110 (<LOD-. serum mirex levels were generally below the limits of detection (Stehr-Green. 2001-2002. 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.html. IARC classifies mirex as possibly carcinogenic to humans. The U. which may vary for some chemicals by year and by individual sample. Smith.140 (<LOD-. 7.102) < LOD < LOD < LOD < LOD .090 (<LOD-.470) .cdc.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 . 110 Fourth National Report on Human Exposure to Environmental Chemicals .064 (<LOD-.310 (.08 (..37) . The geometric mean mirex levels of the Inuit mothers were 8.077 (<LOD-.268) < LOD .92) .610) < LOD < LOD < LOD < LOD . 1995. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.e.510) < LOD < LOD .gov/toxpro2.070-1.. Survey Geometric mean (95% conf.450) 1.090-1.450 (.240) < LOD < LOD < LOD < LOD < LOD < LOD < 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. In addition.062-. 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.410 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .090-1.220 (<LOD-. population from the National Health and Nutrition Examination Survey.055-.059 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.470 (.

330:55-70. New York. 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. Stroup CR. Leininger CC. dichlorodiphenyldichloroethylene. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Smith AG. The human body burden of mirex in the southeastern United States. Profiles of ortho-polychlorinated biphenyl congeners. 1991 pp. Available at URL: http://www. Van Oostdam JC.Organochlorine Pesticides effect. Stehr-Green. Carra JS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kutz FW. 731-915. Eds. Swanson MK. PA. Olson JR. Bottimore DP. Chashchin V. J Toxicol Environ Health 1985. Academic Press.atsdr.97(2):178192. Toxicological profile for mirex and chlordecone [online]. Jr and Laws ER. Handbook of Pesticide Toxicology. Wood PH. Odland JO. 1994-1997 organochlorine compounds. Hansen JC. Gilman A. In Hayes WJ. Sci Total Environ 2004. Chlorinated Hydrocarbon Insecticides. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.html.15:385-394. Environ Res 2005.cdc. Demographic and seasonal influences on human serum pesticide residue levels. J Toxicol Environ Health 1989.120:1-82. 2 Classes of Pesticides. Circumpolar maternal blood contaminant survey. Moysich KB. Kutz FW.gov/toxprofiles/ tp66. Vol. Dewailly E. Inc. Jr. References Agency for Toxic Substances and Disease Registry (ATSDR). Watts DL. Strassman SC. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Rev Environ Contam Toxicol 1991. hexachlorobenzene.27:405-421. Vena JE. 4/21/09 Bloom MS. August 1995. et al. et al.

40 (2. recent sampling of U.80-41.80 (1.80 (2.00 (2.4.20) < LOD 90th 5.30) < LOD < LOD < LOD < LOD < LOD 1.0 (3.40 (2.20-71.30-3.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.5-trichlorophenol.60) < LOD 8.3. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.60 (.0) < LOD 11.Organochlorine Pesticides 2.0) 2. Survey Geometric mean (95% conf.00-8. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.50) < LOD 1.90-33.71 (<LOD-8.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .4.4. hexachlorobenzene. however.4.0) < LOD 5.0) 2.9.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR. Such workers would probably Urinary 2.0) 2.920-3.50 (2.6-trichlorophenol (2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.30-11.03) 9. 2.20) < LOD 5.72) < LOD 1.80) < LOD 1.40) < LOD 6.8) 21.980-3.20 (4.00-3.20-36. Occupational exposures.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. < LOD means less than the limit of detection. other organochlorines.40-11. 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.40 (2.30-40.0) 2.42 (<LOD-8.5TCP and 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.0 (5. population from the National Health and Nutrition Examination Survey.30-27. Trichlorophenols are no longer manufactured commercially.0 (8.60-18.4.00-3.7.0) < LOD 5.4.5-TCP) and 2.0) 14.50-25.0) < LOD 21. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.4.9 and 0.10-3. 1999).980-3. Both chemicals have been detected in air.71 (<LOD-8. and sediments.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2006).5-Trichlorophenol CAS No.57 (<LOD-15.4.9 (<LOD-121) 9.31 (<LOD-9.30-27.6-TCP in any of the samples (U.00 (3.30) < LOD 4.0 (3. 95-95-4 2.0) < LOD 5. surface water.4. 1999). are metabolites of several organochlorine chemicals.40 (.20) < LOD 1.6-TCP were used as intermediates in the production of certain pesticides.50 (.0) 5.940-3.42 (<LOD-12.50 (1.S.0) < LOD 11.7) 24.6-Trichlorophenol CAS No.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 1.40-18.50-63.S.50-16.950 (<LOD-1. may occur by inhalation or dermal routes.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.40) < LOD 1..30-44.4. Exposure to trichlorophenols also may result from metabolism of lindane. and polychlorinated benzenes (Kohil et al. 1976). 112 Fourth National Report on Human Exposure to Environmental Chemicals .40 (. including hexachlorobenzene and hexachlorocyclohexanes.40 (1.27) 696 661 521 696 603 939 Limit of detection (LOD. Formation of 2.5-trichlorophenol (2.60-8.63) 18. 2. EPA.0 (4.60 (4.40) < LOD 4.30-27.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30 (. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.60 (2.900-2. Historically. 2. public drinking water systems did not detect 2. which may vary for some chemicals by year and by individual sample. usually at herbicide production or waste incineration facilities.0 (4.40 (1.40 (2.4.6-TCP).0) 2. soils. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.19 (<LOD-6.0) 2.0 (4.S.

4. 2003).68 (<LOD-8..43 (2.4) < LOD 3. environmental levels) and health effects is available from ATSDR at: http://www.67 (1.44 (1.55 (4.6-TCP levels at the 95th percentile were up to eight times higher than 3.5) < LOD 12.Organochlorine Pesticides be exposed to mixtures of chlorophenols.5-TCP or 2.6-TCP had increased rates of hepatic tumors. In the same 2-6 year old children. NTP classifies 2.24 (3. furans. 1989).4.57 (<LOD-7.html.86 (3.16 (.6) 4.53-3..57 (3. Human health effects from 2.1) 2. Neither 2. However.46 (1.78) < LOD 1.4. and lymphomas.44 (.05-17.5-TCP and limited for 2.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.73 (<LOD-8. At lower doses.90 (4. as being possibly carcinogenic to humans. 1995) were similar. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. 1989).74) 11.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.cdc. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.02) < LOD 7. Fourth National Report on Human Exposure to Environmental Chemicals 113 . urinary 2. animals showed hepatocellular abnormalities..53-3.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.19-4.0) 7.4) < LOD 3.6-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.88-16. 2003.69 (2.3 (5.24) < LOD 1.gov/toxpro2. 7.atsdr.9 (5.4.95 (3.75 (3.2 (2.00) < LOD 4.75 (<LOD-6. the 95th percentile urinary 2. Urinary 2.36 (1. 1995) and up to 19 times higher than the 95th percentile value of 1. leukemias.17) 9.57 (<LOD-7.4.1 (<LOD-58.4.33) < LOD < LOD < LOD < LOD < LOD 2.5) 11. and other chlorinated compounds.47-8.05-8. population from the National Health and Nutrition Examination Survey.20-6..24) < LOD 6.79-4. Laboratory animals chronically fed high doses of 2.4.4.S. the 95th percentile urinary 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.e. Among 6-11 year old children in NHANES 1999-2000..28-25.32) < LOD 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..64 (4.7 (4.6) 4.93-11.4.8 (5..24) < LOD 5.83-12. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al. in addition to dioxins.02-3..78 (3.9) 12.24-11.69-18.3 mg/L reported in German adults aged 18-69 years (Becker et al.8) < LOD 9.37) 16.8) 4. More information about external exposure (i. IARC classifies combined exposures to polychlorophenols.43) < LOD 12.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).67 (1.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.62-20.2) < LOD 5.920-2.2) 2.82 (<LOD-32. 2004).3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .0 mg/L.80 (1.5-TCP nor 2.820-2.4 (6.6) 4.4) 5.19-12.15) < LOD 2.980 (<LOD-1. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.50) < LOD 2.81 (<LOD-9. which includes trichlorophenols. 2003).29 (1. The 95th percentiles for 2.27-17.5-TCP.00-29.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.78-19.60-3.4.68-4. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples. Survey Geometric mean (95% conf.4.6-TCP as reasonably anticipated to be a human carcinogen.16) < LOD 90th 5.37-11..31) < LOD 2.00-19.6-TCP.49 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11. Radon et al.4.13-13.4.

1991).6TCP values.0 (9.14 (2.70-3.0 (20.6-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.0 and 1.0) 17. 114 Fourth National Report on Human Exposure to Environmental Chemicals .70 (2.76) 3.60 (3.4. 1998).0) 11.72-10.28) 24.70) 5.0) 13.36 (1.6-TCP exposure and health effects.3.70) 1.6-TCP (0.00 (4.33-4.23) 3.30-11.69 (3.80) 1.4.3 (11.70 (2.8-15.0-37.20) 4.51-12. 0.80-20. which may vary for some chemicals by year and by individual sample.67-12.00-21.9) 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 2.10-3.46-3.68 (<LOD-2.95) 3.0) 19.5-TCP level of 0.90 (4.09-7.89-6.36 mg/g creatinine.20-3.4 (8.40-4.5-46.5-TCP and 2.30-2.5-TCP and to the median 2.10-3.0-68.35-3.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2. for males in NHANES 19992002 (Agramunt et al.4.40-32.60 (3.53) 2.45-9.4-17.08 (2.7-3.0 (20.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.00 (2.0-38.4.9) 13.0 (6.9 (11.1) 16.59) 4.6TCP causes an adverse health effect.49 (6.0 (11.80-7. Urinary 2.80 (2.6-22.9) 694 677 519 696 602 931 Limit of detection (LOD.7 (13.09) 15.. respectively.28) * 2.63) 90th 15. Survey Geometric mean (95% conf.65) 15..73-9.10) 6.20-23.3-26.2) 12.67) 4.78 (2.6-TCP in urine does not mean that the level of 2.40 (2.40-14.75 (8.74 (2.00 (1.3) 37.0) 12.02) 2.95 (4.2 (14.5-TCP or 2.52-3.00-4.4.4.0) 10.5-TCP and 2.9 (13.3 (11. 2003).4.0-43.90-8.98-11.98-7.6 (11. < LOD means less than the limit of detection. Urinary 2.0 (13.32-4.50-5.18) Selected percentiles ( 95% confidence interval) Sample 95th 25. interval) 2.4.0) 7.4.01-6.0 (6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.6 (12.8) 32.0) 7.1-25.57 (<LOD-2.0-38.0-18.5-TCP (0.8) 18.23-2.95-6.7 (9.4.30-2.58 (1.7-16.55-3.20 (3.5-TCP or 2.60 (2.53) 4.66 (8.48-26.4.70) 5.99) 6.6-17.0-54.0 (15.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.30-33.6 mg/g creatinine) and 2.0 (14.0) 11.5-TCP or 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.40-2.6-TCP level.2-0.0-44.10-2.45 (2.0) 14.0 (7.0 (8.45 (5.0 (15. the median urinary 2.0) 9.45) < LOD 11.8-13.6-TCP than are found in the general population.5-TCP or 2. was about six times lower than the median urinary levels for males in this Report (Radon et al.0 (12.0 (6.4 (10.4.59-6.50 (2.60-37.3-17.32) 3.4 (9.6) 26.80 (2.40) 2.90 (3.0 (14.0 (16.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.31) * 2.0) 15.S. Mean values of 2.58-3.40) 4.4.30) 4.8 (9.0 (8.1 (10.54) 6.6) 21.0) 13.7) 21.07 (<LOD-3..3) 23.92 (2. similar to the limit of detection for this Report (Anderson et al.0-50.60) 6.80-6.40) 2.04) 2.40) 3.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.0-41.80 (3.44) 75th 4. Biomonitoring data will also help scientists plan and conduct research about 2.0) 13.06) * 2.56 (3.2) 25.31 (3.79 (5.74-3.12) 2.52 (2.7 mg/L. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.60-3.7) 33.4 (17.89 (3. In harbor workers exposed to chlorophenol-contaminated river silt.1 (8.90) 2.80-25.47 (3.3) 20. Biomonitoring studies on levels of 2.10) 2.70-6.40 (2.0 (4.70-6.10 (5.26 (2.0) 19.78 (2.40-7.36-5.0) 13.65 (5.85) * 3.6-19.23) 2.20-6.60-21.85 (2.0) 17.4.0) 10.0) 9.70) 3.32) * 3.87-14.4.8-24.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.4.20 (3..6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2004).4. population from the National Health and Nutrition Examination Survey.25-11.0) 6.4.24 (2.18-3.84) 2.5 mg/g creatinine) were similar to the limit of detection for 2.60) < LOD 5.91-4. Finding a measurable amount of 2.0 (14.0) 14.40-2.4.

0) 10.4.00 (3.9) 7.89-2.40 (7.32 (2.6) 12.22-9. Fourth National Report on Human Exposure to Environmental Chemicals 115 .82 (3.9-34.18-4.10-9.28-4.2 (7.87) * 2.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.9-64.4 (11.72-16.3-23.1 (13.49) 4.67-17.01 (3.9) 8.88-7.14-2.59 (2.00) 4.22 (3.23) 4.9 (9.7 (14.88) 4.05 (6.81) 2.76) 4.25 (3.2 (12.00) 4.4 (12.70-9.17) 13.09-3.06) 11.8) 12.56 (7.00 (2.33-2.52 (3.73) 5.6 (6.91 (7.29-4.78 (2.49-3.6 (22.6 (10.63) 4.14-13.5 (8.5) 11.83 (3.33 (7.13 (1.5) 9.8 (8.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.62-15.81-9.21-11.11) 10.54 (2.63 (2.63-15.1 (8.41-6.02 (1.9) 8.22 (<LOD-2.17) 2.25-15.6 (9.38-5.22-2.94-13.4) 9.78) 2.87-6.3-37.2 (13.89) 10.38 (2.60-2. Survey Geometric mean (95% conf.98) 10.1) 14.50 (2.1-21.52 (5.68) 2.47-5.25 (3.95-2.51 (2.38 (4.83-6.6) 8.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.10) 4.15 (1.66-4.53-11.29-4.26-13. interval) 2.43 (2.0 (9.87-7.52) 2.32-19.08-2.42) 2.10 (6.4) 4.63-13.68) 2.29 (6.25-17.53) * 2.53 (3.02) 3.76) 2.65) 2.04-16.19-5.83-5.44 (3.06) 4.77-4.8) 19.6) 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 2.7) 25.63 (<LOD-2.53) 4.63) * 4.05 (3.Organochlorine Pesticides Urinary 2.83-6.27-9.33) * 2.75) 75th 4.99-2.92) 4.72) 32.51) 18.98 (1.18-2.17-4.1-32.6) 13.35 (3.65-21.46-14.4) 8.58 (4.7) 6.87) 2.65-2.8 (7.25-2.88) 1.9) 19.8) 21.88 (2.5 (7.52) 2.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.71 (3.23 (1.5) 11.0 (6.6-31.26 (6.82 (8.6 (9.76-8.9-29.90 (1.2) 19.9-32.60 (4.S.5-28.3 (9.5 (10.96) < LOD 4.0 (11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.43 (<LOD-2.55-2.82-2.82) 2.88) 4.30-2.78) 90th 12.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.91-2.5) 8.20-2.5) 12.15 (6.2 (8.48-2.41 (3.6 (5.43-7.13-6.56) < LOD 11.1) 11.22 (1.50-8.79-17.38) 22.76) 1.33 (1.56-5.24 (1.77) 2.51-21.87 (3.73-22.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.40 (2.0) 8.8) 11.42 (2.88) * 2.3) 8.16-10.06-2.88) 5.65) 18.91 (3.7-36.6 (12.90) 2.9 (9.04-2. population from the National Health and Nutrition Examination Survey.

Falk C. Poschadel B. Baur X. Hanrahan L.atsdr. html.pdf.epa. December 2006 Draft.gov/toxprofiles/tp107. Gregg M. Kohli J.54(3):203-208. Baker S. Pekari K. Becker K. Toxicol Lett 2003.EPA). Can J Biochem 1976. Head SL. et al. Available at URL: http://www.63:57-62. Anderson HA.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).71:99108. Environ Res 1995. Domingo A. Available at URL: http://www. Schulz C. Toxicological profile for chlorophenols [online]. Needham LL. Hill RH Jr. Radon K. Luotamo M. Urinary excretion of chlorinated phenols in saw-mill workers. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Olson J.106(5):279-289. 4/21/09 Agramunt MC. S. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Heinrich-Ramm R. Arch Environ Contam Toxicol 1989. Environ Health Perspect 1998. Corbella J. July 1999. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Shealy DB. et al. Needham LL. U. Domingo JL. Lindroos L. Fast DM. Jarvisalo J. Environmental Protection Agency (U. Hill RH Jr. 206:15-24. Wegner R. Jones D. Bailey SL. Int Arch Occup Environ Health 1991.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. et al.146:83-91. Am J Ind Med 2004. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Safe A. The Great Lakes Consortium. Kaus S.S. The metabolism of higher chlorinated benzene isomers.45:440-445. Holler JS. Seifert B.18(4):469-474.cdc. Burse VW. Szadkowski D. Int J Hyg Environ Health 2003. Pesticide residues in urine of adults living in the United States: reference range concentrations. 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]. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Smith SJ. Aitio A. To T. Seiwert M.

and a low persistence in the environment. General population exposure to organophosphorus insecticides may occur by ingesting contaminated food and from hand-to-mouth contact with surfaces containing organophosphorus insecticides. have accounted for a large share of all insecticides used in the United States. slight to moderate water solubility.. most residential uses have been phased out in the United States as a result of implementation of the Food Quality Protection Act of 1996.DimethyldithioDiethylDiethylthio. 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. Although organophosphorus insecticides are still used for insect control on many food crops. In general.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 . Mammalian elimination halflives can range from hours to weeks. naled) are also registered for public health applications (e. 1993). widely varying degrees of soil leaching or runoff potential. EPA.g. chlorpyriphos) are initially metabolized to the more toxic “oxon” form.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Organophosphorus Insecticides: Dialkyl Phosphate Metabolites General Information Organophosphorus insecticides. Most organophosphorus insecticides undergo hydrolysis with excretion of major hydrolytic metabolites in the urine. moderate to high soil binding. Certain organophosphorus insecticides (e.S. mosquito control) in the United States.g. pesticide applicators. malathion. In general. 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.. less common routes include inhalation and dermal contact. the organophosphorus insecticides have better gastrointestinal than dermal absorption. 2004). Approximately 40 organophosphorus insecticides in a wide variety of formulations are registered for use in the United States by the U. The thiophosphate type organophosphorus insecticides (e. EPA. gardeners.S.. Farm workers. the various organophosphorus insecticides demonstrate low vapor pressures (with some exceptions). with usage declining 45% since 1980 (U.g. florists. An estimated 73 million pounds of organophosphorus insecticides (70% of all insecticides) were used in the United States in 2001. which are active against a broad spectrum of insects. and manufacturers of these insecticides may have greater exposure than the general population.Dimethylthio.

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

Estimates of dose or intake for the general U.. Petchuay et al. 2006. 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. 2006). which may reflect changes in exposure.. 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. 2005) than those presented in U. estimates of dose or intake calculated from urinary dialkyl phosphate levels in studies of pregnant women in one agricultural community (Castorina et al. population (CDC. and these higher levels were associated with a few subtle neurobehavioral test results (Rothlein et al. Bradman et al. 2003) and in another study of workers exposed on reentry to treated orchards (Fenske et al.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites over multiple times of day and over multiple days. 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. 2005).. Lambert et al. Fourth National Report on Human Exposure to Environmental Chemicals 119 .S. In a study of farm workers. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 2006). collection timing. 2005). median urinary levels of DMTP and DMDTP were more than twentyfold higher than median levels in the U. 2005.S.. 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. 2003).. Information is limited with regard to associations between levels of urinary dialkyl phosphates and any health effects.S. 2002. 2003) generally did not exceed doses considered to be safe.. and elimination kinetics (Kissel et al. Koch et al. 2005). 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). population as calculated from urinary dialkyl phosphate measurements were below environmental dose estimates based on multiple routes of exposure (Duggan et al. 2005... representative subsamples from NHANES 1999-2000 and 2001-2002 (CDC.. Also.

36-4.8 (9.90 (1.35-11.91) 4.1-17.52) 6.2) 16.30 (4.01) * * 1.2.70-19.70 (4.70-23.81) 11.26-8.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.S.0) 10.2) 14.670-1.0 (7.86-15.50 (4.21) 9.13-2.20-7.00-19.0) 5.0 (5.954 (.26 (5.40-14.14) * * .90-5.44-3.0) 10.34-3.46) 10.4 (9.5) 15.10 (2.16 (2. 0.60 (5.620-1.50-36.57-7.02-5.3) 17.5-16.68-7.90) 3.1) 95th 13.35-16.0) 5.71 (2.0 (12.9 (8.58 (5.8 (14.840-1.490-2.890 (<LOD-2.39 (3.50 (2.1.0 (9.51) 2.0) 20.0) 7.80 (4.20-30.66) * * 1.00 (1.0 (9.7 (14.5) 20.70) < LOD < LOD 1.93-24.58 (3.55-6.15-12.00-27.0) 12.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 6.19) 9.79 (5.80) 2.0) 10.76 (2.97) 8.70 (2.1) 10.30-4.623-1.40-16.80) 2.42-3.56 (6.0) 11.60-11.0 (6.80) 2.1 (9.970-2.2 (11.2) 16.33 (5.27-15.11 (.80) 11.0 (6.44 (2.37 (3.20 (.2 (7.955 (.5 (11.22 (.20 (2.50-5.2.96-3.81) 11.0 (8.780) < LOD 3.42) .07-10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9-18.97) 90th 7.00-7.99 (5.81) 1.579-1.758-1.70-11.6) 18.8) 19.52-11.08-2.70) < LOD < LOD 75th 3.27-3.0) 15.89) 9.80 (2.83 (5.61) 4.86 (1.7 (12.12-19.15) 14.00 (4.74 (8.2 (7.26-6.1 (10.10) < LOD .860-2.60-25.4) 20.82-12. and 0.0) 6.750-1.981 (.9) 14.2) 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 1.830 (<LOD-3.93 (4.50 (.1-23.45 (2.10 (.00-27.13 (2.40-1.8) 7.70) .4 (9.94) 3.2) 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 1.74 (8.39 (8.2 (14.00) 3.0 (7.60-18.54 (3.10-7.0) 6.05-7.08 (<LOD-2.20 (.4 (7.60) .8) 11.73) * * .08-15. < LOD means less than the limit of detection.40 (.0) 10.60 (1.94) * * .0) 11.23-5.90) 2.0 (8.290 (<LOD-1.6) 7.2 (14.72) 5.90-4.00-12. 120 Fourth National Report on Human Exposure to Environmental Chemicals .80) 4. which may vary for some chemicals by year and by individual sample.32) 1.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.63) 1.80) .0) 5.85 (3.700-1.0 (7.4) 18.40-11.7) 11.810-1.10 (.8 (8.40-19.00) 3.0) 11.17-3. and 03-04 are 0.04) < LOD 1.3-15.32 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-27.5-17.8 (12.12) 4.28) 1.5 (8.740-2.56 (4.8-32.55-8.60) < LOD < LOD 4.20 (.98-5.20 (.03 (.61 (3.44-38.2 (9.530 (<LOD-2. see Data Analysis section) for Survey years 99-00.00 (5.80-22.47) 5.79-7.10 (2.13 (2.56-13.48-7.757-2.9) 8.10) < LOD < LOD 4.16) 4. interval) 1.4 (7.43-12.20-4.290 (<LOD-.70-14.21 (.33-18.38-5.599-1.30 (2.80) .4) 17.0) 9.58 (2.52) * * 1.50) 2.82) 10. 01-02.98-12.35-12.80-24.02) 4.30-6.71-9. population from the National Health and Nutrition Examination Survey.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 1.47) * * 1.53) 4.3) 16.95) 5.56 (1.2 (7.80) 3.2 (9.00-12.40-5.29) * * 1.30 (2.2-20.34-7.0 (7.0) 11.0 (8.8) 7.0) 10. respectively.0 (4.1) 13.80-4.67) 3.600 (<LOD-1.0-28.717-1.3) 14.

03 (2.5-32.75 (3.510-1.61 (1.23 (4.60-9.94 (4.430-1.790 (.56) 7.05 (.62) .95 (3.8) 6.15-10.30 (1.75) 2.28 (2.5) 12.7) 5.9-28.45-5.23) 4.61-29.34) < LOD < LOD .54-15.3) 15. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.820 (.98-5.8) 8.27) < LOD 2.750 (<LOD-1.88-10.5-16.98) .40 (3.46-5.74) 4.7) 12.85 (6.45-11.98) .37 (5.6 (10.1 (10.66 (1.53) 9.80 (6.93) 9.55-20.8) 7.40-14.2) 95th 12.25) 6.5) 7.890 (<LOD-1.549-1.79-3.36) * * 1.4 (4.56) .40-12.47 (3.05 (1.1 (7.40) < LOD < LOD 75th 2.45-5.00-17.924 (.6 (9.996 (.53-11.6) 9.67-19.37-5.89-3.02-2. interval) .98-22.06-2.83) 8.69) 2.40) 4.1-15.60) 2.35 (1.09-11.960 (<LOD-2.5 (4.54-4.7) 18.37-3.1 (11.47) 2.5) 11.67) 1.6) 13.608-1.90-8.44 (2.02-14.31 (3. population from the National Health and Nutrition Examination Survey.83 (7.21-23.88) 2.26) * * .31-14.19 (4.94-23.32-12.566-1.80 (7.855 (.54) .9) 12.710 (<LOD-1.440 (<LOD-2.03) 2.0) 6.69-10.7 (9.82-6.43 (.30) 2.81-5.87 (3.75 (7.0 (8.633-1.03) 2.4) 4.82-26.00 (4.40-5.9 (5.900 (.18 (.80 (2.28 (4.84) 7.39 (2.43) 2.650-1.5) 7.47 (1.40-3.09 (.54-11.75-7.94-9.1 (6.500-1.78 (2.82-14.28) 10.3) 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 1.9) 11.62-5.4 (9.7) 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.8 (10.00-13.04-6.6) 11.72) 11.57 (4.88 (5.69 (4.14 (3.00) 8.574-1.920 (.01-2. Fourth National Report on Human Exposure to Environmental Chemicals 121 .818 (.533-1.932 (.2 (10.2) 9.4) 4.66-34.560-1.41) Selected percentiles ( 95% confidence interval) Total * * 50th .570-1.71) 10.02 (2.47 (3.6) 8.66 (5.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.60) * * .94-22.1) 4.28-9.20-8.34) * * .870-2.38 (1.S.82-14.00-19.94-10.34 (6.56-13.94 (2.7 (8.42) 12.41-12.58) * * 1.3) 5.66-15.75) 14.8) 12.780 (<LOD-1.79-9.37) 9.2) 5.7 (10.9) 16.38) .68) < LOD < LOD 3.9 (9.69) 4.76-4.04 (1.89) * * 1.61-13.2) 8.76) < LOD .4) 13.34 (6.77 (6.57-10.5-20.88-15.890 (<LOD-1.87 (1.540-1.2 (8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-13.03-6.3) 12.93-9.02 (7.960 (.37 (4.56) 4.43 (3.85) 2.8) 16.40-28.1 (8.66 (2.10-13.1) 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 1.830-1.67) 4.57) 4.73 (1.05) .90-5.95) 2.5) 8.47) * * .92-5.46) 2.2) 5.51-5.64-5.883 (.28 (5.07 (.860 (.53 (6.1 (9.87-5.42 (3.1) 4.92-2.57 (6.03 (7.50) 7.2 (6.7) 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 .81 (1.71-2.10 (3.54-2.09) 2.3) 16.61 (1.84 (5.2) 13.29 (2.2) 7.0) 7.9 (9.24-3.98) 9.29) * * .00 (4.773-1.41) .25) < LOD .98 (3.620-1.80) 9.68-4.13) 4.35) < LOD < LOD 3.74) 90th 7.93-5.52) 4.11-6.

see Data Analysis section) for Survey years 99-00.35 (6.82) 8.7) 14.25 (2.72) 2.20) 3.1 (10.18 (3.2) 14.90 (6.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.580-2.6-19.6-41.0 (10.80-21.96) 90th 7.3) 14.24-5.90-31.70 (8.0) 14.90 (1.27 (3. and 0.81-6.90 (2.790 (<LOD-1.80 (2.59-3.34-5.06 (2.740 (<LOD-1.5) 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 * * * * * * .27 (7.78) 5.18) * * * * * * * * 1.74) * * * * * 1.27) 9.6) 18.80-8.70-9.31) 1.75 (3.0) 14.41) 3.51) < LOD 1. which may vary for some chemicals by year and by individual sample.00) 8.24 (2.33-11.50-4.00) < LOD .8-21.70) 2.04 (3.30) 3.46-28.8-20.63-14.70-8.90 (2.6) 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 * * * 1.4) 11.27) .77-3.88) 3.10-4. 122 Fourth National Report on Human Exposure to Environmental Chemicals .0) 19.3 (11.9) 10.7 (11.0-19.0 (15.17 (7.96) 3.10-15.0) 9.9-17.62-17.16-1.15-2.89 (2.14 (6.34-3.80-3.2 (9.0) 11.90) 8.0) 12.80) .4) 7. and 03-04 are 0.90 (2.35) 4.10 (<LOD-1.22-12.28 (7.0) 12.6) 14.0 (14.6 (10.34 (6.9) 95th 14.9) 9.22) 8.15-6.86-10.88) 10.9 (12.95-9.90 (6.0) 13.6) 11.37) 2.40 (2.95 (2.20-8.92-17.4-17.50) 5.7) 22.650-1.0) 18. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7 (10.50) 3.66-13.00-18.0-33.4 (10.0-24.0 (10.0 (7.8-20.34-10.66) 4.0-29.10) 6. < LOD means less than the limit of detection.90-15.80-4.3) 22.60 (6.80-12.01 (2.45 (3.64) 10.31-12.70 (1.3 (9.73) 7.98-9.10 (.00) 3.0) 7.67) 4.42 (1.7) 15.75 (2.49-4.40 (2.50-5.90-9.39 (5.8) 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 1.0 (8.0) 9.S.6) 14.7) 16.670 (<LOD-1.0) 6.90 (6.3) 8.3 (7.58 (1.39-13.90 (6.00 (.00-9.97-4.1-23.00-16.0) 13.61-32.67-10.5 (8.60 (5.8-17.47-6.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10-10.30) < LOD < LOD .8) 8.00-4. population from the National Health and Nutrition Examination Survey.5 (9.58.2 (7.60) < LOD < LOD 2.0 (13.5.37 (3. 0.5-26.70-5.0) 23.61 (3.31-7.1 (10.12 (4.6 (10.0 (5.70-9.80) .80 (5.30) 8.7-21.20 (<LOD-2.99 (3.00) 3.9-14.680 (<LOD-1.89) 2.00-18.9-15.0 (9.0) 12.670 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .4 (14.4 (10.0-24.670 (<LOD-1.30) 3.00) 7.90) 4.0 (9.8) 9.67) 3.910 (<LOD-2.20-4.20) .90-15.8 (12.3) 20.29) < LOD < LOD < LOD < LOD 3.1) 11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.92) 9.9) 16.0) 11.8 (12.40) < LOD < LOD 75th 2.80) 5. respectively.95 (5.80-14.7-19.20) 3.5) 21.80 (2.30) < LOD < LOD 4.52 (6.53 (3.00-4.29-4.5.7) 10.77-14.27) 4.20-18.3) 10.22 (6.3 (12.11-6.60 (2.9 (7.22 (6. 01-02.90 (5.670 (<LOD-1.970 (<LOD-2.3 (6.80-6.3 (9.35-3.5 (8.84-4.46-4.50) .41-5.

6-19.86 (3.88-7.12) < LOD < LOD 4.590 (<LOD-.20-3.89-3.91-9.00) 2.6 (13.93 (<LOD-2.6 (13.42) 8.14 (2.9 (9.63 (2.8 (10.3 (7.2) 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.7 (10.9-25.28-12.7) 12.6) 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 1.75-3.2) 12.91) 3.07-3.55) 16.86-3.5 (11.77) 3.6) 14.95 (2.27) 5.8) 16.7-19.4) 9.42-19.4) 7.950) .890-2.41 (7.89 (2.71) < LOD < LOD 2.68-10.29-2.4) 7.28) 6.4) 6.2 (9.1 (19.7 (8.80) 3.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.6) 6.03) 3.4-15.85-8.0 (13.5) 22. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07 (5.850 (<LOD-1.61 (2.2) 12.6 (10.77 (2.30) 7.88 (1.52-3.810 (<LOD-1.32-8.11-3.42) 7.9 (9.68) .3-15.45) 3.3) 9.94-14.37) 3.05-3.89) 5.1) 13.69-11.78 (4.51-10.11 (5.39-17.29 (2.34) < LOD < LOD < LOD < LOD 3.4 (11.19) 3.09-11.4) 7.30) 2.0 (11.99) 2.77 (2.99 (4.9) 19.7) 14.54 (7.33-10.620 (<LOD-.760 (<LOD-1.S.50 (6.87 (3.58 (4.5 (8.780-1.78-10.1) 20.27-13.25 (4.79-6.44-6.27) 1.92) 3.74-4.82-11.12 (7.32) 2.00 (5.7) 14.06 (<LOD-1.78) 4.1 (13.75-3.79-9.95) 90th 8.72) 4.28 (1.0 (8.53-8.30) 8.8) 14.29) 3.47-9.4) 16.530-1.2 (9.3-21.5) 13.2) 15.5-17.0 (10.27) < LOD .85-17.2) 19.73 (5.89-13.0-19.55 (2. population from the National Health and Nutrition Examination Survey.6) 12.973 (.07) 2.6) 95th 16.93 (2.7) 15.8) 11.4-18.2) 16.72-4.910 (<LOD-1.23-3.6) 7.96-11.93-10.50-17.38 (2.55) .00 (7.78 (6.2-15.74-19.71 (1.7 (11.94 (5.92 (5.3) 8.51-7.9 (9.34-18.00 (<LOD-1.21-21.68-19.2-30.30-5.25-9.89-10.6 (11.89-3.00 (<LOD-1.2) 10.97) < LOD .45) 6.93 (6.64-11.3-17.67 (1.3) 12.38 (.3-34.5 (9.38 (1.3) 6.36 (2.07) 2.2) 8.67 (7.89 (3.21) * * * * * 1.15 (1.5) 10.7 (10. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .00) 8.03 (2.940) < LOD < LOD 1.83 (7.09-11.2) 12.63 (6.0) 14. Fourth National Report on Human Exposure to Environmental Chemicals 123 .0-21.54) 9.4-16.4) 15.6) 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 * * * * * * .54-5.4-16.01-5.5 (15.920 (<LOD-1.9) 16.1 (8.6 (11.6 (12.06) .16 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5 (10.16-14.29 (5.83 (6.15) < LOD < LOD 75th 2.68-4.59-3.70-2.03 (6.81 (7.04) 9.70-35.27) * * * * * * * * 1.6) 13.18) 2.96-10.95) 3.3-17.38) 1.690 (.82-8.1) 10.02-4.38-13.43 (2.6) 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 * * * .97-4.7-23.8 (8.00 (3.33) 3.00 (2.86) 9.9-17.7) 9.48 (2.37-5.5) 8.

respectively.960) .359-.720-1.592) * .22-3.22 (1.59-2.54 (2.09.425 (.240 (<LOD-.10-1.30 (.960) 1.73 (1.58 (1.584) .820 (.48 (1.75-2.650-.10) 1.280-.41 (2.759) * .18 (.740 (.00) 1.95-5.79) .20-3.970) .720-1.35) 1.08 (2.690-.94 (3.510 (<LOD-.29-2.45-4.540 (.1.36-4.41-5.54-2.440-.585) * * .50 (1.720 (.37-2.27 (3.40 (1.03) 1.50) 1.30 (.55 (3.46) 1.96-3.700) .60 (2.83) 1.00-4.09 (.459 (.960) .570 (<LOD-.15) 2.49) 2.88) 1.690-1.90) 2. population from the National Health and Nutrition Examination Survey.96-5.63 (1.31-3.970) 1.960-1.449 (.20 (1.69-4.710 (.592-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.34) 2.32 (1.930-1.77-2.590-.20) 3.70-2.39) 2.17) 1.780 (. and 0.390-.10) 1.510 (.20) 3.960 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.31) 95th 2.600 (<LOD-.388-.710) .01-3.570) * .20-2.80) 3.05-2.91) 2.880) < LOD .94 (2.86 (1.97 (2.990-1.580-1.20) 1.46 (1.95 (2.550 (.33-2.80 (2.570 (<LOD-.94) .730) .20 (2.59-6.50 (1.70 (1.32-1.86) 3.31) 2.50 (1.80) 3.30-3.570 (.22-2.505 (.710 (.860) < LOD < LOD .592) * 50th .17) 1.980) 1.89) .13) .20) 2.26) .32) 3.160 (<LOD-.580-. and 03-04 are 0. 01-02.00 (1.618) * .570 (.90) 3.20 (1.74-5.201-.89-6.68-5.20-1.930 (.75 (2.87-3.65 (2. < LOD means less than the limit of detection.500 (<LOD-.350-.31-3.16) 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.210 (<LOD-.70 (1.83) .80 (1.560-.76 (1.750-1.350-.76-6.467 (.587) * * .620-1.303-.490 (<LOD-.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 * .670) .457 (.455 (.98-3.30) 4.910-1.45 (2.600-1.29) 1.800 (.600-.940) < LOD .460-.04) .18 (1.49) .79) .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 * .25-1.700) .910) 1.80) 3.30-3.30-1.382-.657) * * .390-.2.80) 2.30) 1.16-3. see Data Analysis section) for Survey years 99-00.60) 3.380-.930) 1.26 (2.22-8.42-2.20-2.343 (.04) 1.13) 2.17-4. which may vary for some chemicals by year and by individual sample.30 (1.11-3.780) . interval) Selected percentiles ( 95% confidence interval) Total * .740-.47) 2.60-4.690 (.40 (1.46 (2.30 (.48 (2.98 (2.400) .30) 2.27 (2.740-1.950) 90th 1.00) 2.70 (1.380) .83 (2.60) 2.90 (1. 124 Fourth National Report on Human Exposure to Environmental Chemicals .23-3.910 (.340-.70-7.47 (1.34) 2.380-.95) 2.46-3.90) 2.680-1.820 (.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 * .14-1.11-3.45 (1.S.80) 2.850) < LOD .50 (1.83) 2.14 (1.89) 1.830 (.61 (1.690) .20) 2.57 (2.790 (.16) 1.10) 3.50 (1.01) .22-3.57 (1.90-4.353-.77 (1.54) .73-5.38) 1.10-1.50-2.74) 3.80) 5.810) .260 (<LOD-.50-2.45 (1.597) * .73 (2.01-1.20 (1.10) 1.15) 2.680-1.19-1.30) 4.450 (<LOD-.760 (.98) .550 (.453 (.21) 3.64 (1.398-.570-1.750) 1.83 (2.880) < LOD 75th .08 (2.780 (.00-2.549 (.740 (.949) . 0.336-.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.840 (.749 (.05-3.930) < LOD .880 (.20) 1.78) .

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 * . interval) Selected percentiles ( 95% confidence interval) Total * .60) 1.70 (2.16) 1.72 (1.740) .87 (2.31-1.10) 2.00-1.470 (<LOD-.62 (1.90) 2.17) 2.460) .07) 1.08) 1.67) 1.22) 4.660-.57-2.830 (.300 (<LOD-.270-.08 (2.22-3.75) 6.08-3.580-.23) 3.61-3.740) < LOD 1.07) 1.320-.840) .471-.08-3.72) 1.230 (<LOD-.04-5.460-1.42-8.700 (.73-3.597) * .89-3.60 (1.645) .75 (2.64 (2.377-.00-3.73 (2.89 (1.28 (1.900) 1.38 (1.22 (2.30) 3.95) 1.348-.22-2.80) 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 * .16-1.75-3.850) 1.940-1.77-4.05 (1.490 (.380-1.460 (.42) .36) 3.07) 5.470) .510 (.32) 5.34 (1.04) 95th 2.550-1.14 (2.71) 2.760) < LOD 75th .88 (1.03-1.99) 2.950-2.368) * .690) < LOD < LOD .305 (.500-. population from the National Health and Nutrition Examination Survey.22) .930-1.58 (1.480-1.509 (.253-.485) * * .22) 1.07) 1.65) 2.453 (.67 (1.11 (.580) .560 (.20-7.79) 1.71) .92-8.13 (1.560-.550-.03-2.32 (.97 (1.91 (1.81) 2.62 (2.17-2.535 (.70 (3.02-3.370-.870 (.08-2.790 (.720-1.390) .280 (<LOD-.510-.52) 3.42 (.02-6.23 (.800-1.82) 2.67-3.88) .50) 1.69 (3.44) 2.33) .840) 1.94) .380) .92) 3.57 (3.55-3.560-.08-2.09) .58-6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.77 (3.23) 2.38 (2.390-1.552 (.720 (.590-1.57 (1.60 (2.310-.06-2.25-3.50 (1.750 (.820) .72 (2.57-4.71 (1.08-3.630) * .23) 1.393 (.550) .920) .591 (.760) .61 (3.990-1.45 (1.234 (.32-1.97 (1.910) < LOD .11) 1.700 (.530 (.92 (1.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.640 (.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 * .447 (.30-2.63 (1.99) 1.448 (.53) . Fourth National Report on Human Exposure to Environmental Chemicals 125 .520 (.69 (1.02-3.33 (1.08) 2.22-3.32) 2.24) 4.07-3.98) 1.06) 4.310 (<LOD-.82 (2.04-1.20-2.45 (2.29-4.710 (.43) 2.05-4.670 (.47-4.580 (.730) .520-.05-2.285-.250 (<LOD-.412-.43) 1.11-2.61-3.97) 1.540-.870) .510 (.58) 3.270-.372 (.66) .700 (.42-6.480) .60) .400) .640 (.80) 2.38-3.270 (<LOD-.18-2.97) 2.320-.710 (.750 (.05) < LOD .310 (<LOD-.79 (1.07 (.19 (1.64 (2.830) 90th 1.318-.75 (1.335-.55 (1.840) 1.550-.739) * .800) < LOD .07-2.980-1.84 (2.41 (.67) .44-2.43 (1.330 (<LOD-.61) 2.680 (.300-.17) 2.05) 1.440-1.47 (1.78) 3.77-3.688) * .250 (<LOD-.39) 2.39 (1.76) 1.330-.444-.S.08-3.66 (2.52 (1.47 (1.32) 1.180 (<LOD-.515) * * .72-4.820) 1.43) 2.08-2.23) 2.380-.790) .590) * 50th .16-2.49 (1.742) * * .49-4.00 (3.640 (.710 (.350) .136-.403) .08 (.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.880) 1.20) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.84-6.590 (.400-1.67 (1.

70) 1.1 (22.26 (.0) 18.2 (19.58) 16.50-5.0 (38.79 (1.83-2.470 (<LOD-1.90 (1.70 (1.13 (1.67 (1.54 (3.0-49.0 (38.9-51.5 (24.85) * 2.0 (24.0) 17.53) * 2.63-6.92-5.48-2.66-5.04 (<LOD-2.43-7.87-7.0) 45.70 (1.2-26.1 (25.1) 18.0 (20.7-22.18.57-2.0) 28.20) 1.71) 5.6-22.45) 2.9-21.3) 31.4 (15.90 (1. and 0.10 (7.9) 17.3) 28.690-3.0-53.40) < LOD 1.54 (1.3) 33.86-3.44) Selected percentiles ( 95% confidence interval) Total * 2.0-43.81-3.98) * 2.12 (3.1-19.80-2.5-45.97) 6.05-3.79 (2.17-2.70 (.0) 15.9) 48.2-33.0) 28.00 (.0 (8.10-13.2 (12.0 (8.6) 52.5) 30.8 (26.1-47.9 (27.45) 2.1) 140 (46.0-230) 35.1) 95th 48.3 (10.93-3.0 (13.69) 2.2-39.7) 20.8 (12.71-2.0) 16.9 (10.1-46.46-6.0-41.0) 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 2.30-14.3) 26.0 (6.16) 2.0-41.50-20.9 (19.74-2.0) 4.0-52.9) 38.31-6.1 (25.0 (7.76 (2.02 (2.3 (24.0) 20.50 (2.25-3.7) 47.4.00-24.610 (<LOD-1.8) 41.0) 4.59 (1.6 (9.1 (11. which may vary for some chemicals by year and by individual sample.70-6.0-31.0 (38.57-2.95 (5.82 (1.21 (3.4 (19.44-7.19) 2.19-2.2-27.30) 4.530-4.0-92.32 (2.41) 1.36-2.53) 40.10 (1.0-53.8-21.2-62.0-47.5-74.70 (7.09 (4.10) 39.0 (17.07-5.29-4. 0.30) 11.0-62.7 (28.10) .64-3.8) 62.11) 2.2-47.0 (38.0 (38.61 (1.5) 69.92) * 2.830-3.13 (1.2) 31.7-41.1 (10.71 (4.65 (4.05) 1.80) 90th 38.3 (12.0) 3.0 (38.4) 19.0-39. interval) 1.00 (.80) .0 (25.49-2.6 (15.0-29.30 (.70) 5.0 (20.91 (4. see Data Analysis section) for Survey years 99-00.9 (19.0) 15.86 (1.78) 9.0-260) 34.0) 3.8) 32.1-25.50-7.40) 50th 2.0) 17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (2.0-39.61-2.660-2.14) 5.6-45.0) 32.0 (40.0-69.600-2.27-6.0) 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 2.90) 11.33 (5.06) * 2.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.5.83-2.9 (23.0) 33.0) 31.0 (8.60 (2.78 (1.18) 6.40-4. population from the National Health and Nutrition Examination Survey.0) 20.79-2.8-24.46-2.6-27.0) 42.3 (14.77) 38.0 (21.10 (1.83 (3.0) 6.50-17.2-27.0) 3.0 (33.80) 1.72 (1.96) 5.94 (1.7 (12. 01-02.8) 39.46 (.50-2.0 (11.80-18.77 (1.60) < LOD 1.12) 1.1-40.3 (23.13) 12.98 (1.44) 2.42) 1.80) < LOD 1.52 (4.0) 30.29) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 126 Fourth National Report on Human Exposure to Environmental Chemicals .10-4.21 (4.21 (1.3 (12.0) 5.99 (2.1) 38.0-58.11 (4.0 (38.0-110) 34.830-4.0) 3.9) 18.20-4.0-110) 42.5-40.23) 9.1-20.70) 1.53 (1.04) 3.29-9.26) 75th 11.40) < LOD 2.23-2.83 (1.0) 4.18) 14.75-14.6 (11.8 (22.41) 1.48) 5.53) 1.5-20. < LOD means less than the limit of detection.4 (10.0-62.44) 3.23-2.70-17.0) 19.85 (1.8 (12.S.4) 38.76 (2.48-2. respectively.5-27.4-76.7 (12.64-8.05) * 2.0 (19.3) 38.41) 5.1 (26.1) 38. and 03-04 are 0.0-50.35-6.41-4.90-8.0 (26.0 (32.18) 20.0-41.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 8.81-2.41 (1.88) 1.88) 3.0) 16.2) 16.4-22.59 (1.40-16.58-2.0) 13.0 (37.2-80.8) 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 1.6-54.6 (26.0-58.16) * 1.04-8.06 (1.10 (1.10 (1.

24 (1.2-34.45 (1.7 (24.68 (1.46-6.3-27.5 (41.7-47.8 (7.43) * 2.930 (<LOD-1.6-49.9) 54.7) 66.50 (2.36) 10.36 (4.59-2.86) * 3.22 (.79 (2.0 (23.4-71.75-6.2) 13.79-17.6 (11.80 (1.4) 12.57 (6.2 (8.37-2.75 (1.7) 26.38 (3.5-190) 30.17-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.16 (1.750 (<LOD-1.1 (33.870-3.14 (.0) 25.11) < LOD 1.1-22.66 (1.1) 13.88 (1.2-70.6 (27.80-8.34) * 1.5 (15.870-3.7) 34.8) 11.96) 2.1) 27.9) 3.3 (9.4) 3.7) 15.33) 2.40-4.5) 27.4 (11.66) 8.680-4.7-109) 22.50-5.3) 28.41 (2.28 (1.1-63.0 (32.1) 27.67-3.54-2.6 (24.5 (34.47-17.62 (2.6) 3.58-17.7-38.53) 1.48) 1.18) * 2.58-2.26-2.8-37.0-71.16 (1.35) .37 (1.1) 25.8) 23.51) .67-16.16 (1.83 (.0) 30.59-15.2 (9.06) 1.4) 14.0 (25.26-4.7-20.2) 33.8) 15.0 (39. interval) 1.55 (2.19-6.5) 70.91 (6.95-16.61-2.16-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.19) 5.899-2.4) 12.23-1.07-2.7-37.5 (13.88 (4.54-15.9 (7.70-4.33) < LOD 1.9-95.0-40.12 (1.7 (18.67 (1.09 (5.69-5.27) 50th 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.51) < LOD 1.6) 3.9 (26.9 (10.60) 4.9 (13.75 (1.27-3.90 (.670-1.8) 32.94) 19.25-3.0) 10.63-5.66 (1.2 (15.35 (2.6) 23.61-22.1) 17.7) 30.12) 3.2) 41.93) 5.9) 24.86) * 2.5-36.0) 48.03-2.72) 2.0-70.7-19.97 (1.0 (6.43-2.9 (19.5-97.02) 1.69-18.4-34.18) 3.46-5.07-2.1 (50.2) 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 1.4-67.2 (16.8) 3.99-4.95) 90th 32.28) 1.3 (20.00) 6.7-43.32-3.40 (2.94) 1.0) 47.7) 61.61 (1.2) 36.7) 23.2 (21.0 (23.9-18.47 (1.48 (4.45-1.30) 28.3) 13.6) 7.32 (3.01 (.06) 1.0 (17.83) .75) * 1.17) 2.21 (4.95 (2.4 (9.8-34.4 (12.1) 36.9-52.9-41.00) 1.0) 3.08 (1.29-5.6) 11.9) 24.56) 1.40 (5.6) 112 (40.1) 13.47 (3.88 (1.27) 10.59-2.870-3.33) 1.6) 19.2-28.68) 47.95-16.3-19.4 (21. Fourth National Report on Human Exposure to Environmental Chemicals 127 .44) 9.8-26.20-5.0 (19.20) Selected percentiles ( 95% confidence interval) Total * 1.33-5.15 (.4 (25.19 (1.60 (.3 (10.7 (11.22 (2.1) 25.5 (17.08) 1.88 (4.3 (10.8) 31.38) 5.14-8.06) 75th 9.5 (15.9-36.38-5.4-21.0-118) 29.82 (2.56 (2.70 (1.2) 13.7) 95th 51.43-12.52-4.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.4 (19.3 (8.5-43.1 (25.1 (34.19-14.2) 4.38-1.9) 12.31) 2.2-38.9-37.02 (.2-47.4-39.3-22.57) 4.6-32.6 (7.S.22-2.1 (12.94-20.71 (1.71) 8.0 (14.7 (10.46) 1.890-4.84-13.8-45.0) 13.0) 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 1.1) 52.5 (6.76-2.9 (39.03) 1.67 (1.62) 4.06-1.23) 37.1) 15.39 (1.22-3.3-42.6-51.40-7.4 (25.19) 5.8-43.02) * 1.4 (5. population from the National Health and Nutrition Examination Survey.18-1.35) 1.5 (8.64 (1.71-2.1 (39.2) 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 2.9) 3.82) 1.07) 9.00-16.27 (6.888-1.23) < LOD 2.91-2.860 (<LOD-1.6-38.46-22.96-16.00 (4.7 (18.1-60.52 (1.36-13.2 (22.11-2.

850 (. < LOD means less than the limit of detection.S.640-1.58) .870 (.60) 1.110-.360-.200) < LOD < LOD .410-.162) * * * * * .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 * * * * * * . and 0. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.430-.730-.680 (.450 (.830 (.320 (.410-1.160) .40) .130) .700-1.100 (. respectively. which may vary for some chemicals by year and by individual sample.720) .171) * * .090 (<LOD-.490 (.15) .700-1.400-.080 (<LOD-.120 (<LOD-.310 (.610-1.310-.620 (.820 (.117 (.610-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.220 (<LOD-.00) .380-.10 (.450 (.990) .1.540) .330-.530-.470-1.840) .870) < LOD .370-.650-1.20) . 128 Fourth National Report on Human Exposure to Environmental Chemicals .190 (.830) < LOD .090 (<LOD-.640) . population from the National Health and Nutrition Examination Survey.230-.290 (<LOD-.150) .240 (<LOD-.310 (.700-1.42) .360-.390 (.420-.570) .150 (<LOD-.940 (.850) < LOD .210 (.860) .180) .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.300-1.30) .600 (.30) .870 (.1.730) .550) .090 (<LOD-.760) < LOD .720 (.830 (.410-.700-1. and 03-04 are 0. 01-02.090 (<LOD-.780) < LOD 1.30) .130 (.680-1.540) .430 (.560 (.680-1.080 (<LOD-.210 (.230) .160-.220 (.350) < LOD < LOD < LOD < LOD .610 (.10) .830) .680) .290) < LOD < LOD < LOD < LOD .630 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th . see Data Analysis section) for Survey years 99-00.870 (.820 (.270 (.990) .990 (.140-.140-.650) .260 (.630 (.090 (<LOD-.084-.13) .290) < LOD < LOD < LOD < LOD 90th .280) < LOD < LOD < LOD < LOD .460 (.310) < LOD < LOD < LOD < LOD .650) .370-.930 (.42) .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 * * * * * * * * * .120-.610 (.770) < LOD 95th .840) .36) .12 (.300-. 0.650 (.660 (.170-.190 (.640) .390) < LOD < LOD .130-.099-.03) .870 (.850 (.450 (.140-.860-1.900 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .380-.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 .560 (.740) < LOD .510-1.140) .380-.32) .090 (<LOD-.310) < LOD < LOD < LOD < LOD .720-1.640 (.050-.320-.160) .10) .650-1.410) < LOD < LOD < LOD < LOD .120-.190 (.350) .470 (.540 (<LOD-.10) .770 (.130) .130-.05.870 (.460-.440-1.130-.690-1.

570-.140) .12) < LOD .990) .410-.670 (.730) .850 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .330 (.360) < LOD < LOD < LOD < LOD .360 (.140-.100 (<LOD-.580 (.580) .880 (.180-.090 (.610-1.161) * * .300-.09) .640-1.460 (.140-.01 (.20) 1.03 (.200 (.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.650-1.110) .29 (.300 (.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .550 (.500 (<LOD-.570-1.940) .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.470 (<LOD-.270) < LOD < LOD < LOD < LOD .580-1.410-.380 (.230 (<LOD-.190 (.380-.600) .540 (.330-.080) .200 (.940) .520-.240-.730 (.070 (<LOD-.700-1.110) .750) < LOD 95th .057-.67) .370 (<LOD-.410 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380-1.170 (.310) < LOD < LOD < LOD < LOD .330-.400) .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 .00) < LOD .740 (.150-.540) .140-.116 (.990) .780 (.190 (.290) < LOD < LOD < LOD < LOD 90th . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .060-.230-.570 (.100-.380-.070 (<LOD-.700) .560 (.440-1.230) < LOD < LOD < LOD < LOD .210 (.S.320 (<LOD-.66) 1.280) < LOD < LOD < LOD < LOD .740) < LOD 1.730) .24) .500) .660-1.140-.960) .050 (<LOD-.450) .870) .410 (.670 (.070 (<LOD-.19 (.550 (.380-.03 (.270 (.02) .890 (.090 (<LOD-.860 (.330-.38) 1.080 (.390-.810 (.170 (.540 (.60) .300-.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 * * * * * * * * * .650) < LOD .36 (1.540) 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 * * * * * * .110-.190-.140-.43) .62) 1.260) .340-.880-1.860 (.360-.720 (.710-1.110) .260-.24 (.490-1.670-1.110) .220 (.03) .400 (<LOD-.084-.120) .970) .250-.600-1.390-.800-1.03 (.580) < LOD .070 (<LOD-.450 (.170) < LOD < LOD .360-.86) .410) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.700 (.78) .440 (.080 (<LOD-.760) .220) < LOD < LOD < LOD < LOD .120) .02-1.700 (.500-1.730) .58) 1.510-.780) < LOD 1.14) 1.86) .111) * * * * * .410) < LOD < LOD . population from the National Health and Nutrition Examination Survey.580 (.330 (.720 (.860-2.

90-20.0 (5.62-8.0) 2.14) .0 (13.74) 5.40-4.07-3.0) 3.10 (.90) .800) 90th 13.640 (.20-4.30-7.94-8.32 (1.910) 2.36-3.05 (3.70-17.0 (3.48) 13.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.0 (17.90-9.30) .00) .87) 12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.425-1.20 (1.07 (1.1.30) 95th 19.900 (.11) 13.620-1.10 (3.190-1. respectively.10-9.42) .00-17.730 (.67 (1.49) 17.60) .880) 5.05-3.0 (16.11 (1.55-8.10 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.330 (<LOD-1.49 (1.55-4.0 (17.65) 1.67 (2.15) 14.0 (5.0 (5.47 (3.51-8.S.18) 1.20-4.0) 2. 130 Fourth National Report on Human Exposure to Environmental Chemicals .45 (2.30 (1.750-1.0 (17.510-.0 (5.35) 5.380-.30-3.86) 4.960 (.63 (3.250 (<LOD-.90-28.30 (1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.14) 2.29-10.87) 5.49 (1.40-7.610 (.600 (.720) 2.00 (1.21-3.07 (3.52) 5.0) 2.370-.0 (4.13 (3.960 (<LOD-1.590 (.52 (1.0 (4.90) .53 (2.480-.350-.90 (1.07) 1.97) 20.83-3.580 (.400-1.33 (4.691 (.0) 4.0) 4.46 (1.16) 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 .67) .31) .80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.30 (. population from the National Health and Nutrition Examination Survey.85-3.68) 2.00-17.61 (1.10-3.26 (2.66) 4.00) .20) < LOD < LOD < LOD < LOD < LOD 1.28-9.00 (.97) 20.31-10.360-1.0) 7.1.83-3.0) 2.6) 5.0 (17.0 (7.32-9.0) 2.37) .350-.0) 2.0-38.07 (3.830 (.0) 2.94 (1. which may vary for some chemicals by year and by individual sample.30-6.83) 2.15) 19.76 (1.110 (<LOD-.890 (.70-30.20-17.770 (<LOD-1.90-37.0) 5.96 (1.50) . and 0.0-44.53) 20.53-7.40) 2.99 (1.0) 5.080-1. see Data Analysis section) for Survey years 99-00.39) .0 (6.840 (<LOD-1.03 (.260-.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 * * * * * * .690 (.63) 32.60) 1.90 (2.0) 4.610) < LOD < LOD < LOD < LOD < LOD 2.05 (2.0-40.70-50.0-38.74 (3.640 (.01) 5.800-4.12-1.850) 16.30 (1.70-7.750-2.40-20.99) 19.52 (1.59-5.740 (. 01-02.35-10.0-40.99) 11. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.23-6.840-3.08. and 03-04 are 0.48 (2.0 (17.28) .40-8.30 (2.20 (1.40 (1.800) 17.0-39.11) .14-5.88-3. < LOD means less than the limit of detection.24-7.0) 4.39 (2.40 (1.80 (4.770) 2.70-3.28) 1.36-3.43-4.07-3.51 (2.50) 2.3) 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 * * * * * * * * * .0 (5.40) 1. 0.870) < LOD < LOD .0) 5.82-4.0-38.42) 2.840 (.0) 5.170-1.35) 11.38-3.10-3.94-3.21) 3.70) 2.210-1.90) .12) * * * * * * * * .00) 1.

52 (.580 (.00) .260-.310-.30 (4.18) 1.31) .11) .560 (.8) 4.31) .8) 2.88 (2.580) 1.96-8.540 (.75) 5.50 (4.48-7.22-27.97) .748 (.780-4.5 (9.850-3.86) .710 (<LOD-1.5 (11. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.620-3.55 (3.37) 4.8 (20.47) 5.14 (1.56) .56 (1.60 (1.17) 5.51-44.9) 5.2-38.8) 7.69) 2.29 (4.15) 9.56) 2.8-33.700) 6.48 (4.45 (1.83 (4.660) < LOD < LOD .47-10.340-.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 * * * * * * .474-1.500 (.39) 20.14-6.10-3.10 (2.940-4.830-3.31-18.5) 2.00-19.04 (1.40 (.24) 3.40) 1.84) 9.67 (2.7) 3.240-.32) 9.33 (3.55) 21.1) 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.66-47.820) .57-40.35 (.01 (1.49-2.91) 2.960 (.730-3.47) .330-1.8) 2.430 (<LOD-.890 (.370-1.18) * * * * * * * * .790 (.430) 1.80) 3.25 (1.28-6.3) 3.81-17.0 (9.33-3.5) 7.360 (.5 (8.86 (3.43) .44) .800-2.9) 6.57) 8.740-1.320-1.930) .260-.02 (1.340-.32-6.7) 6.67) 2.670 (.08) .67-6.09-3.33-5.89 (2.17 (1.5) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.48-42.62-17.29-4.06 (.S.270 (<LOD-.630-1.07 (2.50) 11.23-7.25-38.860-2.370) < LOD < LOD < LOD < LOD < LOD 1.82-11.40-2.03) 16.650 (.4) 2.7 (6.390-.02 (.580-1. Fourth National Report on Human Exposure to Environmental Chemicals 131 .18) 95th 21.88) 17.27 (2.700) < LOD < LOD < LOD < LOD < LOD 1.33 (1.540-1.9 (11.21-3.7) 4.61) 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 .65 (2.7 (12.190-1.370 (.36 (.10) 2.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.4-34.12 (4.02-4.13 (2.96) 2.73 (4.64) 30.590) 2.12-4.4 (4.38 (2.51-4.1 (7.85 (1.53) 27.85-3.57) 1.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.840-3.79 (.3) 2.600 (<LOD-1.8) 7.57 (.07-21.33-4.91-4.80 (.450 (.90-6.340 (.470 (.59 (1.05) .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 * * * * * * * * * .47-10.88-3.69-7.44-11.770) .41) 18.2 (8.1 (5.71 (2.67) 1.5-40.970-3.1) 2.50) .150 (<LOD-.04-16.8) 1.83-11.0) 4.02) .650) 90th 10.40-12.11-5.71 (.580) 16.820 (.92 (2.830 (.88 (.74 (2.55) 21.250 (<LOD-.53) .62 (1.790) 11.690-5.98 (4.340-.64-4.31-7.50 (2.22) 2.7) 5.96-25.25-9. population from the National Health and Nutrition Examination Survey.0 (4.270-.41 (4.03) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.77 (.

Ann NY Acad Sci 1997. Barnhart S. Urinary excretion of alkylphosphates in the general population (Italy). 132 Fourth National Report on Human Exposure to Environmental Chemicals . Sci Total Environ 1996. Pilkington A. Garrison RP. Franklin CA. Bouvier G. Environmental and biological monitoring of exposure to organophosphorus pesticides: application to occupationally and non-occupationally exposed adult populations. Kissel JC. Occup Environ Med 2003. Fenske R. Charnley G. Toxicol Ind Health 1998b.111(3):377382. Gillham RA. Bozzi N. Kipen H. The effects of occupational exposure to chlorpyrifos on the neurologic examination of central nervous system function: a prospective cohort study. Eskenazi B. Barr DB. Berent S. Barr DB. Surveillance of occupational. Young AD. Environ Res 2001. Denley HV. et al.32(5):487-496. Sciarra G. Fenske RA. Sartorelli P. Angerer J. Greenhalgh R. neurophysiological.111(13):1640-1648. Strambi M. Keifer MC. Cumulative organophosphate pesticide exposure and risk assessment among pregnant women living in an agricultural community: a case study from the CHAMACOS cohort. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies.177:37-41. Anger WK. Blanchard O. 2005. Fenske RA. J Toxicol Environ Health 1981. et al. Schweitzer SJ. Griffith W. Fenske RA. Lunghini L. Garabrant DH. Neuropsychological performance among agricultural pesticide applicators. and incidental exposure to organophosphate pesticides using urine alkyl phosphate and phenolic metabolite measurements.15(2):164-171. et al. Miller M. Freshwater KJ.38(1):91-97. Costa LG. Reprod Toxicol 1998a. Arcury TA. Giordani B. Momas I. accidental. Quandt SA.12(6):619-645. Peterson JC. Arch Environ Health 1998. Grzywacz JG. Temporal association of children’s pesticide exposure and agricultural spraying: report of a longitudinal biological monitoring study. Harnly ME. Davies JE. J Expo Anal Environ Epidemiol 2005. Davis SW. Am J Ind Med 1997. Amr MM. Leffingwell JT. Lu C. Astroff AB. Abdelrasoul GM. Seta N.837:257-268.49(9):751-760. Long-term use of organophosphates and neuropsychological performance. Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 2000.110(8):829-833. Environ Health Perspect 2002. Hawk R. Eigenberg DA. The effect of the 14-day agricultural restricted entry interval on azinphosmethyl exposures in a group of apple thinners in Washington State.46(4):367-378. McKone TE. Farahat TM. Di-alkyl phosphate biomonitoring data: assessing cumulative exposure to organophosphate pesticides. Abdel-Azis M. Richardson RJ. Chen W.108:521-525. Bradman A. Fenske RA. Neurobehavioural effects among workers occupationally exposed to organophosphorous pesticides. 86:80-87. Organophosphorus pesticide urinary metabolite levels of children in farmworker households in eastern North Carolina. Farahat FM. Daniell W.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites References Albers JW. Demers P. Heudorf U. Centers for Disease Control and Prevention (CDC). Am J Ind Med 2006. Barr DB.59(7):434-441.37(3):382-395. Aprea C. J Expo Sci Environ Epidemiol 2006. Engel LS. Koch D.60(4):279-286. A clinical neurological. Novelli MT. and neuropsychological study of sheep farmers and dippers exposed to organophosphate pesticides. Castorina R. Curl CL. Atlanta (GA). Orsi D. Checkoway H. Organophosphate urinary metabolite levels during pregnancy and after delivery in women living in an agricultural community. Fisker-Andersen J. Barr DB.14(6):869-889. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Regul Toxicol Pharmacol 2003.16(5):417-426. et al. Lu C. Aprea C. Occup Environ Med 2002. Elgethun K. Kissel JC. Correlation of urinary pesticide metabolite excretion with estimated dermal contact in the course of occupational exposure to Guthion. Environ Health Perspect 2003. The relationship between maternal and fetal effects following maternal organophosphate exposure during gestation in the rat. Curl CL. Curl CL. Vaughan TL. Eskenazi B. Jamal GA. Mathieu L. Environ Res 1992. et al. Shebl MM. Fiedler N. Krieger RI. Astroff AB.59(1):217-228. Kedan G. Chukwudebe A. Duggan A. Robinson LR. Environ Health Perspect 2005. Bradman A. Regul Toxicol Pharmacol 2003. Castorina R. Jolley L. Environ Health Perspect 2003. Chevrier J. Sartorelli E. Buchanan D. J Occup Environ Med 2004. Metabolites of organophosphorous insecticides in urine specimens from inhabitants of a residential area. Bravo R. Hansen S. Neurophysiological function in farm workers exposed to organophosphate pesticides. Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets. Kelly-McNeil K.53(1):714. Boccalon P.113(12):1802-1807.7(5):715-731. Biologic monitoring of exposure to organophosphorus pesticides in 195 Italian children. Eaton DL. et al.

Narang A. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Thompson ML. Weerasekera G. 2004. Chronic neurological sequelae of acute organophosphate pesticide poisoning. U. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities.114(5):691-696. Chrislip D. Bravo R. Pesticides in the Diets of Infants and Children. Santana J. et al. Occup Environ Med 2001. 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. et al. Terry AV Jr. discrimination. Petchuay C. Washington (DC): U. Neurotoxicity among pesticide applicators exposed to organophosphates. Jamal GA. Bradman A. low-level exposure to the organophosphate diazinon. Occup Environ Med 1995. Pilkington A. Office of Prevention Pesticides and Toxic Substances. et al. Claypoole K. Arch Environ Health 1988. Lambert WE. 1/12/09 Peiris-John RJ. Aprea C. Ames RG. EPA).20(2):115-22. Stark A. Nell V. National Research Council (NRC). Berry H. Pedersen L. Wickremasinghe AR.12(2):134-141. Stephens R.12(2):153-172. vibration sense and tremor among South African farm workers. Daniell WE. Irish RM. Visuthismajarn P. Lasarev M. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Kidd M. Buchanan D. van der Hoek W. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Calvert IA.S. Takamiya K. Phillips J. 4/7/09 Young JG. McConnell R. Rohlman D. Steenland K. Johnson C. Effects of chronic. Chronic neurological sequelae to organophosphate pesticide poisoning. Lancet. Pesticide industry sales and usage . Scand J Work Environ Health 1998. Barr DB. Masala G.2000 and 2001 market estimates. Savage EP. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Myers JE. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Jenkins B. Schenker M.113(4):504-508. Environ Health Perspect 2005.84(5):731-736. Neurotoxicology 2005. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Arch Environ Health 1975. O’Malley M.nap. London L. Effects of long-term organophosphate exposures on neurological symptoms. 1991. low-level organophosphate exposure on delayed recall. 1993 [online]. Environ Health Perspect 2006. Muniz J. Samuels S. May. Rothlein J. Robson MG. Scherer J. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Hore P. Weisskopf C. Beach J.332(1-3):71-80. Int J Occup Environ Health 2006. and cholinesterase status of date dusters and harvesters in California.epa.345(8958):11351139. Keifer M. Saieva C. Burcar PJ. and spatial learning in monkeys and rats. metabolite clearance. EPA.58(11):702710. Lewis JA.S. Stokes L.php?record_id=2126&page=1. Hansen S. Rodnitzky RL.52(2):190-195. Keefe TJ. Vitayavirasak B. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. McCauley L. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Available at URL: http://books. Ruberu DK. Malathion deposition. Eskenazi B. Lancet 1995.68(3):209-227 Maizlish N. Dinoff TM. J Toxicol Environ Health A 2005. Washington (DC).edu/ openbook. Rothlein J. Lu C. Tumino R. Salvini S. Mounce LM. Seiber J. Russo J.38(4):546-563. S. Smit LA. et al. Levy LS. Prendergast MA.44(4):352-357. The Pesticide Health Effects Study Group. Buccafusco JJ. Neurotoxicol Teratol 1998. Gillham R. A behavioral evaluation of pest control workers with short-term. J Occup Environ Med 2002. Arch Environ Contam Toxicol 2000.26(2):199-209. Am J Public Health 1994. Environmental Protection Agency (U.52(10):648-653.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Gladstone EA. Muniz J. Am J Ind Med 1987. Spurgeon A. et al. Available at URL: http://www.pdf. Caltabiano LM. Frasca G. Neuropsychological effects of long-term exposure to organophosphates in sheep dip.43(1):38-45. Fourth National Report on Human Exposure to Environmental Chemicals 133 .30(2):98-103. Marshall E. National Academy of Sciences. Sci Total Environ 2004. Bull Environ Contam Toxicol 1994. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function.338(8761):223-227.24(1):18-29. Lasarev M. Heaton RK. Rosenstock L.

parathion and methyl parathion are metabolized to para-nitrophenol.” 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.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. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. For example. For general information about the organophosphorus class of insecticides. In addition to reflecting exposure to the parent insecticide. malathion is metabolized to malathion dicarboxylic acid. the level may reflect exposure to the environmental degradation products of these pesticides.5. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report.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 .

60 (2.50-8.and post-construction structural applications for termite control were to be phased out by 2005 (U.35) 2.50 (1.0) 15.7) 13.0 (7.0) 11. but can be detected in streams receiving runoff from application sites.87-6.55-5. 2005).40) 2.80-10.30 (2.0 (10.8-15.30-11.77) 1.51) 1. population from the National Health and Nutrition Examination Survey.0) 12. After 2001.0) 12.8) 9.40 (5.52-12.67 (2.0 (7. Approximately 21-24 million pounds per year were used domestically from 1987-1998. 2002). applied to structures to kill termites.02) 1.S.80 (7.00-8. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.7) 8. Survey Geometric mean (95% conf.16) 2.31-2.50 (2.5.10-17.97-7.81-2.3 (10.10 (5.66-15.97) 7.80) 12.89 (2.92 (1. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.30-1.02 (1.89-2.35) 1.98-15.32-1.60-4.5 (8.60) 5.20-3.90 (1.3) 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 1.13 (1.9) 11.7) 9.91 (1.95 (4.0) 12.67 (2.39) 4.90-4.97) 2.EPA.80) 2. staying bound to soil particles. 2921-88-2 Chlorpyrifos-methyl CAS No.27 (7.50-14.9 (10.20) 10.60-2.60 (4.4-15.25) 1.00) 2. and sprayed to kill mosquitoes.0) 9.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.00-24.19 (1.03) 1.45 (1.02 (7.78 (7.34) 1.9-18.0) 14.90 (6.51 (1.6) 7.0 (9.47-13.0 (7. Approximately 80.20-11.30) 5.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.30-9.17 (1.57 (2.84) 1.0) 12.70 (1.20 (2.3 (8.4 (8.24-3.63 (8.19-3.47-9.S.0) 10.7-23. and dust.50-2.70 (1. in 142 urban homes and preschools in North Carolina.5) 7.0) 10.44 (3.05-5.96) 3.77-15.52-2.0-28.50-4. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.40 (6.90-7.21) 3.60-3.47 (4.40-10. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.70-16.39-2.80 (1.86) 4.61 (1.76 (1.10 (1.74-9.30 (4.51-2.76 (1.70-15.40-26.50 (2.. It also has been applied directly on animals to kill mites.70-17.9) 697 660 521 701 602 947 Limit of detection (LOD.80-8. 2002).43-2.80) 1.8) 10. 1999.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.3) 8.9 (9.50 (2.29) 90th 7.46-2.70) 1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.60-3.0) 12.99-4.97) 2.01) 1. dermal. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al. The general population may be exposed to chlorpyrifos via oral.0) 8.59) 2.71 (6.1) 5.71 (2.37) 5.09 (3.32) 2.40-2. 5598-13-0 General Information The chemical 3.4 (9.15 (1.80) 4.88 (1.68-2.28-3.50-2.38 (3.4.36 (4.63 (1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.09 (2.53 (1.5-24. pre.25) 3. Estimated intakes from diet and water have not exceeded recommended intake limits.0 (7.74 (1.S. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.10 (3.13-3.43-2. USGS.60 (5.0 (13.30 (2. For instance. Fourth National Report on Human Exposure to Environmental Chemicals 135 .44-2.70-11.79-2.20-16.10) 2.90 (3.4 (10.9 (7.30-5.68 (7.64) 3.63 (2.1-16.50-5. interval) 1.20-2.00) 3. and inhalation routes.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.28) 2.5.05) 1. chlorpyrifos was no longer registered for indoor residential uses in the United States.000 pounds are used per year.90 (1.47) 1.00) 1.90) 7.90 (2.20) 2.67 (1.50 (1.37 (1.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.61-7.30-12.77-6.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.90-2.66-4.91) 16. 2007).20 (4.0) 6.59-2.20-4.22) 2. 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.31-2.2 (10.20) 2.20-14. It has low leachability.04-10.50-4.4 and 0.0 (7.90) 3.72) 2.83) 1.26) 7. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.61) 75th 3.30-2.77 (1.71 (1.95) 7.24-1. Exposure can also result from contact with contaminated surfaces.30) 4.40-13.20) 4.22 (1.0) 18.29-1.62-2. and is infrequently detected in ground water (IPCS.97) 4.EPA.0) 8.0) 7.40 (5.0) 10.37 (4.40) 9. Chlorpyrifos is Urinary 3.94 (4. air.04-10.47-11.10 (4.44-5.70-5.90-8. and on plants for days to several weeks.10) 6.30) 4.3 (11.72-4.

48 (1.16 (4.62-7.9 (12.88-8.24-4.83-2.62) 90th 5. 2005.0) 16.58 (1. and producing acute symptoms such as nausea.91) 10.92) 3.82 (2.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.51 (1.53-5.56 (4.5.1-38..1 (10.25-12.86 (1.92 (1.63-2.EPA.82 (3.56) 5.09 (1.30-4. Survey Geometric mean (95% conf.58) 1.78 (1.63 (4.29 (3.44 (1.83-11.47 (1.22) 1. In pesticide applicators.64 (1.97) 3.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.80-6.57) 2.0) 12.39 (2.45-1.24-5.31) 1.68) 1.43 (4.91 (3.1-21. Metabolic hydrolysis leads to the formation of TCPy.72) 1.42-2.91 (4.22 (4. 2006.11) 7.53 (2. population from the National Health and Nutrition Examination Survey.89) 4.05-1.85) 1.6) 9.99-8..82-4.01) 3.23) 14.85 (3.3) 8.71) 3.93 (1.45 (1.57-2. vomiting.66 (1. 2006b).88-9.19-1.72) 2.11-9.95 (1.33-7.80-11.64-2. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.33 (5.35-1.91) 2.5) 5.52 (5.24) 75th 2.83) 1.27-1..47-2.49-2.60-3.16) 6.21-1..22 (6.74) 1.73 (1.69 (1. cholinergic effects. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity. Slotkin et al. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.56 (1.4) 4.75) 6. weakness.17-4.09-3.S.44-6. and seizures.3 (7. 2002).19-2.07) 5.14-8.28) 2.06-4.01) 3..27-7.81 (3.95 (3.87-3.3) 8.3) 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. Thus.86 (3.82) 8. Urinary 3.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.24-24.. Based on animal data and human cholinesterase monitoring during occupational exposure.47 (1. 2005.03) 1.55 (4.91-4.63 (5. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.37 (1.00-8.93) 5.31-1.05-4. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).02 (5.50 (4.25-1.97 (2.32) 1.59) 3. Ricceri et al.47 (5. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.76 (3. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.38) 3. resulting in excess acetylcholine at nerve terminals. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.5 (6.42 (5. 2000).58-5.48 (2.44 (5. Betancourt et al.12) 1.93) 2.44 (6.85-4.88-10.33 (1.55) 1. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.02) 7.88 (1.20-1.55 (1.46 (1.94-14.97 (3. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.80-4. 2005.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.72-2.42 (6.35) 1.81) 2.12-1.80) 3.34-1.58 (1.57) 9.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.01) 1.39) 6.66) 1.06 (1.43-10.91) 1.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .88-8. 2006a..71 (1. 1984).15 (4.08) 6.21-6.64-7..20 (2..19) 6.93 (2.28) 2.76 (2.97) 3.90-9.7) 7.54 (2.24) 5.49-2. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.6) 10.2 (7.79-13.84-6. interval) 1.36) 1.0) 10.6-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.05-8.97-3.86 (1. neurotransmission.98 (7. TCPy is more persistent in the environment than chlorpyrifos itself (U.44 (1.75 (1.19) 3.94-12.70-4.31-4.940-1.14) 1.56) 2.85) 4.26-14. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.56-2. 2006.92-2.65-15.23-1.93 (4.68) 6.S.39 (4.85 (2.00-13.2) 6.8) 9.41 (1.17-4.77) 1.1 (7.22-6.57-2.44 (5.54) 5.0) 6. 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. Howard et al. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.33 (.09-1. paralysis.11 (2.49 (1.39-1.30-1.65-11.09-2.91) 1. and other metabolites. Once absorbed.46 (2.99) 1.33) 2.60 (1.66-11.06 (5.58) 5.96) 3.58 (4.05) 3. TCPy can also occur in the environment from the breakdown of the parent compounds.00 (7.12-3.07) 1.25-11.11 (2.40) 1.24 (1.00) 1.98 (6.24-1.91-13. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.88 (1.49-2.05-3.35) 2.62) 1. Roy et al.3) 9.88) 6.59-2.

Chlorpyrifos exposure and biological monitoring among manufacturing workers. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. Additional information about external exposure (i. Koch et al. CDC. Catenacci G.. Albers JW.Organophosphorus Insecticides: Specific Metabolites 2004. Giordani B. J AOAC Int 1999. Seidler FJ. Barr DB. Environ Health Perspect 2005.. Occup Environ Med 2006. 2005). MacIntosh et al.Reference values of urinary 3.S. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. Clayton CA. 2006). et al.S. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. Environ Health Perspect 2001.. Slotkin TA. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. Lioy PJ. Fourth National Report on Human Exposure to Environmental Chemicals 137 . Betta A.113(8):1027-1031.atsdr. 2005.. Meyer A.S.. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U.epa. EPA at: http://www. 2005.gov/toxpro2. Burgess SC. Aldridge JE. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity.. Perera et al. Biomonitoring Information Urinary TCPy levels reflect recent exposure. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. 2005). 2003.S. et al.. 1999). 2005).EPA.. Burns CJ. In Iowa farm families using several different pesticides.gov/pesticides/.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. representative subsample of NHANES 19992000 (CDC. 2004). Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections..html and from U..63(3):218220. the weighted population mean of TCPy measurements was approximately three times higher (Adgate.. Freeman NC. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Carr RL. Levels of TCPy in the U.e. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. Eberly LE. Magnaghi S.5. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S.. 2002). 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.109(6):583-590. but levels were roughly four to six times higher than the geometric means in the U. environmental levels) and health effects is available from ATSDR at: http://www. 2005).92(2):500-506. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. 2005.cdc. 1992. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. urinary TCPy levels in children were reported not to have increased (Hore et al. 2004).. References Adgate JL.. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al.. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. 2001). Aprea C. the geometric mean urinary TCPy levels were similar in parents and children. 2005). Barisano A. In Minnesota and South Carolina farmers who used chlorpyrifos. Curwin et al. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. population (CDC. Haidar S. 2005). but not chlorpyrifos.. Of 482 pregnant women living in an agricultural community. In a probability-based sample of 102 Minnesota children aged 3-13 years. 2001) and Italy (Aprea et al. U. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Betancourt AM. Whyatt et al. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al.82(2):305-312. 2007). Berent S. Garabrant D. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. 2000). Lotti A. et al. Following crack-and-crevice application of chlorpyrifos in their homes. Toxicol Sci 2006.

Seidler FJ. 4/7/09 Koch HM. Kinney P. Jewell NP. Reid TM.15(3):271-281.org/documents/jmpr/jmpmono/ v99pr03. Mandel JS. Environ Health Perspect 2000. Morgan MK. et al. Levin ED. Steenland K. Environ Health Perspect 2006. Sheldon LS. 1992. et al. Barr DB. Pesticide residues in urine of adults living in the United States: reference range concentrations. Ann Occup Hyg 2007. Howard AS.inchem. Angerer J. Wartenberg D. February 5.10(4):327-340. Barr DB. Lorenzini P. Slotkin TA. Irish R.114(2):260-263. chlorpyrifos.113(2):211-219. Striley C. Hines CJ. Environ Health Perspect 2003. Barr DB. et al. Exposures of preschool children to chlorpyrifos and its degradation product 3. Environmental Health Criteria 198. Slotkin TA. Kromhout H. et al. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Gurunathan S. Pellizzari E. Shealy DB. 1999. Slotkin TA. 2921-882. Interim registration eligibility decision for chlorpyrifos. Hill RH Jr. Tate CA. Adgate JL. et al. Ryde IT. Environ Health Perspect 2005.5. Curwin BD. Neurologic function among termiticide applicators exposed to chlorpyrifos.15(4):297-309. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Alexander BH. Seidler FJ. Dick RB. Herrick RF.5. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Robertson GL. Edwards RD. Levin ED. Environ Health Perspect 2004.108(4):293-300.204(2-3):175-180. Environ Health Perspect 2006b. Lu C. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Bucelli R. Bennett DH. J Expo Anal Environ Epidemiol 2000. Capone F. Acquavella JF. Hardt J. et al. Hore P. Toxicol Appl Pharmacol 2005.nih.6-trichloro 2-pyridinol in their everyday environments. Nolan RJ. Bradman A. Baker BA. Environ Health Perspect 2006a. Freeman N. Jones PA. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Lioy PJ. Executive summary of safety and toxicity information. Scand J Work Environ Health 2005.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. U.155(1):71-80. Freshour NL. Seidler FJ. Toepel K. Heederik D. Barr D. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Tsai WY. Freeman N. J Expo Anal Environ Epidemiol 2005. Fortuna S.niehs. Ricceri L. Bravo R. et al. International Programme on Chemical Safety-INCHEM (IPCS). Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Howell RJ. Available at URL: http://www.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). 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. gov/ntpweb/index. Ryan L. Camann D. Toxicol Appl Pharmacol 1984. Temporal variability of urinary levels of nonpersistent insecticides in adult men.73:8-15. Zhang J. Chlorpyrifos: pharmacokinetics in human volunteers. MacIntosh DL.207(2):112-124. Honeycutt R.114(10):1542-1546. Bravo R. Toxicol Sci 2006. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites.51(1):53-65. Urinary pesticide concentrations among children. Ryan PB. Harley K. National Toxicology Program (NTP). Int J Hyg Environ Health 2001.112(10):1116-1124.9(5):494-501. Hein MJ. Roy TS. Bruun D. Croghan CW. Fenske RA. Available at URL: http://ntp. Gregg M. Robson M. Chuang JC. Sharma V. Jett DA. Environmental Protection Agency (U. Chapman P. Environ Res 1995. Chlorpyrifos. J Expo Anal Environ Epidemiol 2005. et al. Biomonitoring for farm families in the farm family exposure study. Rick DL.S. et al. et al. Weltzien E.6-trichloro-2-pyridinol. EPA). mothers and fathers living in farm and non-farm households in Iowa. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures.71:99108. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Third National Report on Human Exposure to Environmental Chemicals. Head SL. Meeker JD. Chrislip DW. 2005. Baker S. Yang D. Ozkaynak H. Lein PJ.S.htm. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Brain Res Dev Brain Res 2005. Atlanta (GA). Needham LL. Hammerstrom KA.31 Suppl 1:98-104. A longitudinal investigation of selected pesticide metabolites in urine. Saunders JH. Sanderson WT. Eskenazi B.111(2):201-205. 4/7/09 Perera FP. Cometa MF. J Expo Anal Environ Epidemiol 1999. Venerosi A.93(1):105-113. Rauh V.114(5):746-751. Bailey SL.

Pesticides in the Nation’s Streams and Ground Water. Fourth National Report on Human Exposure to Environmental Chemicals 139 .epa. February 2002. The Quality of Our Nation’s Waters. Barr DB. Camann DE. 2007 [online]. Kinney PL. 1992-2001.Organophosphorus Insecticides: Specific Metabolites 01-007.usgs.pdf. Available at URL: http://pubs. Geological Survey (USGS). 6/1/09 Whyatt RM. Environ Health Perspect 2003. revised February 15.S. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. 1/14/09 U. March 2006. Barr JR.gov/circ/2005/1291/.gov/ oppsrrd1/REDs/chlorpyrifos_ired. et al.111(5):749-56. Available at URL: http://www. Andrews HF.

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

200 (<LOD-.S. 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. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf.S.2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.270) < LOD 659 701 920 Limit of detection (LOD.380 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 141 .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.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 .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 .670 (<LOD-1. Survey Geometric mean (95% conf. * 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.200 (<LOD-. population from the National Health and Nutrition Examination Survey. 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 . 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 .

Nguyen JV. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. Eigenberg DA. Barr DB. Reprod Toxicol 1998. September 2000.epa. Sadowski MA.S.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. EPA). 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . Freshwater KJ. Third National Report on Human Exposure to Environmental Chemicals.S. 2005.pdf. Centers for Disease Control and Prevention (CDC). Environmental Protection Agency (U.376(6):808-815.12(6):619-645. Olsson AO. EPA 738-R-00-010. Anal Bioanal Chem 2003. U. Atlanta (GA).gov/oppsrrd1/ REDs/0018tred. Available at URL: http://www.

and forage crops. population from the National Health and Nutrition Examination Survey. 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. seed and foliar applications are planned to be phased out (U. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. an organophosphorus insecticide that is used to control insects on nuts. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. 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. Most granular formulations. Before these restrictions.45 (<LOD-3. It is toxic to birds. diazinon cannot be sold for residential use. Estimated intakes from diet and water do not exceed recommended intake limits (U. which may vary for some chemicals by year and by individual sample. Once absorbed. It is also used for cattle ear tag applications to control flies and ticks and.49 (<LOD-2. 2004).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. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. Prior to 2000. about 13 million pounds of diazinon were used annually on agricultural sites in the United States.S. vegetable. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. Survey Geometric mean (95% conf. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon.EPA. and other metabolites. in some pest strips. and particularly when it was ingested in granular form. 1998. in the past.2 and 0.7. Inhalational and dermal routes of exposure can be significant for pesticide applicators.S. < LOD means less than the limit of detection. but is rapidly absorbed orally (IPCS. Fourth National Report on Human Exposure to Environmental Chemicals 143 .S. since 2004. but these uses have been phased out. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. USGS.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. diazinon produced wild bird kills before use restrictions were in place. 2007). Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. fruits. 2004).05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. Diazinon is not well-absorbed through the skin. aerial.EPA. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. diazinon was widely used in residential and garden application. 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. 1998).

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

References Anthony J. Barr DB.gov/ oppsrrd1/REDs/diazinon_ired. J Expo Anal Environ Epidemiol 2000.gov/circ/2005/1291/.pdf. Liu F. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Barr DB. Ann Occup Hyg 2006. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Environ Health Perspect 2006.44(11):2243-2250. 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. Garfitt SJ. 4/7/09 Lu C. Geological Survey (USGS). In a small number of men visiting fertility clinics in Missouri and Minnesota. 1/14/09 U. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Fenske RA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1992-2001.S. Diazinon. Available at URL: http://www. Brunet RC.114(2):260-263.. Oloffs PC. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Toepel K. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. EPA 738-R-04-006.376(6):808-815. Redmon JB. Baker SE.epa. Bravo R. Kruse RL. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Atlanta (GA). In 23 children. Banister EW. 2005. Pewnim T. International Programme on Chemical Safety-INCHEM (IPCS). Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.37(4):501-507.. Olsson AO. Oloffs PC. et al. Noisel N. revised February 15. 2006). The Quality of Our Nation’s Waters. EPA). Toxicol Lett 2002. Nguyen JV.S. Bouchard M. Biochem Pharmacol 1992. 1998. Centers for Disease Control and Prevention (CDC). Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Needham LL. Beeson MD. Semen quality in relation to biomarkers of pesticide exposure. Swan et al. Interim reregistration eligibility decision (IRED.inchem.usgs.htm. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Available at URL: http://pubs. Banister E. Pesticides in the Nation’s Streams and Ground Water. Environ Health Perspect 2003. Bull Environ Contam Toxicol 1986. Anal Bioanal Chem 2003.S. Environmental Protection Agency (U. U.9(2):117-131. Barr DB. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. 2007 [online]. May 2004. Sadowski MA.50(5):505-515.Organophosphorus Insecticides: Specific Metabolites 2005). Study for Future Families Research Group. Effect of sublethal levels of diazinon: histopathology of liver. Available at URL: http://www. Seifert J. Carrier G. Environmental Health Criteria 198. Driskell WJ. Jones K. Irish R. Swan SH. 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. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Drug Chem Toxicol 1986. Rajendra W. Cocker J. March 2006.111(12):1478-1484. Diazinon. Dumas P. Mason HJ. Drobnis EZ. Third National Report on Human Exposure to Environmental Chemicals. 2006). In 54 Canadian greenhouse workers. Barr DB.10(6 Pt 2):789-798.134(1-3):105-113.org/documents/ehc/ehc/ehc198.

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

1993. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. Of 382 pregnant women living in an agricultural community. environmental levels) and health effects is available from ATSDR at: http://www. IARC considers malathion not classifiable as a human carcinogen. 2001.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. 2000).S. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. 1996..5 and 5.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. 2005). 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. Giri et al. Lu et al. 2006). 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. but isomalathion.EPA.epa. and it is not considered an animal teratogen or a reproductive toxicant. 2005. Malathion itself has not been considered genotoxic (U. Flessel et al. 2003).atsdr. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. 1987.. 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.. 2006)..html and from U.. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. representative subsample from NHANES 19992000 (Adgate. 1999. CDC. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Survey Geometric mean (95% conf.S. 2002. 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 3.50) < 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. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid.... population from the National Health and Nutrition Examination Survey.S.EPA.e. 2005).74 (<LOD-5. 1990).. Fourth National Report on Human Exposure to Environmental Chemicals 147 . Pluth et al. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. 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. but cholinesterase activity was not affected.gov/toxpro2. EPA at: http://www. Additional information about external exposure (i. Thomas et al. 1999).cdc. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. 2004). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Toxicity from unprotected bystander exposure during applications is rare (U..gov/pesticides/.. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. 2006). 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. Human studies of single oral doses between 0.S.

org/documents/jmpr/jmpmono/v2003pr06.73(1):182-94. A longitudinal investigation of selected pesticide metabolites in urine. Harley K. Freeman NC. Albertini RJ. Brunet RC. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . O’Neill JP.S. Griffith W. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.inchem. Atlanta (GA). Centers for Disease Control and Prevention (CDC).S.15(2):164-171. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. htm. et al.gov/circ/2005/1291/. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Third National Report on Human Exposure to Environmental Chemicals. Environ Mol Mutagen 1993. MacIntosh DL. Eskenazi B. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. et al. Reregistration eligibility decision (RED) Malathion. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.77:1009-1010. Samuel O.132(4):794-795. Pesticides in the Nation’s Streams and Ground Water. Lu C. Geological Survey (USGS). Carrier G. Available at URL: http://www. revised February 15. Jaloszynski P. Hammerstrom KA. Weltzien E. Quintana PJ. Lioy PJ. EPA).usgs. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Hertz-Picciotto I. EPA 738-R06-030. 6/1/09 U. Reproductive outcome in women exposed to malathion. 2007 [online]. Toxicol Sci 2003 May. Grether JK. Swan SH. July 2006.22(1):7-17. Mutat Res 2002. International Programme on Chemical Safety-INCHEM (IPCS). Cancer Res 1996.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. and cholinesterase status of date dusters and harvesters in California. Dumoulin MJ. 1992-2001. Bravo R. Needham LL.445(2):275-283. et al. Toepel K. Malathion (addendum). Irish R. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure.114(2):260-263. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Erratum in: Toxicol Sci 2003 Aug. 2005. Curl CL. Bradman A. U. Environ Health Perspect 2006. Neutra R.9(5):494-501. Mutat Res 1999. Gosselin NH. Prasad SB. The Quality of Our Nation’s Waters. Giri S. J Expo Anal Environ Epidemiol 1999. Sharma GD.74(2):following table of contents. Trzeciak A. Nicklas JA. Available at URL: http://www.gov/oppsrrd1/REDs/ malathion_red. 4/7/09 Kissel JC. Harris JA. Szyfter K. J Expo Anal Environ Epidemiol 2005.56(10):2393-2399. Goldhaber M. Thomas D. Flessel P.514(1-2):223231. Clayton CA. March 2006. Hooper K. Jewell NP. Petitti D. Genetic toxicity of malathion: a review. Environ Health Perspect 2001. Giri A.109(6):583-590. Lu C. Malathion deposition. Blasiak J. Environ Health Perspect 2004. Dinoff TM. Barr DB. Available at URL: http://pubs. Eberly LE.38(4):546-553. Fenske RA. Arch Environ Contam Toxicol 2000. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. metabolite clearance. Kedan G.pdf.epa. Ryan PB. Am J Epidemiol 1990. Krieger RI. Rappaport E.112(10):1116-1124. Barr DB. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Barr DB. Pluth JM. Barr DB. Environmental Protection Agency (U.S. Am J Public Health 1987. Bouchard M.

40-4.20) 5. which may vary for some chemicals by year and by individual sample.11-4.50 (1.85 (2.37-4.60) 1. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.70-6.1.70 (2.50-9.910) < LOD .60-5.EPA.700 (<LOD-.33 (1.30-5.10) 4.92-2. with limited applications in agriculture.0) 2.850) < LOD .20-5. Many previous registered agricultural uses of methyl parathion have been cancelled (U.21 (2.S.50 (1. Methyl Parathion. methyl parathion was rapidly absorbed after ingestion. Methyl parathion use is highly restricted.0) 3.45 (1.70 (3. Fourth National Report on Human Exposure to Environmental Chemicals 149 .71 (3.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No. < LOD means less than the limit of detection. Estimated intakes from diet and drinking water have been below recommended limits.90-9.57-4.40-3. Methyl parathion is not registered for residential use in the United States.60-24.80) 2.70-3.0) 4.11) 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 1.70 (<LOD-3.S.36-1. fish.47) 2.37-2.298-00-0 Ethyl Parathion CAS No.10-11.44) 2.300-.01) 695 660 518 679 603 941 Limit of detection (LOD.15-3.19 (. In the 1990s.02-6. and to a lesser extent. Morgan et al.70 (2.74) 5.28 (1.70-3. on cereal grains. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.32-1.12) < LOD < LOD 1.61) < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-1.80 (1.61) < LOD 1.80 (2.01-4.80 (2.10 (3.79) 4.60-36.0) 3.32 (1.770 (.50-14. Given its limited use. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. more slowly absorbed through the skin.40) 1. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.89 (2.20 (2. pulmonary.90 (1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.67) < LOD 1.910) < LOD < LOD . was once a restricted-use insecticide with limited applications on certain agricultural crops.990-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.70 (2. 2007).940 (<LOD-2.72 (3. Once absorbed. It had been applied to cotton.00 (2.26 (1. ethyl parathion..41-4.8 and 0.40) 4. all registered uses were voluntarily cancelled (U. population from the National Health and Nutrition Examination Survey. but by 2003. first registered in 1948.50) 2. and oral routes can occur in pesticide and agricultural workers (Muttray et al.28-4.49 (1.0) 3.32-1.730 (<LOD-.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .50) 1.58) 3.40) 2.50) 3.69 (2.13-1.60-19.69) 4.45) 5.27) 2.40 (1. 2002.EPA.18-3.00 (2..66 (2.30 (1.50) 3.50 (2.62 (1. binds tightly to soils resulting in low leachability.46 (3. and of the chemical nitrobenzene.S.71 (2.22-3. 2006).30-16.30 (2.10 (3. and aquatic invertebrates.21-1.90-11.50 (2.20 (<LOD-2.0) 3.92) 5. and eliminated rapidly from the body after absorption (Kramer et al.0) 3.10) 22.57) 1.790 (<LOD-.910) < LOD < LOD < LOD 1.70) 2.40-4.10 (<LOD-6. 2003).32-3.860 (<LOD-1.50 (1. Ethyl parathion.37) 2.70) 2.91-3. peak domestic use was as high as 5-6 million pounds per year.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .67 (1.34 (3.01) 4.70) 2. Increased risk of exposure via dermal. and has a short half-life in soils and on plants. In animal studies.16) < LOD 1.09-1.60 (4.0 (3.05) 4. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.33) 2.70-6.50 (1.30-3.48) 90th 2. 2000).37-4.. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Methyl parathion has low water solubility.70-6.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. 1977). Both are toxic to birds.00) 3.28 (1. Survey Geometric mean (95% conf.

95) 1.9) 1.55 (<LOD-3.26 (1. and producing acute symptoms such as nausea.500) < LOD < LOD .html and from U.60-2.23) 1.S. 2003. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.09) 2.940 (<LOD-1.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.17) . vomiting.05) 4.00 (1.30-1.07 (1.10) 90th 2.310-.56-2.80 (1.930 (.730-1.90 (1. 1991).06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .930 (.720 (<LOD-.71 (1.2) 2.31) < LOD .540) < LOD . Survey Geometric mean (95% conf.720-1.73 (1.. 2004). resulting in excess acetylcholine at nerve terminals.S.61) 4.13) 4. weakness.37-1.67-2. Methyl parathion is not considered genotoxic.35-3. 2005.79 (1. and other metabolites. cholinergic effects. EPA at: http://www.94-4.29 (2.80 (1.430 (. Lores et al.26) 17.11-4.57-2.2) 2.3) 2.970 (.97 (<LOD-4.640) < LOD < LOD 1.690-1.S.11) 1. gov/toxpro2..07) 2.23) 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 . methyl parathion.. Methyl Parathion.55) 2. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.00 (1.850-1.25) 1.76-14.atsdr.98-7.33-6.70) 3.96 (1.14-3. 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.370 (<LOD-.93 (2.980 (.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .97-10.78 (2. and seizures. gov/pesticides/. 2006.880 (.35-3. Slotkin et al..88 (1.25 (2. U.72-2. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS. paralysis. but lists ethyl parathion as a possible human carcinogen.01-3. 1995).33-3. ethyl parathion..15-10.cdc. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2004).15) 3.530) < LOD < LOD < LOD .7) 3.790-1.44-3. Thus. Additional information about external exposure (i.01 (2.680 (<LOD-1. 1995.08-3.20) .4 (3.38-3. 1978.82) < LOD .82 (2.94-47.84) 3.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .17-4.41-2. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.39 (1.. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.60 (1. 150 Fourth National Report on Human Exposure to Environmental Chemicals . At high animal doses of methyl parathion.950) < LOD .29) 1.86 (2. 1990.04) 1. Parathion and methyl parathion have high acute toxicity in animal testing.830-1.60) 2.71) 1.800-1.91 (1. In large doses.57-7. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.790-.67 (3.840 (. does not inhibit acetylcholinesterase enzymes. Orsorio et al..31-3. paranitrophenol.89 (2. Karanth and Pope et al. accidental exposure.44-3.29) 2. 2006.78) 2.08) < LOD . WHO.20 (3.87 (1.440 (<LOD-. Zurich et al.97 (2.59 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.92 (2. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.21-21. Jaga and Dharmani.88) 1. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.96 (1.33-3. The metabolite. population from the National Health and Nutrition Examination Survey.91) 1.04 (2.Organophosphorus Insecticides: Specific Metabolites Metabolites”).01 (.43) 4..epa. In addition to being a metabolite of methyl and ethyl parathion.00) 2.78-2. environmental levels) and health effects is available from ATSDR at: http://www.30) 3.1) 2.20) 3.79) 1.57) 6. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. and unintentional acute or chronic high-level occupational exposure (Hill et al.13-12.78-2.39) 1.870) < LOD . teratogenic.e.89 (2.16-4.21) 1.EPA considers methyl parathion unlikely to be carcinogenic to humans.10 (1.48-4.83 (1.970 (.400 (<LOD-.77-7.08 (1.

Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Ashley DL.. Weltzien E. Centers for Disease Control and Prevention (CDC). 2002). a range of values several hundred times higher than levels found in the U.15(2):164-171.. Bradway DE. ACGIH recommends a BEI of 0.. Occup Environ Med 1999. Rubin et al. Turner WE. and levels were similar or slightly lower that those in a small convenience sample of the U. Bradman A. 2005). Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. 2004). J Biomed Sci 2002. Lores EM.. Rockhold RW. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Leng G. population (Olsson et al. Dharmani C. Alley CC.215(3):182-190. Hill et al. 2005.S. Laboratory investigation of a poisoning epidemic in Sierra Leone.110 Suppl 6:1075-1078. 2002. Guizzetti M. Lu C. 1999). Pesticide residues in urine of adults living in the United States: reference range concentrations. Slach EF. Moseman RF. Runkle KD. Lin LI. Wellman SE. Atlanta (GA). Parathion-Methyl (addendum). Curl CL. McCann KG. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. and many residents were symptomatic (Barr et al.25(5):599-606. References Barr DB. Moomey CM. et al. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Harley K. Baker S. CDC.33(5):270-276. In a study of workers who handle parathion. 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. Barr JR. Baker SE. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. McClure PC. 4/7/09 Jaga K. Head SL. Cline RE. Jewell NP. Gregg M. Third National Report on Human Exposure to Environmental Chemicals. International Programme on Chemical Safety-INCHEM (IPCS). Morgan DP. Rev Environ Health 2006. McCann et al. Pope C. Hetzler HL.110 Suppl 6:1085-1091. Kramer RE. et al.5 mg (500 µg)/g creatinine for workers at the end of shift. 1995. Hryhorczuk DO.14(4):213-216. Arch Environ Health 1978. Bailey SL. 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.S. Available at URL: http:// www. Environ Res 1995. Hill RH Jr. Barr DB. 2005. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. 1995). et al. Griffith W..21(1):5767. 2005..org/documents/jmpr/jmpmono/v95pr14. Toxicology 2005. Lewalter J. Environ Health Perspect 2002. 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. Environ Health Perspect 2002. Giordano G. Baker RC.9:311-320. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Role of individual susceptibility in risk assessment of pesticides. oral or dermal administration. Hill RH Jr. Karanth S. Costa LG. Kissel JC. Shealy DB. et al. 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.inchem.6(2-3):159-173. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Eskenazi B.htm.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure.56(7):449553. Needham LL. Kedan G. Pathak S.. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.112(10):1116-1124. Neurotoxicol Teratol 2003. Arch Environ Contam Toxicol 1977. Head SL. 2002. Barr DB. J Anal Toxicol 1990. Chicago area methyl parathion response. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. DiPietro E.71:99108. 2005). Pesticide workers may have much higher levels following pesticide applications. general population (CDC. J Expo Anal Environ Epidemiol 2005. Clark JM. Environ Health Perspect 2004. Barr DB. et al. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Methyl parathion: an organophosphate insecticide not quite forgotten.

EPA). Available at URL: http://www. Case No. Osorio AM. Hill G.162(2-3):219-224. 1992-2001.pdf. Available at URL: http://www. Ohio. Yacovac R. Kieszak S. Interim reregistration eligibility decision (IRED) for Methyl Parathion.S.114(10):1542-1546. Hill RH Jr. Facts. Environ Health Perspect 2006. revised February 15.04/106.who. Olsson AO. Ryde IT. Methyl parathion in drinking water. Available at URL: http://pubs. 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. Anal Bioanal Chem 2003. September 2000. Jung D. pdf.epa. Geological Survey (USGS). Esteban E. Rubin C. Rosenberg J. Slotkin TA. May 2003.376(6):808-815.pdf. Available at URL: http://www.D. Mengle DC. R. Monnet-Tschudi F. 1/12/07 U. Costa LG. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Dunlop B. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County.S. 2004. Toxicol Lett 2006. Backer G. Pesticides in the Nation’s Streams and Ground Water. 5/19/09 Zurich MG. et al. Levin ED.S. Seidler FJ.110 Suppl 6:1047-1051.S.epa. 0153.E. Ames RG.usgs. Environmental Protection Agency (U. 1/14/09 U. 2007 [online]. Investigation of a fatality among parathion applicators in California. Sadowski MA. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Barr DB. gov/oppsrrd1/REDs/methylparathion_ired.gov/circ/2005/1291/. EPA-738-FOO-009. Environ Health Perspect 2002.int/water_sanitation_health/dwq/chemicals/ methylparathion. External and internal exposure of wine growers spraying methyl parathion.gov/oppsrrd1/REDs/factsheets/0155fct. Toxicol Appl Pharmacol 2004. Environmental Protection Agency (U. March 2006. The Quality of Our Nation’s Waters. 1995-1996.201(2):97-104. WHO/SDE/WSH/03. U. 6/1/09 World Health Organization (WHO).Organophosphorus Insecticides: Specific Metabolites Muttray A.20(4):533-546. Schilter B.S. Nguyen JV. Ethyl parathion. Am J Ind Med 1991. Letzel S. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Honegger P. Tate CA. EPA).

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

17 (.680 (<LOD-.780 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .500 (.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .27) .64) . population from the National Health and Nutrition Examination Survey.250 (<LOD-.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 .55) .300-1.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .21) < LOD .210-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 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.670 (<LOD-1.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .740 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.820) < LOD < LOD . Survey Geometric mean (95% conf. Survey Geometric mean (95% conf.430 (<LOD-.840) 669 687 929 Limit of detection (LOD.S.2.94) .580-1. 154 Fourth National Report on Human Exposure to Environmental Chemicals .780 (.950) < LOD < LOD 1.470 (.760 (<LOD-.210-. population from the National Health and Nutrition Examination Survey.200-.780 (<LOD-1.610 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07) .840 (. see Data Analysis section) for Survey year 01-02 is 0.930) 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 .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.15) < LOD .S.700-1.850 (. < LOD means less than the limit of detection.700-.780 (.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .740-1.210 (<LOD-.410 (<LOD-1.31) . which may vary for some chemicals by year and by individual sample.

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

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

Kim HS.. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. In developing rodents. Kuhn K. Leng A.8(1):197-202. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Toxicological profile for pyrethrins and pyrethroids. Agrawal AK. Richardson JR. Bernardi MM.251(3):855-859. 2002. Yamada T. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. 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. choreoathetosis. Moniz AC. 2006...atsdr. Shaw IC. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation.html. McCarthy AR. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Elwan et al. Garey J. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. 1998. et al. 2001. et al. neurochemical changes in cholinergic. salivation.. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. J Reprod Dev 2004. Varoli FM. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Shukla Y. Hu et al. Spinosa HS. Garey J. 2005).300(3):161-165. Shin JH.. Wieseler B. 2002). IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Generally.cdc. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Song L. Ranft U. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Neurotoxicol Teratol 2005. Hu JY.1/15/09 Aziz MH. and permethrin) in the Hershberger and uterotrophic assays. dopaminergic. Effects of prenatal exposure to deltamethrin on forced swimming behavior. 1999. Berger-Preiss E. Regul Toxicol Pharmacol 2002.. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. 2005). 1991.. Kuhn KH.27(4):609-614. 2003. Levsen K. Kim TS. Estrogenicity of pyrethroid insecticide metabolites. Kang IH. Fredriksson A. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Miller GW. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. References Agency for Toxic Substances and Disease Registry (ATSDR). Leng G.html. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays.. Lemonica IP. Pauluhn J. Lewalter J. Abell AD. 2002).gov/pesticides/ and from ATSDR at: http://www. Sunami O.atsdr. Caudle WM. and striatal dopamine levels in male and female rats. Yang J. Neurosci Lett 2001. Eriksson and Fredriksson.S. et al. Toxicol Appl Pharmacol 1991. 2001.50(2):245-255.108(1):78-85. J Environ Monit 2006.8(1):18-21. September 2003. 2005). 2004. Kim IY. 2003. Biochem Biophys Res Commun 1998. Leng G. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Wolff MS. Elwan MA. Florio JC. and seizures (ATSDR. Go V.62:101-108. Pogo BG. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. hypersensitivity. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley.. 2000. WHO. Salzgeber SA. Lee SJ.107(3):173-177. 2006. Pyrethroid pesticide-induced alterations in dopamine transporter function. Soderlund et al. cdc. Lazarini CA. Shafer. Idel H. Xenobiotica 1997. Int J Hyg Environ Health 2002. Bernardi MM. 2003. et al. Okuno Y.. bioallethrin and deltamethrin. Neurotoxic effects of two different pyrethroids. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Ray et al. tremor. Toxicol Appl Pharmacol 2006. Moniz et al. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Available from URL: http://www. 2003. Environ Health Perspect 1999. Seth PK. 2005). Kunimatsu et al. Guillot TS. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Wang SL. Sugiri D. fenvalerate. Eriksson P.27(12):1273-1283.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Adhami VM.23(6):665-673. Additional information about pesticides is available from U. Kim et al. Garey and Wolff. Bull Environ Contam Toxicol 1999. epa..211(3):188-197. Wolff MS. Cruz-Casallas PE. McCarthy et al. Leng G. Neurotoxicol Teratol 2001. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Idel H. Kamita Y. 2006). motor activity. EPA at: http://www. Go et al.gov/toxpro2. Lazarini et al..gov/toxprofiles/ tp155. Kunimatsu T. Zhao RC.. Chen JH. Thomson BM.205(6):459-472. In California. Ose K.35(2 Pt 1):227-237.

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

In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin).Pyrethroid Pesticides Cyfluthrin CAS No. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0.. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 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. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. Urinary levels for adults and children in these studies were similar (Heudorf et al. Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. representative 2001-2002 NHANES subsample (CDC. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0. Studies in Germany of 396 children and adolescents (Becker et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al... 2003).S. 2004). median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. 2006).68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin. 2005).. Following an indoor application exposure.S. representative subsample in NHANES 2001-2002 (CDC. 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. 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.2 μg/L) in the U.. 2005.. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. Fourth National Report on Human Exposure to Environmental Chemicals 159 . Thus. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al..95 µg/L. Leng et al. 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. 2003). Baker et al. Cyfluthrin is rapidly metabolized and eliminated from the body. 2005). 2003). 2001. most of which were dermal and respiratory irritations (Spencer and O’Malley. 2006) and 1177 urban adults and children (Heudorf et al. but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment.

2. 160 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.2 and 0.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.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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 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. < LOD means less than the limit of detection.

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. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 161 . 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.

Krieger RI. Angerer J.109(3):213-217. Int J Hyg Environ Health 2006. Hadnagy W. Bernard CE. Rev Environ Contam Toxicol 2006. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Barr DB. Environ Health Perspect 2001. Williams RL.209(3):293-299. Idel H. Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. O’Malley M. Heudorf U.46(3):281-288. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Olsson AO. Int J Hyg Environ Health 2003. Heudorf U. Spencer J. Heudorf U. Hoppe HW. Angerer J. Schulz C. Third National Report on Human Exposure to Environmental Chemicals. Becker K.206(2):85-92.77(1):67-72. Leng G. Seiwert M. Sugiri D. Pyrethroid illnesses in California. Butte W. Ball M. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. J Expo Anal Environ Epidemiol 2003. 19962002. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.13(2):112-119. 2005. Angerer J. Kolossa-Gehring M. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Int J Hyg Environ Health 2006. Centers for Disease Control and Prevention (CDC). Drexler H. Int Arch Occup Environ Health 2004.Pyrethroid Pesticides References Baker SE. Arch Environ Contam Toxicol 2004. Ranft U. Berger-Preiss E.209(3):221-233. et al. Atlanta (GA).186:57-72.

2-Dichlorovinyl)-2.200-.270 (.740 (. The chemical trans-3(2.460 (. but can also reflect exposure to trans-3(2.730 (.880 (.710-1.630) .900 (.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 .140 (.2-dichlorovinyl)2.2-dichlorovinyl)- CAS No.220-.470 (.11) . 1999).300-.160 (<LOD-. Kuhn et al.770) .890 (.820 (.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.07 (. Cyfluthrin. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.380-.350) .13 (.68) .630 (.580) 1.120-.340) . Similarly.1.640 (.68) .24) 1.730 (.380) . Survey Geometric mean (95% conf.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .300 (.460-1. and trans-cyfluthrin.250-.510 (.920) 1.500 (. which may vary for some chemicals by year and by individual sample.230) .200 (.220-.180) .600) .270 (. the presence of trans-3-(2. 1985.68 (. trans-cypermethrin.210) .1 and 0.490-.12 (.740) 1.35) 1.120-.730 (.600-1. cis-cypermethrin.440 (.570-.370-.2dichlorovinyl)-2.490-1.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.50) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.330) .950-2.200-.28) 671 680 518 701 591 957 Limit of detection (LOD.500 (.32) .490-.S.262) * * * < LOD < LOD .160 (.202 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.250 (. and ciscyfluthrin.08) . Fourth National Report on Human Exposure to Environmental Chemicals 163 .15) .or trans-3-(2.310) . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.740-1.510 (.600 (. ciscypermethrin and cis-cyfluthrin.340) .780) .380-.790-1.430-.270 (.370 (.2-dichlorovinyl)-2.and trans-isomers.21) .630) . trans-permethrin.700) .53) . cis-3-(2.580-1.220-.670-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.680-3.570 (.960 (.2-dichlorovinyl)-2.690) .520) .270-. Generally.670 (.44 (.400-.200-.790) .170 (.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.330 (.110-.770-1.410) .340-.670-1.530 (.380-.35) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.180 (.280-.2dichlorovinyl)-2.630-. The presence of cis-3-(2.470-1..740-2.110-. 1985.110-. but it can also reflect exposure to cis-3-(2. < LOD means less than the limit of detection.240) .910-5.43) .120-.220-.890 (.410) .200) < LOD < LOD < LOD .110 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.710) .140 (<LOD-.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.460-.150 (.2-dichlorovinyl)-2.200) .Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.680 (.650-1.80) .420-. 52315-07-8 CAS No.300-. Kuhn et al.790 (. 1999).77 (.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. In the body.120-. transcypermethrin and trans-cyfluthrin.490-1.510 (.670-2.850 (. more of the trans-metabolite than Urinary cis-3-(2.68359-37-5 Cypermethrin Permethrin CAS No. Biomonitoring Information Urinary levels of cis. cis-permethrin.550) .210-.47 (.220) .155-.160 (.610) . population from the National Health and Nutrition Examination Survey.610) .260 (.210) 90th .240) .200) ..280 (.54) .790-1.870) 1.380 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .

the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.270 (.2-dimethylcyclopropane carboxylic acid did not increase.11) .104-.550-1.380 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.11) .320-.150-.220) . post- Urinary cis-3-(2.380-.2dichlorovinyl)-2.540 (.350 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.290 (.67) .430 (.580) .440-.200-..340) .550) .59 (1.12 (.210-.550) . the median and 95th percentile of urinary levels of cis-3-(2.080-.270) .160 (<LOD-. urinary trans-3-(2..690-1.680-1. 2006. 2002).260 (..200 (.24) .170 (. 2002).440-.33) .170) < LOD < LOD < LOD .450-1.530 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.470-1.400 (.890 (.700) . In a study of urban residents in Germany (Berger-Preiss et al. In these volunteers.49) .S.220 (. 2005).540) .710-3.350) . 2005) In a small group of indoor pest-control operators...270) .300) ..810 (.300) . Studies in Germany of 396 children and adolescents (Becker et al.680 (.280-.510-1. 2006).360-1. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al. Other studies have provided evidence that urinary levels of cis.560) .300-.11) 1.390-.33 (.750 (.150-. In the same residents.580-1.700-2.130-. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.250) . Lu et al.2dichlorovinyl)-2.290) ..390 (.21) . Cyfluthrin.320) . Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al. In a study of volunteers.600 (.230-.430-1.640) 1. 2005).370-.590 (.230-.03) 1.400-1.250-.280 (.380) .830) .800 (. 2006.150-.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.37) . population from the National Health and Nutrition Examination Survey.340-.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .80) .500 (.250-.640-1.59) .640-.920 (.170 (. representative NHANES 2001-2002 subsample (CDC.530 (. 164 Fourth National Report on Human Exposure to Environmental Chemicals .2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.840 (.260 (. Survey Geometric mean (95% conf. 2006).140-.890) .290) . 2004..200-.250 (<LOD-.120 (.Pyrethroid Pesticides 2.11 (.880) .and trans-3-(2.182) * * * < LOD < LOD .2-dichlorovinyl)-2.420 (. 2005). 2001) showed urinary levels of cis.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .59) .260-.250) .550 (.700) . 2001. 2005). urinary levels of cis-3-(2.590) .2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.180 (. 2004).12-2.410) .710 (.550-1..640 (.220 (.680-1.560) 1.640-1.03) 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 .340) . Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.31) .2-dichlorovinyl)-2.290-.440 (.190) .520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .750-1.230 (.540 (.840 (. Schettgen et al.450 (.260 (.180-.270-.300 (.67 (.29 (..370-.190 (.S. 2006) and 1177 urban adults and children (Heudorf et al.250-.450-.190) .2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U..430-. 2003).and trans-3(2.390-.570) .780 (.780) 1.200) .300 (.370-.440 (.900 (.250) 90th .2-dichlorovinyl)-2.230-.260) . median urinary levels of trans-3-(2.240 (<LOD-.2-Dichlorovinyl)-2.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.138 (. 2003).

77) 2.54) 4.49-3.54 (1.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.49-5. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.48) 4.14-2.60-4.and trans-3-(2.11-2.400-.850-1.520-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.14-6.S.610) 1.22 (1. Survey Geometric mean (95% conf.4.41-14.4 and 0.08-6.620) < LOD 2.2-dichlorovinyl)-2.470 (<LOD-.490 (<LOD-.490-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.5) 2. Finding a measurable amount of cis.81) 2.10) 2.420 (<LOD-.95) 2.07 (1.560 (.43) 2.560 (.60) 1.76-3. Biomonitoring studies on urinary levels of cisor trans-3-(2.460-.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .76-4.26 (.08) 1.20 (.19 (2.35) 1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.19 (3. The maximum post-application urinary levels.410-.910-1.50 (1.07-3.40 (1.17-1.08-4.56) 2.970 (.920-1.750) .680-1.710 (. however.25-3.730) .20 (.90) 1.68) 1.800-1.55-5.49-3.Pyrethroid Pesticides application median urinary levels of summed cis.03-1.39-5.60) .25 (1.760) .01 (1.780 (.95) 3.63) 1.42) 1. 2005). Urinary trans-3-(2.400 (<LOD-.68) 2.14) 1.or trans-3-(2.520) .85) 4.20 (.03-1.89 (2.830-1.2-dichlorovinyl)-2. 2005).940 (.2-Dichlorovinyl)-2.66) .55-4.77 (1.55-3. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 165 .17 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.840-1.69) 1.16) 1.500-.13) .23 (.480-.87 (1.94 (1.410 (<LOD-.2dichlorovinyl)-2.460-.63) 1.560 (.97-11.910-1. which may vary for some chemicals by year and by individual sample.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .62 (1.470 (.530) .01) 4.91 (1.700) .39 (1.77) 1.68-2.660) 1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.28 (2.64-4.580 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.820) .56 (1.28 (1.410-.410 (<LOD-.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.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.810-1.42 (2.19) 1.670) .69 (1.56 (1.23) 2.7) 2.68) 1. population from the National Health and Nutrition Examination Survey.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 .860) .58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .12-6.84 (1.670) .11-1.37 (1.440 (<LOD-.500 (.17 (.59 (1.41 (1.27 (1.66) 691 680 518 690 595 954 Limit of detection (LOD.68-3.56) 2.700-1.09 (. trans-Cypermethrin.500) .550 (.570) 90th 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 .20-2.530 (<LOD-.87-8.35 (1.07-3.91) 1.2-Dichlorovinyl)-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.570 (<LOD-.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.08 (.98 (1.780 (<LOD-.930-1.74) .56-2.770) < LOD 2.87) 1.64 (1.07) 2.570-.640) .37 (1.00 (1.410-.48 (1.740) .31 (2.30-6.850) . population from the National Health and Nutrition Examination Survey.28) 2.48-2.610-.520 (<LOD-.30-3.660) .540) .70 (.850) 1.27-2.44) 2.47 (1.19) .45 (1. trans-Cypermethrin.22-2.470 (.20 (1.31 (.580 (.19 (1.720 (<LOD-.33 (1.87) 1.800-1.68) 3.42 (.Pyrethroid Pesticides Urinary trans-3-(2.33-1.60) 2.13) 1.42) 1.15) 2.56-5.760 (.07-1.65) 1.75 (1.900 (<LOD-1.47-2.00) 5.87 (1.530 (. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.880 (<LOD-1.00) 1.29) 1.61) 1.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .02-1.780) 90th 1.65 (2.S.720-1.81 (2.91 (1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.13) .39 (1.36) 2. Survey Geometric mean (95% conf.45-2.970 (.480-.880-1.16 (1.87-3.57) 3.880 (.800-1.57 (1.700-.80) 1.67 (2.500-.35) 1.07-2.750) .580) .730) . 166 Fourth National Report on Human Exposure to Environmental Chemicals .33-2.15-3.700 (.07) 2.86 (2.34-4.00-5.91-11.15) 3.00) 1.08 (.12 (.39) 1.40-2.22) 1.15-3.11) .41) 1.670) .11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.440-.34-3.820-2.780) .36 (1.47-2.74) 2.570 (.56 (1.700 (.15-3.470-.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .15 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.55 (2.850-3.560 (.12-1.720-1.27-2.60 (1.60) 2.3) 2.55 (2.89) 2.31) 1.26 (1.55 (2.22-1.

Angerer J. Angerer J.134(1-3):141-145. Angerer J. Heudorf U. Leng G. J AOAC 1985. Butte W. Centers for Disease Control and Prevention (CDC). Angerer J. Int J Hyg Environ Health 2003. Sugiri D. Atlanta (GA). Biological monitoring of workers after the application of insecticidal pyrethroids. Schulz C. Int J Hyg Environ Health 2002. Environ Health Perspect 2001. Kuhn K. Heudorf U. George DA. Seiwert M. Third National Report on Human Exposure to Environmental Chemicals. Idel H. Bull Environ Contam Toxicol 1999. Heudorf U.62:101-108. et al. Bartell S. Hadnagy W.Pyrethroid Pesticides References Becker K.109(3):213-217.206(2):85-92. Ranft U. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Hardt J. Pearson M. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.114(9):14191423. Ball M. Kolossa-Gehring M. Wieseler B. Drexler H. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Angerer J.68(6):1160-1163. Int J Hyg Environ Health 2006. Leng G. Berger-Preiss E.209(3):293-299. Ranft U. Barr DB. Environ Health Perspect 2006. Idel H. 2005. Angerer J. Indoor pyrethroid exposure in homes with woollen textile floor coverings. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Drexler H. Int Arch Occup Environ Health 2004. Berger-Preiss E.77(1):67-72. Lu C. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int J Hyg Environ Health 2006. Heudorf U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Hoppe HW. Schettgen T.209(3):221-233. Permethrin and its two metabolite residues in seven agricultural crops. Sugiri D. Levsen K. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Bravo R. Idel H. Leng G.76(7):492-498.205(6):459-472. Int Arch Occup Environ Health 2003. Fourth National Report on Human Exposure to Environmental Chemicals 167 .

. In the NHANES 2001-2002 subsample. 2004). 2006) and 1177 urban adults and children (Heudorf et al.2-dibromovinyl)2.Pyrethroid Pesticides Deltamethrin CAS No.2-dibromovinyl)-2.2-dibromovinyl)-2. 2005). 52918-63-5 General Information Cis-3-(2.2dimethylcyclopropane carboxylic acid formed in the environment.. 2001.2-dibromovinyl)-2. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.2-dimethylcyclopropane carboxylic acid of 0. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2-dibromovinyl)-2. Baker et al. Thus. (2004) reported a geometric mean concentration of cis-3(2. 168 Fourth National Report on Human Exposure to Environmental Chemicals .2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. 2005).2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.2-dibromovinyl)-2. Studies in Germany of 396 children and adolescents (Becker et al. in detection of cis-3-(2.2-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. 1990).39 µg/L.. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.. Following residential spraying with deltamethrin for malaria protection in Mexico. Deltamethrin can degrade to cis-3(2.S. Outside the U. Finding a measurable amount of cis-3-(2. Biomonitoring Information Urinary levels of cis-3-(2. in some situations replacing the use of DDT.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.5 μg/L) than the detection limit (0.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. 2005). deltamethrin has been used against mosquitoes that carry malaria.2-dibromovinyl)-2. 2001) showed that urinary levels of cis-3-(2. 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. Urinary levels for adults and children in these studies were similar (Heudorf et al.3-0. mean peak urinary levels of cis-3-(2..2-dibromovinyl)-2. urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.2-dibromovinyl)-2.1 μg/L) for the NHANES 2001-2002 subsample (CDC..

2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.Pyrethroid Pesticides Urinary cis-3-(2. < LOD means less than the limit of detection. 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.2-Dibromovinyl)-2.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.1 and 0. Fourth National Report on Human Exposure to Environmental Chemicals 169 .1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. which may vary for some chemicals by year and by individual sample.

Pyrethroid Pesticides Urinary cis-3-(2. Survey Geometric mean (95% conf.S. 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.2-Dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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. population from the National Health and Nutrition Examination Survey.

Lopez-Guzman OD. Hoppe HW. Environmental Health Criteria 97. Environ Health Perspect 2001. et al. Drexler H. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Butte W. Int J Hyg Environ Health 2006. Angerer J. Batres LE. Kolossa-Gehring M. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Angerer J.org/documents/ehc/ehc/ ehc97. Int J Hyg Environ Health 2006.109(3):213-217. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.77(1):67-72. Heudorf U.209(3):293-299. 5/26/09 Ortiz-Perez MD.htm. et al.113(6):782-786. Angerer J. Angerer J. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. International Programme On Chemical Safety (IPCS). Carranza C. and genotoxicity in exposed children. toxicokinetics. 2005. Schulz C. Environ Health Perspect 2005. Deltamethrin. Grimaldo M. Ball M.209(3):221-233. Int Arch Occup Environ Health 2004. Third National Report on Human Exposure to Environmental Chemicals. Heudorf U. Torres-Dosal A. Seiwert M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Centers for Disease Control and Prevention (CDC). Heudorf U. Atlanta (GA).Pyrethroid Pesticides References Becker K. [online] 1990.inchem. Available at URL: http://www.

39515-41-8 CAS No. Baker et al. 2003. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 52918-63-5 use and house dust levels (Lu et al. 2006). CDC. (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. 2005). CDC. Following residential spraying with deltamethrin for malaria protection in Mexico.. Saieva et al. In one study of 145 urban residents in 80 private homes in Germany. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 2005). Becker 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. 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. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect.S. 2005). representative NHANES 2001-2002 subsample (CDC. 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. 2004). 52645-53-1 Tralomethrin CAS No. Thus. In the New York City study. 2006. A study of 396 German children (Becker et al. CDC. 2003.. Fenpropathrin Permethrin CAS No.. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. 2005). the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. In a small group of indoor pest-control operators. 2002. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides...Pyrethroid Pesticides Cyhalothrin CAS No. 2003). 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. Hardt and Angerer. 2005). median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. 68359-37-5 Cypermethrin Deltamethrin CAS No. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC.. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above.52315-07-8 CAS No. 2005). the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. 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. 2005). 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. 2005. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. 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 .

46) 2.12) 4.810) 1.190-.320) .320) .44) 5.46) .273 (.43) 3.314 (.510-.280 (.52-5.270) .49-2.277-.62-6.960 (.325 (.450 (.288 (.35 (1.34 (2.352-.353 (.25 (2.32 (1.230-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.64) 697 680 524 701 603 957 Limit of detection (LOD.560-1.83-11.78) 1.800) 1.190-.226-.246-.600 (.16-1.56-5.360) .12 (.240 (.26) 2.440) .253-.200-.601) .297 (.321 (.1.25-4.267 (.710 (.330) .39) 2.271-.238-.530-.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 .276-.270 (.300 (.63-3.04) .298 (.550-.330) .800 (.640 (.670 (.190-.45 (2.25-1.01 (1.160-.220-.210-.420) .230 (.13) .33) .78) 6.29-1.210-.25-7.750) .590-.507 (.48-2. interval) . Fourth National Report on Human Exposure to Environmental Chemicals 173 .311 (.93 (1.38 (2.430-.630) .53) 1. Deltamethrin.340) 75th .350-.230-.1) 3.34-6.740 (.530-.28) 1.49-2.65-2.610) .250 (.05) 1.27-2.490-.42-2.27-11.45-5.387) .13 (.71 (1.730 (.490) .427) .840-1.38 (2.384) .374) 99-00 01-02 99-00 01-02 99-00 01-02 .340) .328 (.364) .35 (2.34) 8.55 (1.570-1.14-6.230-.54) 1.320) .700-1.560-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.26) 2.36) 1.266-.586) .41 (1.81 (1.30 (1.510-.295) .428-.30 (.740 (.92-3.850) .373) .990) .520 (.41) 3.470-.12) .250 (.434) .750) .290 (.240 (.288-.265-.355) .1) 3.300 (.90) 1.62) 5.48-2.940) 1.49 (1.32-21.292-.51-6.570-.850) .49 (1.390) .292 (.320 (.32 (2.26-2.03 (3.406) .620-1.78 (1.700 (.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.180-.430-.870 (.260-.18 (1.320) .16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .369) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30) 3.33 (1.86 (1.18 (2.247-. Survey Geometric mean (95% conf.05) .27-2.250-.21 (2.340) 1.760 (.75 (1.830-2.260 (.230 (.1) 3.160-.52-4.41-3.830) 90th 1.04-5.590 (.65 (1.16) 1.41-2.560-.73) 1. population from the National Health and Nutrition Examination Survey.51-3.78) 1.200-.02-6.680 (.233-.650 (.417 (.89-71.260 (.60) .750-1.250 (.300 (.53-3.79) 3.454 (.62-8.35) 2.336 (.227-.33 (2.820) .50 (2.8) 3.72 (1.25 (2.1 and 0.710 (.300) .315 (.190-.35) 1.63 (3.820) .76 (1.780) 4.69) 3.35) 2.595) .314) .23 (2.362) .370) .200-.S.260 (.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .69 (1.

410) .240 (.860-1.630) .229-.64-5.09 (.32 (2.238-.35 (1.330) 1.261 (.372) .510 (.63) 1. Survey Geometric mean (95% conf.299-.55) 3.280 (.67 (1.43 (2.37) 1.36 (1.11 (.210 (.04 (.36-6.234 (.17-1.62) 1.370-.73-4.311 (.250 (.49 (1.410-.246 (.250 (.534) .730-1.86 (1.150-.280) .216-.860 (.510 (.09-2.401) .35) .810) 1.274-.362 (.210 (.35-3.930) 1.39) 1.19 (2.740) . population from the National Health and Nutrition Examination Survey.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .930) .37 (1.330) .330) .09) 3.94 (1.95) 1.226-.328) .720 (.83 (1.05-3. Deltamethrin.270 (.490 (.380-.02 (2.210-.19-6.440-.650) .304) Selected percentiles ( 95% confidence interval) Sample 95th 3.320) .55 (1.49) 1.40) 2.700-1.840-1.610 (.22 (1.278) .670) 3.15-2.61-2.270-.480-.590) .91) 9.173-.350 (.270) .27) 1.00) 5.21-4.91-4.53 (1.312 (.357) .25-5.480 (.230) .510 (.670) .200-.49-2.580) .230-.760) .220-.54 (1.13-1.13-1.350) .272) .387) .370 (.330) 75th .280 (.560 (.270 (.25-2.330 (.88-5.03 (.329) .272 (.860-1.43-64.10 (2.84 (1.264 (.590-1.44) 2.580 (.90) 3.21 (1.178-.378 (.220 (.200-.309) .570) .43) 1.35) 1.365) 99-00 01-02 99-00 01-02 99-00 01-02 .11 (.720) 90th 1.240-.225-.440-.400-.240 (.75-8.420-.640 (.63-3.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .290) .280-.730) .49) 3.750-1.240-.09-2.40 (1.240-.270) .06-3.460-.290) .25) 2.17 (.41-4.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.730) .329) .240 (.60) 1.400-.280 (.540 (.321-.309 (.200-.550 (.240 (.190 (.00) 1.74) 3.07) 2.07-5.04 (3.590) .640 (.400) .16-4.335-.0) 3.490-.250) .550 (.48 (1.300-.67 (1.202-.96 (1.677) .490 (.52) 2.19) 2. interval) .423 (.437) .280) .446) .62) .160-.190-.83) 1.323 (.550 (.03-1.44 (1.13 (.00) 1.290-.227 (.80) 4.51-7.500) .390-.73) 1.60-4.200-.91 (2.91) .72 (1.440-.261-.S.81 (1.271-.230-.590) .274 (.224-.530-.02-1.88) 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 .190-.67) 1.310) .275 (.41) 1.380 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.52 (1.960-1.43 (1.450 (.240-.530-.300-.460-.316 (.253) .

111(1):79-84. Olsson AO. Lopez-Guzman OD. Centers for Disease Control and Prevention (CDC). Berger-Preiss E. Angerer J. Carranza C. Batres LE. Grimaldo M.209(3):221-233. urban cohort.76(7):492-498. Angerer J.206(2):85-92. Leng G. Barr DB. Ranft U. Idel H.113(6):782-786. Obel J. Torres-Dosal A. Leng G.205(6):459-472. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Ranft U. Godbold J. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence.114(9):14191423. Barr DB. Hoppe HW. Atlanta (GA).46(3):281-288. Ortiz-Perez MD. Kolossa-Gehring M. Seiwert M. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Arch Environ Contam Toxicol 2004. Pearson M. Idel H. Int J Hyg Environ Health 2003. et al. Hadnagy W. Deych E. Environ Health Perspect 2005. 2005. Int J Hyg Environ Health 2006. Sugiri D. Lapinski R. Third National Report on Human Exposure to Environmental Chemicals. Berkowitz GS. Hardt J. toxicokinetics. Berger-Preiss E. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Liu Z. Int Arch Occup Environ Health 2003. et al. and genotoxicity in exposed children. Levsen K. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Environ Health Perspect 2006. Biological monitoring of workers after the application of insecticidal pyrethroids. Exposure to indoor pesticides during pregnancy in a multiethnic. Ball M. et al. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Bartell S. Becker K. Sugiri D.Pyrethroid Pesticides References Baker SE. Bravo R. Int J Hyg Environ Health 2002. Lu C. Environ Health Perspect 2003.

340) .128 (.099 (.190 (.260 (. to a lesser extent.190-.100 (.180 (.350) .410) .210) .360 (.132 (.105 (.080) .200 (.710) .120 (.110-.176 (.180) .132 (.200-.120-.180 (.154) .146 (.140-.145 (.110-.128 (. People are exposed to antimony primarily through food and. 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.230 (.240 (.220 (.360) .220) 95th . 01-02.S.310 (.190-.157) .114) .230-.200 (.460 (.270 (.440) .300 (.270) .150 (.160) . Antimony enters the environment from natural sources and from its use in industry. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.350-. and excretion of antimony vary depending on its oxidation state. Dermal contact with soil.112-.130-.400 (.156-.230) .090) 75th .154-.100) .400) .310-.115-.Metals Antimony CAS No.130 (.360 (. storage batteries. 176 Fourth National Report on Human Exposure to Environmental Chemicals .280) .200 (.108-.250 (. < LOD means less than the limit of detection.180-.070 (<LOD-.200 (.290 (.310 (.310 (.087-.190-.123 (. and as a fire-retardant in textiles and plastics.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 .220) .170-.330 (.280-.350-.260 (.320-.090 (<LOD-.140) .150 (.280 (.470) .130-. or other substances containing antimony is another means of exposure.310) .430 (.350-.440) .330) .230) .410) .117-.160) .160-.150-.140 (.400 (.270 (.270 (.170-.460 (.160-.260) .320-.420) .130) < LOD .300-.220) .184) .140) .390 (.175 (.070-.180-.300-.110) . 0.093 (.180 (.115) .460) .180-.310 (.250 (.080 (<LOD-.119-.220 (.460 (. see Data Analysis section) for Survey years 99-00.240-.330) .109-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.390-.400) .125 (.220-.260) .180 (.160 (.250-. and pewter.120) .430 (. Antimony can exist in one of four valences in its various chemical and physical forms: -3.210 (.160) .135) * .390-.150-.340 (.150) 90th .240) .260) .090 (.320 (.470 (.320-.130) .130-.144) . metal bearings.200 (.320) Total .178) .260-.120 (.230-.180 (.280-.320 (.250-.350) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.270 (.200-.164-.140 (. population from the National Health and Nutrition Examination Survey.390) . respectively.080) .430 (.131-.140 (. and 0.340 (.240 (.530) .280 (.190-.570) .148-.440 (.150) . solder.137) .100-.130 (.150 (.200) .130) .04.140) .133) * .470) .120-.120 (.310) . 0.270) .170-.130 (. castings.600) .103) .070 (<LOD-.120-. sheet and pipe metal.490) .510) .190) .130 (.130) .160-.170) .130 (.160) .310-.240 (.190) .108 (.190 (.170-.180-.240 (.120-.170 (. enamels.400-.134-.190) .330) .370) .330 (.136-.207) .350 (.390) .350 (.270-.130-.260-.170 (.350) .126-.136) * .120-.220-.140 (.130 (.220-.250-.200 (.160 (. It is used in metal alloys.330-.250-. +3.240-.140) .290-.100-.240 (.220) . coal-fired plants. and +5.180) .210) .390-.095-.200-.210-. distribution. and glass.110-.150-.330) .079-.370-.160) . ammunition.150) .110-.150-.120 (.130 (.490 (.210) .137) .300) .190 (.117-.150) .160 (.190) .210) .120) .150-.160) . which may vary for some chemicals by year and by individual sample.095 (.350 (.350 (.360-.390) .154) .230 (.145) Selected percentiles ( 95% confidence interval) 50th . from air and drinking water.500) .130 (.119) .320-.160-.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 .190) .320) .190 (.200) .280-.400 (.560) .200) . Stibine is a metal hydride form of antimony used in the semiconductor industry.280-. interval) .230) .390) .088-.360) .098-.280) .120-.120-.200-.200) .230-.210) .120 (.300 (.120-.220-. ceramics.120) .250) .120-.350) . 7440-36-0 General Information Antimony is found in ores or other minerals.080-. water.190-.122 (.130-.350 (.090-.04.170-.300) .130-.210-.090-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and 03-04 are 0.161) .260 (.280) .300-.100 (.140) .210 (.330 (.134 (. It is also used in paints.126 (.400) .280-.180 (.280) .500) .07.230 (.141-.140) . fireworks.120) .230-.110 (.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.220-.410-.220-.250 (.290-.197) . and refuse incinerators that process or release antimony.169 (.142 (.158 (. Workplace exposures can occur at smelters.180-.300) .130-. The absorption.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 .143 (.330-.230-.190 (.

298 (. 1988. 1954).261) .085) .120 (.079 (<LOD-.186) .187) .272) .208 (.115 (.120 (.135) .127) .333-.159-.144-.159-.310) .146-.181) .123) . Fourth National Report on Human Exposure to Environmental Chemicals 177 .122 (.135 (.159-.313-.385 (.080 (<LOD-.139 (.143) Selected percentiles ( 95% confidence interval) 50th .205-.286 (.250 (.116 (.173-.308-.178 (.176-. 1944).068 (.138) * .139 (.156 (.156-.092) .233 (.109 (.112 (.099-.338) .200-.320-.300) .176 (.115) .209 (.118 (.114 (.130) .131-.121) .267-. skin.320 (.108-.414) .130) .189 (. interval) .095-.248) .116-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.078 (. Acute antimony poisoning may cause a metallic taste.278) .167 (.069-.343 (.228-.124-.405) .117-.104-.195-.183) .106-.235-.081) .242-. species.143) .163 (.320) .173 (.195-.152) .068-.146-.107-. diarrhea.113-.115 (.194-.209-. resulting in hemolysis with abdominal and back pain (Dernehl et al.271-.147-.104-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.265-.203) .138-.238 (. Histopathologic inflammatory and degenerative changes in the lung. and kidney have been demonstrated in high dose animal studies depending on the dose.250-.444) .438) .127 (.167 (.200-.192) .076-.084) .300 (. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.310) .113) .277 (.129 (. and route of exposure (Elinder and Friberg.188) .429) .430) . 1986).096-.120 (.192-. 1953).131 (.143 (.075 (.230-.137 (.170 (.207) . 1973).225) .199-.338 (.198) .185 (.741 (.220) .250-.214) .130) .250-.318-.317) .127) .315) .400 (.172-.229-.188-.308) .118 (.071-.112-.333 (.352) .138 (.173) .480) .182 (.206-.124) .154-.131) .317) .133) .135) .109 (.300) . Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.132 (.209) .143) .153-.280 (..338 (.167-.263-.108 (.244-. abdominal pain.138-.253 (.126 (.200) .075 (.111-.417) .164-.160 (.318-.333 (.089) .211) .195 (.268) .192 (.310 (.171) .152) .175 (.245) .352 (.082) .136) .132) .162-.257) .107-.295 (.333-1.364 (.147) .256 (.082) .280-.107-.444) .163 (.086 (.122 (.117-.115-.741) .241-.103-.233) .727) .098) .239-.225 (. Inorganic antimony salts irritate the mucous membranes.250) .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. myocardium..391) .247) .125-.265 (.097-.108-.109-.320-.173 (.176 (.253-. liver.181) .140) . 1962).373) .224 (.115-.267) .080 (.178-.121 (. 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.255-. and eyes.238) .098-.429 (.288 (.213 (..371 (.217 (.421) .250-.391) . 1995).146-.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 .102-.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 .333-.135 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.255) .145) ..227-.241-.148-.123 (.380 (.161) .236 (.185 (.077) .208-.143) 90th .203) .238) .193 (.119-.321) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.082 (<LOD-.209) .500) .119-.149-.228 (.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 .357) .108-.148-.124-.281-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.250 (..266 (.119 (.113-.485) .076-.135) .126) .117-.061-. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.333) .074 (.425) . and ulcers (Werrin.317) .167 (.127) .191 (.471 (.357-.150-.148) * .127) .095-.092-.151) . and gastrointestinal symptoms such as vomiting.164) .099-.417) .069-.114 (.30) .098-.129) .364 (.134) .204-.140) < LOD .179-.130 (.150-.111 (.196 (.200-.081 (<LOD-.278 (.125 (.146) .100 (.269 (.294) Total .102-.114 (.120 (.128-. population from the National Health and Nutrition Examination Survey. 1958) and occupational exposures (Briegner et al.103-.087) .267 (.105-. Ming-Hsin et al.230) 95th .193) .153 (.112 (.447 (.129 (.226 (.Metals than for trivalent compounds (Elinder and Friberg.124 (.222 (. 1986).259 (.333 (.129) * .126-.121 (.115 (.233-.S.471) .263 (.149) .164 (.320 (.181) .086) 75th .333-.276 (.228 (.106-.248-.161) .185-.

J Clin Pathol 1998. Biological assessment of exposure to antimony and lead in the glass-producing industry. References Berman JD. Delves HT. O’Regan M. Environ Health Perspect 1998.. which may be due to methodologic. Luedersdorf R. Sci Total Environ 1994.S. Industrial antimony poisoning... EPA. HH. 26-42. Chest 1973. Friberg L.. Bailly R. Chia-Yu H. Schacke G.. Sabbioni E. Review of elements in blood. Sabbioni E. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Industrial Medicine and Surgery (Dec. Delves HT.521-523. 1990. Wade A. 20012002. clinical efficacy.13:361-362. Carelli G. Buchet JP. stibine. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al.. 1995. eds. Minoia C. Gallorini M. gallium. Trace element reference values in tissues from inhabitants of the European community I. Antimony trioxide is rated by IARC as a possible human carcinogen. 1997). VI. Ju-Sun P. Arch Dis Child 1997. 1998) or compiled reference ranges (Hamilton et al. Dernehl CU. Lenert G. Br J Ind Med 1991. Petrucci F. even when exposure levels were below workplace air standards (Bailly et al. Kentner et al. 1987). Ludersdorf et al. Costeloe K.51:238-240.html. Cullen A.76:432436. Yang C-Y. 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. New York: Elsevier. Gebel TW. gov/toxpro2. or exposure differences. External and internal antimony exposure in starter battery production. Liao Y-H. Liao Y-H et al. 1991. Vouk VB. Int Arch Occup Environ Health 1995. pp. Stasney J. In: Friberg L.10(3):560-586.cdc. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Ming-Hsin H. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Stocks J. Elinder CG. and hydrogen sulfide. and a drinking water standard has been established by the U. Earlier measurements in general populations (Minoia et al..)1954. Biomonitoring of a worker population exposed to low antimony trioxide levels. Cordasco EM. Arsine.158:165-190. Pozzoli L. 2002. Schaller KH. Chen J-R. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Roland H. Ho C-K.64(2):182-185. Piatnek DA. et al. Pulmonary edema of environmental origin. respectively. 2005. Iavicoli I. Yu H-S. Chemotherapy for leishmaniasis: Biochemical mechanisms. Suchenwirth R. Stead FM..16: 33-39. Antimony in blood and urine of infants. Shao-Chi C. Dezateux et al. Matthews T. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Wu M-T. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Mahieu P. Mayer P. arsenic. Iavicoli et al. Urinary antimony in infancy.46:931-936. J Occup Environ Med 2004. Paschal et al. Rev Infect Dis 1988. Biological monitoring of exposures to aluminum. Handbook on the toxicology of metals. Dezateux C. Atlanta (GA).48:93-97. Centers for Disease Control and Prevention (CDC). Dunkelberg. Lauwerys R. and antimony in optoelectronic industry workers. Kiberd B. 1998. population. Hamilton EI. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Apostoli P. Third National Report on Human Exposure to Environmental Chemicals. Bolten C. indium. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Information about external exposure (i. Element reference values in tissues from inhabitants of the European community. Leinemann M. environmental levels) and health effects is available from ATSDR at: http://www. Chin Med J 1958. 1998). Fuchs A. Industrial Medicine 1944. Nordberg GF.e. et al.. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Mayne P. and future strategies. Antimony.106:33-39.76(2):103-115. Nau CA. 1994) have reported values slightly higher than those in this Report. Pietra R. 1986.67:119-123. Kentner M. Konings J. Caroli S. 2004. 2nd ed. Stone FD. Kuo-Juie Y. Alimonti A. Cheng-Wei L.Metals to antimony have been established by OSHA and ACGIH. Pilgrim L... Briegner H.atsdr.. Semisch CW. Skulsukai G. Weltle D.59:469-474. Van der Venne MT. and 2003-2004. et al. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Int Arch Occup Environ Health 1987. J Trace Elem Med Biol 2002.

Pirkle JL. et al. Morrow JC. Chemical food poisoning. blood. 27:38-45.99-108. Trace metals in urine of United States residents: reference range concentrations. Sampson EJ. and serum of Italian subjects. Renes LE. Antimony poisoning in industry.Metals in urine.95:89-105.76(1):53-59. Industrial Hygiene and Occupational Medicine 1953. Ting BG. Jackson RJ. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Sci Total Environ 1990. Werrin M. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Paschal DC. Environ Res 1998.

1) 1281 1276 03-04 03-04 03-04 9.8) 7.8) 17.4 (31.6 (32. sodium arsenite.4) 13. to a lesser extent. retaining walls.90-8.30 (7. aluminum.80-9. ocean and fresh waters.Metals Arsenic CAS No.5-52. Also. mental disorders.5) 43.29 (8.5) 66. and arsenosugars. and as a cosmetic to lighten complexion. Arsenic and its compounds have had many uses in the past and present as medicines.9-34.2 (41.3) 10. interval) 8.10-10.34-9.90 (5. population from the National Health and Nutrition Examination Survey.9-46.41 (7.57) Selected percentiles ( 95% confidence interval) 50th 7. Gallium. arsenocholine.7-83.6) 11.55 (7. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. Arsine (AsH3) is a reactive.1 (38.5 (40. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.2 (51.2) 15. copper arsenates. and foods.5 (34. and produce.2 (13.10) 10.5) 95th 65. and.1-18. as alloy in metal bearings. were used as treatments for syphilis.8) 7.90-8.90 (7. The United States no longer produces arsenic from mining but imports about 22.70 (6.08 (5. the smelting of copper.10 (6.0 (14. and gray forms). and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.7) 24. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. meats. see Data Analysis section) for Survey year 03-04 is 0. General population exposure to inorganic arsenic can occur through consumption of drinking water and.80) 6.000 metric tons annually.4 (26.84) 8. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.2-61. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1) 15.2 (12.4) 60.8) 33.1-40.90) 75th 16.0 (43.0 (11. +3 and +5).4) 40. Before the 20th century.6 (9.19-9. In the last century.9 (8.50-14.7-95.3-19.9-62.5 (14. referred to as inorganic arsenic compounds. gaseous hydride manufactured in small quantities for use in the semiconductor industry. and play sets.84) 8.5-41.4-65. Water sources contain mostly inorganic arsenate.30) 17.9 (17.6-141) 53.90-7. Arsenic trioxide is approved to treat acute promyelocytic leukemia.77) 6.1) 290 725 1542 03-04 03-04 9. 2005).1) 7.5-178) 46.70) 8. and as homicidal poisons. 2001). Although it is still widely used in the United States.2-93.4 (7.7) 65. from coal burning.3-15.6 (15.10-7. Various arsenic compounds were used in paint pigments and for tanning animal hides.66-8. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. In nature. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.90-11.2) 46. 180 Fourth National Report on Human Exposure to Environmental Chemicals .S. grain.13-8. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.00 (6. and indium arsenides are used in the semiconductor industry.40) 7.12 (6.8) 30. Survey years 03-04 Geometric mean (95% conf. cancers.6-43.3) 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 7.0 (15.2-20.2-17.4 (48.30 (6. psoriasis. such as arsenopyrite (FeAsS) and realgar (As4S4). black.0-60. trimethylarsine oxide. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. it is found in over 200 crystalline or mineral forms.97) 8.50 (8.02-8. particularly arsenic trioxide. or rarely as elemental metalloids (yellow.6 (13.8) 34.5 (23.34-10. pesticides.8 (48.20 (8.8-77.5-19.5) 41. cacodylic acid.70-9.8-61. arsenic compounds. solders.74.1 (32.8) 29.12-10. though in some locations arsenite may be prevalent (WHO.5 (36.3-111) 78. to a lesser extent.27) 9. Arsenic is measurable in most soils. Arsenic trioxide (As2O3.0 (22. arsenic as elemental metalloids may be used in some ammunition.9) 21.00-9.6) 618 722 1074 Limit of detection (LOD.4 (24.0-19. alloys. lead hydrogen arsenate.90-14.90 (7. arsenites. and other metals.80 (5.7 (11. and in lead-acid storage battery grids. mostly for use in wood preservation (ATSDR.9) 68. lead. semiconductors. and arsenates (oxidation states of -3. Since the 1940s.25-9.90) 16.7) 90th 37.6-35.

7-17.38-10.5-17.4 (11.31 (6.4 (24.4-64.6-17.7-188) 27.01) 7.04) 7. 2006. 1988).93-8.1) 24.86-17.8) 27.33 (6.0-38.5) 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. shellfish. Fish. interval) 8. cacodylic acid and monosodium methyl arsenate.0) 12. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.99-9.25-9.S.8) 22. 2001).11 (5. Smoking tobacco is also a source of inorganic arsenic.23-7.10-8.3-41. 2007.0-26.7) 28. mine tailings).30-9.4 (26.5-120) 40. arsenic does not show biomagnification in the food chain (WHO.0 (31.7-34.18 (5. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.47 (6.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U. Extremely high groundwater arsenic levels. Steinmaus et al.S.12-10.1) 7.64 (7.6) 45.4 (42. 2007.41) 6.81-9.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .4 (12. Gamble et al.20-9. Tseng.58-10. and arsenosugars.. Though modest bioconcentration occurs in some aquatic life.59) Selected percentiles ( 95% confidence interval) 50th 7. arsenocholine. 2001.8-32. After absorption.7 (9.96) 12. Chowdhury et al.8-62.66-8..88) 7.45) 5.2) 40.0 (17.2) 15. 2001).1 (11.3 (24. age.8 (11.0) 33.5) 290 725 1542 03-04 03-04 8.3) 9.44-11. 2001).7-18. Survey years 03-04 Geometric mean (95% conf.13) 8. so exposure to the general population is extremely limited. population from the National Health and Nutrition Examination Survey. as observed in Bangladesh where millions of people have been exposed.1) 6. Arsenate is reduced in the body to arsenite (oxidation state +3). are used in enclosed ultraclean operations within the semiconductor industry.04 (5.1 (14. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.32 (5. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.40) 8.66 (7. 2001). though some reduction may occur in the gut prior to absorption. and contact with CCA-preserved wood structures.4) 32. kelp. trimethylarsine oxide (TMAO). 2001). but is poorly absorbed dermally (WHO. The semiconductor dopants.61 (7. and folate status (Chen et al.1-36.1) 8.S.8 (12.9 (45.88 (5.0) 1281 1276 03-04 03-04 03-04 8.66-8.8 (27.47-6. gallium arsenide and indium arsenide.93-9. selenium. 2001.33-10. Direct exposure to DMA and MMA may result from use of the two pesticides.3-53. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.8 (21..3) 6. and some other seafood can contain organic forms of arsenic including arsenobetaine.4 (40.7) 95th 50.00 (6. WHO.24 (7.3 (27. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.7 (11. In aquatic sediments. organic arsenic can be converted back to methylated and inorganic arsenic. dust.75 (5.5 (9. NRC. WHO. EPA.07-9.7 (25.7-35.35) 7.8 (20. 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.4) 54.2-15.44) 6.6 (10. Inorganic forms of arsenic demonstrate high acute toxicity.10-16.0) 26.2) 90th 30.2-46..g. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al. 2003. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. 2007. 2001).0) 14. inorganic arsenic is widely distributed within the body.9) 13.2 (12..76 (6. 2001).9) 53. 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.47 (7.8-75.0) 42. U.51) 75th 14. 2006.75) 13.6 (17. In aquatic organisms.9-56.01) 11.3-64..6 (35.5) 17. 2001). Children may have additional exposures from ingestion of contaminated soils (e. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.25 (6.0-18. dose level. EPA’s maximum contaminant level (Hughes.0-69.3-62.06 (4. have caused clinical arsenic poisoning.50 (6.1) 58.28-7.

S.20 (<LOD-1. 2006. including inhibition of numerous enzymes.50) 1. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. Cellular glucose uptake. 2001).Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. 182 Fourth National Report on Human Exposure to Environmental Chemicals . 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. Acutely. fatty acid oxidation. including drinking water sources with elevated arsenic levels (e. 2004.60) 1. some of these effects may take years to develop. 2007.10 (<LOD-1. 2007.. and altered gene expression. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. 2004). Arsenic has many actions demonstrated in cellular studies. which may vary for some chemicals by year and by individual sample... 2007). Chronic arsenic exposure in humans is considered to be a cause of skin. < LOD means less than the limit of detection. Chronic human intake of arsenic at less than acutely toxic doses..0.g. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. Cohen et al. increased oxidative stress. arsenic trioxide) includes hemorrhagic gastritis with nausea. vomiting.80) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. which can lead to dehydration and shock. noncirrhotic portal hypertension.50) 621 725 1078 Limit of detection (LOD. apoptosis. 2001).. 2001). Chile). and diarrhea. Studies of arsenic at levels typical of U.20 (<LOD-1.10 (<LOD-1. 2001). WHO.S. respectively. and hyperpigmentation of the skin (NRC.S.. lung. and endothelial injury (Kumagai and Sumi.g.. hematocytopenias. 2000.EPA. drinking water have not been associated with increased cancer rates (Schoen et al. 2006) or when exposure occurs in smokers (Chen et al. hypertension. Bredfeldt et al.10 (<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 < LOD 90th < LOD Sample size 1.20 (<LOD-1.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. and childhood neurodevelopmental effects in observational human studies. hepatotoxicity. U... hyperkeratosis. and bladder cancer (IARC. The U. Taiwan.10 (<LOD-1..30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. interference in signal transduction pathways.S. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. 2006. see Data Analysis section) for Survey year 03-04 is 1. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. 2001.. substitution in phosphate metabolism. NRC. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. cell transformations. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. peripheral vascular disease. 2001). cytotoxicity. With chronic exposure. Raml et al.10 (<LOD-1. and it also will inhibit succinate dehydrogenase. and production of glutathione may be affected as well. WHO. The organic forms of arsenic occurring in seafood have little known toxicity. Survey years 03-04 Geometric mean (95% conf. WHO. Bangladesh. Cardiac arrhythmias.. Such actions may lead to decreased energy production. WHO. population from the National Health and Nutrition Examination Survey. Although arsenate is reduced in the body to arsenite. gluconeogenesis. and DNA repair inhibition (Cohen et al. food residue. NRC.EPA has established drinking water.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1.60) 1. 2001.30) 1. 1998. 2004). 2006. renal failure. Chronic elevated arsenic intakes have been associated with diabetes. 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. and by uncoupling oxidative phosphorylation (NRC. 2001). but additional or confirmatory research is needed (Kapaj et al. can cause peripheral sensorimotor neuropathies.20 (<LOD-1. leading to a decrease in adenosine triphosphate energy production.

Meza et al.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2..75 (<LOD-2. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. had decreased since the prior 1990– 1992 survey..18) 3.. 2006). Calderon et al. 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. arsenic has been fetotoxic and teratogenic. Pellizzari and Clayton. 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.41) 3. 1992.. Josyula et al. population (Rubin et al.html..19) 3.. 2000. Shalat et al. 2004. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al.. In animal studies. Consequently. 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. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. 2003. 2004. 1999).. 2008.18 (<LOD-3. Compared with this Report.Metals compounds. Caldwell et al. population from the National Health and Nutrition Examination Survey. Additional information about external exposure (i.. population in NHANES 2003–2004 (Schulz et al.S.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2.. In a Nevada town where groundwater levels were naturally elevated. 2006. 2007.. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 1999. 2008).. Valenzuela et al. environmental levels) and health effects is available from ATSDR at: http://www.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.S. although urinary arsenic levels were not associated with CCA contact (Shalat et al. 2006). 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. 1998. 2007. 2006.. WHO. 2008). urinary arsenic levels have been accepted as a good biomarker of dose (WHO. DMA produced bladder cancer in some chronic rat studies (Cohen et al... Pellizzari and Clayton 2006).61 (<LOD-3.. 1986).04 (<LOD-3.33 (<LOD-3. 1999.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and were about two-fold lower than those for the U. Offergelt et al..S. Pellizzari and Clayton. 2006).. Vahter et al.S.33 (<LOD-3..cdc. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. 2001).00) 1.atsdr. 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.80 (<LOD-4. gov/toxpro2. Levels of total urinary arsenic in the U. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.75 (<LOD-2. 2001).. Shalat et al. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al.50) 1. and the FDA has established a bottled drinking water standard. but generally only at maternally toxic doses (WHO. Survey years 03-04 Geometric mean (95% conf. Caldwell et al. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2006).e. 2000).. median urinary total arsenic levels in 4052 adults varied with seafood intake. 2001)..69 (<LOD-3. In the German Environmental Survey III of 1998. 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. 2006.

Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1-25. 2001. geometric mean levels were about 70-fold higher than for the U.43-1.800 (.90-7. 2000.4 (16. DMA and MMA.900 (.g. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.700-1. and two methylated metabolic products. 2005. 1985. arsenite.83) Selected percentiles ( 95% confidence interval) 50th 1.2-35.. 2006). China. population (Sun et al.29 (1.8 (12. Individually measurable species resulting from inorganic arsenic exposure are arsenate.20-3.30 (1. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.800) 1. Measurable organic arsenic species in this Report are three biologically generated environmental forms. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80 (3.8-50. Chowdhury et al.2-38...800-1.1) 18.00) 3. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. interval) 1.00-1. 2007) with higher levels of arsenic in the drinking water. population from the National Health and Nutrition Examination Survey.19 (. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.e.. Tseng et al.. Valenzuela et al.17-1.00 (.30) 10.40) 75th 5.00-12. population (Ahsan et al.70-21. Some noncancer effects of arsenic (e..S. When seafood intake is avoided.5) 32. and 0.20 (1..6 (25.80 (.20 (.11-1. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.3) 95th 35.50) . Survey years 03-04 Geometric mean (95% conf.4) 31. and TMAO.1-51.1) 45.93) 1. 2005..70) 6. population in the NHANES 2003–2004 subsample. arsenocholine.20) 7.6) 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.. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. The higher percentiles of total urinary arsenic levels in the U.7 (21. dermal keratosis.20-190) 31.50) . 2008). 4. 2007).8) 35.9) 13..20 (4. After recent seafood ingestion.. arsenite. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.. population showed a higher contribution of arsenobetaine (Caldwell et al. For residents of Inner Mongolia. 1.7 (13.5) 621 725 1078 Limit of detection (LOD. Caldwell et al.20-25.66 (1. 2000.1-94.62) 2. see Data Analysis section) for Survey year 03-04 is 0. vasospasm. respectively. Caldwell et al.48-2.3 (9..10 (4.68) . MMA. Caldwell et al. 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.Metals other areas of the world (Ahsan et al.20) 3.0) 4.9-23.8 (17.6 (11.8. 2003).05) < LOD .00-4.30 (2.00 (1.7) 13. 1990. in NHEXAS 1995–1996. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. and TMAO were detected in only 7.80-5.45 (1.0-23. which may vary for some chemicals by year and by individual sample. 2008).S..5 (26. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.400-. arsenocholine. In the residents of a Chilean town who consumed water with high levels of arsenic..31-1.900-1.60-3.70 (3.3) 1284 1284 03-04 03-04 03-04 1. 2008).871-1.80) 1. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.6 (13.50-6. Pellizzari and Clayton.10) 8. and duration of exposure are also considered important.. Caceres et al.0 (27.. Sun et al.3-39.20) 18. Aposhian et al.55 (1.700-1.2 (6.40) 5. In most human studies.4.8-40.5) 29. < LOD means less than the limit of detection.40-7.4) 23. arsenobetaine. 2008).S.90-29.6. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al. 1996..0) 29.600 (. 2008..5) 292 728 1548 03-04 03-04 1.S. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.40-6. 2008.6.800-4.7) 15.10) 4. Arsenate. Also.6-44.9 (6. 2000. and other factors such as nutrition.37 (1.500-1.20 (2.9 (7.800 (.70-21.80 (4.50) 90th 16.74 (1. when seafood organic arsenic is subtracted).7-22.28) 1. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.3% of a representative sample of the U.S.0 (26. with DMA..00-6.70 (5. These associations are stronger at higher urinary levels.3) 35.4-35. WHO. 2001). methylation capacity.30) 2.3 (21. In the late 1980s.60) 1. 184 Fourth National Report on Human Exposure to Environmental Chemicals .5 (14. Blom et al. 2005.

4) 32. 2006. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.15-1.S.39-3.32-7.4) 292 728 1548 03-04 03-04 1.6 (9. 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.959-1.65 (1. population from the National Health and Nutrition Examination Survey.15-4. 1998.05) 1.5 (18. Survey years 03-04 Geometric mean (95% conf.4) 13.82) Selected percentiles ( 95% confidence interval) 50th 1.Metals as with DMA.. interval) 1. 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.81 (4.29 (4.78-5.47 (2.3 (10.2 (12. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.55) 1.7) 9.68 (1. which is below the ACGIH BEI (Caldwell et al.19-2.1-36.400-.9 μg/L.44 (1.25-7.29-14.40) 1.76-27.67) 1. Caldwell et al. 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.53 (.3 (10. Offergelt et al. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.40 (1.2 (13. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Information about the biological exposure indices is provided here for comparison.638) 1..1-18.43) 75th 5.83) 2.6-32.4-21.36) 2.16 (.5 (18.612-1.54 (1.93 (1..S.00 (3. Vahter et al.4-28..50-7.9-18. 2001).1 (26.3-24.64-29. Fourth National Report on Human Exposure to Environmental Chemicals 185 .37-2. 2001)..9 (13.80-153) 17.5-20.7) 30.6-46.30-1. Sun et al.5) 17.3) 95th 29.12) < LOD .43) 14.82) 4.88) 2.73-6.1) 26. The 95th percentile of the U.4-82.67) 4.91) 90th 16. In recent years. 2003. 1992.88 (5.877 (. 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.833-1.25 (.531 (.5) 26.6 (6.83) 8.15-1.80) .51) 5. 2007). WHO.901-2.2 (4.30) 1.18-1.00 (1.61-6.909-1.45) 1.51-2. 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.91 (4.4 (11.9) 14. 2008).4 (24.10 (.62-6..8) 29..6-29.2 (12.50-15.70) 5.9) 32.58 (3.72) 12.13-39. 2008).6) 19. not to imply a safety level for general population exposure.21) 5. population for the sum of inorganic related species was 18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.28) 1.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.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 * * 1.11 (.47 (1.78 (3.938-1.14 (1.3) 1284 1284 03-04 03-04 03-04 1. 1986.786-1.0-36.0 (9.9 (25.7) 17.79 (1.05 (..

population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. Survey years 03-04 Geometric mean (95% conf.6.Metals Urinary Arsenocholine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 0. which may vary for some chemicals by year and by individual sample. 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. 186 Fourth National Report on Human Exposure to Environmental Chemicals . Survey years 03-04 Geometric mean (95% conf.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 < 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.S. Urinary Arsenocholine (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 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.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 1.2.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey years 03-04 Geometric mean (95% conf.44) 2. Survey years 03-04 Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 1.S. Urinary Arsenous (III) Acid (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. population from the National Health and Nutrition Examination Survey.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 2.08 (<LOD-4.40 (<LOD-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.95 (<LOD-2.76) < 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.S.80) < LOD 621 725 1078 Limit of detection (LOD.00 (<LOD-2.29) < LOD 621 725 1078 < 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. 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 1.00 (<LOD-3. Fourth National Report on Human Exposure to Environmental Chemicals 187 . 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.

0 (10.2) 10.9 (7.90) 2.80-5.20-12.00-8.61-11.0-16.84-8.00 (6.00 (7.00) 6.15) 4.11) 4.20-4.85 (3.39-3.6-18.00) 9.24-4.34-4.82) 3.34 (3.00 (3.0 (14.03 (3.70-4.00) 90th 11.80-6.09 (7.00-11.9) 11.12-4.00) 7.71 (4.12 (3.45) 3.92-12.98) 4.0) 10.31-4.0) 14.74) 90th 9.80) 2.17 (2.05) 3.00-7.0) 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 4.49-4.00 (5.05) 5.9 (11.00-4. interval) 3.37 (3.0 (13.0 (12.00) 3.0) 13.00-3.57-5.55 (2.69 (3.03-6.0-12.73) 6.00-10.00-15.5) 95th 13.9) 13.8) 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 3.0) 12.14) 3.00-3.7) 12.00-12.82-9.62) 4.00) 6.28) 2.0) 11.91) 75th 5.97-3.00 (5.00) 75th 6.0) 9.34) 3. Survey years 03-04 Geometric mean (95% conf.00 (3.90) 5.50 (4.72 (4.29-4.0) 292 728 1548 03-04 03-04 4.5 (11.32-10.27 (2. interval) 3.00) 5.0 (12.00 (3.0) 16.16-11.8) 7.00-11.00-4.34-4.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (9.27-2.33) 3.00 (5.14) Selected percentiles ( 95% confidence interval) 50th 3.65-8.60-4.0) 17.00-13.94-3.30) 3.80 (4.86 (2.0) 17.3 (8.00) 6.0) 95th 16.95-4.57 (3.0 (13.44 (2.31) 4.00 (6.1 (8.0 (10.00-4.67) 9.3 (7.4 (7.0-19.82-5.00 (7.44) 5.00-4.10) 6.32 (8.0) 11.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .78) 4.88 (4.37 (2.50-5.95-3.S.33-4.7 (10.86-7.17-4.7) 1284 1284 03-04 03-04 03-04 4.34 (3.00-7.0 (11.00) 6.67) 8.81 (5.6) 1284 1284 03-04 03-04 03-04 4.9) 12. see Data Analysis section) for Survey year 03-04 is 1.69 (3.80-3. population from the National Health and Nutrition Examination Survey.59 (6.0-18.69-3.70-12.0 (10.89 (3.16 (4.00-4.18 (6.94) 3.3 (8.70) 5.20) 11.06) 5.8) 7.0) 16.17-6.00 (6.95 (4.24) 3.48 (3.9) 5.00-4.70 (3.49) 10.60-3.00 (3.00) 12.0 (8.0) 9.90 (3.77 (3.0) 621 725 1078 Limit of detection (LOD.27-5.00-7.00) 4.61-16.79 (3.00 (5.00 (3. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.7-16.5) 12.00) 3.16 (2.86-21.7) 13.05) 10.73 (3.27 (3.00-15.00-5.46 (4.84-18.78 (4.0-17.70-3.1-18.00) 4.0 (10.32 (4.08 (2.71-4.1-15.0) 9.50-15.6 (9.48 (2.00-22.71) 3.00-11.0 (8.00-7.42) 3. Survey years 03-04 Geometric mean (95% conf.60-7.1-22.45 (8.0-25.00-15.74 (2.11 (3.19) Selected percentiles ( 95% confidence interval) 50th 3.52) 3.00 (4.0 (9.S.13-4.45) 8.10) 3.0) 13.6) 292 728 1548 03-04 03-04 3. population from the National Health and Nutrition Examination Survey.95-6.00-9.00-12.00 (3.80) 7.60-6.0 (9.30 (7.92) 3.00 (5.71 (3.65-6.0-17.38 (3.25 (4.0-16.69-6.7.22) 4.

60-2.9.50 (<LOD-1.88 (1.10-1.20 (1.28 (1.18-1.80-2.53-2.43-3.37 (1.71-2.36 (1.90) 2.50) 621 725 1077 Limit of detection (LOD.60 (2.35-3.96-2.58) 2.85) 1.22 (1.62) 2.15-1.63 (<LOD-1. Survey years 03-04 Geometric mean (95% conf.80 (1.00 (1.30-1.70-2.80 (2.30 (2.10 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.53 (1.20 (1.70-2. 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 1.77) 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 1.816 (<LOD-.00-1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.10 (.36) 1.61-3.00 (<LOD-1.00) 2.86) 3.57) 95th 2.900-1.07 (1.70-2.31-3.10-1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .50 (1.40 (2.40-3.60) 2.80) 1.10 (<LOD-1.30-1.52 (2.10) 95th 2.40) 2.40-2.16 (2.00-4.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50 (1.30) 2.70) 2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00 (<LOD-1.80 (1.31 (1.30) 1.70-3.10 (. < LOD means less than the limit of detection.40-2.20-1.30 (1.11-1.90) 1.61) 2.80) 1.20 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.46 (1.93) .33 (1.79) 2.00-2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.00) 2.88 (1.30 (1.33 (1.17) 2.985) 1.50) 1.90 (1.20 (1.07-3. which may vary for some chemicals by year and by individual sample.20) 2.00) 1.50-2.S.80 (1.54) 90th 2.86) 2. population from the National Health and Nutrition Examination Survey.60) 2.80-2.82-2.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.90) 2.S.00) 1.00 (2.88-2.10) 2.30 (1.85) 2.853-1.60 (1.18-1. see Data Analysis section) for Survey year 03-04 is 0.23) 1.82-2.81) 1.70-2. Survey years 03-04 Geometric mean (95% conf.10 (1.00-2.45) 3.84-3.00) 1.34) 2.40) 1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.30) 1.07) 2.40-3.00 (2.60) 1.00-1.80 (1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.20 (1.46-2.20-3.90 (2.10-3.05-1.30) 90th 1.20 (1.22) 3.73-2.40) 1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.50 (2.40 (1.30-2. population from the National Health and Nutrition Examination Survey.14-1.86 (2.86 (2.28 (1.

which may vary for some chemicals by year and by individual sample. 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. Survey years 03-04 Geometric mean (95% conf.0. see Data Analysis section) for Survey year 03-04 is 1. Survey years 03-04 Geometric mean (95% conf.Metals Urinary Trimethylarsine oxide 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 < 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. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. Urinary Trimethylarsine oxide (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. population from the National Health and Nutrition Examination Survey. 190 Fourth National Report on Human Exposure to Environmental Chemicals .S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Arsenic: signal transduction.84(5):1093-1101. 8/7/08 Ahsan H. Sumi D. Caceres DD. Chanda CR. Moldeus P.13(8):693697. Chowdhury UK. Graziano JH. Environ Health Perspect 2006. Updated September 2004 [online].36(2):99-133. Gamble MV. J Environ Sci Health A Tox Hazard Subst Environ Eng 2003. Sengupta MK. Gurzau A. J Expo Anal Environ Epidemiol 2003. Arsenic exposure to smelter workers. Rahman MM. Beck BD. et al. Chem Res Toxicol 2000. Jakubowski M. Hughes MF. Gandolfi AJ. Eldan M. Le XC. Le XC. The effect of variable environmental arsenic contamination on urinary concentrations of arsenic species. Human health effects from chronic arsenic poisoning--a review. Hudgens E. Cellular metabolism of arsenocholine. Toxicol Appl Pharmacol 2006. cigarette smoking. Arsenic methylation patterns before and after changing from high to lower concentrations of arsenic in drinking water. Jagadish B.107(8):663-667.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Burgess JL. Ahsan H.gov/toxpro2. Josyula AB. Smith AH. MMA(V). Some Drinking-water Disinfectants and Contaminants. Toxicological profile for arsenic. Atalah E.104(11):1200-1207. Bhattacharya P. Monomethylarsonous acid induces transformation of human bladder cells. Bredfeldt TG. International Agency for Research on Cancer (IARC). Norin H. Eblin KE.24(3):298304.11(4):265-269.pdf. Pattern of excretion of arsenic compounds [arsenite. Fourth National Report on Human Exposure to Environmental Chemicals 191 . et al. Rahman A. Hsueh YM. Trzcinka-Ochocka M. Kapaj S. Kurzius-Spencer M. arsenate. House dust and inorganic urinary arsenic in two Arizona mining towns. Reidy JA. Peterson H.fr/ENG/Monographs/vol84/ volume84. Cohen SM. Blom S. Linderholm H. Coble K. Folate and arsenic metabolism: a double-blind. Documentation of biological exposure indices.114(11):1790-1796. Annu Rev Pharmacol Toxicol 2007. J Appl Toxicol 1988. Chen CL. Cancer Epidemiol Biomarkers Prev 2007. Healy SM. Matczak W.41(10):2399-2428. Hsu LI. Cincinnati (OH): ACGIH Worldwide. Wu MM.98(2):151-159. Pilsner JR. Chen SY. Hopenhayn-Rich C. Int Arch Occup Environ Health 1998. Loomis D. Methylated arsenicals: the implications of metabolism and carcinogenicity studies in rodents to human risk assessment. Bolgiano D. Sandstrom M.47:243-262. Liu X.292(24):2984-2990. Ingested arsenic.iarc. 7th edition. Occurrence of monomethylarsonous acid in urine of humans exposed to inorganic arsenic. Associations between drinking water and urinary arsenic levels and skin lesions in Bangladesh. Kumagai Y. Exposure to inorganic arsenic in drinking water and total urinary arsenic concentration in a Chilean population. Ye X. Zheng Y. Environ Res 2005. Parvez F. Chiou HY. Calafat AM. Aposhian HV. Kalman DA. J Health Popul Nutr 2006. Needham LL. 8/7/07. Clinical and neurophysiological studies. Stute M.16(2):207-213. O’Rourke MK. Environ Health Perspect 1996. and biotransformation involved in cellular response and toxicity. Environ Health Perspect 1999. Moore LE. Parvez F. et al. Biggs ML. Summary of Data Reported and Evaluation. and lung cancer risk: a follow-up study in arseniasis-endemic areas in Taiwan. et al.116(7):893-897. Hysong TA. transcription factor. including Arsenic. Burbacher T. Excretion of arsenic in urine as a function of exposure to arsenic in drinking water. Razniewska G. van Belle G.42(12):1195-1201. J Occup Environ Med 2000. J Environ Sci Health A Tox Hazard Subst Environ Eng 2006. Chen Y. September 2005 [online]. Poplin GS. McClellen H. placebocontrolled folic acid-supplementation trial in Bangladesh. Hysong TA. Calderon RL. Wong LY. Lagerkvist B. Biological monitoring of occupational exposure to arsenic by determining urinary content of inorganic arsenic and its methylated metabolites. DMA(V)] in urine of children compared to adults from an arsenic exposed area in Bangladesh. et al. Perrin M. Scand J Work Environ Health 1985. Gurzau ES.atsdr. Lewis AS. American Conference of Government Industrial Hygienists (ACGIH).89:145-151.cdc. et al.html. Hughes J. A prospective study of blood selenium levels and the risk of arsenic-related premalignant skin lesions. Reduction in urinary arsenic with bottled-water intervention. Thomas DJ. et al. Sturup S. Lu X. Slavkovich V. Lodh D. JAMA 2004. Available at URL: http://monographs. Pino P. Hall M. Ryhage R.13(3):211-218.216(1):69-79. Concentrations of the sunscreen agent benzophenone-3 in residents of the United States: National Health and Nutrition Examination Survey 2003-2004. Environ Health Perspect 1990.8(2):119-127. Schreinemachers D. Arnold LL.38(1):87-113. Montesinos N. Environ Health Perspect 2008. et al. 2001. Available at: http://www. Thor H. Biomarkers of exposure: a case study with inorganic arsenic. Liber K. van Geen A. Roy S. Cebrian Garcia ME. Slavkovich V. Mash EA.71 Suppl:S29-32. Crit Rev Toxicol 2006. Kalman DA. Am J Clin Nutr 2006. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Volume 84. Amigo H. Ilievski V. Christakopoulos A.

210(3-4):271-297. A pilot study of children’s exposure to CCAtreated wood from playground equipment.org/documents/ehc/ ehc/ehc224. National Research Council (NRC). J Anal Toxicol 2006. Toxicol Appl Pharmacol 2005. Environ Health Perspect 2006. Yang MH. Available at URL: http://www. Nolinder P.57(2):79-91. Vahter M.49(6):387-393.367(1):80-88. Thio-dimethylarsinate is a common metabolite in urine samples from arsenic-exposed women in Bangladesh. Tseng CH. Moore LE. Flanders WD. Fact Sheet: Drinking Water Standard for Arsenic. Roels H. Environmental Health Criteria 224. CruzGonzalez MB. urinary arsenic speciation.Metals Kwon E. 3rd Ed. Garcia-Montalvo EA.96(2):119126. Nygren A.114(8):1293-1296. Sci Total Environ 2006. Br J Ind Med 1992. U.epa. Marshall G. et al. Int J Hyg Environ Health 2007. Geneva 2001.epa. Jones RL. Fok N. Yuan Y. Morton J. Biggs ML. Wang Z. Arsenic on the hands of children after playing in playgrounds. Lauwerys RR. Twenty years of the German Environmental Survey (GerES): human biomonitoring--temporal and spatial (West Germany/East Germany) differences in population exposure. Shipp M.30(5):293-301. Jimenez M. Investigating childhood leukemia in Churchill County. World Health Organization (WHO). Solo-Gabriele HM. Garcia-Vargas GG. Holmes AK. Environ Health Perspect 2006. Mason H.211(2):175.htm. Urinary trivalent methylated arsenic species in a population chronically exposed to inorganic arsenic. Sun G. Rumpler A. html. 8/8/07 192 Fourth National Report on Human Exposure to Environmental Chemicals .36-37. using a routine LC-ICP-MS method. EPA). GSTM1 and T1.113(3):250-254. Mexico. Environmental Protection Agency (U. Assessing the measurement precision of various arsenic forms and arsenic exposure in the National Human Exposure Assessment Survey (NHEXAS). Boca Raton (FL). Liaw J. Environ Health Perspect 2005. Rubin CS. Burgess JL. Arsenic. Erratum in: Toxicol Appl Pharmacol 2006.115(4):648-652. Genetic polymorphisms in MTHFR 677 and 1298. et al.gov/iris/subst/0278. Arsenic in drinking water-2001 update. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 2007. Schulz C. et al. Environ Res 2004. Valenzuela OL. Buchet JP. von Ehrenstein O. Kalman D. Li B. Naranmandura H. Borja-Aburto VH. Kieszak SM.inchem. Guidelines for Biological Monitoring. inorganic.S. Steinmaus C. Raml R. Offergelt JA. Arsenic methylation. Hoet P. Huang YK.115(1):151-157. Seifert B. EPA). urinary arsenic metabolites and human diseases: current perspective. Belson MG. Goessler W. Chem Res Toxicol 2007. Calderon-Aranda ES. Boeckx M.gov/safewater/arsenic/regulations_factsheet. J Toxicol Environ Health A 2007.S. Integrated Risk Information System. Meza MM. Arsenic in Drinking Water. Li L. Zhang H. Pellizzari ED.S. Sun X. 2001. Arsenic and Arsenic Compounds. et al. Environ Health Perspect 2007. 8/7/07. Jhangri GS. and metabolism of arsenic.htm. Li X.222(3):374-380.K. Available at URL: http://www. In:Industrial Chemical Exposure. Environ Health Perspect 2004. Vahter M. Huang YL.25(1):1-22. 2nd ed. Arsenic drinking water exposure and urinary excretion among adults in the Yaqui Valley. Lewis Publishers. Toxicol Appl Pharmacol 2007. 1998 [online]. et al. Fleming LE. Urinary arsenic metabolites in children and adults exposed to arsenic in drinking water in Inner Mongolia. et al. Conrad A. Lu X. Environ Health Perspect 2007. Lauwerys R. Ibata K. Increased mortality from lung cancer and bronchiectasis in young adults after exposure to arsenic in utero and in early childhood. Black K. Seiwert M. Tseng CH. Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites. Arsenic. Becker K. EPA 815-F-00-015. Jin Y. Friberg L. Buckley BT.114(2):220-227.112(14):1375-1380. Toxicity of dimethylmonothioarsinic acid toward human epidermoid carcinoma A431 cells.20(8):1120-1125. Available at URL: http://www.70(2):159-170. Ferreccio C. Kopplin MJ. Int Arch Occup Environ Health 1986. Rahnster B. Environmental Protection Agency (U. Francesconi KA. and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. pp. Ochi T.S. Washington (DC) National Academy Press. Speciation of arsenic compounds in urine from occupationally unexposed and exposed persons in the U. 2001. 8/7/07 U. Nevada. Kolossa-Gehring M. Clayton CA. Shalat SL. China. Rey OA.206(3):299-308. Smith AH. Sonora. et al. Arsenic exposure. January 2001 [online]. Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers. Chen CJ. Suzuki KT. Chung CJ. Gandolfi AJ. Xu Y.

97 (1.54) 1.43) 6.70-6.71) 2.85) 1.20-8.93-8.86 (4.41) 1.01 (4.57 (5.05% of the earth’s crust.29-5.20-8.61 (3.54 (2.62) 1.80 (1. 0.38) 8.78) 1.56) 4.20 (1.16 (1.40) 7.37-8.10) 5.66) Selected percentiles ( 95% confidence interval) 50th 1.27 (1.30) 4.65) 3.50-6.59-11.90-13.00-76.20 (3.30 (5.35) 5.50) 2.12-1.34 (1.01-7.65) 1.54 (6.48) 1.54-8.40 (5.71-9.73 (6.15 (6.56) 1.90 (6.28-1.35-1.94-6.76) 1.87-14.90-9.8) 5. fireworks.14 (6.36-1.60) 1.50 (1.50 (1.9) 5.32-1.62 (1.60-6.21-2.99-5.10) 3.50 (1.60-2.4) 7.40 (1. and 0.76-7.87-3. soluble forms of barium.87 (6.40 (1.54) 1.22-1.73 (5.60 (1.8 (6.34 (2.44-2.05-2.70-2.71) 1.63) 1.47) 4.10) 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 1.21 (1.70-2.20) 2. 7440-39-3 Medically.44-5.39) 1.82) 2.85 (2.80 (5.03 (1.20-1.63) Total 1.14-6.19) 2.50 (1.63 (1.39 (1.60) 3.90) 2.50 (5. glass.50 (6.S.39 (1.10 (2.40 (4.40 (5. Workers employed by industries that make or use barium compounds can be exposed to barium dust.40) 7.87 (5.24 (4.95-6.43 (1.49-1.43) 2.56 (1.35-1.50) 4.78-2.43 (1.64 (1. depilatories.26-1.12 (2.06-1.80) 6.50 (4.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 2001). Barium compounds are also used commercially in paint.29) 5.15 (2.21 (1.28) 90th 5.56 (1.31 (2.60) 4.80-5.30) 3. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and ceramics.53-5.15-1.95 (4.57-7.19-1.46) 1.1) 9.51 (1.30-1.87) 7.88) 7.52 (4.88) 1.72) 1.69 (1.65-1.37) 5.4) 9.00 (2.72) 75th 3.18-1.38 (1.50-1.91) 2.40 (5.20-1. barium sulfate and barium carbonate).71 (2. and 03-04 are 0. Small amounts of barium can be released into the air during mining and other industrial processes.34 (1.50 (3.51) 1.14-1.80 (2.63 (8.20-8.48-4.76 (3.98) 1.80) 1.60-3.00-8.61 (1. respectively. such as brazil nuts.70) 1.81-2.11-1.11 (2.56 (2. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.g.46-1.55-7.50-6.80-3. Certain foods.46) 1.61 (5.54) 2.Metals Barium CAS No.70) 4.70) 1.43) 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. The general population can be exposed to low amounts of barium in air.70-8.70 (1.90 (1.90) 1.36-1.04-2. Barium salts have also been available as rodenticides.25-1.15 (1.18) 3.35 (2.70) 3.74-3.78) 1.50-1.80 (1.00 (1. 01-02.52 (1. In single dose animal studies.36 (4.86 (4.20-6.12 (2.74) 3.81-2.30 (1.11 (3.49) 4.27) 2.78-3.65) 1.36 (1.51) 2.41-1. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).50 (4.65 (5.73) 3.35 (3.00) 1.63 (5. population from the National Health and Nutrition Examination Survey.30 (5.50 (1.20-1.44 (1.59) 3.30) 2.37) 1.76-2.43 (5..61 (1.30) 5.60-6.25 (1.25-11.30-5.67) 6.20-1.30) 5.54-1.15) 5.10-5.40-13.65-5.86-4. Barium compounds are used by the oil and gas industries to make drilling muds.08 (6.12) 7.57) 3.30 (2.92) 2.99 (4.50 (4.77 (3.63 (2.73-5.50) 2. it combines with other chemicals such as sulfur or carbon and oxygen.70-5.4) 6.06-2.39) 4.35 (1.56 (6.82) 1.12.09 (2.50 (2.68 (1.24-1.30) 8.00) 6.22-1.87-7.50) 1.80-7.48 (6. water.12) 6. Some barium salts are freely soluble in water.91) 6.16) 5.18 (6.38) 2.64) 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 2.70) 7.80 (1.33 (1.31-2.48-4.00) 4.30) 5.47-1.31.70) 5.82-6.24-1.96-2.26) 5.08-8.00) 1.80 (2.73) 1. whereas others are practically insoluble (e.88) 4.45 (1.60 (2.90) 4.63) 1.49 (1. In nature.07 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.41-3. interval) 1.35-4.10-4.49) 2.54-1. see Data Analysis section) for Survey years 99-00.62 (1.17-1.75-3.02 (7. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.49-9.38 (1.48) 1.49) 8.26-7.81-3.51) 7.90 (4.75) 2.30-3.36) 5.87-9.20-5.93-2.80) 7.49) 11.84) 5.72) 4.76-3.90) 2.39-1.37 (4.10 (4.77-3.30-2.32) 8.40) 3.60-10.15-1.29-1.00-3.93 (4.80-2.30-2.20 (4.91 (2.61 (2.64-3.70-3.62) 1.53) 2.86) 6.21-8.09 (1.11 (3.55-3.32-7.90-2.53) 1.26) 2.70 (5.8) 9.77) 1.10 (3.86-5. rubber.66 (4.85) 1.15-11.30 (3.34) 2. bricks. such as barium chloride.22) 6.65-8.2) 6.42 (1.71) 95th 6.88 (5.12. tiles.40 (1.74-2.45) 7. and food.37-1.47-1. Fourth National Report on Human Exposure to Environmental Chemicals 193 .60) 1. are high in barium (Genter.30-1.27 (1.61-8.04-6.

86) 5.08-1.15-4.45-6.10 (6.777-1.97 (4.28-6. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter. diarrhea.53 (2.81-6. NTP.08-2.16-1.06) 2.2) 6.24-6.45 (3.61) 2.02-5.45) 1.29-4.55) .24-1. 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.04) 5.54 (1.47 (2.69-9.42) 1.04) 1..46) 1. population from the National Health and Nutrition Examination Survey.49 (1.963 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. paralysis.55 (4.43-6.60 (5. hypertension. 1984.45-1.28) 5.09) 6.00) 4.39 (2.16 (1.69 (5.45) 95th 6.39 (2.78 (2. 1989).52-10..06) .62 (1.31 (1.11) .51-3.36 (3.2) 5.10) 3.36 (5.47-8.96) 7.32 (2.73-2.23-1.54) 2.64 (1.54 (2.68 (2.01 (4.59 (1. Following intravenous injection in animals.0) 5.41) 5. Toxicity from soluble barium salts is rare.51 (1.30 (1.59-7.73-4.62) 2.48) 2.57) 2.39-1.13-3.80) 4.88 (2.46-22.76 (3.46 (2.57 (6.03) 3.52-4. 1985.11) .81-6.92 (4.70) 4.22-1.28-1.48-3.72) 4.40 (1.44-2.00 (2.67-6.68 (3.59 (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 1.39 (3. Chronic high doses in animals resulted in kidney damage (McCauley et al.65 (5.56) Selected percentiles ( 95% confidence interval) 50th 1.84-5.29 (1.98 (2. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.34-1.41 (1.29-7.41) 4.37 (1.51) 4.60 (2. such as those used in medical radiographic procedures.915 (. water solubility.68-3.26-1.50) 1.00-7.53) .44-2.47) 1.55-6.Metals was eliminated primarily in feces and to a lesser extent.03-1.20-1.59) 2.29) 1.99 (4.16) 11.47) 10.25-11.47) 4.14-2.34) 1. chemical form.58-6.4 (5. and route of exposure.36-1.74 (5.47 (5.880-1.45-1.24) 3.76 (2.18 (1.76) 2.01 (5.46) 2.40 (1.77) 1.20) 4.76 (4.33-4.56-3. 1990).62 (2.60 (2.38) 1.77) 1.31-1.34-3. weakness.68-3.91 (3.22-1.89 (2.24-11.39-1.96 (4.42) 1.36 (3.26-1.31 (4.45-8.56) 4.0) 7.55 (5.50) 1.46) 3.4) 5.66 (1.25) 4.48 (1.56 (1.24-3.40 (1.76) 2.82) 1.35-1.10-1.92) 2.19-1.55-5.70) 1.74) 1.38) 1.58 (2.30) 2.10) 6. Insoluble barium salts.84) 2.97 (5.52) 7.13-2. Barium is not rated for human carcinogenicity.36 (1.84-2.19-2. vomiting.49 (1.23-2. interval) 1.39) 4.51) 6.35-1.01) 1.881 (.3 (6. in urine.32 (1.26-4.76-3.33 (1. Perry et al.85-5.56 (1.89) 90th 4.0) 6.79-5. The health effects of exposure to barium compounds depend on the dose.77) 5.41 (1.54) 1.39 (2.64 (1.57-5.48-5.72) 6.64) 7.81-7.31-1.48-1.23-5.96 (4.82) 1.91-2.41 (2.59) 1.37) 2.86 (2. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.42 (4.754-1.31) 5.75) 1.38-7.29-1.00-1.68) 3.75) 2.37 (1.38 (1.48 (1.49-1.02) .21 (1.97-3.59) 1.49-1. Wones et al.03) 1.60 (1.68 (3.75-22.8) 4.52 (3.20 (1.02) 4.49-1.03) 2.38 (1.11-2.04 (2.02 (3.68) 1.921 (.25 (1. a benign condition that may occur among barite ore miners.26) 4.27) 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 .96) 4. 2001).38) 4.38 (4.50 (4.77) Total 1.00) 6.24 (5.36-1.891 (.33-1.36-2.90-2.832-1.00) 4.3) 6.19-1.65 (2.38-1.5) 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. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves. are not absorbed when administered.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 2.87) 1.S.96-6.62 (4.97-4.97) 1.43) 1.63) 1.34 (1.905 (.703-1.33) 1.33) 6.63-4.27) 7.61 (4.00 (3.39-5.99 (2.32) 2.58 (4.51 (3.75) 1.18 (1.51 (1.79) 1.75-3.30 (1.91 (3.31-1.33 (5. 1986).47) 1.29-3.52) 2.71 (5.32 (1.58) 4.64 (1. 1994. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.28-7.32) 2.28 (1.29 (3.00 (5.64 (1.05-1.2 (3.26-1.99) 1.03-1.37-1.38-5.24-6.73) 2.29-4.48 (1.77) 1.57-7.96) 4.84 (3.51) 4.44 (1.10-2.00) 1.24 (3. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.72 (2. Symptoms following acute high dose include perioral paresthesias.58) 1.80) 3.35-3.55 (1.00 (3.77-5..27-3.27-1.28-11.50) 2.64) 7.96) 4.76) 1.33 (1.86-7.36 (1.75) 2.24-1.39-10.26-1.20-8.80-6.22-4.19-1.45 (1.38 (4.88 (6.710-1.40-1.83) 2.22-2.27 (2. and cardiac dysrhythmias.34-5.91) 2.70) 10.37-2.12) 2.83) 3.74) 1.55 (1.20-2.58) 75th 2.53-21.57-10.60 (1.52) 1.

2005.. Patty’s toxicology. Comparison of representative ranges based on U.gov/ntp/htdocs/LT_rpts/tr432. [online]. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Centers for Disease Control and Prevention (CDC). Barium. et al. et al. 2000) to levels in NHANES 1999-2000 and 2001-2002. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Minoia C.nih.. p. Environ Res 1998. Cohressen B.. Pirkle JL. Pietra R. Jr. 2001-2002. strontium.html?charset=iso-88591&url=http%3A//ntp. Perry HM. Powell C. Sampson EJ. Calabrese EJ.gov:8080/cs. 84-94. 4/8/09 Paschal DC. and serum of Italian subjects. In Friberg L. Clin Chim Acta 2000.atsdr. Genter MB. Magnesium.85:355-359. In: Calabrese EJ.S. et al. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding.197210. Available at URL: http://ntp. Reeves AL. 1986. Costa R. calcium. Information about external exposure (i. LA. Douglas BH.cdc. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no.niehs. p.296(1-2):71-90.64(1):13-23. 1984.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. Zschiesche W. 1994. Morrow JC. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. pp. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Frohman. Lack of effect of drinking water barium on cardiovascular risk factor.html. Jackson RJ. National Toxicology Program (NTP). ed. NTP. ed. Weltle D. Perry EF. Nordberg GF. 2001.. New York: Elsevier. Pozzoli L. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000.. References Brenniman GR. Apostoli P.nih. 2nd Ed. Levy.. patient population and literature reference intervals for urinary trace elements. eds. Trace metals in urine of United States residents: reference range concentrations. Vol 2: Specific Metals.e. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). 221-252 Komaromy-Hiller G. Princeton (NJ): Princeton Scientific Publications. Advances in modern toxicology. Paschal et al. 1990. Ting BG.. 1992).S. Investigations into the effect of drinking water barium on rats. and 2003-2004 (CDC. J Toxicol Environ Health. Exposure to soluble barium compounds: an interventional study in arc welders. Howerton K. New York: John Wiley & Sons. barium. Atlanta (GA). et al. Laurie RD. Handbook on the Toxicology of Metals. Epidemiological study of barium in Illinois drinking water supplies. 231-249. Wones RG.niehs. 5th ed. eds. Kopp SJ. Sci Total Environ 1990. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. A study of 46 elements in urine.76(1):53-59. Vouk VB. Ash KO. and radium In: Bingham A. Stadler BL.. 1989. Environ Health Perspect 1990. Schaller KH. Fourth National Report on Human Exposure to Environmental Chemicals 195 . and a drinking water standard has been established by U. In: Inorganics in drinking water and cardiovascular disease. blood. Gallorini M. Biomonitoring Information Levels of urinary barium reflect recent exposure. the welders had no obvious adverse clinical effects (Zschiesche et al. 1985. 1998).28(3):373-388. Princeton NJ: Princeton Scientific Publications. Trace element reference values in tissues from inhabitants of the European community I.95:89-105.gov/toxpro2. McCauley PT. 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. Inc. EPA. Minoia et al.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. 2005. p. Third National Report on Human Exposure to Environmental Chemicals. PS. environmental levels) and health effects is available from ATSDR at: http://www. Int Arch Occup Environ Health 1992. Sabbioni E..

130 (<LOD-. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. aircraft. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. and refined beryllium is used in mirrors and special metal alloys for the automobile. population from the National Health and Nutrition Examination Survey. Two types of minerals.13. 01-02. electrical. In studies of laboratory animals. see Data Analysis section) for Survey years 99-00. x-ray machines. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. soil. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. and machine-parts industries. and from breathing tobacco smoke. eating food. In medicine. Beryllium compounds are commercially mined. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 7440-41-7 General Information Pure beryllium is a hard gray metal. computer. 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 .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 . are mined for commercial recovery of beryllium. coal. < LOD means less than the limit of detection. and can be found in mineral rocks.13. bertrandite and beryl. and dental bridges.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. or drinking water containing the metal. which may vary for some chemicals by year and by individual sample. and 03-04 are 0. and 0. beryllium is used in instruments. 0.150) < 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 .140 (<LOD-. respectively. near some hazardous waste sites. Exposure to beryllium occurs mostly in the workplace. 196 Fourth National Report on Human Exposure to Environmental Chemicals .13.S. the lightest of all metals. Low-level beryllium exposure in the general population can occur through breathing air. nuclear. and volcanic dust.130 (<LOD-. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. * 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. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. or berylliosis. population from the National Health and Nutrition Examination Survey.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.346 (<LOD-. 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. EPA. 2002). 1990). which produces pneumonitis.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 . Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. Fourth National Report on Human Exposure to Environmental Chemicals 197 . Maier..281 (<LOD-. NTP considers beryllium to be a known human carcinogen.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 . 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 . including contact dermatitis and subcutaneous nodules. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. respectively. based upon excess lung and central nervous system cancers in studies of workers.S. Skin exposure can result in delayed hypersensitivity reactions.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. Chronic beryllium disease. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.231 (<LOD-. and drinking water and environmental standards have been established by U. 2003. IARC has classified beryllium as a human carcinogen. S.

20012002. plasma and urine and a critical evaluation of reference values for the United Kingdom population.12 to 0.S. Clin Chest Med 2002.23:827-839.76(1):53-59. population were generally undetectable in NHANES 1999-2000. Van der Venne MT.157:388-398. Ash KO. Pietra R. Hamilton EI. 1990. 1998).1 μg/L).95:89-105.. A study of 46 elements in urine. 2001).158:165-190. Kriess K.. Morrow JC. et al. Environmental Health Criteria. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Centers for Disease Control and Prevention (CDC).296(1-2):71-90. References Apostoli P. VI. Sabbioni E. International Programme on Chemical Safety (IPCS).gov/toxpro2. 0. it is likely that urinary beryllium levels in the U. In other studies. Review of elements in blood. Pozzoli L. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Environ Res 1998. Trace element reference values in tissues from inhabitants of the European community I. Am J Epidemiol 2003. 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. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Third National Report on Human Exposure to Environmental Chemicals. Genetic and exposure risks for chronic beryllium disease. and 2003-2004. patient population and literature reference intervals for urinary trace elements.13 μg/L. Sabbioni E. Minoia et al. Schaller KH. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect.S. 198 Fourth National Report on Human Exposure to Environmental Chemicals . environmental levels) and health effects is available from ATSDR at: http://www. Costa R.org/documents/ehc/ehc/ ehc106. Gallorini M.e. Jackson RJ. less than 0. Howerton K. Hamilton et al. Maier L. Atlanta (GA) 2005. Paschal et al. HLA-DPB1 and chronic beryllium disease: a HuGE review. Comparison of representative ranges based on U. Sampson EJ. Pirkle JL. Sci Total Environ 1990.atsdr.74:162-166. Sci Total Environ 1994. Andrew M.cdc. Trace metals in urine of United States residents: reference range concentrations. and the 95th percentile for males in NHANES 2001-2002. 106. Available at URL: http://www. Ting BG.htm. Given these results.inchem..Metals (i. Levels of beryllium in urine for the U. Beryllium [online]. Clin Chim Acta 2000. Element reference values in tissues from inhabitants of the European community. and serum of Italian subjects. 3/27/08 Komaromy-Hiller G. 2000. They reported urinary beryllium levels ranging from 0. Paschal DC.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. McCanlies EC. Int Arch Occup Environ Health 2001.S. Weston A.html. 1990. which approximate this Report’s limit of detection.e. population are lower than levels in workers. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. and the fact that most NHANES participant levels were undetectable. Minoia C..15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. blood. Apostoli P. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. et al.

500 (.400) .10 (.331) .400 (.500 (.300 (<LOD-.20) 1.800-1.300) .600) . respectively.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 .367-.40) 1.700-1.300-.900-1.70) 1.00-1.600 (. The predominant commercial use of cadmium is in battery manufacturing.800) .S.700) .300 (.600 (.400) < LOD . and nonferrous alloys.255) .40 (1.30) 1.300-.449) Selected percentiles ( 95% confidence interval) 50th . lead.300) .30) .00-1.400 (. Since 2001.600) .300) .10) 1.378-.368-.20-1.50 (1.10) 1.500-.70) 1.usgs.500 (.366) * * .400-.337) .460) . U.700) .400) .400-.424) * .400) .60 (1.400-.326 (. interval) .200) .361-.500-. 01-02.400 (.500 (.441) * .500 (.40-1.300-.600) .500-.600-.400) .00 (. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.300-.600 (.500-.20) 1.304 (.386-.400-.513) .427) * .60 (1.40 (1.90) 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 * * * * * * .300) .600) 1.425 (.600 (.00) .500-.600 (.500-.500-.400) < LOD .00-1.10 (1.200 (.600-1.200-.30-1.700 (.900-1.300 (.300) .500-.344) .600) . as zinc sulfide) and to a lesser extent. malleable.400 (.300 (.426-.300-.800) 1.400 (.600 (.300 (<LOD-.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3. which may vary for some chemicals by year and by individual sample.300-.10 (1.700) .300-.10 (1.600) .00-1.00-1.40 (1.300-.382 (.400-.500-.600-.10 (1.304-.200-.60) 1.300 (.500) . and 03-04 are 0.00 (.300-.700) .20-1.30) 1.500) .900-1.600 (.200) .00-1.300 (.10) 1.900-1.90) 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) .300) 75th . bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.20-1.400 (.400) .300-.900-1.333 (.300 (<LOD-.400) .300-.70) 1.20) .S.50) 1.00 (.500-.500-.420 (.500-.200-.400) . during refining of lead and copper from sulfide ore.60) 1.400) .300 (.403 (.300) .00-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00 (.266-.400 (.283 (.200 (<LOD-.400-. Other uses include pigment production.200 (.500-.30-1.400 (.50-1.300) .10) 1.300 (.600-.00-1.50-1.20 (.10 (1.700) .20-1. EPA.20-1.500 (.00 (.600) .40 (1. 0.20-1.80 (1.393 (.50 (1.200 (.400) .300 (. and incineration of municipal waste materials.300) .289-.500-. plastic stabilizers.600 (.300) 1.Metals Cadmium CAS No.30-1.700) .300) .700) 1.275-.500-.600 (.376-.400-.421 (.800-1.70) 1.300-.900 (.216-.359-.50-1.400) .900 (.300-.800) .400 (.40 (1.900-1.700) .400 (.300 (.30-1.300 (. 7440-43-9 General Information Cadmium is a soft.235 (.395 (.300-.452) .40-1.398) < LOD < LOD < LOD < LOD < LOD < LOD .00 (1.300-.400) < LOD < LOD < LOD .600 (.900-1.304 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .300-.10) 1.400-.10) 1.300 (.400 (.30-1.700-1.400 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (.20) 1.50-1.400) .500) .60 (1.60) Total * .500 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.400) .200 (<LOD-.378 (. see Data Analysis section) for Survey years 99-00.00 (.00 (1.500) .500-.800 (.20) .600) 90th 1. and 0.50 (1.309-.600 (.00 (.296-.30) 1.S.00 (.400 (.14.700-1.400-.400 (.00-1.300 (.500-.400) .500 (.300-.20) 1.30 (1.500 (.900-1. cadmium use has declined in response to environmental concerns (http:// minerals.300-.60 (1.60-1.60) 1. population from the National Health and Nutrition Examination Survey.80) 1.500) .10) 1. < LOD means less than the limit of detection.20 (1.600 (.20-1.500) .20) 1. Cadmium also may be emitted into the air from zinc.200-.300 (<LOD-.300) .300-.3.600 (.300 (.300) .20) 95th 1.400-.300-. coatings and plating.80) 1.500) .20) 1.60 (1.50) 1.300) .900-1.300-.600) .200-.50 (1.20) 1.20) 1.300) .403) .300 (.800 (.50) 1.600) .gov/minerals/pubs/commodity/cadmium).313 (.500-. or copper smelters (U.00 (.40 (1.412 (.900-1.400 (.470) * .300-.00 (.362-.468 (.600 (.400) < LOD .400 (.400-.400) .40) 1.700) .10 (1.40 (1.10) 1.10 (1.600) .

381-.279 (.520-.206) .462 (.157) .530 (. and various seeds.366) .848 (. drinking water is a source for cadmium intake.519) .210 (.03) .717-.492 (.440 (.482) . 2003. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.43) 1.22 (1.167-.412) .187 (.426 (.980) .080 (.481) .272-.261-.290-. With chronic exposure.733) .456-. Diamond et al.393-.081) .263) ..151-.458 (.219 (.490) . Cadmium in soil is absorbed by plants.243-.362) .705-.140 (.12 (. an inducible metal binding protein.270 (.680 (.295) .284) .20-1.313) .114-. ingestion through food is the largest source of exposure.817 (.239 (.714-1.700-.466 (.232 (.253-.067-. To a lesser extent. Cadmium is absorbed via inhalation and ingestion.211-.210 (.160-.980) .231) .470-.265 (.38) 1.607) .01) .13-1.24) 1.281 (.179-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.240-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.101) .S.203) .232) .128 (.180 (. however.640) .890 (.38) 1.107-.820 (.940-1.211 (.214-.960 (.192-.390 (.713) .251) .440 (.136) . copper) and protein. interval) .440-.150) .202 (.83) 1.200-..189-.310 (.115-.229) .36) 1.07-1.28-1.135 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.790 (.28 (1.226) .480) .320) .255) .229-.148-.06-1.545 (.372) .282 (.210) .51 (1.817 (.330-.387) ..229) ..190-.200 (.190-.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.351-. 2003).246) .339) .13 (.210) .06..919) .109 (. For nonsmokers who are not exposed to cadmium in the workplace.336) .28) 1.092) .820-1.452 (.17 (.20) 1.153-.207-. whose body burdens of cadmium can be approximately twice that of nonsmokers.260-.366-.134) .Metals 2000).219 (.233) .171-.126) .237-.061-.892 (.310) .120 (.989-1.436-. Cadmium absorption may be increased with iron deficiency (Berglund et al.12-1. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.110-.19) 1.077 (. 1994). Kikuchi et al. Horiguchi et al.47) 1.17 (.199 (.316 (.249) .493-.06) ..322 (. and 0.173) .220 (. and 03-04 are 0.06.540) .977) .447 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers.200 (.41 (.20 (1.216 (.766 (.25) 1.01-1.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .223 (.191-.730-.141 (.261-.234 (.800-.193 (.02-1.170-.241) .455 (.810-1.148) .201 (.280 (.196-.17) .087-.065-.300 (.** Survey Geometric mean (95% conf.121 (.741-1.15) 1.06-1.839 (.13) .230 (.445 (. 2001).633 (.498-.302 (.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.918-1. population from the National Health and Nutrition Examination Survey.48 (1.430-.100-.813 (.800 (.507) .450 (.394-.20 (1.875 (.500) .206 (.623) .836-1.550 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.858 (.580) .227 (.150-. Renal tubular and glomerular damage.589 (.240) .300) .191 (.092 (.260 (.233) .270 (.078 (.191-.257-.820) 1.222) .170 (. see Data Analysis section) for Survey years 99-00.209 (.388-. respectively.596) .733-.181 (.559 (.189-.10 (1.82) 1.354) .510) .060-.748-1.475 (.285-. potatoes.04 (.25 (1.433-.806) .875) .34) 1.38) .633-1.195-.15) .061 (<LOD-.551) .763-.880) .450 (.22 (.479) . calcium. **All results are corrected for molybdenum oxide interference in the ICP-MS method.210 (.500) 90th .350 (.38) .238) .210 (.980 (. 1999.700-.067-.519) . 2003).74) 1.230) . zinc.289-.175 (.990) .165-.551 (.360) .980-1.262) . 0.160) .490) 1.610) .510-.238-.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 .210 (.299) .200-.090) .177-.972 (.892-1.192-. 2003).208-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .04 (.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 .09-1.204 (.15 (.277 (.860) 1.220-. wheat.077 (.112-.202-.72) 1.184-.130 (.260-.183-.160) .193-.855-1.175 (. rice.870) .170-.329 (.32 (1.30-1.169-.194-.220-.700-.247) .198) .135-.843-1.476-.230) 75th . a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.01 (.221 (.257) .273 (.255) .52 (1.963-1.818 (.090) .283 (.686-.17 (.430) .219 (.221) .886) .790 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.539) .255) . 200 Fourth National Report on Human Exposure to Environmental Chemicals .960) 1.326) .390-.265) .886-1.980-1.189) .366-.235) .400-. 01-02.753-.109-.390-.306 (. 2004a.530) .308) .190-.445 (.203 (. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.06. including many food crops such as cereal grains.20 (1.400-.157-.327 (.160 (.57) 1.423-.249-.220) .178-.890-1.

181-.433-.204-.719 (.876-1.233 (. 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.** Survey Geometric mean (95% conf.150-.740 (.201-.404) .421 (.091 (.281) .919 (.340) .431) .100 (.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .154 (.267 (.137 (.545) . Horiguchi et al.432 (.289) .234-.157-.194-.224 (.826-1.281) .884) . can result from high dose chronic exposure.181) .668-.377-.161-.795) 1.178-.440) .541) .163) .245 (.537-.228-.219 (.650-. Jarup et al.470) .538) . 2004).352) .187-.205 (.630-.268 (.051-.929) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.190 (.828) ..074-.414 (.979 (.418-.184-.472) .688-. 2004b).263 (.716) .440) .156-.190 (.166 (.261-.388-.229) .147 (.112) .338 (.941 (.209) . 1999).931 (.423 (.415) .232) . 1999). Olsson et al.159 (.690-.391-.278) .501 (.288) .382-.096) .792 (.303) .253 (.168-.343-.241) .225) .722-.221-.783 (.438-. 2002.21) 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 .183 (.364) .962) .261) .086 (.607) .404 (.300-.091 (.123-.104) .700 (. 1996.518) .077-.311) .126 (..16) .693 (.813-1.078-.865 (.113-.101) .423-.708-1.147-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.318 (.757 (. 2002.531 (.131-.184) . two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al. 1999).336-. Staessen et al.247-.252 (.398-.106) .826-1.122 (.209) Selected percentiles ( 95% confidence interval) Sample 95th .12) 1.856 (.218) .071 (.191) .098) .177) .441-.084-.247-.490 (.289) .143) .261 (.10) 1.210 (.473 (.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.536 (.873 (.227-.13) .220 (.308 (.909-1.678 (.07) .270 (.199 (.917) .238) .350) .158-.856) .769 (. However.387 (.090 (.247-.187) .00 (.412 (.551) .181 (.083-.950) .446) . interval) .293-..449) .754) .234 (.653) .757) .191 (.182) .273 (.232) .516-.687 (.280 (.686 (.779 (.162 (.136-.712 (.239-.414-.107) .174-.690-.208-.085-.146-.666-.156) .985 (.288 (.806-1.316) .874-1.085 (.208 (.700) . During the 1950’s and 1960’s.225) .16) 1.381-.438) 90th .063-.426-.140-.783) .484 (..622 (.507-.02 (.335 (.067-.S.500-.140-.266) .818) .178) .470) .06 (.830-1.559-.727-.331 (.614) .094) .215 (.645-.591 (. 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.175 (. 2000.716-.168-.288-.839) .07 (.617 (.927-1.253) .631) .185) .256-.917 (. population from the National Health and Nutrition Examination Survey.830) .075 (<LOD-.725-1.481 (.175-.813-.222-.38) .219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .687-.130-.267 (.784) .170 (.156 (.850) ..562-.147-.221 (.17) .182) .434 (.093 (.283 (.192) .159 (.240) .255-.678-.387-.234) .250) .242) .236-..207) .104) .198) .304-.444-.663 (.202 (.143-.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 .084 (.282 (.171-.827) .691-.163 (.212 (. 2002.144-..111-.316 (.199-.00 (.08) .998) . 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.274) 1. Fourth National Report on Human Exposure to Environmental Chemicals 201 .173-.197-.833-1.210) .206-.182) .292) .136-.091) .729 (. 2003.560-.238-.940 (.767 (.123-.487 (.176 (.148 (.075-.906) .189-.097) .263-.183) .667) .211 (.304) .135) .491-. most often a result of occupational exposure (Roels et al.418) .235) .176 (.297) . Noonan et al.329 (.09 (.078 (. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.216-.200 (.137-.210 (..296 (.647-.802 (. At lower environmental exposures. 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.175 (..266-.185 (.154-.308) .157-.143-.184-.321) .696-.226) 75th .674-1.181 (.382) .940-1.476) .170-.05) 1.191-.718 (.207-.173 (.196 (.533) .325 (. 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.240) .479 (..850) .767) .219 (.789 (.223) .168 (.818) .690 (.

Moriguchi et al. Jin et al.S. 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).. 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. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect.. Cadmium can produce lung. 2003. 2003).. 1996.. 2006). 2003. Wennberg et al. 2002.26 and 3... Jarup et al... intermediate in former smokers and lower in never-smokers (Becker et al.46 mg/gram of creatinine) (Ezaki et al.... 2002).. 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. 1999). 2004.. Wilhelm et al. Olsson et al. 1996).. Women had higher blood and urine cadmium levels compared to men of similar ages. Mannino et al. 2004b.. Information about external exposure (i. Friedman et al. Creatinine-corrected urine cadmium values in U.. Staessen et al. Ezaki et al. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. Ezaki et al. with peak values observed in the fifth to sixth decades (CDC. 2003. Becker et al. 2000). Animal studies have demonstrated reproductive and teratogenic effects. Horiguchi et al. In adults aged 60 years and older. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. 2006. Suwazono et al. 2005). decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. 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. 2002. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al.. environmental levels) and health effects is available from ATSDR at: http://www. maternal blood or maternal urine and birth weight (Nishijo et al. 2000. 2004. 2002). 2003. 2004).e.. 2003. 2004. Further research is needed to address the public health consequences of such exposure in the United States. 1999. has resulted in severe. 2002... 2002).. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood.. approached these values associated with subclinical changes in renal function and bone mineral density. 2002. 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.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al.. Olsson et al. Noonan et al.html. 2005.. potentially fatal pneumonitis (Fernandez et al. Olsson et al.gov/ toxpro2.. Komaromy-Hiller et al... Becker et al. 2006. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Becker et al. 2005. as may occur from welding cadmium-alloyed metals.. Acute and heavy exposure to airborne dusts and fumes. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al.S. Jarup et al. Salpietro et al.. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC.atsdr. 2002). 2002) and length at birth (Nishijo et al. respectively.. In postmenopausal women. 2002). respectively... 2006). not to imply a safety level for general population exposure. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles... EPA. However. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH.S. Horiguchi et al. In the typical environmental exposure. For NHANES 19992000. and drinking water and environmental standards have been established by U.cdc... CDC. Staessen et al. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. Wennberg et al. 2005. 2002.. 2005.1 mg/L (Alfven et al.. Staessen et al. 2003. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures.. 2002. data (CDC. 2000. Occupational standards are provided here for comparison only. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. Zhang et al.. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. 2004.. Both IARC and NTP consider cadmium a human carcinogen. 2004b).. 1999). urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney. 1988). 2000.

Olfactory function in workers exposed to moderate airborne cadmium levels. Chislovska NV. Berglund M.354:1508– 1513. Tsukahara T.296(1-2):71-90. Jarup L. Kundiev YT. Venables KM. Mannino DM. Environ Health Perspect 2002. Vahter M. Thayer WC. Consonni D. Mucha A. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Sasaki S. Furuki K. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. 196:114-123. Costa R. Takebayashi T.148(1-2):11-20.45:43-52.102:83-89. J Toxicol Environ Health 2003. et al. Comparison of representative ranges based on U. Kumagai N. possibly better than b2microglobulin. Wang H. Becker K. Jones RL. et al. Ye T. Grubb A. et al. Lukyanova EM. Agency for Toxic Substances and Disease Registry (ATSDR). Kaus S. Lancet 1988.205:297-308. Fayers PM. Greves HM.atsdr. Int J Hyg Environ Health 2002. iron deficiency. 1999 [online]. Krause C. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Atlanta (GA). et al.95:20–31. Nomiyama T. Nerbrand C. Centers for Disease Control and Prevention (CDC). et al. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Bregante G.57:668-672. Oguma E. Fukui Y. 2005. Savage-Brown A. Stock AL. Serra J. Mascagni P. Third National Report on Human Exposure to Environmental Chemicals. Furuki K.cdc. Bellerup P. Seiwert M. Horiguchi H. Schulz C. patient population and literature reference intervals for urinary trace elements.46:372-374. Ash KO. Oguma E. Bernard A. Dekio F. et al. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study.76:186-196. Machida M. Lidfeldt J. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. et al. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Jarup L. Kikuchi Y. Komaromy-Hiller G. Cadmium fume inhalation and emphysema.000 women in the Japanese general population: a nationwide large-scale survey. Okamoto S. et al. J Occup Health 2003. Occup Med 1996. Sanz P. et al. 206:15-24.59:497].gov/toxprofiles/tp5. Bo M. Sasaki S. Thorax 2004. Hotz P.1(8587):663-667. Fukui Y. Nordberg G. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Miyamoto K. Moriguchi J. Carlsson MD. Ikeda Y. Akesson A. Darbyshire J. Hellstrom L. ShkiryakNizhnyk AZ. Environ Res 2004b. References Akesson A. Vahter M. 4/8/09 Alfven T. Alfven T. Seiwert M. Pickering CA.S. Occup Environ Med 2000. Chiappino G. environmental.24:717-724. Howerton K. Choudhury H. diabetes mellitus. Toxicol Lett 2004. Ikeda Y. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Nermell B. Fatal chemical pneumonitis due to cadmium fumes. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group.html. 102:10581066. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Lison D. Environ Health Perspect 1994. Neurotoxicology 2003. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.59:194-8. Ukai H. Jin T. Toffoletto F. Gadea E. Machida M. Lancet 1999. Int J Hyg Environ Health 2003. Holguin F. Davison AG. Schulz C.S. Becker K. Persson B. Int Arch Occup Environ Health 2003. Palomar M.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.110:699-702. Fourth National Report on Human Exposure to Environmental Chemicals 203 . population. Ezaki T. Friedman LS. Toxicological profile for cadmium update. et al. Fernandez MA. Taylor AJ.13(11):1627-1631. Diamond GL. Available at URL: http://www. Tsukahara T. Ezaki T. Horiguchi H. Comprehensive study of the effects of age. et al. Lundh T. Uemura T. Seifert B. Lauwerys R.66(Pt A):2141-2164. Kaus S. Environ Res 2004. Environ Health Perspect 2005. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction.96:353-359. Lepom P. Miyamoto K. Zhu G. Moriguchi J. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Toxicol Appl Pharmacol 2004a. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Environ Res 2006. Buchet JP. Clin Chim Acta 2000. Elinder CG. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Anthropometric.

Environ Health Perspect 2002. In: Clarkson TW. Sager PR. Nordberg GF. Nakagawa H. Lison D. Lybarger JA. Okubo Y. Tanebe K.gov/ttn/atw/ hlthef/cadmium. Usefulness of biomarkers of exposure to inorganic mercury. Cadmium compounds. Bensryd I. Lundh T.39:2507-2515. Noonan CW. Japan. 151-168. Nordberg GF.59:394-397. Schwenk M. dietary intake. Emelianov D. Wang JX. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Lauwerys R. Fan YG. Roels HA. 2000. United States Environmental Protection Agency (U. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan.209:301305. Revised 2000 [online]. cadmium. Revised and new reference values for arsenic. et al.html. Wilhelm M. and risk of fractures: prospective population study. created 1992. Liu QF. lead. Merlino MV. Roels HA. Nishijo M. Relationship between newborn size and mother’s blood cadmium levels. Cadmium carcinogenesis. Zhu HD. lead. New York: Plenum Press. Buchet JP. Gallmans G. J Perinat Med 2002. Honda R. Hoet P. Available at URL: www. 2004. Lijnen P. Kathman SJ. Staessen J. 4/8/09 Waalkes MP. Lundh T. et al.S. Vangronsveld J.30(5):395-399.84 (Section A):4455. Tawara K. Mutat Res 2003. et al.epa. Environ Health Perspect 2002. Schultz C. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Toyama. Nakagawa H. J Cardiovasc Risk 1996. Nordberg M. Minciullo PL. Kuznetsova T. Nakagawa H. eds. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Suwazono Y.533(12):107-120.21(3-4):251-262. Roels H.110:1185-1190.Metals Nishijo M. et al.353:1140-1144. Nogawa K. Oskarsson A.59(1):22-25.100:330-338. Stelitano A. et al. Campagna D.110:151-155. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. and mercury in the population of northern Sweden. pp. Saito S. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Kobayashi E. Kido T. Salpietro CD. iron status. Staessen JA. Mueller PW. Stegmayr B. Gangemi S. J Environ Sci Health B 2004. Bergdahl IA.3:26-41. Jansson J-H. Tanebe K. Ottosson H. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. forearm bone density. Honda R. Biological monitoring of cadmium. Cadmium in blood and urine – impact of sex. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Time trends in burdens of cadmium. Zhang YL. Biological monitoring of toxic metals. Arch Environ Health. 2001. Friberg L. et al. EPA). Sarasua SM. Ginucchio G. Int J Hyg Environ Health 2006. Skerfving S. Hazard Summary. Lancet 1999. Bruiglia S. Zhao YC. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. and former smoking – association of renal effects. age. Thijs L. Ren Fail 1999. Environ Res 2006. Occup Environ Med 2002. Environmental exposure to cadmium. Olsson IM. lead. Wennberg M. Environ Res 2000.

62) 4.30-10. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.25 (3.90) 5.91-8.14.20 (6.70-8.4) 10.6 (9. For absorbed cesium salts.64-10.12-5.9) 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 4.40-11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 11.92-13.00-8.35-5.77 (4. and cardiac arrhythmia (ATSDR.50) 5.3) 10.86-12.66 (7.87 (4.98 (7.90 (4.70) 7.17 (6.39) 7.00) 7.56-11.74) Selected percentiles ( 95% confidence interval) 50th 4.89-5.81) 4.26-11.53 (6.8 (10.2) 11.2-12.49) 4.50 (4.32-5.12-11.89) 4.14.6 (11.9 (10.21) 90th 9.Metals Cesium CAS No.7 (10.72) 4.7 (10.90-10.5-13.1-12.56 (4.60-6.60-12.93 (4.6 (9.83-4.22-4.84-9.20-7.27 (7.8 (11.08 (7.1) 11.1 (10.33 (5.80-10.61-6.63) 6.5-16.2.36 (3. interval) 4.0-13. Most human exposure to cesium occurs through the diet.40-5.46) 7.08-5.7 (11.3-13.95-4.84-5. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4) 95th 11. Fourth National Report on Human Exposure to Environmental Chemicals 205 .7) 11. 01-02.60) 7.16-6. population from the National Health and Nutrition Examination Survey.80-13.5-14.05-5.3 (8. and high-power gas-ion devices.01-8.9) 12. Whether cesium compounds are carcinogenic is unknown.40 (4.80-11.0-15.9 (11.98 (7.7 (9.95 (3.54) 4.90-8.50 (4. the body half-life is estimated to be 70-109 days based on 137Cs exposures.88 (8.09) 5.6 (9.2-13.61) 7.00-10.90-12.64) 4.63 (4.84) 8.S.60-7.2 (9.47-4.94) 4.59-5.08-5.40) 5.5-14.99-11.8) 9.26) 7.34 (4.86 (7.69-6.7 (9.36) 3.60) 5.82) 5.40-11.24) 4.6 (11.99-6.80 (8.77 (9. and as polymerization catalysts.00-8.97 (7.6) 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 4.20-8.59 (5.05-5.82-4.0 (9.07-11.42) 6.64) 5.4 (10.20) 5.97) 4.60-7.27-5.45-8.04 (4.40-5.1) 11.44 (8.60 (7.86-11.0) 12. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.50 (7.3 (8.32) 4.29) 4.1 (11.60 (8. photographic emulsions.83) 6.8) 12. and 03-04 are 0.10-5. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.42-7.77 (9.94 (4.7 (10.81) 9.4) 9.60) 7.3) 9.45-5.20-4.80 (4.9) Total 4.80-6.84 (4. respectively.87 (4.20) 8.25) 4.97) 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. although cesium was generally of low toxicity when given to animals.30 (6.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3) 10.53-11.55 (4.3) 10.05) 5.30-5.70 (8. semiconductors.25-5. diarrhea.64 (4.70 (6.5 (10.0) 12.5) 12.35 (4.20) 7.32 (3.33 (6.4 (9.0) 10. infrared lamps.52-9.90) 9. cesium hydroxide is corrosive and irritating at high concentrations.8) 11.50-7.60-5.40-5.00) 6.73-11.3) 12.99-11.39-4.10-9.62 (5.09-5.9) 11.87) 5.80-10.80) 7.56) 5.7 (9.29 (4.52) 7.72-7.13 (8.95) 5. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.59-5.94-4.55-11.47-8.0) 9.87-7.10-7.56 (4.80 (4.9 (10.5) 9.2 (9.71-5.63-4.77-8.1-12.1) 10.00) 4.64-5.03-4.70 (8.38) 5.54-11.7) 11.7) 10.50) 9.84) 5.57-5.31-8.6) 10.96 (6.94 (4.89) 5.90) 5.35 (4.81-14.64) 5.81 (4.10 (6.97-7.99) 7.80 (8.71-8.2-13.26) 4. Little is known about the health effects of this metal.15-8. Radioactive 137Cs has been used medically to treat cancer.6) 11. scintillation counters.0 (10.8 (10.04) 7.70 (9.1) 9.26 (3.03 (4.74-5. nausea. Inorganic cesium compounds are used in photomultiplier and vacuum tubes. see Data Analysis section) for Survey years 99-00.40) 5.16-6.91 (7.4) 10.42) 7.81) 4.34) 9.10 (8.03 (4.20-5.70 (5.00 (7.71-9.1 (9.07) 4.87 (4.80 (8.73-5. soil.8) 12.9 (11. 0.40-7.1-13.7-14.17-6.7 (8.40-5.90-10.30 (6.30) 7.6 (9.80 (4.17) 4.36 (6.00-4.59) 7.90 (6.02 (4.12) 5.4-13. 2004).33-5.8) 9.10-8.0) 11. However.71 (8.0) 12.3-15.90-12.22 (4.70) 5.30) 5.4) 11.49) 75th 7.76-6.4 (9.27) 4.2-14.9 (11.08) 7.5 (8.62 (5.37) 7.10 (8.70) 5.55 (7.05) 5.3-13. and 0.60-6.80-10.13 (5.49 (5.79 (4.99) 9.14 (4.21 (4.90) 7.49 (4.13 (7.4) 12.43 (5.70 (6.90-10.40) 7.8) 11.74 (4. and clay.9 (11.37) 5.13-8.50 (4.68) 9.00-9.2) 12.3) 10.08 (6.20 (4.23-4.50 (6.59-5.8) 12.5) 10.9) 8.23) 9.68 (7.90) 4.8-13.20) 4.7) 10.67 (4.01) 7.43-8.70 (4.1) 9.2-13.71 (4.01-6.71) 4.12 (4.10 (6.4) 12.70-5.

78 (3.90-8.50) 4.31-6.42 (4.64) 4.17) 9.03-5.70) 6.5) 9.08) 3.7) 10.26-6.47) 6.21-4.70) 7.09 (4.06) 4.29) 5.40) 6.96-4.26 (4.75-11.56) 3.47 (7.27 (6.01-8.90 (7.7) 10.86 (4.0 (7.84-11.33-3.44) 3.51 (3.24 (3.06 (5.54 (3.97-5.03) 5.2) 11.00-10.66-6.64 (4. Two small studies of European populations reported urinary cesium levels similar to U.14 (6.39 (5.77 (6.30 (7.04-5.50 (7.43-11.72) 4.28) 8.75 (7.87 (5.51 (4.47) 6.42-4.10 (5.37) 4.66 (5.06) 5.39) 8.83-6.29-3. (2000) found urinary cesium levels that were slightly lower than those reported for the U.67 (5.25) 4.13 (3.15) 95th 8.84-7.20-4.4) 10.04-11.13-9.56 (4.8 (9.31 (4. population.97-4.43-6.49) 3.18-6.84-7.43 (4.85) 5.14) 4.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.19-3.55) 4.9 (9.99) 4.16) 5.94 (5.50) 4.08 (5.65-3.73-4. Komaromy-Hiller et al.44-9.51 (7.53 (6.87) 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 5.27 (6.40-5. population from the National Health and Nutrition Examination Survey.50) 8.74-11.41) 4.51 (3.28 (4.78 (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.00-8.99-9.94) 7.53 (4.84-9.3) 9.85) 4.42 (5.64) 9.5 (9.06 (3.60-20.38-12.07-4.54 (5.30-4.98 (7.58 (6.7-12.35 (4.44-5.80) 6.6 (9.33 (5.07) 8.59) 4.58-5.96 (4.20-4.71 (7.12) 3.72 (4.41) 9.05-3.45-6.95) 8.79) 6.79) 9.12 (3.74) 3.27) 4.58) 8.22-11.92) 3.17-4.0) 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 .51) 4.18) 8.91) 5.64-6.3-15.61 (7.24-4.58 (4.81 (4.59-8.68-11.29-3.15-4.79 (5.44 (8.9 (10..8) 6.37-3.47) 7.65 (6.91) 5.96) 4.05-4.82-4.95-12.04) 6.08) 4.36-10.20) 5.1) 11. 2005.26 (3.6 (9.00-5.41-4.64) 5. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.75 (6.74 (4.56) 4.98 (6.90-3.20-4.38 (3.S.77 (7.30-4.95) 4.63-6.89-4.62-8.90-8.12-6.07 (5.0) Total 4.10 (3.8) 10.2 (8.29) 4..35 (3.74 (5.33-8.5) 7.73 (3.05 (4.28) 7.10-4.3) 11.20-8.55-5.42-6.63 (7.88-4.46 (8.50 (6.S.48-6.05) 6.82) 7.03-6.36-3.68) 4.60 (3.25) Selected percentiles ( 95% confidence interval) 50th 4. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.10) 7.18-7.54 (4.50 (5. and were also roughly similar to those in this Report.29) 4.68) 6.87-4.41 (5.27 (8.63-6.53) 6.43 (8.0) 7.79) 4.18 (7. 2004).22) 6.30) 10.33 (5.63 (4.00) 6.61-3.14-7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.04) 5.38) 10. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.99-9.76-9.98) 5.95 (3.53) 3.93-9.41 (4.66 (6.43) 8.15 (7.92 (5.41 (8.88-10.81 (4.66 (5.21-3.43 (3.65-4.22 (3.70 (7.31-4.03) 6.91-6.3 (8.38 (3.08-7.52-5.63) 6.47 (4.14-6. interval) 4.72-5.14-4.99-4.96) 4.93-7.00-5.45 (4.91) 4.46) 6.42-4.30 (4.77) 4.83-7.16-5.58) 3.44 (4.41-7.46 (7.63 (6.51 (4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.48) 90th 7.30 (3.09) 8..55 (3.17) 4.40) 7. population results shown in this Report (Alimonti et al.91-7.35) 3.96-4.50) 4.74) 75th 5. 1990).77-5.07) 8.28 (5.13-9.14) 4.48) 7.3 (9.00 (8.8) 5.21-5.56-10.78) 4.95) 10.05) 3.57) 3.68 (4.10 (3.97) 8.76-6.84-9.68) 3.27-6.67) 5.95 (5.79-5.39) 5.54 (4.35-11.67 (6.34 (5.87) 5.21 (2.15-11.30) 10.08 (3.47) 4.13) 7.46-8.98) 5.19-6.83) 8.64 (8.91-9.78) 4.16-8.00-9.99 (3.08 (6.9) 10.50-5.46-4.00-4.11 (5.02 (5.S.05-3. Minoia et al.02-4.43 (4.08-3.91 (5.38-7.11 (5. Using clinically submitted specimens.2 (8.08) 4.60) 3.6) 6.62) 5.56) 4.27-4.24-10.17 (6.09) 4.3 (10.77 (4.85-4.60-10.60 (5.35-7.16-8.95-6.91 (5.5) 9.71) 6.3) 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 3.2) 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 3.31 (4.36-6.23 (7.

cdc. Paschal D. New Mexico. Comparison of representative ranges based on U. Sewell CM. Wood CM. blood. Centers for Disease Control and Prevention (CDC). Mott JA. Rapid Commun Mass Spectrom 2005.2004 [online]. Wolfe MI. Howerton K. Gallorini M. cesium. Minoia C. Apostoli P. Trace element reference values in tissues from inhabitants of the European community I. J Expo Anal Environ Epidemiol 2004. Pietra R. Komaromy-Hiller G.atsdr.html. Clin Chim Acta 2000. Mincione G. Assessment of urinary metals following exposure to a large vegetative fire. Gatti A. A study of 46 elements in urine.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Ronchi P.14:120-128. and serum of Italian subjects. Sabbioni E. et al. Available at URL: http://www. Costa R. antimony and tungsten. 2000. Toxicological profile for cesium. Forte G. Atlanta (GA) 2005. Spezia S. 4/8/09 Alimonti A.296(1-2):71-90. Voorhees RE. Fourth National Report on Human Exposure to Environmental Chemicals 207 . patient population and literature reference intervals for urinary trace elements.gov/toxprofiles/tp157. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium.S. et al.19:3131-3138.95:89-105. Sci Total Environ 1990. et al. Pozzoli L. Ash KO. Third National Report on Human Exposure to Environmental Chemicals.

660) . 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. Cobalt occurs naturally in airborne dust.259-. varnishes.434 (.880 (.890-1.340) .680) .810) .570) .16 (. 208 Fourth National Report on Human Exposure to Environmental Chemicals .454 (.480 (.52 (1.470) .53) 1.950 (.430) .540-. and kitchenware.22-1.07.333-.44) 1.520 (.01-2.540-.12) 1.570 (.930-1.15 (1.710) .620-.520 (.352 (.480-. interval) .610-.860 (. hard metal (alloys of cobalt and tungsten carbide).285 (.32 (1.39) 1.374 (.03 (.339 (.520-.950-1.680 (.350-.450) .404) .940 (.25-1.60 (1.00) .410) .390-. The cobalt used in U.600-.360-.520) . automobile airbags.540-.410-.410 (.29 (1.32-2.900-1.515 (.487) .16 (1. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.24 (1.370 (.405-.398 (.410 (.04-1.S.07.460 (.15-1.45 (1.750 (.16-1.310 (.390 (.790-.435 (.700) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.550-.33 (1.590 (.16 (1.01-1.270-.300 (.81) 1.355-.450) .420) . and fertilizers.463-.23-2.460) .369 (.940-1.32) 1.550) 90th .890) .418 (.S.400-.920) 1.03) 1. and 03-04 are 0.640) .48) 1. diamond-polishing wheels.950-1.430-.650-.870 (.670-.331-.07 (.340-.380 (.32) 1.431) .01 (.390 (.710) 1.380-.20 (1.05) 1.386) .02-1.14) .428-.410) .375 (.301 (.620-.660) .75 (1.520) .36) 1.520-.316 (.33-1.850-1.760 (.600 (.450-.370-.Metals Cobalt CAS No. Cobalt compounds are used as catalysts in producing oil and gas.419) Selected percentiles ( 95% confidence interval) 50th .28 (1.42) 1.564) . 01-02.670-.68 (1.416) .370-.380-.940-1.47 (1.26-2.08) .308-.26) Total .28-2.430 (.590-.770) .420) .03-1. It is emitted into the environment from burning coal and oil and car and truck exhaust.900) .59 (1.12) 1. hard metal or in combination with other elements.430 (.338-.490-.510) 1.496) .690-.333-.610) .910-1. and inks. population from the National Health and Nutrition Examination Survey.04-1.460 (.03) 1.740-.670 (.305-.530) .16-1.980-1.330 (.760) .313) .520-.06 (.710 (.890-1.380 (.520-.334) .900) .570) .300-.26-1.523) .880-1. and magnetic recording media.430 (.13) 1.583) .430) .900-1.690-.14-1.660-. steel-belted radial tires.900) .580 (.830-1.465) .670 (.09) .620) . Usual human exposure is from food sources.270-.16) 1.26) 1.790) .410 (.50 (1.890) 95th 1.47) 1.320 (.350 (.740 (.610) .22 (1.520 (.490-.340-.330) .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 .450) .07-1.810-.390) .291-.37-1.336-.790 (.410-.680 (.388-.460-.650 (. Cobalt is used as a drying agent in paints.46 (1.740-.980) .410-.520 (.350-.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 .398) .500) .540-.16) 1.393-.310-.359 (. seawater.950 (.469-. and 0.730) 1.820 (.580 (.890-1.550 (.47 (1.64) 1. see Data Analysis section) for Survey years 99-00.920-1.610 (.21) 1.394) .500 (.530-.630 (.350-.343 (.47) 1.420 (.01 (.06 (.290-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.06-1.04) 1.850-1.581) .379 (. industry is imported or obtained by recycling scrap metal that contains cobalt.410 (.750 (.820 (.519 (.28 (1.800-.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 .810) .330-.17 (1.427-.590-.460) .600) .370-.640) .364-.390 (.05 (.350) 75th .04-1.650 (.03 (.560 (.08. Cobalt compounds are also used in manufacturing battery electrodes.820 (.414) .373-.750 (.23) .570-.470 (.850) .870-1.530 (.930) .340 (.840) .56) 1.630 (.294 (.373) .543) .690 (.48) 1.319) .630-.327-.700) .360-.540) 1.377-.99) 1.800-.670 (.452 (.08-1.22) 1.81) 1.348-.499 (.17 (1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.370) .620-.371 (.07-1.930 (.580 (.399) . 0. blue-colored pigments. large appliances.590) .461 (.348-. and in synthesizing polyester and other materials.640) .502) .750-.360-.950) .09 (.92) 1.280-.17-1.04 (.65) 1.870 (.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.480 (.417) .17 (.431) . and soil.19) .680) .05 (.850) 1.03) .960-1.09 (.67) 1.24 (.28 (1.440-.450-.380 (.340) .73) 1.270-.450) .460) .316-.372) .800) .424) . shiny.367 (.32 (1.410 (.50) 1.570-. It is also a component of porcelain enamel applied to steel bathroom fixtures.379 (. respectively.

660-.352 (.683-.326-.537 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH..324) .300) .785) .630-.515 (.616-.393 (.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 .847) .500-.689 (.11-1.513) .554 (.388 (.259 (.554 (.368 (.396) .402 (.282 (.744) 1.329-. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.757-1.753-.30 (1.376 (. Smith et al.548 (.898 (.895-1.274-.457 (.50 (1.635 (.733-1.417 (.463-.990-1.247 (.600-.250) .495 (.434-.534-.644 (.00) . an essential human nutrient.563-.760-1.333 (.585) .50) 1.302-.756 (.00 (.461) .838 (.781-1.272-.282-.542 (.319-. or using diamond-polishing wheels that contain cobalt metal.562) .355) .14 (.804) 1.33) .449) .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 .533 (.452-.296-.598 (. refining or processing alloys.388 (.392 (.955) .534 (.850 (.679-..313-.55) .16 (.638-1.983-1.313-.349) .872 (.500-.669) .647) .36) 1.257-.983) .378-.310) .279 (.547 (. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.02 (.781) 95th 1. Exposure in the workplace may come from electroplating.457) .736-.421) .291 (.09) 1.327 (.408 (.513 (.829) .850-1.394) .723 (.435 (.Metals fabricated from cobalt alloys (Lhotka et al.278 (.861-1. in the feces.251-.248-.952 (.06 (.328 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.348) .425-.29 (1.471-.342-.362) .728) .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 . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.505) .00 (.407) . population from the National Health and Nutrition Examination Survey.703-.382-.976 (.313-.821 (.552 (.582-. 1994).963) .234 (.433) . A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.248-.911-1.611) .304) .15 (.467-.830 (.290 (.740-1.753) 1.487-. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.334) .17) .386 (.848 (.54) 1.384) .378 (.297) .594) .378-.29) .00) .273 (.324-.949) .417) . Once absorbed and distributed in the body.503-.842) .487-.23 (1.294-.04-1.33) 1.975 (.737 (.561) .12-1. 1994. 1972).608 (.593) .857-1.337 (.44 (.488) .508-.662) .279) .316 (.667-1.10 (.290 (.03-1.673-.560-.475 (.429) 1.268 (.630-.353 (.626-..297-.281) .83) 1.960 (.990) .303-.591 (.298 (.29 (1.271 (.344-.428-.28) 1.634-.00 (.16) .369 (. respectively.879-1.365) .481) 90th .57) 1.407 (.694) .439) .278-.829-1.900-1.237-.523 (.409) .296) .861 (.314 (.343-.426 (.S.419) .361-.905) .313-.353-.346 (.215-.529 (.12 (.500 (.738 (.256-.581) .333-.368) .938-1.929) .25 (.362 (.333-.932-1. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).479-.750-.259) .964 (.471-. 1979).543) .306) 75th .289) .27) 1.50) 1. interval) .25 (.393-.595) . and to a lesser extent.455 (.479) .632-.275-.368) .963) .275-.387) .16 (. 2003).361 (.329 (.606 (.243-.309) .293 (.259-.328) .313 (.343 (.378-.396) .358 (.391 (.35) ..49) 1.457-.700 (. A portion of cobalt retained for long periods is concentrated in the liver.777-.15) 1.700 (.774 (.19) .550-.468) .35) 1.792 (.562) .331-.381) .955) .728 (.708) .844 (.03 (.339-..239-.27) 1.317 (.640) .707) . Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.435-.313-.60) 1.895-1.36) 1.00-1.513-.361-.16 (1.851 (.599) .60) 1.391) Selected percentiles ( 95% confidence interval) 50th .301-.792-1.29 (1.442-.611) .833-1.691 (.917) .438) .963-1. using hard metal cutting tools.277-.360) .444 (.449-.29) 1.826-1.574-.786-.824 (.404-.304-.290 (.380-.352 (.609) .425) .963-1.471 (.335 (.462) .306 (. cobalt is excreted predominantly in the urine.727 (.73) 1. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al. Cobalt is absorbed by oral and pulmonary routes.615) .333-.738 (.04 (.328 (.337) .704-.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 .363) .469-.522) .327-.301) . 1972).10-1.938) .286) .361 (.821-3.523 (.257 (.11-1.10) .667-1.750) .362-.352) .280-.937 (..00 (.372) .365-.10) Total .24) .323) .400 (.476-.

1999). Urinary measurements mainly reflect recent exposure. Information about external exposure (i. Am J Med 1972. Krause et al. A clinical and pathological study of twenty-eight cases. White and Sabbioni.50(13):95-104. usually in combination with tungsten carbide (Cugell et al. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. Information about the BEI is provided here for comparison. has been associated with exposure to dusts that contain cobalt. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. 1988). Rubin A. Toxicol Sci 1999. A 1982-1992 surveillance programme on Danish pottery painters.gov/toxpro2. 1994. 4/3/08 Christensen JM. 1988)... 2001). 1993). Swennen et al. Sci Total Environ 1994. Grumbein SL.. although substantial occupational exposures have produced elevated urinary levels for many weeks. 1993). Morgan WKC. Haseman JK. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals. Poulsen OM. Daniel et al..S. 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.html.gov/ exposurereport/. et al. For workers exposed to cobalt in the air.. Blood and urinary concentrations as estimators of cobalt exposure. Lauwerys and Hoet. Iavicoli et al. 1955). Linnainmaa and Kiilunen.Metals Toxic effects of cobalt have been encountered in workplace settings. 1992).. Lison et al. 2001. References Alexander CS.. 2005. Cugell DW. not to imply that the BEI is a safe level for general population exposure.. Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. Alexandersson R. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. Centers for Disease Control and Prevention (CDC)..S. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al.. 2005 [online]. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. 1994). 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. Cobalt-beer cardiomyopathy. 2003. 1985.. population results in this Report (Kristiansen et al.cdc. 1998).. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis. 1997. environmental levels) and health effects is available from ATSDR at: http://www.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005.e. Sills RC. Lisi. 1990). Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations.atsdr. population (CDC. 2003. Hailey JR.49:56-67. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al. 2003).. 2001. 1997). “Hard metal” disease.43(4):299-303. Roycroft JR. Available at URL: http://www. Thomassen et al... Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. Dunstan et al.. 1994. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al. Arch Environ Health 1988.53:395417. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al... 210 2006. Perkins DG. Bucher JR..cdc. 1998). 2006.. 1972).. 1989).... Cobalt was once added as a foaming agent to beer. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. Shirakawa et al. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. MacDonald et al. with mean levels that were about 15-20 times higher than in the general U. 2001.

Smith T. A report of two cases from mineral assay laboratories and a review of the literature. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Unwin P. 2001. Int Arch Occup Environ Health 1997.44:124-132. Edmonds CJ. Gross RT. Kraus T. Int Arch Occup Environ Health. Carnes WH. Sci Total Environ 1994. Peltier A.21(2):189-195. Leghissa P. Cannon SR. Occup Environ Med 2001.87(5):628-631. Cleland D. Thomassen H. Dunning SP.150. Angerer J. Pradhan C. Kriss JP.36:732-734. X. Robinson C. Christensen JM. Lisi P. Ghat IS. Laippala P. HoffmannB. Swennen B. Zobelein P.28(5):1121-1128. Am J Epidemiol 1998. Science 1988.150(1-3):167-171. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Schramel P. Ziaee H. Hedge AG. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Steffan I. McCalden RW.95:29-37. Palmroos P.45:246-247. Long-term clearance of inhaled 60Co. Chest 1989. Co-sensitivity between cobalt and other transition metals. Mosconi G. Am J Ind Med 2003. Oksa P. Lung cancer risk in hard-metal workers. Mutat Res 2003. Sabbioni E. Cresti R. Daniel J.Metals effects of cobalt. Dickel H. Meier R.216:253-270. Shirakawa T. De Boeck M. Goto S. Vitali MT. Chess DG. et al.51(7):447450. Hoher T. Bunn HF. Kato M. J Bone Joint Surg Br 2005. Rorabeck CH. McMinn DJ. Molders J. J Orthop Res 2003. Biological monitoring of workers exposed to cobalt metal. J Rheumatol 2001.22:359367. Jarvis JQ. Br J Ind Med 1993. cobalt salts. Industrial Chemical Exposure: Guidelines for Biological Monitoring. The release of metals from metal-onmetal surface arthroplasty of the hip. White MA. Lauwerys RB. J Trace Elem Med Biol 2006.148:241-248. Sabbioni E. Sabbioni E. Pisati G.88(4):443448. Outcome of occupational asthma due to cobalt hypersensitivity.” Contact Dermatitis 2001. and hard metal dust.204:147-160.242:1412-1415. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Salama A. Wild P. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up.157:117121. Sci Total Environ 1998. Zhuber K. et al. et al.69(3):193-200. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. salt. Swennen B. Falcone G. Absorption and retention of cobalt in man by whole-body counting. Lhotka C. Blunn G. Clin Orthop Relat Res 2003. Boca Raton (FL): Lewis Publishers. oxides.34:620-626. Sanghrajka AP. Uitti J.150:177-183. Ichikawa Y. Zweymuller K. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Weyher I. Schaller KH. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Hammon E. Epidemiological survey of workers exposed to cobalt oxides. Roto P. Meyer zum Buschenfelde K-H. Kristiansen J. Schank M. J Occup Med 1992. Lasfargues G. Sci Total Environ 1994. 1985. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Buchet JP. Bozec C. Health Phys 1979.48:172-173. Respiratory health of cobalt production workers. Cobalt cardiomyopathy. Linna A. Bourne RB. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein.55(4):269-276. Kuska Y. Thakker DM. Cobalt and antimony: genotoxicity and carcinogenicity. Diepgen TL. Goldberg MA.50(9):835-842. Trace element reference values in tissues from inhabitants of the European Union. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Bacis M. Hoet P.406:282-296. Iversen BS. Heki S. Fujimura N. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Kusaka Y. Health Phys 1972. Weber A. Lauwerys R. Barnaby CF. Romazini S.20(1):25-31. Lison D. J Bone Joint Surg Br 2006. Tilley S. DeSantis V.58(10):631-634. Zedda S. Sci Total Environ 1997. Lauwerys R. Occupationallyinduced “isolated cobalt sensitization. Salvatori S. Stanescu D. Kiilunen M. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Contact Dermatitis 2003. Buchet JP.(1-3):133-139. Szekeres T. Goto S. Lison D. et al. Radulescu M. Linnainmaa M. a study of 13 elements in blood and urine of a United Kingdom population. and cobalt metals. Lison D.533:135-152. Alessandrelli M. Occup Environ Med 1994. Iavicoli I. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. 3rd ed. et al. Arch Intern Med 1990. Thabe H. Kirsch-Volders M. Moulin JJ. MacDonald SJ. et al. Dunstan E.

30) 1.10) 3.30-1.30 (3.30 (1.17) .20) 2.80-3.10) 1.20-1.37-1.69 (1.69 (1.37 (1.70 (1.80) 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 1.40) 1.69) 1.43-1.80) 1.50) 3.14-1.70 (1. Lead has a variety of uses in manufacturing: storage batteries.60-1. plastics.00 (4. malleable.00) 3.90 (3.30 (2.60 (1.20 (1.60 (3.30 (2.10) 3.70) 1.10-2.00 (1.20-1.80 (1. ammunition.00 (4.66 (1.01 (1.20 (3.3.50-6.10) 2.60-1.50 (2.20) 4.70 (2.60) 1.20) 4.90) 1.20 (3.80) 1.40 (4.30-5. and 03-04 are 0.70) 3.49-1.00) 6.40) 2.09) 1.10 (1.80-4.40-3.40-2.78 (1.80 (4.90 (3. population from the National Health and Nutrition Examination Survey.10-8.80 (1.80) 2.60) 1.50) 1.20 (2. population was aerosolized lead emitted from combustion engines that used leaded gasoline.60) 3.90) 2.60 (2.40-2.20) 3.00 (2.20-4.51 (1.80-2.00) 5.28.40) 4.90 (1.50) 2.00-1.00) 3.60) 3.10 (1.60 (2.20 (4.20-3.S.50-2.10-1.32-1.80) 2.10-1.40-6. see Data Analysis section) for Survey years 99-00.60) 2.50) 1.30 (4.30) 2.10-2.50-1.60 (1.10-1.60) 4.Metals Lead CAS No.00 (1.93-2.90) 1.90 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.56 (1.80 (1.70) 1.40) 1.00) 2.60) 3.87) 1.50-5.83 (1. antique-molded or cast ornaments.20) .40) 2.86) 1.986) .10 (2. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.00 (5. interval) 1.60-6.40 (1.60) 3.50 (2.90) 3.52-1.70-6.90-4.90) 2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00-4.50-4.20-2.50) 4.80-3.70) 1.80 (5.80-4.25 (1.50) 7.30-1.10-3.50 (4.04-1. the main source of lead exposure for the general U.30 (2.20) 3.65 (1.10-2.30 (2.80 (2.20 (1.77 (1.10 (2.30-4. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.60 (3.80 (2.946 (.02) 1.90 (1.25) 1.30-6.62-1.00-4.31) 1. leaded glass.90-4.30-2. metal alloys (e.48) 1.60 (1.60 (1.62) 1.40) 1.90) 2.60) 4.50-1.70) 3.10) 4.10 (1.60) 2.60 (2.50-1.20 (3.10-3.80 (1.60) 4.00-5.90) 5.10) 1.90-6.53) 1.20) 3.60) 1.20 (3.60 (1.37 (1.70) 4.70 (5. bronze).75) 1.90-2.55-1.20 (2.80-5. ceramic glazes.43 (1.36-1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .S.70-1.00 (6.40 (5.69) 1.45-1.40-1.19 (1.70-1.62 (1.50-3.40-1.10-2.40-1. respectively.60) 2.60 (1.50-2.87 (1. Before the 1980’s.50 (2.90-2.60 (3.30-1.50 (1. 7439-92-1 General Information Elemental lead is a soft.43) 1.80 (2.50 (3.36) 1.10) 5. solders.40 (1.50 (1.80) 1.60-4.80-3.40) 2.60) 2.60 (2.900 (.00-2.70-2.50) 75th 2. and for radiation shielding. Lead was used in plumbing for centuries and may still be present.80-3.40) 3.70-1.00) .50 (1.50 (3.30 (4.30 (2.900 (.60) 5.30 (2.10 (2.00) 1.14-1.30 (1.70-2.90-2.20 (3.00-4.50) 5.50 (1.70) 1.89) 1.00) 1.46 (1. 0.899-.60-2.10-6.80) 2.900-1.90-4.20 (3.52-1.20-3.80 (1.23 (1.68-1.80 (4.800-1.40-1.60-2.20) 90th 3.90-4.10-2.70 (2.20) 5.50 (2.20 (3. 01-02.50) 2.66) 1.30 (1.75-1.60 (2.40-1.70-3. lead was added to gasoline and residential paints and used in soldering the seams of food cans.80 (3.36-1.90) 2.60-3.20 (1.14-1.40) 5.00-6.12-1.25 (1.00) 1.10-6.3.50-2.90) 1. blue-gray metal that occurs naturally in soils and rocks.50 (2.70 (2.72) Selected percentiles ( 95% confidence interval) 50th 1.70-5.34-1.60-1.20) 3.00) 1.20 (1.80 (1.40-4. and 0.60-4.g.70) 4.50 (4.10) 2.70 (3. In the past.40-3.00) 2.30 (1.30 (4.00) 2.60 (2.40) 2.40 (3.60) 1.30-1.90) 2.50) 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 2.50) 1.00) 4. Since lead has been eliminated from gasoline.60 (4.40 (2.40 (1.90 (2.40) Total 1.43 (1.70) 2.40-3.30) 2.10 (4.30 (2.878-1.10-2.50-1.70) 4.10-3.60 (3.80) 2.50) 5.70-4.90) 3.90 (2.70) 4.40 (2.00-1.55 (1.30-2.95) 1.50) 1.71-1. Lead is most often mined from ores or recycled from scrap metal or batteries.80 (5. brass.90 (3.60) 4.50-2.30-2.60) 2.60-1.30-1.75 (1.70-2.55-1.50-5.50-4.10-4. such as lead phosphate and tetraethyl lead. Elemental lead can be combined with other elements to form inorganic and organic compounds.90 (4.70 (1.70 (3.81) 1.40-1.80) 1.51) 1.20 (1.22 (1.96-2.70 (1.30-1.50-3.30-2.70) 3.00 (3.43) 1.60) 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 2.40-2.40-5.20-2.80) 3.52 (1.80) 1.10-4.90-2.60) 5.39-1.50) 4.45 (1.40-6.00) 4.40 (1.90 (3.91) 1.00) 1.30) 2.75-2.70) 1.60 (1.32-1.80-4.10 (3.942 (.20-6.30) 5.20-3.50-1.10-3.30) 95th 5.10) 3.00) 2.39) 1. dense.20) 1.60) 1.20-3.10) 1.90-3.

691-.50) 1.640 (.00-1.04) .10-1.90 (1.1.931) .659 (.30) 1.40 (1.960 (.40-3.700 (.00 (.900) .40) 2.808 (.10-3.10) 1.10 (.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 1.857) .600-.50) 3.558 (.600 (. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.59) 1.00 (1.660) .59-2.700-.Metals occupational (e.90 (1.40 (1.10-1.605) .600) .700-.80) 1.40-1.688 (.20 (1.90 (1.90-3.g.818) .40) 1.710-1.52-1.97) 4.800-.30) 2.848 (. and 0.70) 1.40) 1.60) 2.960-1.535-.04) 2.33-2.30-2.923 (.600) .564 (.50 (2.553-.50 (2.11) 2.S.40-5.800 (.790 (.13-3. CDC.70 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.900) .40) 2.50-2.30) 2.90-3.20-1.00 (1.70 (2.10 (1.773) . lead-contaminated dust in indoor firing ranges.50-2.30-1.650) 1.506-.29) 2.60 (1.90) 2.66 (2.80) 3.935) 1.540-.900-1.00-2.526-.86 (1.10-1.700 (.10) .70 (2. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.60-3.90-2. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70 (1.800) .986) .. and 03-04 are 0.729-.540 (.89) 2.20-1.700-.920 (.62-4.49) 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 .795 (. 1991).78-2.50) 2.752 (.02) 1.700 (.03-2.20-2.20 (2. older plumbing systems with leaded pipes or lead soldered connections.700 (.80) 2.30 (3.700 (.00-2.66 (2. stained glass framing.990) 1.700) 1.70) 1.00-1.800) .11 (1.00) 2.80) 2.573 (.20 (1.10-1.35 (.00-2.50-1.20 (1.04-2.60 (2.900-1.33 (2.915-1.60-2.710-.22) 1.900-1.920 (.862) .900 (.900) .572-. and contact with soil.616) .13) .690) 75th 1.731 (.800 (.90 (2.580-. 01-02.40 (1.800 (.700-.840 (. lead-based painted surfaces undergoing renovation or demolition.90) 2.20 (2.00 (2.70) 1.590 (.800 (.30-1.30) 2.70) 2.785) .50) 1.00) 2.940 (.80) 2.29 (2.970-1. 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.10) 2.02 (.40-1.14 (1.910-.730 (. Approximately half of the absorbed lead may be incorporated into bone. However.00 (1.637-.600 (.14 (1.628) 1.828) Selected percentiles ( 95% confidence interval) 50th . Fourth National Report on Human Exposure to Environmental Chemicals 213 .27 (1.600-.800) .70) 3.620) 1. or water contaminated by mining or smelting operations.600-. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.600-.04 (.64) 2.677 (. respectively.86) 95th 2. dust.674) 1.31-3.680) 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 1.766 (..86) 1.701) .60-1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.1.30-1.49 (1.900) .00) .12) 90th 2. interval) .745-.33.708-.80) 1.815 (.800-.30 (2.20) .591 (.00) 1.810-1.500-.40-1.757-.18-1. imported children’s trinkets and toys.40) 3.850 (. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.900) .50) 2.50 (1.10-1.900) .833-1.90) 1.27) 1.820-1.40 (1.40) 1.900 (.636 (. pewter utensils and drinking vessels.10-3.579-.642 (.30-1.90 (2.40) 1.30) 1.680) . absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone. 2007.90-2.80) 3.70-2.20) 1.570-.30) .23) .625 (.10-5.604 (.40) 1.82 (1.80 (1.75) 3.20) 1.30) 1.20 (1.480-.72) 1.80 (2.749) .30-3.07-1.671-.17 (1.600-.10 (. In the blood.40 (2.70 (2.700-.07 (.40) 2.86-2.900-1.800-1.23-4.09) 1.24-1.60 (1.613) .640-.50) 1.990) 2.941) .651) .75) 4. population from the National Health and Nutrition Examination Survey.960-1.833 (.78-2.20) .51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70-3.82 (2.30) 1.20 (2.20) .50 (2. bullet fragments retained in human tissue.50 (1.718) .10 (1.20) 1.60 (1.30) 1. see Data Analysis section) for Survey years 99-00.40 (2.800) .00 (1.52 (1.04 (.30-5.14-1.641-.80-2.20 (1.661-.610 (.620 (. 0.80) 2.556-.40 (2.10 (.50-2.60-2.10-3.80) 1.900 (.738) .50-3.20-2.695 (.41) 2.800-1.753 (.680-.78-2.19 (1.90) 2.700 (.680-.40 (2.80 (1.595-.20 (3.03 (1.62) Total .80-2.579-. lead-containing folk remedies and cosmetics.00-1.630 (.822-1.40) 2.700) .31 (1.40 (1.10) 2.20) .40-1.589-.20 (1.40-2.80) 2.10 (1. or after soluble lead compounds are ingested.06) .70) 3.44-2.800) . battery and radiator manufacturing) and recreational sources.560-.955-1.90-4. 2000).60 (1.625-.32 (1.700-1.52-1.10 (1.10) .30 (1.60-3.20-1.91) 2.90 (2.73 (1.00) .00) .90-2.00) .90-2.21 (2.80-3.

383-.828) .655-.917-1.992-1.61) 3.78-4.742) .28) 2.625 (.01) .63) 1.404 (.26) Total .73) 2. 1993).758) .408-.428) . BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger. zinc.667-.380-.36-2.72) .31 (2.607-.796-1.988-1.98 (1.709 (.668-.06 (.946-1.66) 2.677 (.718) 1.52) 1.633 (.03) 90th 1.639) .66 (1.22) 1.03) 2.698) .404 (.659-. Nash et al.938-1. O’Flaherty.64) 95th 2.00 (1.71 (1. 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.02-1.11 (1.722 (.37-1.88-2.10) 1.50-2.00 (.29 (1.693 (.22) .644 (.64 (1.83) 1.48 (1. 2007).677) .933-1.623 (.621 (.85) 1.72-2.64) 2.02) 1.41-1.990 (.876-1.608-.900 (.583-.79) 1.56 (1.639 (. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.635 (.45 (1. 1996).841-1.510-.828-1. Lead can cross the placenta and enter the developing fetal brain.06) .712 (.615 (.09-1.657) 1.72-2.853-1.04-3.18) 1.26) 2.746) .43) 1.703) .436) .673) .86 (1.918 (.52 (1.579-.25-1.14) 1.05 (.508) .94-2.682) .898) .632 (.608 (.98-2.87) 1.88) 1.11 (.988 (.63) 4.460-.38 (2.44) 1.812-1.27 (1.98) 2. through the inhibition of certain enzymes.400) .06) 1.43-1.920-1.810 (.681-. and iron.17-1.918-1.05-1.535) .765) . and paralysis.652 (.649 (.11-1.615 (.702) .07 (.734) .671 (.65 (1.962 (.88 (1.43 (2.731-.56-2.47) 1.33) 2.702) .710) .69 (1.47 (1.914-1.50-2.541-.701) .03 (1.43) 2.618 (.569 (.763) .50) 1.838) .571-.47 (2.720 (.03) .Metals 90% of the body lead burden in most adults.31 (1.561-.62-1.588-.981-1.11 (.790) .66 (1.44 (1.40-1.957-1.07) .11) .78 (2.58) 1.31) 1.06 (1.586-.61) 1.71-2.492-. Schwartz.963-1.85-2.612-.870 (.679-. abdominal pain.15) 1.603-.940 (. BLLs and associated toxic effects differ in children and adults.05-1.97) 1. 1991.604-.08) .893) .85-2.04) 2. 1995.730) 1.50 (1. kidney injury.587-. based on prospective population studies.19) 1.432 (.15-2.28) .667-.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 . encephalopathy. CDC.23 (1.74 (1.681-.97) 1.622 (.79 (1.50-2.662) 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 1.11 (1.781-1.696 (.793-1.94 (1.33-1.22) 1.933) .05 (1.593 (.07-1.. hair.721 (.670) 1. The toxic effects of lead result from its interference with the physiologic actions of calcium.09-1.992-1.03) .50-1.08-2.18 (1.644) .914 (.56) 3.31 (1.61) 1.09) 1.22-2.551-.617-.688) .75-2.971 (.914 (. and through binding to ion channels and regulatory proteins.529-.34-1.28-1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.09-1.41 (1.55 (1.718) .20-3. Staessen et al. 1995).01 (.18) 1.887 (.655) 75th 1. Approximately 70% of lead excretion occurs via the urine.03) 1.92) 2.14 (1. population from the National Health and Nutrition Examination Survey.667) .44 (1.638 (.19-5. 2004.83 (2.683-.11) 1.15-3.85 (1.18) 2.20) 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 .03) 2. interval) .67-4.53) 1.755 (.588-. 1993.601-.79) 2.977) 1.606-.975-1.404-.20) .645-.707 (. The skeleton acts as a storage depot.774 (.55 (1.64-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.592-.10 (.37-1.851) .89-2.62-2.88) 2.677-.35) 2.676) .645-.00 (1. scant amounts are lost through sweat.594-.654) . seizures.88) 2.679) 1.53-1.15) 1.82) 1.686) .722 (.62) 2.605-.00 (1.08) .03-2.15-2.59-3.00) .603 (.03 (.639 (.33 (1.469 (.51) 1.938 (..97 (1.862-.609 (.12-1.77) 2.461) .70 (1.33) 1. with a half-life of years to decades.800-.10 (1.46 (2.496 (.43 (1. In 1991.742) Selected percentiles ( 95% confidence interval) 50th .18) .62-3.41) .75 (2.51 (1.0) 3.56-3.926 (.698) .641 (.739) .31) 1.571-.38 (2.97-18.655) .658 (. 2003. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.89-5.25-1. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.375 (.342-.702-.979 (.03) 1.46 (1.96 (1. and nails (Leggett.725) .997-1.03 (.594-.648 (.38 (2.882-1.65-2.708 (.49 (1.20) .559-.61) 1. For instance.753) .61) 1.701 (.17 (.24 (1.725) .700-.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 .03 (.68 (1.603-.73-2..720 (. Large amounts of lead in the body can cause anemia.S.39-1. with lesser amounts eliminated via the feces.22-1.639 (.623 (.

atsdr. residing in housing built before the 1950’s.S. and low family income (CDC. almost double the geometric mean of 1.S.e. CDC.g. BLLs reflect both recent intake and equilibration with stored lead in other tissues.. respectively. environmental levels) and health effects is available from ATSDR at: http://www. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. EPA. usually with BLLs greater than 40 mg/dL. 2003..75 µg/dL in U.. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC.html. Urine levels may reflect recently absorbed lead. Borja-Aburto et al. Muntner et al. and spontaneous abortion (Baghurst et al.. 2003. with overt encephalopathy.07 µg/dL (Becker et al. 2006).S.2 µg/dL in males and 3.... Staessen et al.. NTP considers lead and its compounds reasonably anticipated to be human carcinogens.. though there is greater individual variation in urine lead than in blood and greater potential for contamination.7 µg/dL and 4. and organic lead compounds not classifiable with respect to human carcinogenicity. adults in the 19992000 NHANES sample (Apostoli et al.0 µg/dL in females (Soldin et al..Metals µg/dL or higher as the level of concern in children. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. Schwartz.4% of children had BLLs of 10µg/dL or higher (CDC. reduce sperm count. 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. Jones et al. Pirkle et al.. 1996. Schwartz et al. 1996. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. the prevalence rate has declined annually since 1994 (CDC.5 per 100. 2003). higher than 100-200 µg/dL). At low environmental exposures.3 million children tested had BLLs of 10 mg/dL or higher (http://www. 1984.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 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. Surveillance data reported by U. 2000).. 2007). 2002).. However.. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. premature delivery. may alter sperm morphology. 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. 2002a). 2000). 1995. and peripheral neuropathy generally occurring at much higher levels (e.. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. 2002. Payton et al..000 adults.. Fourth National Report on Human Exposure to Environmental Chemicals 215 . More recently. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. Information about external exposure (i. Data submitted through state public health programs from 2006 showed that 1.cdc.. particularly in the skeleton.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.S.. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. adults in the 1999-2000 NHANES sample. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al.. 1996. adult residents.gov/toxpro2. 2006). urban residence. 1999). 2001). 2005b. 2003. both the geometric mean (1. Korrick et al. 2009). when the geometric mean BLL was 2. 1991. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. lead in women may be associated with hypertension during pregnancy. In NHANES 1999-2002 in children 1-5 years old. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al.S... 2005b). In occupationally exposed adults.6%) were lower than those from NHANES 1991-1994.. IARC considers inorganic lead compounds probable human carcinogens. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. 1987. and decrease fertility (Alexander et al.cdc.xls). 2005a). Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.6% in NHANES 1988-1991 to 1. which is an 84% decline. 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.S. 1999). Telisman et al. the geometric mean BLL was 3.4% in NHANES 1999-2004. Bellinger 2005. The U. Lanphear et al. 1994). High dose occupational lead exposure. 1998). A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. approximately 11. Overall. Both drinking water and ambient air standards for lead have been established by the U. seizures. For example. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. including minority race or ethnicity.21% of approximately 3.

Birth Defects Research (Part A). Kuehnemann TJ. Leggett RW. Farias P. Lead and hypertension in a sample of middle-aged women. Managing Elevated Blood Lead Levels Among Young Children. et al.cdc. JAMA 1996. Lead. Int J Hyg Environ Health 2002. Third National Report on Human Exposure to Environmental Chemicals.cdc. Weiss ST.htm.82:60-80. Neri A. Centers for Disease Control and Prevention (CDC).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. Checkoway H. Rios C.htm. Adult blood lead epidemiology and surveillance—United States.8(3):395-401. Available at URL: http://www.10:43-50. Weiss ST. Pediatrics 2004. Wager C. Age-specific kinetic model of lead metal in humans. Inorganic and Organic Lead Compounds. et al. Hänninen H. Pediatrics 2009. Payton M. Ronchi L. Hu H.115:521-529. Toxicological profile for lead. Brody DJ. 1988-2004. Lepom P.gov/mmwr/preview/mmwrhtml/ mm5532a2. Atlanta (GA). Pirkle JL.cdc. Atlanta (GA). Kaus S. van Netten C.html. MMWR Morb Mortal Wkly Rep 2006.73:409-420. Caldwell KL.1542/peds:2007-3608. IARC Monogr Eval Carcinog Risks Hum 2006. Neurotoxicol Teratol 2004. 2005. Available from URL: http://www. Sparrow D. Bellinger D. Batuman V. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . 4/14/09 Centers for Disease Control and Prevention (CDC). Kim R. N Engl J Med 2003. Lanphear BP. Coresh J.275:1177-1181.gov/nceh/lead/publications/ books/plpyc/contents. et al. Hu H. Rojas LM. Acquisition and retention of lead by young children. Auinger P. 4/14/09 Alexander BH. Blood lead reference values: the results of an Italian polycentric study. Dietrich K.101(7):598-616. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Ga.htm.89:330-335. 2005b. Sci Total Environ 2002. Becker K. Aro A. Am J Public Health 1999. Jacobson SW. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Baghurst PA. Stanek KL. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Roberts RR. 4/14/09 Centers for Disease Control and Prevention (CDC). Henderson CR. JAMA 1996. Speizer FE. Manton WI. Bellinger D.53:411-416. Environ Res 2000. Scand J Work Environ Health 1984. 2002 [online]. CDC.gov/nceh/lead/ CaseManagement/caseManage_main. Atlanta. Cory-Slechta DA. Rotnitzky A. Homa DM. Vimpani FB. Mantere P. Borja-Aburto VH.26:359-371. Kaufman JD.cdc. et al. Hertz-Picciotto I.150(6):590-597. Canfield RL.htm. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Seiwert M. Neurotoxicol 1987. Hu H. Neurodevelopmental effects of postnatal lead exposure at very low levels. Blanco J. Available at URL: http://www. Blood lead levels—United States. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. The relationship of bone and blood lead to hypertension. 4/14/09 Centers for Disease Control and Prevention (CDC).54(20):513-516.287:1-11.348:15171526. Ewers TG. Teratogen update: lead and pregnancy. Public Health Rep 2000. Am J Epidemiol 1999. Bavazzano P. Jusko TA. Korrick SA. Meyer PA. gov/mmwr/preview/mmwrhtml/mm5420a5.113(4):1016-1022. Blood lead levels measured prospectively and risk of spontaneous abortion.cdc. Korrick S. Cox C.123:e376-e385. Hernberg S. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Apostoli P. Vupputyuri S. Ganzi A. Occup Environ Med 1996. McMichael AJ. Robertson EF. 1991 [online]. Reese YR. Muller CH. Sparrow D. Baj A. Jacobson JL. Rotnitzky A. Schulz C. et al.atsdr. MMWR Morb Mortal Wkly Rep 2005a. Luukkonen R.gov/toxprofiles/tp13. Environ Health Perspect 1993. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Cox C. 4/14/09 Centers for Disease Control and Prevention (CDC). doi:10. Chiodo LM. Semen quality of men employed at a lead smelter. Wigg NR. Preventing Lead Poisoning in Young Children.87:1-471. 2003-2004. Aug 2007 [online].205:297-308. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Krause C. Angle CR. Available at URL: http://www. Jones RL. Muntner P. 1999-2002.275(15):1171-1176. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Hunter DJ.55(32):876-879. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http://www. Lanphear BP. References Agency for Toxic Substances and Disease Registry (ATSDR).

Magder L. Pizent A. blood pressure and cardiovascular disease in men. JAMA 2003. Schwartz BS. Environ Health Perspect 2000. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine.Metals results from NHANES III. Paschal DC. Exposure of the U. Wilhelm M. Osterloh JD. Staessen JA. et al. Lee BK. Rocic B. Physiologically based models for bone-seeking elements. Telisman S. Clin Chim Acta 2003. Pirkle JL. population to lead: 1991-1994. Schwenk M. Lustberg M.9:303-327. Hu H. Soldin SJ. Schulz D. Hanak B. Semen quality and reproductive endocrine function in relation to biomarkers of lead.106:745-750.108(1):45-53. Cvitkovic P. Blood lead concentrations in children: new ranges. zinc. and hypertension in perimenopausal and postmenopausal women. et al. Jurasovic J. Kaufmann R. cadmium. IV. Kidney Int 2003. stable lead isotopes to determine release of lead from the skeleton.S. O’Flaherty EJ. Schwartz J. Hickman T. and tibia lead with neurobehavioral test scores in South Korean lead workers. 50:31-37. Lee GS.140:821-829. Blood lead. Lead. Brody DJ. Gunter EW. Am J Epidemiol 2001. Low-level lead exposure and blood pressure. Flegal AR. Soldin OP. blood pressure. J Hum Hypertens 1995. Roels H. Association of blood lead.118:16-29.153(5):453464. Sparrow D. Gavella M. Low-level lead exposure and renal function in the Normative Aging Study. Stewar WF. Lee SS.289(12):1523-1531. Use of endogenous. Lauwerys RR. Smith DR. dimercaptosuccinic acidchelatable lead. lead. Nash D. Rubin R. Kaufmann RB.209:301305. Toxicol Appl Pharmacol 1993.63:1044-1050. Kinetics of lead disposition in humans. Int J Hyg Environ Health 2006. Am J Epidemiol 1994.104(1):60-66. Payton M. Revised and new reference values for arsenic. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Environ Health Perspect 1998. Weiss ST. Environ Health Perspect 1996. Hwang KY. cadmium. Arch Environ Health 1995.327:109-113. Amery A. Sherwin R. and copper in men.

300 (.80 (1. The kinetics of the different forms of mercury vary considerably. 1999 ..50) 1.g.00 (. merbromin).S. synthetic organomercury compounds were once used in pharmaceutical applications.g.10-3. may contain inorganic mercury. interval) .30-6.50) 5.50-2.600 (.80 (1. and dental amalgam.860-1.800-1.30 (1. to form inorganic mercury compounds or salts.00) 4.50) 2.00 (2.40) 3. and mining and smelting. 1994. Some cosmetic skin creams from countries other than the U.30) 1.80 (3. Hursh et al.781 (.50-3.500 (. and mercury compounds are still used as preservatives (e.326 (.. inorganic. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.90) 95th 4. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.02) .814 (..800-1.700 (. Elemental mercury is a shiny.400-. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.700-.285-.700-. solid-waste incineration. thimerosal. Accidental spills of elemental mercury.472-. Poorly absorbed from the gastrointestinal tract.20-4.672) . Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. 218 Fourth National Report on Human Exposure to Environmental Chemicals .90 (4.776 (. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach. constitutes the main source of dietary mercury exposure in the general population.900) 1.900) 75th 1.600) 1.490 (.800 (.70 (3.30 (2.800 (.20 (2. have often required public health intervention (Zeitz et al.90-3.418-.70 (1.40 (3. Apart from methyl mercury.80 (1. Other major uses include electrical equipment (e.60) 1.30-2.300) .10) . After elemental mercury is absorbed. sulfur.60-2.30) 5.655-.800-1. phenylmercuric acetate) or topical antiseptics (e.800 (.40-1.00 (.70 (4.30) 3. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.563 (.Metals Mercury CAS No.00 (2. Also..80) 1.700) .50-1. with the highest concentrations occurring in the kidneys (Barregard et al.40) 1.500) .80) 3. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal). elemental mercury is absorbed mainly by inhaling volatilized vapor.753-1.2.700-.20) 2.927) .419 (.90 (1.500-.300-. and is distributed to most tissues.700) .30-5. The ingestion of methyl mercury. which can bioaccumulate in aquatic and terrestrial food chains.60-6.689-. 1993).800-1.500-. 2002).00) 1.00 (2.703-. Woods et al..903) Selected percentiles ( 95% confidence interval) 50th .60) 2085 2293 3478 Limit of detection (LOD.20-4. IARC. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.797 (.00 (1.S.40-2. electrical lamps.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 . Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. Survey years 03-04 Geometric mean (95% conf. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).60 (1.g.60 (1.900) 1.50) 4.20-3.00-5. see Data Analysis section) for Survey year 03-04 is 0.40-2. or oxygen.60-6. Kingman et al.30) 1.40 (4..00 (.70 (1. mercuric chloride).700-.. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.12) .00) .00) 3.900 (.90) 90th 3.70-2.574) .900) 1. 2007).70) 911 856 2081 4525 03-04 03-04 .800 (. thermostats and switches).30) 4132 4241 03-04 03-04 03-04 .40-1.800-1. Atmospheric elemental mercury can be deposited on land and water. In addition..60 (2. thermometers. predominantly from fish and other seafood.400 (. an organic form of mercury. 1998.40 (3.60-5. such as chlorine (e.g.60-3.00) 1.363-.900) .714-.40 (4.877 (.372) .00-1.400-.700-.886) .500 (.00 (.. sphygmomanometers and barometers.979 (.90 (1.80) 4.90) 3.30-4. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.30) 3. population from the National Health and Nutrition Examination Survey. and organic forms.919) .484) . which create an episodic potential for volatization and inhalation of mercury vapor. 1980.60) 1.40-3.

60) 3.30) 1.30-4. 1993). McDowell et al.70 (1..40-2. 2004.20-3.00 (1.00) 1..700-.200-. Methyl mercury is incorporated into growing hair.300 (..374) .06 (.30-6.. 1993).00) 4. thereafter.30 (. 2003).500-. 1973).40-1.700-1.395) .70 (1. 2003).00) 1.800 (.30 (1.500-1. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.40 (1.14.27) ..70-3.00-2. 1994) and then undergoes slow dealkylation to inorganic mercury. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al. 1991.. National Health and Nutrition Examination Survey. Vimy et al.60 (1.10) .738-.300 (.200-. for both acute and chronic exposures. 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.919) .30-3.S.30) 1.377 (.30-6.900 (.00) .318 (.02 (.343 (.269-.300) .10 (3..50-12.80) 579 527 370 436 588 806 Limit of detection (LOD. Smith et al..600) .300 (.10-3.30-4.317 (.299-.10 (5... interval) Selected percentiles (95% confidence interval) 50th .50 (2.697-. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.70-5.50) 1.60 (1.60) 2..00 (2.800-1.14 and 0.. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.800 (.664-1.541-.50) 3.900 (.500 (. Sandborgh-Englund et al.940) Race/ethnicity (females. Suzuki et al.700-1.800) 1.90 (1.200-.73) 1.40) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.297-. a measure of accumulated dose (Cernichiari et al. 2005).600 (.600) .900 (.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 .800) ..50) 2.06-1. 1992. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.300) . Geometric mean Survey years (95% conf.3) 4. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .800 (. 1998). 1971).377) .10 (1.00 (2.90) 5.90 (4.60) 1. 1969.10 (.20) 1.30 (1. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.00-3.50-2.300) .90) 2.475) .70) 1..00-6.300) .7) 4. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al. 1984.90) 2.824) 1. 1975.700 (.400-. Smith and Farris.667 (.0) 4.726-1.40-2.50-3.80-3.200 (.20 (2. 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.200-..268-.00) 6. Methyl mercury enters the brain and other tissues (Vahter et al. Jonsson et al.20) .407) .900-1. 1995. 1994). Fourth National Report on Human Exposure to Environmental Chemicals 219 .329 (.70) 4.00-2.200-.70 (1.700-.300) .70-5...70-3.70) 4.10 (1.500-.800-1.70-6. 1992).50) 95th 2.200 (.Metals the tissues to mercurous and mercuric inorganic forms. 1992 and 1999.500-.60 (3.800) .10 (. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.30-5.265-.60 (3. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.40 (1.00) 7.10) 1.40) 2.800) 75th .20-3.30-6. Excretion occurs by renal and fecal routes. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al..60 (2.20) .00-1.30-11.820 (.90) 3.20 (.00-2. 1999).90) 90th 1.23) . 1999-2002.60 (1.10) . After exposure to elemental mercury.700 (..80 (3.10 (1.40) 5.29) .50) 1..90 (4.300 (. Vahter et al.. 1990).944 (.700 (.800-1.307 (.833 (.800) 1. Miettinen et al. 1996).30-2.80 (1. and a useful marker of exposure in epidemiologic studies (Grandjean et al.20-2.01) .30) 3. with most elimination occurring through in the feces (Sherlock et al.80) 1. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.369) 1. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.00) 2.35 (1.00 (3.90 (3..20-11.500-. population.500-.20-3.90 (1.60) 1.300) . 1994.825-1.30 (1.256-.200-.700 (. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.700) 2. 1998).50 (1.10-1. Myers et al.871-1.900-1.500 (.00 (2. 1996.

600 (. Factor-Litvak et al. 1998..600) . insomnia. typically after a latent period of weeks to months.700 (. population from the National Health and Nutrition Examination Survey..600 (. depression. Sakamoto et al.500-. which may vary for some chemicals by year and by individual sample.42. gingivitis. Sakamoto et al. Drexler and Schaller. The constellation of findings may include anorexia.. Oskarsson et al. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.600) . the existence of a causal relation is unresolved (Chan and Egeland.. 2004. 1951.700 (. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. sensory impairments.600-.600 (. At levels below those that cause acute lung injury.600) .500) . 2000).600 (. anorexia. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. cerebellar ataxia.500-. and progressive constriction of the visual fields.700-. Rice. hearing impairment.700 (. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. short-term memory loss. 1963)..700 (.600 (. 2004). 1996).500 (<LOD-.700-.500-. Once absorbed. Bellinger et al. DeRouen et al. 2005.600-.600) . 1995. Overt poisoning from methyl mercury primarily affects the central nervous system. Smith et al. Rissanen et al.. Salonen et al.700) .600 (. overt signs and symptoms of chronic inhalation may include tremor. dysarthria.600) .. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. 2006. and cerebral palsy (NRC.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .700) 2007 2240 3406 Limit of detection (LOD. Acute.600 (.600) .. 2006.S.. 220 Fourth National Report on Human Exposure to Environmental Chemicals .600 (.Metals may be more efficient for inorganic mercury (Grandjean et al.500-.700 (. limb deformities. 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.800) .. irritability. 2002.600) .600-. 2004. and sleep disturbance (Bidstrup et al.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . maculopapular rash.500-. dysarthria.500-. 1983)... 2000.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . and neurocognitive and behavioral disturbances. 2003). 2004). < LOD means less than the limit of detection. 1970. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.600-. ataxia... Inorganic mercury exposure usually occurs by ingestion. and pinkish discoloration of the hands and feet (Tunnessen et al. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.800) .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 . Smith et al.500 (<LOD-. 1993). hypertension. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al.600) .500-. see Data Analysis section) for Survey year 03-04 is 0. 1987). In recent epidemiologic studies. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al... 2005).500-. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. Vupputuri et al. altered physical growth. 1995.700-. particularly irritability. 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. causing parasthesias. Survey Geometric mean (95% conf.600) ..500-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700 (. 2000.500 (.500 (. pain in the extremities. Stern 2005.

89) 3. population from the National Health and Nutrition Examination Survey.433 (. Kingman et al. Benes et al. Among the three racial/ethnic groups. Over the NHANES 1999-2006 survey periods. Grandjean et al.76-4.05) 1. and the age-related changes differed across the groups (Caldwell et al.97) 2.430) . Biomonitoring Information In the general population.60-2. However.610-1..480 (. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women... see Data Analysis section) for Survey year 03-04 is 0.940 (. 2001.770-1.gov/mercury and from ATSDR at: http:// www.18) 2.65) 1.396-.930-1.420 (. particularly methyl mercury.77-2.88-3.96 (1..19 (1.30) 3.Metals standard for inorganic mercury has been established by U.870-1.19 (2. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning. 1995. military veterans (mean age 52.555) .78 µg/L for adults and 0.400 (. From 1996 through 1998.13-2. 2006). Information about external exposure (i.88) 287 722 1529 03-04 03-04 . 2003).08 (1. 1998).S.330-.840) 1. Total blood mercury levels increase with greater fish consumption (Dewailly et al. average age 9.20 (1.60) 619 713 1066 Limit of detection (LOD. Sanzo et al.33 (2. total blood mercury geometric mean levels in females aged 16-49 years did not change.280-.330-.08 (1.14-2.447 (. and increased slightly in non-Hispanic white children (Caldwell. 2003). 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.e.54 (2.530) .90) 2.67-3. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.250) .88 (1.442-.28) 1.42) 95th 3.304) . 1998).16 (1.cdc.870-1..700 (.340-.960 (.34-3.S.epa.93 (1.463) . These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al. aged 18 to 69 years.03-4. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.39-3..99-6. range 40 years to 78 years) had an average total blood mercury concentration of 2. Survey years 03-04 Geometric mean (95% conf.46 µg/L for children. 2001. In Germany the geometric mean for blood mercury was 0.290-. the median concentration of blood mercury was 0.63-2.55 µg/L.530-. the total blood mercury concentration is due mostly to the dietary intake of organic forms. total blood mercury increased with age.313-.96 (1.76-3.410-.430 (.360 (.890 (.840-1. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.476 (.atsdr.530) .213-. interval) . 758 children.60 (1.520) .382-.549) .360-.492) Selected percentiles ( 95% confidence interval) 50th .05) 3.330-.00 (. EPA at: http://www.580) .66) 3. slightly higher total blood mercury levels were found in U..16 (.31) 1266 1272 03-04 03-04 03-04 . who participated in a 1998 representative population survey (Becker et al...14) 90th 2.23) . 2009). 2002). Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.370) . EPA.350-. 2004. In NHANES 19992002.420 (.440 (.26 (1.12 (.360-. During the same survey periods.534) .358 (.406-. Fourth National Report on Human Exposure to Environmental Chemicals 221 ..430 (.46) 3.S.58 µg/L for 4645 adults.254 (.14. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.85-2.460) .460 (.330 (. 2009).61) 1.. 1997.700-1.160-..8 years. et al..413-. Mahaffey et al. A cohort of 1127 U.52) 2.68 (2.24) 1.S.01 (. adult women in several ethnic subgroups (Hightower et al.200 (.509) .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 .408) . These distinctions can help interpret mercury blood levels in people.24 (2..9 years).840-1.480) 75th 1.S. average age 33 years.509) .00) 1.405-. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.78-2.441 (.416 (.76-3.23) 2. Schober et al. 2000).495 (.09 (2.31) 2.29) 1. environmental levels) and health effects is available from the U.67-2.07 (.570) .gov/toxprofiles. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.

2009).06 (.587 (.990) .87 (1.652) . not to imply a safety level for general population exposure. population from the National Health and Nutrition Examination Survey.32 (1.280-.400) . reversible increase in urinary N-acetyl-glucosaminidase.86) 95th 2.85) 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 .79 (1.S.391-.417) .443 (.333-.620-.687) .56) 1266 1271 03-04 03-04 03-04 . DeRouen et al..630) . Survey years 03-04 Geometric mean (95% conf.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .00) 90th 1. and on average.289) .31 (1.619-.306 (.46-2.246-.11-2.11) 1.12-3.00) 286 722 1529 03-04 03-04 .61) 1.1 µg/L.06 (.358) . Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.970 (. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.11) 2.362 (.79) 1. a biomarker of perturbation in renal tubular function.485 (.480) .01) 2. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.368) .1 µg/L for each surface with a dental amalgam (Kingman et al. et al. Czech (Benes et al.16) 1. 2006). interval) .54 (2.909 (.447 (.276 (.309-.217 (.347) .391) .535) 1.588) .00 (.969-1.714-1.13 (1.07) 1. An expert-panel report recently prepared for the U.301-.88-2.28 (.88-2.545 (.455-.297 (.25 (.41-2.486) Selected percentiles ( 95% confidence interval) 50th .800-1.404-. Department of Health and Human Services noted that several studies have observed a modest.498) 75th .67 (1. 1998).77 (2.04-3.464 (.44) 1.784) 1.40 (1.532 (.87) 2. mean urinary mercury was 3.88 (1. 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.385-.196-. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.307-.S.67 (1. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.76 (1. Levels in U.32-2.376-.667-1.455-.343 (. 2003).78-4.62 (1. 2002) adult population surveys were similar to those in a U.768 (. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.64-2.40-1.S.875-1..472-..599) .S.537) . Information about the biological exposure indices is provided here for comparison. 2005).785-1. Langworth et al.225-.255 (.508 (.476 (.275) .208-.09) 1.65 (1.30) 1.03) 2.566) . and Italian (Apostoli et al. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects. Urine mercury and the number of dental amalgams were correlated.365 (.23-2.455) . In the study of U.463 (. 2006. 2002).Metals 2000).30) 2. 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..696 (.964-1.63) 1. 2009).S.365 (.447-. Urinary mercury levels in recent German (Becker et al. women of childbearing age have generally been much lower than these levels (CDC.616) .21) 1.525 (. military veterans with dental amalgams. 1992)..400-. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell. 1988..35 (1.39) 1.392-..384 (.. the urine mercury increased by approximately 0.522-..18-1.265-.51-2. et al..13-2.

636-.560-.824) .31-1.Metals Urinary Mercury−Females Aged 16-49 Years Old.55) 90th 3.650 (.37) 1.631-.500-.56) 3.622-.99 (3.61-6.475-.92) 4.806) .42) 2.79) 3.620 (.650 (.03-2.46-4.560 (.52) 3.97 (1.540 (.76) 2.03 (.706 (.97) 2.62 (3.23-1. 16-49 years) 99-00 01-02 .14) 3.450-.30 (2.30 (1.516 (.05 (3.610-.21 (2.09-1.17) 95th 5.37 (1.809) . National Health and Nutrition Examination Survey.658 (.30 (2.16) 5.710 (.10-2.846) .32-3.410-.579-.637) .07) 1.582-.39-3.S.50-4.84 (2.25) 2.46 (1. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.47) 1.650) 1.833) . National Health and Nutrition Examination Survey.87-4.07-5.92) 2.502-.91 (2.61) 1.03 (.99 (2.665) .565 (.24-1.540-.709) .92) 3.77) 1.632 (.639 (.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.42-3.744) 1.596 (.831) .21 (1.14 and 0.54) 595 531 381 442 594 826 Limit of detection (LOD.45) 2.740 (.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .27 (1.600 (.909-1.508-.91-7.83-3.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .580 (.53-3.24) 6.892) . Geometric mean Survey years (95% conf.15 (2.21-3.45-3.70 (2.06 (.22-3.719 (.81-6.68) 3.00 (3.79) 1.13 (2.23-1.799) .699) 1.68 (3.831) .85-3.46) 3.45 (1.44) 3.724 (.62 (4.526-.98 (5.832-1.580-.65) 1.62 (1.606 (.772 (.59-5. interval) Selected percentiles (95% confidence interval) Survey years 50th .670) 75th 1.615 (.68-3.50 (2.47) 1.710) 1.77) 2.14-2.691) .S.97) 2.56) 4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.85) 4.57-4.657 (.05 (2. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.624-.72) 1. 16-49 years) 99-00 01-02 . population.520-.10-4.04-10.655 (.709) 75th 1.557-.13-4.45-2.69 (1.50 (1.686) .28 (1.32) 2.76 (1.14-1.27 (2.95 (2.685 (.760 (. 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.522 (.27-1.07-2.41 (2. 1999-2002.45) 95th 3.790) .850-1.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .18) 3.38) 4.721 (.592 (.966) .97) 2.00 (2.56 (1.32 (1. Geometric mean (95% conf.03) 1.45) 2.605-.76-5.51) .3) 5.742-1.16-5.84 (2. population.774) .520-.04-1.94) 1.99-2.51 (3.18 (3.910) .616-.81 (3.99) 1.89 (2.35 (1.710 (.15-1.420-.664) .31 (1.65-4.41-6.55-3.578-.48 (2.553-.41 (1.501-.14.426-.00) 2.41 (1.43-1.387-. interval) Selected percentiles (95% confidence interval) 50th .35) .42) 90th 2.22 (.930) .870) .810) .69-3.656-.09-1.569-. 1999-2002.723 (.30-2.

Jones RL. Kline J.50:17-27. Cardenas A. Krause C. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Vahter M. Sandborgh-englund B. Arch Environ Health 1992. Echeverria D. Barregard L. Bernardo M. Persson G. Budtz-Jorgensen E. Sallsten G. Weihe P. Osterloh JD. Lebel G. Lapham LW. Cernichiari E. Lepom P. Becker K. Atlanta (GA). Sallsten G. Roels H. Schaller KH. Centers for Disease Control and Prevention (CDC). Schutz A.149:301-305. Weihe P. Cernichiari E.77(2):124-129.111:719-723. Ayotte P. Cerna M. Trachtenberg F. and heart diseases. Fish consumption.19:478-484. Leitão J. Martin MD. Cent Eur J Public Health 2000. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. et al. I. Woods JS. Levallois P. Smid J. Am J Epidemiol 1999.205:297-308. Debes F. 2007 TLVs and BEIs. Subrt P. mercury exposure. Kaus S. selenium. ACGIH. Gagliardi T. 206:15-24. Sci Total Environ 2002. Skerfving S. Nutr Rev 2004.2:856-861. White RF. Total blood mercury concentrations in the U. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. et al. Lauwerys RR. Harvey DG. Factor-Litvak P. Bidstrup PL. Arch Environ Health 2001. Impact of maternal seafood diet on fetal exposure to mercury. Snihs JO. McKinlay S. Mercury derived from dental amalgams and neuropsychologic function. Cox C.295(15):1775-1783. Br J Ind Med 1993. Int JHyg Environ Health 2002. Health effects of dental amalgam exposure: a retrospective cohort study.72:169-173. Grandjean P. population: 19992006. Kjellstrom T. Biennow M. Seiwert M. Cianciola ME. Seiwert M. Cu. JAMA 2006. Weber JP. Chronic mercury poisoning in men repairing direct-current meters. Schuzt A.. et al. The concentration levels of Cd. Jorgensen PJ. et al. Cincinnati (OH): Signature Publications. Becker K. Third National Report on Human Exposure to Environmental Chemicals. Falk R. Barregard L. Sallsten G. Dewailly E. and lead. Jacobs D. Cortesi I. Martins IP. Cernichiari E.8(2):117-119. and Se in blood of the population in the Czech Republic. Leroux BG. Tissue levels of mercury determined in a deceased worker after occupational exposure.56(4):350-357. Tavares M. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Castro-Caldas A. Apostoli P.61:65-69. 224 Fourth National Report on Human Exposure to Environmental Chemicals . Bates MN. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. et al. Caudill SP. Clarkson T. Conradi N. Kaus S. Lancet 1951.295(15):17841792. Videro T. Environ Res 1998. Rosenbaum G. Cutress T. Locket S. Drexler H. Kinetics of mercury in blood and urine after brief occupational exposure. Martin MD. Zn. Int J Hyg Environ Health 2003. et al. Caldwell KL. Myers GJ. Barbon R. Niklasson B. Mangili A. Drago I. Environ Health Perspect 2005. Int Arch Occup Environ Health 1999.S. Daniel D. Arch Environ Health 1969. Schulz C. Pb. et al. Chan JM. Mortensen ME. Application to workers exposed to mercury vapour. Jarvholm B. Assessment of reference values for mercury in urine: the results of an Italian polycentric study. Neurotoxicology 1995. Schulz C. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Benes B.33:1-9. Buchet JP. Markers of early renal changes induced by industrial pollutants. Seifert B. Enzymuria in workers exposed to inorganic mercury. Garrett N. Bonnell JA. Elia G. Int J Hyg Environ Health 2009. Brewer R. Int J Epidemiol 2004. Luis H. Ekman L. Arch Environ Health 1992. Bruneau S.212:588-598. Barregard L. Metabolism of methyl mercury (203Hg) compounds in man. Greitz U. Woods JS.Metals References Aberg B. 2005. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo). Marsh DO. Barregard L. Attewell R.62(2):68-72. Egeland FM.113(10):1381-1385. Hasselgren G. Grandjean P. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure. Spevackova V. Bellinger DC.289:1324. Jorgensen PJ. Int Arch Occup Environ Health 1988. Bernard AM.7(3):176-184. 52:19-33. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. Berglund B.16(4):705-710. Aposian HV. Geier J.47(3):185-195. Fawcett J. DeRouen TA. Begg M. Hg. Cejchanova M. J Toxicol Environ Health 1997. Hultberg B. Environ Health Perspect 2003. JAMA 2006. Townes BD. Bjornberg KA.

Circulation 1995. Kubota M. Environ Health Perspect 2004. Korolainen A. Nyyssonen K. Greenwood MR. and polychlorinated biphenyl and other organochlorine concentrations in human milk. Environ Health Perspect 2006. Nyyssonen K. McDowell MA. Br J Ind Med 1993. Liu XJ.51(3):234-241. Arch Toxicol 1996.3dimercaptosuccinic acid (DMSA). Hallen IP. Elimination of 203Hg-methyl mercury in man. Amalgam tooth fillings and man’s mercury burden. Miettinen JK.77(4):615-624.71(1):29-38. IARC Monographs on the Evaluation of Risks to Humans. Seppanen K. Environ Res 2004. Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillings in lactating women. Needham LL. Ekstrand J.70(5):310-314. Nakai K.59(5):692-706. Murata K. Hum Exp Toxicol 1994. Fourth National Report on Human Exposure to Environmental Chemicals 225 . Elinder CG. Elimination of free and protein-bound ionic mercury (203Hg2+) in man. Pellizzari E. The effect of ethanol on the fate of mercury vapor inhaled by man. and any death in eastern Finnish men. Declining risk of methylmercury exposure to infants during lactation. Rahola T. Environ Res 1995. Blood mercury reporting in NHANES: Identifying Asian.114(2):173-175. and Exposures in the Glass Manufacturing industry. Rahola T. Barregard L. Satoh H. Maternal and fetal mercury and n-3 polyunsaturated fatty acids as a risk and benefit of fish consumption to fetus. Tillander M. Sakamoto M. Kantola M. Sampson EJ. Hair mercury levels in U. Skerfving S. Halbach S. Salonen JT. Mercury concentrations in urine and whole blood associated with amalgam exposure in a US military population. Fish oil-derived fatty acids. methylmercury transport across the placenta via neutral amino acid carrier. Circulation 2000. et al.77(3):461-467. Brown LJ. J Pharmacol Exp Ther 1980. Yasutake A. Sandborgh-Englund G. Toxicol Appl Pharmacol 1999.iarc. Ann Clin Res 1971. Oskarsson A. Allen J. selenium. 2000. The US EPA reference dose for methyl mercury: sources of uncertainty. Hirayama K. Clarkson TW.13:496-501. Seto DS. Mehaffey KR. Hursh JB. Environ Physiol Biochem 1975.90:185-189. Clickner RP. Hernandez GT. Native American. Lagerkvist BJ.48:247-53.49(6):394-401. Johanson G. Cox C. Palumbo D.Metals Grandjean P. Relation of a seafood diet to mercury. Br J Ind Med 1992.112(11):1165-1171.112(5):562-570.103:2766-2679. Sakamoto M. Acute mercurial intoxication treated by hemodialysis. et al. Osterloh J.5:252-257. Lakka TA. Sandborgh-Englund G. Lancet 2003. Rice DC. Environ Health Perspect 2004. Rissanen K. Boeckx M. 1993. Myers GJ. Volume 58. Decrease in mercury concentration in blood after long term exposure: a kinetic study of chloralkali workers. Washington (DC). Weihe P. Hattula T. Schultz A. et al. and the risk of acute coronary events— The Kuopio Ischaemic Heart Disease Risk Factor Study. Burse VW. Roels HA. Hattula T. Cadmium. Blood organic mercury and dietary intake: National Health and Nutrition Examination Survey. Dillon CF. Akagi H. Albertini T. Arch Environ Health 1996. National Academy Press. Kauhanen J. Langworth S. lipid peroxidation. Adachi T. docosahexenoic acid and docosapentaenoic acid. Voutilainen S. arsenic. cardiovascular. Cernichari.95:406-13. Kubota M. Beryllium. Rissanen T.91:645655. Schutz A. Langworth S. Korpela H. Ann Clin Res 1973. Environ Res 2002. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study.214(3):520-527. Toxicological effects of methylmercury. Sundquist KG. Ohlin B. Davidson PW.fr/ENG/Monographs/vol58/index. KajiwaraY. Sanchez-Sicilia L. Mercury in biological fluids after amalgam removal. Environ Sci Technol 2004. Salonen JT. and the risk of myocardial infarction and coronary. Bolger PM.5:214-219. Shamlaye CF. Nakamoto S. Ceulemans E. et al. and multiracial groups. Urinary excretion of mercury after occupational exposure to mercury vapor and influence of the chelating agent meso-2.361:1686-1692. Elinder CG.38:3860-3863. Kolff WJ. 7/15/09 Jonsson F. Nakano A. National Research Council (NRC). Hattula T. Fernando R. Bodurow CC. Ann Intern Med 1963. Pacific Islander. J Dent Res 1998. J Dent Res 1998. Miettinen JK. Sallsten G. Schutz A. Vesterberg O. Rahola T. Br J Ind Med 1991. The distribution and biological half-time of 203 Hg in the human body according to a modified whole-body counting technique. Lauwerys RR. Hightower JM. Mercury.S. Available at URL: http:// monographs.155(2):161-168. Patterson DG Jr. 1999 and 2000.50(9):814-821. A compartmental model for the kinetics of mercury vapor in humans.php. children and women of childbearing age: reference range data from NHANES 1999-2000.3(2):116-122. Renal and immunological effects of occupational exposure to inorganic mercury. Kingman A. O’Hare A. Matsumoto S. Demuth S. Intake of mercury from fish. International Agency for Research on Cancer (IARC).

Am Ind Hyg Assoc J 1970. Stern AH. Acrodynia: exposure to mercury from fluorescent light bulbs. Toxicol Appl Pharmacol 1996. Aguinagalde FX. Matsuo N. Smith PJ. Lind B. Environ Health Perspect 2002. Environ Res 2005. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect 2003.2:117-131. Amiano P. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Nakazawa M. Blood mercury levels in US children and women of childbearing age.128(2):25125-25126. Tunnessen WW. Hall LL. Vimy MJ. Leitao JG. McMahon KJ. Most B. Environ Health Perspect 2007. et al.110:129-132. Allen PV. Patil LS.98(1):133-142. The hair-organ relationship in mercury concentration in contemporary Japanese. Daniels JL. Azpiri MA. Effects of occupational exposure to elemental mercury on short term memory. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Bolger PM.79:786789. Orr MF. Vahter M. Sherlock J. Toxicol Appl Pharmacol 1994. Takahashi Y. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Turner MD. et al. Lorscheider FL. Leroux BG. Amurrio A. Martin MD.97(2):195-200. Arch Environ Health 1993.48(4):221229. Mooney TF. Goldberg J.115(10):1527-1531. Langolf GD. The contribution of dental amalgam to urinary mercury excretion in children. Fisher HL.258(4 Pt 2):R939-945. Vorwald AJ. Guo S. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Yoshinaga J. Sinks TH.124:221-229. Bernardo MF. Hislop D. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Stern AH. Newton G. Schober SE. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Pediatrics 1987. DeRouen TA. The kinetics of intravenously administered methyl mercury in man.111(12):1465-1470. Public Health Nutr 2001. McDowell M. Topping G. Toxicol Appl Pharmacol 1994. Hum Toxicol 1984.40:413-419. Br J Ind Med 1983. Baser M. Kaye WE. Smith JC. Farris FF. JAMA 2003. Smith AE. Effects of exposure to mercury in the manufacture of chlorine. Mottet NK. 1993-1998. Vupputuri S. Methyl mercury pharmacokinetics in man: a reevaluation. Zeitz P. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Jones RL. Dorronsoro M. Longnecker MP. 1999-2000.289(13):1667-1674. Smith RG.31:687-700. Am J Physiol 1990. Environ Res 2005. Shen DD. et al.37:245-252. Imai H.4(5):981-988. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Burbacher T. Osterloh J. Smith JC. Whittle K. Friberg L.Metals Sanzo JM. Hongo T. Sandler DP. Suzuki T. Woods JS.

7-92.7) 45.5) 80.2 (83. semiconductor and battery industries have begun to use molybdenum. More recently.4) 41.0) 55.8-94.5 (81.7-96.7-51. 2001.6-42.0 (43.9 (32.6) 71.7) 75th 84.6-111) 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 52.1) 46.1-55.3) 37.3 (55.3 (38.5) 44.5 (74.7) 78.0 (41.0-56.4) 45.6) 71.1) 59.3-44.0 (81.5 (37. inks. 1996).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 78.4 (34. and 1. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.3) 83.6) 51.4) 76.8) 75.1-52.7 (71.S.Metals Molybdenum or ore deposits.4 (48.5-52.8-108) 87.7) 46.7 (44.3 (84.1) 126 (106-147) 109 (94.2 (49.8) 44.3-91.6 (43.9 (73.9 (44. 0. aldehyde dehydrogenase.1-59. 7439-98-7 General Information Elemental molybdenum is a silver-white.2 (61.6-62.1) 57.5 (41.7 (58.6 (55.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.6) 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 (99.2) 53.1-63.4 (80.7-47.2 (40.8 (82.2-53.5 (67.3) 85.2-59.1 (71.7-73.6 (40. At a daily oral molybdenum dose of 24 µg.0) 84. Compounds of molybdenum are also used as corrosion inhibitors.8) 39.7-60.9) 62.2 (63.0-38. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.5-46.3 (55.8.3-115) 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.5) 80.9 (78.5-41.9) 34. 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 (71. In humans.5 (48.9-85.6 (73.9-56.0 (48.2) 40. Fourth National Report on Human Exposure to Environmental Chemicals 227 .3) 47.5 (43.5-66.7 (51.6-72.1) 82.3) 65.0-101) 82.5-52.2) 37. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.5-68.2 (55. 1997). chemical reagents in hospital laboratories.0) 54. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.5-65.3-47.4 (48.5) 47.7 (37.2 (69.0) 62.7-68.9 (34.8-49.7 (50.8.6-58.6 (52.0-77.0) 97.1) 35.1-44.3-108) 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 47.2 (38.7-105) 69.4-61.0 (46.3 (73.3 (79. which exert homeostatic regulation over molybdenum balance. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2001). see Data Analysis section) for survey years 99-00.1-52.0 (42.0) 39.8) 48.0-65.3 (37.4 (72.3 (46.5 (41.4 (79.6-82.2-37.2) 52. hydrogenation catalysts.9 (33. and 03-04 are 0.9) 67.7) 86. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.0) 45.2-79.7-41.9 (52.5 (49.2 (49.7 (36.6-96.6-46.8) 40.8-46.2) 48.4) 52.3 (47.7 (45.0-110) 90.4-82.9 (37.8-90.7) 57.5) 60.5. and xanthine oxidase (Kisker et al. urinary excretion over six days CAS No. WHO.8-106) 88.0-85.2-91.4) 56. population from the National Health and Nutrition Examination survey.0-100) 63.2-42.1 (38.8 (85. respectively.3) 41.2-70.4-75.2-59.4-52.6) Selected percentiles ( 95% confidence interval) 50th 50. 01-02.3-75.4) 42. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.1 (34.0-62.8 (42..1 (91.2 (56.6) 93.0-53.5-91.7-84.0 (42.3 (64.3) 54.1) 60.6 (55. Excretion occurs predominantly via the kidneys.6 (40.2) 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 (98.3 (53.7 (73.0-71.6-55. lubricants.1-51.9-55.6) 53.9-109) 97.0 (76. and in pigments for ceramics.1-88.9-55. and paints.9 (40.5) 85. interval) 45.8 (67.1-48.7-122) 93.7-91.5-124) 108 (92.0) 60.4) 49.7) 78.2) 79.8) 46.9-82.9-83.7-39.7-50.7) 77.2) 41.7) 51.

5 (59.0) 53. EPA.2 (52.8 (75.3-68.1-67.5-70.S.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.7) 112 (95.9-45.0) 39.1-109) 89.4-76.3) 61.5-119) 90.4-118) 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 .1 (42. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.9-61.3) 43.0) 36.2 (69.2) 42. 1995). 1999).3 (71.7 (66.6 (59.4 (40.1 (37.6-63.2 (37.6 (38.0-120) 85.4-66.9 mg/kg/day and established a tolerable upper intake level of 0.3 (58.5 (35.8-65.0-133) 119 (88.2-65.1) 56.2) 58.1 (38.5 (50.8) 39.8-52.2) 37.1) 40.4-39.3 (36.1) 65.2 (57.3) 64.8) 38.0 (58.4 (37.6 (57.9 (40.9 (64.7-38.3-59.9-118) 91.2-41.2-46.4) 40.8-47.5 (38.3) 44.9-42.2 (33.8 (56.1 (39.6) 48.4-41..4 (59.4) 89.1 (33.7-43.7-52.2 (40. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.5-60.4-107) 85.2-47. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.3-43.3-46. In industry.0) 39.8-118) 81.5) 90th 108 (97.2-121) 107 (92.4 (78.1-38.6 (71.4) 122 (107-133) 109 (99.4 (44. 1961.9 (49.5-99.7-100) 77.Metals was 18% of the ingested dose.3) 57.8-42.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.1-43.9-117) 57.1-79.7) 53. of the ingested dose (Turnlund et al.5-45.7-44.4) 60.1 (82.5 (39.6) 39.0-46.4) 116 (101-126) 104 (88.5 (40.9-40.5) 71.3) 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 85.7) 75th 63.1-39..5) 73. and clinical or epidemiologic evidence of adverse effects is limited..2 (43.0 (74.1-100) 86. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.1-41.0) 33.8 (36.0-46. Based on studies finding adverse reproductive effects in rats and mice.9) 44.5 (40.0) 72.9-68.1-127) 90.2-96.7 (75.5-62.8) 71.4 (53.1-43. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0-41.4) 77.2-40.3-56.6-76.7-40.5 (41.5) 60.9 (64.7) 41.1 (30. 2001).9 (36.8) 38. U.7-93.5-97.3-115) 98.2) 38. Molybdenum is generally considered to be of low human toxicity.2 (73.8-46.03 mg/kg/day in humans (IOM. interval) 43.0) 38.5) 72.9) 40. but available epidemiologic data are scant.9 (73.1) 101 (83.2-49.6 (36.1) 43. and urinary levels reflect intake from all sources.1 (54.1 (44.3 (55.3) 41.2) 37.4) 58.3-45.5-46.2-80.7) 62.5) 63.0) 62.9 (39. at daily oral doses of 95 µg and 428 µg.4-185) 106 (94.0-38.3 (37.2 (40.3 (83. 1997).9 (79.3-52.8) 45.0 (35.9-41.6) Selected percentiles ( 95% confidence interval) 50th 41.3 (71. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2 (40.9-96.0) 88.7 (77.0-56.5 (34.9-71.1-112) 78.7) 57.4) 47.9-87.8) 79.5-48.2) 42.9) 41.0) 44.4 (67.8 (37.1-45.6-78.6 (36. 1993).1-39.6-61.5 (36. Biomonitoring Information Molybdenum is an essential element for health.1-81.2) 39.4 (56.4) 44.6) 43.3 (36.3) 40.5 (39. urinary excretion over six days rose to 50% and 67%.9 (39.1 (40.2) 43.6) 39.9) 92.8) 61.5-50.3 (37.9) 31.1-40.3 (51.8-66.5 (65.8-84.5-69.5 (41.6) 36.0 (80.8-67.4-120) 101 (84.6 (42.6-88.5 (35.3-141) 109 (81.1-34.7-120) 87.S.1) 37.6-41.3 (53.7-137) 129 (109-155) 112 (97.6-45.2) 55.2) 39.7) 45.2-103) 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 42.1 (38.9) 79.7) 42.0-103) 103 (90.8) 37.8 (57.4-42.1) 37. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.9 (35.2 (36.4-106) 85.3) 56.7) 115 (93.2 (50.4) 48.8) 62.5-92.4) 61.6-63.5-44.8 (90.9-45.5 (37.3) 37.3-102) 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 40.5 (79.8-47.6-61.5 (54.7 (30. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.5 (78.4 (55.5 (65.5 (83.5 (80.2-96. respectively.5 (37.1 (49.3-44.5-35.7-62. population from the National Health and Nutrition Examination survey.

Keyes WR. (DC): National Academy Press. Schleyerbach U.Metals in urine for the U. X.gov/index. Occupational risk factors of lung cancer: a hospital based case-control study.62(4):790-796. EPA). Zhurnal Obshchey Biologii 1961. 16:1313-1319. manganese.. Molybdenum absorption. Menne C. 2001. chromium. arsenic. iodine. edu/openbook. pp. Minoia C. Available at URL: http://books. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. vanadium.nap. Sabbioni E. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Rees DC. van Sprundel MP. Kristiansen J. Minoia et al. Ronchi A. Molybdenum. 4/14/09 White MA. excretion. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al.123(1):81-85. Food and Nutrition Board. Molybdenum in infancy: methodical investigation of urinary excretion.. copper. silicon. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. 1998). and zinc: a report of the Panel on Micronutrients. Shmavonyan DM. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Available at URL: http://ntp. National Toxicology Program (NTP). 144-154.S. Available at URL: http://www. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. 4/14/09 Iversen BS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. iron. White and Sabbioni.epa. Yarovaya GA. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Molybdenum 1993 [online]. Analyst 1998.niehs. Washington. U. 2005). Kisker C. In: Trace elements in human nutrition and health. boron. Aprea C. 420-441. molybdenum.S.15(2-3):149-154. 2005. J Trace Elem Med Biol 2001. Rapid Comm Mass Spectrom 2002. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Van Meerbeeck JP. 56:322-327. A study of 13 elements in blood and urine of a United Kingdom population. Peiffer GL. 2001). Am J Clin Nutr 1995. Trace element reference values in tissues from inhabitants of the European Union. Sabbioni E. Schindelin H.php?record_id=10026&page=420.. Sciarra G. White MA. Koval’skiy GA. Institute of Medicine (IOM). Sci Total Environ 1998. 1996. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. 4/14/09 Sievers E. Third National Report on Human Exposure to Environmental Chemicals.htm. Christensen JM. Turnlund JR. Droste JHJ. Occup Environ Med 1999. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online].216:253-270. Molybdenum-cofactorcontaining enzymes: structure and mechanism. References Centers for Disease Control and Prevention (CDC). Dietary reference intakes for vitamin A.S. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population.nih. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. World Health Organization (WHO). Atlanta (GA). pp.66:233-267.22(3):179-191. TR-462. Weyler JJ.gov/iris/ subst/0425. nickel. Gatti A. Vermeire PA. vitamin K. 1998. Schaub J. 2002. Geneva: WHO. Turci R. Ann Rev Biochem 1997. 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. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. Environmental Protection Agency (U. et al.

Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. and iron. cisplatin. however. population from the National Health and Nutrition Examination Survey. 01-02. and as drugs (e..04. Platinum compounds are used in electrodes.g.07. 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.Metals Platinum CAS No. jewelry.S. 1998). < LOD means less than the limit of detection. respectively. which may vary for some chemicals by year and by individual sample. 7440-06-4 General Information Platinum is a silver-gray. Important properties of platinum are resistance to corrosion. as oxidation catalysts in chemical manufacturing. 230 Fourth National Report on Human Exposure to Environmental Chemicals . Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. carboplatin) in the treatment of cancer. strength at high temperatures. and 03-04 are 0. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. thick-film circuits printed on ceramic substrates. see Data Analysis section) for Survey years 99-00. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. and high catalytic activity. dental alloys. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 0. and 0.04. 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. copper.. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al.

. 1969. inorganic salt..Metals doses or at biomonitored levels from low environmental exposures are unknown. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. whereas soluble platinum compounds (e. Toxicity is determined by the type of compound (e. 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. cutaneous..g.g. population from the National Health and Nutrition Examination Survey. 2000). Information about external exposure (i. 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. 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. Saindelle et al. or recommended for the metal form by NIOSH (Czerczak and Gromiec.. 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. Platinum metal and insoluble salts can produce eye irritation.. 1969). Animals exposed to cholorplatinate salts used in industry have demonstrated severe hypersensitivity with asthma-like symptoms and anaphylactic shock (Parrot et al.. Fourth National Report on Human Exposure to Environmental Chemicals 231 . intravenous medicinal use. 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. metallic. or organometallic). When ingested or inhaled. Platinum metal is biologically inert.g.S. oral). 1975b). and duration of exposure. 1975a. inhalational. Most absorbed platinum accumulates in the kidneys and is excreted in urine (Moore et al. route of exposure (e.e. The pharmaceutical cisplatin is an animal carcinogen and reasonably anticipated to be a human carcinogen as determined by NTP.

Part 1: monitoring of urinary concentrations. Rommelt H. Kaus S. Occup Environ Med 1998. Blanks R.70(3):205-208. Neuendorf J. Huber R. Levels of platinum in urine for the U. Hauff K. Cohrssen B. Schierl R. Pethran et al. Seifert B. Herr et al.. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations..9:152-158.. International Programme on Chemical Safety (IPCS). Kelly J. Pethran A. J Expo Anal Environ Epidemiol 2003. Carelli G. Schulz C. 206:15-24. Urinary platinum levels associated with dental gold alloys. Gromiec JP. rhodium.. Biomarkers 1999. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Kulka U. Saindelle A. Schierl R. Parrot JL.04 µg/L) in this Report. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In: Bingham E. New York: John Wiley & Sons. Ensslin AS. van de Weyer C. Occup Environ Med 2004. 1998). Biomonitoring of traffic police officers exposed to airborne platinum. eds. and platinum. Nowak D. Fruhmann G.htm. Begerow J.. population were below the limit of detection (0. Uptake of antineoplastic agents in pharmacy and hospital personnel. References Becker K.. Saindelle A. Platinum.01 µg/L (Becker et al. Hall L. palladium. Gieler U. Br J Pharmacol 1969.. 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. 1999.207(1):69-73. Herr CE.4(1):27-36. Senofonte O. 5th ed. 2000. Hysell D. ruthenium. and in blood and urine in the United Kingdom. Ruff F: Platinum and platinosis.10:63-71. 2003). Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Boos KS. Raab W. Schierl et al. Hysell D. Available at URL: http://www. Powell CH. Environ Res 1975a.56(3):283-286.htm. 2003. Stilianakis NI. Schierl. Environ Health Perspect 1975b. Jankofsky M. 1991 [online]. Platinum concentrations in urban road dust and soil.S. Environmental Health Criteria 125. 2003. Kavanagh P.org/documents/ehc/ehc/ehc125. 1997.61(7):636-9. pp. Int Arch Occup Environ Health 1997. osmium. 2001). Schulz C. Seiwert M.13(1):24-30. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Ewers U. Herr et al. which elevate urinary platinum by five to twelve-fold (Begerow et al.005 µg/L (Iavicoli et al. Influences on human internal exposure to environmental platinum.76(1):5-10. Patty’s Toxicology.inchem. Urinary excretion of platinum from platinum-industry workers. Nickel. et al. Petrucci F. Hebert R. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Grimm CH. Allergy and histamine release due to some platinum salts.. Wilhelm et al. and gold excretion of patients after insertion of noble-metal dental alloys.19:685-691. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Int J Hyg Environ Health 2004. Thornton I. Moore W Jr.. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. 2004. Duneman L:Long-term urinary platinum. 289-380. Ruff F: Histamine release by sodium cholorplatinate. Angerer J. 1998). 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. Schierl R.. Alimonti A. Arch Environ Health:1969. Campbell K. Schierl R. Biomonitoring Information Urinary platinum levels reflect recent exposure. Kuster W. Arch Environ Health 2001. Pethran A. palladium. Several studies have shown that background concentrations in general populations were usually less than 0. Int Arch Occup Environ Health 2003. 3/31/08 Moore W Jr. Analyst 1998.Metals the International Programme on Chemical Safety at http:// www.123(3):451-454. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Iavicoli I. Farago ME.org/documents/ehc/ehc/ ehc125.inchem. et al. et al. Kazantzis G. et al.55(2):138-140. Turfeld M. Fries HG. 232 Fourth National Report on Human Exposure to Environmental Chemicals . 2003. International Journal of Hygiene and Environmental Health 2003. Czerczak S. Crocker W. 2004).. 2004) or less than 0.35:313-321. Bocca B. Wilhelm M.

350-.430-.330) .400) .Metals Thallium depilatory cosmetics.290) 90th .180) .200 (.390) .330) .480) .420) .290) .480) .S.167-.420-.170-. Fourth National Report on Human Exposure to Environmental Chemicals 233 . it has not been specifically mined or refined in the United States since 1984.192) Selected percentiles ( 95% confidence interval) 50th .340-.400 (.180) 75th .450 (.420 (.290) .350-.320) .230) .170) .360 (.154-.150-.440 (.250 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.390) .450 (.190 (. In addition.196) .182-.370 (.400) .270 (.350 (.173) .360) .470 (.490 (.360-.310 (.330-.270 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.260-.370) .200) .02.410-.150-.170-.170-.440-.290-.300 (.200 (.450) .420) .160-.350-.400 (. 2005).147-.430 (.270-.230) .340-.490) .160 (.400 (.200) .330-.370 (.210-.210) .380-.390-.350-.159 (.150-.390 (.400 (.370 (.310 (.370 (.170-.178) .510 (.330-.220 (.210 (.400) .220 (.300) .520) .350) .240-.145-. representing distribution into other tissues.145-.430) .480) .420) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.190 (.320) .320 (.190 (.200) .172 (.270) .149 (.520) .188) .270 (.360 (.430 (.180 (.470) .230-. Human health effects from thallium at low environmental CAS No.135-.450 (.160-.202 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.239) .145 (.440) .170-.191 (.180-.400-.400-.200-.240) .480) .370-.250-.360-.380 (.460-.510) .370 (.243) .172) .420-.390) .450 (.220) .173-.170-.290 (.280) .200 (.171 (.158) .200-.450 (.240) .520 (.430-.590) .410-.360 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.260-.420) .250-.153-.147-.200 (.400 (.250 (.360-.450 (.350 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.320) .159 (. From these and other sources.160-.150-.190-.270) .470) .180-.156-.330-. population from the National Health and Nutrition Examination Survey.400) 95th .330) .280-.220) .270-.146 (.490) .420-. however.430) .160-.159 (.200) .490) Total . In the United States.202 (.350-.400-.350-.215) .220 (.165 (.390-.330-.410 (.210 (.147-.330) .201 (. 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.200-.430 (.290 (.144 (.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 .310) .370-. interval) .173) .430 (.410) .290 (.440 (.380) .197-.410-.370-.410-.280-.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 .240) .470) .300) .290) .220) .180 (.410 (.300) .156) .250-.560) . thallium was obtained as a by-product of smelting other metals.170) .220 (.290-.300-.370 (.218) .163) .250-.450 (. 0.310 (.250-.340) .330-..225) .200-.183) .280) .160 (.300 (.206) .181-.160-.490) .217 (.170 (.390-.450 (.290 (.500) .480) . the latter being the current major industrial consumer of thallium in this country.280 (.260 (.260-.190 (.230-.230-.190 (.410 (.290 (. see Data Analysis section) for Survey years 99-00.190 (. respectively.500) .370 (.167-.360-.200 (.160 (.550 (.02.170) .196) .162-.280 (.380 (.157-.185-.200) .180-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.230) . 01-02.270 (.260 (.172 (.202) .280) .440 (.185 (.340-.240-.340) .350) .500 (.180-.410 (.148-.220) . Thallium disappears from the blood with a half-life of several days.170 (.183) .390-.270 (.201 (.250-.187-.177) .270-.200) .410 (.380-.290 (.440) .690) .260 (.400-.218) .167 (.310-.200 (.400) .360-.460) .420) .370-.320-.02.300 (.470 (.420) .420) .160 (.330-.440 (.197 (.250) .260-.360 (. thallium readily crosses the placenta and also distributes into breast milk.430-.150-.290) .340-.260-.280 (. and 0.400-.160 (.155 (.170 (.520) .217) .390) .140-.220 (.440) .137-.460 (.230 (.150-.260) .250-.300) .370) .450 (.133-.184 (.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 .410 (.410-.176 (.630) .250-.500) .410-.220) .220-.390 (.179-.170-.590) . and 03-04 are 0.230) .220) .156) .175) .180 (.240-.340 (. In the past.134-.420-.640) .

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

Celier D. et al.1 mg/m3 (Marcus.gov/toxprofiles/tp54. X. Brockhaus et al. Available at URL: http://www. Sci Total Environ 1990. Cassot G. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Pietra R. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U..cdc. with concentrations ranging up to 76. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Pozzoli L.html. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Atlanta (GA). Challeton-de Vathaire C. 1990. Sabbioni E. 1981. 1985). Schaller et al. Centers for Disease Control and Prevention. (1981) studied 1. Apostoli P. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al.. Trace element reference values in tissues from inhabitants of the European community I.. 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. Schmidt M. population) are thought to correspond to workplace exposures at the threshold limit value of 0. J Soc Occup Med 1985. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Martin J-C. 1992 [online]. et al. Raithel HJ. Gallorini M. Trace metals in urine of United States residents: reference range concentrations.S. Wiegand H. Sampson EJ. References Agency for Toxic Substances and Disease Registry (ATSDR). Int Arch Occup Environ Health 1980. Ting BG. Paschal DC. 2005) and are shown with results from NHANES 2003-2004 in this Report. 2005.113(1):47-53. Marcus RL. Boisson P. Paschal et al. 2005. 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.216:253-270. Dolger R. Investigations of thallium-exposed workers in cement factories. Trace element reference values in tissues from inhabitants of the European Union. Toxicological profile for thallium. 1998).atsdr. et al. Morrow JC. Valentin H.35(1):4-9. White and Sabbioni. Schaller KH. White MA. Kramer U. Sci Total Environ 1998. Minoia C. blood. Environ Res 1998. Fourth National Report on Human Exposure to Environmental Chemicals 235 . A study of 46 elements in urine. Investigation of a working population exposed to thallium. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Buhlmeyer G.76(1):53-59. Ewers U. Pirkle JL. Radiat Prot Dosim. Int Arch Occup Environ Health 1981.48(4):375-389. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Soddemann H. 1980. Sabbioni E.. Third National Report on Human Exposure to Environmental Chemicals. Brockhaus A. A study of 13 elements in blood and urine of a United Kingdom population.95:89-105. Jackson RJ. Manke G. 1998.Metals (CDC.265 people living near a thallium-emitting cement plant in Germany. 7/15/09 Blanchardon E. and serum of Italian subjects.5 μg/L. Minoia et al.47(3):223-231.

060-.060-.300 (. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.180-.070) .570 (.250-.150 (.120-.113 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.560 (.060 (.350) .360 (.510 (.100) .070 (.080-.120) .050-.200 (.460 (.300) 95th .070) .230) .060-.310-.113 (.410 (. Evidence is lacking for the carcinogenicity of tungsten.120) .080) .190-.135) .137 (.260 (. 01-02.400 (. filaments for incandescent lamps.160 (.380) .082-.092 (.380-.204) .670) .071 (.084) .320 (.092 (. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.320) .490 (.120) .560) .250-.097-.050-.190-.370) .120) .270 (.53) .310-.082 (.190 (.560) .104) .120) .240 (.330 (.060 (. and as catalysts in the petroleum industry.082 (.380 (. mainly as scheelite (CaWO4).340-.058-.160-. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).100-.095-.580) .350) .310-.270 (.04.070 (.120-.110) .080-.510-.071-.370-.090-.076 (.113 (.116) .111-.210 (.095-.220 (.200) .190-.088) .S.470) .107 (. and 03-04 are 0.060 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.180 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .380-.056-.091) .360 (.100) .160) .810) .100 (.065 (.080 (.160-.470 (. Tungsten is used mainly for producing hard metals.520) .440) .300-.520) .620 (.130-.150 (.081 (.510-1.100 (.230) .190) .450 (.290-. Little information is available on the toxicity of tungsten.190 (.180) .270-.430) .280 (.090) .220-.050-.060 (.260 (.300 (.270-.410-.110-.180) .160) .330) .088 (.092) .100) .470) .080-.087-.140 (.430 (.290-. see Data Analysis section) for Survey years 99-00.340-.560) . and for producing ferrotungsten.140-. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.062 (.320-.350 (.110-.082) .370 (.310 (.132) .390 (.180-.310) .170 (.290) .093-.060 (.090 (.230-.060-.230-.650) .084-.530 (.140 (.087) .250) .096-.123-.270-.400 (.190-.110 (.160-.430 (.130-. Occupational exposure is from dusts released during grinding or drilling of hard metals.520) .260-.210 (. and 0.070-.140-.073) .130) .140 (.060-.160 (.550 (.130) .120-.080) .086 (.280-.100) .560) .400) .360-.370-.390) .110-.290-.950) .590) .420-.101-.320-.500) . respectively.065-.500 (.200-.320 (.830) .210 (.062 (.090) .310-.101 (.570 (.170-.04.220) .370 (.130 (.070) .180-.109) .550) .250) .210) .090 (.350-1.158 (.120 (.077-.350) .260-.113 (.073 (.180) .130) .090-.360) .073-.070-.260-.330-.430-.122) .640 (.230-.170) .090-.150) .130) .120-.066-.400-.090) . which is used in the steel industry.130-.250) .090 (. Tungsten compounds are used as lubricating agents.070) .210-.620) .500 (.330-.460 (.180-.430 (.380 (.250) .620) .120-.078-.090) .110 (.180 (.064-. which are used in rock drills and metal-cutting tools.073-.480) Total . bronzes in pigments.00) .800) .310-.070-.080 (.290 (.100-.096 (.270 (.090-.400 (.090-.076 (.093 (.180) .490) .770 (.340-.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.550) .090-.069-.070-. population from the National Health and Nutrition Examination Survey.470-.070-.250) .450-.170 (.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 .080 (.100) .160 (.690) .130-.130 (.110) .270-.100-.230-.400 (.530 (.069) .250) .150 (.090-.110 (.630) .790) .220) . 0.130) .140 (.460) .240-.105) .070 (.800) .470 (.210 (.170) .530 (.550) .120-.380-.060-.160-.260) .084 (.120) .170) .210 (.460) .430-.060 (.370 (.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 .460 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.100) Selected percentiles ( 95% confidence interval) 50th .151) .110 (.Metals Tungsten CAS No.080 (.105 (.056-.380-.080) 75th .04. interval) .093) .140) 90th .300 (.080) .280 (.360 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.126) .110 (.220) .170) .290) .050-.090-.160 (.420-.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 .068) .360-.160 (.340) .330) .133) .230 (.300) .080 (.100 (.150-.074-.100 (.

103-.063-.071 (. or exposure that a control group of non-metal workers had mean levels differences.279 (.089 (.301) . Using neutron activation analysis to 2000.201) .500) . 2001).138) .222) ..109-.484) .083) .083 (.245-.151 (.(Kraus et al.088) .237) . measure urinary tungsten.143 (.088) .072 (.148) .084) .060-. Patients with medically-inserted tungsten found at increased levels in drinking water.197 (.284) .180-.124 (.074-.329-.258 (.078) .075-.065) .117) .152-.340 (.554) .080-.133) .111 (.278-.067 (.065-.333 (.071) .217-.068 (.201 (.065 (.354) .057-.426) .168 (.084 (.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 .158) .124-.049-.287) .214-.105 (.120) .059-.091) .354-. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.317 (.158) .146 (.555 (.199 (.197) .179-.326) .089) .098) .098-. Nicolaou et al.107-. similar to those in this Report (Schramel et al.294 (. 1998).302-.452-.078 (.073 (. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.136-.138 (.359 (.079) .344-.217-.308) .073 (.080-.093-.098 (.071-.116) .061-.082 (.080 (.333) .071) .181 (.179-.158) .253) 95th ..375) .148 (.144 (.086) .079 (.081 (.308) .068-.275 (.358) .153-.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 . (1987) found possibly due to methodologic.333 (.121 (.184 (.093) .300 (.083-.216 (.392) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.158 (.167-.144-.066 (.108) .098-.431) .077-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.083 (.072-.279 (.106 (.122 (.119 (.200-.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 .823) .169 (.153) .216 (.122-.090-.667) .091) .300) .091) .139) . 1997).224) .431) .073 (.199 (.126-.267-.176-.439 (.122-.465) .S.100 (.120) .087) .188-.069 (.054-.333 (.100) .216-.279 (.331-.237) .880) .329 (.119-.383 (.104-.341 (.079) .353 (.055-.339 (.071) .379 (.197) .465) .250-.439) Total .255 (.253 (.139 (.301) .136 (. 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.317-.145 (.081 (.082) .070 (.108-.060 (.078 (.090-.240-. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.075 (.063-.258-.061-.138 (.283) .077) .605) .063-.169) .302-.125) .167) .250 (.116 (.347 (.206-.059-.218 (.339 (.079 (.058-.286-.086-.208-.069 (.174 (.414) .081-.094-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.099-.293 (.060-.215) .261-.072-.075) .150-.255 (.161) .187) .095) Selected percentiles ( 95% confidence interval) 50th .364 (.215 (.069-.439 (. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U. 2005).306) .150-.267) .087 (.064-.078-.075-.634 (.426) .083) .063 (.077-.190) .216-.198-.109 (. 2003.410-.125 (.078) .265 (.117 (.091 (.360 (.084) .100) .130 (.096) .139-.216-..092) .211 (.067 (.431) .231-. population (CDC.063 (.056-.285) .136-.333-. interval) . population.084 (. and 2003-2004 (Paschal et al.079) .074 (.333 (.482 (.079) .300-.054-.174) . population from the National Health and Nutrition Examination Survey.209-.333-.059 (.386) .250 (.121-.053-.359 (.300-.203-.091) .484 (.157) .270 (.497 (.150 (.094) .065-.098-.057-.299 (.315-.237-.436-1.063-.200-.075 (.214) .091 (.727) .667 (.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 .085 (.222-.28) .074) 75th .086) .197-.065 (.186 (.073 (.233-.453) .074-.094) .146 (.085-.081) .582) .133) 90th .105 (.116-.071 (.067-.080 (.059-.164 (.064-.086) .176-.272-.S.462) .071 (.255-.436) .231 (.165) .066 (.065-.739) .074) .136-.301) .154) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.136-.167-.143-.085) .131-.077) .412 (.155-.082) .333) .095-.062 (.385 (.198) .205-.061-.167) .317) .075) .353 (.797) .130-.381) .170-.538) .133) .154) .056-.146) .S.459) .070 (. 2001-2002.253-.

Cancer Clusters.58(10):631-634. 2004). Zobelein P.Metals blood. Sampson EJ. thallium. The determination of metals (antimony.(2):73-77. Catheter Cardiovasc Interv 2004.69(3):219-223. 4/15/09 Centers for Disease Control and Prevention. Atlanta (GA). Trace metals in urine of United States residents: reference range concentrations. 2005. platinum. Centers for Disease Control and Prevention. 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. Angerer J. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Feuerbach S. bismuth. Churchill County (Fallon). Morrow JC. Kraus T. Weber A. Nevada Exposure Asssessment.76(1):53-59. Lenhart M. Pirkle JL.cdc. et al. cadmium. Jackson RJ. Link J. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis.htm. Manke C. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Angerer J. References Bachthaler M. Schramel P. Available at URL: http://www. Paschal DC. Int Arch Occup Environ Health 1997. Schramel P. Occup Environ Med 2001. J Trace Elem Electrolytes Health Dis 1987. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. palladium. Nicolaou G. Paetzel C. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. lead. Sabioni E. mercury. Mosconi G. Ting BG. Third National Report on Human Exposure to Environmental Chemicals. Schaller KH. Environ Res 1998. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds.. Seghizzi P. and hair (Bachthaler et al. tellurium. [online] 2003. 238 Fourth National Report on Human Exposure to Environmental Chemicals .gov/nceh/clusters/Fallon/study. Wendler I. Pietra R. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. urine. Cassina G.62:380-384. National Center for Environmental Health.

013 (.008 (.045) .031 (.027) .014 (.010) * .027 (.008-.023 (.009) .007-.013 (.011) .062) .018) .005-.016) .024-.009 (.008-.012 (.018) .033) .023 (.043 (.019 (.008-.009 (.042 (.012-.010) .037) Total .005. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.007-.020-.021-.010) .008-.007 (.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.030 (.009) .009-.037 (.006-.014 (.017-.019-.022-.008) .034) .020-. in some ceramics.018) .009) * .007-.008-.053 (.088) .021) .033 (.004. Since the 1990’s.007-.013-.005-.013 (.033 (.028 (.066) .024-.039) .027 (.007-.051) .016) .010) .021) .019-.006-.011) .009) .007 (.017-.011-.017) .008 (. milling.010 (. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.114 (.007-.017) .012-.009) .015 (.007-.014 (.044 (.011-.009 (.009) .008 (. Uranium has many commercial uses.023) .017-.Metals Uranium CAS No.279) .009-.041 (.023-.010-.011) .013-.008 (.018 (.063) .008-.028-.046 (.016) .030-.035) .027-.011-. and 0.008-.041 (.012-.004.020) .006 (.017) .015 (.045) .007 (.009-.006-.047 (.064 (.027) .008-.060 (.029 (.008) .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 .007) .007-.031 (.073) .029-.054) .037) .026-.021 (.035-.008) . respectively.006-.009) . population from the National Health and Nutrition Examination Survey.006-.023 (.015-.027) .037) .010 (.032 (.026 (.011-.020-.016-.034-. Variable concentrations of uranium occur naturally in drinking water sources.020) .019-.007 (.009-.007-.017 (. Thus.009-.016) .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 .030 (.007) .012 (.008 (.023-.039-.020-.011-.009) Selected percentiles ( 95% confidence interval) 50th .054) .009-. Fourth National Report on Human Exposure to Environmental Chemicals 239 .009-.011 (.008 (.026) 95th .052 (.014 (.008) .037) .007-.010-.015) .024 (.017-.014 (.009) .012 (.009-.007-. and 234U.012-.005-.011) .008 (.050) . 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.010-.011 (.017-.025-.023-.007) .007-.158) .006-.013) .046) .040) .026 (.038 (.040-.008 (. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).027-.007 (.016-.026-.022-.009) .006-.028 (.027 (.008 (.009 (.012 (.009) .046-.013-.010) .010-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.010-. 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.022-.006 (.006-.007) 75th .046 (.007 (.008 (.046 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.010 (.027) .027 (.020 (.030) .049) .012) .053) .009) .017) .048) .015) .012-.031 (.009) .054-.017 (.018) .009 (.012 (.008 (.007-.026 (.050) .014 (.009 (.010) .007 (.010) .021 (. and as an aid in electron microscopy and photography.015 (.007-.007-.012 (.069) .008 (.012) .033-.056) .036-.013) 90th .018-.72%).042) .018 (.036) .067) . In workplaces that involve uranium mining.010 (.009 (. 0.009-.023-.056) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.007 (.010) * .012) .016-.012) .028-.072) .011-.034-. and 03-04 are 0.S.026) .021-. 01-02.006-.012-.008 (.007) .023) .010 (.031 (. interval) .067) .030 (.008 (.007) .036-.036) .009 (.006-.023) .038) .016 (.065) .028 (.007-.009) .017-.007-.008 (.049) .007 (.040-.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 .009 (.048 (.013 (.006-.029-.011) .008 (. 235U (about 0.031 (.006-.027-.010) .005-.006-.017) .009) .013 (.127) .010) .036 (. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.013 (.008) .040) .011-.022) .009 (.065) .036 (.055 (.016) .040 (. nuclear fuel.010-.037-.009-. including nuclear weapons.043) .006 (.006 (. or processing.013 (.026) .015 (.031-.021 (.022 (.021) .008 (.007 (.040 (.039) . human exposure occurs primarily by inhaling dust and other small particles.020-.046 (.005-.007 (.007-. see Data Analysis section) for Survey years 99-00.019-.011) .011) .035) .016) .024-.

006-.011-.021-.056) .010) .019 (.006) . After exposure to soluble uranium salts. with much slower elimination from bone.020-.008-.013 (.028) .024) .009 (.006-.008) .027-.006-.028 (.024) .010) . the shrapnel acts as a source of chronic.014) .058) . After long term or repeated exposure.015 (.010-.030 (.008) .053) .009) .005 (.034-.018-.006-.006-.008 (.014) .027 (.008-. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.011 (.008) .018-.006 (.026-.013) .013 (.048) .020-.018-.021 (. low level exposure.010-.008-.026 (.009 (.010) .024) .026 (.020 (.015-.041) .024) .010-.029) .011-.009-.007) .010-.010) . In cases of retained DU shrapnel. interval) .016) .018) .009) * .007 (.016-.063) .007 (.034 (.008) .005-. 0.010) * .014-.007 (.077) .027-.012 (.007 (.006-.061) .015 (.013 (.010-.006-.034 (.009) .026) .006-.009) .014-.017) .016) .024-.010-.009 (.016 (.009-.028) .006 (.020 (. kidneys.009-.032) ..007 (.048) . the initial half-life of uranium is about 15 days (Bhattacharyya et al.019-.039) .029 (.028) .008 (.007 (.017) .007-.006-.029) .009-. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.037 (.007) .015 (.014 (.034 (.018-.004-.013 (.005-.011) * .009) .050) .032) .029) .007 (.044) .030) .006 (.009) Selected percentiles ( 95% confidence interval) 50th .007-.011-.034) .008) .010 (.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 .017-.006-.011-.022) .004-.013 (.034 (.S.009) .054) .010) .015) .027 (.039) .010-.025 (. 240 Fourth National Report on Human Exposure to Environmental Chemicals .029 (.005-.005-.006-.009 (.030) .027) .022-.059 (.022 (.006-.053) .014-.024 (.005-.009-.016) .016) .010) .008 (.025 (.015-.008) .007 (.008 (.007 (.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 .023-. liver.027 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.022 (. which represents distribution and excretion.042) .018 (. where limited absorption occurs (less than 5%). Survey years 99-00 01-02 03-04 Geometric mean (95% conf.010-.025) 95th .010 (.008) .009 (.146) .027) .010-.047) .010 (.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.019-.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 .015-.025-.051) .007 (.016) .006-.010-.008 (.012 (.006 (.008) .012 (.005 (.020) .033 (.010 (.008 (.008 (.006 (.013 (.006) .011-. Inhaled uranium-containing particles are retained in the lungs.016) .017 (.022 (. 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 (.Metals impact.016) .030 (.009) .010 (.017) .015) .012) .042-.020 (.019 (.011-.011) .021 (.017 (.012) .007) .007-.010-.007 (..045 (.033 (.013 (.039) Total .025-.009) .016-.007-.021 (.015-.270) .006) .008 (.013) .051) .021) . 1992).015) .031-.007 (. which can occur occasionally from high occupational exposure. 2003).008 (.024) .012 (.007 (.022-.007-.006-.012) .019-. Radiation risks from exposure to natural uranium are very low.028-.080) .067) .012 (.024 (.030-.009) .031 (.025-.011-.007-.005-.100 (.007-.018-.006-.024-.033 (.050) .019) .007 (.034 (.012 (.012-.027-.006) .007 (. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Health effects from uranium exposure result from chemical toxicity to the kidney.005 (.012-.008 (.006 (.009-.007-.014 (.017-.016-.040 (.014) 90th .021 (. Depending upon the specific compound and solubility.007-.011-.005 (.009) .043 (. population from the National Health and Nutrition Examination Survey. After inhalation. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.008-.058) .029 (.007 (.034-.017-.017-.005-.019) .029) .007 (.013-.006-.009) .011-.019-.011) .025-.008) .009) .008) .006-.007 (.050 (.008) 75th .033) .013 (.024 (.006-.006-.006-.026 (.013) .007 (. 2005).039) .030 (.015 (.028 (.024-..007-.051) .014) .011) .028) .051 (.035 (.011 (.007 (.035 (.012 (.019-.015) .016-.019 (.008) .016) .020-.033 (.006-.042) .030-. Uranium is eliminated in feces and urine.008-.020-.015-.008-.074) .027-.013 (.006) .006-.006-.006-.022-.1%-6% of an ingested dose may be absorbed.013 (.

Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Thomas RG. In the same study. Health Phys 1992. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Karpas et al. The U. Mil Med 2003. the geometric mean urinary uranium concentration was 0. Zimmerman I. and 2003-2004 (Dang et al.. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Sci Total Environ 1991. respectively.atsdr.011 μg/L (McDiarmid et al. 28 soldiers who may have been exposed to DU by inhalation. 1-49. Benedik L. Health Phys 2000.. (Kurttio et al. Guidebook for the treatment of accidental internal radionuclide contamination of workers.. 41 (1). Ejnik JW.65 μg/L). Carmichael AJ. population. Third National Report on Human Exposure to Environmental Chemicals. 2004). had a mean urinary uranium concentration of 0.61 μg/g creatinine.1996.066 μg/g creatinine (Gwiazda et al.. References Bhattacharyya MH.. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. et al. Determining the normal concentration of uranium in urine and application of the data to its biokinetics.. 2002). Stradling GN. EPA. 2000). Tolmachev et al.110 to 45 μg/L (Ejnik et al. IARC and NTP have no ratings for uranium human carcinogenicity. 2006.Metals injury associated with elevated urinary uranium levels (Kurttio et al.. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000.S. Six workers in a depleted uranium program showed concentrations of 0. (May et al. Pillai KC. Boyd P. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population.gov/ toxpro2.078 μg/L (ranging up to 5. 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.1992. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. environmental levels) and health effects is available from ATSDR at: http://www. the median urinary concentration was 0. Dang HS. 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...55 μg/L (median 0. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. and no consistent effects on multiple endpoints of kidney function were found. the median urinary uranium concentration was 2.162 μg/L) (Orloff et al. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al.S. 1994. Hamilton MM. 2001-2002. 2000). with emphasis on quality control. 2006).e. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. Metivier H. Uranium content of blood. 2004). Byrne AR. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.. McDiarmid M. 2006). 2004)...78:143-146. Pullat VR. Vol. Komaromy-Hiller et al. Muggenburg BA. NRC.cdc. Drinking water and other environmental standards have been established by U. 2002.. 2006). 2005. 2004). Centers for Disease Control and Prevention (CDC). but in whom no shrapnel was embedded. eds. In a study of 105 persons exposed to natural uranium in well water. pp. 1978).S. In: Gerber GB. 2003. Information about external exposure (i.S. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al.html. In 17 U. Squibb K. ingestion. soldiers evaluated before. 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.. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U.. Radiation protection dosimetry.. Hamilton et al.. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. urinary levels of uranium were as high as 9.107:143-157. Horan P. Kent (England): Nuclear Technology Publishing. although slightly increased during and after deployment. Galletti.168(8):600-605. Fourth National Report on Human Exposure to Environmental Chemicals 241 . or wound contamination. A cohort of 46 U. 1991. Atlanta (GA). McDiarmid et al..S. during. Durakovic A.S. Breitenstein BD.62:562-566. 2006). Volf V. Dietz LA. 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. in that the levels were below their respective detection limits (Byrne et al. 1992. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.

Hancock RG.81:45-51. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Saha H. McDiarmid MA. McDiarmid M. Gucer P. Environ Res 1999. Hamilton EI. Squibb K. 242 Fourth National Report on Human Exposure to Environmental Chemicals . McDiarmid MA. Charp P. U. Comparison of representative ranges based on U. Harmionen A. Pekkanen J. Auvinen A. et al.110(4):337-342. Paschal DC. Auvinen A. Orloff KG. Oberbroekling KJ. Health Phys 2004. Environ Health Perspect 2002. Kidney toxicity of ingested uranium from drinking water. Squibb K. U. Cremisini C. Lorber A. Roiz J.71(6):879-85. Komulainen H. plasma and urine and a critical evaluation of reference values for the United Kingdom population. et al. Uranium daily intake and urinary excretion: a preliminary study in Italy.22–Bioassay at uranium mills. Health Phys 2003. Nuclear Regulatory Commission (U.87:51-56. Halicz L. Smith D. Kuwabara J. et al. Marino R. Oliver M. Lewis BM. Gwiazda RH. Inductively coupled plasma mass spectrometry as a simple. et al. Radiat Environ Biophys 2005. Washington (DC): NRC. patient population and literature reference intervals for urinary trace elements. Saha H. Li WB.Metals Galletti M. Scott K. Ash KO. Wilson PD. Clin Chim Acta 2000. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Pinto V. Van der Venne MT. Paretzke HG. Jackson RJ. Jarrett JM. Environ Res 2004. Makelainen I. Howerton K.44:29-40.S. Kane R. Engelhardt SM. Biokinetic modeling of uranium in man after injection and ingestion. Biologic monitoring for urinary uranium in Gulf War I veterans. May LM. Ting BG. Renal effects of uranium in drinking water. Salonen L. Ejnik J. concentration and daily excretion of uranium in urine of Japanese. Andrews WS. Noguchi H. et al. Nuclear Regulatory Commission (NRC) Guide 8. Sampson EJ. Kurttio P. Komaromy-Hiller G. Review of elements in blood. Roth P. Oeh U. rapid.79(1):11-21. Int Arch Occup Environ Health 2006. Costa R.94:319-326. Metcalf S.158:165-190. Ough EA.86:12-18. Health Phys 2004. Karpas Z. Human exposure to uranium in groundwater. Uranium and thorium in urine of United States residents: reference range concentrations. D’Annibale L. Bennett LG. et al. Kurttio P. Sci Total Environ 1994. Am J Kidney Dis 2006. Element reference values in tissues from inhabitants of the European community. Tolmachev S.67(8-10):697-714.82(4): 527-532. VI.91(2):144-153. Kalinsky V. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Salonen L. NRC). Heller J.85:228-235. Shelly T. Health Phys 1996.S.S. Marko R. Health Phys 2006. Englehardt SA. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Health Phys 2002. Katorza E. Hollriegl V. J Toxicol Environ Health A 2004. Wahl W. Mistry K.47(6):972-982. Karpas Z. Sabbioni E.S. July 1978.296(1-2):71-90. Pirkle JL. Cordero S.

20-11.70-9.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0 (10.0) 12.80-15.80-6.70 (3.66) 3. lettuce) can be the main sources of intake for humans (FDA. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.0) 10. In addition.47-4.0 (11.30) 6.EPA. 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.90 (2.20) 4.80) 7.0-17. 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.0 (8.62 (3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .89-3. or ammonium salt.0 (9.40-5.30 (5.51 (3.0 (11.0 (11.80 (3.65) 3.20 (2.g.93-4.30-7.70-5.10-11.0) 11.0) 13.S. but has strong oxidant properties in the presence of concentrated acids. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.0) 8.18-3.10 (2. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.90-9.79 (2.0) 13. and certain plants with high water content (e.0 (8.10 (7.00-5.20-4.0 (11.11) 3.0-17.60 (4.0 (8.75 (3. and electroplating.30) 6.0 (8.40 (8.30-19. 2007). Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0 (9.10 (5.40-7.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.10-7.07-4.0) 11.46) 3.0-17.0 (9.40 (3.10) 3.75-3.0) 11.51 (3.90) 6.45-4.90-6.60) 8.0) 16.0-19.10) 3.40-4.00) 3. 1998).30-6.40-4.50-11.40) 3.50 (3.50) 11.0) 15.80 (3.50) 5.32 (3.0 (11. milk.90-3. 2002).20-12.20 (4.90 (5.88) 3.38) 5.50-3.67-5.90-3.70-7.20-3.00) 7.02 (3.30 (2.60 (7.00) 3.0-14.60) 3..05. 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.01 (2.0) 10.80 (6.0) 13.0) 10.40) 3.54 (3.50) 5.90-9. 2005). 2005).0 (9.35 (3.40 (3.0) 14.00) 5.60-6.11) 4.0 (11.40 (4.70 (3.50 (8.30-7. Survey years 01-02 03-04 Geometric mean (95% conf.0 (12.20 (7.10-12. leather tanning.80) 3.93 (4.50-7.0) 19.90 (3.0 (11.39-4.22 (2.20 (2.0-23.60-7.93-3.70-12.90-12.10) 5.0) 14.05 (2.0 (11.87-3.10) 12.68) 4.0) 9.40 (5.0) 9.70-3. Other manufactured uses include fireworks.50-4.80-8.0) 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 3.26 (2.0-18. fabric dyeing.30-17. Drinking water.31) 2.00-6.03) 3.44-4.0-17.74-3.0) 9.0) 9. and reducing agents.16) 3.60 (4.0 (9.10 (6. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.0-20.70) 3. interval) 3.90-10.76 (3.84) 14.90-11.05 and 0.40-13.20) 3.S.40 (5.0-15.80) 12.40) 6.29-3.5 hours and has a small estimated volume of distribution (Crump and Gibbs. population from the National Health and Nutrition Examination Survey.10-4.49-3.0) 13.0-17.20 (8.0) 14.40) 90th 10.0) 15.10-11.00) 4. potassium.90-11.20 (4.0) 13.S.0-18.0) 708 617 681 652 1228 1092 Limit of detection (LOD.0 (12.40-6.70-3. It is normally found and produced as the anion of a sodium.50 (5.0 (11.0) 13.0 (13.60) 5.12) 3.80-12.0 (9.0 (12.90 (5.09) 3.20) 7.80 (7.40) 4.90 (5.40 (5.50) 6.. laboratory analysis.30 (5.0 (9.0 (11.90) 5.96 (3.0) 8.70-6.0) 13.Perchlorate Perchlorate (Urbansky.0-17. certain catalytic metals. Perchlorate is stable under most environmental and physiological conditions.00-6.10 (6.70-11. matches.90 (4.08-3.80-4.19 (3.50-4.80) 75th 6.20 (6.0-15.21 (2.22-5. Perchlorate was added to the U.40-11.40) 3.20-4.70 (3. and limited applications in pharmaceutics.80-4.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.0) 9.0) 13. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.0-29.0) 9.56) 3. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.10) 5.0-18.50) 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.0) 95th 14.40) 2.0 (8.81) Selected percentiles ( 95% confidence interval) 50th 3.81-16.20 (5.0 (12.40 (4.30 (2.76) 4.19-4.

89 (2. Steinmaus et al.84) 2.0) 9.87-3..93-8.0) 12.00-2.3) 11.08 (3. 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.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.80) Selected percentiles ( 95% confidence interval) 50th 3.70 (4.10-3.30-5.61-5.60-5.25) 5.0-44.20 (6.0-19.16-3. 2002.0 (10.36 (8.30-10.02) 3.0) 7.91) 4. 2005).60) 8.0-14.46 (3.09) 3.98) 3.3 (10. 2000).99 (5. 2005.87 (7.99-3.60 (3.6) 12.0 (9.93-5.54 (2.80-3.1-22.33-12. U.90 (2.50-9.S.20 (4.0) 12.60-5.08) 3.2) 8.Perchlorate inhibition (RUI).07 (2.4 (10.09 (7.90-15.24 (4.20) 3.10 (2.40 (3.70-4.10) 3.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.46-4.00) 3. and the presence of other substances known to affect thyroid function (e.70-3. 2005).75) 3.5 (13. Lawrence et al.10 (6.EPA.10 (4.0 (8.56-3.22-4.67) 5.76-3.S.30 (3.30 (6..82 (5.44) 3.64) 5.4) 8.90 (7. 2002).0-14..S.4-16.52-9.10) 13. 1999.0) 4.20-3.90-2. Also.87 (5.0) 13.50) 9.51-4.4 (11.10 (1.1-14.25) 5.3-14.0) 12..22 (2.90) 5.97-5.1 (11.50 (6. although iodine intake was higher than U.60-11. population from the National Health and Nutrition Examination Survey. interval) 3. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability. in a representative sample of U.70 (2.4 (11.1-16. Many factors may be important in consideration of perchlorate action on the thyroid: dose.00 (2.35 (2.25 (3.50) 95th 12.93-5. age. menopausal status..93-7.0) 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 . perchlorate is negative in most genotoxic assays (U. However.12 (6.60-11.19-10.26) 4..87) 7.02-4.0-17.7 (11.61 (5.95 (2.64-3.53 (2.S.50) 5.39) 2.33 (7.93) 3.60) 10.0) 6.76 (3.70-15. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.29-6.10-7. In the U. During gestation and infancy.20-3. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.26 (3.90-20.05 (4.04-3.3) 12.40 (4.0) 10.0) 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. Greer et al. 2002.39-4.40-10.S.4 (8. Li et al.60-15. 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.37-13.87) 2.80 (7.34-3.30) 75th 5.0 (9.45) 3. women with urinary levels of iodine less than 100 micrograms per day. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.30) 5.12-2.00 (4.18-3.43) 6. thiocyanate.80 (4.40) 17. 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. 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.80-3.2) 8.74) 7. chronicity of exposure.00-11.0) 13.60-8.04-3.10) 6.46-13.58) 2.3) 8.6-17.70) 10.56 (3.50) 6. Lamm and Doemland.60-8.35) 3.0 (11.40) 3.89-3.40 (3. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.39 (3.50 (3.90-3.50) 2.1-13.0) 12.20 (7.60-6.20-10.24-2.81-3.54 (3.30-5.83 (5.20-9.22-6.6) 20.30) 90th 9. Survey years 01-02 03-04 Geometric mean (95% conf.. up to 68% RUI has been demonstrated.0 (8.EPA.0 (9.90-9.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.51 (3.5) 8.30) 3.71 (5. gender. medications).S. 2001.70-5.45-2. NAS.15-12. 2003.80 (7.32) 5.19-6.61-10.86) 4.20) 8.0) 14.. 2006...35 (4.96) 2.29) 2.8 (11. levels and sufficient in most participants (Tellez et al.72 (3.66) 3.90-11. 2005).30 (5.33-6.44-6.00-3.60-3. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.50-3.47) 2. nitrate.50-5.g.90 (4.00) 4. 2005. dietary iodine intake.52 (8.0) 9.00) 9.41-9.0 (11.59) 3.21 (2.S.1) 8.03 (2.90 (2. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.20-4.42 (3.37 (4.20 (2.0) 11.25) 5.70 (2.22-4.77 (3. levels.4) 13.20 (3.0 (11.1 (8.10) 4. 2007).50) 2.40 (7.00 (6.10 (4.70) 2.60) 3.14 (2.73) 3.40) 5.

Greer SE. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Blount et al. Braverman LE. Environ Health Perspect 2002. et al. Pirkle JL. Sesser DE. population. Environ Health Perspect 2006. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Kirk AB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. J Occup Environ Med 2000. Osterloh JD.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653.17(4):400-407. 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. 2005. Kelsh MA. Available at URL: http://www. Goodman G. Steinmaus C. Environ Health Perspect 2005. Byrd D. Jackson WA. Erratum in: J Occup Environ Med 2004. 2007). The effect of perchlorate.90(2):700-706. 6/2/09 Greer MA.S. Lamm SH. Neonatal thyroxine level and perchlorate in drinking water. Li FX.cdc. Lawrence JE.42(2):200-205. Caldwell KL. Pirkle JL. Buffler PA. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Environ Sci Technol 2006. Lamm SH. et al. Dasgupta PK. 2001-2002.115(9):1333-1338. CFSAN/Office of Plant & Dairy Foods. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Abarca CR. 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. Pino S. Perchlorate Exposure of the US Population. J Occup Environ Med 2003.html and from ATSDR at: http://www. Blount BC. Valentin-Blasini L. Washington (DC): National Academy Press.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. National Academy of Sciences (NAS). Blount BC. most of the population is considered to be below the U. Lau EC. Magnani B.45(10):1116-1127. 2005).46(5):509. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Landingham CB. Environ Health Perspect 2007. Tellez RT. Health Implications of Perchlorate Ingestion.S.. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data.fda. Gibbs JP. EPA reference dose (Blount et al. Lamm SH. Howd R. Deyhle GM. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Dyke JV. Crump KS. Primary congenital hypothyroidism.S. Valentin-Blasini L. Additional information about exposure and health effects is available from the U. Barnard JC.gov/safewater/ccl/perchlorate/perchlorate. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Chacon PM. Also.40(21):6608-6614. Daaboul JJ. 2005). Rutherford GW. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Braverman LE.html. and environmental perchlorate exposure among residents of a Southern California community.10(8):659-663.114(12):1865-1871.41(5):409-411. Lamm S. et al. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. newborn thyroid function. Low dose perchlorate (3 mg daily) and thyroid function. and nitrate on thyroid function in workers exposed to perchlorate long-term. Richman K. National Research Council of the National Academies. Lawrence J. J Expo Sci Environ Epidemiol 2007.gov/toxpro2. Crump KS. Benchmark calculations for perchlorate from three human cohorts. Pleus RC. thiocyanate. Osterloh JD.110(9):927-937. Thyroid 2000. May 2007..113(8):10011008.atsdr. Miller MD. Analysis of relative source contributions to the food chain. Li Z. Doemland M. Cross M. Braverman LE. epa. Food and Drug Administration (FDA). J Clin Endocrinol Metab 2005.EPA at: http://www. (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. et al. Thyroid 2001. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.. Page Last Updated: 05/28/2009. 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. References Blount BC.htm. Skeels MR.11(3):295. Perchlorate in the United States. Erratum in: Environ Health Perspect 2005. Mauldin JP. Pino S. He X.113(11):A732. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002.

Perchlorate. Thyroid 2005. Drinking Water Contaminant Candidate List. Environ Sci Pollut Res Int 2002.9(3):187-192. 246 Fourth National Report on Human Exposure to Environmental Chemicals .1/15/06 U.15(9):963-975.S. Perchlorate as an environmental contaminant.Perchlorate pregnancy and the neonatal period. cfm?substance_nmbr=1007.S.gov/iris/quickview. Available from URL: http://cfpub. EPA/600/F-98/002 Washington (DC). Integrated Risk Information System (IRIS). EPA). Urbansky TF. Revised 2/11/05. 1988.S. Environmental Protection Agency (U. No. EPA). Doc.epa. U.S. Environmental Protection Agency (U.

Olsen et al. semiconductor. Production rates and emission rates have fallen since 2002 after conversion to a new synthesis process. finalized perfluorochemical polymer products. A major application of one important fluoropolymer. Perfluorooctanesulfonyl fluoride (POSF) was synthesized as a polymerization starting material. Worldwide annual production of PFOA was estimated to be 260 metric tons in 1999 (Prevedouros et al. as a solubilization aid in the synthesis of polytetrafluoroethylene. There are many other fluorocarbon type chemicals which are not addressed here. 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 . perfluorooctane sulfonamide. furniture. U. PFOS) (Hekster et al. Fluoropolymers have applications in waterproofing and protective coatings of clothes. low volatility (as salts or ionized) and can remain in the environment and bioconcentrate in animals (e. Because of their properties.. perfluorooctane sulfonate. electrical and electronics.. 2006). and also as constituents of floor polish. and their oxidation products.S. chemical processing.. Perfluorononanoic acid (PFNA) was an impurity in the process that produces PFOS.S.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. and other products. U.. and alcohols which are by-products. chlorofluorocarbons and investigational blood substitutes. EPA.. Global production that year for POSF materials was 3700 metric tons (Prevedouros et al. Other PFCs (including small amounts of PFOA) can also form as side-reaction by-products in the synthesis of POSF (e. and textiles. PFOSA). fluoropolymer products are used in a wide range of industries including aerospace. In addition.g. amides. automotive. or form as degradation products during its reaction to create the intermediate reacting monomers. Perfluorohexane sulfonate (PFHxS) has also been used to synthesize the fluoropolymers used in firefighting foams and some carpet treatments. several pathways (during manufacturing) can lead to formation of PFOS or other sulfonyl-containing PFCs as residual contaminants in the final polymer products. Discussed here are perfluoroalkyl acids. building/construction. MeFOSE and EtFOSE have been used in food packaging and textile treatments. has been the heat-resistant non-stick coatings used on cooking ware and other protected surfaces. manufacture of POSF-based products began ending in about 2000. end products. Other perfluoroalkyl carboxylates of various chain lengths were also formed in the process used prior to 2002. adhesives. or processing aids used in the synthesis of fluoropolymers. N-methylperfluorooctanesulfonamidoethanol (MeFOSE) and N-ethylperfluorooctanesulfonamidoethanol (EtFOSE).. PFOA is usually not a residual contaminant in non-stick surfaces made of polytetrafluoroethylene. and fire protection. current manufacturing Perfluorinated Chemicals in this Report practices reduce the formation of these by exclusively using fluorotelomers (Prevedouros et al. fire retardant foam. POSF-based polymers have been used in a wide variety of products such as waterproofing. However. such as perfluorochemical telomers.g. 2006). 2006). respectively. primarily as its ammonium salt. Perfluorooctanoic acid (PFOA) has been manufactured since the 1950s. polytetrafluoroethylene. or form in the final product (e. 2005.. N-methylperfluorooctanesulfonamidoacetic acid (Me-PFOSA-AcOH) and N-ethylperfluorooctanesulfonamidoacetic acid (EtPFOSA-AcOH). The PFCs have limited water solubility. textiles.. 2003. and insulation of electrical wire. 2003). may be markers of food or consumer exposures.g.

PFCs have been identified in surface coastal and ocean waters (Yamashita et al... The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. 248 Fourth National Report on Human Exposure to Environmental Chemicals . Excepting PFOS and PFOA. 2002. population from the National Health and Nutrition Examination Survey. 2005.8 years (Olsen et al. In some cases.. 2003). EPA. 2004).. C5... human toxicokinetics.S.. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. may metabolize or degrade to PFOA (Dinglasan et al. 2006.. 2006a. All sources of human exposure are uncertain. or effects of other PFCs. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. Prevedouros et al. 2004. Keller et al. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. in a wide variety of marine and land animals (Kannan et al. environmental fate. hepatotoxicity.. peroxisomal proliferation. Lau et al. 2003.. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins.S. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. by high protein binding in plasma and other proteins. kidney. 2003). 1995. 2004. 2004...e. the 8-2 telomer.. 2003a and 2004a). 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. growth retardation and delayed sexual maturation (Kennedy et al. 2005). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5 years and for PFOS.. Unlike many organohalogen contaminant chemicals.. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Kannan et al. Some of the effects in animals may be mediated through peroxisomal proliferation. The PFCs often measured in human serum are listed in the table.. Vanden Heuvel et al. there is limited information on the sources. heptadecafluoro-1-decanol. endocrine and immune effects. U. C7). 2000. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. Bookstaff et al. see Data Analysis section) for Survey year 03-04 is 0. 2005. and in human blood and semen (Calafat et al. Taniyasu et al. 2005). 1990).. and β-oxidation of lipids (Kudo et al. 1993).Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). thymus and spleen. Olsen et al.. pancreas. Lau et al. It is unclear if environmentally degraded telomer products are a major source of other PFCs.. Guruge et al. including immunologic effects and tumor induction... in part. which may vary for some chemicals by year and by individual sample. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. For instance. The elimination half-life of PFOA in humans is roughly estimated to be 3. approximately 4. Survey Geometric mean (95% conf. 2004. 2007a). 2007). but probably include dietary sources (Kannan et al. Tittlemier 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. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. and in offspring. PFOA has been reported to cause liver..4. but still can have long residence times in the body... 2005). C6. 2004). PFOA is mostly excreted in the urine in animal studies. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. 2005.

population.10) * 03-04 03-04 * * < LOD < LOD < LOD .800 (. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.500-1. or increased cancer rates (Alexander et al.500) .800 (.500) 90th .600 (.500 (. Cook et al. 2003a). and changes in thyroid hormone concentrations (Grasty et al. 2004a. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.400 (<LOD-.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 . PFOS. PFOA. Harada et al.500) .S.300 (<LOD-. Lau et al. the potential to estimate risks to humans from animal doses is uncertain..20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. 1992. 2007b). 2004. Fei et al.. hepatotoxicity. Olsen et al. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.. reproductive. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. 2003).. 2003a.500) .400-1. elderly and children...400-.40) . see Data Analysis section) for Survey year 03-04 is 0..00) .Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. PFOS.300-1.10 (.900 (.400 (<LOD-. Thibodeaux et al. 2007)..600 (. 2003a).800 (. U. 2007a.. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.500) . Olsen et al. At doses causing maternal toxicity.600-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. EPA.S. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. possibly related to lung immaturity (Lau et al.. 2004b). Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. 1999.500-. EPA.700) .3. which may vary for some chemicals by year and by individual sample. 2005). and there was no clear evidence of excess all-cause or diseasespecific mortality.80) 640 1454 03-04 03-04 * * < LOD < LOD . 2007b. developmental and teratogenic effects were demonstrated in offspring. Fourth National Report on Human Exposure to Environmental Chemicals 249 .600 (. 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. In comparing three separate reports on adults.80) 485 538 962 Limit of detection (LOD.800) 1. Olsen et al. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al.400-1. < LOD means less than the limit of detection.800 (...500-3.20) . U. 2004. 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. Survey Geometric mean (95% conf. 2007a. However.00) .10) . development in offspring was stunted and hypothyroxinemia was observed.500 (<LOD-1..300 (<LOD-. 2003a. and humans. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. perfluorohexanesulfonate (PFHxS). animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.500 (.800) 1. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.. population from the National Health and Nutrition Examination Survey. 2003. 2003).400-1.500-1. 2001. interval) Selected percentiles ( 95% confidence interval) Sample 95th ..50) .900 (.S. At high but non-toxic maternal doses of PFOS.10) ..00 (. Kennedy et al. Animal studies of PFOS have demonstrated weight loss.300 (<LOD-. 2003).. monkeys..400-1.00) ..S.400) . 2003. 2003a.900 (. 2003.400-1.400 (<LOD-. 2004).500-1. 2004).700 (.500-1. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.108 times higher than background serum levels in humans (Butenoff et al.. 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. PFOA. 2005).400-. thyroidal). the median PFCs values tend to be roughly similar in these age categories (Olsen et al. In such studies. 2007.

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

3.500 (<LOD-. see Data Analysis section) for Survey year 03-04 is 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-.S.600 (.900) < LOD .400 (<LOD-.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .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 .400 (.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) 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.400 (<LOD-.300 (<LOD-.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.400) .0. which may vary for some chemicals by year and by individual sample.500-. see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.S. Fourth National Report on Human Exposure to Environmental Chemicals 251 . which may vary for some chemicals by year and by individual sample.300 (<LOD-.600) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500) 485 538 962 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Survey Geometric mean (95% conf.

70-5.30 (1.40 (1.73-2.30 (2.12) .91) 2.10 (.70) 2.00) 1.900-1.3 (9.60-4.40 (1.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.80-4.86 (1.10) 6.20 (1.44 (2.60-4. see Data Analysis section) for Survey year 03-04 is 0.20 (1.50 (1.40) 640 1454 03-04 03-04 1.00 (5.50) 2.700-1.70-2.80-4.50) 2.60) 1.50 (4.26) 2.20-1.90) 8.70-2.00-6.20) 03-04 03-04 2.20) 485 538 962 Limit of detection (LOD.3.30) 3.00 (.10-5.S.50 (2.90) 3.900-1.10) 8.05-2.900 (.809) 1.30) . interval) 1. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80 (4.30 (6.00) 3.90 (2.70) 13.50-6.800 (.721-1.60-3.90) 1. interval) .60 (1.30 (3.14 (.20) 2.900-1.900-1.10) 4.00 (2.10-9.20-3.60) 9.30-6.10) 6.70) 1.72) 1.20-1.70) 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 1.20) 1.90-2.984 (.20-1.20-2.40-3.50 (1.54) .1) 485 538 962 Limit of detection (LOD.30-9.00 (1.93 (1. population from the National Health and Nutrition Examination Survey.50 (4.90 (4.900-1.56-1.900-1.72 (1.60 (1.50 (1.50-3.20) .77-2.80-3.60 (1.40) 640 1454 03-04 03-04 2.10 (.27) 1.87-2.67-2.80-7.20 (1.70) 1.10 (4. 252 Fourth National Report on Human Exposure to Environmental Chemicals .1.60-3. population from the National Health and Nutrition Examination Survey.0) 8.17-1. Survey Geometric mean (95% conf.80-8.01 (1.09 (.80) 4.70-6.20) 1. see Data Analysis section) for Survey year 03-04 is 0.60-2.30) 3.00-8.50-10.60-2.70-7.70) 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 1.600-.40) 1.60 (6.963 (.08) 2.51) 1.40-1.852 (.10 (1.40) 4.40) 2.00 (1.90-10.42 (1.816-1.0) 1053 1041 03-04 03-04 03-04 1.800-1.966 (.80) 90th 2.60-7.03) 1.900) 1.80 (1.50 (1.90 (4.861 (.92 (1.697-1.30) 3.10) 4.30) 03-04 03-04 .80) 5.80) 1.40 (2.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.S.60-2.90) 90th 5.00) 2.80-7.50) 6.40 (1.689 (.90 (1.40 (1.90) 1.80-2.00 (1.17 (1.62-2.20 (6.70) 2.20 (6.10) 1.90 (1.10 (4.70 (1.04) .30 (1.30 (1.50-6.60-8.90) 1.00 (1.80-12.10) 5.826-1.586-.80-4.80) 3.00-1.30 (1.00) 1.6) 7.20 (1.80-6.50 (6.70 (2.60) 3.10) 75th 1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.00-7.30 (2.90 (1.80-8.00 (.30-2.5) 8.40) 1.10 (.20-1.80-3.90 (1.5) 5.80 (1.900 (.40-1.10) 75th 3.10) 1.834-1.40) .835-1.60) 2.70-10.30 (7.10) 1053 1041 03-04 03-04 03-04 .700 (.50 (6.70) 3. Survey Geometric mean (95% conf.90-19.10-9.00-1.30-12.912-1.16) .

4 (17. population from the National Health and Nutrition Examination Survey.6) 9.3 (35.50) 7.47-4.90 (5.96 (3.8-81.1-35.3) 41.5) 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 21.0) 485 538 962 Limit of detection (LOD.2-22.1) 57.5-23.30 (3.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.6-24.5-62.1-52.5 (28.4 (19.70 (5.6) 42.3) 485 538 962 Limit of detection (LOD.4 (28.5) 9.82) 4.0-66.0-16.70 (5.10 (6.1.10 (3.7-33.2) 45.9 (19.4-42.0 (27.9) 22.50-13.3 (17.7-53.8) 27.80 (7.70-7.80 (6.2 (27.20-5.30-5.6 (35.20-9.4-25.70-9.9 (22.2 (16.7-23.7 (43.99-3.1) 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) 640 1454 03-04 03-04 4.67-4.10 (3.2) 30.3) 28.40) 90th 7.9 (17.00 (5.30) 7.9) 22.9 (13.07-4.90-12.50) 4.80-4.2 (21.70) 4.20 (4.S.4) 56.5) 18.7 (7.20-4.21-3.70) 6.30-3.00 (3.60 (5.20) 5.70-10.95 (3.9-38. interval) 3.60) 03-04 03-04 3.40) 75th 5.40) 3.1-36.10) 5.4 (19.80-12.60-6.9) 27.70 (3.30 (5.S.4) 75th 30.3-22.40-6.00) 3.1 (19.1 (23.40) 5.5) 19.7 (43.85-4.50-4.7-30.3 (35.79) 4.4.60) 8.50 (3.80 (6.1 (24.4) 640 1454 03-04 03-04 23.27) 4.5) 1053 1041 03-04 03-04 03-04 14.6) 1053 1041 03-04 03-04 03-04 3.0) 21.84-3. population from the National Health and Nutrition Examination Survey.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.91) 3.7 (35.20) 7.6) 7.8-30.5-33.7 (19.8-22.5) 57.65-4.6 (44.5) 32.9-23.90-4.0-70.60-9.1-25.90 (7.50 (4.37 (2.5) 8. Survey Geometric mean (95% conf.60 (6.20 (4.8-22.30 (3.2 (28.6 (42.0) 90th 41.4) 20.2 (18.60 (3.3) 42.2-57.3-61.6-50.8 (45.80) 8.30) 6.7 (35.6) 35.53) 3.8) 46.6-45.0) 21.6 (19.70-5.6) 18.7) 39.20) 4. Survey Geometric mean (95% conf.9-19.60-13.11 (2.5 (28.0) 03-04 03-04 19.2) 30.40-6.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.20) 5.47 (4.8 (37.5-21. interval) 20.18 (3. see Data Analysis section) for Survey year 03-04 is 0.0-20.5) 7.4) 21.3 (44.60 (7.3 (28.60-14.0) 36.35) 3.90 (7.90 (7.60 (6.20) 10.9) 9.50-6.7-69.40-17.00 (5.40 (4.7-49.70) 3.10-3.40 (6.8) 32.80-9.89 (3.2 (19.7 (13.90-4.6) 62.8-22.6) 21.8-78.30-8.60 (4.30-11. see Data Analysis section) for Survey year 03-04 is 0.80 (5.4 (23.70-7. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.40-10.4-17.0) 43.0 (20.1-33.1-24.90) 6.30-6.40-14.20) 7. Fourth National Report on Human Exposure to Environmental Chemicals 253 .8-35.0) 23.8 (34.1) 15.

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 .300-.300) .200-.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200-.200-.S.300) . population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th .200-.300) .Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500) . population from the National Health and Nutrition Examination Survey.300-.300) .300 (.300 (.2.S. < LOD means less than the limit of detection.300 (.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .500) .200-.300 (.200-.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) .300 (.300) .300 (. 254 Fourth National Report on Human Exposure to Environmental Chemicals .200-.300) . which may vary for some chemicals by year and by individual sample.400 (<LOD-.300 (.300 (. < LOD means less than the limit of detection.300 (.300-.300-. 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. see Data Analysis section) for Survey year 03-04 is 0.300 (. see Data Analysis section) for Survey year 03-04 is 0.300) .200-.300 (.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 .500) < LOD 485 538 962 Limit of detection (LOD.200-.300 (.200-.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .500) 485 538 962 Limit of detection (LOD.300 (.300 (. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.4.

900-1.10 (.70) 1.00) < LOD .40) < LOD < LOD .00 (.700) 90th 1.10-1.600 (<LOD-.10 (.10) .700) .10 (1.00 (.10) 1.60) 640 1454 03-04 03-04 * * < LOD < LOD . population from the National Health and Nutrition Examination Survey.10 (.900-1. Survey Geometric mean (95% conf.6.30) 1.30) . see Data Analysis section) for Survey year 03-04 is 0. Survey Geometric mean (95% conf.900 (.600 (<LOD-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 .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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900-1. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th .60) 485 538 962 Limit of detection (LOD.800) . < LOD means less than the limit of detection.30 (1.900) 1.20 (1. see Data Analysis section) for Survey year 03-04 is 0.30 (1.900-1.800) .600) .10) 1.600 (<LOD-1.3.700) 1.900 (<LOD-1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .10-1.10-1.700 (<LOD-.10) .40) 1.80) 1.700 (<LOD-.900-1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (<LOD-1.10-1.10-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .50 (1.700 (<LOD-. < LOD means less than the limit of detection.00 (.20) 1.900) 485 538 962 Limit of detection (LOD.300 (<LOD-. which may vary for some chemicals by year and by individual sample.10) * 03-04 03-04 * * < LOD < LOD .50 (1.00 (.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .30) 1.300-2.700) 1. which may vary for some chemicals by year and by individual sample.900) .80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .S.30 (1.20-1.00-1.400 (<LOD-1.500 (<LOD-.900-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (<LOD-2.600 (<LOD-1.80) 1.30) 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 .90) .800 (<LOD-.400 (<LOD-.900-1.700 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.700 (<LOD-.S.700 (<LOD-.

et al.1968--2003. Polyfluoroalkyl chemicals in the U. et al.63:490496. Seacat AM.39(1):80-84. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Seneviratne HR. Chem Biol Interact 2000. in vivo. Mandel JH. Rev Environ Contam Toxicol 2003. Wijeratna S. et al. Butenhoff JL. and perfluorinated contaminants in livers of polar bears from Alaska. O’Connor JC.40:21282134. Rodricks J. Bandai N. Caudill SP. Suzuki E. Environ Sci Technol 2005. Watanabe T. Mandel JH. Environ Sci Technol 2005. Kannan K. Kuklenyik Z. Grasty RC. Tully JS. J Environ Monit 2005. Perfluorinated chemicals in selected residents of the American continent.34(4):351-384. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Sasaki S. Wong LY. Environ Health Perspect 2007. Inoue K. Perkins RG. et al. Hurtt ME. Toxicol Appl Pharmacol 1992. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Taniyasu S.179:99-121. The influence of time.7(4):371-377. de Voogt P. Reidy JA. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Needham LL.39(3):363-380. Harada K. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Reidy JA. Dinglasan MJ. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Bookstaff RC. J Occup Health 2004. 2007b. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002.41:2237-2242. Koizumi A. Fluorotelomer alcohol biodegradation yields poly. Occup Environ Med 2003. The toxicology of perfluorooctanoate. Calafat AM.68(6):465-471. Lau CS. Moore RW. Hurtt ME. Environ Health Perspect. Cook JC. Kamiyama S. Chlorinated. Environmental and toxicity effects of perfluoroalkylated substances. Regul Toxicol Pharmacol 2004. O’Connor JC. and ex vivo studies. Corsolini S. Hekster FM. Ingall GB. Witter FR. Yun SH. Butenhoff JL. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Cook JC. Environ Health Perspect 2007.134(1):18-25. Kuklenyik Z. Kuklenyik Z. Murray SM. Mandel JS. Olsen GW. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Bignert A. Laane RW. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Kannan K. Yamashita N. Mohotti KM. Yoshinaga T. Tarone RE. Calafat AM. Arendt MD.Koizumi A. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Needham LL. Reidy JA. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat.99(2):253-261. Fillmann G. Characterization of risk for general population exposure to perfluorooctanoate. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Morikawa A.115(11):1677-1682. Needham LL. Jarnberg U. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth.and perfluorinated acids. Toxicol Sci 2001. Grey BE. Day RD. Saito N. Caudill SP. Apelberg BJ.S. Liu RC. Moore JA. Peterson RE. Toxicol Appl Pharmacol 1995.38(17):4489-4495. Saito N.39(23):9057-9063. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Katakura M. Loganathan BG. Frame SR. Birth Defects Res B Dev Reprod Toxicol 2003. Harada K. Reidy JA.124(2):119-132. Burris JM. Needham LL. Inoue K. Taniyasu S. Kennedy GL Jr. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Calafat AM. McLaughlin JK. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Environ Sci Technol 2004. Kudo N. Gaylor DW. Environ Sci Technol 2006a. Kannan K.115(11):1670-1676.Perfluorochemicals References Alexander BH. Kumar KS. Yoshinaga T. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats.38(10):2857-2864. Environ Sci Technol 2005.115(11):1596-1602. Calafat AM. Environ Sci Technol 2004.60(10):722729.46(2):141-147. brominated. et al.113(2):209-217. et al. Evans TJ. Halden RU. Tully JS. Olsen J. Fei C. Guruge KS.104(2):322-333. Cook JC.S. Hurtt ME.39(23):9101-9108. Environ Sci Technol 2007a. Aguilar-Villalobos M. Edwards EA. Falandysz J. Frame SR. Kawashima Y. Olsen GW. Ye Y. Herbstman JB. Toxicol Appl Pharmacol 1990. Keller JM. Mabury SA. et al.60(1):44-55. Yamashita N. Environ Res 2005. Biegel LB. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Kuklenyik Z. Chemosphere 2006b. Olsen GW. Rogers JM. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Biegel LB. Calafat AM. Crit Rev Toxicol 2004. Holmstrom KE.

45(3):260-270. Huang HY. Bronson R. The developmental toxicity of perfluoroalkyl acids and their derivatives. Toxicol Sci 2002. et al. Kannan K. (Erratum in: Toxicol Sci 2004.37(12):2634-2639. et al. Yamashita N. Church TR. Coordinate induction of acyl-CoA binding protein. Gamo T. Butenhoff JL. fish. htm. Butenhoff JL. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. perfluorooctanoate andother fluorochemicals in human blood. Burris JM.) Tittlemier SA. Pepper K.68(1):249-264. Stanton ME. Nesbit DJ. J Occup Environ Med 2003b. Butenhoff JL.113(5):539-545. Richards JH. Mar Pollut Bull 2005. Buck RC.S. Butenhoff JL. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Burlew MM. Horii Y. Horii Y. A global survey of perfluorinated acids in oceans. Historical comparison of perfluorooctanesulfonate. Lundberg JK. J Children’s Health 2004b. Mandel JH. Olsen GW. et al. fast foods. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Kawashima Y. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Thibodeaux JR. Olsen GW. Environ Health Perspect 2005.26(1):47-51. Peterson RE.41(9):799-806.111(16):1892-1901. Hanson RG. Helzlsouer KJ. J Ag Food Chem 2007. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Reagen WK. Burris JM. et al. EPA). Washington. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Olsen GW.Perfluorochemicals Kudo N. birds. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation.perfluorohexanesulfonate. Hansen KJ. Olsen GW. Olsen GW. Sources.55:3203-3210. Sterchele PF.54(11):1599-1611. Burris JM. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle.74(2):369-381. Thibodeaux JR. Taniyasu S. J Occup Environ Med 1999.2(1):53-76. Toxicol Sci 2003. Biol Pharm Bull 2003. Mair DC. fish. et al.epa. Hansen KJ. Case MT. I: maternal and prenatal evaluations. Ehresman DJ. Rogers JM. Grey BE. Chemosphere 2007b. II: postnatal evaluation. Environ Sci Technol 2003. 2003a. Olsen GW. Seacat AM. Taniyasu S. Chemosphere 2004a.111(16):1900) Olsen GW.S. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Ehresman DJ. Ellefson ME. Prevedouros K. U. Butenhoff JL. Lundberg JK. van Belle G. Toxicol Appl Pharmacol 2004. Hanson RG.68:105–111. Rogers JM.51(8-12):658-668. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Cousins IT. Grey BE. Hansen KJ. Mandel JH. Moisey J. Burris JM. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. et al. (Erratum in: Environ Health Perspect.82(1):359. Cao XL et al. Thomford PJ. Environ Health Perspect 2003a. Seacat AM.gov/opptintr/pfoa/pfoara. Seymour C. Hansen KJ. Biochim Biophys Acta 1993.. Froehlich JW. Mandel JH. 2007a. Hanari N. Environ Health Perspect. Mandel JH.198(2):231-241. Rogers JM.40(1):32-44. Miller JP. Korzeniowski SH. Lau C. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Olsen GW. Petrick G. Lau C. Yamashita N. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators.115(9):1298-1305. Zobel LR. Butenhoff JL. Burris JM. Environ Sci Technol 2006. 1/15/06 Vanden Heuvel JP. and food items prepared in their packaging.74(2):382-392. Available from URL: http://www. and perfluorooctanoate in retired fluorochemical production workers. Kannan K. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Larson EB. Barbee BD. Environmental Protection Agency (U. Toxicol Sci 2003. Olsen GW. Church TR. Hansen KJ.1177(2):183-190. 2003. fate and transport of perfluorocarboxylates. and humans from Japan. Half-life of serum elimination of perfluoroo ctanesulfonate. Church TR.

. fragrances. several of the phthalates produced testicular injury. indoor and ambient air.. followed by inhaling indoor air. and other oxidized metabolites included in this Report. 2004. Infants may have relatively greater exposures from ingesting indoor dust containing some phthalates (Clark et al. and sediments (Clark et al. 2002).. 1998). 1998. Okubo et al. garden hoses.. phthalates can be released into the environment during use or disposal of the product. urinary metabolite and air phthalate concentrations are roughly correlated (Liss et al. plastic raincoats.. Harris et al. Absorbed monoester metabolites are usually oxidized in the body and.. Albro and Lavenhar. some medical devices and pharmaceuticals. lubricating oils. dietary sources have been considered as the major exposure route. 1985. automotive plastics. inflatable recreational toys. and. however. Nielsen et al. People are exposed through ingestion.. which are then absorbed (Albro et al. Dirven et al. shampoo. Because they are not chemically bound to the plastics to which they are added. vinyl tiles and flooring. liver injury. 1982. 2003). detergents. 1985. lotions.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. and personal-care products. excreted in urine largely as glucuronide conjugates (Albro et al.. 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 . There are numerous products that contain phthalates: adhesives. 2001. Phthalates are metabolized and excreted quickly and do not accumulate in the body (Anderson et al. such as soap. 2000. Zacharewski et al. corresponding monoester metabolites. In chronic rodent studies. 1989).. In vitro studies showed that certain phthalates can bind to estrogen receptors and may have weak estrogenic or anti-estrogenic activity (Coldham et al. to a lesser extent. water sources. Ingested phthalate diesters are initially hydrolyzed in the intestine to the corresponding monoesters... 2001). dermal contact with products that contain phthalates. 1982. and teratogenicity. but in vivo studies did not support phthalates having estrogenic effects (Milligan et al.. Various phthalate esters have been measured in specific foods. 2003). 1993). liver cancer.. blood product storage bags. Phthalates are often used in polyvinyl chloride type plastics.. Human milk can be a source of phthalate exposure for nursing infants (Calafat et al. in humans.. Parks et al. The table shows the phthalate diesters. indoor dust. and nail polish.. 1997.. 2005). solvents. In settings where workers may be exposed to higher air phthalate concentrations than the general population. hair spray. 2003. The intravenous or parenteral exposure route can be important in patients undergoing medical procedures involving devices or materials containing phthalates. Pan et al. Mortensen et al. Human health effects from phthalates at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Phthalates are also used as solubilizing and stabilizing agents in other applications. Phthalates have low acute animal toxicity. inhalation. 1995). but these effects either have not been demonstrated when tested in non-human primates or are yet to be studied. and toys (ATSDR. Jobling et al. 2006). such as plastic bags.. intravenous medical tubing. 1997. deodorants. For the general population.

gov/toxpro2. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. and Sertoli cell abnormalities in the male animals and.cdc..805:49-56. 2000b.. 4/20/09 Albro PW. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). The Handbook of Environmental Chemistry.. and extent of metabolite conjugation to glucuronide (Albro et al. Corbett JT. Toxicological profile for di(2-ethylhexyl)phthalate update [online].. Hauser et al. efficiency of intestinal absorption. reducing estrogen production.. ovarian abnormalities in the female animals (Jarfelt et al. Peck and Albro. 2001. Food Addit Contam 2001. Anderson WA. Drug Metab Rev 1989. Information about external exposure (i.21:13-34. 2002.gov/ toxprofiles/tp9. 2004). Silva MJ. Evaluation of a recombinant yeast cell estrogen screening assay. Toxicological profile for di-n-butyl phthalate update [online].nih. 2000a.. Hoppin et al. gender. 2004. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. 2003.html.cdc. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Connor C.. Jordan S.45:19-25. dibutyl phthalate (DBP). 2004.gov/toxprofiles/ tp135. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites..Phthalates and metabolites have been tested.atsdr. Jongeneelen FJ. 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. van der Broek PH.atsdr. In animals. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. McKee et al. However. These differences may contribute to species-specific differences in toxicity (ATSDR..3.gov/ reports/index.. 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. 1982. 2002). Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 ..html. 2004. Calafat AM. which may be a pathway to the development of liver toxicity and cancers in these animals. 227-262. Pharmacokinetics.. 1982). interactions with macromolecules and species differences in metabolism of DEHP.18(12):10681074. Herbert AR. at very high levels. 2003. Dave M. 2006). Scotter MJ. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. testicular atrophy. 1985.html). 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. Population estimates of concentrations of specific phthalate metabolites may differ by age. Rhodes et al. 105:734-742.e. NTP-CERHR. High doses of di2-ethylhexyl phthalate (DEHP). A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Springall C. 2007. Kessler et al. Vol. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. Environ Health Perspect 1997.cdc. Assessment of critical exposure pathways. Springer. and race/ethnicity (Silva et al. J Chromatogr B 2004. References Agency for Toxic Substances and Disease Registry (ATSDR). Castle L. Available at URL: http://www. atsdr. variation also occurs in the same person during repetitive monitoring (Fromme et al. Albro PW and Lavenhar SR... and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. but there are known species-related differences in the hydrolysis of diester phthalates. at higher doses. 2001). 2005. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. 2000c. pp. phthalates produced anti-androgenic effects by reducing testosterone production and. Massey RC. Clark K. 2006). Silvapathasundaram S. Part Q: Phthalate Esters.. 2005). Hauser et al. McDonnell DP. 2001. Sauer MJ. Slakman AR. The monoester metabolites are thought to mediate toxic effects for some of the phthalates.html. Cousins IT. Metabolism of di(2-ethylhexyl) phthalate. Lovekamp-Swan and Davis. Available at URL: http://www.niehs. Mackay D.New York. 2002). Also. Needham LL. 2007). phthalates have been shown to induce peroxisomal proliferation in rodents. Environ Health Perspect 1982. Schroeder JL. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al.. In Staples CA (ed). Matthews HB. Coldham NG. Dirven HA. 2004. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. 1986).

National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. 6/2/09 Okubo T. NTP-CERHR. Reynolds T. McKee RH. Silva MJ. Koch HM.html. Harris CA. Available at URL: http://cerhr. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Sumpter JP. Baird DD. Ryan L. Skakkebaek NE. Jobling S. Park MG. Int J Hyg Environ Health 2007. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Filser J. Am Ind Hyg Assoc J 1985.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. 2006 [online]. Chen Z. Tsukino H. Bolte G. consumer milk.25(2):293-302. Epidemiol 2005. Anal Bioanal Chem 2005. Available at URL: http://cerhr. Yokoyama Y. Ladefoged O.112(17):1740].18(1):122.382:10841092. Environ Health Perspect 2004. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate.105:802-811. 6/2/09 NTP-CERHR. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Silva MJ. Environ Health Perspect 2003. Jacobsen H. Numtip W. Hum Reprod 2007. Scand J Work Environ Health 1985. Jarfelt K.195:142-153. Stringer WT. Singh NP.nih. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Research Triangle Park (NC). Kalita JC. and infant formula by tandem mass spectrometry (LC-MS-MS). David RM. Andersson A-M. gov/chemicals/dehp/dehp-eval. Leffers H. 2000a [online]. et al. Boehmer S. Davis BJ.11(5):381-387. Biol Pharm Bull 2003. Giwercman A. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Akesson B.16(4):487-493. Main KM. Angerer J. Available at URL: http://cerhr. Milligan SR.html.nih. Balasubramanian AV.niehs.46(11):643-647. Silva MJ. Available at URL: http://cerhr. 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 . 2000c [online]. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP).106(1):23-26. 2000b [online]. 6/2/09 NTP-CERHR. Davis BJ. Pan G. Duty S. Meeker JD. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Liss GM. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Environ Health Perspect 1997. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. White R. Nielsen J. Kessler W. Suzuki T. Hoppin JA. Hagmar L. Jonsson BAG. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Drexler H. Sumpter JP. et al. J Androl 2004. Gans G. Hauser R. Grote K. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Duty SM. Environ Health Perspect 1998. Yoshimura M. Lovekamp-Swan T.22(3):688-695. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets.gov/chemicals/ phthalates/dbp/dbp-eval.210:21-33. Research Triangle Park (NC).niehs. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Fromme H. Richthoff J. Mortensen GK. Csanády G. Ryan L.103:582-587. Rylander L. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).niehs.111(2):139-145.nih. Calafat AM. Borch J. Park S. Chahoud I. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Wang P. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Hauser R. 6/2/09 NTP-CERHR. Research Triangle Park (NC). DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Kano I. Henttu P. Kano K. et al. Research Triangle Park (NC). Butala JH. Brock JW.26(8):1219-24.Phthalates in human urine samples.gov/chemicals/dehp/dehp-eval.nih. Dalgaard M. Reprod Toxicol 2004. Mechanisms of phthalate ester toxicity in the female reproductive system.19(4):505-515. Urinary phthalate metabolites and biomarkers of reproductive function in young men. The estrogenic activity of phthalate esters in vitro.html. Meeker JD. Albro PW. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Environ Health Perspect 1995. Environ Health Perspect 2002.niehs. Zhang S. Reprod Toxicol 2005. Skerfving S. Brock JW. et al. Calafat AM. Hass U. Toxicol Appl Pharmacol 2004.html. Int Arch Occup Environ Health 1993. Determination of phthalate monoesters in human milk.64(8):555-560.110(5):515-518. Hanaoka T.112(17):1734-1740. Reproducibility of urinary phthalate metabolites in first morning urine samples. Hartle RW. Parker MG.

Phthalates phthalate (DEHP): a cross-sectional study in China. Zacharewski TR. 112(5):A270]. Reidy JA. Batten PL. et al. Barr DB. Peters JM. Crit Rev Toxicol 2006. Orton TC. Silva MJ. Clemons JH. Environ Health Perspect 1986. Ostby JS.114(11):1643-1648.58:339349. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Environ Health Perspect 2004. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Barlow NJ. Hodge CC. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Malek NA. Cunningham ML. Toxicol Sci 2000.112(3):331-338.65:299-308. Fielden MR. Pratt IA. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Rusyn I. Lambright CR. et al. Klinefelter GR. Meek MD. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man.S. et al. Environ Health Perspect 2006. Peck CC. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Wu ZF. Jackson SJ. Caudill SP. Matthews JB. Bratt H.45:11-17. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Environ Health Perspect 1982. Rhodes C. Albro PW. Parks LG.46:282-293.36:459-479. Urinary levels of seven phthalate metabolites in the U. Toxicol Sci 1998. Abbott BD.

3) 15. it can be released into the ambient air during use or disposal of the products.6) 13.7) 23.3-130) 122 (88.7-82.4 (53.3-12.2) 12.8) 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. interval) 15.8 (50.0) 20. Food crops take up BzBP.2-116) 122 (102-143) 101 (84.1 (55.4) 51.7) 40.7-170) 169 (134-198) 152 (99.7-25.0 (30.3-18. including MBzP. can produce developmental and reproductive toxicity in rodents.2) 15.5-36.S.4) 33. because it is not bound to products in which it is incorporated.4 (48.5 (55.3-27. and to a lesser extent. IARC considers BzBP not classifiable with respect to human carcinogenicity.3-125) Total 15.3 (30.2) 22. and 03-04 are 0.3 (12.5-14.8-18.2) 13.7-16.4-16.2-16.5-33.0) 32.7-119) 99.4) 35.7 (13.2 (43.8-35. 01-02.0 (34.9-47.6) 35.7-16.0 (26.8-98.3) 94.3-91.4) 80.6) 29.4 (10.6-38.1) 14.3 (13.6-17.1-90.9-87.8 (71.1 (13.5) 15. 262 Fourth National Report on Human Exposure to Environmental Chemicals .1) 31.4 (32.8 (38.1-120) 52. 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.7-172) 103 (74.4) 35.9-16.9) 12.9 (70.0-85.6 (13.1 (20.5-94.0 (23.2 (47.7 (53.4 (53. population from the National Health and Nutrition Examination Survey. some personal care products.9) 18.6-116) 122 (102-142) 101 (85.1 (13.4 (32.8-41.4) 12.4 (13.5 (27.0) 90th 67.9 (28.9-14.1-116) 122 (93.2-115) 113 (91.4 (10.2-31.9 (39.6-132) 103 (84.8-121) 79.3-75.0 (30.1) 67.0) 70.5) 65.4) 65.8-13. High dose BzBP and its monoester metabolites.5 (67.6) 16.2 (19.5-35.2) 14.6) 63.9) 13.2-39.3.9 (12.3-21.0) 23.8) 33.5-145) 138 (106-241) 143 (127-179) 120 (99.1 (14.9 (21.1-15.8 (14.4) 38.1-16.3 (33.3) 23.6-18.9 (16. BzBP can be released into the environment during its production and.3-18.1-16.0) 33.4-120) 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 13.8-64.0-55.1 (14.6 (21.5-25.8-133) 89.0 (43.3 (12. and 2003-2004 were generally similar those reported in U.0 (33.3-43.4-92.3 (12.8) 63. 2001-2002.8 (71.6 (41.3) 37.5 (47.2-17.8) 24. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.4-25. respectively.5-84.1-35.1-43.8-14.1-214) 166 (116-191) 145 (110-213) 88.3 (29.2-19.7 (80.8-72.6) 67.2-16..3-74.4) 14.6) 50.6 (12.6) 14.6) 95th 103 (94.8-76.7-17.4) 108 (96.4) 49.9) 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) 66.6) 24.9) 43.6-72.2) 78. sealants.7-58. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.6 (13.6 (13.0 (27.8-17.2 (25.9-27.6) 14.7-14.7-15.9-190) 86.4) 98.6 (53.4 (68. car care products.3-34. and 0.4-15.7) 38.7 (11.2) 17.2 (14.6) 13.6 (66.5-18.5-36.8. 2000). 2000).6-150) 94.2 (10.1-61.2) 32.1-15. particularly male animals (McKee et al.0 (14.6) 25.6-92.1) 13.9 (11. vinyl tile.3 (29.4 (27.8-16.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.Phthalates Benzylbutyl Phthalate CAS No.9 (13.2-155) 91.0-106) 58.1 (32.7-35.3-161) 99.0 (11.7 (12.9-49.7 (82.9) 14.5) 30.7-13.3 (54.3) 13.5) 82.1) 12.4 (63. 2004.4 (31. and diet is the major source for general population exposure.4 (29.2-33.4-127) 80.1-38.5) 55.8 (21.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.3) 13.8) 14.5 (76.1 (58.0) 34.5 (66.8 (12.8 (10.5 (57.7 (15.6-43.6) 35.2) 33.8-48.6 (13.6-79.0 (12.8 (28.9) 15.5-97.0) 24.5 (26.1) Selected percentiles ( 95% confidence interval) 50th 17.5) 15.4) 71..7 (51.6) 37.6-39.0 (55.1-39.5-41.9 (22.9-62.5) 27.S. residents (Blount et al.9) 49.1) 32.5-40. NTPCERHR.2-40.5 (61.0 (20.4) 75th 35.4-24.0 (15.1 (10.5-62.1 (19.3 (44.9-30.6 (32.1) 29.1-18.1.5 (13.3-88.8 (86.7-16.3 (22.1) 76.0 (15.2-38.6-92.1) 68.0-130) 101 (86.2) 69.8 (30.3) 54.9-28. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4) 81.0) 16.2) 14.9) 14. 0.5) 16.2 (19.2-183) 101 (78.7 (70.2 (11. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.5) 23.8-14.2-20.8) 28.4) 129 (98.8-16.3) 63.8 (80.0-26.6) 15.6-29.3-82.9 (12.4-62.8-17.8 (53. see Data Analysis section) for Survey years 99-00.4 (59.9) 11.

5 (48.7 (11.1-120) 77.8-14.6-99.7-12.9) 64.4 (34.1-58. population from the National Health and Nutrition Examination Survey.8 (10. 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.4 (13.5 (49.5) 41.8) 13.3-11.5-31.8) 24.8 (13.7) 38.7 (23.0 (33.4) 50.4 (69.8) 53.5) 14.1 (46.0 (12.4 (33.8-85.2) 11.5) 17.8-16.3 (23.8-48.4 (46.0 (41.95-14.4-90.9 (12.9) 24.8-15.2-49.6 (11.7-56.3 (12.7-397) 70.9 (51.8-80.3) 21.2) 32.6 (36.2-15.6 (14.1 (41.8) 68.8 (69. 2005).5) 95th 77.7 (55.4-17.6 (57.3) 90.5) 23.3 (39.8 (11. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.1) 17.0 (41.1) 24.1 (11.1 (19.2) 26.6 (11. in young Swedish men (Jonsson et al.2-13.3) 13.3) 13.3-34.S.9-40.8) 56.0 (67.5-23.6-81.1 (13.8 (64.4-23.9) 11..2-26.4-42.1 (15.. Hauser et al.0) 13. 2007).1-29.. 2004).6 (19.4 (21..8) 34.2-15.9 (22.1 (21.1-12.6 (51.5-99.5-29.2 (56.0) 24.0 (62.1) 27.1 (43.5-26.6) 75th 25. In an annual sample of German university students.. 2007). 2003).1 (53.3) 16.6-47.1) 142 (99.4-93.5) 20.8 (50.1) 24.8) 33.7) 56.1 (34.4-142) 134 (116-176) 136 (85.6) 38.8 (30.6-12.4-19.5 (56.8-173) 195 (121-305) 229 (99.7 (59.4) 25.6 (30.7-123) 77.9-83.4 (11.4) 21.6-20.5 (42.8 (12.4 (12.5 (12.4) 13. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8-60.1) 39.69-11.4 (11.4 (25.0-26.0) 12.8) 108 (75.7-15.8) 26.7-61.0) Selected percentiles ( 95% confidence interval) 50th 13.6) 53.Phthalates York City (Adibi et al.8) 15.4-14.4 (26. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2-78.4-116) 73.7-20.4) 12.5) 78..5-42. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al. interval) 14. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.2) 15.3) 13.8-39.4) 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 12.2) 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 12.7 (19.4) 28.0-27.8) 16.9-104) 62.7-19.5-38.5 (10.5) 13.7 (18.4-27.5-58.8-27.7) 11. 2003).4) 104 (89.7 (54.4 (11.7-20.1 (14. and females compared to males (Silva et al.4-79.9) 100 (80.8-64.3) 14.2 (41.4 (10.7) 19. In NHANES 1999-2000.3-38.3) 55.2-12.6-86.5 (11.3 (13.7 (11.5 (9.2-13.8-15.5-13.1-12. 2006).9 (24.0 (11.0 (10.2-21.9-16.0-48.8) 71.3-73.2 (40.8 (46.0 (12. 2005.0-53.6 (30.2-51.9 (55. 2004.1-79.4) 17.8-13.7-14.9-14.5-79.4-18. 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.8 (49.3) 29.0) 24.1-27.7 (11.9) 12.9-23.0) 49.3) 14.6) 30.7-19.2-117) 95.1 (21.9 (9.6) 73.9 (12.1) 23.1 (23.7-15. and in a small sample of German residents (Koch et al.3 (38.0-90.0 (13..8-69.3 (24.5-26.3) 67.9 (24.3) 37.7-31.6 (15.5 (10.4 (74.0) 11.4 (63.1) 12.8) 33...4) 51.4-15.3 (35. A small study of African-American women in Washington.2 (69.6-26.9-13.1 (18.4-102) 70.9 (10.8) 53.9 (15.6-13.7-29.9) 52.0-15.8-13.0) 15.4) 15.9-62.6 (22.6-40.0-51.1) 80.2) 11.8-14.9 (43.73-12.5-16.1-35.3) 12.3) 36.7-69.4-99.6) 58.7-90.9-115) 57.5-61.5) 16.2 (27. Weuve et al.4) 13.8) 46.3) 89.5 (35.4) 60.8-13.1 (13.9) 11.7 (12.7) 25.3-16.0) 60.9 (54.0 (49.6-15.1 (25.1 (21.4 (60.8) 80.8-34.5-58.7 (13.1) 35.9) 12.1-14.0-109) 65.7 (38.6 (11.9) 42.2) 11.9 (10.9) Total 14.6) 12.1 (21.3 (60.5) 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 . 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.8) 54.7 (13. 2002).8 (57.7 (14.9-69.4) 14.6 (34.2) 67..4-14.2-17.6) 12.9) 12.6 (24.5-76.4) 90th 50. in men attending a Boston infertility clinic (Duty et al. 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.6) 13. adolescents compared with adults.0 (38.8-42.4) 44.9-28.3 (15.9 (29.9-13. 2002.9 (15.3-64.7) 46.7-14.5) 46.9 (39.5-57.1 (9.3) 73.8) 11.1-125) 86. Hoppin et al.7 (21.6) 25.2-57.6-116) 74.3) 18.7) 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 40.2) 12.5) 10.5-213) 49.4-60.

J Androl 2004. et al. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Research Triangle Park (NC).110(5):515-518. Reproducibility of urinary phthalate metabolites in first morning urine samples. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP).niehs.210(3-4):319-333. Silva MJ. Duty S. Brock JW. Environ Health Perspect 2003.Phthalates References Adibi JJ. Sampson EJ. Rossbach B. Blount BC. et al. Pirkle JL. Reidy JA. Drexler H. Meeker JD. Caudill SP. Silva MJ.111(14):1719-1722. Malek NA. Silva MJ. Third National Report on Human Exposure to Environmental Chemicals.114(9):1424-1431. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. NTP-CERHR. Brock JW. Koch HM. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Centers for Disease Control and Prevention (CDC).18(1):122. Chen Z. Ryan L. Environ Health Perspect 2002. Hauser R. Duty SM. Rylander L. Ryan L. Caudill SP. McKee RH. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Schettler T. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. 2005. Urinary phthalate metabolites and biomarkers of reproductive function in young men. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Poland. Hilborn ED. Silva MJ. Environ Res 2003. Caudill SP. et al. Environ Health Perspect 2004. Hagmar L. Calafat AM. Gans G. Eckard R. David RM. Jacek R. Levels of seven urinary phthalate metabolites in a human reference population. Atlanta (GA). Available at URL: http://cerhr.22(3):688-695.nih. Angerer J. Brock JW. Dobler L. Baird DD. Hodge CC. Hum Reprod 2007. Hu H. Perera FP. Needham LL. 2000 [online]. Butala JH. 4/20/09 Silva MJ. Reprod Toxicol 2004. Bull Environ Contam Toxicol 2002. Phthalate monoesters levels in the urine of young children. Singh NP. et al. Calafat AM.html. Epidemiol 2005. Giwercman A.S. Jedrychowski W.112(3):331-338. Barr DB. Needham LL. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Sanchez GN. Camann DE.108(10):979-982. et al. Davis BJ. Wittassek M. Jonsson BAG. Barr D.gov/ chemicals/phthalates/bb-phthalate/bbp-eval.93:177-185.68:309-314. Weuve J. Koch HM. 112(5):A270]. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Wiesmuller GA.25(2):293-302. Helm D. Hoppin JA. Int J Hyg Environ Health 2007. Urinary levels of seven phthalate metabolites in the U. Environ Health Perspect 2006.16(4):487-493. Green RA. et al. Environ Health Perspect 2000. et al. Prenatal exposures to phthalates among women in New York City and Krakow. Richthoff J.

97) 4.20) 7.91) 4.Phthalates Di-n-butyl Phthalate CAS No.50-2.80-5.50) 2. Koch et al.5) 18.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.6-14.3 (13.40 (6.0-25.73 (2.70-4.S. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.70-8.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.40 (2. In addition..0) 13.80 (5.80 (5. 2004.33 (2..7-31.30) 2..9 (16.40 (2.7 (9.20 (6. OSHA has established a workplace air standard for external exposure to DBP.1 (13.00-11.6 (10.8) 40.3 (16.5) 18.68 (2.81 (3. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.30-13.3 (19.4) 5.50) 8.10 (4.6 (29. 2000.7 (7.7) 18.40-17.22) 3.6) 26. Studies of children found age-related differences in urine MBP levels.37) 6.90-2.5) 22.50 (3.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.8) 21. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.30) 10.30-6.6) 12.22 (3. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.85-6. 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.7) 15.0) 12. 2007).80-5.40-12.96) 3.20-12.6) 16.2-33.90 (3.46 (2.43) 6.2 (11.60-6. population from the National Health and Nutrition Examination Survey.00 (7.5) 12.50-6.30 (4.7-18.5-29. 2005).17) 4.17 (2.00-6.30-3. NTP-CERHR.90 (4. in men attending a Boston infertility clinic (Duty et al.7-20.1) 22. CDC. Fourth National Report on Human Exposure to Environmental Chemicals 265 .5 (17.9) 10.73-5.10 (4.1-25.7 (16.2-14.6-18.56 (5. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.80 (2.5-16.00) 6.7 (18.80 (2.46 (3.1-12.50) 5.20-2.30-2.50) 90th 12.02) 4.84) 4.S.30) 10.5 (11.40) 5.1-20. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.0) 24. Biomonitoring Information Median concentrations reported in the NHANES 19992000.50-4. and also in some printing inks.0 and 0.40 (7..56) 3.30 (1.2) 5.5-16. residents (Blount et al. pharmaceutical coatings.40 (3. When total DBP metabolites have been measured.9-14. and insecticides. 2005).8 (9.28-5.90 (6.30-11.66) 2.46-5.30) 5.00) 10.50) 7. they have been referred to as monobutyl phthalate (MBP). 2000).56-4.0) 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. in a small sample of pregnant women in New York City (Adibi et al.3 (13.3 (16.90-7.55) 2.9 (16.5-24.20-9.30) 6.6) 10.3 (11.00-4.97-7.24-8. Survey Geometric mean (95% conf.00) 4.48 (2.59) 3.10 (3.56 (3.4) 22.40-3.07 (3.7) 7.6) 17.0 (11.2 (8.60) 3.2-22.97) 2.90 (4.00-6.82-3.55 (3..6 (13.7 (17.1) 25.3-48. mostly as MnBP (Anderson et al.3-20.4) 12.5) 19.10) 3. about 65% to 80% of a dose is eliminated in urine within 24 hours.6 (9.10-9.40-4.3-18.40-5.19-3.00) 7.0-18.70) 5.6 (13.0 (13.5 (27.30 (3.3-30.49-2.70-4.0) 20.1-17.3-24.90-4.6 (14.4-12. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.0 (13. 2004.60 (2..5) 14.1) 16.6) 16. 2005). 2001). 2005.72-3.6-20.70) 3.10) 8.2 (12.4 (14.40-3.80) 75th 5.0) 9.80 (3.50) 18.7-31.20-12. DBP can produce reproductive toxicity in male rodents (McKee et al.60 (4.90) 12.9) 15.67 (5.46) 2.50 (6.6-26. Following oral administration of DBP to humans.60 (5. 2003).3) 33.30-7.60 (8.7) 14.3. Hauser et al.5 (10.5) 25.00-9.0 (19. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.7 (17.9-23.6 (10.20 (7.70 (2.7) 4.00 (5.4 (20.5 (20.71 (2.30-6.0-14.90-4.6) 17. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.8) 677 652 703 699 1216 1088 Limit of detection (LOD.40-9.20 (3..40-4. interval) 2.10-2.1 (8.5) 23.10) 9.20) 4.26 (2.0-38.63) 3.3-43.44-2. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.10-9.6 (11.00) 4.3 (18. 2003).10) 2.20-6.3) 18.6 (14. 84-74-2 Di-isobutyl Phthalate CAS No.6-34. and in a small sample of Japanese adults (Itoh et al.3-19. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.4-27.3) 3.11-3.50-10.70 (5.25) 01-02 03-04 01-02 03-04 01-02 03-04 4..10) 11..

1-12. ranging from more than one-tenth the NHANES median (Itoh et al. 2007)..24) 3. 2005).33 (3.47-12..58-4.82) 4.91-6. Between 1998 and 2003.37) 3.79 (4.13 (2.08) 75th 4.6 (12.64-10.52) 3.3) 13.93-6.73 (5.57 (3.22 (2.3) 16.86-4.6) 11.2 (11.81 (3.17-12.2) 9..20 (7. 2004).51) 2.54 (2. 2006).84 (8.57-4.02-10. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.27-12.7) 10.07-5.56-15.94 (5.4 (12.1) 10.32) 7.6 (8.92 (7.46) 3.0-18.67-5. An analysis of NHANES 2001-2002 showed similar age.6) 13.11-2.95) 10.46 (2. to about two to fourfold higher (Fromme et al.8 (8.76-3.56-4.3) 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.15-4.66) 2.07 (2.78) 9.31 (7.72-7.33) 3.03-11. 2004).9 (11.28 (4.33 (2.65-11.6-19.7 (9.32 (3. 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.5) 15.31) 2.29-8.3) 13.99-4.13-6.8 (10. respectively.86) 6.18 (1.65 (4.05) 2.94-12.78-8.96 (3..Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.36-2.8-18.1-24.69-7.64-7.2) 24.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC. interval) 2.55-6.72) 5.46-11.1) 4.38-10.00 (3.8) 10.43) 3.11) 5. population from the National Health and Nutrition Examination Survey.43) 3.0 (8.74 (4.57 (3.76-3.66 (8.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .20-2.09-2.21) 10.66) 10.80) 7. 2002.9 (9.82 (4.18) 3.1-15.80 (3.9 (15.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.88 (2.7 (11.3) 28.29-3..76 (3.43) 3. In an analysis of NHANES 1999-2000.81 (6.00-7.81) 9.10-5.95-3.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.04) 3.52 (2. Survey Geometric mean (95% conf.2-15.03-7. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.4) 7.62-12. Over this time.6 (9.99) 7.98 (2. while MnBP declined (Wittassek et al.69 (2. than adults in NHANES subsamples during the same time period.2 (10.34 (3.42) 2.85 (2.0) 7.0) 11.36-7. Weuve et al.69) 6.66) 4.47 (3.5) 13.7 (13.20-4.0) 15.26-2.83 (2.14 (4.21 (5.5 (9. 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.8 (9.56) 5.17) 90th 8.95) 2.18) 4.1) 11. 2007).58-3.74-3..53-5.11 (5.18-4.68) 3.51) 15.7 (21.54 (4.3 (13.45) 3.00-3.20 (2.76-15.65-4.02 (7.7) 11.03 (5.35) 3.61-3.59 (4.S.30 (6.8-36.08-2.6 (8.78) 8.39) 5.00-3.26 (2.15) 3.0 (12.5 (11.8-18.18 (4.20-3.69) 4.4) 23.52-3.0) 3.6 (10. up to four and 13 fold.54) 2.79-6.68 (2.1) 15.80-3.53-3.89-5.20 (2. 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.1-25.75 (4.5-19.19 (2.68) 5.6 (15.97-2.84 (4.53-4.51) 5.8-13.7) 3.25) 5.52-20.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.1) 7.0 (10.2-13.47-5.44 (3.1) 13.75 (6. samples from German university students had consistently higher median urine levels of MnBP and MiBP.38 (6.9-40.33-9.01-2.56) 2.41 (2.9-16. the students’ median values for MiBP levels remained relatively unchanged.9) 12.1 (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 2.79-8.04) 7.31) 2.18-10.3 (17.04-5.2) 8.89 (3. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.39-3.62 (6.30) 2.4-16.81) 4.94) 6.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.32 (7.6-19. 2005).and gender.7) 19.31 (2.28-13.64-7.7-28.9-26.17 (2..89) 6.4) 15.1 (11.

5-42.8-29.6 (90.1 (21.5) 95.6 (22.2-49.7) 92.4 (35.0-19.9 (17.1) 19.5) 31.5) 19.0-73.2-33.6-33.0 (17.4-42.6 (65. population from the National Health and Nutrition Examination Survey.6) 20.6) 38.3-40.0-24.9-28.7-53.5-47.4 (71.7) 124 (98.9-87.4 (23.1 (19.1 (18.1) 46.7-116) 95.6-143) 127 (99.5) 40.5) 85.5) 21.5-47.1.5) 36.9-33.7 (43.5) 36.4 (25.1 (26.1) 23.9-92.6 (26.0 (20. referred to as monobutyl phthalate (MBP).2-159) 92.7 (18.0) 21.3) 36.8-25.3 (42.2-23.8-123) 101 (90.0-32.5 (29.3) 23.2) 42.4 (84.2 (19.4-26.4 (19.5) 47.1) 25.0 (72.1) 23.3-79.3-24.1-75.3) 26.7-42.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.9-101) 77.6-36.5-53.5) 26.1-20.0) 30.3 (17.4-60.1) 47.4) 22.0) 20.6) 71.3-21. interval) 24.0-24.6-37.6-24.1 (28.7-111) 64.5-117) 95.7-106) 69.3 (56.1 (17.0 (78.3 (51.0 (23.7-34.7-92.2-114) 73.7) 28.7 (33.3-60.7 (28.6) 46.2-22.3) 40.3 (37.0) 38.0-51.4) 59.4 (35.9-79.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.0 (31.7-20.7 (70.6-20.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.2 (17.8) 23. *In the 1999-2000 survey period.7-91.9) 21.2 (18.7-42.3-85.3 (36.1-24.5-44.2 (58.6-44.9 (17.0 (36.2 (75.2 (79.3-136) 137 (107-162) 119 (90.7 (24.0 (25.4-25.1 (19.4) 20.6-113) 108 (90.8-111) 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 23.3) 19.0) 120 (98.2-63.1-22.6 (16.4 (38.2 (74.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26. Survey Geometric mean (95% conf.4 (35.8-119) 90.3 (60.5-121) 106 (94.7-117) 118 (108-143) 93.7) 42.1 (51.6 (44.7 (18.2) 62.2 (21.0 (30.4 (21.5) 37.1 (16.7 (16.2-32.7-34.8 (57.8) 43.2-87.6 (55.1) 23.1 (19.6) 21.9-42.5) 34.S.5) 17.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.7 (38.1 (62.2) 68.3-96.9 (20.2-93.4-31. Fourth National Report on Human Exposure to Environmental Chemicals 267 .4-20.2) 32.2 (59.5 (59.2 (78.2-56.8) 48.0 (45.5 (59.3 (30.2) 26.2-21.4-18.4-159) 107 (84.9) 46.1) 36.6 (48.2 (20.6) 17.1 (41.7 (19.1-80.4.1 (19.7 (22. 1.6) 35.4 (35.8-42.5 (30.8) 19.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.8) 75th 51.7) 52.9) 26.5-43.5) 24.6-29.4) 64.0) 84.4 (72.7-24.6-49.3-76.4) 52.0) 117 (104-131) 112 (84.7-26.9-53.2) 20.6) 80.6-69.9) 75.7-127) 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 22.7 (64.0) 31.3) 24.0-58.3) 21.6 (61. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.0 (18.1) 20.0-26.8-22.1-82.0-21.3 (23.9) 36.1-27.9-22.7-124) 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.6-29.8) 62.4 (36.3-67.5) 65.6-40.1-92.5-27.9 (79.1 (31. 01-02.7) 74.2 (25.9.8 (19.5 (74.9) 18.2-24.9) 71.9) 29.4-44.8-132) 95.3 (30. and 03-04 are 0.1) 17.9-22.7 (51.3 (23.2) 38.1-51.1 (36. see Data Analysis section) for survey years 99-00.6 (19.0 (15.6 (32.2) 90th 98.3-145) 85.2 (21.1) 31.1-29.5 (28.9-114) 116 (97.6-31.1 (58.5) 20.6) 39.9 (79.6-48.1 (54.3) 18.0) 27.8) 58. and 0.5) 78.1 (34.1) 30.7-121) 97.5-60. respectively.0-19.

6-19.0 (71.9 (30.3-38.9) 49.6) 23.3 (71.0 (27.6 (27.0) 108 (71.7-39.4 (56.6-128) 96.4 (16.8-24.7) 19.6-23.0) 94.5 (18.1 (21.9-68.8 (16.5 (15.6) 24.8 (33.6-44.2) 74.0) 70.2-86.2-27.5) 84.1) 20.6 (41.7-80.1 (32.8 (22.6-32.3 (52.3) 33.1 (29.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.3 (17.5-15.2-16.9 (56.2) 16.4 (17.5) 134 (93.3-32.4 (50.2 (38.5-30.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.7 (12.9 (19.1) 42.9-36.2-22.0-47.9) 19.9 (39.6-24.1 (61.3 (48.8 (13. interval) 22.4) 21.7 (19.7-26.3) 35.4 (33.3-17.1-99.9 (35.3 (46.9) 20.1 (15.3-81.9-105) 85.5-18.3) 33.6-119) 63.3 (16.8-235) 137 (108-198) 88.1-99.6 (25.3) 21.4) 16.8-24.0 (69.1-21.0) 41.1) 17.8 (18.8 (50.9 (21.7-51.0-17.9-84.9-49.9-14.1) 37.9 (30.0) 53.4-135) 71.8 (18.9 (35.8) 17.4 (16.7 (57.9) 28.6) 24.8 (25.1-23.0 (26.5-70.4 (17.9) 30.0 (50.0-60.9) 39.5 (64.6 (19.3-21.0 (16.6-50.2 (35.5) 21.0 (15.7-20.3 (21.3-71.3 (60.9-34.0 (70.7 (14.0 (43.4 (19.8) 23.6-92.9) 91.6-155) 91.2-106) 64.9 (64.5-37.7 (20.2) 65.2-61.4 (31.5) 17.7-37.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.3 (52.6 (57.6-26.2) 31.4 (50.9 (20.1) 22.8) 28.6) 38.6-53.4-164) 96.3) 19.3-114) 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 17.4 (31.8 (65.0) 81.0 (61.5 (81.7-42.8) 40.3 (76.7 (54.0 (18.5-23.2) 159 (102-263) 147 (93.1) 50.6 (25.1) 44.1) 21.3 (17.8 (17.0 (19.3 (19.6) 14.7 (81.8-23.S. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.0) 29.4 (45.8-32.4 (20.0) 26.5 (18.4-34.1) 53.4) 19.4 (13.0) 25. population from the National Health and Nutrition Examination Survey.2) 59.6-43.0-113) 104 (83.7 (16.2 (83.8) 75th 38.3-20.9) 62.2 (19.2 (19.3-26.6) 65.8) 19.4-76.7) 42.6) 18.5-64.0 (18.5-142) 81.5-21.6-27.6-24.1 (34.8-43.7 (43.2-22.0 (20.6-22.7-28.7 (73.2-73.2-18.2 (16.0 (52.4-72.5-16.5-76.0 (34.3) 17.9-68. 268 Fourth National Report on Human Exposure to Environmental Chemicals .4-131) 81.4-103) 117 (83.8) 20.3) 19.3) 20.9 (73.6 (29.3 (24.9) 14.2-108) 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.6 (17.6) 25.3 (42.0-90.1 (56.6-74.4 (53.5 (30.8) 13.3-106) 74.6 (72.5) 82.5) 91.6 (61.3) 67.8) 17.2-85.4 (18.4) 15.1) 35.2) 21.4) 15.1-32.4 (23.7 (60.8 (18.4-61.5 (14.5) 60.3 (69.6) 39.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.3-18.7 (27.5-41.0) 28.3 (55.8) 30.4 (47.3-23.1-128) 97.0) 35.7-19.6) 64.2-21.3-49.6-23.9 (30.9 (16.4) 20.8) 34.0) 19.3 (17.8) 35.4-47.5-142) 89.9) 52.3) 59.7-21.6) 31.6-28.7-78.4) 62.7 (28.9-70.9) 24.8) 22.7 (60.0) 75.7-23.6-42.1-18.3-78.7) 36.3-39.9 (58.9-100) 86.6) 37.2-28.5-22.6-16.4 (68.4) 53.6) 34.8) 34.2-179) 84.4 (37.0) 59.4) 51.4-65.6 (74. Survey Geometric mean (95% conf.6-44.3-21.3 (28.7-19.9-38.0) 55.8) 63.5) 39.0-75.0-41.6 (31.9-56.8) 17.1 (46.1-62.7) 20.9-26.4 (31.1) 20.3) 52.6) 83.4-24.9 (37.0-19.1-83.3) 18.3-40.2-48.0-38.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.5) 90th 68.2-22.1) 61.0-92.8) 20.

Richthoff J. Yoshida K. Green RA. Reidy JA. Available at URL: http://cerhr. J Androl 2004.niehs. Giwercman A.210(3-4):319-33. Wiesmuller GA. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Springall C. Drexler H. Ryan L. Bull Environ Contam Toxicol 2002. Camann DE. Drexler H.nih. 112(5):A270]. Masunaga S. Duty SM.111(14):1719-1722. Needham LL. et al.Phthalates References Adibi JJ. Scotter MJ. Dobler L. Caudill SP.208:237-245. Koch HM. et al. Research Triangle Park (NC). Eckard R. Urinary levels of seven phthalate metabolites in the U. 2000 [online]. Silva MJ. Atlanta (GA). Silva MJ. Levels of seven urinary phthalate metabolites in a human reference population.html. Food Addit Contam 2001. Hauser R. Jedrychowski W. Chen Z. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Hagmar L.16(4):487-493. Environ Health Perspect 2003. Caudill SP. Anderson WA. Koch HM. Meeker JD. Silva MJ. Silva MJ. Hum Reprod 2007. Singh NP. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Gans G. Epidemiol 2005. Rylander L.22(3):688-695. Environ Health Perspect 2000. Wittassek M. Int J Hyg Environ Health 2005.210:21-33. Int J Hyg Environ Health 2007. Koch HM. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Sampson EJ. Phthalate monoesters levels in the urine of young children. Centers for Disease Control and Prevention (CDC). NTP-CERHR. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Barr D.18(1):122.S. Duty S. Barr DB.112(3):331-338. Environ Health Perspect 2006. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. 4/20/09 Silva MJ. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Angerer J. Castle L.114(9):1424-1431. Reprod Toxicol 2004. Malek NA.93:177-185. Itoh H. et al. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.18(12):10681074. Schettler T. Calafat AM.gov/chemicals/ phthalates/dbp/dbp-eval. Environ Health Perspect 2004. Caudill SP. Bolte G. Brock JW. Hu H. Urinary phthalate metabolites and biomarkers of reproductive function in young men.108(10)979-982. et al. Needham LL. Brock JW. Jacek R. David RM. Perera FP. McKee RH. Massey RC. Sanchez GN.68:309-314.25(2):293-302. Hodge CC. Ryan L. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. et al. Jonsson BAG. Butala JH. Rossbach B. Pirkle JL. Third National Report on Human Exposure to Environmental Chemicals. Int J Hyg Environ Health 2007. Hilborn ED. Fromme H. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. 2005. Environ Res 2003. et al. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Helm D. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Boehmer S. Calafat AM. et al. Weuve J. et al. Blount BC. Prenatal exposures to phthalates among women in New York City and Krakow. Angerer J. Poland.

500) < LOD 1.700) .50) .400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .S.500) 1.00-2.400) 1. population from the National Health and Nutrition Examination Survey. 270 Fourth National Report on Human Exposure to Environmental Chemicals .300-.400-.300 (.2.400-.400-.200-.600) .500) 1. 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.300-.300-.50) .900-1. Survey Geometric mean (95% conf.300-.400 (.400) 1.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.600) .00-3.700) .400-. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.300 (<LOD-.00 (<LOD-1.70 (1.70 (1.400-.600) .500) 1.00) .600 (.300-.500) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300 (.400 (<LOD-.300-.300-.80) .200 (<LOD-. polyvinyl acetate.400 (<LOD-.500 (. and 03-04 are 0.200-. 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) < 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 1.400 (.500) . People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.300-.200-.00 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. including nitrocellulose. and polyvinyl chloride.500 (.400-.500 (.500) < LOD < LOD .300-.00 (<LOD-1.9.400 (<LOD-. 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.10 (. which may vary for some chemicals by year and by individual sample.300-.500 (.400 (.500) < LOD < LOD .20) . 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.200-.700) .500) .600) < LOD .600) .500 (.400 (. < LOD means less than the limit of detection. only levels at or above the 90th percentile could be characterized. 01-02. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.300 (.70) .300) < LOD .500 (.70) .300 (.10 (<LOD-1.90) . and 0.400 (<LOD-.Phthalates Dicyclohexyl Phthalate CAS No. 0.600) . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.500 (.400 (.500) . and polymers.400-.300) < LOD . In this Report.200-.300 (.300 (.500-. see Data Analysis section) for Survey years 99-00.400 (.200-.10 (<LOD-2.400) < LOD < LOD .10) .400 (.10 (<LOD-1.3. resins. respectively.300 (.400) < LOD 1.500 (.500 (.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 .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 .

00 (<LOD-3.270) < LOD .53) .400-.590 (.740) < LOD < LOD .590 (<LOD-.630 (<LOD-.770) < LOD 2.530-1.660) < LOD < LOD .670 (<LOD-.00) .22 (<LOD-1.830) 1.390 (.330 (.43 (1.290-.67 (1.880 (.S.310) < LOD .530-.690 (.690) < LOD < LOD .250 (.510 (.16) .82) .770-1.500-.44) .06) .330 (.310-.33) .910 (.220 (<LOD-.450 (. Survey Geometric mean (95% conf.510-.490) .17) .670-1.740) .940 (.630 (<LOD-.610 (.500 (.910 (.16 (<LOD-3.450 (.260-.240-.480 (.06) .770-1.500) 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 .400-.660) .12-1.10) .690-1.910 (.530) 1.82 (1.590) 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 .790-1. Fourth National Report on Human Exposure to Environmental Chemicals 271 .770-1.620) < LOD .420-.74) .170-.770 (.53) .14 (<LOD-3.54) .360-.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 1.410 (.470) 3.530) 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.11) .500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .54-6.910 (.470 (. 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.420-.710) .05) .380 (.36-1.350-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.530 (.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.500) 3.560) 1.420-.34) .370 (<LOD-.690) < LOD 2.33 (<LOD-3.800-1.380-.54 (<LOD-2.950 (.18) .

9 (61.3-103) 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. Products that may contain DEP include perfumes. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. 2003) and African-American women in Washington.3 (74. deodorants. In contrast.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75.Phthalates Diethyl Phthalate CAS No.3 (82.. Biomonitoring Information MEP levels in the NHANES 1999-2000. see Data Analysis section) for Survey years 99-00. and hand lotions. population from the National Health and Nutrition Examination Survey. 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. 0.4 (62.7) 71. shampoos. 2007).S.9. and 03-04 are 1. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. respectively.1 (71. particularly those containing fragrances.2. 272 Fourth National Report on Human Exposure to Environmental Chemicals . People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine..2-102) 95. 2002).8-111) 85. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. DC (Hoppin et al. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 01-02. colognes.. and 0. soaps.7 (70. 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.9-92.5) 81. 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 91.4.1-93. and also in men attending a Boston infertility clinic (Hauser et al. 2001-2002.

2002). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2003) were slightly lower than levels found in NHANES 2001-2002. 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.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79.2 (66.0 (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. 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. 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.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 .5-113) 122 (93. 2004). Median MEP levels found in a small sample of German residents (Koch et al. 2005). 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.3-105) 87.6 (77.6 (65.. Analysis of NHANES 2001-2002 showed similar findings. Other population estimates also differed by sex and race ethnicity (Silva et al.. This age-related trend is opposite the direction seen for other phthalates.9 (82..7-110) 81.5-114) 101 (87.Phthalates 2002 (Brock et al.S. In an analysis of NHANES 1999-2000.9-110) 96. with adjusted geometric mean levels of urinary MEP that increased with age (CDC.

Brock JW.93:177-185. Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 2002.110(5):515-518. Reproducibility of urinary phthalate metabolites in first morning urine samples. Caudill SP. Drexler H. Hum Reprod 2007. Needham LL. Hauser R. Environ Res 2003. Silva MJ. Environ Health Perspect 2004. Reidy JA.111(14):1719-1722. Ryan L. Prenatal exposures to phthalates among women in New York City and Krakow. Caudill SP. 274 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Davis BJ. et al. Koch HM. Camann DE. Jacek R. Poland. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Perera FP. Meeker JD. Silva MJ. Environ Health Perspect 2003.68:309-314. Jedrychowski W. Singh NP. Hilborn ED. Duty S. Angerer J. Barr D. Atlanta (GA). Urinary levels of seven phthalate metabolites in the U. Baird DD. et al. et al. Brock JW. Bull Environ Contam Toxicol 2002. Barr DB. Phthalate monoesters levels in the urine of young children.22(3):688-695. Rossbach B. Centers for Disease Control and Prevention (CDC). 112(5):A270]. Malek NA.S.112(3):331-338.Phthalates References Adibi JJ. Hoppin JA. 2005. Hodge CC. Silva MJ.

6) 14.86) 2.10 (3.60) 9.4) 22.80-3.40) 4.60 (6. interval) 3.10 (2.10-3.8 (19.00-3.9-19.90) 7.9 (29.9) 18.3-64.3 (10.40-12.40) 2.10) 3.1-17. 2002.70-2.1-27.60) 90th 14.77 (2.21 (2.70 (5.7) 6.00) 19.1982). respectively.15 (1.2) 6. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).30-6.9 (17.7-32.23 (3.0) 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 3.4) 20.0 (9.7 (14.9-48.10-2.30-8.2 (7.79) 2.80 (2.2) 4.9 (17.86) 2.27 (3.1-17.2) 42. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.50-5.5 (25.62) 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 5.96-5.50-11.30 (4.6 (10.3 (19.90) 4.93) 6. Fourth National Report on Human Exposure to Environmental Chemicals 275 .57 (3.60) 4.80-5.7) 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 3.42) 3.90 (1.30 (6.40) 8. 1.9) 13.40) 9.3-49.70 (7.37-4.10) 2.12 (4. population from the National Health and Nutrition Examination Survey.4-40.3 (24.27) 2.6 (12.90-11.7-18.57-7.5) 21.10 (4.82 (3.60) 7.56 (2.1-48.9) 15.0 (21. Concentrations in plastic materials may reach 40% by weight.40 (2.1) 19.87-2.4 (16.70-4.6-130) 31.30) 2.5 (12.4) 13.6-28.8 (17.8) 17.5-17.5 (30.0-29.54) 4.00 (2.0) 23.50) 4.67-4.90-8.40-9.7) 22.25-3.4-27.30-13.7 (17.0-18.50 (3.32 (3.50 (7.50-14.20 (1.70-6.00-3.70) 16.5) 19.70) 2.00) 2. and in humans.9-57.50-6.80 (1.30-11.4) 7.5) 23.8) 15.07-4.70 (3.50-3.24-4.10 (3.20 (3.0 (17.0 (14.70-5.40) 11.10) 3.5 (18.10-5. Following ingestion.50-3.2) 29.50) 9.82) 3. and 03-04 are 1.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70-8.92) 4.1 (8.2) 23.85 (3.3) 52. ATSDR.80 (8.94-3.90) 1. 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.03-2.80) 13.40-1.00) 2.5) 43.4) 6.2-28.50 (3.2 (10.5 (24.2-39.4) 23.80 (4.0.40-8..7) 27. and blood product storage and intravenous delivery systems.80 (8.90) 4.9 (15.6-23.69) Selected percentiles ( 95% confidence interval) 50th 3.1-29.80) 9. mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).40 (4.23 (2.10-11.1) 25.9-26.9 (26.84) 3.0 (19.9) 5.30 (3. which is used for many consumer products.5) 37.5-28.3) 28.4 (13.00 (4.70-3.0 (13.10) 3.10 (4.00) 5.20 (3.6) 9.5 (12.1 (10.3-26.91-3.92-2.40) 4.60) 10.40) 75th 7.4-42.5-27.9) 13.26-2.5) 40.90) 3. packaging film.5 (12.50-2.35 (1. After parenteral administration.1 (8.5 (18. see Data Analysis section) for Survey years 99-00.90 (4.2 (29.20 (3.50-16.3-25.0-18.00) 11.0) 35.4-20.7-58.9-55.00 (5.50-6. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.16 (2.70 (2. 1982.5 (31.9-49.50-5.85) 4.S.21 (2.3 (11.51) 4.40-11.7) 8.60) 8.0) Total 4.10-3.2-17.90-3.68 (3.6) 5.10-4.10) 4.80-4.43 (3.0 (16.84 (2.70 (1.70 (3.60) 3.50 (2.9 (16.50-8. as glucuronide conjugates (Albro et al.9 (7.30 (7.2 (31.1