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CDC Chemical Exposure Fourth Report 2009 Americans

CDC Chemical Exposure Fourth Report 2009 Americans

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Sections

  • Introduction
  • What’s New in this Report
  • What’s Different in this Report
  • Data Sources and Data Analysis
  • Interpretation of Report Data: Important Factors
  • Interpretation of Report Data: Important Factors
  • Chemical and Toxicological Information
  • Acrylamide
  • Blood Tribromomethane (Bromoform)
  • Blood Trichloromethane (Chloroform)
  • Urinary Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone)
  • Urinary Bisphenol A (2,2-bis[4-Hydroxyphenyl] propane)
  • Urinary 4-tert-Octylphenol (4-[1,1,3,3-Tetramethylbutyl] phenol)
  • Urinary Triclosan (2,4,4’-Trichloro-2’-hydroxyphenyl ether)
  • Pentachlorophenol
  • ortho-Phenylphenol
  • Herbicides
  • Acetochlor
  • Alachlor
  • Atrazine
  • 2,4-Dichlorophenoxyacetic Acid
  • Urinary 2,4-Dichlorophenoxyacetic acid
  • Metolachlor
  • Urinary Metolachlor mercapturate
  • 2,4,5-Trichlorophenoxyacetic Acid
  • Urinary 2,4,5-Trichlorophenoxyacetic acid
  • Carbamate Insecticides
  • Carbofuran
  • Propoxur
  • Organochlorine Pesticides
  • Organochlorine Pesticide
  • Aldrin
  • Dichlorodiphenyltrichloroethane (DDT)
  • Endrin
  • Hexachlorobenzene
  • Hexachlorocyclohexane
  • beta-Hexachlorocyclohexane
  • gamma-Hexachlorocyclohexane
  • Mirex
  • Organophosphorus Insecticides: Dialkyl Phosphate Metabolites
  • Urinary Diethylthiophosphate (DETP)
  • Urinary Dimethylthiophosphate (DMTP)
  • Urinary Diethyldithiophosphate (DEDTP)
  • Urinary Dimethyldithiophosphate (DMDTP)
  • Urinary 3,5,6-Trichloro-2-pyridinol
  • Coumaphos
  • Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol
  • Diazinon
  • Urinary 2-Isopropyl-4-methyl-6-hydroxypyrimidine
  • Malathion
  • Urinary Malathion dicarboxylic acid
  • Pirimiphos-methyl
  • Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one
  • Pyrethroid Pesticides
  • Cyfuthrin
  • Urinary 4-Fluoro-3-phenoxybenzoic acid
  • Urinary cis-3-(2,2-Dichlorovinyl)-2,2-dimethylcyclopropane carboxylic acid
  • Urinary trans-3-(2,2-Dichlorovinyl)-2,2-dimethylcyclopropane carboxylic acid
  • Deltamethrin
  • Urinary cis-3-(2,2-Dibromovinyl)-2,2-dimethylcyclopropane carboxylic acid
  • Antimony
  • Arsenic
  • Barium
  • Beryllium
  • Cadmium
  • Cesium
  • Cobalt
  • Lead
  • Mercury
  • Molybdenum
  • Platinum
  • Thallium
  • Tungsten
  • Uranium
  • Perchlorate
  • Perfuorochemicals
  • Serum Perfluorobutane sulfonic acid (PFBuS)
  • Serum Perfluorododecanoic acid (PFDoA)
  • Serum Perfluoroheptanoic acid (PFHpA)
  • Serum Perfluorohexane sulfonic acid (PFHxS)
  • Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH)
  • Serum Perfluorooctane sulfonamide (PFOSA)
  • Serum Perfluoroundecanoic acid (PFUA)
  • Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH)
  • Phthalates
  • Benzylbutyl Phthalate
  • Urinary Mono-benzyl phthalate (MBzP)
  • Urinary Mono-isobutyl phthalate (MiBP)
  • Urinary Mono-n-butyl phthalate (MnBP)
  • Dicyclohexyl Phthalate
  • Urinary Mono-cyclohexyl phthalate (MCHP)
  • Diethyl Phthalate
  • Urinary Mono-ethyl phthalate (MEP)
  • Di-2-ethylhexyl Phthalate
  • Urinary Mono-2-ethylhexyl phthalate (MEHP)
  • Urinary Mono-(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP)
  • Urinary Mono-(2-ethyl-5-oxohexyl) phthalate (MEOHP)
  • Urinary Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP)
  • Di-isononyl Phthalate
  • Urinary Mono-isononyl phthalate (MiNP)
  • Dimethyl Phthalate
  • Urinary Mono-methyl phthalate (MMP)
  • Urinary Mono-(3-carboxypropyl) phthalate (MCPP)
  • Urinary Mono-n-octyl phthalate (MOP)
  • Phytoestrogens
  • Non-Dioxin-Like Polychlorinated Biphenyls
  • Polychlorinated dibenzo-p-dioxins CAS
  • Polycyclic Aromatic Hydrocarbons
  • Polycyclic Aromatic Hydrocarbon
  • Fluorene
  • Naphthalene
  • Phenanthrene
  • Pyrene
  • Benzene
  • Chlorobenzenes
  • Chlorobenzene (Monochlorobenzene)
  • Blood Chlorobenzene (Monochlorobenzene)
  • Blood 1,2-Dichlorobenzene (o-Dichlorobenzene)
  • Blood 1,3-Dichlorobenzene (m-Dichlorobenzene)
  • Blood 1,4-Dichlorobenzene (Paradichlorobenzene)
  • 1,2-Dibromo-3-Chloropropane (DBCP)
  • Blood 1,2-Dibromo-3-chloropropane (DBCP)
  • 2,5-Dimethylfuran
  • Ethylbenzene
  • Halogenated Solvents
  • Dichloromethane (Methylene chloride)
  • Blood Dichloromethane (Methylene chloride)
  • Blood Trichloroethene (Trichloroethylene)
  • Blood Tetrachloroethene (Perchloroethylene)
  • Other Halogenated Solvents
  • Blood 1,2-Dichloroethane (Ethylene dichloride)
  • Blood 1,1-Dichloroethene (Vinylidene chloride)
  • Blood cis-1,2-Dichloroethene
  • Blood trans-1,2-Dichloroethene
  • Blood 1,1,1-Trichloroethane (Methyl chloroform)
  • Blood 1,1,2-Trichloroethane
  • Blood 1,1,2,2-Tetrachloroethane
  • Blood Tetrachloromethane (Carbon tetrachloride)
  • Hexachloroethane
  • Methyl tert-Butyl Ether (MTBE)
  • Blood Methyl tert-butyl ether (MTBE)
  • Nitrobenzene
  • Styrene
  • Toluene
  • Xylenes
  • Appendix A. Procedure to Estimate Percentiles
  • Appendix B. Changes and Edits to Results Released in the Third Report
  • 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

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

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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

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Fourth National Report on Human Exposure to Environmental Chemicals

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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

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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

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Fourth National Report on Human Exposure to Environmental Chemicals

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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

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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

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Fourth National Report on Human Exposure to Environmental Chemicals

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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

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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

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2-Dichloroethane (Ethylene dichloride) 1.2'.2'.4-Tribromodiphenyl ether (BDE 17) 2.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .2.3-Dichlorobenzene (m-Dichlorobenzene) 1.4-Dichlorobenzene (p-Dichlorobenzene.5.3.1-Trichloroethane (Methyl chloroform) 1. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.2-Dichloroethene Dichloromethane (Methylene chloride) 1.5.2-Dichloropropane 2.3’.5'-Hexabromodiphenyl ether (BDE 153) 2.1-Dichloroethene (Vinylidene chloride) cis-1.1.4'.4’.4. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4'-Tetrabromodiphenyl ether (BDE 47) 2.4.5'-Tetrachlorobiphenyl (PCB 49) 2.gov/exposurereport/chemical_selection.2-Dichloroethene trans-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-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2'.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.1.4.4. Paradichlorobenzene) 1.4.3'.4.4.cdc. Table 1. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.6.4'.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 2.6-Heptabromodiphenyl ether (BDE 183) 2.2-Dichlorobenzene (o-Dichlorobenzene) 1.4’.6-Pentabromodiphenyl ether (BDE 100) 2.5. The process for selection is described at http://www.2'.4.5'-Tetrachlorobiphenyl (PCB 44) 2.3.2'.2'4.2'.5'.2-Trichloroethane Trichloroethene (Trichloroethylene) m.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.4'.4'.2'.4.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.4.2'3.1-Dichloroethane 1.6'-Hexabromodiphenyl ether (BDE 154) 2.2’.What’s New in this Report What’s New in this Report In this Fourth Report.1.4'-Tetrabromodiphenyl ether (BDE 66) 2.3.2'.5.4'-Tribromodiphenyl ether (BDE 28) 2.3.4'-Pentabromodiphenyl ether (BDE 85) 2.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.3-Tetramethylbutyl] phenol) Triclosan (2.2'.5’.5-Pentabromodiphenyl ether (BDE 99) 2.4.html.4'.4.1.

. 2003-2004) have been re-computed by use of this improved procedure. Percentiles for all three NHANES survey periods (1999-2000.1). Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period.g.. Details of this procedure are provided in Appendix A. Only slight differences should be noted when one compares the recomputations to previous releases of the Report.5-dichlorophenol for the 1999-2002 survey periods. Explanations for each change are provided in Appendix B.4-dichlorophenol and 2. the presence of an interference) that produced results of inadequate quality. Data for other pesticides are included only for 1999-2000 and 2001-2002. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. urinary 2. 2001-2002. five results that all have the value 90. Fourth National Report on Human Exposure to Environmental Chemicals 3 .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.g. and these data will be included in the next release of the Report.

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

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

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

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

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

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

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

3 (55.S.7-64. In the general population. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.0-58.S. and well below doses known to cause nerve damage or carcinogenicity in animals.7) 58.6-66. and in some cosmetics.S. are heated at temperatures used for frying and baking.0-108) 152 (139-175) 126 (111-142) 108 (86. and cosmetics (NTP-CERHR.3-71. glycidamide.S.3 (53.6) 90.5 (74. soil conditioners.6-104) 82. 217 million pounds of acrylamide were produced commercially in the U.2 (58.0) 57.5 (52.8 (81. EPA.0.1-64. the main source of exposure is from the diet. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.9) 57.5) 58.1-64. People may be exposed to acrylamide from foods. FAO/WHO.0 (69.9-61. and is either metabolized to the reactive epoxide.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.2-93. gels.0 (57.5) 66.7) 75th 79. EPA. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.2) 57.1 (47.5 (79. acrylamide has produced upper airway irritation following inhalation of high levels. in some sealing grouts.8-55.9) 75.3) 63.4 (53.5 (44.4-76. such as potatoes and some grains. or to glutathione conjugates (Calleman et al. 2002).4-60.7) 73. Elimination occurs mainly in the urine as mercapturic acid conjugates.8 (57.9 (69.9 (54.4 (54. Polyacrylamides are useful water-compatible polymers used in water treatment. Tareke et al.8-57.. Acrylamide is not thought to accumulate in the body at environmental doses.7-60. and from dermal contact with products that contain residual acrylamide.8 (52.6 (81. smoking. Survey Geometric mean (95% conf.6-61..7) 96.7 (55.2-77.4) 57. 2005.9-52. 2005).1) 53. ocular and dermal irritation from direct contact with acrylamide containing materials.0) 85.0 μg/kg for adults (FAO/ WHO.6) 71.0-49.1-61. Recently.5-85.4 (59.9 (60.6-75.4-60.3) 70.8 (91.9-105) 86.4) 57. but are generally above the U. 2005). 2004).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. Commercially.2 (62.6) 73.0 (53.7 (58. 1990.4) Selected percentiles ( 95% confidence interval) Sample 95th 192 (168-217) size 7101 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 54. pulp and paper production. Estimated intakes in children are about twice that of adults (DiNovi and Howard.4 (54. Fourth National Report on Human Exposure to Environmental Chemicals 11 .0-66.2 μg/kg/day (U.9) 58. EPA reference dose of 0. 1994). 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. acrylamide is synthesized and used in the production of polyacrylamide polymer. (NTP-CERHR. widely distributed in tissues. Since acrylamide has limited volatility and high water solubility.3-2.7 (63. but can covalently bind to form adducts with proteins. and in the synthesis or compounding of dye materials. 2005). In humans.5-80.4) 100 (89. 2005). as an absorbent in disposable diapers.9) 63.1 (73. 2006.2-59.2-118) 98.1) 62.6 (51. it was discovered that acrylamide is formed when starch-rich foods.2-91.2-70. see Data Analysis section) for Survey year 03-04 is 3.6 (56. Fennell et al. population from the National Health and Nutrition Examination Survey.S.6-108) 61. 2005).0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD. Natural substances in the food are converted to acrylamide.6) 50. interval) 61. mineral processing. in permanent press fabrics. These estimated intakes are hundreds of times lower than occupational exposures.1 (83.4-83.7 (65.1 (88.1-57. In 1997.1) 55.2) 57..4-89. FDA. drinking water.7-64. and binding agents. Animal studies indicate that acrylamide is well absorbed.6-65.1) 46.1 (52.0 (67. 2006).4 (51.2 (75. and an average daily intake is estimated as 0.3) 86.2-114) 163 (147-191) 96.2-67. 2004. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.Acrylamide Acrylamide CAS No.7) 54. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.1) 101 (95.

9-77..2 (72. 2008). to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.0-62.3-101) 95.2) 65.2) 87.5) 75th 85. Rice. respectively) are markers of integrated acrylamide exposure over the preceding few months.2-68..int/ ipcs/food/jecfa/summaries/summary_report_64_final.. thyroid.pdf. Survey Geometric mean (95% conf. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.4) 83. Additional information is available from U. EPA..4 (61. altered gene expression in testicular tissues (Yang et al.0 (75.1 (70. 2006). scrotal. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. male germinal cell injury. Axonal degeneration.7 (84.8-61. adrenal.. 2009).9 (81.1-60.5) 87.4 (57.epa. most non-smokers had levels less than about 100 pmol/gram hemoglobin.9) 75. 2005). 2005.2-91..0-93.8 (51..9) 65. Hagmar et al.2 (63.7) 90.1 (82. 2005.4 (81. 1997..1) 56.9-76. 2005. Animal studies have shown that acrylamide can cause nerve damage (neuropathy). Klaunig et al. Puppel et al. U. 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.S. dominant lethality).6-62.1 (56. EPA. 2002.5-64..8) 45. glycidamide (NTP-CERHR. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.Acrylamide occupational exposures. 2005. 2005. and neuronal DNA reactivity (Doerge et al...8 (44.7 (57.0-103) 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 64.9-78. In addition.9-64. 2005. 2006.7) 61. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 12 Fourth National Report on Human Exposure to Environmental Chemicals .. probably through its epoxide metabolite.7-86. NTP-CERHR. 2005. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al. although different analytic methods can affect results..5-94.8) 60.9 (58. 2005).9 (57. 2006).0. Glycidamide has been shown to react with DNA (Doerge et al. Levels of AHA and GHA reported the NHANES 20032004 sample are generally similar to those seen in several previous studies of non-occupationally exposed subjects (Bergmark et al. Mucci et al. 2005) have been demonstrated in animals. presynaptic nerve terminal binding (LoPachin. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. and cancer (mammary. AHA levels have been shown to increase with dietary intake (Hagmar et al. 2004. 2005).8-49. 2005.5) 71.5 (83..3) 59. and other sites) (FAO/WHO. Puppel et al.who.7-64.7 (61. 2001).8-48. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.3) 59. 2008). 2005).9) 87.4) 53.1-70.9-62.3) 59.3 (56.6-90.0) 94.1) 62. reproductive effects (reduced litter size.9) 59. 2005.7-62..1-62.S.6 (66.4) 46.6-64.9-138) 143 (130-159) 96. Acrylamide is clastogenic and can produce dominant lethal mutations.0 (80. Schettgen et al. see Data Analysis section) for Survey year 03-04 is 4.7) 60. uterine. 2005. Vesper et al.1 (57. fetal death.. U. 1997.4-65. After exposure ceases.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. Maniere et al.1-56.5 (59. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.5-92.4 (90..5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.2) 55. interval) 59.1 (66..4-103) 79.0) 118 (103-126) 121 (112-134) 113 (94. 2004). Vesper 2005) and smoking (Bergmark. 2005. 2005) and sperm DNA adducts (Xie et al.1) 60. EPA at: http://www.3) 85.5 (56.7 (87.5) 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.4-59.5 (42.4-98. 2003.7) 74..2-90..5-66.S.2 (56.6 (90. population from the National Health and Nutrition Examination Survey.0 (70. 2002.0 (52. Schettgen et al.4 (56. 2006) have been demonstrated after acrylamide dosing.4 (51. IARC classifies acrylamide as probably carcinogenic to humans.3-78.S.

Bruze M. Duale N. Toxicol Sci 2005.120(1):45-54. smokers and nonsmokers. July. 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.43:365–410.nih. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. et al.Acrylamide In occupational settings. Bergmark E. Mutat Res 2005. Toxicol Sci. Mechanisms of acrylamide induced rodent carcinogenesis. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Wilson KM. [Epub ahead of print] Dybing E.. 8-17 February 2005. April 13-15. Paulsen JE. National Toxicology Program. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Malmberg B. Fennell TR. Chem Res Toxicol 1997 Jan. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Scand J Work Environ Health 2001. Chicago. Nordander C. Illinois. 2001). Food and Drug Administration (FDA).10(1):78-84. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Tian G. 2/3/09 Hagmar L. Adv Exp Med Biol 2005. He F. Hagmar L. Magnusson AL. Snyder RW. 2001.. 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. Zhang S. Summer SCJ. 054472. Costa LG.Toxicol Appl Pharmacol 1994.html#u1004. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. da Costa GG. Bergmark E.561:21-37. 1994). Italy.niehs. Beland FA. Costa LG. 2/3/09 Perez HL. 2004. Wirfalt E. Perez et al. Calleman CJ. Maniere I.580(1-2):157-165. Farmer PB. Acrylamide neurotoxicity: neurological. Axmon A. 2/3/09 Klaunig JE. LoPachin RM. Godard T. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. 1993. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR).cfsan. Hagmar et al. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Twaddle NC.85:447-459.561:49-62. et al. Available at URL: http://cerhr. Mucci LA. Tornqvist M. Tornqvist M. Acrylamide intake through diet and human cancer risk. J Agric Food Chem 2008. Andersen M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. NIH Publication No. Paulsson B. Food Chem. References Bergmark E. Spicer R.27(4):219-226. Aprea P. 2006. Calleman CJ. Osterman-Golkar S. 1999). He F. Joint FAO/WHO Expert Committee on Food Additives. Uncertainties.fda. Fennell TR. Available at URL: http://www. Calleman CJ.. Adv Exp Med Biol 2005. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. February. Rosen I. Mutat Res 2005. 64th Meeting: Summary and Conclusions (FAO/WHO). Toxicol 2005. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation.. et al.who. 2005. Kautiainen A. morphological and molecular endpoints in animal models. Chem Res Toxicol 1990.126(2):361-371. Cheong HK. DiNovi M and Howard D.. CFSAN/Office of Plant and Dairy Foods. Burgess J. Bjellaas T. Bridson WE. 2009 Jan 8. Yang JS. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Toxicol Appl Pharmacol 1993. McDaniel LP. Human exposure and internal dose assessments of acrylamide in food. Metabolism and hemoglobin adduct formation of acrylamide in humans. Churchwell MI. Rome. Wu Y. and Research Strategies. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al.580(1-2):119-129. In another study. 6013-6019.pdf. et al. Laurentie M. 2004 Acrylamide in Food Workshop: Update Scientific Issues.gov/chemicals/ acrylamide/Acrylamide_Monograph.pdf. et al. Alexander J. 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. Kamendulis LM. The Updated Exposure Assessment for Acrylamide.int/ipcs/ food/jecfa/summaries/summary_report_64_final.3:406-412. Guffroy M. Haugen M. Becher G. Churchwell MI. Survey data on acrylamide in food: individual food products. Doerge DR. Doerge DR. Mutat Res 2005. gov/~dms/acrydata. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. smoking habits and gender. Available at URL: http://www.580(1-2):131-141. Bergmark E. Granath F.56.

Toxicol Lett 2002. Mutat Res 2005. Angerer J. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Lee MH. Sun H. The carcinogenicity of acrylamide.S. 2/3/09 Vesper HW.20(6):959-64. Reprod Toxicol 2005. Tareke E. J Agric Food Chem 2008. Tjaden Z. Vesper HW. September. Myers GL. Rydberg P. Eriksson S. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Liu K. Han DU. Tornqvist M. Licea-Perez H. Chemical Summary for Acrylamide.epa. Environmental Protection Agency (U. Office of Pollution Prevention and Toxics.Acrylamide glycidamide by gas chromatography-mass spectrometry. Rossbach B. U. Kutting B.epa. Toxicol Lett 2006. Karlsson P. Fu D. et al. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions.274(1):59-68. 2/3/09.134(1-3):65-70. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. propylene oxide. Adv Exp Med Biol 2005. Toxicological effects of acrylamide on rat testicular gene expression profile. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Anal Biochem 1999. Ospina M. Puppel N. et al. Agudo A. Drexler H. Yang HJ. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Int J Hyg Environ Health 2003. EPA). Integrated Risk Information System (IRIS). Mutat Res 2005 Feb 7.txt. Acrylamide. Hemoglobin adducts of ethylene oxide. a carcinogen formed in heated foodstuffs. Analysis of acrylamide.S. Schettgen T. Environmental Protection Agency (U. Choi JH. Angerer J. Lee SH. Vesper HW. Rapid Commun Mass Spectrom 2006.gov/iris/subst/0286. Rice JM. Chae C. Schettgen T. Ospina M. Jin Y. Fueller F.gov/chemfact/s_acryla. Drexler H.207(6):531-9.206(1):9-14.580(1-2):3-20. Gray JG.56(15):6046-53. Xie Q. Ingham L. Smith A. Angerer J.580(1-2):71-80. Benetou V.163(2):101-8.S. Schettgen T.19(4):527-34.S.htm. Meyers T. Available at URL: http://www. revised 1/3/06. Marko D. Han CH.50(17):4998-5006. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Drexler H. 1994. J Agric Food Chem 2002. Available at URL: http://www. Meyers T. EPA). Liu Y. Weiss T. Slimani N. U.561:89-96. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Int J Hyg Environ Health 2004. Broding HC. Letzel S. Hallmans G. Washington (DC). Ding X. Tjønneland A. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study.

360) .077) .950-1.015 ng/mL.066) .54) 1.210 (.94) 1.16) .70) 2.20) 1.428-.96) 2. DHHS.090-..62) 2.770-1.071 (.740-1.620-1.110) .14-1.70-2.630 (. 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.190-.050) .040 (. acute respiratory illness.350-.080) < LOD < LOD .320) .621-1.110 (. and 03-04 are 0.110 (.075 (.111-. emphysema.230) .44) 2.92) 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 .84-3.05) 1.070-.050 (<LOD-.726) .39) 3.050 (.22) 2.220) .66) 1.059-.770) . Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.088-.790) . 2006).073) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 15 .660) .060 (<LOD-.21-1.505 (.23 (1.850 (.19) .89) 1.077) .260) 1.087 (.180) .15 (2.68 (1. and 17% had an LOD of 0.180) . acute respiratory infections.062 (.110-.213) .131 (.120-.04 (1.600-1.87-3.108) * .910-1.060-.96 (1.300) .140-.310-1.42-4.470-.160) . ear problems. 2004).180) .95) 1.030-.302) .020-. stroke.580-1.510 (.12-4.370-.75) 1.860 (.070) .76 (1.39 (1.840) 3.197) .160-.500 (.040 (.047-.280 (.28) .030-.160 (.20 (.540 (.230 (. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.070 (<LOD-.62 (2.310) 90th 1.65 (1.15) 2.30) 2.154-.930 (. and various other disorders (U.99) 2.740-1.00) .800 (.710 (.180 (.02 (.160) .88 (1.50 (1.48-2.080) < LOD .140 (.20-2.66-3.S. and 0.148-.240 (.630 (.53 (1.12 (1.120 (.080-.090-.150) .058 (.55 (1.44 (2.200) 1.234) .190-.050 (<LOD-.057-.160 (.68) .40) .5% nicotine by weight (Kozlowski et al.188) .260-1.047-.32-2.17 (1.00) 1.68) 2.55-2.163) .080 (.21 (.167 (.S.63 (2.Cotinine Cotinine CAS No.12) 1.57) 2.14) .33-2.12 (2.120 (.480-1.78) 2.66 (1.45) 1. 2004).32-2.630 (.080 (.23 (2.77 (1.070) .053 (<LOD-.130 (.198) * .089) Age group 3-11 years 99-00 01-02** 03-04 .820) .086 (.950 (.080-.42 (1. Survey Geometric mean (95% conf.180 (.030 (.052 (<LOD-.520 (.20 (1.09-3.63-2.060) .05 ng/mL.960-1.130) . The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.120 (. and exacerbated asthma (U.450-.126) .670) .99) 2. 1998).106-.150) .110 (.163 (.050-.063) .050 (<LOD-.990) .11) .28-1.83-2.580 (.23 (.068) .015.061) < LOD .120 (.076-.44) 2.540-.220-.990 (.400-.920 (.430-1.770) . see Data Analysis section) for Survey years 99-00.124 (.570-1.49) 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.110-.77 (2. population from the National Health and Nutrition Examination Survey. DHHS. which may vary for some chemicals by year and by individual sample.120) .30) 2.068) .100-.480-.48-3.S.690 (.310-1.059-.92 (1.02) 1.094) .066 (.506 (.110 (. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob. respectively.087-.220) .040-.350-.140 (.997-3.60-2.137-.43 (1.88 (.137 (.14) .050-.570 (.533-.030-.050) .350 (.164 (.308 (.02) 1.312) .120 (.120-.050 (<LOD-.060 (<LOD-. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.115-.54 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.060-. < LOD means less than the limit of detection.50-4.087) < LOD < LOD .110) .09-3.145) .96-4.50) 3.47-3.38-2.410) . Children exposed to ETS are at increased risk for sudden infant death syndrome.93) .071) . 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) .175 (.187) .85 (1.625) .50-1.34 (1.18-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.153-.19-2.26-1.49) 1.49) 1.900-1.180) .190-.040 (.052 (<LOD-.144 (.060 (.110 (.104-. maternal exposure during pregnancy can result in lower birth weight.20) .060-.043-.23-2.164 (.30) * .216 (.730 (.140-.080-. 83% of measurements had an LOD of 0.01 (1.193) .201) .01) 3.080-.084) .19) 1.44 (1.32) 1.040-.09-2.180) .05.17) .054 (. cardiovascular disease.620 (.53-4. Cigarettes contain about 1.090-.77 (1.21-1.070) 75th .17 (.110-.54 (1.139) * .35 (2.160 (.81-2.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .142-. ** In the 2001-2002 survey period.060 (.310) .22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .79) 3.066-.

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

S. Department of Heath and Human Services. 1988-1991. Sosnoff CS. Respiratory nicotine absorption in non-smoking females during passive smoking.cancer.S. Maurer KR. Summary of Data Reported and Evaluation [online] 2004. Absorption and metabolism of nicotine from cigarettes. Jacob III P. Curtin LR. Cotinine as a biomarker of environmental tobacco smoke exposure. Filter ventilation and nicotine content of tobacco in cigarettes from Canada.7:369-375. Aiba M. Third National Report on Human Exposure to Environmental Chemicals. 1991. In Report on Carcinogens. Schwartz SS.nih.S. 1999. [online].fr/ENG/Monographs/ allmonos90. Coordinating Center for Health Promotion. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.275:1233-1240. U.niosh.gov/tcrb/monographs/10/. George CF. Warner K. Summary of Data Reported and Evaluation [online] 1986. Houseman TH. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Etzel RA. 1988-1991. BMJ 1975. Environ Health Perspect 2006. 4/13/09 U. Ethnic differences in N-glucuronidation of nicotine and cotinine. Pickett MA. the United Kingdom. Pharmacol Rev 2005. Atlanta (GA): 2005. Pollack HA. 4/13/09 International Agency for Research on Cancer. Soliman S. Jarvis MJ.php. Available at URL: http://www. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Exposure of the U. Department of Heath and Human Services. 4/13/09 Centers for Disease Control and Prevention (CDC). JAMA 1998. DHHS). J Pharmacol Exp Ther 1999.291(3):1196-1203. 4/13/09 Perez-Stable EJ. Tobacco related exposures. International Agency for Research on Cancer.php.pdf.4:313-316. Herrera B. Pirkle JL. Tobacco Smoke. Dollery CT.94(2):314-320.S Department of Health and Human Services (U. Vol 83. Mehta NY.iarc. Vogler GP. Lewis PJ. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. 2004.S Department of Health and Human Services (U.280:135-140. Kira S.S. National Institute for Occupational Safety and Hygiene (NIOSH). Hukkanen J. Available at URL: http://monographs.57(1):79115.cdc.gov/eid/rmca/critdocs/ criteriadoc/33. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 .63:139-43. Caudill SP. Pechacek TF. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Benowitz NL. Coordinating Center for Health Promotion. Jacob P III. Vol 38. Jacob P. Office on Smoking and Health [online] 2006.gov/ntp/roc/eleventh/profiles/ s176toba. Am J Public Health 2004.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Clin Pharmacol Ther 1994. Nicotine metabolism and intake in black and white smokers.S. iarc. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Available at URL: http://monographs.S. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency.niehs. et al. Bernert JT. et al. population to secondhand smoke: 1988-2002. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Centers for Disease Control. Bernert JT.15:302-307. Smoking and Tobacco Control Monograph 10 [online].surgeongeneral. Racial/ethnic differences in serum cotinine levels among adult U. Tob Control 1998. Sweeney CT. Benowitz NL. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. National Center for Chronic Disease Prevention and Health Promotion. Pirkle JL. Pechacek TF. 11th ed. Turner DM. Giovino GA. Herrera B. Tob Control 2006. Jacob P III. U. cigarette smokers: the Third National Health and Nutrition Examination Survey. Centers for Disease Control and Prevention.280:152-156. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Caraballo R. Flegal KM. Available at URL: http:// cancercontrol.gov/library/ secondhandsmoke/. Perez-Stable EJ. Centers for Disease Control and Prevention. Richter PA. Int Arch Occup Environ Health 1991. JAMA 1998. Modin G. References Armitage AK. Brody DJ. National Toxicology Program (NTP). Strauss WJ. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.18:188-204. and the United States. June. Benowitz NL. Fong I. available at URL: http://mtn. U. Brody DJ. Benowitz NL. IARC Monogr Eval Carcinog Risks Hum. Mowery PD. Tobacco Smoke and Involuntary Smoking. Epidemiol Rev 1996. Available at URL: http://ntp. Kozlowski LT. Trends in the exposure of nonsmokers in the U. DHHS).fr/ENG/Monographs/allmonos90.S.114(6):853-858. JAMA 1996. Benowitz NL. Metabolism and disposition kinetics of nicotine.pdf. Schober SE. 4/13/09 National Cancer Institute (NCI). 4/13/09 Iwase A. 1999-2002. IARC Monogr Eval Carcinog Risks Hum. Giovino G.56:483-493.

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

N-Diethyl-meta-toluamide (DEET) N. Sudakin and Trevathan. DEET is not genotoxic.130-.130-.110 (. DEET is also used in combination with dermal sun screens (U.110-.130-.gov/pesticides/.180 (.100-.. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. 134-62-3 General Information N. About 3-8% of dermally applied DEET is absorbed. population from the National Health and Nutrition Examination Survey. 2002). Survey Geometric mean (95% conf.100-.S. 1998). Neurological effects in humans. There are over 225 insect repellents brands containing DEET.100-.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 .210 (. including seizures and encephalopathy. EPA.100 (<LOD-.110 (. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. 2005). DEET is not a developmental or reproductive toxicant in animals (U.130) < LOD . and they range in concentration from 4% to 100%.N..130 (.100-. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.110 (. < LOD means less than the limit of detection.120-. After absorption.epa.N-Diethyl-meta-toluamide (DEET) CAS No. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . 1995.110 (<LOD-. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.S.EPA. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. 2003). and it has not been rated by IARC or NTP with respect to human carcinogenicity.140-. (Kolpin et al.130-.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.130 (.140 (.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 .190) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.180 (. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown..100-. 2002). DEET is not registered for use on agricultural commodities.140) < LOD .140) < LOD .N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.110 (<LOD-.S.220 (. have been reported as result of self-poisoning by ingestion or excessive dermal application.110-.EPA at: http://www. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.250) < LOD . Additional information is available from U.130) < LOD .180 (.560) < LOD .120-.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 . Its use is recommended for prevention of several vector-borne diseases. 2003).449 and 0.160) < LOD .270) 688 678 518 700 598 956 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.150) < LOD . 1998). DEET has low acute toxicity.EPA.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 19 .180) < LOD .S.520) < LOD .240) < LOD .130 (.170 (.S. Urinary N. DEET can be applied to clothing and the skin to repel biting insects.100-.170 (.140) < LOD . One survey detected DEET in 74% of sampled streams in the U.110 (.1. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. (U.

330 (.500 (.270-.370) < LOD . 2005)..410 (.280-1.230-.350-. 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. In this survey period. representative subsamples from NHANES 2001-2002. 2007).140-.410 (.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 .350) < LOD .170-. Urinary DEET levels as high as 5.130 (<LOD-. Survey Geometric mean (95% conf.150) < LOD .500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .N. 20 Fourth National Report on Human Exposure to Environmental Chemicals .290-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.320) < LOD .S.230) < LOD . population from the National Health and Nutrition Examination Survey.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.270 (.190-.200 (. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.190 (.240-.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.240) < LOD .S.190 (<LOD-..250) < LOD .330 (.440) < LOD . Urinary N.410-.350) < LOD .93) < LOD .150-.490) < LOD .250-.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.230-.250 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.630) < LOD .190 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .320 (.390-.300 (.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.270) < 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 .370-. 1992).270 (<LOD-.280 (.480 (. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.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 .640 (. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.

S.25:95-100. 1999-2000: a national reconnaissance. N.S. 4/9/09 U.gov/teach/chem_summ/ DEET_summary. Washington (DC): U.S. Selim S. U. 2005 Kolpin DW. J Toxicol Clin Toxicol 2003.36(6):1202-1211. Environmental Protection Agency (U. et al. Chemical Summary.EPA).S. Environ Sci Technol 2002. Available at URL: http://www.2:341352. Schoenig GP.16(1):10-13.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography.epa. and excretion of N. Human exposures to N. pp. Sudakin DL. Grzywacz JG. Quandt SA. U.115(8):1254-1260. EPA.EPA).S. Bell JW. Page BC. Tapia J. EPA 738-R98-010.S.epa.N. Lowry LK. Smallwood AW. Diethyltoluamide (DEET). Trevathan WR. Hartnagel RE Jr. Atlanta (GA).gov/oppsrrd1/REDs/0002red. pdf. Pharmaceuticals. J Anal Toxicol 1992. Thurman EM. Available at URL: http://www. Reregistration Eligibility Decision (RED): DEET. Environmental Protection Agency (U. Toxicity and Exposure Assessment in Children’s Health. DEET: a review and update of safety and risk in the general population. Third National Report on Human Exposure to Environmental Chemicals. hormones. Meyer MT. Centers for Disease Control and Prevention (CDC). Environ Health Perspect 2007. Gabriel KL.N-diethyl-mtoluamide following dermal application to human volunteers. 1993-1997.S. Zaugg SD.EPA. Veltri JC. and other organic wastewater contaminants in U. Barr DB.41(6):831-839.pdf. 2005. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Osimitz TG. September 1998. Chen H. Furlong ET.N-Diethyl-meta-toluamide (DEET) References Arcury TA. 1-118. metabolism. Fundam Appl Toxicol 1995.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. Int J Toxicol 2002. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Absorption. streams. Barber LB. DeBord KE.

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

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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

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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

J. Szigeti-Buck. K. Timms BG. 32 Fourth National Report on Human Exposure to Environmental Chemicals .nih.S. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. An evaluation of the possible carcinogenicity of bisphenol A to humans. Thurman EM. Belgium. Reidy JA. Rubin C. Hlywka JJ.116(1):39-44.Environmental Phenols References Akingbemi BT. and Hardy MP. Harazono A. Gender differences in the levels of bisphenol A metabolites in urine. Department of Health and Human Services. Myers CB. Twomey K. Zacharewski TR. Kim JC. Available at URL: http://cerhr. Cha SW. Available at URL: http://cerhr. Ispra.europa. Reprod Toxicol 2001.gov/chemicals/bisphenol/BPAFinalEPVF112607. vom Saal FS. Brussels. and other organic wastewater contaminants in U. Cohen JT. National Institutes of Health.pdf. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents.niehs. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Kuklenyik Z. Brine DR. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Italy. Bradley S. Kawamura N. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Available at URL: http://ec. 4. 2/4/09 European Commission. National Institute of Environmental Health Sciences. Hara K. and Hajszan. C. Serizawa S. Park S. Munro IC. Environ Sci Technol 2002.gov/chemicals/bisphenol/bisphenol. Han SY.. Fujii S.. 1999-2000: a national reconnaissance. Howdeshell KL. Hum Ecol Risk Assess 2004. Toxicol Sci 2002. Richter CA. J Am Dent Assoc 2006. Hughes C. Koulova AI. Kroes R.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Haighton LA. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. National Toxicology Program. N. 5: 505-523. Ekong J. November 26. Kiguchi M. Available at URL: http://ntp. MacLusky. Ema M. Proc Natl Acad Sci USA 2005. et al. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Calafat AM. Barton L. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Endocrinology 2008. Occup Environ Med 2002. Meyer MT. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Tyl RW. T. Barber LB. U. In vitro and in vivo interactions of bisphenol A and its metabolite.nih. Wong LY. Furlong ET. Pyo MY. Yang M. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Calafat AM.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325.14(2):149-157.S. Matthews JB.pdf .pdf . 2002. Kim CS. Shin HC. bisphenol A glucuronide. 2007. Environ Health Perspect 2005. Needham LL.pdf. Rat two-generation reproductive toxicity study of bisphenol A. et al. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Ye X. Pharmaceuticals. Marr MC. August 2001. Han SS.69(22):2611-2625. Tsugane S. Available at URL: http://ecb. Imai H.Scientific Committee on Toxicity. Chem Res Toxicol 2001. Caudill SP. Gray GM. Arakawa C. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. niehs. Environ Health Perspect 2008.10:875-921. Needham LL. Exposure of the U.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Calafat AM. et al. Sottas CM. Nippon Eiseigaku Zasshi 2004. 2/4/09 Fujimaki K. Yoshinaga J. Biochem Biophys Res Commun 2003. Klinefelter GR. Doull J.36(6):1202-1211. niehs. Koh WS. Endocrinology 2004. Research Triangle Park.. Kim YH. Keimowitz AR. Life Sci 2001. Reidy JA. Ecotoxicity and the Environment (CSTEE). Regul Toxicol Pharmacol 2002.59(9):625-628.149:988-994. DirectorateGeneral Health and Consumer Protection. Human Health. streams. Joint Research Centre Institute of Health and Consumer Protection. May 22. Ikka T.35(2 Pt 1):238-254. 2008. Zaugg SD. hormones.145:592-603.59(4):403-408. September. 2/4/09 Ouchi K. Leranth. Chung MK. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Hanaoka T. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).780(2):365-370. Barr DB. McConnell EE.312(2):441-448. European Commission.nih.S. Lynch BS. Needham LL. Bisphenol A.jrc. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP).113(4):391-395. Watanabe S. with estrogen receptors alpha and beta. 2003. Watanabe C. Joskow R.102(19):7014-7019. Kolpin DW. NC.pdf.eu/ health/ph_risk/committees/sct/documents/out156_en.137(3):353-362. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Thomas BF. 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. Barr JR. Rhomberg et al.68(1):121-146. Cunha G. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Furukawa M.

Lordo RA. Food Chem Toxicol 2002. Arch Environ Contam Toxicol 2003.Environmental Phenols Volkel W. Witorsch RJ. Dekant W.15:12811287. vom Saal FS. Jang JY. Colnot T. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. bisphenol-A. III. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Kim SY. Large effects from small exposures.40(7):905-12. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Csanady GA. Yang M.44(4):546-51. Morgan MK. Fourth National Report on Human Exposure to Environmental Chemicals 33 . An observational study of the potential exposures of preschool children to pentachlorophenol. Lee SM. Nagel SC.103(1):9-20. Hughes C. Welshons WV. Sheldon LS. Filser JG. Chang SS. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration.147(6 Suppl):S56-69.113(8):926-33. Chuang JC. Kawamoto T. Vom Saal FS. Environ Health Perspect 2005. and nonylphenol at home and daycare. Endocrinology 2006. Chem Res Toxicol 2002. Biological monitoring of bisphenol a in a Korean population. Environ Res 2007. et al. Wilson NK.

Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. The alkylphenol ethoxylates enter the environment through human use of products containing them. is used to manufacture alkylphenol ethoxylates.00 (1.80) 2.20-2. 2002).300 (<LOD-.300 (<LOD-. and to alkylphenoxycarboxylates. leading to inhalation as another potential exposure route (Rudel et al.369 (. industrial cleaners.500) . an alkylphenol. Urinary 4-tert-Octylphenol (4-[1.g.10) 1. orally administered 4-tert-octylphenol was well absorbed.30) 90th 1.400 (.50 (1. In 1999-2000.300 (<LOD-.500) 75th .20-2. 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. 2006.10) 2.300 (<LOD-.70 (1. which are anionic surfactants used in detergents.S. 34 Fourth National Report on Human Exposure to Environmental Chemicals .30-2. Less frequently.20) 1. the various alkylphenols have also been used as emulsifiers and modifiers in paints. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.10 (..600-1.477) . The alkylphenols can bioaccumulate in some fish.274-. and emulsifiers.1.500) . In rats.Environmental Phenols 4-tert-Octylphenol CAS No.50) 1. and was quickly eliminated from the blood (Certa et al.500) . impaired steroidogenesis..600-1. pesticides.507) * < LOD . which may vary for some chemicals by year and by individual sample.50-3.20) 2..600-1.600) 1. over 500.40) * 03-04 03-04 03-04 .2. and the polyethoxy chain may consist of up to 50 ethoxy units.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Disposition in humans has not been studied sufficiently.60) . Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. < LOD means less than the limit of detection.900 (.60-3.10-2. altered estrus cycles and reproductive outcomes.. During the 1980s and 1990s.300-.600) . They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).90) 2. Bian et al.50) . and some of their degradation products are toxic to aquatic life.900 (. population from the National Health and Nutrition Examination Survey. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.000 tons of alkylphenol ethoxylates were produced annually worldwide. and impaired spermatogenesis (e.400 (.357 (.40) 1.70 (1.20 (1.60-3.30 (1.500 (.500-1. 4-octylphenol monoethoxylate was detected in 43.268-.600-1. 2004).400 (.60-3. Katsuda et al. 2003.30) 1.400) 1.3.600) . including 4-tert-octylphenol.60-3.40) 2. testicular atrophy.5% of 139 U.20) 314 715 1488 03-04 03-04 * * .50) 1. Laws et al. streams in 30 states (Kolpin et al. to shorter chain alkylphenol ethoxylates. Several alkylphenols. have demonstrated estrogenic effects particularly when injected at high doses in animals. see Data Analysis section) for Survey year 03-04 is 0.30 (1. and from contact with some personal care products and detergents.200-.30 (1. 140-66-9 General Information 4-tert-Octyphenol.900 (. 1996). and through manufacturing waste streams (Warhurst. and some personal care products. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.20-2. fish) and drinking water. 2002).00) 1229 1288 03-04 03-04 03-04 * .700-1. through sewage.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 . 1995.80 (1.900 (.60-3. 1997. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.60-3.300 (<LOD-.30) 2.600) ..00 (.600-1.40 (1.299-.60) 613 652 1092 Limit of detection (LOD.30 (.20-2.80 (1.g.50-2.60) 1.389 (. Indoor and to a lesser extent.S.20-2. did not bioaccumulate.20-2. Ying et al. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. textiles.00 (.. 2000.10 (.70 (1.50) 1.900 (.10 (1..800-1.40) 2. altered neonatal sexual development.. 2000.500-1. Saito et al.600-1.70 (1. Blake and Boockfor.497) * .30 (1.80 (1.. Survey Geometric mean (95% conf. In the 1990s.200-..90) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50) .300-.40) 1.

43) 1.40-4.270 (.25) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. or their corresponding ethoxylates with respect to human carcinogenicity.00 (.540-1.610) .890-2. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.170-.. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.640-1.43-3.435 (.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 .40 (1.349) * < LOD .78) 3.269 (.337-.50 (2.Environmental Phenols Myllymaki et al.530) .59 (1.300 (<LOD-.11-2.76 (2.207-..270-. Yoshida et al. 2000. Kawaguchi et al.11) 1.1. In a small number of adult Japanese volunteers.620) . IARC and NTP have not rated octylphenol. Calafat et al.550-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. Survey Geometric mean (95% conf.81 (1.S.68-2.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2001.500-1. Urinary 4-tert-Octylphenol (4-[1.62 (1.53-3.54) * 03-04 03-04 03-04 . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.3...740 (. Fourth National Report on Human Exposure to Environmental Chemicals 35 . 2005.370 (<LOD-..470-1.630-1.03 (1.00) 2.85 (1. 4-tert-Octylphenol is not considered directly genotoxic.78 (1.10-2.71) 2.730-1. 2001).280-.160-.03 (1.11) 2. Sweeney et al. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.43) 1. 1999).420) .740 (.41) .260 (<LOD-.25-2.860 (.470) 75th .450) 1.470-1.08) 1.03-6.31-2.850 (.270 (.910 (.00) 2.570) .00 (.64 (. population from the National Health and Nutrition Examination Survey.199-.78) 1228 1286 03-04 03-04 03-04 * .276 (.25) 90th 1.00) 1.33) 3..22) .380 (<LOD-. 2003. It is unclear if estrogenic or other effects occur in animals through oral dosing.73) 2. representative subsample of NHANES 2003-2004.05-2.62 (1. 2004. 2004).320 (<LOD-.02-4.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.410 (.S.15) 1.400) . at lower or environmentally relevant doses (Blake et al.14) 314 713 1487 03-04 03-04 * * .65-3. Nagao et al.06 (2.620-1.20 (1.33 (2.62) .460 (.60 (1.770 (.36-3.59) 1.560) . Tyl et al. nonylphenol. 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.18-4.29) 2.67-2.384) * .450) .68) 2.17 (.31 (1. 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.96-4.

Yoshimura S. Taya K.37(20):4543-53. Makino T.18(1):43-51. Chen J. Wiegand HJ.121(1):21-33. Calafat AM. bisphenol A and methoxychlor in rats. Two-generation reproduction study with para-tert-octylphenol in rats. McCoy GL.15(6):683-692. Toxicol Appl Pharmacol 2005. Thurman EM. Indoor air pollution by alkylphenols in Tokyo. et al. Karjalainen M. Pharmaceuticals. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Toxicol Lett 2001. Myllymaki SA. Tyl RW.S. Carey SA. Yoshida M.36(6):1202-1211. et al. Paranko J. Furlong ET. Environ Sci Technol 2002. Boockfor FR. Kawaguchi M. Raychoudhury SS. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Nagao T. Haavisto TE. Saito Y. Phthalates. Brine DR. Spengler JD. et al. Indoor Air 2004. Inoue K. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Environ Health Perspect 2008.foe. Environ Sci Technol 2003.207(1):59-68.57(2):255-266.co. Nicol L. Yoshida M. Qian J.14(5):325-332. Watanabe G. 2/4/09 Ying GG. Onuki A. Sakui N. Toxicol Sci 2000. streams. Kookana R. Arch Toxicol 1996. prolactin. Warhurst AM. Blake CA. Brooks AN. Williams B. 1999-2000: a national reconnaissance. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. hormones.71(1-2):112-122. Inoue K. Myers CB. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. 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. Ono H. Blake CA. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. and testosterone. Sweeney T. Saito I. Needham LL. Bolt HM. Food Chem Toxicol 2006. Katsuda S. Watanabe G.116(1):39-44.folliclestimulating hormone.uk/resource/reports/ethoxylates_alkylphenols. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Biol Reprod 1997.Environmental Phenols References Bian Q.pdf. Maekawa A. Fail PA. J Chromatogr B Analyt Technol Biomed Life Sci 2004.799(1):119-125. Camann DE. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Marr MC. Meyer MT. and sertoli cell number. Usumi K. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Reprod Toxicol 2004. Available at URL: http:// www. Laws SC. Ferrell JM. Takai N. 1995. Wang X. Toxicol Appl Pharmacol 2000. Taya K. Horie M. Katsuda S. Exposure of the U. and other organic wastewater contaminants in U. pesticides. Seely JC. Regul Toxicol Pharmacol 1999.141(7):2667-2673. Korn LR. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Endocrinology 2000. polybrominated diphenyl ethers. Reidy JA. testis size. Toppari J. Izumi S.165(3):217-226.S. Nakagomi M. Boockfor FR. Kawaguchi M. Muller AM. Estrogenic activity of octylphenol. Ye X. and other endocrine-disrupting compounds in indoor air and dust. Nair-Menon JU.30(2 Pt 1):81-95. 2003. nonylphenol. Barber LB. Ito R. Zaugg SD. Anal Chim Acta 486:41-50. Millette CF. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Wong LY. et al. Bodman GJ.54(1):154-167. Environ Int 2002. Certa H. Cooper RL. Roche JF. Yoshimura Y. Rudel RA. Fedtke N. Maekawa A. Brody JG.44(8):1355-1361. Song L. Okada F. Seto H.28(3):215-226. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Kolpin DW. Reprod Toxicol 2001. Xu L. Takenaka A. alkylphenols.

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

6 (30.72-13.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.38-18.5) 13.5) 20.8-112) 30.4) 25. interval) 12.8) 9.3-67.9 (33.4.4 (38.5) 11.00-8.1) 13.48-10.8-85.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6-111) 33.6 (10.5 (11.20-11.9 (8.6) 90th 212 (172-241) 03-04 03-04 03-04 9.8) 116 (39.3) 10.8 (21.45-10.18 (5.60 (8.6-14.4) 73.7) 292 (151-432) 132 (78.3 (26.8) 7.6-15.9) 32.0 (36.70-16. Urinary Triclosan (2.90-10.74 (5.0) 9.55 (4.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1) 7.2 (27.7 (39.1) 11.2 (10.0-73.7 (28.1 (45.50) 10.6) 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 9.6-14.0) 49.3 (11.7 (11.2-14.60 (6.1 (15.32-14.5) 66.1) 14.4 (12.4) 75th 43.21 (6.45 (5.2 (25.S.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.4-19.8-63.8) 14.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.6) 31.6 (12.54 (8.9) 8.1-39.9-61.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.3-35.4) 51.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.94 (7.89-11.43-13.6) 12.0) 65.1 (8.20-13.0-19.4) 317 (231-433) 144 (96.5-86.20 (7.92-12.3) 47.7) 123 (36.2-46. Survey Geometric mean (95% conf.45-13.0 (26.93 (7.4-18.6 (9.48 (8.7 (9.1) 9.0-213) 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 .9 (11.0 (8.9) 75th 47.6-37.10-9.80 (5.10) 84. see Data Analysis section) for Survey year 03-04 is 2.29-12.S.2-58.6-20.20-10.1) 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 9.30-14.2) 13.4 (32.3 (8.50-10.16 (6.1) 50.6) 10.2) 9.7) 10.40-17.2) 12.0-15.1) 9.6-65.2 (13.0 (34.22-10.11-11.4 (11.0-15.2 (11. Survey Geometric mean (95% conf.9 (50.2-58.86-12.4) 357 (225-456) 203 (87. population from the National Health and Nutrition Examination Survey.3) 6.9-236) 193 (90.9) 7.6) 39.8-127) 37.Environmental Phenols Urinary Triclosan (2.4) 90th 249 (188-304) 03-04 03-04 03-04 8.3-31.7 (14.1) 9. interval) 13.00 (4. population from the National Health and Nutrition Examination Survey.4) 7.3-15.20 (7.1) 9.40-11.2 (37.3.8-60.4.0 (11.3 (9.82 (8.5-14.

Skirrow RC.7/2. Kolpin DW. Percutaneous penetration and dermal metabolism of triclosan (2. 4’-trichloro-2’-hydroxydiphenyl ether. Katsura E.66:1052-1056. Ferrer I.50(1-5):153-156. Reidy JA. phthalates. Mar Environ Res 2000. Foran CM. et al. Benson WH. Chemosphere 2007. Wigmore H. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. and other organic wastewater contaminants in U. Meyer MT. Odham G. Hernando MD. Watanabe N. Moss T. Chelimo C.4’-trichloro-2’hydroxydiphenyl ether). Hong HC.67(4):532-537.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Williams FM. Matsumura N. et al.S. Anal Chim Acta 1004. Aguera A. et al. Food Chem Toxicol 2000. J Toxicol Environ Health A 2006. Pinney SM.Environmental Phenols References Aiello AE. IMS Ind Med Surg 1969. Photolytic degradation of triclosan in freshwater and seawater. Environ Sci Technol 2002.4. Calafat AM. Hirano M. Clapson DJ. Wong LY. Arch Environ Contam Toxicol 1988. Bhargava HN. streams. Mezcua M. Britton JA. Nagao Y. J Invest Dermatol 1976. Pharmaceuticals.28(9):1748-1751. Aquat Toxicol 2006. Wolff MS. Osachoff H. Biol Pharm Bull 2005. and phenols in girls. Pharmacokinetics of triclosan following oral ingestion in humans. Ekstrand J.36(6):1202-1211. Shiratsuchi H. Ogawa H. Sandborgh-Englund G.45 Suppl 2:S137-S147. Ebersole R. Leonard PA. Lyman FL. Thurman EM. Windham G. Howes D. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Pilot study of urinary biomarkers of phytoestrogens. Zaugg SD. Br J Clin Pharmacol 1987. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Gilbert RJ. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. et al.115:116-121. Fernandez-Alba AR. Furia T.S. Bennett ER. Ishibashi H. Needham LL.24(3):209-218. population: 2003-2004. Gunderson MP. Gomez MJ. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Okui T. Barber LB.80(3):217-227. 1999-2000: a national reconnaissance. Levy SB. hormones. Urinary concentrations of triclosan in the U. Kaneshima H. Furlong ET. Aranami K. Veldhoen N. Ye X. Williams PE.23(5):579-583.38(2):64-71. Evidence of 2. Environ Health Perspect 2007.38(4):361370. Readman JW. Bodey GP. Developmental evaluation of a potential non-steroidal estrogen: triclosan. 4. Environ Health Perspect 2008. The oral retention and antiplaque efficacy of triclosan in human volunteers. Triclosan: applications and safety. Erratum in: Aquat Toxicol 2007. Am J Infect Control 1996.116(3):303-307.524:241-247. Teitelbaum SL.69(20):1861-1873. Adolfsson-Erici M. Larson EL.. Kanetoshi A.17(5):637-644. Toxicology of 2.83(1):84.

350-1.350) < LOD .350-1.350) < LOD < LOD 75th .350-. bactericide.350 (.00 (.350-2. utility poles and fence posts).83 (2.350 (.98 (1.30 (.350) < LOD . PCP use in the U. population from the National Health and Nutrition Examination Survey. so it is relatively non-persistent. 2002. ingestion of contaminated food or water.350) 90th . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.350-.350 (.350-.30) 1.350) < LOD .350 (. Effects including hyperthermia.350-.390 (.00) 1. plants.350) < LOD .350 (.350) < LOD .890 (.62 (.350 (.350) < LOD .530) 1.58-2. the elimination half-life may be a week or more (Uhl et al.960) 1. and it is used primarily as a preservative for wood to be used outdoors (e.350) < LOD .S.510-5.30 (.350-. Human exposure to PCP has become less common.00) 2.37) . The parent compound and conjugates. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350 (.500-2.350-2. and possibly of lindane (IPCS.48 (. After absorption.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (1.350-.350 (.350-2.990-2.590-1.350 (.350-.25 and 0.350 (.350) < LOD .350-.350-.75) 2.480-2. 1997).45-2. In the environment. along with small amounts of tetrachlorohydroquinone and conjugates. PCP is absorbed rapidly and well by all exposure routes.350-..76) 1. with repeated or chronic exposure. PCP is degraded by sunlight and metabolized rapidly by microorganisms.350 (.350 (. 1979).350-.32 (.48-2.78) 1.650) 1.350-. are eliminated in the urine. Since 1984.350 (.770 (.37 (.60) 1.60) 1.g. herbicide.42) 696 680 521 696 603 951 Limit of detection (LOD.64) 1. PCP is eliminated over a few days (Braun et al.10 (.30) . high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.90 (1.76) .30 (1.67) 1. and animals. < LOD means less than the limit of detection.350-. which may vary for some chemicals by year and by individual sample.S.23 (.10 (<LOD-1.350 (.18 (<LOD-1.350 (. Kohli et al.350 (. Survey Geometric mean (95% conf.350-1.65 (.350) < LOD . mollusicide. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.10) 1.47-3.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350-. PCP cannot be used on wood in residential or agricultural buildings.58-2. After a single dose.5.90) 1. PCP has been detected in soils.350) < LOD . algaecide and insecticide.350-.510-3.94 (1.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .350) < LOD . PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350 (.350-.90) 2.350-. 1976.50) 1.00) 1.30) 1.350) < LOD .350 (.54-2.04) 1.860-2. and metabolic acidosis were observed in CAS No.10) 1.73 (1.350) < LOD .70) 2. 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.350 (. hypertension.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 . and dermal contact with PCP-treated products.40 (.33) .. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.350 (.80) . 40 Fourth National Report on Human Exposure to Environmental Chemicals .51) 1.33-2.91 (1.650 (.350-.850-2.47-5.680-1.350-.890-1. water and sediments because of the large amounts that were produced and used historically.09) .390 (.94 (1.630 (.70) .350 (. PCP is distributed to most tissues and is not extensively metabolized.350-1.08-3.350) < LOD .65 (..350-2.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350-. Acute..01 (<LOD-1.. General population exposure to PCP may occur by inhalation of contaminated air.350) < LOD .660 (. has been restricted.980 (. air.350) .350) < LOD . To-Figueras et al. other polychlorinated benzenes.990 (<LOD-2.350-. 1986).350-.350-2.

40) 1.19) 2.800-1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .440 (. Among adults in the NHANES 1999-2000 subsample.650 (. respectively) (Becker et al.56) 1.950-1.00) 1.10 (1.320) < LOD .250 (.40-2.82) 1. 1989).48-2. respectively) (Seifert et al. and adversely affected thyroid function (U.S. 1991).920 (.26 (1.510-.730) < LOD .94 (1.900-1..19) 2. Fourth National Report on Human Exposure to Environmental Chemicals 41 .16 (.67 (1.360-.560) < LOD .Fungicides adults and children severely exposed to PCP through ingestion.470 (.06 (.490) < LOD .700-2.35) 1.67-3.310-.300 (.260 (.84-4.67 (1. Urinary Pentachlorophenol (creatinine corrected) Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.35-2.html.300 (.360 (.40) 1.220-.590-1.570 (.75) 1.290-.09-1.610 (.30) 1.52 (<LOD-1.270-. environmental levels) and health effects is available from the U.69 (1.650 (.83 (1.380-.gov/ toxpro2.270-.06-3.40) 1. inhalation.25 (1.330-.950-1.67 (1. EPA at: http://www.08 and 5. 2000).6 and 14.00-1.25) 1.94 (1.29-3.18) .78) 1.35) 1..73 (1. The U. population from the National Health and Nutrition Examination Survey.34 (.epa.25 (1. In NHANES 2001-2002 subsamples.310) < LOD .370 (.79) 1.52 (<LOD-1.800) < LOD 1. children in the 1980’s. More information about external exposure (i.320) < LOD < LOD 75th .0 mg/L.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .57 (1.84) 1.710-1. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.25-1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.19) 2.320 (. 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.35-2.21-2.240-.830) < LOD .. EPA has developed standards for PCP in drinking water and the environment.850 (.780-1.430) < LOD .10-2.320) < LOD .950-1. carcinogenic. 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.25-2. chronically administered high doses of PCP were hepatotoxic.500 (.36) .650) 90th 1.e. 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. 2003).52 (1..500-.67-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.09 (<LOD-2.16-1.9 mg/L. 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.30) 1.cdc.510-.94-3..780) < LOD .30-2. or skin absorption.90) 1.gov/ pesticides/ and from ATSDR at: http://www. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500-1..11) 2.67 (1.92) 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. 2003).580-.67-2.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .400 (.340-. OSHA has established an occupational standard.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 .S.78) 1.21 (.26 (1.250 (.18 (1.EPA.13 (.57 (.S.300 (.350) < LOD .30 (.19 (1. 1995).51) 1.910-1.52) 1.590) < LOD . Survey Geometric mean (95% conf. Death can result from seizures and cardiovascular collapse.420) < LOD ..82 (1.560-.630 (. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.S.06) 1.290-.75 (<LOD-2.430-.67 (1. and the FDA has established a standard for bottled water.40) 1.95) 3.990 (..55) 1.S.290) < LOD .00-1.220-.25-2. In animals.atsdr.760 (.84 (1. In a small sample of U. 2004.280) < LOD .40) 1. Pentachlorophenol is not mutagenic or teratogenic. van Raaij et al. 1989).560) < LOD .

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

645) * .50) .20) < LOD 1.570-1.600) < LOD 1. are antimicrobial agents used as bacteriostats.00 (1.50) 1.740 (.80-3.690) < LOD .22 (.860 (.630) < LOD . sodium ortho-phenylphenate (SOPP).90) . but OPP and SOPP are still used on pears and citrus (U.386-.S. formulate.90) 1. < LOD means less than the limit of detection.00) . fungicides. population from the National Health and Nutrition Examination Survey. 1998).590-2.85) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90) 2. Both chemicals degrade within hours to weeks in the environment (U. or 2-phenylphenol) and its water-soluble salt. Timchalk et al.389-.61) 2. Cnubben et al.490 (<LOD-.30-7.370-. Available evidence suggests that OPP does not accumulate in the body.90) . interval) .570-.600) < LOD 75th .3 and 0.570 (. 2002.90 (1.50 (1.20-2.10) .23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .07 (.370-. Estimated human intakes have been below recommended intake limits (U.420 (<LOD-.830 (.60-3.80) 1. OPP is still used as a disinfectant fungicide for industrial applications.50) < LOD .890 (.552 (.. 2006).30) < LOD .20 (1.636) * . however.496 (.610 (.EPA.80 (2.820 (.540-2.19 (.500-2.600) < LOD .14 (<LOD-3.50) < LOD .632) Selected percentiles ( 95% confidence interval) Sample 95th 2.490 (<LOD-.50) < LOD .640) < LOD .02) 1.10-2.780) < LOD .00 (1.880-2.00) < LOD .27 (.497 (. 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.760-2. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.490 (<LOD-.970 (.349-.433-. in paints.20 (.60-2. and sanitizers. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.610-1.930 (.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 .00 (1.30) 1.40-7.600-1.450 (<LOD-.S.33 (.09) 2.40-5.710) 3.567 (. In the past.890) 1.10) 2.20-3.S. 2006).10 (1.370-.696) * .450 (<LOD-.770 (. Workers who manufacture.638) * .600-1. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley. on ornamental plants and turfs.560-8.50-2.10) 1.742) * .498 (.20 (1.750-2.10) .550-1.20) < LOD 2.50 (1.23) 695 680 520 695 603 953 Limit of detection (LOD.00 (1.840-1.389-. it was used in home sanitizers for surfaces. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.30-2.580-1. General population exposure can occur via dermal. and as a wood preservative. 2006).80) 1.34) 1.Fungicides ortho-Phenylphenol CAS No.90 (1. whereas SOPP is not volatile and is more water soluble. Most agricultural food applications have been revoked.03) 1. EPA.50-4.00-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.836) * .710-2.800-3.490 (<LOD-.480-1.. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.28 (.10) .770 (.402-. 2006).10-1.570 (.60 (1.17 (.450 (<LOD-.508 (. Survey Geometric mean (95% conf.60 (1.40-5.570-2. such as fruits and vegetables.690-1.470 (<LOD-.890 (. Both have been used in agriculture to control fungal and bacterial growth on stored crops.790) 2.S. OPP is volatile. leaving the chemical residue OPP.20) 2.950) < LOD . OPP is considered to be moderately toxic after acute oral doses in animal studies.493 (.390-. inhalational.28-3.509 (.50-3.92 (.10) 1.30) < LOD 90th 1.EPA.520 (.600) < LOD .350-1.3.860) * 99-00 01-02 99-00 01-02 99-00 01-02 . 90-43-7 General Information Ortho-phenylphenol (OPP. 1998.466 (.40-2. 1989).22) 2..40 (. SOPP is applied topically to the crop and then rinsed off.621) * .88) 1. Fourth National Report on Human Exposure to Environmental Chemicals 43 .30 (1.490 (<LOD-.50 (1.600-1. and it has limited water solubility. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.10 (1.76) 1.60 (1.670) 2.00) .30) < LOD 1. which may vary for some chemicals by year and by individual sample.624) * .364-.410-.850 (. or apply these chemicals may be more highly exposed than the general population.

58) 2.840 (.420 (<LOD-.403-.64 (2.21 (.. IARC has classified SOPP as a possible human carcinogen.61 (2.38) 2.51-3.600-1. or developmental toxicity was observed (Bomhard et al. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.24-2..08-1.09-6. 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.900-1.590) * .453 (.750 (.61 (1.EPA 2006).28 (<LOD-4.20) < LOD 3..560-2.gov/pesticides/.EPA 2006).06-5.670) < LOD .52 (.473) * . Smith et al.69 (1. but no neurologic. 1998.89 (1. or.44 (1.670 (.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 . U.800-1. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.620-1.43-2. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.910-1.06 (1.11-1.06-4. 1993. U. 1984.496 (. 1997.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .17 (.620-1.12) < LOD 1.EPA at: http:// www.640-1.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.78 (2.484) * . 1986).96-4.32) 1.248-.27) < LOD .550) < LOD .91 (1.460-.75 (1. In high dose animal studies. 2005).. 1999. 1984.17) 2. Zhao et al.93 (1.21) 1.670 (. Detectable levels were seen in over half the U.93) .07) 2. less likely.29) 1.770-2.570) < LOD 1.97 (2.S. CDC. leading to production of two metabolites. and it has classified OPP as not classifiable with respect to human carcinogenicity.910 (<LOD-1.61 (.4) 3.33) .93) 1.320 (<LOD-.26) 1.750-2.96 (1.05-2.11 (.950) < LOD .690 (.343 (.53) 1.440 (..361-.580) < LOD . 44 Fourth National Report on Human Exposure to Environmental Chemicals .780 (. Ito et al. interval) .93) .09-3. Murata et al.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.32) 3. by possible genotoxic mechanisms (Hagiwara et al.550 (.420 (<LOD-.00 (..500) < LOD .810-1. Additional information is available from U.epa.43 (1.38-3.410 (<LOD-.29) 1. 2002.47) ..09 (1. Brusick.880-1.11) 4.568) * .40-13.510 (<LOD-.980 (. 2002.S.353-.470) < LOD .940-2.88-4.74 (1.59) .S.96 (1.84 (1.291-.17 (.810) < LOD .610) < LOD 1.382 (.Fungicides anemia.28 (2.750 (.00 (1.508) * .24-2. reproductive.455-.S.650-1.480-.444 (.. Volunteers exposed to 0. Pathak and Roy.18) 2. Biomonitoring Information Urinary OPP levels reflect recent exposure.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .21-2. 2000.380 (.301-.46) < LOD 1.59) 1.31) < LOD .970) 1.38) 1.02 (.08-2..30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .270-.01) 1. 1992.329-. Kwok et al. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.13) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.81) 1.791) * . Survey Geometric mean (95% conf.11 (.666) * .980 (<LOD-1.470 (<LOD-.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. 1999.S.12-2.04-4. 2002). 2005).311-..360 (<LOD-. 2005.43) 3. Nakagawa et al.08) 1.550-.410 (<LOD-.75 (1.0) 1. OPP was not found to be mutagenic.25-6.780-14.900) < LOD . Bomhard et al.86 (1.11) < LOD 90th 1.510-.514 (.385 (.860 (.43-2.560) < LOD 75th .62) . Urinary ortho-Phenylphenol (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.860 (.656) * .33-2.990) < LOD . ortho-phenylhydroquinone and ortho-phenylbenzoquinone.580-1.96) 1.910 (. population from the National Health and Nutrition Examination Survey.

EPA 739 R-06004. St John MK. Bartels MJ.20(5):851-857. McNett DA. Fukushima S. Available at URL: http://www. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. EPA-560/5-89-003.epa. July 28. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Elliott GR. J Chromatogr B Biomed Sci Appl 1997.50(11):3351-3358. Hakkert BC. Eastmond DA. Xenobiotica 1998.S. Gierthy J. Richter M. Murata M. Moriya K. Herbold BA. 2006. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Pathak DN. Freyberger A. 4/13/09 Onstot JD.43(7):14311437. Shirai T. Kwok ES. Timchalk C. Coelhan M. Environmental Protection Agency (U.35(2 Pt 1):198-208. Bormett GA. Toxicol Appl Pharmacol 1998. Nakagawa Y. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. J Agric Food Chem 2002.. National Toxicology Program (NTP). Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Tayama S. et al.54(16):5731-5735.gov/oppsrrd1/REDs/ phenylphenol_red.nih. Crit Rev Toxicol 2002. Bomhard EM. Bartels MJ. Christenson WR. et al. Vogel JS.159(1):18-24. Sangha GK. IARC Sci Publ 1984.17(8):411-417. Available at URL: http://ntp. Shibata M. Zhao S. Regul Toxicol Pharmacol 2002. U.pdf. Roberts AL.pdf. Identification of SARA compounds in adipose tissue. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Bartels MJ. Hirose M.45(5):460-481. 1989. Biochem Pharmacol 1992. Glas K. Inoue S. Meuling WJ. U. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Brusick D.(56):399-407. Roy D. Toxicol Appl Pharmacol 1999. Imaida K. Office of Toxic Substances. Fukushima S. Comparative metabolism of orthophenylphenol in mouse. Mendrala AL. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol.S. Atlanta (GA). rat and man. Smith RA. van de Sandt JJ. Moldeus P. Hagiwara A. Hum Exp Toxicol 1998. Bartels MJ.Fungicides References Appel KE.22(10):809-814.286(2):309-319. Ito N.S. 2005. 4/9/09.niehs. Stanley JS.150(2):402-413. Third National Report on Human Exposure to Environmental Chemicals. EPA). Mutat Res 1993. Brzak KA. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. J Agric Food Chem 2006. Centers for Disease Control and Prevention (CDC). Cnubben NH. Environmental Protection Agency (U. 90-43-7) in Swiss CD-1 mice (dermal studies). Moore GA.74(2):61-71. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Cano M. Turteltaub KW. Buchholz BA. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol.gov/ntp/htdocs/LT_ rpts/tr301. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry.EPA). The carcinogenicity of the biocide ortho-phenylphenol.703(12):97-104. Drugs. March 1986.S. Environ Mol Mutagen 2005. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Arnold LL. Christenson WR. Arch Toxicol 2000. Hagiwara A. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Leser KH. Food Chem Toxicol 1984. Kawanishi S.32(6):551-625. Timchalk C. Narang A. Eadon G. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Carcinogenesis 1999. Ito N.28(6):579594. Brendler-Schwaab SY. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Sangha G. Bromig KH. Selim S.

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

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

< LOD means less than the limit of detection. see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf.Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. 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. 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. * 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 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. Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1.S. * 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 .

17(6):559-566. Bravo R.S. Kinney PL. Available at URL: http://www. EPA). Available at URL(non U. Wilson AG. et al. Kolpin DW. Striley CA. Furlong ET. Olsson AO. March 2006. J Expo Anal Environ Epidemiol 2005.37(4):10881093.108(12):1151-1157. sulfonamide. Andrews HF. Environ Health Perspect 2000. Federal Register: January 24. Hsiao JJ. Burkhardt MR. Hladik ML. Volume 65. Barr JR.html. Comparative metabolism and elimination of acetanilide compounds by rat. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.11(4):353359. Ward EM. Environ Health Perspect 2003. Feil VJ. Hein MJ. Rose RL. Feng PCC.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100.cce. Sci Total Environ 2000. Sci Total Environ 2000. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Kier L. Centers for Disease Control and Prevention (CDC). Hines CJ. Linhart SM. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Environ Sci Technol 2005.EPA): http://pmep.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. reservoirs and ground water in the Midwestern United States. Camann DE. epa. and metolachlor herbicides in rats. and other herbicides in rivers. Battaglin WA. J Expo Sci Environ Epidemiol 2007. Lefevre PA. Davison KL. Whyatt RM. 2000.S.248(2-3):115-122.cornell.Herbicides References Ashby J. J Agri Food Chem 1989. Coleman S. 2005. Jefferies PR.111(5):749-756. Hodgson E. imidazolinone. Curwin BD. Wratten SJ.S. Environmental Protection Agency (U. 5/30/06. Environmental Protection Agency (U. Thurman EM. et al. Reynolds SJ. Barr DB. Green T. Linderman R. Dialkylquinonimines validated as in vivo metabolites of alachlor. Barr DB. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Larsen GL. pages 3682-3690. 5/30/06 U. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Barr DB. Quistad GB. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Number 15. Sanderson WT. Hum Exp Toxicol 1996. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.S.39(17):6561-6574. Third National Report on Human Exposure to Environmental Chemicals. Roberts AL. Tinwell H.248(2-3):123-133. EPA). acetochlor. Casida JE. EPA 738-R-00-009. Occurrence of sulfonylurea. Deddens JA.pdf. Heederik D. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Alavanja MC.15(9):702-735.S. 1998. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Atlanta (GA). Xenobiotica 1994. U.24(10):1003-1012. Peter CJ. Acetochlor (Harness) Pesticide Petition Filing 1/00.15(6):500-508. et al. Chem Res Toxicol 1998.

gov/pesticides/.EPA. 1998). USGS. 2003).. about 20-25% of the U. soybeans. the latter may account for some observed effects (Davison et al. including corn. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates.S.S. as measured through conversion to deethylamine. 1989. 1998.S. WHO.EPA considers alachlor to be a probable human carcinogen at high doses. Jefferies et al. Estimated human intakes have been below recommended limits (U.EPA. 1999. NTP and IARC do not have ratings regarding human carcinogenicity. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. Hill et al. 1998). 1998). Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1995. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1998.6-diethylaniline and its reactive metabolite.. ranged from 0. 1997. 2005. Hines et al. (2003) showed that 2.. In animals. 1996). though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. formulators. WHO. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. U. In animal studies.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. stomach. 2003). but shows little bioaccumulation. corn cropland was treated with alachlor. mean values of urinary concentrations of alachlor metabolites.S. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment.1 mg/L at various collection times (Sanderson et al.EPA.. 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. 2000.S. 1995). alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. hemosiderosis. 1994.EPA. Hladik et al. 50 Fourth National Report on Human Exposure to Environmental Chemicals .Herbicides Alachlor CAS No. and on non-crop land for general weed control. Additional information about is available from U. In a study of applicators and workers exposed to alachlor. 1998. 2000. Kolpin et al. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al.. and uveal degeneration. 1996. U. 1988. In chronic animal testing. Feng and Wratten. In 1993-1995.. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect.S.1 to 1. 1999 and 2007. U. whereas 60% of applicators had detectable amounts. WHO.. 2003).S. U. and field workers. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. Tessier and Clark.. peanuts and other crops. but another metabolic pathway can produce 2. 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. 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. IPCS. alachlor has demonstrated hepatotoxicity. mercapturate conjugates were predominant metabolites. Because it can be absorbed through skin. Alachlor has low potential for acute toxicity. Alachlor has a soil half-life of a few weeks. EPA at: http://www.S. Since the late 1980s alachlor use has been declining.EPA. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. It is absorbed by plants and inhibits plant protein synthesis. 2005). Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. WHO. Alachlor itself is not considered mutagenic.. 2003).epa. but has not shown developmental or reproductive toxicity in mammalian systems (U. but not likely at low doses. 1996.. the dermal exposure route is potentially significant for applicators.

population from the National Health and Nutrition Examination Survey. 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.S.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. 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. Urinary Alachlor mercapturate (creatinine corrected) Metabolite of Alachlor 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.18. * 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. Fourth National Report on Human Exposure to Environmental Chemicals 51 . Survey Geometric mean (95% conf.

Andrews HF. Life Sci 1988. Biagini R.39(17):6561-6574. World Health Organization (WHO).usgs. Reregistration Eligibility Decision (RED) Alachlor. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.47(6):503-517. et al. Brown KK. et al. Kier LD. Kinney PL. MacKenzie B. Brown MA. Kolpin DW. Wratten SJ. Available at URL: http:// www. Identification of a major human urinary metabolite of alachlor by LC-MS/MS.111(5):749-756.43(9):2504-2512. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Available at URL: http://water. Available at URL: http://www. Environ Health Perspect 2003. Thurman EM. Barr DB. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Thake DC.248(2-3):115-122. Environmental Protection Agency (U. J Ag Food Chem 1995. Chem Res Toxicol 1998. reservoirs and ground water in the Midwestern United States. Hull RD.epa. U. Barr JR. EPA). 1996. Background document for development of WHO Guidelines for Drinking-water Quality. Jefferies PR.18(6):363-391. J Agri Food Chem 1989. Sacramento. Feng PCC. 2005. 1997.pdf.44(18):1325. 2/27/09 Jefferies PR. 2003.S. 1998. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Furlong ET.S. Lau H.248(2-3):123-133. California.gov/oppsrrd1/ REDs/0063. Peter CJ.Herbicides References Battaglin WA.php. Linhart SM. Driskell WJ. and metolachlor herbicides in rats.S. Hill RH Jr. Gilliom RJ). Sci Total Environ 2000. 1999. Biagini RE. Comparative metabolism and elimination of acetanilide compounds by rat. and other herbicides in rivers. Larsen GL. 1999. 2007. Supplemental Technical Information (available on-line only). 98-4245 (by Barbash JE. No. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Feil VJ.htm. Kimmel EC.11(4):353359. Davison KL. Geological Survey (USGS). Shoemaker DA. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Kolpin DW. Centers for Disease Control and Prevention (CDC). Hladik ML. who. International Programme on Chemical Safety (IPCS). Mutat Res.int/water_sanitation_health/dwq/chemicals/en/alachlor. Quistad GB. Erratum in: Life Sci 1989. Casida JE.395(2-3):159-171.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Circular 1291. Roberts AL. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Geological Survey (USGS). Available at URL: http://www. Xenobiotica 1994. Ann Occup Hyg 2003. Wilson AG. World Health Organization. Atlanta (GA). Am Ind Hyg Assoc J 1995. WHO/ FAO Data Sheets on Pesticides. December 1998. Burkhardt MR. Bull Environ Contam Toxicol 1996. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.S. Geneva. Environ Sci Technol 2005. sulfonamide. Casida JE.pdf. Tolos W. Whyatt RM. revised February 15. Heydens WF. Occurrence of sulfonylurea.37(4):10881093. Hill AB. ALACHLOR.56(9):883-889. Hines CJ. Deddens JA. Hum Exp Toxicol. 1992-2001. Quistad GB.inchem. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Dialkylquinonimines validated as in vivo metabolites of alachlor. Tessier DM. Casida JE. 86.43(25):2087-94. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Sci Total Environ 2000.24(10):1003-1012. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Third National Report on Human Exposure to Environmental Chemicals. acetochlor. Hsiao JJ. Martens MA. 4/2/09 U. Striley CA. EPA 738R-98-020.org/documents/pds/pds/pest86_e. Camann DE. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Clark JM.56(6):853-859. Hines CJ. March 2006. imidazolinone. Henningsen G. Alachlor in Drinking-water. 2/27/09 U. DNA adduct formation by alachlor metabolites. Sanderson WT. Thelin GP. Shealy DB.

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

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

Stoker TE. J Toxicol Environ Health 1994. 3/11/09 Laws SC.30(2):244-247.. Available at URL: http:// www. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Toxicol Lett 1993. Stoker TE. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Cooper RL. et al. Toxicol Sci 2003.47(6):503-517. Toxicol Sci 2000. Collins A. Wetzel LT. In small studies of Maryland residents in 19951996 (MacIntosh et al. Centers for Disease Control and Prevention (CDC). Environ Health Perspect 2001.. A risk assessment of atrazine use in California: human health and ecological aspects. Ann Occup Hyg 2003. Available at URL: http://www. Jones AD. Catenacci G. Proc Natl Acad Sci USA 2002.atsdr. 2007). Blewett C. Ferrell JM.htm. 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. 2000).69(2):217-222. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Geneva. Tyrey L. Grzywacz JG. Barr DB. Brown KK. Moseman RF. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Agency for Toxic Substances and Disease Registry (ATSDR). Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). 1993). et al. Goldman JM. et al. Carr WC Jr. Stevens JT. Hines CJ. Perry et al. Steroids 1999.15(6):500-508. Cottica D. Biological monitoring of human exposure to atrazine. 2005). Mendoza M.. Wetzel LT. Hermaphroditic. 2003. Lucas AD. Toxicological profile for atrazine. WHO/ FAO Data Sheets on Pesticides. Toxicol Sci 2000. Maroni M. Chen H. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Lioy PJ. Barr DB. Third National Report on Human Exposure to Environmental Chemicals. Bradway DE.43(2):155-167. References Adgate JL. et al. Cooper RL.53(2):297-307. levels of atrazine mercapturate were generally not detectable (CDC. Eberly LE. 82. Sanborn JR. Gillis JH. In a study of 60 farm worker children. et al. Striley CA.html.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Freeman NC. Pest Manag Sci 2005. Stoker TE.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al.76(1):190-200.. Hayes TB. Quandt SA.inchem. ATRAZINE. Ferrell JM. J Expo Anal Environ Epidemiol 2005. World Health Organization. International Programme on Chemical Safety (IPCS). Biagini RE. Simpkins JW. Barbieri F. 2005.. Curwin BD. Cooper RL. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . 3/11/09 Arcury TA. Seiber JN. In a small number of field workers. Heederik D. In the NHANES 2001-2002 subsample. Pfeifer KF.115(8):1254-1260.64(9):672-678. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Gillis JH. Bersani M. Laws SC. Schmid J. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products.. Noriega N. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Deddens JA. atrazine was detected in only four children (Arcury et al.61(4):331-355.gov/toxprofiles/tp153. Goodrow MH.cdc. Lee M.org/documents/pds/pds/pest82_e. Aldous CN. McElroy WK. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. J Toxicol Environ Health 1994.99(8):5476-5480. Hein MJ. Eldridge JC. Saiz SG. Environ Health Perspect 2007. Extrom PC. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.109(6):583-590. Sanderson WT. Breckenridge CB. The geometric mean of urinary atrazine mercapturate was 1. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Eldridge JC. Shoemaker DA.. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. 1996. Tapia J. Vonk A. Atlanta (GA). Stuart AA. 2005). Clayton CA. 2001). 2001 [online]. Atrazine disrupts the hypothalamic control of pituitary-ovarian function.43(2):155-167. J Agric Food Chem 1982. No. Fleenor-Heyser DG. Reynolds SJ. diamino-S-chlorotriazine and hydroxyatrazine. Barr DB. Ferioli A. Gammon DW.58(2):366-376. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. et al.

The Quality of Our Nation’s Waters. Crit Rev Toxicol 1997. Washington (DC). U.php.pdf. MacIntosh DL. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .epa. Breckenridge CB.S. EPA Office of Pesticide Programs. Environmental Protection Agency (U. Sanderson JT. Pesticides and Toxic Substances.usgs. Timchalk C. Toxicol Sci 2000.195(1):23-34. 6/1/09 U. Guidici DL. Wood C. J Toxicol Environ Health A 1999. 2003b. White paper on potential developmental effects of atrazine on amphibians. Environmental Protection Agency (U. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Pesticides in the Nation’s Streams and Ground Water. J Expo Anal Environ Epidemiol 1999. A review of epidemiologic studies of triazine herbicides and cancer. Available at URL: http://www. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Interim Reregistration Eligibility Decision For Atrazine. Office of Prevention. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells.61(1):27-40. Guidici DL. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Laws SC. May 2003a. Cooper RL. Geological Survey (USGS). Rayner JL. van den Berg M. Toxicol Appl Pharmacol 2004. Fenton SE. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Ann Epidemiol 2000.58(1):50-59.10(7):479. Hammerstrom KA. Case No. Available at URL: http://water.epa. Laws SC. March 2006. Perry M. EPA). Osborne DW.S.6(1):107-116.S. Toxicology 1990. Tortorelli J.pdf. Langvardt PW. 0062.S. Stevens JT. Kastl PE. A longitudinal investigation of selected pesticide metabolites in urine. Toxicol Sci 2002.S. revised February 15. Wetzel L. Needham LL. 1992-2001.67(2):198-206.27(6):599612. Sathiakumar N.9(5):494-501. Lansbergen GW. Chem Res Toxicol 1993.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Available at URL: http://www. Dagenhart D. Stoker TE.182(1):44-54. Delzell E.56(2):69-109. 3/11/09 U. Cooper RL. Circular 1291. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Environmental Fate and Effects Division.gov/oppsrrd1/REDs/ atrazine_ired. Supplemental Technical Information (available on-line only). Singzoni B. EPA). Dryzga MD. Toxicol Appl Pharmacol 2002. Boerma J. A risk characterization for atrazine: oncogenicity profile. Christiani D. Stoker TE. Ryan PB. 2007.Herbicides development of a biomarker of exposure.

S.2.230-.05-2. by direct contact with agricultural and residential areas after applications.230 (<LOD-.4-D were used in the U. and mecoprop).910) 1.21) 1. but at higher levels they are herbicidal.420-. myotonia.30 (<LOD-2.48) < LOD 1. headache. 4-D.560-1.810-1.330 (.210-.910) < LOD .610 (.370-.260 (<LOD-.610-..660) 1.890 (. < LOD means less than the limit of detection.27 (1.55 (1.70) 1.4-D can be applied either as an aqueous salt or as oil-soluble esters.07 (.27-2.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (<LOD-1.4-D have been below recommended intake limits (U. It is rarely detected in ground waters (USGS. It was first registered with U.24 (. population from the National Health and Nutrition Examination Survey. MCPA.250 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 57 ..S.43) 1. 2.550-1.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .490) < LOD < LOD < LOD .4-dichlorophenoxyacetic acid (2.930 (.40) 1.4-D has low acute toxicity.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . Kohli et al. dizziness.S. and by consuming food or drinking water contaminated with 2. Human health effects from 2.51 (1.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.Herbicides 2.490 (. 2.440-1. 2. 2005).690 (. 1977). with a half-life of several days to several weeks.930-1.400) < LOD .22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .690 (.32 (1.80) 1.S.4-D may occur during residential applications. 2.540-.20 (.60) 1.4-D or exposed for prolonged periods. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.410) < LOD .22) < LOD .16) < LOD .27 (.420) < LOD . At low levels. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. renal and hepatic injury. General population exposure to 2. Similar to other chlorophenoxy herbicides. it acts as a plant growth hormone.10) < LOD 1. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. and delayed Urinary 2.310) < LOD . 1989.960-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.670-1.350) < LOD < LOD < LOD . nausea.13) < LOD .760 (.310 (. 94-75-7 General Information Widely used throughout the United States. abdominal pain.730 (.680-1.08) < LOD .740 (. in 2001 (U. 2007).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 . 2004). It is not well absorbed through the skin. Recent estimates of chronic intakes of 2. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. Survey Geometric mean (95% conf. agricultural.EPA in 1948. these herbicides can enhance plant growth.10 (<LOD-1. Sauerhoff et al. As much as 62 million pounds of 2. the chlorophenoxy herbicide 2.4-Dichlorophenoxyacetic Acid CAS No. which may vary for some chemicals by year and by individual sample.. Once absorbed.S. 1974. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.210 (<LOD-.690-1.320) 90th .4-D) controls broadleaf weeds in residential.250 (<LOD-. It is poorly bound in soils.10 (<LOD-1.890) < LOD .02-1.EPA. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00-2.EPA.690 (.4-D is rapidly absorbed via oral and inhalation routes.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.66) < LOD 1.03) 695 659 520 668 589 892 Limit of detection (LOD.560-. hypotension.952 and 0. and aquatic environments.

680) < LOD .S.14 (.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD ..560-.3.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.610-.EPA.590 (<LOD-1.24) 1. 2006.330-. Hill et al.380-. U. thyroid.340 (. In previous samples of the U.4-D reflect recent exposure. 2003. eyes.440 (.560-.640 (.410) < LOD < LOD < LOD .670 (.4-D levels were detectable in less than a quarter of the individuals studied.660) < LOD . 2.S. 2005. adrenals and gonads (NTP.39) < LOD 1.890) < LOD 1.350 (<LOD-. IOM.Herbicides neuropathy (Bradberry et al.. or to contaminants in the herbicide formulations (specifically 2.380 (<LOD-..73) .790) 1. other exposures.780-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. 1995. 2005). Additional information is available from U.. 2005).520-.810-1.410) 90th .780 (. 1980.EPA at: http://www.980) < LOD 1.EPA.27-1.17 (.32 (<LOD-2.720 (.. and evidence of histological injury to the kidneys.780) . CDC.890-1.19) .990-1. Epidemiological studies have reported associations of several types of cancer.05) . 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..810-1.550-. 1989). 2.epa. urinary 2..410 (<LOD-. Frank et al.. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. Post-application levels in farmers and home gardeners were dependent on Urinary 2.470) < LOD .700 (. 2002.4-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.13 (.40) 695 659 520 667 589 892 < 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. 2.S. IPCS.08 (.EPA.390) < LOD < LOD < LOD . Kutz et al.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .13 (.740 (. U..08 (.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .610-.590 (<LOD-1.490 (.4-D are eye irritants. 2005).820-1. 2000). Knopp et al.480 (.S.270-.7.570) < LOD . 1994).56) .S. myotonia.670 (<LOD-1. 2001. Survey Geometric mean (95% conf.790) < LOD . 1996.4-Dichlorophenoxyacetic acid (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. Average post-application urinary levels of 2.4-D production plant workers and a few forestry workers spraying 2. Kolmodin-Hedman and Erne..380 (<LOD-. It is unclear whether these associations are related to the chlorophenoxy herbicides. 1992). developmental. 1985.EPA 2005). population (Hill et al.620-. 2002.35) < LOD . and of adults and children (Baker et al. 58 Fourth National Report on Human Exposure to Environmental Chemicals . Pearce and McLean.920) < LOD 1.580-. 2004). 2005.850) < LOD .410) < LOD 1. in small samples of children (Hill et al. 1995). 2005). 2005. IPCS. U.gov/pesticides/.08 (.670 (.4-D does not have significant reproductive.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 .S.270 (<LOD-. 1996.16) 1.930-1.S. liver. or teratogenic effects in chronic rodent studies (Charles et al. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.41 (1. 1996. U. 2005. Acute high doses administered to laboratory animals produced ataxia. IPCS.380) < LOD . IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.660 (. The acid and salt forms of 2.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. Biomonitoring Information Urinary levels of 2.340-.

cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Bus JS. Stephenson GR. Biomonitoring of herbicides in Ontario farm applicators. Selected pesticide residues and metabolites in urine from a survey of the U.nih. Ritter L.18(4):469-474.4-dichlorophenoxyacetic acid (2. Occup Environ Med 1994. Mandel et al. Hein MJ.. Mandel JS. Estimation of occupational exposure to phenoxy acids (2. Frank R. Available at URL: http:// www.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study.31(2):121-125. Beasley VR. Heederik D.niehs. Finding a measurable amount of 2.gov/index. 3/17/09 Institute of Medicine (IOM). Barr DB. 2005). Hill RH Jr. International Programme on Chemical Safety-INCHEM (IPCS). Khanna RN. 2003. Gregg M. References Arbuckle TE. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Kutz FW.edu/catalog. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Gupta BN. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. J Expo Anal Environ Epidemiol 2000. Reynolds SJ. general population.4-D.4-D) epidemiology and toxicology. 3/17/09 Knopp D. Toxicol Sci 2001. Available at URL: http://ntp.inchem. Tables. Baker S.4-dichlorophenoxyacetic acid in man. Erne K. 2005). Harris SA. Dhar MM. In farm families. 2005. the number of acres to which it was applied (Curwin et al. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. van Ravenzwaay B. Head SL.4. Alexander BH.4-dichlorophenoxyacetic acid (2.51(3):152-159.71(2):99-108.nap. Developmental toxicity studies in rats and rabbits on 2. To T. Carter-Pokras OD. Baker SE. Cook BT.php?record_id=10603.5-T). 914. Centers for Disease Control and Prevention (CDC).Herbicides the time since application..4-D in urine does not mean that the level of the 2. Washington (DC): National Academies Press. J Expo Anal Environ Epidemiol 2005 Nov. Shealy DB.31 Suppl 1:98-104. Driskell WJ. Ripley BD.31 Suppl 1:90-97. J Environ Sci Health B 1992.htm. Holler JS. National Toxicology Program (NTP).4-D). the amount of pesticide applied.4-D will result in an adverse health effect. Beeson MD. Exposure of homeowners and bystanders to 2. Fast DM. Arnold EK.4:427-435.60(1):121-131. Available at URL: http:// www. Survival and Growth Curves from NTP Toxicity Studies. geometric mean urinary levels of 2. Dichlorophenoxyacetic acid. Barr DB.. Harris et al. et al.37(2):277-291. Acquavella JF. Bailey SL. Board on Health Promotion and Disease Prevention.4-D): exposure and urinary excretion. Crit Rev Toxicol 2002. Needham LL. Solomon KR. Scand J Work Environ Health 2005. Vet Hum Toxicol 1989.S.4:318-321.4-D were highest in the farmers who applied the 2. Honeycutt R. 2005. Cole DC.15(6):500-508. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Arch Environ Contam Toxicol 1985.4-D than levels found in the general population. Updated March 7. Biomonitoring for farm families in the farm family exposure study. Tandon JS. Smith SJ. Assessment of exposure to 2. Xenobiotica 1974. et al. Garabrant DH. and the use of protective clothing or equipment (Arbuckle et al. 1992). Absorption and excretion of 2. Hill RH Jr.32(4):233-257. Sirons G J. Environ Res 1995. Pesticides residues in food: 1996 evaluations Part II Toxicology. Pesticide residues in urine of adults living in the United States: reference range concentrations.4-D and 2.4-dichlorophenoxyacetic acid and its forms. Chapman P.4 dichlorophenoxyacetic acid (2. TOX-63: TOXICITY REPORT CURVES. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Curwin BD. 2006.. Baker BA. Needham LL.4-. TOX-63 Peroxisone Project (2. Third National Report on Human Exposure to Environmental Chemicals. Brody D. Forestry workers involved in aerial application of 2. et al. Hanley TR Jr. Kolmodin-Hedman B. Atlanta (GA).4-Dichlorophenoxyacetic Acid). Scand J Work Environ Health 2005. Veterans and Agent Orange: update 2002.27(1):23-38. 2005 Charles JM.4:97-100. Sircar KP. Murphy RS. Biomonitoring studies of 2. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.org/documents/jmpr/jmpmono/v96pr04. Sanderson WT. Wilson RD. J Toxicol Environ Health 1992. Campbell RA. Philbert MA. Review of 2.4-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. Arch Toxicol Suppl 1980.10(6 Pt 2):789-798. Arch Environ Contam Toxicol 1989. 2. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Kohli JD.

revised February 15.2000 and 2001 market estimates. Office of Prevention Pesticides and Toxic Substances. May. 3/17/09.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. 4/2/09 U.gov/oppsrrd1/ REDs/factsheets/24d_fs.8:3-1U. Pesticides in the Nation’s Streams and Ground Water. EPA 738 F-05-002. Toxicology 1977.4-D RED Facts.epa.S. June 2005.4-dichlorophenoxyacetic acid (2.EPA.S.php. Pesticide industry sales and usage .Herbicides Sauerhoff MW. Braun WH. Geological Survey (USGS). Available at URL: http://www.pdf.S. Blau GE. 2004.usgs.htm. 1992-2001.EPA).epa. 2. Available at URL: http://water. March 2006. The fate of 2. The Quality of Our Nation’s Waters. 3/17/09 U. gov/oppbead1/pestsales/01pestsales/market_estimates2001.EPA). Available at URL: http://www. Supplemental Technical Information (available on-line only).4-D) following oral administration to man. 2007. S. Gehring PJ.S. 60 Fourth National Report on Human Exposure to Environmental Chemicals . Environmental Protection Agency (U. Circular 1291. Washington (DC): U.S. Environmental Protection Agency (U.

S. U. mercapturate conjugates were the predominant metabolites. 1995.S. 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.. 2005..7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al.. Metolachlor has a soil half-life of a few weeks to three months and is degraded microbiologically and photochemically to at least five different products. 1994.. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. It is absorbed by plants and inhibits plant protein synthesis. Hladik et al. Hines et al. Estimated human intakes have been below recommended limits (U. metolachlor levels in water have exceeded lifetime human health advisory levels (U. metolachlor was quickly absorbed after dermal or oral doses. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample. This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment. 1999. Fourth National Report on Human Exposure to Environmental Chemicals 61 . 2003). WHO. so applicators.S. 1995). lacrimation.S. though the 95th percentile for males was 0. 2000.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine. 2005).S. Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. (2003) showed that 2. 2005). Davison et al. People exposed to metolachlor will excrete metolachlor mercapturate in their urine. and convulsions were observed at lethal doses in animal studies. 1995). 1998). Jefferies et al. The geometric mean metolachlor mercapturate was 4. 2007. soybeans.epa. formulators.EPA.Herbicides Metolachlor available from U. and on non-crop land for general weed control. 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. Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect. 2000. and field workers may have significant exposures via this route. Metolachlor has low potential for acute toxicity (U.gov/pesticides/.EPA considers metolachlor to be a possible human carcinogen. USGS.EPA. Biomonitoring Information CAS No. but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. 1995).. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. Occasionally in the past. 2003). 2003). In animal studies. In animals. NTP and IARC do not have ratings regarding human carcinogenicity. 2007. Feng and Wratten. Metolachlor is well absorbed dermally. Salivation. EPA. and eliminated in urine and feces over two to three days (WHO. EPA at: http://www. 1989. including corn. sorghum and other crops.S.EPA. Metolachlor did not show developmental or reproductive toxicity in chronic animal studies. and it was not mutagenic in mammalian cells (U. Gilliom. whereas 60% of applicators had detectable amounts.. Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. General population exposure may occur through the consumption of contaminated food or drinking water.. in both ground and surface waters (Battaglin et al. Kolpin et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.200 μg/L (CDC. WHO.

see Data Analysis section) for Survey year 01-02 is 0.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.200 (<LOD-.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .670 (<LOD-. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor 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 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 .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.240) 679 701 957 Limit of detection (LOD.2. 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 .200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. 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.440 (<LOD-. 62 Fourth National Report on Human Exposure to Environmental Chemicals .S.

Larsen GL.248(2-3):123-133.epa. Reynolds SJ. reservoirs and ground water in the Midwestern United States. 1998. California. Barr DB. Xenobiotica 1994. sulfonamide. 1999. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Environmental Protection Agency (U. Thurman EM. Kolpin DW. Furlong ET.11(4):353359. J Agri Food Chem 1989.S. R. Centers for Disease Control and Prevention (CDC). Ann Occup Hyg 2003. Wratten SJ. Environ Sci Technol 2007. Peter CJ.gov/oppsrrd1/ REDs/0001. Reregistration Eligibility Decision (RED) Metolachlor.111(5):749-756. Atlanta (GA). Hodgson E. 2005. Linderman R.usgs. imidazolinone. Camann DE. revised February 15. Sacramento.15(6):500-508. 3/26/09 U. 4/2/09 U. Hladik ML. Thelin GP. 98-4245 (by Barbash JE. Available at URL: http://water. Deddens JA. April 1995. Shoemaker DA. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Sanderson WT. usgs. Environ Health Perspect 2003. Hein MJ. Barr JR.24(10):1003-1012. EPA 738R-95-006. Circular 1291. Dialkylquinonimines validated as in vivo metabolites of alachlor. World Health Organization (WHO). Finding minimal herbicide concentrations in ground water? Try looking for their degradates.gov/nawqa/ pnsp/pubs/wrir984245/text.pdf. Ward EM. Occurrence of sulfonylurea. 2007. Hsiao JJ. Third National Report on Human Exposure to Environmental Chemicals. et al. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Curwin BD. 6/1/09 Whyatt RM. Supplemental Technical Information (available on-line only).108(12):1151-1157. Quistad GB.S.int/water_sanitation_health/dwq/chemicals/ metolachlor. Sci Total Environ 2000. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Heederik D. Available at URL: http://water. Available at URL: http://www. et al. Feng PCC. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Metolachlor in Drinkingwater. J Expo Anal Environ Epidemiol 2005. March 2006. and other herbicides in rivers. Jefferies PR. 1992-2001.html.pdf. U.php. Pesticides in U. Geological Survey (USGS). and metolachlor herbicides in rats. Davison KL.gov/nawqa/pnsp/pubs/files/051507. Feil VJ.37(4):10881093.usgs.248(2-3):115-122.S. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Available at URL: http://water. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.47(6):503-517. Roberts AL. Gillion. Geological Survey (USGS). Environ Sci Technol 2005.ESTfeature_gilliom. Environ Health Perspect 2000. Coleman S. Sci Total Environ 2000. Gilliom RJ). Rose RL. Casida JE. 2003.39(17):6561-6574. Brown KK.S.S. Alavanja MC. Barr DB.41:3409-3414.Herbicides References Battaglin WA. Burkhardt MR. Biagini RE.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Striley CA. Andrews HF. Available at URL: http://www. Chem Res Toxicol 1998. Kolpin DW. Kinney PL. acetochlor. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.pdf 3/30/09 Hines CJ. Comparative metabolism and elimination of acetanilide compounds by rat. EPA).who. streams and groundwater. Background document for development of WHO Guidelines for Drinking-water Quality. Linhart SM. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.

1974). At low levels. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. abdominal pain.5-T (Holson et al. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 2007). Agent Orange).5-T and 2. the general population is unlikely to be exposed to it. Although 2.4.5-T is eliminated mostly unchanged in the urine.S.. Nelson et al.4. 2. dizziness... Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2.4.4-D were used as defoliants in the Vietnam War (e. Survey Geometric mean (95% conf.4.5-trichlorophenol and other degradates. and delayed neuropathy (Bradberry et al.5-Trichlorophenoxyacetic acid (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. nausea. which may vary for some chemicals by year and by individual sample.4.4. myotonia.4.5-Trichlorophenoxyacetic Acid CAS No.4. population from the National Health and Nutrition Examination Survey. it is not well absorbed through the skin. but higher levels are herbicidal.. ranging from several weeks to many months.4. Given the commercial unavailability of 2. these herbicides can enhance plant growth. Mohammad and St. with an elimination half-life of approximately 19 hours (Arnold et al.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. Chlorophenoxy herbicides act as plant growth hormones.. 2. Kohli et al.5-T has been rarely detected in ground waters (USGS.4. Human health effects from 2.5-T.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. The half-life of 2.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.7.4.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.2 and 0.4. 2004). 2.4. 93-76-5 General Information 2. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. renal and hepatic injury. and concern about contamination with 2.g. Ester forms of 2. Epidemiological studies have reported associations of several types of cancer. headache. < LOD means less than the limit of detection.4. 2.5-T in soil varies with conditions.Herbicides 2.5-T was once applied as either an aqueous salt or as an oil-soluble ester.5-T degrades to 2. 1986. 1989. Once absorbed into the body.5T is rapidly absorbed via oral and inhalation routes. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.4.4. 64 Fourth National Report on Human Exposure to Environmental Chemicals . 1992). 1992..3. 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.1. hypotension.5-T use as a herbicide in 1985. Omer.

000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.S. Finding a measurable amount of 2.4. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.4. urinary levels of 2. 2005).7. 1996.4. 1992). 1980).4.4.5-T reflect recent exposure. Biomonitoring studies on 2. population from the National Health and Nutrition Examination Survey.EPA.4. * 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 65 .4.EPA at: http://www.Herbicides or contaminated herbicides. 2.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2..8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. It is unclear whether these associations are related to the chlorophenoxy herbicides. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. other exposures. Biomonitoring Information Urinary levels of 2.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.gov/pesticides/. 2005. U. Pearce and McLean.S. Additional information is available from U. or to contaminants in the herbicide formulations (specifically 2. Survey Geometric mean (95% conf. 2002. Urinary 2.5-T does not mean that the level will result in an adverse health effect. 2003. similar to results of NHANES II (19761980).5-T also were below the limit of detection (Kutz et al. IPCS. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. Mean urinary levels of 2.S.4.5-T than levels found in the general population.3. 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.epa. 2004). IOM.4.5-T itself is not mutagenic. in which urinary levels of 2.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.5-T were generally below the limit of detection.

Cook BT. St Omer VE. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . LaBorde JB. Wolff GL. Fundam Appl Toxicol 1992. et al. Toxicol Rev 2004. Gaines TB. Arch Toxicol Suppl 1980.5-trichlorophenoxyacetic acid (2.32(4):233-257.19(2):286-297. Developmental toxicity of 2.4. 3/17/09 Institute of Medicine (IOM).epa. Pearce N. Sircar KP. Estimation of occupational exposure to phenoxy acids (2. Environmental Protection Agency (U. 3/17/09 Kohli JD.37(2):277-91. Vet Hum Toxicol 1989. Pesticides residues in food: 1996 evaluations Part II Toxicology.S.php?record_id=10603. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. 2005. Third National Report on Human Exposure to Environmental Chemicals. Washington (DC): U. Brody D.inchem.23(2):65-73. Dichlorophenoxyacetic acid. Selected pesticide residues and metabolites in urine from a survey of the U.4-D/2. Absorption and excretion of 2. Khanna RN. et al. Holson JF. Review of 2. Holson JF.8(5):551-60.4. Nelson CJ. Poisoning due to chlorophenoxy herbicides. Sheehan DM. Gaylor DW.31 Suppl 1:1825. Pesticide industry sales and usage . Proudfoot AT. Gaines TB.EPA).Herbicides References Arnold EK. Gupta BN.4-D and 2.5-T). Developmental toxicity of 2. LaBorde JB.org/documents/jmpr/jmpmono/v96pr04. II. Veterans and Agent Orange: update 2002.4.5-t mixture. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.5-trichlorophenoxyacetic acid (2. 2003. Behavioral and developmental effects in rats following in utero exposure to 2. Mohammad FK. 914. Crit Rev Toxicol 2002. Bradberry SM. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice.5-T in four-way outcross mice.5-trichlorophenoxy acetic acid in man. general population.4:318-21. Neurobehav Toxicol Teratol 1986.31(2):121-125. Office of Prevention Pesticides and Toxic Substances. McCallum WF. Dhar MM. 2. Beasley VR.pdf. Tandon JS. McLean D. Kutz FW. International Programme on Chemical Safety-INCHEM (IPCS).4.edu/catalog.S. Agricultural exposures and non-Hodgkin’s lymphoma. I. Washington (DC): National Academies Press. Vale JA.4-dichlorophenoxyacetic acid (2.htm. Multireplicated dose-response studies with technical and analytical grades of 2. Centers for Disease Control and Prevention (CDC).2000 and 2001 market estimates. Kolmodin-Hedman B. Murphy RS. Fundam Appl Toxicol 1992.4-. Available at URL: http://www. May. Available at URL: http:// www.nap. J Toxicol Environ Health 1992. discussion 5-7. S.5-T). Board on Health Promotion and Disease Prevention. Available at URL: http:// www. Garabrant DH.4-D) epidemiology and toxicology.5-T).S.4. Philbert MA.4. Scand J Work Environ Health 2005.19(2):298-306. Arch Int Pharmacodyn Ther 1974.4. Atlanta (GA). Erne K. 2004.4. 210:250-255. Carter-Pokras OD. U. gov/oppbead1/pestsales/01pestsales/market_estimates2001.EPA. Nelson CJ.

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

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

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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.

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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.

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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.

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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

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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)

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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.

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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

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

8 (18.8) < LOD 8.120) .3 (18.062 (.073-.3 (13.100 (.6 (14.070-.096-.149) .0-21.103 (.048 (<LOD-.180) .117) < LOD . Survey years 01-02 03-04 Geometric mean (95% conf.1-19.120-.0 (15.1) 15.150 (. population from the National Health and Nutrition Examination Survey.0 (11.4 (12.130-.100-.30 (8.116) .110-.5 (16.124) .1) < LOD 9.130) .160) .190) .3 (18.083-.50 (8.089 (.4) 21.8-24.4-17.064 (.0) < LOD 9.110) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.088-.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.140-.5-15.109 (.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .075) < LOD .1 (18.2) 12.6) 16.1) 13.070) .S.130-. < LOD means less than the limit of detection.130-.3 (14.1) 15.4) < LOD < LOD 16.084-.1 (13.4) 19.059 (. which may vary for some chemicals by year and by individual sample.8-17.108-.40-9.8-17.110 (.110) .0) 21.090-.80-10.100) .093) .098 (.6-24.140) . which may vary for some chemicals by year and by individual sample.70 (7.112) 95th .120 (.7 (<LOD-15.8-25.10 (<LOD-16.062-.6-24.130) .056-.0) 19.1-18.7 (14.4-18.00 (8.8 (9.090-.8) 14.086-.8.5) 15.50) 15.242) .138 (.053 (<LOD-.090 (.054-.4) 539 456 484 487 980 885 Limits of detection (LOD.9-23.070 (<LOD-.4 (12.8 (11.2-15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170) . Survey years 01-02 03-04 Geometric mean (95% conf.90) 90th 15.103 (.101) .6 (15.6) 9.6) 19. see Data Analysis section) for survey years 01-02 and 03-04 are 10.080 (.080-. population from the National Health and Nutrition Examination Survey.062 (.063-.190) .7-19.069) < LOD < LOD .055 (.130 (.054-.2) 11.060) . 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 .5-17.130) .1) 20.120 (.3-21.80-9.1-24.180) .139 (.5) 19.140 (.60-10.100) .0-25.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.058) < LOD .2) 15.9 (12.102 (.1) 14.S.4) 95th 20.100-.100-.7) 15.077-.7 (15.147 (.160 (.6 (15.120 (.9 (12.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .5-17.064) 90th .109-.8-19.077 (.3 (19.9 (13.2) 14.113 (.9-38.1-16.40-10. 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 9.6-33.4) 14.80 (<LOD-10.0 (10.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.7-22.5) 21.4) 20.4) 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 8.080) .0 (10.090 (<LOD-.110 (.112-. Fourth National Report on Human Exposure to Environmental Chemicals 79 .138) .139 (.150 (.9 (14.049-.1) 10.5 and 7.8) 15.158) .054-.9 (13.147) 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 .2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10. 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.9-22.090-.109-.30 (8.110 (.160 (.5 (<LOD-11.00-14.

Chapin RE. Available at URL: http://pubs. Grandjean P. Academic Press.htm. Kanthasamy A. Environmental Health Criteria 91. J Occup Environ Med 2005. et al. bioaccumulation. et al. Serrano FO. New York. PA.usgs. Needham LL. 15. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Food and Drug Administration (FDA). Part A 2000. 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. Jr and Laws ER. 2 Classes of Pesticides.64-65 Spec. Carlson JN.html. Kitzazwa M. Aldrin and dieldrin: A review of research on their production environmental deposition and fate.109(Supp1):113-139.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). David VL. Brock JW. Stehr-Green. are nonestrogenic in transfected HeLa cells.59:229-234.html. Inc. Toxicological profile for aldrin/dieldrin [online]. J Toxicol Environ Health 1989. Daniel SE. Olea N.atsdr. 4/21/09 Hoyer AP. Organochlorine exposure and risk of breast cancer. pp. Edwards JW. Shore RF. 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. McIntosh LJ. Demographic and seasonal influences on human serum pesticide residue levels. Jorgensen T.cdc. Pesticides in the Nation’s Stream and Ground Water. 1992-2001. 6/1/09 Ward EM.150:263-271. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Mumtaz MM.gov/ circ/2005/1291/.14:95-102.47:1059-1087. 4/21/09 Jorgenson JL. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Available at URL: http://www. and epidemiology in the United States. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. 4/21/09 Bates MN. Cox. International Programme on Chemical Safety (IPCS).27:405-421. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. 1991. Chung KL. Andersen A. Patterson DG Jr.fda.inchem. No:429-436. September 2002. Mink PJ.cfsan. Kanthasamy AG. Teta MJ. United States Geological Survey (USGS). Smith AG. Corrigan FM. Anantharam V. Finley B. plasma dieldrin. Sonnenschein C.org/documents/ehc/ ehc/ehc91. August 2008. Available at URL: http://www. Environ Health Perspect 1995. Tully DB. Handbook of Pesticide Toxicology. Ellis H.91(1):122-126.103(Suppl 7):113-122. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Patterson DG Jr. Psychopharmacology (Berl) 1987. Organochlorine insecticides in substantia nigra in Parkinson’s disease.gov/toxprofiles/ tp1. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. VT. Aldrin and Dieldrin [online]. Sanchez-Ramos J. Turner W. toxicology. Lancet 1998. Six high-priority organochlorine pesticides. Facca A.66(4):229-234. Roy ML. Vol. Narahashi T.352:1816-1820. Fernandez MG. J Toxicol Environ Health. Reprod Toxicol 2000. Mann D. Grajewski B. Buckland SJ. Ginsburg KS. References Agency for Toxic Substances and Disease Registry (ATSDR).9:1357-1367.54:1431-1443. Chemosphere 2004. Environ Health Perspect 2001. Cancer Epidemiol Biomarkers Prev 2000. Wienburg CL. Priestly BG. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Revised Feb. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Chlorinated Hydrocarbon Insecticides. 731-915. Toxicol Lett 1992. Eds. either singly or in combination. Soto AM. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Schulte P. Hartvig HB. Basit A. Exp Neurol 1998. Int Arch Occup Environ Health 1994. Garrett N. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Song S. 2007 [online]. Frey JM. 1989. Neurotoxicol 2005. Jr. and lymphocyte sister chromatid exchange. Available at URL: http://www. Rosellini RA.gov/~dms/ pesrpts. Li AA.26:701-719. In Hayes WJ.

8-20. 57-74-9 Heptachlor CAS No.6) 9. and 03-04 are 14. Survey Geometric mean (95% conf. and 7.10-11.69-10.8-33. lawns.5-42.6) 8. Technical grade chlordane had contained 7% trans-nonachlor.8 (42.3-45.1-25.7) 28.63 (8.3) 18..4) < LOD < LOD < LOD 23.3 (21. 1994).9) 39.8) 53.S.2 (37.7-56.5) 44. from the early 1950’s until the mid-1980’s.7) 19.5-44.9-21.3 (9.9) 36.9 (11.4-51.8) 27.1 (<LOD-12.1) 30.6) 39. As a result of the manufacturing process.8 (18.5) 21.30-11.3) 10.8-43.1 (11.2) * 12.2 (28.8) 52.1 (44.6-24.1 (15.3 (26.36-11.9-38.6-24.5) < LOD < LOD < LOD < LOD 13.2 (36.3) 10.1-65. Chlordane is not currently produced or used in the U.8 (40.4 (35.3 (28.1) 16.3-45.0-12.9-42.9 (21.1) 22.9) 13.6) 9.4-45.37 (8.2 (39.0-33. 01-02.2) 33.6-53.5-41.Organochlorine Pesticides Chlordane CAS No.9 (17.7 (<LOD-32.2-26.90 (8.9) 11.1) * 11.2) < LOD 11. respectively. heptachlor use has been limited to treatment of fire ants near power transformers. chlordane was used to kill termites and other insects on agricultural crops.6) 49. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.6 (9.4) 29.4) 39.0 (20.0) 41.5 (41.20 (<LOD-11.2 (10.2) < LOD 11.8-73.0) 75th 20.9) 10.4-21.1-50.2-28.74 (<LOD-10.6) 48.9) 23.6) 11.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6 (43.2) 34.8-33.7-39.3 (11.4 (31.0-18.2 (9.20-10.1 (<LOD-12.4 (30.5 (31.6) 36.9 (26.6) 23.6) < LOD 11.5 (<LOD-12. foods high in fat such as meat.5) 38. 1994.8) 18.3) 41.5) 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. the technical grade product of each chemical contains 10%-20% of the other chemical.9 (15.9) 31. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.S.7-14.4) 12. and in soil. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.9 (31.89-10.2 (21.0-67. Since 1992.70 (<LOD-10.0 (<LOD-12. Until 1988. and dairy products are the usual sources of exposure to these chemicals in the general population.0) 31.20-11.1 (20.0 (26.9 (15. 10.0 (37.5-38.3 (27.8 (17. population from the National Health and Nutrition Examination Survey.7) 42. < 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.5) 56.8-32.0) 27.2 (41.4 (<LOD-12.4 (10.7) 9.5.0-13.9) 23.3-24.8.8) 44.2) 37.0) 21.7 (17. Fourth National Report on Human Exposure to Environmental Chemicals 81 .1-51.3-49.5-65. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.3) 37.2) 36. buildings.7-25.9 (36.10-18.0) 37.5) 10.9) 11. which may vary for some chemicals by year and by individual sample.1-19.5) 37.7) 35.2) 22.6-18.7 (19.S.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.9 (18. 2007).5) 9.2-49.8-31.9 (29.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.9 (11.5-43.10 (8. 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.0 (32.8 (10.8-23. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.1-25.7 (34.9-21. see Data Analysis section) for Survey years 99-00.1 (17.2-56.4) < LOD 11. fish.5) < LOD < LOD 9.5 (34.8-42.6) 20.8-61.0-25.9) 37.1 (16.1 (25.9) 17.4 (22.4-14.7 (10.5 (8.3-43.2-49.2) 46.7 (34.3-32.6) 48.6-12.7) 19.7 (<LOD-13.6-45.5-32.5-13.4) 18.0 (16.1-15.3 (20.7-12.6 (9.8 (17. 2007).1) 30.8) 52.3) 18.4) 37.7 (42. 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.7-70.5.3 (25.5-40.7 (43.2-21.7) 31.1) * 11.1 (40.9 (26.6 (25. 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.4 (30. Consequently.8 (10.4) 22.1) < LOD < LOD < LOD < LOD < LOD 8.1 (27.1 (<LOD-12.5-47.1) 90th 34.82-11.6 (16.9-40.3 (<LOD-19.5 (33.4-40.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.0-61.7 (32. in addition to trace amounts of numerous other related compounds (ATSDR.9) 47.0) 20.

1991). Smith. OSHA has established occupational exposure criteria.070 (<LOD-. and heptachlor epoxide in foods and bottled water.340) .091) .119 (.112 (. 2002.130 (.077) .077) . Shindell and Ulrich.126) . 1991.246-.083 (.140-. 1981).189 (.079) .350 (.204 (.120-.Organochlorine Pesticides (Dallaire et al.300) .430) .380) .150-.080 (.140 (..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 * * * * .320) . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.290-.231) .057-.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .120-. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.130-.230 (.070 (<LOD-.208 (. 2006).230 (.190-.440) .320 (.302) .150 (.100-.150) .070) .260 (.227) < LOD .300-.063 (.270 (.056 (.400) .064) < LOD .079) < LOD < LOD < LOD .310) .350) .510) .130-. dermal.070) < LOD < LOD < LOD < LOD < LOD .140) . 2007.108-. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.180-.189-.190-.216-.130 (.063-. 2007).066-. EPA has established environmental criteria for chlordane and heptachlor.160) .150 (.170) .080) . Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.280 (.070 (.061-. Chlordane and heptachlor are absorbed after oral.070-.260-. 1986).170) .106-. Elimination of all these chemicals from the body occurs over months to years. 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.130) . and breast milk is a major excretion route in lactating women.286 (.146) < LOD < LOD .450) .400) .290) .055-.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .080 (. Le Marchand et al.140 (.140 (.120 (.287) .146) .073) < LOD < LOD < LOD < LOD .073 (.150 (.207 (.210 (. 2001.067 (.148-.258 (.370 (.450) .092) .170) .110-.340) .070-.090) .130-. to heptachlor. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf. which is also persistent in the body (ATSDR.160 (. and alterations in immune function of offspring.240-.200 (.050 (<LOD-.070-.310) .068) .090) .310-.200-.242-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .083) .330 (.310 (.082 (.160) .270 (.240-.080) .373) .410) .149 (.270 (.280) .199-.269 (. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.068) 75th .126 (. chronic doses of heptachlor have produced liver enlargement and injury. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.130-.100 (<LOD-.128 (.048-.245-.280 (.066-.220-. 82 Fourth National Report on Human Exposure to Environmental Chemicals . heptachlor.315 (.160) .130) .070 (<LOD-.230) .140 (. Rogan.110 (<LOD-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.070 (<LOD-.077) .063) * .350 (.100 (.066 (<LOD-.271 (.058 (. 1977a.430) .066 (.100-.320 (.115 (. Takahashi et al. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.280-.165-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity. In laboratory animal studies.370 (.S. 1996.071 (.180-.225 (.230-.200-.230-. and inhalation exposure.133) 90th .130 (.250 (.300) .360) .062) < LOD .348) . The major metabolite of heptachlor is heptachlor epoxide.300) .075 (. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.240) ..260 (..207) .310) .203-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.063 (.180) . population from the National Health and Nutrition Examination Survey.250-.076) < LOD .210-.058-.286 (.170) .280-.253-.300) .280-.065-.210 (. neonatal mortality.057 (.190-. FDA established allowable residues of chlordane.057) * .140-.320) .220-.087-. and the U. characterized by seizures and paralysis.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .077) .130-.080) .049 (<LOD-.230-.200-.250 (.060 (<LOD-. The U.260 (.148) .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. 1977b. IARC.104) .069 (<LOD-.223) .220 (.290-.063 (.136) .053-..104-.290-.370 (.170-.560) .063 (.050-.180) . Acute.063) .240 (.053-.290 (.068-.290) .120-.320 (.047 (<LOD-.S.074-.320 (.213) * .115-.S.300 (.168-.258-.090-.170) .058-. 1986).

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

6-21.8) 15.3) 18.5 (<LOD-21.0 (11.7-18.5.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.4) 18.9-29.6 (13.0-16.6) < LOD < LOD < LOD 27. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.9-16.8 (18.8 (15.5) < LOD 14.6-17.2) 15.1-29.8) 13.20 (<LOD-9.8) 19.1 (19.5 (11.7 (13.1-16.3 (<LOD-25.6 (12.2) 26.8-24.8 (<LOD-23.9-23.7 (16.7 (10.4 (<LOD-19.6) 22.6 (16.9) 15.6) 14.8) 20.8) 19.6) 13.9 (12.9-29.8. and 03-04 are 14.4 (15.90 (<LOD-9.0-19. respectively.7-19.1-38.2-27.0 (15.8) 13.2 (18.8) 16.6 (11.8) 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 8.50) < LOD < LOD < LOD 17.8-24.5 (11.8 (18.1) 20.3) 23.3) 22.5 (18.8-23.1-15.1 (16. which may vary for some chemicals by year and by individual sample.2-17.2 (<LOD-16.5 (10.5) 19.2 (<LOD-25.S. < LOD means less than the limit of detection.3) 27.40) 15.6 (<LOD-27.6 (14.6.4) 21. population from the National Health and Nutrition Examination Survey.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.2) 20.8 (13.10-13.3-18.9-25.2-27.0-54.8) 14.3) 18.6 (8.2 (<LOD-62. 84 Fourth National Report on Human Exposure to Environmental Chemicals . 01-02.5) 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 7.4 (11.0-17. and 7.9 (15. 10.4 (<LOD-54.0-17.8 (13.8-24. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8) 21.3) 18.3) 16. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00.4 (11.3 (13.1) 13.0) 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 13.2-16.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) 13.8-46.1) 23.5 (<LOD-32.0) 13.3) 10.6 (16.7-25.

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

0 (16.5) 36.8-110) 59.0-23.7) 17.4-67.5) 14.2 (36.5-111) 68.7) 52.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.1) 17.4 (12.2 (14.2) 20.4 (30.0-68.7-113) 68.4-52.7-21.9 (15.4-22.4 (67.6 (56.2-17.3) 16.9 (51.7-77.9-65.7) 35.9 (28.2) 39.1 (65.9) 51.5 (25.7) 73.8-19.5.0 (13.8 (45.7) 78.5-36.1 (17.5) 19.2 (59.8) 19. see Data Analysis section) for Survey years 99-00.4-36.2 (15.5 (44.7-18.5-69.7 (13.7 (11.0 (62.7) 14.1) 31.5.7-20.9-89.1-20.1 (22.4 (16.8 (26.1) 17.7) 78.7-29.5) 48.0-23.7-34.5 (15. respectively.4) 16.5) 35.8) 47.6) 13.5) 22.8 (17.6 (57.1-34.0) < LOD < LOD 8.8.70 (<LOD-12.7 (59.6-82.7-38.6-19.8 (12.0) 33.9) < LOD < LOD < LOD 20.8-21.0) 19.2 (64.2-21.3-30.3-74.1-18.0-38.0-93.3) 18.2 (26.0-37.0-123) 74.4 (11.1) 30.4) 59.8 (<LOD-20.1) 17.0-24.9 (29.5 (15.0 (19.5) 78.9 (51.6) 56.9) 14.2 (27.0) 13.5) 77.2 (60.2-18.2) 34.8 (42.5 (45.8 (28.7 (30.0-22.1 (48.3 (45.7 (59.2) 19.7) 56.3-86.8) 51.1-16.9-20.86-13.5-20.3 (58.0 (48.2-18.1) 32.8-16.0) 49.4) 19.8 (13.6-20.0 (15.4) 107 (84.1) 78.2-23.7 (28.3) 32.8 (13.9 (16.6-22.9 (<LOD-14.0-93.6 (15.3-58.3 (56.5 (13.8-129) 74.6) 54.10 (<LOD-11.6 (52.7-22.8 (26.6-54.2 (25.8 (16.9 (15.3) 15.0-143) 112 (68.3) 36.3-50.8 (11.8 (28.9 (36.1) 78. < LOD means less than the limit of detection.0 (16.2) 59.9-65.0-59.9-45.3) 30.3) 30.2 (7.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.1-22.9-36. interval) 18.9-40.8-16.4-23.1-16.6 (56.6 (<LOD-14.3-57.6) 82.3-39.4) 20. and 03-04 are 14.4 (28.6) 25.3 (16.6-88.7 (35.6) 10.6-66.5) 30.0) 40.2-16.8 (71.6 (50.8-67.8 (15.0 (13.4) 48.4) 55.2) < LOD 10.3) 25.9-22.3) 32.1) 17. 86 Fourth National Report on Human Exposure to Environmental Chemicals .1 (10.9-58.4-35.9-69. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5) 9.8-90.4-18.3 (14.7 (18.1) 18.8-19.6) 84.1) 18.6) 34.1) 62.0) 75th 31.9-64.0-113) 68. population from the National Health and Nutrition Examination Survey.3 (14. 10.9) 14.7) 28. 01-02.1) 16.9-35.6 (16.0 (14.7-35.0) 18. Survey Geometric mean (95% conf.0 (42.7-17.7-160) 86.5-19.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.7) 15.6 (12.9 (47.3) 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.1-55.9 (66.1) 17.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.1) 17.1-51.8 (28.5-87.1) 17.2-37.0 (42.3-21.5-17.3 (17.8-77.5-95.8 (19.7) 59.5) 14.9 (19.3) 19.0 (60.8-41.4 (45.8) 80.7 (74. which may vary for some chemicals by year and by individual sample.9) 51.8-79.8 (49.6 (32.1-34.0 (29.8 (26.7 (16.8 (30.8-90.3) 18.2) 17.0 (15.5) 26.2-88.2) 30.6) 60.0) 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 (41.6) 56.3 (49.7-23.1-126) 67.1 (47.5) 20.2 (14.5) 90th 55.1-28.0-20.S. and 7.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.4-62.7-32.2 (19.1) 14.3-32.

161) .096-.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.390) .237) .409-.141) .141) .461 (.317 (.098-.120) .288 (.161-.930) .134) .310-.400) .330-.130) .108) 75th .110 (.160 (.093-.300) .150) .160-.324 (.450) .091-. Fourth National Report on Human Exposure to Environmental Chemicals 87 .340-.440) .202 (.112 (.220 (.594) .177-.128 (.098 (.108) .180-.470 (.490-.470-.680) .430-.060) .116 (.124) .380 (.104-.20) .090 (.210 (.171-.111 (.090) .120-.078-.390) .371) .210-.109 (.119) < LOD < LOD < LOD .130) .047-.565) .130) .370 (.108 (.114) .186 (.250) .240-.260) .470-.106 (.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .280) .090-.430-.460-.116-.080-.310-.470 (.279-.510 (.145-.420 (.081-.099-.120) .220 (.497-.520 (.310) .590 (.390 (.490) .550 (.127) < LOD < LOD .510-.242) .150) .090-.094 (.062 (.190-.320-.540) .360-.367) .210) .130 (.285-.130) .690) .104 (.093-.395-.180-.240) .080) .310-.390-.440-.400 (.093) .084-.417 (.111-.210) .410-1.355 (.290-.100-.103 (.100 (. interval) .573 (.651) .830) .680 (.230 (.069-.095-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .055 (<LOD-.360-.170 (.410-.350 (.420) .116) .270-.190-.106 (.630) .211) 90th .041 (<LOD-.190-.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.630) .220) .220 (.220 (.205 (.080 (.490 (.840) .061-.120-.630) .559) .400-.250) .100 (.100-.079-.520 (.480) .830) .090 (<LOD-.580 (.234) .640 (.113) .125) .110 (.085-.240) .106 (.080-.190-.330 (.800) .060 (<LOD-.320-.395) .210 (.183 (.260) .110 (.960) .120 (.110) .130) .069) .220 (.191 (.097) .129) .400 (.580 (.173-.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .430-.125 (.110-.090-.180-.120 (.110 (.390 (.400-.300-.085-.098 (.520) .590) .460) .327 (.113) < LOD .210-.343 (.110 (.092 (.060-.397-.190-.099-.340) .135 (.126) .460) .390 (.091) .186-.340-.370 (.405) .310-.158-.500) .092 (.250) .080-.690) .105 (.220 (.068-.090-.310 (.220 (.081 (.085-.390 (.122) .286-.458 (.130) .117) .131) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.684) . Survey Geometric mean (95% conf.600) .301-.112 (.240) .350-.100-.090-. population from the National Health and Nutrition Examination Survey.470 (.S.490 (.096) .190-.089 (.109 (.080-.580 (.079-.272-.120-.119) Selected percentiles ( 95% confidence interval) Sample 95th .087 (.330-.130) .082) .122) .414 (.240 (.110 (.590 (.210) .130 (.096-. which may vary for some chemicals by year and by individual sample.232) .220 (.210 (.098) .054-.070 (.120 (.071 (<LOD-.093-.600 (.237) .760 (.103 (.090-.120) .288-.100-.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 .140) .078 (.120) .

Lawrence River (Quebec. Smith AG. Takahashi W. Takei G. Saidein D. Dendle WH. Available at URL: http://www. Organochlorines in Swedish women: determinants of serum concentrations.atsdr. Sci Tot Environ 2006. Circumpolar maternal blood contaminant survey. Charles MJ. Bjerselius R. 4/21/09 Dallaire F. et al. 4/21/09 Baker DB. Academic Press.111:349355. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Toxicological profile for chlordane [online]. 6/1/09 Rogan WJ. Senie R. Environ Health Perspect 2002.gov/ntp/ htdocs/LT_rpts/tr009. JAMA 1988.org/ documents/cicads/cicads/cicad70.pdf.nih.html. Available at URL: http://ntp. 9/25/07 International Programme in Chemical Safety (IPCS). Dewailly E. 1986. Darnerud PO. Wolff MS.gov/ntp/ htdocs/LT_rpts/tr008.28:497501. Aune M. August 2007. Distribution of polychlorinated biphenyls. Covaci A. 79.inchem. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Environ Health Perspect 2003.8:1-123. et al. Chlorinated Hydrocarbon Insecticides. Available at URL: http://www. Available at URL: http://ntp. In Hayes WJ. Poland. Jr.cdc. International Agency for Research on Cancer (IARC). Hertz-Picciotto I. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. 1963-1967. Toxicological profile for heptachlor and heptachlor epoxide [online].gov/toxprofiles/tp31.110(8):835-838.niehs. Siegel BZ. Wohlleb JC. Environ Health Perspect 2002. Mortality of workers employed in the manufacture of chlordane: an update. Chlordane and heptachlor [online]. Organochlorine exposures and breast cancer risk in New York City women.pdf. Granath F. Atuma S. Organochloride pesticide residues in human milk in Hawaii. 88 Fourth National Report on Human Exposure to Environmental Chemicals .Summaries & Evaluations. Eds. Brower S. Royce W. Jr and Laws ER. Canada). Chashchin V. Environ Res 2000.org/documents/iarc/ vol79/79-12. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum.org/site/foundation/ research/projects2. LeMarchand L. Kolonel LN. International Agency for Research on Cancer (IARC) .html. Inc. Wong L. 6/1/09 National Toxicology Program (NTP). Drews K. 2001. 731-915. Handbook of Pesticide Toxicology. Concise International Chemical Assessment Document 70 Heptachlor [online]. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Muckle G. Berkowitz GS. Voorspoels S. Tartter P.nih. Bioassay of chlordane for possible carcinogenicity. Laliberte C. National Toxicology Program (NTP).niehs.330:55-70. Ayotte P. Head SL. 1991 pp. New York. 4/21/09 James RA. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort.41:145–148.htm. Dewailly E.html. Loo S. Bull Environ Contam Toxicol 1981:27:506-511. Jaraczewska K. Pollutants in breast milk.9:1-109.372:20-31.110:617-624. Stehr-Green P. et al. Vol.atsdr. A Report to the Hawaii Heptachlor Research and Education Foundation. Vol.259(3):374-377. 1994-1997 organochlorine compounds. Lulek J.heptachlor. Sci Total Environ 2004. Baker DB. Glynn AW. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Hawaii Med J 1991. Available at URL: http://www. 1993. Arch Pediatr Adolesc Med 1996. et al. Available at URL: http://www. 2006. Bleiweiss IJ. Available at URL: http://www.50(3):108-118.inchem. Shindell S and Ulrich S. Hansen JC. 2 Classes of Pesticides. Arch Environ Health. Van Oostdam JC. Bioassay of heptachlor for possible carcinogenicity. J Occup Med 1986. Gilman A.htm. maternal serum and milk from Wielkopolska region.150:981-990. Natl Cancer Inst Carcinog Tech Rep Ser 1977a.cdc. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). KalubaSkotarczak A.84:151-161. May 1994. gov/toxprofiles/tp12.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Keller JA. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Willman E. Odland JO. Barker J. 1979-1980.

9 (10.5) 23.5 (23. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.7 (15. Both Serum p. continues to be the primary source of DDT exposure.6 (9.0) 40.2-95.3) 28.8-39.5-54. including 1. fish.7) < LOD 18.S.0) 26. particularly meat.6 (31.9-34. although DDT and DDE intakes have decreased over time (FDA. 1991).6 (25. after World War II until 1972.2-bis(p-chlorophenyl) ethane (DDD).9) 17.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 89 .0-35.1 (33.7) 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. and 03-04 are 20. resulting in fetal exposure.8-26.7 (19.9 (21.3 (<LOD-31.3 (<LOD-21.4) < LOD < LOD < LOD 61. or dermal exposure. respectively.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. Food imported from countries that still use DDT may contain the chemical or its residues.0) 19.9) 14. which is a mixture containing p.p’-DDT (15%-21%). 1988). 2008. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.4) < LOD 17.2 (<LOD-40.9 (<LOD-20. particularly for endemic vector and malaria control. and dairy products. DDT was used at one time as a treatment for head and body lice.0-15. air.1) 31.70 (8. when virtually all use of it was banned.8-23.3-236) 24.5-36.1-27. Only a small proportion of DDT is metabolized and excreted (Smith.8) 30.3) 21. and 7.2 (11. Survey Geometric mean (95% conf.2) < LOD < LOD 9. p.p’-DDD (4% or less). food. 2002.3-16.0 (18.0 (10. Smith. population. These chemicals are highly persistent in soil.6-33.3) 21. It is still used in some countries.10 (<LOD-12. 1991).5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.5 (15.1 (23.1’-(2.6 (<LOD-25. DDT can be absorbed after ingestion.5) < LOD < LOD 9. It was produced and used in the U.7) 12.4 (23. as well as in plant and animal tissues.5 (23. and trace amounts of several related compounds. 17. In the body. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2) 30.50-11. see Data Analysis section) for Survey years 99-00.9 (10.3-590) 293 (104-541) 48.0-27. The biodegradation half-life of DDT in soil varies from 2 to 15 years.2) 155 (59.1’-dichloro-(2.4. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.8. DDT is converted in the environment to other more stable chemical forms.5 (14.3 (27.9) < LOD < LOD 9.2-65.10-13. DDT and DDE can cross the placenta.8) 36. DDT usually refers to the technical product. and water.8-17.0 (21. < LOD means less than the limit of detection.8) 15.9) 29.1 (<LOD-39. inhalation.0-37.5) 25. 01-02.7. depending on conditions.0-53.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.7-16.3) 22.00 (<LOD-10.S.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.S.9-28. In the general U.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. o.90 (<LOD-12.8) 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. DDT is converted to DDE and several other metabolites.6 (22. 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.0) 20.9 (10.p’-DDT (65%-80%).0-155) 83.1-71. Gunderson.0 (18. sediments.

570-4. and leukemia have also been inconclusive (ADSDR.105-.120 (<LOD-. 2006. 2006).34) .069) .084 (. Jusko et al. have not been consistently demonstrated (Beard.260) .. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.220) .130-.201 (. lung cancer. 1998). tremor.095) < LOD .p’-DDE can produce anti-androgenic effects (Gray et al. 2002. Calle et al.059-.00 (.627) .420) ...112 (.180 (.230) . Gladen and Rogan. overt signs of acute human toxicity include vomiting..170-.146 (. In laboratory animals. interval) Selected percentiles ( 95% confidence interval) Sample 95th ..064 (. 2001).114-. DDT may bind to estrogen receptors (Chen et al.. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.128 (.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.330-4.313 (.290) .065-. 1956). In high dose. 2001). although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.240 (.063 (<LOD-.130 (<LOD-.00) .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 .130 (<LOD-. and altered behavior after neonatal exposure (Eriksson and Talts. which may vary for some chemicals by year and by individual sample. Hayes et al. A workplace standard for DDT has been established by Serum p.071 (.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .230) . Snedeker.343) < LOD . 2001).079) < LOD < LOD . other organochlorines. and duration of lactation.180-.086 (..051 (<LOD-.190 (. 1997).203) .189-. resulting in exposure to nursing infants (Rogan.080-.400) . and seizures. polychlorinated biphenyls. and o.146 (..078-.150 (<LOD-.250-1. premature delivery.26) 1. Beard.061) < LOD < LOD < LOD . 2002.160-. 2006. 2004. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. Jusko et al. 2002. accidental exposures. Survey Geometric mean (95% conf.. 2006. 2002. 2006). Mariussen and Fonnum.170 (.400 (. Longnecker et al.150-. 2001).075) 1.143) < LOD < LOD .220) . Studies of DDT exposure and pancreatic cancer.054-.140-.048 (<LOD-.071-.078 (.098-.180) .074-. Animal studies reported reduced fertility. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown. dioxins and furans).190-1.01) . reproductive organ abnormalities.Organochlorine Pesticides chemicals are excreted in breast milk. 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.150 (<LOD-..132-.62 (.150) . 1996).530) .142 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.180 (.240) .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 .p’-DDD and p.106) < LOD < LOD . population from the National Health and Nutrition Examination Survey.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 ..106) .150-. Reproductive effects in humans affecting birth weight.108 (.200 (.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. 90 Fourth National Report on Human Exposure to Environmental Chemicals .068-.140) .190 (.087 (. 1995.106-. fertility..250 (. Gray et al. 2000.130 (<LOD-.530 (.g.120-.S.170) . 2006).180) .

html. 2003. 2005). Compared to females in the NHANES 1999-2000 subsample. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. 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. see Data Analysis section) for Survey years 99-00. 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. population from the National Health and Nutrition Examination Survey.epa. 1998. Fourth National Report on Human Exposure to Environmental Chemicals 91 . and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. In general. 2004). compared to levels observed in this Report (Anderson et al. mean serum levels of DDT and DDE in the U.8.S.7-119) 113 (100-140) 93...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.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. 1991). Since the 1970’s. Declining DDE levels over time have also been observed in the German population.. for males and females in the NHANES 19992000 subsample (Pavuk et al...S.atsdr. population declined by about fivefold to tenfold. 2003). In a population-based sample of men and women from eastern Slovakia. 01-02. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. 1989).Organochlorine Pesticides OSHA and a guidance established by ACGIH. and 03-04 are 18.cdc.gov/ pestcides/ and from ATSDR at: http://www. 2002. Link et al. and 7.. IARC classifies DDT (p.6 (81. More information about external exposure (i. 8. EPA at: http://www. A study of New Zealand adults sampled in 1996-1997 reported median DDE levels that were about threefold higher than the median for adults in the NHANES 1999-2000 subsample (Bates et al. Heudorf et al. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. Biomonitoring Information DDE persists in the body longer than DDT. 2004). 2002. environmental levels) and health effects is available from the U.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..gov/ toxpro2.e. 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. Smith. respectively.. respectively. NTP considers DDT as being reasonably anticipated to be a human carcinogen.S. Stehr-Green.3.p’-DDT) as a possible human carcinogen.6.

0 (9.1 (8.1) 7.43-4.69 (2.46 (1.18 (6.46 (1.6) 8.534-.34 (7.01-1.14 (1.59 (4.48-4.59 (1.26-2.09-1.81-18.68 (2.590 (.65 (1. 2004).5) 16.71 (6.75 (4.31-12.32 (1.50 (2.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.34-3.56-2.3) 16.81) 11.04 (6.57 (1.45 (1.18-4.43 (5. 1991).85-10.6) 12.43-8.66) 3. 1971)..520 (. population from the National Health and Nutrition Examination Survey.84 (3.37-16.623 (.30 (1.01) 1.7-20.30-1.88 (2.20 (.68) 2.24 (1.96) 1.46-2.13-2.51) 3.66) 4.55-9.p’-DDT.37-4.54-7.60-13.59 (1.03-1.48 (6.30-1. 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.52-6.80 (2.66) 1.58) 75th 3.14-9.05 (3.81 (7..41-12.01-5.963-1. or p.62-6.37-10. Survey Geometric mean (95% conf.36-11.57-2.5) 7.34) 2.0) 2.47 (1.33-1.36) 3.57-3.50-17.860 ng/L) and DDE (about 14.59) 6.06) 1.40-8.00 (6.01-11.81-5.8 (13.31-2.69 (.63 (1.890-1.53 (2.92 (3.7 (8.80) 1.23 (7.76-3.8 (14.6 (17.5) 5.97-4.68-4.58) 1.70-3.21) 3.6 (8.8 (13.p’-DDT.18) 1.39) 1.61 (1.25-14.9 (26.500-.516 (.57 (3.600) . interval) 1.91) 3.635) 1.57 (1.9 (15.29 (1.53-15.69 (1.25-16.75 (8.44) 1.93 (7.12-1.01-15.22) .7-48.97 (3. 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.77 (1.64) 3.02) 1.03-4.2) 26.56-6. serum levels of o.17 (3.91 (6.31 (1.5) 22.456 (.p’-DDT (Stehr-Green.70) 1. Finding a measurable amount of p.38 (1.6) 11.80) 3.27-1.16 (2.10-5.611-1.10) .32 (1.870 (. less than one percent had detectable serum levels of o.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.5) 10.25) 1.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.49 (1.25) 8.13 (1.39 (3.84-3.3) 10.6) 9. 2004).3-43.18-3.S.04-1.54) 8.38 (1.02 (2.85-4.8) 15.6) 9.90-8.18-1.28) 1.1) 40.40 (3.730) .796 (.488-.32-9. In a subsample of NHANES II (19761980) participants.3 (8.45 (1.36 (3.14) 2. o.15-4.10) 2.41 (1.05) 1.82 (1.96) .55 (2.8-90.56) 2.91-3.65) 1.14) 2.11-1.16-1.34) 6.37 (1.69) 4.2 (19.9) 7.75) 1. 2001-2002 and 2003-2004 subsamples.92 (3.76) 1.9) 5.02-8..49 (1.25 (1.19) 4.24) 1.71) 12.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.82) 1.75) 6.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.01-11.90) 22.00) 7.32) 1. considerably higher than levels in this Report (Smith.9-38.91-2.71) 32.2) 19.92) 1.430-.51) 1.26-10.01) 1.66) 1.76 (2.36-1.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .18-1.35) 1.51-8.49) 8.4) 14.61-2. In the NHANES 1999-2000.66-4.37-1.965-1.72) 1.13) 4.22 (7.07) 1.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect. Serum p.12 (.32-1.72) 1.26 (1.87 (5.3) 13.66-2.419-.0 (12.4) 9.53) 1.47) 3.8 (9. 2005).32-1.56-3.9-17.39-2.53) 7.51 (1.00 (.57) 2.4) 13.99) 1.75) 2.78 (4.40-4.7) 9.557) 1.43-4.22-1.2 (6.1 (9.63 (1.24-17. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.63-15.77 (1.p’-DDT were below the limits of detection.63 (6.06) 3.40-4.52 (3.7) 13.4 (12.19-14.561 (.12 (6. 1989). Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.57-13.81 (1.26) 3.21) 90th 7.6) 9.14-1.07 (5.11 (2.07) 1.2 (9.680-1.88-35. 309 versus 268 ng/g lipid.820-1.2 (9.1) 12.4-19. High mean levels of whole blood DDT (about 3.6 (7.6 (9. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.646) .76) 1..80) 1.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.10-1.6) 13.726) .85 (1.64-2.52 (1.2-32.51-15.51-49.01-1.66-17.7) 16.Organochlorine Pesticides nearby agriculture (Botella et al.79) 4.3 (9.87-16.83 (1.58) 1.69) 8.00-1.6) 9.25 (.27) 3.39-1.71 (5.4 (8.30 (1.49 (6.385-.34-11.59) 3.0) 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 .994-2.17-3.36-2.7-19.54 (1.

8.7. 17.S. 01-02.4. * 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.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. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. 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. respectively. Fourth National Report on Human Exposure to Environmental Chemicals 93 . and 7.Organochlorine Pesticides Serum o. which may vary for some chemicals by year and by individual sample. and 03-04 are 20. see Data Analysis section) for Survey years 99-00.

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

html. Exposure of women to organochlorine pesticides in Southern Spain. Zhou H.gov/ toxprofiles/tp35. Aune M. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Needham LL. Maternal serum level of 1.1-dichloro2. Saiyed HN. Hurd C. dichlorodiphenyldichloroethylene. Zhou H. Greenfield TA. Olea N. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Furr J. Vorojeikina DP. 4/21/09 Gladen BC. et al. Brock JW. 4/21/09 Anderson HA. Klebanoff MA.21(1-2)37-48. Bloom MS. Bates MN. Becker K. Katz SH. Lancet 2001.355:7889. Calle EE. Gabrio T. Baker RJ. Olson JR. Jr. et al.205:297-308. Available at URL: http://www. Hayes WJ. Herrman T.71(6):1200-1209.58:1185-1201. et al. Darnerud PO.358:110-114. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Organochlorines in Swedish women: determinants of serum concentrations. et al. and HCB residues in human blood in Ahmedabad.155(4):313-322. Olea-Serrano MF. et al. Crespo J. et al. Barr DB. FDA total diet study. Arnold SF. Henley SJ. Falk C. Chemosphere 2004. Longnecker MP. Klebanoff MA.gov/~dms/ pesrpts.54:1431-1443. selected elements. Hum Reprod Updat 2001.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Link B. Fourth National Report on Human Exposure to Environmental Chemicals 95 .72:261265.96:34-40. Patterson DG Jr. Wolf CJ.85:504508. Rogan WJ. et al. Hediger ML. Jr.7(3):248-264. Ostby J. Granath F. Kaus S. Lambright C. Beard J. Food and Drug Administration (FDA). Needham LL. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Environ Health Perspect 2004. Notides AC. Durham WF. Environ Res 2005. Zoellner I.206:485-491. Biomonitoring of persistent organochlorine pesticides. Davis MD. Toxicological profile for DDT. Botella B. Piechotowski I. Organochlorines and breast cancer risk. Gladen BC. Gray KA. J Assoc Off Anal Chem 1988. Burse VW. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Hanrahan L. Olson J. Eriksson P. Kashyap R. and polythelia among male offspring. Cerrillo I. Int J Hyg Environ Health 2003. Drexler H. Koepsell TD.17(6):692-700. DDT and human health.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.112(17):1761-1767.html.53(8):1161-1172. Environ Health Perspect 1998. Environ Health Perspect 2003. and dichloro(diphenyl)ethylene (DDE).. Klebanoff MA. hypospadias. Glynn AW. Chen CW. and DDD [online]. Am J Public Health 1995. DDE. Kulkarni PK. Levels of DDT. India. CA Cancer J Clin 2002. Frumkin H. Rivas A. Sci Tot Environ 2006. Ellis H.97(2):178192. Int J Hyg Environ Health 2002.cdc. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Lepom P. Cueto C. Schulz C. Effects of environmental antiandrogens on reproductive development in experimental animals. Buckland SJ.atsdr. Thun MJ. Swanson MK. and other chemicals. Heudorf U. Available at URL: http://www.106(5):279-289. lindane (g-HCH). Willman EJ. Zaidi SS. Bull Environ Contam Toxicol 2004. dietary intakes of pesticides. April 1982 to 1984.fda.52:301-309.111:349355. Moysich KB. Vena JE. et al. Krause C. Am J Epidemiol 2002. Chemosphere 2005. Gray LE Jr.162:890-897. hexachlorobenzene. Paepke O. Profiles of ortho-polychlorinated biphenyl congeners. Epidemiology 2006. Seiwert M. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. DDE and shortened duration of lactation in a northern Mexican town. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Angerer J. Jusko TA.cfsan. August 2008. Longnecker MP. Maternal DDT exposures in relation to fetal and 5-year growth. Savitz DA. HCH. Neurotoxicol 2000. Biochem Pharmacol 1997. Needham LL. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Atuma S. JAMA 1956. Bjerselius R. Environ Res 2004. et al. Charles MJ. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. September 2002. Talts U. The Great Lakes Consortium. Bhatnagar VK. Gunderson EL. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Garrett N. Parks L. Brock JW.

Lubet R. PA. Comparative pharmacodynamics of CYP2B induction by DDT. 2 Classes of Pesticides. Deichmann WB. Thomas PE. 731-915. Schecter A. Chemosphere 2004. Jones CR. Smith AG. Chlorinated Hydrocarbon Insecticides. Toxicol Appl Pharmacol 1971. New York. Fox S. Lynch CF. Arch Pediatr Adolesc Med 1996. Nims R. Chovancova J. DDE. Petrik J. J Toxicol Environ Health 1989. Pollutants in breast milk. et al. Neurochemical targets and behavioral effects of organohalogen compounds: an update.150:981-990.54:1509-520. 1991 pp. Fonnum F. Inc. Jr. Demographic and seasonal influences on human serum pesticide residue levels. children and newborn infants.27:405-421.20(2):186-193.36:253-589. Snedeker SM.53:455-477. Environ Health Perspect 2001. and dieldrin. Reddy AB. Pesticides and breast cancer risk: a review of DDT.Organochlorine Pesticides Mariussen E. Vol.109:35-47. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Crit Rev Toxicol 2006. J Toxicol Environ Health Part A 1998. Rey AA. Jr and Laws ER. and DDD in male rat liver and cultured rat hepatocytes. Pavuk M. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Stehr-Green. Handbook of Pesticide Toxicology. Eds. Astolfi E. Rogan WJ. Radomski JL. DDE. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Cerhan JR. Academic Press. In Hayes WJ. et al.

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. Because it is metabolized so rapidly. rodenticide and avicide.50) < LOD < LOD < LOD 5. 1992). characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. IPCS. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.. Endrin was used as an insecticide. Endrin has been detected in soils. Depending on soil conditions. anti-12hydroxyendrin.09 and 7. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 97 . 2008).30 (<LOD-6. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. and occasionally at low levels in sediment and surface waters. 72-20-8 General Information Endrin. Ketoendrin is a major photodegradation product (IPCS. 1996. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. Endrin is absorbed rapidly after ingestion. endrin can persist for years.S. 1992).40 (<LOD-6.20 (<LOD-5.S. At high doses. Smith. An epidemic of acute endrin poisoning. 1979.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.S. Endrin does not accumulate in body tissues (IPCS. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40-5.10 (<LOD-5. 1992).S.10 (<LOD-5.S. 1991). have been cancelled by the U. 1987). unlike aldrin and dieldrin. In the body. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. is no longer manufactured in the U.. Hepatic effects of endrin exposure have included necrosis. EPA. population from the National Health and Nutrition Examination Survey. fatty infiltration. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. 1991). 1981). unless the dose is high and the exposure is very recent. 1992. endrin has been detected with declining frequency in U. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. endrin usually is not detected in serum of exposed individuals. < LOD means less than the limit of detection. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used.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 5.50) < LOD 5. inhalation or dermal exposure routes.8. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. Over time. or discarded.. or from contact with contaminated soils and sediments in areas where endrin was applied. Kavlock et al.30) < LOD 5.40) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. which may vary for some chemicals by year and by individual sample. 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. total diet surveys (FDA. Endrin was not widely used as a termiticide.Organochlorine Pesticides Endrin CAS No.20 (<LOD-5.60 (5. a stereoisomer of dieldrin.. and inflammation (Smith. All uses of the pesticide in the U. manufactured.

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

Rowley DL. 1991. Jr. Saleem M. pp. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Whitehouse DA. Schulte P.64-65 Spec. 731-915. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. et al. Hardjotanojo W. Burse VW.13:155-165. Hanisch RC. Eds.html. Patterson DG Jr. August 2008.html. Buckland SJ. Available at URL: http://www. Grajewski B. Inc. Pediatrics 1987.79(6):928-934. Handbook of Pesticide Toxicology. 4/21/09 Bates MN. Smith AG. Convulsions caused by endrin poisoning in Pakistan. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. et al.21:141-150. II. Kavlock RJ. Olea-Serrano MF. Environmental Health Criteria 130.gov/~dms/ pesrpts.9:1357-136. Olea N. Chernoff H. 1992. Exposure of women to organochlorine pesticides in Southern Spain. Toxicological profile for endrin [online].fda. Ginsburg KS. Turner W. Sokal D.96:34-40.54:1431-1443. Cancer Epidemiol Biomarkers Prev 2000. Rab MA. Patterson DG Jr. Environ Res 2004. Narahashi T. Botella B. Chernoff N. No:429-436. Chemosphere 2004. Ward EM. 4/21/09 International Programme on Chemical Safety (IPCS). et al. Perinatal toxicity of endrin in rodents.inchem.atsdr. Rivas A. Gray JA. Crespo J.cfsan. Gray LE. Ellis H. Jr and Laws ER. Cerrillo I. Needham LL. Academic Press. Andersen A. Available at URL: http://www. Hanisch RC. Fetotoxic effects of prenatal exposure in hamsters. Food and Drug Administration (FDA).org/documents/ehc/ehc/ ehc130. Frey JM. Vol. August 1996. New York. Gray J. 2 Classes of Pesticides. Fetotoxic effects of prenatal exposure in rats and mice. Toxicology 1979. Perinatal toxicity of endrin in rodents. Fourth National Report on Human Exposure to Environmental Chemicals 99 . et al. 4/21/09 Kavlock RJ. Roy ML. Endrin [online].cdc. Rogers E. In Hayes WJ.gov/toxprofiles/tp89. Toxicol Lett 1992. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Available at URL: http://www. Liddle J. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. I. Gray LE. Garrett N. Toxicology 1981.htm. Chlorinated Hydrocarbon Insecticides.

4. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.9 (25.8 (22.3-20.6) < LOD < LOD 24.6-44.2 (17. 01-02.5-18. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.4-16. population from the National Health and Nutrition Examination Survey.0-25.0 (25.3-26.2 (14.2-31.2-15.5-33.9) < LOD < LOD 15. 2..6-trichlorophenol (2. and foods with a high fat content.9-20. particularly by consuming fish.6) < LOD < LOD 26. wildfowl. and sediment (Barber et al. HCB is well absorbed after oral administration. and has been detected in soil.5 (13.4.9) < LOD < LOD 16.9 (14.6-33.9) < LOD < LOD 20.4 (11. Survey Geometric mean (95% conf.2 (13. Urinary metabolites include pentachlorophenol (PCP).1-20.4 (18.9-24. < LOD means less than the limit of detection. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.7) * * 14. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.8 (15.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (14. The FDA dietary surveys have shown that over time.4.6 (24.4) < LOD < LOD 22.7 (27. Therefore.9-32.3 (22.4-15.7 (19.8) < LOD < LOD 27. and 7.4 (22. 2005). Although it is not manufactured as an end-product in the U.1 (14.5) < LOD < LOD 18.8-15.S.5-14.7-26. and 03-04 are 118.0-28.4.3) * * 15.3) < LOD < LOD 29.3 (16. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR. 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.3-22.1) * * 15.2) < LOD < LOD 29. Gunderson.1 (14.9) < LOD < LOD 28.3) 24.5-trichlorophenol (2.9) < LOD < LOD 19.7 (15.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.6 (21.2 (24.0 (18.7-30.5-TCP) and 2.4) < LOD < LOD 14.0-16.7) < LOD < LOD 24. 31.5 (14.3 (20.7-15.9-30.1) < LOD < LOD 15.3 (12.1-16.9 (25.4) < LOD < LOD 23.4 (18..7-16. and accumulates in fatty tissues where it persists for years. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..7 (15.4) < LOD < LOD 19. The general population may be exposed to HCB through diet.8.S.7-29.0) < LOD < LOD 15.6-26.0) < LOD < LOD 15. water.4) < LOD < LOD 18.4. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.9 (23.6-TCP) (To-Figueras et al.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. primarily as a fungicide and seed treatment until the U. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.5-14. 1988).4) < LOD < LOD 33.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. air.0 (18. distributes widely throughout the body.6-32. which may vary for some chemicals by year and by individual sample.0.2-15.S.9) 19.7-22.9-17.S.0) < LOD < LOD 24.6) < LOD < LOD 25. and elimination occurs by renal and fecal routes.9-15.1 (17.6) < LOD < LOD 26.9) < LOD < LOD 20.7-21.3 (14.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.2) < LOD < LOD 13. 2008. 1976).2 (14.1 (13.0-19. see Data Analysis section) for Survey years 99-00. or game taken from areas with HCB contamination.6 (23.. 1997).6) < LOD < LOD 14.0) * * 15.7-16. 2002).5-15.5 (13.7) 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 * * 16.8 (26. respectively.3) < LOD < LOD 20. 100 Fourth National Report on Human Exposure to Environmental Chemicals .Organochlorine Pesticides Hexachlorobenzene CAS No. HCB is slowly metabolized. HCB has been detected in fewer foods since the 1980s (FDA.6-19.3 (22. EPA cancelled its use in 1984.5-15. breast milk is an additional route of elimination in nursing women.

very high.gov/pesticides/ and from ATSDR at: http://www.060-. environmental levels) and health effects is available from the U.145-.132) < LOD < LOD .196) < LOD < LOD .065 (.097) < LOD < LOD . population from the National Health and Nutrition Examination Survey.S.092 (.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. Chronic feeding studies in animals have demonstrated kidney injury.157-.163 (. and the FDA has established a bottled water standard for HCB.099) < LOD < LOD .147 (.129) < LOD < LOD . Survey Geometric mean (95% conf.086-.203) < LOD < LOD .258) < LOD < LOD .171 (. anorexia.087 (. This condition.123 (.169-.090 (. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown. acute doses produce central nervous system depression and seizures.155) < LOD < LOD .085-.127-.113-.186 (.090-. Schmid.S. 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. and many died before 2 years of age (Peters et al.Organochlorine Pesticides chemical. Infants were exposed transplacentally and through breast milk.178-. thyromegaly.098 (.086) < LOD < LOD .121 (.135-. and weakness. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.095-.107) < LOD < LOD .102 (.091-.118-.gov/toxpro2.092 (.148-.160 (.157 (. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.118) < LOD < LOD .089-. 1960). With chronic exposure.123 (.145-..163) < LOD < LOD .095) * * . IARC classifies hexachlorobenzene as possibly carcinogenic to humans. HCB interferes with normal heme synthesis.e.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .081 (.094) < LOD < LOD .099) < LOD < LOD .S.109) * * .191 (. arthritis. immunologic abnormalities.html.114-.176-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD . and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.073-.092-.141) < LOD < LOD .175) < LOD < LOD . EPA has established a drinking water standard.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 * * .099) < LOD < LOD ..102) < LOD < LOD .126) .100) < LOD < LOD .095) < LOD < LOD 75th < LOD < LOD 90th * * .152) < LOD < LOD .epa. More information about external exposure (i.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .097) .081-.090 (.088-. as well as hypertrichosis.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 * * .159-. reproductive and developmental toxicities.156 (.069) < LOD < LOD .118-. 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. EPA at: http://www.095 (.147-.179 (.111-.088-.167 (.097 (. and liver and thyroid cancers (ATSDR. The U.089-.122) < LOD < LOD .163-. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.088-.078 (.083) < LOD < LOD .085) * * .125 (.082-. Fourth National Report on Human Exposure to Environmental Chemicals 101 .atsdr.130) < LOD < LOD .173) < LOD < LOD .182 (.203) < LOD < LOD .225 (.062-.069) * * .094 (. which may vary for some chemicals by year and by individual sample.190 (.095 (.086-.090 (.174-. Biomonitoring Information Serum concentrations reflect the body burden of HCB.114-.115 (.cdc. 2002).140 (.120 (.143-.064 (. 1982.092 (.111) < LOD < LOD .077-.104 (. ACGIH has developed workplace exposure limits for HCB.072-.079 (. In humans.107-.123 (.176) < LOD < LOD .

1986. Herrero C. Canada). The metabolism of higher chlorinated benzene isomers. Bjerselius R. 2005). Lackmann. Biol Neonate 2002.205:297-308. et al. Muckle G. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al.135(4):400404. Glynn et al. 2002. August 2008. 2002. Kohli J. only 4. 1999). Bryan GT.. As a result of the lower limit of detection in NHANES 2003-2004.110(8):835-838. Dewailly E. September 2002. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area.atsdr. 2003). Santiago-Silva M.gov/~dms/ pesrpts. Arch Dermatol 1999. Krause C. Schwartz JM. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Kemper FH. 2006). Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. 2002) and among children (Link et al. Link et al. van Wijk D. Zoellner I.349:144. Paepke O. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher... J Exp Sci Environ Epidemiol 2007.. Fenster L.html. Organochlorines in Swedish women: determinants of serum concentrations.71(6):1200-1209. Toxicological profile for hexachlorobenzene update [online]. 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.cfsan. FDA total diet study. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Chemosphere 2005. but overall. Piechotowski I. 4/21/09 Glynn AW. Biomonitoring of persistent organochlorine pesticides. Barr DB.81(2):82-85. J Assoc Off Anal Chem 1988.. Gabrio T. et al. Ozalla D. Sweetman AJ.44 mg/L. Eskenazi B.77:173182. In Spain. Sala M. Sci Tot Environ 2005. Bertram HP. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. dietary intakes of pesticides. Available at URL: http://www.gov/ toxprofiles/tp90. Laliberte C. 1989).. Bradman A. Atuma S. HCB detection in serum also was proportional to age. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect.cdc.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.fda. Herrman T. Muller C. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. trends and processes. et al. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.58:1185-1201. Gocmen A. In a representative sample of the 1998 German adult population. Kaus S. Link B. 2002. Hexachlorobenzene in the global environment: emissions. and the geometric mean concentration of HCB in whole blood was 0. Can J Biochem 1976. Seiwert M. In the 1976-1980 NHANES subsample.17:388–399. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Schulz C. Environ Health Perspect 2002. Food and Drug Administration (FDA). Otero R. Becker K. distribution. Lackmann GM. Bertram et al. Lecha M. Jones D. April 1982 to 1984. Cripps DJ. more HCB levels were quantified. HCB levels were directly related to age. 2005. Safe A.. 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. Over the past two decades. Available at URL: http://www. Darnerud PO. Gunderson EL. et al. and other chemicals. levels. Granath F.54(3):203-208. Reference values updated. however. 102 Fourth National Report on Human Exposure to Environmental Chemicals . 4/21/09 Barber JL. Lackman.39(12):744-749.111:349355. References Agency for Toxic Substances and Disease Registry (ATSDR).9% of participants had quantifiable levels (Stehr-Green. Arch Neurol 1982. Peters HA. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Jones KC. Lepom P. Dallaire F. Dogramaci I. Lawrence River (Quebec. IARC Sci Publ 1986. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Aune M. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Environ Health Perspect 2003. Bradman et al. Ayotte P... respectively. 2002). 2005). Int J Hyg Environ Health 2002. selected elements. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. 2002.html.. Holland NT.

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

50) 8. See the section “What’s New” at the beginning of this Report for details.7-166) 70.6 (10.9-56.3 (42.6) 35.6) 16.80 (6.3 (13.0) 71.7 (62.9 (30.S.5 (14.3 (26.2 (50.4-50.5528. 2005).7) 32.6-47. commonly known as lindane. and 03-04 are 9. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.3-56.1-32.8 (10.4 (52.20-16.46-11.7) 10.3 (42.4) 51.Organochlorine Pesticides Hexachlorocyclohexane CAS No.3 (62.7) 27.4 (16.S.3-85.8) * * * * * * 15.4) < LOD < LOD < LOD 46.8 (33.5 (24. 58-89-9 General Information Hexachlorocyclohexane (HCH).3) 34.6-37.5 (8.1 (18. Technical grade HCH is a mixture of all four isomers.8) 12.7) 10.5) 11. which may vary for some chemicals by year and by individual sample.9 (32.2) 13. environmental levels declined.1 (12. containing about 64% alpha and 10%-15% gamma isomers.87 (9.1-49.9-24. 6.0-21.8 (21. Lindane has a half-life of about two weeks in soils and water. gamma.8.0-20.68 (<LOD-10.1) 12.1-27.7-96.1) 31.4) 11.8-16.5) 67.3) 14.4 (8.5 (37.2 (34.6) 36.2-17.70-12.0) 8.0 (33. water.3) 37. and delta.2 (31.6-89.2 (9.6 (17.1 (11.7 (35.70 (6.0) 7. It is no longer produced or sold in the U.7 (30.70-19. population from the National Health and Nutrition Examination Survey.4) 901 1067 952 992 1224 1007 Females 11.1-15.2-52.0 (19.6 (16.7-96.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.8) 7.6 (22.36.8 (17.6-14. beta.1 (21.2-98.6-62.1 (9.9 (62.6) 47.1-36.2) 142 (99.8) 95th 68. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.4) 10.9-21.9 (40. 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.3-38. 608-73-1 beta-Hexachlorocyclohexane CAS No.8-87.30-11.2-67. respectively.43 (<LOD-9.0-70.9-14. In 2006.0 (8.7-20.6 (33.7 (<LOD-16.4) 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. including alpha. exists in several isomeric forms.7) 23. EPA cancelled agricultural uses of lindane (ATSDR. each result has been multiplied by 1. HCH isomers.3) 25.6-42.8-19.1-16.8) 52.8) 27.8 (64.4) 21.1 (16.6) 50. However.8-54. formerly referred to as benzene hexachloride.90-8.5) 22.04-10.7 (29.4 (12.6-20.7 (13.5-123) 49.2 (18. the U.8 (9.7) 18.70 (8.66-12.9-81.56-12.4 (50.8 (23.2 (29.1 (30.5) 14.8) < LOD 10.4 (11.9 (50.0) 17.9) 81.7) 73.1-37.6) 18.9-178) 48.7 (53. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-199) 134 (85.4-45.0) 35. As pesticide applications of HCH were increasingly restricted or eliminated. 104 Fourth National Report on Human Exposure to Environmental Chemicals .1-32.61-12.2-42.0-34. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR. soil.2-22.5 (16. 01-02.0-23.1) 12.7-26.6) 653 758 589 1240 1533 1370 20 years and older 10.0 (14.2 (48.7) 97. see Data Analysis section) for survey years 99-00.2) 62. 2005).7-69.5 (11.76.5) 40.4-73.4) 27. < LOD means less than the limit of detection.6-135) 69. so they can accumulate in fatty tissues of animals.60-13.5) 16.0-70. and 7.4) 44.6 (40.3) 51.5) 29.2-20.90-8.1) 71.2-87.2-46.5-29.8 (32.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.4-111) 84.0) 41. interval) 9.1 (9.2) 36.8) 39. **In survey period 2001-2002.7-69.0 (35.9) 15. 319-85-7 gamma-Hexachlorocyclohexane CAS No. particularly alpha and gamma have been detected widely in air.8-68.5 (43.9 (9.0 (<LOD-12.6-18.7) 56. and sediment as a result of historic production and use.90) 7.9-51.9) 17.9) 45.1) 13.2) 9.4) < LOD 9.0 (37. and have been used either as fungicides or to synthesize other chemicals.80 (<LOD-14.7 (25.9 (11.1 (27. The other isomers can be formed during the synthesis of lindane.0-111) 70.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.9 (26.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14. The gamma isomer.S. HCH isomers are lipophilic.89 (<LOD-9.5) 90th 42.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.2-55.

1977).700) .080-. The beta isomer accumulates in fatty tissues and is metabolized more slowly.070 (.244-. 1983). and memory loss (Nigam et al.350 (. which may vary for some chemicals by year and by individual sample.103-.081-.521 (.330-.200-.250-.580 (.100) .065 (.620) .110) . U.083 (.144 (.05) . The U.587) 653 758 589 1240 1533 1370 20 years and older .350) .125) < LOD < LOD < LOD .120) . When animals were chronically fed lindane at high doses.080 (.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th . Workers who directly handled HCH have complained of headache. 2008. for lindane.062 (. After dermal application of lindane 1% lotion.5528.057-.056-.077) < LOD .051-.710) .150) .103) 90th . Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.200 (..090-.410 (.150 (.047-.140 (. Rogan.480) .130) . 1986).170-.086) < LOD < LOD < LOD < LOD < LOD < LOD . EPA has established a drinking water standard.092 (.100-.050 (.174) . Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.050-.254) 95th .080 (.131-. Distribution is mainly to fatty tissues.310) .560) .216 (. each result has been multiplied by 1.690) .32) .139 (.100-.160 (.103 (.120 (.S.190) .160-.450-.470) . 1971. See the section “What’s New” at the beginning of this Report for details.220) .S.068-.360) .057 (<LOD-.380 (. probably by blocking inhibitory neurotransmitters in the central nervous system.090 (.140) ..404) .160) .140) .175 (.048 (<LOD-.01 (.260) . ingestion.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .077) < LOD .080) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.150) .Organochlorine Pesticides exposure to HCH is through the diet. the serum half-life was about 20 hours among children (Ginsburg et al.370-.120-.050-. **In survey period 2001-2002.680) .190-1.250 (.070 (.060) .319) .064) .340-.180-.191-.040-.390-. hepatic enzyme induction. respectively.501) .062 (.090 (.400) .065 (.120-.480 (.050-.080-.290) .190-. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.073-.100) .124-.290) .191-.260-.130 (.290 (.150-.091) .460 (.200-.050 (.230-. HCH isomers are absorbed after inhalation.410-. 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.146-.372 (.250 (. or dermal exposure.190) .250 (.210-.260) .281 (.050-.320 (. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.220-.078 (.560 (.570 (. tremors. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.059-.510) .100 (.410) . Fourth National Report on Human Exposure to Environmental Chemicals 105 .214) .057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .294-.118 (.222 (.167 (.120) .220-. 1996. OSHA and ACGIH have established workplace standards and guidelines.840) .096) .382-..173-.110-.460) .280-. Gunderson 1988).120 (.450 (.050 (<LOD-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.410) .390 (.100 (.170-.056-.089) . 1981).250) .287 (.910 (.450) .083) .050 (<LOD-.290 (. and FDA has established a bottled water standard and food residue tolerances for lindane.240-.420-.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 .360-.234 (.210 (.330 (..305) .220 (.067 (. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.119) .057-.308-.120-.360 (.310) .S.070) . resulting in a half-life of about seven years.210) .661) 901 1067 952 992 1224 1007 Females .620-1.070-. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.280-.098 (.120 (.442 (.600) .069) .067) .297-.072 (.240 (.051 (<LOD-. 2002).270 (.080-.090 (.058 (<LOD-.130-.064 (.118-.210 (. and nephropathy developed (IPCS.310 (.050) .100-.089-. paresthesias. and seizures.340) .070-.250-.580-1.110) ..400) .412 (.110) . Saxena et al.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.221-.070-.140) .470 (.080) * * * * * * .814) . population from the National Health and Nutrition Examination Survey.331 (. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways. enlarged livers. interval) .480 (.290 (.37) 1.300-. ataxia.

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

. 1998). 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).S. which may vary for some chemicals by year and by individual sample. Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. 2003). 2005). Radomski et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. 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. 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. respectively. 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 .. In a small study of adults who consumed sport fish from the Great Lakes. 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. population from the National Health and Nutrition Examination Survey...Organochlorine Pesticides 2001-2002 survey period (Link et al. 1971). in this Report (Nigam et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Heinrich R. Krause C. Available at URL: http://www.cdc. Metabolism of gammahexachlorocyclohexane in man. Aune M. Radomski JL. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Placental transfer of pesticides in humans. dietary intakes of pesticides. org/documents/jmpr/jmpmono/2002pr08. Available at URL: http://www. Ellis H. Maass R. Visweswariah K. Bottimore DP. Needham LL. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Becker K.html. Needham LL.9(4):417-424. Stehr-Green.html. J Assoc Off Anal Chem 1988. Piechotowski I.inchem.58:1185-1201.72:261265. Cancer Causes and Control 1998. Seiwert M.111:349355.91:998-1000. et al. et al. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Saiyed HN. Reisch JS. Rothman N. Darnerud PO. et al. and other chemicals.96:34-4Food and Drug Administration (FDA). Chemosphere 2005. Atuma S. India. Bai KM. April 1982 to 1984. Nigam SK. Gabrio T. Wood PH. Garrett N. Toxicological profile for hexachlorocyclohexanes update [online]. Environ Res 2004. Lowry W. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Int Arch Occup Environ Health 1983. Rivas A. Brinton LA. Absorption of lindane (g benzene hexachloride) in infants and children. Buckland SJ.71(6):1200-1209. FDA total diet study. Exposure of women to organochlorine pesticides in Southern Spain. et al.52(1):59-67. gov/toxprofiles/tp43. Pollutants in breast milk.205:297-308. Int Arch Occup Environ Health 1986.atsdr. Lepom P. Karnik AB. 4/21/09 Kutz FW. Sturgeon SR. Saxena MC. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Siddiqui MKJ. selected elements. Bhargava AK. Link B. Gunderson EL. The Great Lakes Consortium. Majumder SK. Zaidi SS. et al. Brock JW. Needham LL. Int J Hyg Environ Health 2002.150:981-990. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. 2002. Kaus S. Chemosphere 2004. 4/21/09 Anderson HA.120:1-82. August 2008.cfsan. Arch Toxicol 1981. Burse VW.27:405-421. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States).48:127-134. Angerer J.54:1431-1443. Environ Health Perspect 1998. Bjerselius R. August 2005. Deichmann WB. Hanrahan L. Rey AA. Schulz C. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Arch Pediatr Adolesc Med 1996. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.htm. Granath F. Herrman T. Raju GS. Environ Health Perspect 2003. Krishna Murti CR.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Olea-Serrano MF. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. children and newborn infants. Cerrillo I. Bull Environ Contam Toxicol 2004. and HCB residues in human blood in Ahmedabad.gov/~dms/pesrpts. Glynn AW. International Programme on Chemical Safety (IPCS). Demographic and seasonal influences on human serum pesticide residue levels. Olea N. J Toxicol Environ Health 1989. J Pediatr 1977. Zoellner I.20(2):186-193. Kashyap R. available at URL: http://www. Patterson DG Jr. Bhatnagar VK. Lindane. Toxicol Appl Pharmacol 1971. Kutty D. Organochlorines in Swedish women: determinants of serum concentrations. Rogan WJ. et al.106(5):279-289. Levels of DDT.57(4):315-320. Bates MN. Rev Environ Contam Toxicol 1991. 4/21/09 Ginsburg CM.fda. Crespo J. Biomonitoring of persistent organochlorine pesticides. Falk C. Potischman N. et al. Olson J. Astolfi E. HCH. PA. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Kulkarni PK. Paepke O. VI. Occupational exposure to hexachlorocyclohexane. Botella B.

5 (9. Survey Geometric mean (95% conf.6) < LOD < LOD < LOD < LOD 71.0-374) 11. where it has a half-life of 12 years..5-82.1 (13. and 03-04 are 14.S.7) 8.2 (7.5-425) 40.40 (<LOD-13.2-230) 13.1 (8.8) < LOD 15.5 (<LOD-115) 153 (30. Formerly. which may vary for some chemicals by year and by individual sample.70 (<LOD-15.4 (8. < LOD means less than the limit of detection.S. resulting in exposure to newborns and nursing infants.3 (15.90-29.7 (12. 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. 1995). aquatic organisms.4-230) 18.1 (<LOD-65.3-225) 15.70-24. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. and 7.6) 9. where it was applied directly to soil and by aerial spraying.4) < LOD 15.10-37.3 (15. Mirex can cross the placenta and be excreted in breast milk. 1991). disposal.6 (<LOD-108) 9.5-291) 11. Occupational exposure is limited to workers at sites where mirex contamination is present.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. Fourth National Report on Human Exposure to Environmental Chemicals 109 . water.6 (<LOD-31.10 (<LOD-15. Mirex has been detected in air.6-305) 15. In studies conducted in the 1970’s and 1980’s. especially those from persons living in the southeastern U. animals.5 (<LOD-42. 2385-85-5 General Information Mirex has not been produced or used in the U. mirex was detected in human adipose samples. Mirex binds strongly to soil. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.7) < LOD 66.8 (12.8 (<LOD-73.Organochlorine Pesticides Mirex CAS No. soil.6 (<LOD-23.70-40.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4) < LOD 63. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. after which it is widely distributed in the body and stored in fat. Mirex is absorbed through the skin and from the gastrointestinal tract. 01-02.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.0 (12.2) 51.S.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. respectively. since 1977. it is a highly persistent chemical in the environment. sediments. Mirex is not metabolized in the body. (Kutz et al.S.0 (<LOD-108) < LOD < LOD 50. population from the National Health and Nutrition Examination Survey. 1985. 10.8. see Data Analysis section) for Survey years 99-00.0 (14. 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. and foods.5.S.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.7 (<LOD-47.6.1) 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. Some states and the U.. or pesticide application.

which may vary for some chemicals by year and by individual sample.470) . 110 Fourth National Report on Human Exposure to Environmental Chemicals .635) < LOD .090 (<LOD-.79) .470 (.. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue. Survey Geometric mean (95% conf.310 (.079 (<LOD-. 2004). and 4. The U. Biomonitoring Information In the NHANES 1999-2000. In addition.08 (.053-.02) .170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . IARC classifies mirex as possibly carcinogenic to humans. 1991).054 (<LOD-.080-1.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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.140 (<LOD-.e. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.052-.79) . Laboratory animals fed high doses developed liver enlargement and liver tumors.37) .610) < LOD < LOD < LOD < LOD . environmental levels) and health effects is available from the ATSDR at: http://www.080-1. 1989).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 .410 (. More information about external exposure (i.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 .450 (. as well as in a subsample of NHANES II (1976-1980) participants.170) < LOD .510) < 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. reproductive toxicity included decreased fertility and testicular damage.106 (.Organochlorine Pesticides exposures are unknown.220) .077 (<LOD-. 7. and 2003-2004 subsamples.S. The geometric mean mirex levels of the Inuit mothers were 8.102) < LOD < LOD < LOD < LOD .370 (.7 ng/g of lipid.090 (<LOD-. 2001-2002. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . In samples obtained between 1994 and 1997.112 (.070-1.064 (<LOD-.090-1. Smith.110 (<LOD-.062-. 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.92) .41) . 2005).170-3. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.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 .268) < LOD .256 (.73) ..gov/toxpro2.100 (<LOD-.220 (<LOD-.atsdr.430 (.093 (.690) .090-1.html.090-1. 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.cdc. population from the National Health and Nutrition Examination Survey. EPA has established environmental standards for mirex.8. serum mirex levels were generally below the limits of detection (Stehr-Green.100 (<LOD-.090 (<LOD-.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1995.089-.059 (<LOD-.055-.106) < LOD . 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.S.108 (.450) 1.470) .

27:405-421. Odland JO. Leininger CC. Carra JS. Circumpolar maternal blood contaminant survey. August 1995. Eds. Jr. J Toxicol Environ Health 1989. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Van Oostdam JC. Watts DL. Olson JR. Handbook of Pesticide Toxicology. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Stehr-Green. dichlorodiphenyldichloroethylene.97(2):178192. et al. Gilman A.atsdr. Profiles of ortho-polychlorinated biphenyl congeners. Toxicological profile for mirex and chlordecone [online]. J Toxicol Environ Health 1985. Kutz FW.15:385-394.cdc.Organochlorine Pesticides effect. 1994-1997 organochlorine compounds. Chashchin V. Environ Res 2005. Chlorinated Hydrocarbon Insecticides. Stroup CR. 2 Classes of Pesticides. PA. In Hayes WJ. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Inc. Smith AG.120:1-82. Bottimore DP. 731-915. Demographic and seasonal influences on human serum pesticide residue levels. Sci Total Environ 2004. hexachlorobenzene. Moysich KB. New York. Hansen JC.330:55-70. Vol.gov/toxprofiles/ tp66. Vena JE. Wood PH.html. Jr and Laws ER. Rev Environ Contam Toxicol 1991. 4/21/09 Bloom MS. 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. Kutz FW. Strassman SC. Available at URL: http://www. Academic Press. 1991 pp. et al. The human body burden of mirex in the southeastern United States. Swanson MK. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. References Agency for Toxic Substances and Disease Registry (ATSDR). Dewailly E.

31 (<LOD-9.4.57 (<LOD-15.S.00 (3.6-TCP were used as intermediates in the production of certain pesticides. 1999).6-Trichlorophenol CAS No. Exposure to trichlorophenols also may result from metabolism of lindane.30-3.50-16.0 (4.40 (2.60) < LOD 8.40 (2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.4.20 (4.30-27. population from the National Health and Nutrition Examination Survey. EPA.6-trichlorophenol (2.0 (4.50 (1.7) 24.63) 18.Organochlorine Pesticides 2.30-11.27) 696 661 521 696 603 939 Limit of detection (LOD.3.00 (2. Survey Geometric mean (95% conf.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4.10-3.9. surface water.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . Historically. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. are metabolites of several organochlorine chemicals. 1999).03) 9.7. < LOD means less than the limit of detection.20) < LOD 5. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.980-3. Trichlorophenols are no longer manufactured commercially.40 (2.980-3.42 (<LOD-12..27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.0) 2.60 (.71 (<LOD-8. Such workers would probably Urinary 2.90-33.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.0) 2.30-40.8) 21.40-11.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.40 (.0) < LOD 5.80 (1. soils.60-18.0) 5.9 and 0. 2006).60 (2. which may vary for some chemicals by year and by individual sample.4.0) 2.5-TCP) and 2. Formation of 2.S.0 (3.40 (2.20-36.900-2. and polychlorinated benzenes (Kohil et al.4.4.60-8. public drinking water systems did not detect 2. 2.0) < LOD 11.0) 14.30-44. 112 Fourth National Report on Human Exposure to Environmental Chemicals . and sediments.30 (. other organochlorines.40) < LOD 6.30-27. however.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR. including hexachlorobenzene and hexachlorocyclohexanes.60 (4. may occur by inhalation or dermal routes.00-3.950 (<LOD-1.30) < LOD 4.80-41.4.0) 2. 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.0 (8.40 (1.00-3.6-TCP in any of the samples (U.0) 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.940-3.5-trichlorophenol.20) < LOD 90th 5.40) < LOD 1.50-63.5-trichlorophenol (2.40-18.20) < LOD 1.0 (5. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.4.80 (2. recent sampling of U. hexachlorobenzene.0) < LOD 21.0) < LOD 5.5-Trichlorophenol CAS No.6-TCP).30) < LOD < LOD < LOD < LOD < LOD 1.19 (<LOD-6.50 (2.00-8.27) 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 1.9 (<LOD-121) 9.0) < LOD 11.4.4.50 (.71 (<LOD-8. Both chemicals have been detected in air.S. Occupational exposures.0) < LOD 5.920-3. 1976).0 (4.42 (<LOD-8.40 (1.40 (.72) < LOD 1.20-71.30-27. 2.0 (3. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.80) < LOD 1.40) < LOD 4. 95-95-4 2.50) < LOD 1. usually at herbicide production or waste incineration facilities.4.4. 2.5TCP and 2.0) 2.50-25. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.

4.67 (1.74) 11.6-TCP..980 (<LOD-1.44 (1.44 (.2) < LOD 5. leukemias.68-4. 1989).5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.atsdr.86 (3.47-8.html.820-2.13-13.2) 2.00) < LOD 4. Among 6-11 year old children in NHANES 1999-2000. NTP classifies 2.88-16.0) 7. IARC classifies combined exposures to polychlorophenols.. Laboratory animals chronically fed high doses of 2.05-8. as being possibly carcinogenic to humans.6-TCP levels at the 95th percentile were up to eight times higher than 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.82 (<LOD-32. which includes trichlorophenols.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 2.16 (.5-TCP and limited for 2. Fourth National Report on Human Exposure to Environmental Chemicals 113 .4 (6.24-11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) < LOD 3. Human health effects from 2..5-TCP nor 2.36 (1. 2004). and lymphomas. furans..19-12.53-3..9) 12.8) 4.64 (4.4. The 95th percentiles for 2. However.00-19. Survey Geometric mean (95% conf.50) < LOD 2.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.31) < LOD 2.17) 9.gov/toxpro2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.6) 4.43 (2. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.57 (3.93-11.Organochlorine Pesticides be exposed to mixtures of chlorophenols.24) < LOD 6. animals showed hepatocellular abnormalities. the 95th percentile urinary 2.75 (<LOD-6. 7.29 (1.4.53-3. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.24 (3.80 (1.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Radon et al.7 (4.68 (<LOD-8.69-18. urinary 2.4.cdc.4) 5. Neither 2.28-25.1) 2.4.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1995) and up to 19 times higher than the 95th percentile value of 1.6) 4. At lower doses.16) < LOD 90th 5. 2003).69 (2. 2003.43) < LOD 12.4.02) < LOD 7.6-TCP as reasonably anticipated to be a human carcinogen.20-6.78-19.4.6-TCP had increased rates of hepatic tumors.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).60-3. the 95th percentile urinary 2. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.4.55 (4.00-29.4.2 (2.6) 4. in addition to dioxins.4.5-TCP.79-4.. and other chlorinated compounds..57 (<LOD-7.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .S.67 (1. 2003). Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.920-2.27-17.4.3 (5.4) < LOD 3..90 (4.5) < LOD 12.24) < LOD 5.33) < LOD < LOD < LOD < LOD < LOD 2.5-TCP or 2.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.24) < LOD 1.81 (<LOD-9.05-17.49 (1..0 mg/L.4.15) < LOD 2.37-11.8 (5.57 (<LOD-7.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.95 (3.78) < LOD 1. 1989). recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al. In the same 2-6 year old children.32) < LOD 4.46 (1.5) 11. More information about external exposure (i.75 (3.19-4.3 mg/L reported in German adults aged 18-69 years (Becker et al. 1995) were similar.8) < LOD 9.37) 16.e.73 (<LOD-8.02-3.4.1 (<LOD-58.83-12. environmental levels) and health effects is available from ATSDR at: http://www. population from the National Health and Nutrition Examination Survey.62-20.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. Urinary 2.9 (5.78 (3.

40-2.59-6.6-22.78 (2.25-11.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.04) 2.10) 2.3) 37.0-41.0 (11.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.7) 33.9 (11.53) 4.0-50.0-68.0 (15.50 (2.70) 1.48-26.9 (13. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.0) 17.92 (2.6-19.6 mg/g creatinine) and 2.51-12.4.1 (8.89-6.0) 12.35-3.14 (2. Urinary 2. 1998).02) 2. Biomonitoring data will also help scientists plan and conduct research about 2.5-TCP and 2.9) 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 2.4.7-3.0) 6.5-TCP or 2.8-24.45) < LOD 11.0-37.00-4.40-32.0 (6.0 (7.0) 17.40) 3.67) 4.0) 15.90 (3.67-12.5-TCP or 2.95 (4.0-38.53) 2.99) 6.74 (2.5-TCP and to the median 2.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.23) 3.0-18.70) 5.80-7.8) 18.4-17.70-6.4.75 (8.20 (3.8-13.8 (9.5-TCP or 2.4.6-TCP (0.69 (3.80-20.9) 694 677 519 696 602 931 Limit of detection (LOD.79 (5.4 (10.55-3.2 (14.3 (11.07 (<LOD-3.20-3.30) 4.4.10-3.80 (2. 0.60 (3.00-21.5 mg/g creatinine) were similar to the limit of detection for 2.5-TCP or 2.76) 3.40) 4.78 (2.0 (8.31 (3.3) 20. 2003).23) 2. < LOD means less than the limit of detection.84) 2.7 (13.8) 32.0) 19.65) 15. respectively.0 (16.4..09) 15.73-9.40-14.0 (14.5-TCP and 2.70) 5.80) 1. Finding a measurable amount of 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6TCP causes an adverse health effect.52-3.63) 90th 15.46-3.70 (2.56 (3.0) 13.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.4.0) 10. Survey Geometric mean (95% conf.00 (4.01-6.6TCP values.1 (10.47 (3.90 (4.20-6.0-54.10 (5.68 (<LOD-2.70) 3.4.40) 2.3) 23.0 (14.12) 2.54) 6.0 (4.10) 6.0 (6.40 (2.80 (3.20-23.0 (20.6-TCP level.70-6.49 (6.33-4.44) 75th 4.9) 13.4.70 (2.08 (2.32) * 3.2) 25.0) 13.30-33.45 (2.6) 26.4.0 (20.60) 6.4.7 mg/L.32-4.30-2.6-TCP than are found in the general population.1) 16.3 (11.60-21.36 (1.0 (12.3-26. 114 Fourth National Report on Human Exposure to Environmental Chemicals .58 (1.0) 14.45 (5.30-11.36 mg/g creatinine.4.58-3.4 (9.0) 9.2-0.60 (3. was about six times lower than the median urinary levels for males in this Report (Radon et al.57 (<LOD-2.87-14.80-6. similar to the limit of detection for this Report (Anderson et al.0 (6. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.0) 10. interval) 2.40-2.90) 2.26 (2.. Mean values of 2.66 (8.0 (15.52 (2.8-15.4.30-2.0-44.36-5.0) 13.4.40 (2.60) < LOD 5.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002. 2004)..50-5.6-TCP exposure and health effects.6-TCP in urine does not mean that the level of 2.80-25.40-7.60-3. 1991).3.4 (17.3-17.20) 4.4.74-3.0) 11.09-7. Urinary 2.5-TCP level of 0.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.1-25.31) * 2.0) 13.10-3.91-4.0-38.0) 9.28) 24.90-8.6 (12.23-2.0 (13.4 (8.85 (2.S.18-3. Biomonitoring studies on levels of 2.6-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.4.10-2.4.00 (2.00 (1.0 and 1.0) 14.6 (11.0) 19.28) * 2.85) * 3.60 (2.40-4.89 (3.24 (2. the median urinary 2.4.06) * 2.45-9.70-3. In harbor workers exposed to chlorophenol-contaminated river silt.7-16.6-17.60-37.59) 4.98-11.98-7.2) 12.7 (9.95) 3.65 (5.0-43.95-6.80 (2.72-10.0) 7.32) 3.0 (8.20 (3.0) 11.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.5-46.4.0 (9.5-TCP (0.0 (14.6) 21.7) 21..40) 2. for males in NHANES 19992002 (Agramunt et al.4.0) 7.

00) 4.42) 2.62-15.48-2.98 (1.01 (3.82 (3.09-3.8) 12.41 (3.4 (11.6) 8.2 (8.43 (2.91 (7.72-16.44 (3.22 (<LOD-2.46-14.33-2.88-7.88) 4.7 (14.20-2.9 (9.98) 10.76) 1.33 (1.5 (10.78) 2.0) 10.21-11.00) 4.5) 12.17-4.83 (3.82) 2. Fourth National Report on Human Exposure to Environmental Chemicals 115 .25 (3.14-13.3 (9.83-5.53 (3.22-9.73) 5.25-15.60 (4.79-17.15 (1.5) 11.73-22.05 (3.8) 11.50 (2.51-21.13-6.94-13.56 (7.28-4.51 (2.32-19.25-17.4 (12.50-8.52 (3.10) 4.60-2.7) 25.17) 13.22 (1.25-2.65) 2.18-2.9) 8.25 (3.53) * 2.89-2.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.8 (8.6 (9.38 (4.56) < LOD 11.52) 2.49-3.95-2.08-2.9-29.6) 12.1-21.88) 1.13 (1.24 (1.15 (6.83-6.71 (3.47-5.66-4.23 (1.83-6.26 (6.90) 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.53) 4.76) 4.63-13.5-28.91 (3.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.63 (2.4) 8.27-9.1 (13.63) 4.5) 11.52) 2.65-21.88) * 2.02 (1.49) 4.67-17.9-64.88) 4.9) 8.91-2.90 (1.52 (5.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.1) 14.77) 2.81) 2.8 (7.1-32.9) 7.40 (7.42 (2.2) 19.35 (3.3-23. Survey Geometric mean (95% conf.6 (22. population from the National Health and Nutrition Examination Survey.2 (12.5 (7.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.82-2.6-31.18-4.92) 4.59 (2.65-2.6 (10.22 (3.6) 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 2.77-4.43-7.11) 10.3) 8.54 (2.76) 2.33 (7.9-32.29 (6.05 (6.81-9.5) 9.0) 8.3-37.7-36.1 (8.68) 2.38-5.88) 5.16-10.14-2.00 (2.88 (2.00 (3.87) * 2.63) * 4.51) 18.32 (2.87) 2.75) 75th 4.38) 22.22-2.65) 18.0 (6.0 (11.9 (9.4) 4.87-7.0 (9. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33) * 2.55-2.Organochlorine Pesticides Urinary 2.78 (2.06) 4.6 (6.63 (<LOD-2.04-16.99-2.02) 3.2 (7.5 (8.4) 9.S.4.9-34.10-9.87 (3.76-8.56-5.63-15.6 (12.7) 6.58 (4.2 (13.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.29-4.8) 19.38 (2.8) 21.23) 4.6 (9.1) 11.89) 10.87-6.19-5.70-9.30-2.06) 11.04-2.53-11.41-6.10 (6.26-13.5) 8.96) < LOD 4.6) 13.06-2.6 (5.68) 2.72) 32. interval) 2.29-4.40 (2.82 (8.43 (<LOD-2.9) 19.78) 90th 12.17) 2.

Baker S. Luotamo M. Needham LL. et al. Poschadel B. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.pdf. Toxicol Lett 2003. S. U. Domingo JL.gov/toxprofiles/tp107.epa. Hill RH Jr.54(3):203-208.45:440-445. Can J Biochem 1976. Bailey SL. Am J Ind Med 2004. To T. Environ Health Perspect 1998. Schulz C. Anderson HA. Wegner R. Environ Res 1995. Safe A. Radon K. Available at URL: http://www. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.cdc. Domingo A. Jarvisalo J. Needham LL. Falk C. Head SL. 206:15-24.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Baur X.106(5):279-289.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. December 2006 Draft. Arch Environ Contam Toxicol 1989. 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].18(4):469-474.63:57-62. Aitio A. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Smith SJ. Seifert B. Jones D. Environmental Protection Agency (U. The metabolism of higher chlorinated benzene isomers. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals .EPA). Seiwert M. html. Toxicological profile for chlorophenols [online]. Hanrahan L. The Great Lakes Consortium. 4/21/09 Agramunt MC. Heinrich-Ramm R. Corbella J. July 1999. Hill RH Jr. Shealy DB. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Pesticide residues in urine of adults living in the United States: reference range concentrations. Available at URL: http://www. Pekari K.atsdr. Urinary excretion of chlorinated phenols in saw-mill workers. Kaus S. Gregg M. Becker K. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Int J Hyg Environ Health 2003. Burse VW. Holler JS. Lindroos L. Int Arch Occup Environ Health 1991. et al.S. et al.71:99108. Olson J. Fast DM. Kohli J. Szadkowski D.146:83-91.

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

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

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

0 (5.89) 9.5) 20.7) 11.60-18.43-12.45 (2.08-2.01) * * 1.0) 10.61 (3.70 (2.14) * * .79 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2) 16.0-27.50-36.20-4.13 (2.954 (.70) < LOD < LOD 1.00) 3.0-28.90) 3.50 (4.60) .0 (9. interval) 1.16 (2.98-5.290 (<LOD-.3) 17.8) 11.2.90) 2.30-4.51) 2.58 (2.9) 8.1 (9.33 (5.00-12.20 (.16) 4.860-2.95) 5.1) 13.98-12.30-6.00) 3.26 (5.42-3.00-7.40 (.63) 1.13-2.50 (2.32 (.04) < LOD 1.20-7.2 (14.530 (<LOD-2.60-11.0 (8.0 (6.58 (5.13 (2.5-17.890 (<LOD-2.30 (2.53) 4.4) 17.91) 4.56 (6.22 (.750-1.0) 11.19) 9.20-30.70 (4.81) 1.26-6.8 (12.52-11.9 (8.7 (12.810-1.48-7.1) 95th 13.00-27.44-3.717-1.757-2.4) 18.67) 3.80 (2.5 (11.4 (7.4 (9.5) 15.0) 20.83 (5.08 (<LOD-2.80) 2.60-25.3) 14. and 03-04 are 0.44 (2.02-5.81) 11.2 (9. 01-02.15-12.0) 5.2.5-16.0) 6.8 (8.97) 8.12-19.0) 11.39 (3.23-5.55-8.670-1.10) < LOD < LOD 4.840-1. and 0.8) 7.80) 11.780) < LOD 3.0 (7.0 (7.74 (8.8) 7.52) 6.30 (2.40-19.21 (.90 (1.68-7.32) 1.0 (4.80 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.97) 90th 7.955 (.4 (7.20 (.74 (8.56-13.00-12.36-4. population from the National Health and Nutrition Examination Survey.40-11.55-6.1.2 (9. which may vary for some chemicals by year and by individual sample.970-2.12) 4.10 (2.60) < LOD < LOD 4.79-7.58 (3.7 (14.71 (2.86-15.02) 4.0) 12.0 (7.35-16.27-3.47) 5.00 (5.34-7.1 (10.50) 2.0 (12.830 (<LOD-3.70-14.46) 10.10) < LOD .47) * * 1.600 (<LOD-1.2 (7.56 (4.2) 16.82-12.20 (.0) 10.80-4.05-7.0) 7.11 (.71-9.70) .81) 11.10 (.72) 5.10-7.03 (.4) 20.60 (5.40-14.00-27.93-24.0) 6.0 (8.8 (14.758-1.90-4.37 (3.35-11.1-23.700-1.8-32.70-11.0) 5.26-8.0 (8.80) 4.5 (8.70) < LOD < LOD 75th 3.2) 14.0) 10.9) 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 1.9) 14.56 (1.3-15.54 (3.80) .29) * * 1.35-12.93 (4.6) 18.20 (.20 (2.2 (14.28) 1.4 (9.579-1.10 (.80) .38-5.981 (.0) 6.34-3.86 (1.80) 2.1-17.70-19.33-18.27-15.08-15.42) .0) 10.1) 10.82) 10.6) 7.8 (9.07-10.0) 5.30 (4.3) 16.00 (1. respectively.99 (5.623-1. < LOD means less than the limit of detection.90-5. 0.39 (8.21) 9.85 (3.73) * * .80) 2.17-3.80-24.290 (<LOD-1.52) * * 1.620-1.50-5.40-16.8) 19.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.50 (.61) 4.0) 9.490-2.0 (6.0 (9.2 (11.57-7. 120 Fourth National Report on Human Exposure to Environmental Chemicals .40-5.2-20.10 (2.0) 11.70-23.599-1.66) * * 1.740-2.76 (2.0) 10.94) * * . see Data Analysis section) for Survey years 99-00.94) 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 1.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.2 (7.0) 15.0 (7.15) 14.80) 3.96-3.00-19.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80-22.44-38.40-1.0) 11.2) 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 1.2 (7.00 (4.60 (1.9-18.

9) 11.03-6.71) 10.5) 7.6) 13.67) 4.5) 12.1 (9.3) 5.2 (6.883 (.73 (1.05 (.37-3.29) * * .650-1.78 (2.31 (3.75 (7.14 (3.87-5.1 (6.68) < LOD < LOD 3.870-2.69) 2.9) 16. population from the National Health and Nutrition Examination Survey.80 (7.75 (3.20-8.94-23.79-3.710 (<LOD-1.81-5.54-11.56-13.11-6.6) 11.19 (4.93-9.13) 4.85) 2.960 (.28) 10.03 (2.60) * * .890 (<LOD-1.84 (5.61-29.855 (.28-9.34) * * .28 (2.72) 11.55-20.46) 2.98-5.76) < LOD .2) 7.28 (4.25) 6.66 (5.8) 12.40-28.56) 4.00-17.92-2.7 (8.57-10.83) 8.6) 9.60-9.45-5.2 (10.790 (.37-5.924 (.04-6.750 (<LOD-1.31-14.95 (3.09) 2.95) 2.45-11.932 (.67-19.4 (9.02 (7.00 (4.02-2.3) 16.76-4.574-1.07 (.566-1.44 (2.633-1.0) 7.58) * * 1.54-4.43 (.02 (2.7) 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 .37 (5.93-5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.47 (1. Fourth National Report on Human Exposure to Environmental Chemicals 121 .36) * * 1.23) 4.75) 2.57) 4.3) 15.29 (2.10-13.38 (1.00-13.75-7.996 (.40-3.50) 7.1) 4.40-12.94 (4.82-26.860 (.15-10.430-1.47) 2.94-22.24-3.87 (1.03) 2.53-11.5 (4.03) 2.98) .54-15.42 (3.74) 4.4 (4.40) < LOD < LOD 75th 2.80) 9.45-5.540-1.5-16.09 (.30) 2.28 (5.09-11. interval) .85 (6.9 (5.7 (9.1 (11.533-1.92-5.93) 9.87 (3.61 (1.7 (10.79-9.38) .98-22.89) * * 1.84) 7.43 (3.82-6.60) 2.39 (2.00 (4.82-14.570-1.00-19.773-1.34) < LOD < LOD .94 (2.830-1.83 (7.8 (10.61-13.57 (4.90-8.7) 12.68-4.5) 7.41) Selected percentiles ( 95% confidence interval) Total * * 50th .4) 13.89-3.2 (8.69 (4.960 (<LOD-2.03 (7.00) 8.7) 18.41-12.62-5.81 (1.47) * * .51-5.74) 90th 7.26) * * .05) .88 (5.98 (3.71-2.56) 7.25) < LOD .69) 4.40 (3.61 (1.37) 9.2) 8.1-15.27) < LOD 2.3) 12.80 (2.88) 2.21-23.2) 13.5) 8.4) 4.57 (6.30 (1.04 (1.818 (.S.41) .90-5.32-12.23 (4.9 (9.66 (1.8) 7.6 (9.94-9.52) 4.6 (10.05 (1.67) 1.1) 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 1.6) 8.8) 8.69-10.510-1.34 (6.620-1.549-1.3) 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 1.1 (7.7) 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.920 (.75) 14.900 (.1 (8.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.54-2.560-1.7) 5.5-13.01-2.10 (3.42) 12.2) 95th 12.47 (3.66 (2.820 (.98) .54) .5) 11.06-2.40) 4.8) 6.46-5.9-28.43) 2.780 (<LOD-1.64-5.47 (3.56) .608-1.02-14.2) 5.5-32.18 (.40-5.500-1.66-34.35 (1.0 (8.2) 5.9 (9.1) 4.9) 12.34 (6.80 (6.440 (<LOD-2.37 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 4.53 (6.82-14.53) 9.890 (<LOD-1.88-10.98) 9.77 (6.5-20.88-15.66-15.94-10.8) 16.0) 6.35) < LOD < LOD 3.2) 9.40-14.62) .1 (10.

89) 2.80-14.9 (7.0) 14.70-5.30) < LOD < LOD .3 (9.73) 7. see Data Analysis section) for Survey years 99-00.63-14.42 (1.8) 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 1.6 (10.31-12.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0-29.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.22 (6.5 (9.98-9.4) 11.8 (12.60 (5.00) 7.80-12.35) 4.0) 7.95 (5.90 (2.0) 13.9 (12.33-11.70 (1.90) 4.8-17.84-4. which may vary for some chemicals by year and by individual sample.9) 10.90 (2.00) < LOD .1 (10.S.90 (1.650-1.0) 9.9-17.5 (8.0 (8.30) 8.80 (2.12 (4.90-15.6) 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 * * * 1.2 (7.86-10.30) < LOD < LOD 4.4 (10.0-19.50-4.97-4.46-28.5) 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 * * * * * * .01 (2.6-41.17 (7.35-3.8-20.2) 14.3 (11.22 (6.74) * * * * * 1.20) .64) 10.790 (<LOD-1.0) 12.0) 14.0) 9.27) 9. < LOD means less than the limit of detection.4 (14.00-16.1-23.3 (9.34-5.34-3.61-32. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (9.3 (7.90 (6.27) 4.90) 8.27 (7.20-8.53 (3.81-6. 0.0) 11.6) 14.67) 4.95-9.3) 8.60) < LOD < LOD 2.7) 10.00) 3.70) 2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .00-9.75 (3.27) .88) 10.00-4.00-18.41) 3.80-8.0-24.0) 12.00-4.30) 3.66) 4.45 (3.62-17.7) 15.4 (10.20-4.27 (3.59-3.14 (6. population from the National Health and Nutrition Examination Survey.49-4.0) 11.37 (3.5 (8.9-14.00) 8.39 (5.20) 3.52 (6.24-5.7) 22.670 (<LOD-1.0 (7.80-21.0 (15.3) 14.60 (2.75 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 5.70 (8.15-2.670 (<LOD-1.00) 3.9) 95th 14.740 (<LOD-1.20-18.00-18.0 (14.80-6.31-7.6 (10. and 03-04 are 0.92) 9.910 (<LOD-2.20 (<LOD-2.90 (6.31) 1.35 (6.50-5.7) 14.0-24.670 (<LOD-1.22-12.04 (3.00 (.82) 8.5) 21.5.16-1.89 (2.10-4.6) 14.92-17.6) 11.70-9.96) 3.11-6.680 (<LOD-1.10) 6.50) 5.88) 3.6) 18.20) 3.40 (2.72) 2.670 (<LOD-1.58.9-15.5-26.25 (2.34 (6.80-3.90 (5.0 (10.80-4.0 (5.4-17.30) 3.29) < LOD < LOD < LOD < LOD 3.80 (5.0 (9.3) 22.7-19.70-8.90 (6.06 (2.1 (10.0) 23.8-20.6-19.3 (6.28 (7. 01-02.0 (13.80) . 122 Fourth National Report on Human Exposure to Environmental Chemicals .9) 9.24 (2.3 (12.8) 8.0) 13.8-21.50) .90-15.7) 16.77-3.50) 3.47-6.51) < LOD 1.99 (3.0-33.46-4.29-4.0) 6.1) 11.41-5.3) 20.80) .5.34-10.90 (6.2 (9.10-10.7-21.80 (2.58 (1.37) 2.8 (12.77-14.3) 10.90 (2.90-9.9) 16.39-13.15-6.96) 90th 7.7 (11.0 (10.8) 9. and 0.78) 5.7 (10.70-9.61 (3.66-13. respectively.4) 7.90-31.60 (6.10 (.95 (2.18 (3.0) 19.970 (<LOD-2.40) < LOD < LOD 75th 2.67-10.0) 12.22) 8.0) 18.580-2.18) * * * * * * * * 1.67) 3.10 (<LOD-1.40 (2.10-15.

99) 2.21) * * * * * 1.6) 952 1187 945 997 1331 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * .3-34.28) 6.29 (5.0-21.38-13.00 (3.74-19.39-17.47-9.86) 9.42) 7.94 (5.54) 9.4) 16.03) 3.97-4.3) 6.52-3.37-5.29-2.2) 15.27) 1.19) 3.2) 16.6) 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 1.940) < LOD < LOD 1.4-18.8) 16.96-11.5 (8.4) 15.973 (.1) 13.910 (<LOD-1.89 (2. Fourth National Report on Human Exposure to Environmental Chemicals 123 .01-5.8 (8.25-9. population from the National Health and Nutrition Examination Survey.33) 3.7-19.12) < LOD < LOD 4.20-3.34) < LOD < LOD < LOD < LOD 3.12 (7.5-17.1 (8.15 (1.89-10.68-19.3-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6) 12.79-6.02-4.0 (13.6) 13.48 (2.8 (10.03 (2.33-10.4) 6.82-8.77 (2.29 (2.8) 11.80) 3.38 (2.28-12.78 (4.88-7.2-30.93 (2.5) 10.590 (<LOD-.00) 8.11 (5.2-15.50 (6.16 (3.73 (5.S.74-4.71) < LOD < LOD 2.5 (15.8) 14.63 (2.86-3.75-3.4-15.89 (3.4 (11.30) 8.7 (10.79-9.29) 3.92 (5.41 (7.6 (11.530-1.950) .7) 14.1) 10.9) 19.28 (1.81 (7.32) 2.77 (2.07) 2.89-3.3-17.83 (6.85-17.0-19.7 (8.18) 2.9 (9.00 (<LOD-1.3-15.2) 10.92) 3.9-17.78) 4.2) 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.36 (2.4) 7.71 (1.00 (7.00 (<LOD-1.6 (11.93 (<LOD-2.27) * * * * * * * * 1.780-1.6 (13.54-5.78 (6.30) 7.43 (2.7) 15.810 (<LOD-1.06) .0 (10.27) 5.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.3) 9.27-13.4) 7.5) 13.05-3.91-9.3-21.88 (1.06 (<LOD-1.00 (5.6) 7.50-17.78-10.45) 6.760 (<LOD-1.2) 19.09-11.5 (9.30) 2.3 (7.67 (1.3) 12.70-2.4-16.53-8.55 (2.00) 2.890-2.2) 12.95) 90th 8.2 (9.7 (10.2) 12.55) 16.1 (13.68-10.6 (13.07 (5.27) < LOD .75-3.07) 2.51-7.0) 14. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .91) 3.87 (3.4) 7.83 (7.95) 3.5) 8.51-10.69-11.5 (11.59-3.2 (9.6 (10.58 (4.34-18.9-25.9 (9.72) 4.21-21.920 (<LOD-1.15) < LOD < LOD 75th 2.6) 6.3) 8.85-8.2) 8.6-19.6) 95th 16.54 (7.67 (7.6) 14.0 (11.6) 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 * * * * * * .14 (2.04) 9.25 (4.37) 3.1) 20.23-3.44-6.82-11.11-3.93 (6.6 (12.30-5.7-23.38 (.620 (<LOD-.5 (10.95 (2.00 (2.99 (4.68) .96-10.03 (6.93-10.86 (3.38) 1.5) 22.9) 16.94-14.1 (19.38 (1.61 (2.850 (<LOD-1.07-3.7) 12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.42-19.42) 8.70-35.64-11.7) 9.7 (11.89-13.45) 3.16-14.63 (6.4) 9.72-4.32-8.68-4.690 (.97) < LOD .77) 3.0 (8.89) 5.09-11.55) .7) 14.89-3.9 (9.2) 12.4-16.

83) 2.759) * .450 (<LOD-.41-5.930-1. 0.620-1.13) .77-2.930 (.01-3.14-1.31) 2.36-4.388-.86) 3.46) 1.730) .94 (2.350-.30 (.830 (.04) 1.27 (2.73 (2.950) 90th 1.10) 1.690 (.60-4.453 (.30) 1.00 (1.05-3.580-1.96-3.S.550 (.22-3.78) 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 * .90) 2.20-2.449 (.710 (.16-3.990-1.960) 1.40 (1.343 (.820 (.749 (.455 (. 01-02.600-1.949) .59-2.00-2.720 (.46 (2.95 (2. and 0.45 (1.05-2.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.57 (2.16) 2.303-.34) 2.73-5.910) 1. and 03-04 are 0.70-2.570-1.13) 2.760 (.980) 1.98) .960 (.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.50-2.89) 471 575 296 664 822 690 814 1122 919 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .340-.585) * * .10-1.740 (.657) * * .89) .240 (<LOD-.80) 2.30-3.45 (2.30 (1.584) .10) 3.20 (1.88) 1.810) .17) 1. interval) Selected percentiles ( 95% confidence interval) Total * .670) .83 (2.850) < LOD .710) .570 (.86 (1.597) * .40 (1.457 (.740 (.20-1.08 (2.600 (<LOD-. 124 Fourth National Report on Human Exposure to Environmental Chemicals .73 (1.17) 1.47) 2.54 (2.54-2.10-1.78) .75 (2.970) .79) .90 (1.90-4.54) .89) 1.95-5.382-.08 (2.570 (<LOD-.31) 95th 2.201-.20-2.390-. respectively.780) .380) .960) .592) * 50th .80 (2.50 (1.700) .11-3.48 (1. which may vary for some chemicals by year and by individual sample.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 * .80) 3.45-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.510 (<LOD-.690-1.1.38) 1.50-2.600-.09.49) .425 (.690-.260 (<LOD-.97 (2.910 (.65 (2.37-2.750) 1.83 (2.459 (.690) .26 (2.860) < LOD < LOD .970) 1.98-3.880) < LOD 75th . see Data Analysis section) for Survey years 99-00.930) 1.79) .650-.83) 1.70 (1.618) * .460-.77 (1.720-1.91) 2.76 (1.25-1.80) 3.59-6.83) .820 (.89-6.47 (1.549 (.540 (.58 (1.20) 3.16) 1.20) 3.90) 2.580-.29) 1.490 (<LOD-.35) 1.790 (.80 (1.380-.50 (1.00-4.31-3.280-.60) 2.70-7.30-3.160 (<LOD-.910-1.30) 4.32 (1.69-4.90) 3.680-1.336-.10) 1.03) 1.510 (.398-.505 (.880) < LOD .70 (1.22-2.00) 1.39) 2.30) 2.22 (1.30) 4.20) 2.48 (2.740-1.800 (.87-3.55 (3.20 (1. < LOD means less than the limit of detection.50 (1.74-5.390-.80) 2.590-.01-1.60 (2.80) 5.700) .22-8.26) .550 (.98 (2.11-3.353-.10) 1.940) < LOD .41 (2.94) .09 (.32-1.17-4.440-.61 (1.49) 2.780 (.840 (.15) 2.76-6.20) 1.04) .2.01) .380-.500 (<LOD-.15) 2.80) 3.46 (1.96-5.570) * .31-3.64 (1.20 (2.467 (. population from the National Health and Nutrition Examination Survey.33-2.960) .592-.00) 2.592) * .20-3.400) .720-1.359-.42-2.30 (.63 (1.210 (<LOD-.21) 3.680-1.20 (1.70 (1.570 (<LOD-.350-.18 (1.740-.587) * * .27 (3.780 (.50 (1.20) 2.30 (.18 (.29-2.23-3.560-.20) 1.930) < LOD .710 (.22-3.570 (.74) 3.19-1.57 (1.750-1.68-5.46-3.75-2.32) 3.95) 2.94 (3.960-1.45 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.34) 2.50 (1.50) 1.30-1.60) 3.14 (1.880 (.

32) 2.20-2.52) 3.31-1.07-2.00-3.50) 1.800-1.88) .60 (1.670 (.380) .310 (<LOD-.08-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.24) 4.72) 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 * .380-1.58 (1.47 (1.36) 3.61-3.08-2.28 (1.920) .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 * .76) 1.980-1.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.07 (.07) 5.60) .57-2.485) * * .45 (1.89 (1.730) .510 (.08-3.34 (1.80) 2.08-3.32-1.77-3.32 (.73 (2.597) * .840) .23) 1.688) * .580) . interval) Selected percentiles ( 95% confidence interval) Total * .05-4.790 (.335-.08 (.04) 95th 2.16) 1.330-.580 (.460 (.742) * * .22-2.840) 1.16-2.448 (.00-1.630) * .55-3.591 (.60) 1.19 (1.08 (2.17) 2.320-.530 (.03-2.640 (.71) .71) 2.280 (<LOD-.590-1.67 (1.490 (.32) 1.41 (.20-7.97 (1.88 (1.81) 2.09) .95) 1.850) 1.13 (1.08-2.270 (<LOD-.07) 1.53) .830 (.61) 2.06) 4.43) 1.84-6.453 (.39) 2. population from the National Health and Nutrition Examination Survey.930-1.32) 5.820) 1.07-3.510 (.39 (1.99) 1.97) 2.92-8.08) 2.70 (3.22) 4.372 (.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 * .230 (<LOD-.560 (.680 (.700 (.72) 1.89-3.377-.11 (.57 (1.305 (.78) 3.75 (2.44) 2.30) 3. Fourth National Report on Human Exposure to Environmental Chemicals 125 .18-2.02-6.540-.900) 1.49-4.02-3.66 (2.33) .447 (.740) < LOD 1.800) < LOD .72 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (.910) < LOD .08) 1.60 (2.520-.180 (<LOD-.760) < LOD 75th .750 (.75-3.710 (.23) 2.550-.700 (.645) .61 (3.11) 1.535 (.42) .23 (.950-2.460-1.42-6.310-.25-3.66) .470) .03-1.79 (1.368) * .90) 2.22 (2.550) .84 (2.43) 2.560-.67) 1.520 (.760) .440-1.87 (2.38 (1.57 (3.64 (2.550-1.97) 672 678 478 509 694 552 595 948 744 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.82) 2.72-4.55 (1.471-.136-.23) 2.71 (1.44-2.16-1.460) .38-3.47-4.550-.552 (.640 (.42 (.77-4.29-4.444-.S.45 (2.820) .318-.509 (.70 (2.880) 1.62 (2.403) .82 (2.92) 3.47 (1.05-2.08-3.370-.30-2.400-1.52 (1.300 (<LOD-.590) * 50th .94) .42-8.320-.00 (3.400) .67-3.61-3.07) 1.72 (2.08-2.67 (1.590 (.43 (1.07) 1.50 (1.02-3.22-3.05) < LOD .04-1.640 (.22) .62 (1.04-5.270-.990-1.710 (.390-1.20) 1.500-.690) < LOD < LOD .515) * * .75) 6.830) 90th 1.92 (1.77 (3.310 (<LOD-.234 (.99) 2.790) .393 (.58) 3.75 (1.739) * .380-.480) .510-.64 (2.300-.740) .05) 1.720-1.22-3.250 (<LOD-.22) 1.750 (.720 (.65) 2.10) 2.17-2.17) 2.79) 1.11-2.660-.57-4.350) .250 (<LOD-.470 (<LOD-.38 (2.06-2.870) .05 (1.67) .870 (.91 (1.73-3.330 (<LOD-.49 (1.840) 1.253-.97) 1.940-1.33 (1.98) 1.14 (2.58-6.710 (.69 (3.412-.285-.560-.270-.97 (1.43) 2.69 (1.580-.23) 3.63 (1.480-1.348-.390) .

83 (1.45) 2.0) 33.5-27.20) 1.29-4.20 (2.90 (1.11) 2.00 (.0-39.86-3.06 (1. population from the National Health and Nutrition Examination Survey.97) 6.25-3. 0.79 (2.57-2.470 (<LOD-1.83-2.9 (27.70-6.0-41.61-2.88) 3.50 (2. 01-02.0) 30.0) 3.0-260) 34.71-2.00-24.53 (1.0 (25.10 (7.10) .10 (1.6-27.0 (6.0 (24.80) .0-41.0 (26.0 (21.0) 6.00 (.19) 2.1) 38.29-9.1 (10. which may vary for some chemicals by year and by individual sample.80) 1.3) 31.5) 30.70) 1.0-49.9) 38.81-2.80) 90th 38.2-80.0 (20.0 (7.48-2.2 (19.41) 1.11 (4.0 (8.830-4.18.0-110) 42.0 (11.23) 9.14) 5.0) 4.0) 8.63-6.8 (12.660-2.90 (1.31-6.0) 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 2.18) 20.60) < LOD 1.8 (22.5-45.0-31.40-16.9) 17.9 (23.71) 5.65 (4.41 (1.45) 2.59 (1.10 (1.50-2.18) 14.33 (5.0) 32. < LOD means less than the limit of detection.32 (2.70 (.0 (20.0) 20. and 03-04 are 0.49-2.52 (4.0) 28.9-21.8) 41.2-39.4 (19.16) 2.6-45.43-7.85 (1.6 (11.3 (14.13 (1.830-3.04 (<LOD-2.83 (3.06) * 2.0) 4.26) 75th 11.5 (24.53) 1.8-24.40) < LOD 2.77) 38.0-43.64-3.1 (25.12 (3.3 (24.0-29.0-110) 34.1-46.0 (32.71 (4.3 (12.6 (9.48) 5. and 0.60 (2.6) 52.87-7.0 (38.0-53.76 (2.8 (12.5.1-25.70 (1.92-5.2) 31.0) 16.30-14.78 (1.0 (17.79 (1.26 (.9-51.36-2.82 (1.8 (26.59 (1.0) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (38.0) 18.04-8.0 (38.81-3.77 (1.70) 5.0) 3.66-5.7-22.09 (4.57-2.2-26.98) * 2.21 (1.7) 47.05) * 2.0 (38.0) 42.7 (28.70-17.0) 16.4) 19.0-58.91 (4.30) 11.0) 17.0) 4.53) * 2.16) * 1.83-2.5) 69.40) < LOD 1.46-2.1) 140 (46.50-20.0) 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (13.3 (12.80-2.76 (2.30 (.58-2.10-4.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90) 11.0-41.35-6.0-52.7) 20.2-27.29) 2.1-47.0) 15.2 (12.7 (12.600-2.4 (10.21 (3.7-41.3) 38.48-2.85) * 2.4) 38.64-8.0 (37.90-8.6-54.05-3.7 (12.6 (15.99 (2.8) 32.1-40.0 (40.2) 16.17-2.1-19.70) 1.53) 40.44) Selected percentiles ( 95% confidence interval) Total * 2.18) 6.12) 1.23-2.8) 39.44) 2.40) 50th 2.3 (23.6-22.0) 19.30) 4.0 (38. interval) 1.67 (1.41) 1.2-62.61 (1.530-4.5-74.13) 12.1 (22.1 (25.70 (7.0-92.41) 5.50-5.9) 48.69) 2.1-20.1) 18.10 (1.3) 33.0-69.0 (38.610 (<LOD-1.9) 18.5-20.92) * 2.2-27.10 (1.10) 39.41-4.3) 28.40-4.23-2.4-22.50-17.0-58.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0) 5.0) 15.94 (1.58) 16.78) 9.2-47.42) 1.0-50.690-3.4-76.93-3.19-2.0-53.96) 5.79-2.10-13.27-6.44-7.0) 45.9 (19.5-40.0 (8.1) 95th 48. respectively.8) 62.4.46 (.54 (1.21 (4.0) 20.13 (1.1 (26.80-18.04) 3.46-6.0 (19.0-62.44) 3.S.0-47.20-4.54 (3. see Data Analysis section) for Survey years 99-00.72 (1.0 (8.0-62.70 (1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1) 38.75-14.9 (10.0) 28.0) 3.8-21.05) 1.0 (33.6 (26.80) < LOD 1.0-39.9 (19.88) 1.50-7.0-230) 35.2-33. 126 Fourth National Report on Human Exposure to Environmental Chemicals .4 (15.95 (5.0) 31.74-2.98 (1.3) 26.0) 17.0) 13.3 (10.1 (11.02 (2.07-5.86 (1.0 (38.

8 (7.6) 23.56) 1.7-38.2) 36.33) < LOD 1.1 (25.9) 24.35 (2.67-16.59-15.19) 5.19) 5.5 (34.2-70. interval) 1.4 (9.46-5.80-8.16-2.11) < LOD 1.4 (5.75) * 1.2-28.86) * 3.88 (4.71) 8.2) 41.95-16.53) 1.7 (24.3-22.88 (4.84-13.27 (6.06-1.1) 27.30) 28.3-27.680-4.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.1) 36.66 (1.4-67.4) 12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.47 (1.16 (1.46) 1.7 (11.95 (2.22-2.4 (12.70 (1.00) 6.88 (1.1 (34.5) 27.7-37.0-70.59-2.0 (39.S.51) < LOD 1.1 (12.41 (2.33) 2.5 (17.66 (1.9-37.9 (26.40 (2.0 (23.3 (10.88 (1.38-5.0-71.0 (23.4 (21. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.63-5.48 (4.1) 52.1 (39.36 (4.58-2.18) 3.870-3.23-1.38 (3.5 (8.02) 1.4 (25.0) 3.0 (25.95) 90th 32.08) 1.07-2.06) 1.4-34.86) * 2.899-2.15 (.21 (4.6) 3.83) .94) 19.5 (15.45 (1.59-2.79-17.61 (1.4) 14.5 (15.930 (<LOD-1.1) 17.1) 13.9 (10.1) 27.82) 1.48) 1.16 (1.23) < LOD 2.4-39.22-3.1-22.6) 19.7-43.37 (1.06) 1.2 (8.38-1.52 (1.6) 11.5-43.3-42.6 (11.6-32.6 (7.34) * 1.2 (9.06) 75th 9.3 (10.5 (6.26-4.9 (13.4 (25.67 (1.2 (16.1) 13.0) 25.0 (19.1-63.7) 26.9 (39.7 (10.60 (.1 (50.44) 9.8) 23.8-37.6) 112 (40. population from the National Health and Nutrition Examination Survey.91 (6.17) 2.83 (.71-2.1) 25.24 (1.32-3.8) 32.2-38.0-118) 29.00 (4.0-40.80 (1.6) 3.36-13.12) 3.90 (.58-17.0) 952 1187 945 996 1330 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.1 (33.4 (11.61-22.670-1.72) 2.2) 33.2 (15.67-3.0) 47.09 (5.46-6.9-18.51) .2) 13.3 (20.7) 30.07) 9.8) 11.64 (1.11-2.9-36.08 (1.5-36.9 (7.6 (27.91-2.32 (3.9) 54.2) 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 2.7-19.1-60.9) 12.29-5.03-2.27) 10.00-16.61-2.19-6.890-4.28 (1.01 (.46-22.50-5.2 (21.28) 1.82 (2.40-4.22 (.56 (2.68) 47.39 (1.0) 30.14 (.7 (18.57 (6.3) 28.75-6.5 (41.60) 4.0 (14.0 (17.0) 13.35) 1.97 (1.96) 2.9) 3.02) * 1.43) * 2.2) 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 1.0 (32.8-43.5-97.870-3.6-38.66) 8.54-15.79 (2.7-20.52-4.23) 37.8-45.6-51.3) 13.8-26.9 (19.62 (2.37-2.1) 15.8-34.33-5.69-18.33) 1.0 (6.9-95.70-4.27) 50th 2.9-52.93) 5.19-14.36) 10.888-1.4) 12.7-109) 22.3-19.94-20.2-47.8) 31.8) 15.7) 23.16 (1.40-7.57) 4.7) 95th 51.20-5.18) * 2.71 (1.22 (2.03) 1.4 (19.40 (5.5) 70.69-5.27-3.0) 10.68 (1.2) 4.35) .3 (9.6) 7.9-41.67 (1.75 (1.95-16.45-1.19 (1.4-21.94) 1.2) 13.02 (.6-49.9) 3.9) 24.6 (24.38) 5.07-2.3 (8.7) 15.26-2.1) 25.7-47.96-16.2-34.54-2.76-2.750 (<LOD-1.18-1.5 (13.99-4.20) Selected percentiles ( 95% confidence interval) Total * 1.7) 66.7) 34.50 (2.7) 61.25-3.870-3.4-71.47 (3.12 (1.75 (1.43-2.43-12.2) 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.31) 2.17-3.4) 3.860 (<LOD-1.7 (18.62) 4.8) 3.5-190) 30.55 (2.47-17. Fourth National Report on Human Exposure to Environmental Chemicals 127 .2 (22.0) 48.14-8.00) 1.

310 (.870 (.700-1.10) .200) < LOD < LOD .160-.650-1.130-.090 (<LOD-.130) .090 (<LOD-.700-1.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.460-.730-.080 (<LOD-.160) .870 (.640) .780) < LOD 1.240 (<LOD-.42) .140-.171) * * .390 (.410-.230-.150 (<LOD-.930 (.720-1.830 (.320 (. respectively.320-.610-1.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.120 (<LOD-.117 (.870 (.090 (<LOD-.190 (.330-.03) .610 (. 128 Fourth National Report on Human Exposure to Environmental Chemicals .660 (.640) .990) .00) .160) .360-. < LOD means less than the limit of detection.310 (.840) .850) < LOD .310-.05.650) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) .080 (<LOD-.130 (.30) .10) .760) < LOD .740) < LOD .130) .050-. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.310) < LOD < LOD < LOD < LOD .1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .S.60) 1.220 (<LOD-.850 (.310) < LOD < LOD < LOD < LOD .770) < LOD 95th .700-1.350) .680 (.510-1.290 (<LOD-.180) .380-.540) .140-.370-. see Data Analysis section) for Survey years 99-00.400-.870 (.280) < LOD < LOD < LOD < LOD .210 (.20) .540) .940 (. 0.450 (.560 (.630 (.870 (.162) * * * * * .10) .820 (.290) < LOD < LOD < LOD < LOD .110-.410-1.15) .300-1.084-.690-1.12 (.370-.10 (.130-.650-1.700) 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 .170-.530-.830) < LOD .210 (.720 (.560 (.680) .100 (.650 (.840) .430-.830 (.270 (.350) < LOD < LOD < LOD < LOD .900 (.42) .32) .610-.730) .720) .090 (<LOD-.150) .990) .190 (.090 (<LOD-.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 * * * * * * * * * .770 (.410) < LOD < LOD < LOD < LOD .300-.490 (.13) .630 (.58) .440-1.090 (<LOD-.470-1.290) < LOD < LOD < LOD < LOD 90th .700-1.410-.620 (.450 (.380-. and 03-04 are 0.570) .550) .850 (.260 (.460 (.860) .680-1.820 (.870) < LOD .360-.610 (.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 * * * * * * .099-.190 (.1.640-1.860-1.990 (.140-. and 0.120-.650) .680-1.36) .540 (<LOD-.220 (.140) .420-.130-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380-.390) < LOD < LOD .640 (.120-.830) .450 (.30) . 01-02.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .600 (.470 (.230) .430 (.30) .

720 (.750) < LOD 95th .600-1.24 (.880-1.057-.410 (.890 (.600) .161) * * .19 (.110) .960) .860 (.700-1.220) < LOD < LOD < LOD < LOD .300-.410) < LOD < LOD .490-1.03 (.140-.60) .20) 1.410 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .330 (.780 (.120) .510-.230) < LOD < LOD < LOD < LOD .410-.720 (.43) .660-1.500) .380-1.080 (.710-1.860 (.320 (<LOD-.060-.09) .78) .310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.330-.580 (.380 (.390-.360-.570-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .500 (<LOD-.070 (<LOD-.230-.370 (<LOD-.140-.270 (.550 (.550 (.230 (<LOD-.190 (.170 (.990) .810 (.800-1.070 (<LOD-.760) .360) < LOD < LOD < LOD < LOD .070 (<LOD-.180-.080 (<LOD-.450 (.730) .390-.700) .940) .410) .970) .470 (<LOD-.110) .170 (.650-1.24) .740) < LOD 1.36 (1.940) .340-.730 (.01 (.540 (.090 (.580) .520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .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-.02) .310) < LOD < LOD < LOD < LOD .86) .200 (.240-.780) < LOD 1.580-1.14) 1.210 (.270) < LOD < LOD < LOD < LOD .870) .260) .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.540) .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 * * * * * * * * * .080) .400 (<LOD-.850 (.700 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.360-.360 (.650) < LOD .02-1.140-.300-.580 (.260-.140) .380-.860-2.990) .084-.100-.450) .03) .86) .140-.440 (.670 (.500-1.570 (.570-1.560 (.290) < LOD < LOD < LOD < LOD 90th .640-1.460 (.03 (.67) .300 (.670 (.03 (.110) .380-.220 (.330-.520-.38) 1.330 (.090 (<LOD-.670-1.880 (.29 (.730) .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 .440-1.580) < LOD . population from the National Health and Nutrition Examination Survey.700 (.050 (<LOD-.120) .280) < LOD < LOD < LOD < LOD .170) < LOD < LOD .00) < LOD .540 (.250-.110) .111) * * * * * .12) < LOD .740 (.S.66) 1.070 (<LOD-.380-.190-.190 (.58) 1.140-.410-.100 (<LOD-.330-.610-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (.116 (.730) .62) 1.150-.400) .

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.26 (2.86) 4.12-1.800) 17.610) < LOD < LOD < LOD < LOD < LOD 2.00) .0-38.20-17.10-3.90-28.0) 4.90-37.46 (1.83) 2.36-3.510-.350-.190-1.770 (<LOD-1.88-3.0) 2.55-4.0 (17.28-9.640 (.10 (.170-1. which may vary for some chemicals by year and by individual sample.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 .691 (.35-10.94-3.70-17.00 (1.0) 7.0 (5.11) 13.70-3.30-6.740 (.15) 14.20-4.30-7.370-.48) 13.62-8.0 (5.40-7.67 (2.87) 12.0 (4.31-10. 0.38-3.15) 19.0 (5.07 (1.40-4.0 (3.70-30.37) .05-3.47 (3.10-9.35) 5. and 0.18) 1.0-38.0 (7.770) 2.74 (3.28) .0) 2.60) 1.870) < LOD < LOD .52 (1.330 (<LOD-1.82-4.31) .0 (6.0-39.0 (16.40) 1.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.43-4.49) 17.0-40.59-5.0) 5.76 (1.30) .0 (17.0 (5.40 (1.40-8.90) .10 (3.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.97) 20.0 (5.0) 2.580 (.360-1.21) 3.800-4.14-5.0) 2.600 (.39 (2.07 (3.6) 5.70-50.960 (.210-1.42) 2.53 (2.14) 2.28) 1.350-. and 03-04 are 0.07-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 5.67 (1.63) 32.250 (<LOD-.70) 2.0 (17.85-3. 130 Fourth National Report on Human Exposure to Environmental Chemicals .55-8.910) 2.880) 5.39) .30 (.70-7.99 (1.42) .87) 5.400-1.50) 2.380-.94 (1.890 (.05 (3.730 (.425-1.45 (2.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.0-40.33 (4.260-.07) 1.S.0) 4.90-20.110 (<LOD-.14) . respectively.0-44.53-7.29-10.590 (. see Data Analysis section) for Survey years 99-00.60) .90) .32 (1.1.99) 19.40) 2.01) 5.61 (1.00-17.480-.83-3.20-4.74) 5.68) 2.32-9.00) 1.24-7.20) < LOD < LOD < LOD < LOD < LOD 1.10 (3.90-9. population from the National Health and Nutrition Examination Survey.90) .0) 2.11) .07 (3.900 (.83-3.53) 20.07-3.80 (4.50) .10-3.0 (4.40-20.620-1.51 (2.96 (1.05 (2.750-2.0 (17.97) 20.0) 2.35) 11.0-38.99) 11.640 (.00) .20 (1.30 (1.690 (.51-8.52) 5.840-3.720) 2.08.830 (.49 (1.0 (13.48 (2.0) 5.66) 4.49 (1.850) 16.0) 4.1.750-1.30-3.12) * * * * * * * * .52 (1.20 (1.30 (1.11 (1.65) 1.30) 95th 19.90 (2.00 (.23-6. 01-02.90 (1.0 (17.63 (3.00-17.40 (1.610 (.67) .080-1.0) 2.0) 3.0) 5. < LOD means less than the limit of detection.13 (3.840 (<LOD-1.800) 90th 13.62) 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 * * * * * * .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 * * * * * * * * * .03 (.30 (2.94-8.840 (.36-3.960 (<LOD-1.30 (1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.21-3.0) 4.

4 (4.86 (3.660) < LOD < LOD .28-6.930) .3) 3.4) 2.3) 2.59 (1.370-1.33-4.830-3.07-21.03) 16.21-3.10-3.360 (.580-1.600 (<LOD-1.960 (.55) 21.18) * * * * * * * * .90-6.8) 1.66-47.1 (5.340-.580) 1.04 (1.5 (8.27 (2.04-16.11-5.260-.5 (11.91) 2.60 (1.310-.7) 4.8) 4.67) 1.38 (2.80 (.85 (1.17 (1.30 (4.8) 7.17) 5.48-42.71 (.64-4.4-34.65 (2.39) 20.7 (6.5-40.450 (.890 (.45 (1.55) 21.8) 2.71 (2.75) 5.57 (.25 (1.69) 2.02) .12 (4.370 (.700) 6.2-38.31-7.86) .96) 2.2 (8.474-1.77 (.580 (.57-40.98 (4.13 (2.33-3.540 (.14-6.240-.650) 90th 10.190-1.860-2.18) 1.96-25.50) .33 (1.150 (<LOD-.22) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8) 7.770) .790) 11.88 (2.47-10.89 (2.67 (2.9 (11.47) 5.430) 1.44) .57) 8.1) 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 * * * * * * .03) 2.31) .780-4.57) 1.62 (1.7) 3.07 (2.940-4.820 (.00) .0 (4.43) .8-33.85-3.53) .970-3.55 (3.67-6.64) 30.7) 6.1) 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.40 (.73 (4.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.620-3.00-19.67) 2.S.01 (1.8 (20.56) .14 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 4.96-8.56) 2.97) .15) 9.41) 18.18) 95th 21.740-1.11) .37) 4.81-17.44-11.730-3.10) 2.260-.590) 2.06 (.92 (2.40-12.5) 2.10 (2.9) 5.12-4.51-44.48 (4.82-11.80) 3.74 (2.83-11.91-4.02-4.790 (.02 (1.820) .1) 2.748 (.5 (9.33 (3.9) 6.88-3.33-5.08) .630-1.800-2.650 (.56 (1.23-7.270-.330-1.340-.840-3.05) .88) 17.52 (.7) 5.49-2.1 (7.51-4.53) 27.250 (<LOD-.41 (4.560 (.700) < LOD < LOD < LOD < LOD < LOD 1.69-7.32) 9.88 (.7 (12.25-38.580) 16.40) 1.62-17.35 (.22-27.5) 7.6) 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 * * * * * * * * * .390-.31-18.47) .270 (<LOD-.340 (.850-3.25-9.500 (.50 (2.340-.670 (.50 (4.8) 2. Fourth National Report on Human Exposure to Environmental Chemicals 131 .09-3.84) 9.0 (9.31) .02 (.24) 3.540-1.61) 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 .32-6. population from the National Health and Nutrition Examination Survey.48-7.690-5.36 (.29 (4.5) 2.40-2.370) < LOD < LOD < LOD < LOD < LOD 1.47-10.830 (.470 (.29-4.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.83 (4.710 (<LOD-1.430 (<LOD-.79 (.320-1.50) 11.

Buchanan D. Richardson RJ. Momas I. Charnley G. Garrison RP. Neurobehavioural effects among workers occupationally exposed to organophosphorous pesticides. Garabrant DH. Third National Report on Human Exposure to Environmental Chemicals. Shebl MM. Fisker-Andersen J. accidental. Franklin CA.7(5):715-731. Freshwater KJ. Urinary excretion of alkylphosphates in the general population (Italy). et al. Centers for Disease Control and Prevention (CDC). et al.46(4):367-378. et al. Duggan A. Demers P. Bravo R. Fenske R. Farahat TM. Bozzi N. Davis SW.59(1):217-228. McKone TE. Denley HV. Bouvier G. Bradman A. Aprea C. A clinical neurological. Krieger RI. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Abdelrasoul GM. Seta N. Kelly-McNeil K. Peterson JC. Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets. Arch Environ Health 1998. Occup Environ Med 2003. Barr DB. Harnly ME. Mathieu L. Miller M.32(5):487-496.14(6):869-889. Eigenberg DA. Blanchard O.111(13):1640-1648.110(8):829-833. Toxicol Ind Health 1998b. Ann NY Acad Sci 1997. Chevrier J. Farahat FM. Robinson LR. Young AD. Greenhalgh R. and incidental exposure to organophosphate pesticides using urine alkyl phosphate and phenolic metabolite measurements. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. J Expo Anal Environ Epidemiol 2005. Environ Res 2001. Neurophysiological function in farm workers exposed to organophosphate pesticides. Fenske RA. Castorina R. Davies JE. neurophysiological. Bradman A. et al. 2005. Checkoway H. Neuropsychological performance among agricultural pesticide applicators. Environmental and biological monitoring of exposure to organophosphorus pesticides: application to occupationally and non-occupationally exposed adult populations. Barr DB. Grzywacz JG. J Occup Environ Med 2004. Curl CL. Kipen H. Griffith W. Sartorelli E. Anger WK. Environ Health Perspect 2003. and neuropsychological study of sheep farmers and dippers exposed to organophosphate pesticides. Lu C. J Toxicol Environ Health 1981. Barr DB. et al. Am J Ind Med 1997. Quandt SA. Am J Ind Med 2006. Heudorf U. Chukwudebe A. Astroff AB. Regul Toxicol Pharmacol 2003. Sciarra G. Kissel JC. Curl CL. Engel LS. Fenske RA. Strambi M. Abdel-Azis M. Kissel JC. Giordani B. Metabolites of organophosphorous insecticides in urine specimens from inhabitants of a residential area. Occup Environ Med 2002. Elgethun K. Hansen S. J Expo Sci Environ Epidemiol 2006. The effects of occupational exposure to chlorpyrifos on the neurologic examination of central nervous system function: a prospective cohort study. Fiedler N. Eaton DL.16(5):417-426. Schweitzer SJ. Barr DB. Long-term use of organophosphates and neuropsychological performance. Kedan G. Amr MM. Curl CL.15(2):164-171. Koch D. Organophosphorus pesticide urinary metabolite levels of children in farmworker households in eastern North Carolina. Aprea C. Barnhart S. Environ Health Perspect 2005. Surveillance of occupational. Environ Res 1992. Environ Health Perspect 2000. Environ Health Perspect 2002. Pilkington A.12(6):619-645. Gillham RA.38(1):91-97. Lu C. Temporal association of children’s pesticide exposure and agricultural spraying: report of a longitudinal biological monitoring study. Jamal GA. Atlanta (GA). Eskenazi B.53(1):714. Angerer J. Novelli MT. Biologic monitoring of exposure to organophosphorus pesticides in 195 Italian children. Chen W. Keifer MC.837:257-268. Correlation of urinary pesticide metabolite excretion with estimated dermal contact in the course of occupational exposure to Guthion. Berent S. Costa LG. et al.108:521-525. Fenske RA. Sci Total Environ 1996. Hawk R. Boccalon P. Leffingwell JT.59(7):434-441.37(3):382-395.49(9):751-760.111(3):377382. Jolley L. Organophosphate urinary metabolite levels during pregnancy and after delivery in women living in an agricultural community. Eskenazi B. Di-alkyl phosphate biomonitoring data: assessing cumulative exposure to organophosphate pesticides. 132 Fourth National Report on Human Exposure to Environmental Chemicals . Astroff AB. Sartorelli P.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites References Albers JW. Daniell W. The effect of the 14-day agricultural restricted entry interval on azinphosmethyl exposures in a group of apple thinners in Washington State. Cumulative organophosphate pesticide exposure and risk assessment among pregnant women living in an agricultural community: a case study from the CHAMACOS cohort. Lunghini L. Orsi D. Arcury TA. Castorina R. 86:80-87. Environ Health Perspect 2003. 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Aprea C. Malathion deposition. Marshall E. Lancet. Prendergast MA. et al. Chronic neurological sequelae of acute organophosphate pesticide poisoning. et al. Jenkins B. Hore P. Eskenazi B. Johnson C. Int J Occup Environ Health 2006. vibration sense and tremor among South African farm workers. Dinoff TM. J Toxicol Environ Health A 2005. Lewis JA. O’Malley M. Levy LS. S. Kidd M. low-level organophosphate exposure on delayed recall. et al. EPA. Scherer J. Ruberu DK. Weisskopf C. National Academy of Sciences. Salvini S. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Neurotoxicol Teratol 1998. et al. Daniell WE. Am J Ind Med 1987. Neurotoxicity among pesticide applicators exposed to organophosphates. Pesticide industry sales and usage . J Occup Environ Med 2002. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Environ Health Perspect 2005. Chronic central nervous system effects of acute organophosphate pesticide intoxication. low-level exposure to the organophosphate diazinon. Arch Environ Health 1975. Takamiya K. Terry AV Jr. Jamal GA. Sci Total Environ 2004. Thompson ML. Stark A.26(2):199-209. Available at URL: http://books. Pedersen L. Wickremasinghe AR.20(2):115-22. Calvert IA. Narang A. Tumino R. Masala G. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. 4/7/09 Young JG. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Hansen S.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI.84(5):731-736. Washington (DC): U. et al. Robson MG. Visuthismajarn P. Occup Environ Med 2001.edu/ openbook.S. Rodnitzky RL. and cholinesterase status of date dusters and harvesters in California. Myers JE.30(2):98-103. Occup Environ Med 1995. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Stephens R. U.pdf. 2004. Santana J. The Pesticide Health Effects Study Group. Lancet 1995. Seiber J. Muniz J.43(1):38-45. Neurotoxicology 2005. Lu C. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Keefe TJ. Savage EP. Berry H. Rothlein J. Chrislip D. Mounce LM. Irish RM. Lasarev M. metabolite clearance. Available at URL: http://www. Keifer M. Scand J Work Environ Health 1998.345(8958):11351139. Arch Environ Contam Toxicol 2000.php?record_id=2126&page=1. May.44(4):352-357.332(1-3):71-80. 1993 [online].52(10):648-653.epa. Spurgeon A.2000 and 2001 market estimates. Rosenstock L. An epidemiological study of the relations between exposure to organophosphate pesticides and indices of chronic peripheral neuropathy and neuropsychological abnormalities in sheep farmers and dippers. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Bravo R. Heaton RK.24(1):18-29.113(4):504-508. Russo J. Effects of long-term organophosphate exposures on neurological symptoms. Environmental Protection Agency (U. Am J Public Health 1994.114(5):691-696. Steenland K. and spatial learning in monkeys and rats. Lambert WE. 1/12/09 Peiris-John RJ. Nell V. Gladstone EA. Burcar PJ. Frasca G. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Effects of chronic. Office of Prevention Pesticides and Toxic Substances. Buchanan D. Pilkington A. Phillips J. Vitayavirasak B. McConnell R. Weerasekera G.338(8761):223-227. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Caltabiano LM. Claypoole K.12(2):134-141. Beach J. Rohlman D. van der Hoek W. Samuels S. 1991. National Research Council (NRC). Buccafusco JJ. Lasarev M. Bull Environ Contam Toxicol 1994.nap. Washington (DC).S. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Ames RG. Petchuay C. Stokes L.12(2):153-172. Arch Environ Health 1988.58(11):702710.52(2):190-195. Environ Health Perspect 2006. Schenker M. Smit LA. McCauley L. Muniz J.38(4):546-563. London L. Barr DB. Chronic neurological sequelae to organophosphate pesticide poisoning. Bradman A. Saieva C. Pesticides in the Diets of Infants and Children. discrimination. Rothlein J. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Gillham R. A behavioral evaluation of pest control workers with short-term. EPA).68(3):209-227 Maizlish N.

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

28) 2. Chlorpyrifos is Urinary 3.0) 7.9-18.52-2.20 (2.01) 1.91) 16.90 (1. and on plants for days to several weeks.79-2.03) 1.20-4.00-8.97) 4.5.59) 2.92 (1.EPA. 2007).7) 8.80) 2.90 (3.10) 2.46-2.0) 12.S.43-2.98-15.76 (1.38 (3.10 (1.0) 10.62-2.60 (2.84) 1..67 (2.80-8.0-28.63 (8.30-11.47) 1.60-3.61 (1.16) 2.and post-construction structural applications for termite control were to be phased out by 2005 (U.94 (4. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.77) 1.13-3.2 (10.67 (2.51 (1.0) 9. and dust.00) 3.09 (2.30) 4. The general population may be exposed to chlorpyrifos via oral.50 (1. although some tolerances for specific food crops have been reduced in the past to avoid exceeding recommended intake limits for total dietary intake in special groups (U.0 (7.0) 15.0) 11.7) 9.50 (2.20) 10.24-1.90-7.40-26.80-10.29-1. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.0 (7.66-15.5-24. 1999.30) 5.39) 4.60-3.20-14.50 (1.30-9.0 (13.00-24.99-4.28-3.13 (1.30 (2.35) 1.51-2. but can be detected in streams receiving runoff from application sites.70-5.52-12.9) 697 660 521 701 602 947 Limit of detection (LOD.74 (1.22 (1.36 (4. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.19-3.39-2.21) 3.63 (1. It also has been applied directly on animals to kill mites.26) 7.70-17.90) 3.47-9.8-15.40-13.60-2. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.77-15.96) 3.91 (1.4.57 (2.70) 1.70 (1. USGS.9 (9.61) 75th 3.00) 1.60 (4.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.20) 4.17 (1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl. 5598-13-0 General Information The chemical 3.95 (4. applied to structures to kill termites.64) 3.97-7.25) 3. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.29) 90th 7.3 (8.1) 5.30-5.20-16.22) 2.80 (7.68 (7.15 (1.05-5.4 (10.20 (4.5 (8. and inhalation routes. in 142 urban homes and preschools in North Carolina.45 (1.0) 14. Approximately 80. Fourth National Report on Human Exposure to Environmental Chemicals 135 .61-7.50-2. 2002).80) 1.50-8.59-2.9 (10.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.20-11.40) 2.70 (1.7) 13.10) 6.24-3.89-2.10 (4.30) 4. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.0) 12.40-2.0) 12.5) 7.3) 8.9 (7.60) 5.4 (8.20-2.89 (2. Exposure can also result from contact with contaminated surfaces.40 (6.67 (1.70-15.90 (6.86) 4.0) 10.87-6.76 (1.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.37 (4.20) 2.30 (4.63 (2.9) 11.5.0) 10. air.30-1. Approximately 21-24 million pounds per year were used domestically from 1987-1998.55-5. For instance. and sprayed to kill mosquitoes.0) 6.97) 2.97) 7.20-3.44-2.0 (9.09 (3.8) 9.0 (10.80) 4.02 (1.00) 2.40 (5.0) 12.EPA.35) 2.50 (2.20) 2.81-2.71 (1.53 (1. After 2001. It has low leachability. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.71 (6.31-2.80) 12.50-5.74-9.90) 7. 2921-88-2 Chlorpyrifos-methyl CAS No.0) 18.0) 12.05) 1. dermal.4-15.66-4.90-8.27 (7.3) 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. and is infrequently detected in ground water (IPCS.77-6.50-14.50-4.10-17.30-2.95) 7.02) 1.6) 7. Survey Geometric mean (95% conf.4 (9.43-2.71 (2.37 (1.37) 5.78 (7.3 (11.40-10.32) 2. 2005).90 (2.30 (2.S. Estimated intakes from diet and water have not exceeded recommended intake limits.88 (1.0 (7.3 (10.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.50-4.70-11.97) 2.8) 10.90-4.19 (1.72-4. interval) 1.34) 1.50-2. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.1-16.0) 8.47-13.90 (1.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.40 (5.04-10.0 (7.50 (2.0) 8.80 (1.47-11.S.10 (3.68-2.32-1.60 (5.04-10.72) 2.90-2.44-5.40) 9.77 (1.51) 1.000 pounds are used per year.44 (3.47 (4. staying bound to soil particles.10 (5.4 and 0. population from the National Health and Nutrition Examination Survey.70-16.7-23.02 (7.30-12. 2002).83) 1.25) 1.60-4.0 (7.31-2. chlorpyrifos was no longer registered for indoor residential uses in the United States. pre.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.

92) 3.88-8.43 (4.02 (5.97) 3. Slotkin et al.57-2.16 (4.76 (2.35) 2.42 (6.63 (5.53-5. 2006a.55) 1.50 (4.11 (2.84-6.54) 5.1 (10.88-10.5 (6.88 (1. and other metabolites. The metabolite TCPy does not inhibit acetylcholinesterase enzymes. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.56 (1.72) 1.82 (2.63 (4.49-2. TCPy can also occur in the environment from the breakdown of the parent compounds.89) 4.02) 7.91 (4.71 (1.93 (2.14-8.60-3.7) 7. Metabolic hydrolysis leads to the formation of TCPy.43-10.57-2.39) 6.54 (2.00) 1. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.01) 3.8) 9.33) 2.39 (2.80-6.90-9.0) 6.0) 10.32) 1.24 (1.58) 1.97) 3.3) 8.25-12. weakness.52 (5.06 (1.56) 5.6) 10.6) 9.S.59) 3.47 (1.15 (4. 2002).88) 6.33 (1..22-6.69 (1.06-4.9 (12.93) 2.56-2.97-3..75) 6.24-24.26-14.19) 6.49-2.0) 12.91) 2.58 (1.51 (1. 2005.3) 8.28) 2.12-3.6-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. and seizures.47 (5.11 (2.00-8. 2005.19) 3. TCPy is more persistent in the environment than chlorpyrifos itself (U.03) 1.2) 6.09 (1. Thus.80-4. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.28) 2. 2006.91-13.80) 3.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.17-4.05-3.09-2.05-4.23-1.97 (2.21-1.14) 1.00 (7. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.93 (4..33-7.85) 4.62) 90th 5.22 (4.49-2.22) 1.86 (1.48 (2.22 (6. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.91-4.S.66-11.11) 7.64-2.07) 5.1 (7.98 (7.79-13.47 (1.93 (1.01) 3.1-38.72-2.3) 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..64-7.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.27-1. interval) 1.17-4.33 (5.83-2.85 (3.65-11.77) 1.95 (1.42-2.37 (1.64 (1.74) 1. 1984).7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .86 (1. paralysis. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.81 (3.92 (1.33 (..00-13.34-1.85-4. Based on animal data and human cholinesterase monitoring during occupational exposure.29 (3.59-2.96) 3.63-2. cholinergic effects.49 (1.82) 8.87-3.72) 2.11-9.2 (7.36) 1.62) 1.65-15.68) 1.56) 2.88-9.55 (1.83) 1.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.97 (3.25-1.05-8.44-6.58 (4.91) 1.83-11. In pesticide applicators.91) 10.25-11.39-1. Howard et al.82 (3. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.5.09-3.3 (7. neurotransmission. 2006.81) 2.47-2.53 (2.68) 6. population from the National Health and Nutrition Examination Survey.58 (1.75 (1.88 (1. 2006b). Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.01) 1. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al. resulting in excess acetylcholine at nerve terminals. 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.35-1.62-7.21-6.24) 5.55 (4.71) 3.44 (5.07) 1.58) 5. Survey Geometric mean (95% conf.24-5.19-2.31-1.86 (3.05) 3.09-1.0) 16.40) 1.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.38) 3.66) 1. Betancourt et al.31-4.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.1-21.41 (1.20 (2. 2000).46 (2.58-5.60 (1.30-1. Ricceri et al. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.45-1.44 (6.27-7.44 (1.91) 1.80-11.70-4.12-1.95 (3. and producing acute symptoms such as nausea.88-8.66 (1.44 (1.76 (3.92-2.24-1.EPA.91 (3.30-4.57) 9. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).42 (5.48 (1.73 (1.31) 1.05-1.57) 2.5) 5.. vomiting.940-1.4) 4.35) 1.23) 14.82-4..85 (2.08) 6. Once absorbed.99) 1..16) 6.12) 1. 2005.93) 5.19-1.39 (4.20-1.94-12.24) 75th 2.56 (4.78 (1.94-14.45 (1.85) 1.06 (5.24-4.3) 9.46 (1. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis. Roy et al. Urinary 3.98 (6..44 (5.99-8.

2006). 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. Curwin et al. 2005. Lioy PJ..epa..cdc.atsdr. 2007). Environ Health Perspect 2005. Catenacci G. but not chlorpyrifos. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. Barisano A. Slotkin TA. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect.82(2):305-312. In Minnesota and South Carolina farmers who used chlorpyrifos. Whyatt et al.. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. 2005). 2001) and Italy (Aprea et al. Environ Health Perspect 2001. Garabrant D. J AOAC Int 1999. 2000).. Of 482 pregnant women living in an agricultural community. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al.gov/toxpro2. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos.Reference values of urinary 3.html and from U.5.S. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. Albers JW. Betancourt AM. 2004). Aldridge JE. Meyer A. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP.. Carr RL.109(6):583-590. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U.. 2005). EPA at: http://www. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. Lotti A. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. representative subsample of NHANES 19992000 (CDC. Haidar S.. Chlorpyrifos exposure and biological monitoring among manufacturing workers. 2005.63(3):218220. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. 2002). Toxicol Sci 2006. Magnaghi S. et al. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Perera et al. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC.92(2):500-506. References Adgate JL. MacIntosh et al.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Berent S. Occup Environ Med 2006.S. the geometric mean urinary TCPy levels were similar in parents and children. Burns CJ. Aprea C.. Koch et al. 2005). 2004).EPA.. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. Burgess SC..gov/pesticides/. Betta A. Freeman NC. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. 1992. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. but levels were roughly four to six times higher than the geometric means in the U... 1999). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005). 2001). Giordani B.S. 2005. population (CDC. Additional information about external exposure (i. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. Seidler FJ. urinary TCPy levels in children were reported not to have increased (Hore et al.e. Clayton CA. Eberly LE... In Iowa farm families using several different pesticides. 2003. Levels of TCPy in the U. 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. et al. CDC. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. U. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Following crack-and-crevice application of chlorpyrifos in their homes.113(8):1027-1031.S. environmental levels) and health effects is available from ATSDR at: http://www.S. Barr DB. In a probability-based sample of 102 Minnesota children aged 3-13 years. Biomonitoring Information Urinary TCPy levels reflect recent exposure. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC.. 2005). et al. Fourth National Report on Human Exposure to Environmental Chemicals 137 .Organophosphorus Insecticides: Specific Metabolites 2004.. 2005).

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Lioy PJ.73:8-15. Barr D. gov/ntpweb/index. Pesticide residues in urine of adults living in the United States: reference range concentrations. Lein PJ. Bradman A. Howell RJ. Morgan MK. Jewell NP. Wartenberg D.15(3):271-281. Baker S. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Freshour NL. et al. Hore P. Lorenzini P. Tsai WY. Fortuna S. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Bruun D. Robertson GL. Steenland K. Bailey SL. Barr DB. Kromhout H. Cometa MF. Saunders JH. et al. Chlorpyrifos: pharmacokinetics in human volunteers.S. Chuang JC. Ann Occup Hyg 2007. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Meeker JD.5. Toepel K. Sanderson WT.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Slotkin TA. EPA). 4/7/09 Perera FP. Environ Health Perspect 2006. Toxicol Sci 2006. Bucelli R. Atlanta (GA).org/documents/jmpr/jmpmono/ v99pr03. U.

Available at URL: http://www. March 2006.111(5):749-56. 1992-2001.Organophosphorus Insecticides: Specific Metabolites 01-007. Barr DB. Barr JR.gov/circ/2005/1291/.usgs. Andrews HF.pdf.epa. 1/14/09 U. Kinney PL. 2007 [online]. Environ Health Perspect 2003. et al. Fourth National Report on Human Exposure to Environmental Chemicals 139 .gov/ oppsrrd1/REDs/chlorpyrifos_ired.S. February 2002. The Quality of Our Nation’s Waters. Pesticides in the Nation’s Streams and Ground Water. Geological Survey (USGS). Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Available at URL: http://pubs. revised February 15. Camann DE. 6/1/09 Whyatt RM.

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

< LOD means less than the limit of detection. 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. Fourth National Report on Human Exposure to Environmental Chemicals 141 .200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380 (<LOD-.2. 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 .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 .270) < LOD 659 701 920 Limit of detection (LOD. Survey Geometric mean (95% conf. 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 .S.S.200 (<LOD-. see Data Analysis section) for Survey year 01-02 is 0.670 (<LOD-1. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey.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. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

2005. Third National Report on Human Exposure to Environmental Chemicals.12(6):619-645.pdf. EPA). Freshwater KJ.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. U. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . Barr DB. Sadowski MA. September 2000. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.epa. Available at URL: http://www. Olsson AO.S.gov/oppsrrd1/ REDs/0018tred. Environmental Protection Agency (U. Eigenberg DA. Centers for Disease Control and Prevention (CDC).376(6):808-815. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. Anal Bioanal Chem 2003. EPA 738-R-00-010.S. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. Nguyen JV. Atlanta (GA). Reprod Toxicol 1998.

seed and foliar applications are planned to be phased out (U. which may vary for some chemicals by year and by individual sample. 2007). Survey Geometric mean (95% conf. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). diazinon was widely used in residential and garden application. Before these restrictions. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. Prior to 2000.45 (<LOD-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS.S. about 13 million pounds of diazinon were used annually on agricultural sites in the United States.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 143 . USGS. 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. and other metabolites.EPA.S. Diazinon is not well-absorbed through the skin. Inhalational and dermal routes of exposure can be significant for pesticide applicators. and particularly when it was ingested in granular form. 1998. but these uses have been phased out. but is rapidly absorbed orally (IPCS.2 and 0.49 (<LOD-2. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. 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. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. and forage crops. 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. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. < LOD means less than the limit of detection. 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. Most granular formulations. Once absorbed. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity.7. diazinon produced wild bird kills before use restrictions were in place. It is also used for cattle ear tag applications to control flies and ticks and. an organophosphorus insecticide that is used to control insects on nuts. diazinon cannot be sold for residential use. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects.S. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00 and 01-02 are 7.EPA. Estimated intakes from diet and water do not exceed recommended intake limits (U. 1998). in some pest strips. since 2004. vegetable. It is toxic to birds. in the past. aerial. fruits.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. 2004).

diazinon does not accumulate in tissues (IPCS. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure.e.atsdr.49 μg/L.. EPA at: http://www. 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. Thus.. respectively (Baker et al. respectively. animal carcinogen. 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.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. teratogen..epa.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.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. 1992). 2003). weakness.. 1986 Rajendra et al. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. The U. and indoor applications have been documented. 1998). At high doses. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. Diazinon is not considered to be a mutagen. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.S. Seifert and Pewnim. Intoxications in humans from intentional overdose. Additional information about external exposure (i. In addition to being a human metabolite of diazinon.76 (<LOD-3. subsamples of NHANES 1999-2000 and 20012002. In the U. agricultural. In two nonrandom samples of United States adults and children.cdc. 144 Fourth National Report on Human Exposure to Environmental Chemicals .html and from U.72 (<LOD-4.45) < 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.S. 2000. Survey Geometric mean (95% conf. Olsson et al. or reproductive toxicant (IPCS.. 2002).45 and 1.gov/toxpro2. environmental levels) and health effects is available from ATSDR at: http://www. paralysis. cholinergic effects. vomiting. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection.S. population from the National Health and Nutrition Examination Survey. in the 2001-2002 subsample (CDC. and producing acute symptoms such as nausea. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1.S.EPA considers diazinon unlikely to be carcinogenic in humans. 1986. In animals. resulting in excess acetylcholine at nerve terminals.gov/pesticides/. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. Diazinon has moderate acute toxicity in animal studies. and seizures.

(2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. 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. Study for Future Families Research Group. 2006).Organophosphorus Insecticides: Specific Metabolites 2005). May 2004.. Anal Bioanal Chem 2003. Dumas P. et al. Pewnim T. International Programme on Chemical Safety-INCHEM (IPCS). urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Toxicol Lett 2002.10(6 Pt 2):789-798. Beeson MD. Liu F. Oloffs PC. Third National Report on Human Exposure to Environmental Chemicals. Biochem Pharmacol 1992. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Diazinon. Kruse RL.134(1-3):105-113. Banister EW.376(6):808-815.htm. Irish R. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. 4/7/09 Lu C. Environ Health Perspect 2003.usgs. Geological Survey (USGS). Needham LL. Environmental Health Criteria 198. Fenske RA.44(11):2243-2250. Effect of sublethal levels of diazinon: histopathology of liver. Drobnis EZ. Swan SH. Ann Occup Hyg 2006. 2005.gov/circ/2005/1291/. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. 2007 [online]. Environ Health Perspect 2006. Bull Environ Contam Toxicol 1986. Noisel N. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. References Anthony J.gov/ oppsrrd1/REDs/diazinon_ired. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. revised February 15.50(5):505-515. Available at URL: http://pubs. Banister E. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Barr DB. Driskell WJ. Interim reregistration eligibility decision (IRED. March 2006. Centers for Disease Control and Prevention (CDC). A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.. Barr DB. Drug Chem Toxicol 1986.114(2):260-263. Redmon JB. Environmental Protection Agency (U. EPA). Toepel K.inchem. Brunet RC. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses.9(2):117-131. Seifert J.111(12):1478-1484. Swan et al. Diazinon. Oloffs PC. Carrier G. In 23 children. In 54 Canadian greenhouse workers.S. EPA 738-R-04-006. Cocker J. Atlanta (GA). 1/14/09 U. J Expo Anal Environ Epidemiol 2000. 1998. The Quality of Our Nation’s Waters. Barr DB. Sadowski MA. U.org/documents/ehc/ehc/ehc198. Olsson AO. Jones K. Pesticides in the Nation’s Streams and Ground Water. Semen quality in relation to biomarkers of pesticide exposure. In a small number of men visiting fertility clinics in Missouri and Minnesota. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. 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. Bravo R. Baker SE.S.pdf. Available at URL: http://www. Nguyen JV. Available at URL: http://www.S. 2006).epa. Bouchard M. Barr DB. Rajendra W.37(4):501-507. Mason HJ. 1992-2001.

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

S.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. environmental levels) and health effects is available from ATSDR at: http://www. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. representative subsample from NHANES 19992000 (Adgate. 2006).cdc.S. Toxicity from unprotected bystander exposure during applications is rare (U.. 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.74 (<LOD-5. 2001. 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. 2006). 1990). 2000). Giri et al. Of 382 pregnant women living in an agricultural community.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS.gov/toxpro2. EPA at: http://www. Human studies of single oral doses between 0. 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. Fourth National Report on Human Exposure to Environmental Chemicals 147 . 1996..html and from U. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample.EPA. 2005).S. 1999. Lu et al. IARC considers malathion not classifiable as a human carcinogen. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. Flessel et al. CDC. Malathion itself has not been considered genotoxic (U. 1987.. 2005.epa. 1999). Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. but cholinesterase activity was not affected.gov/pesticides/. 2002.5 and 5.. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. 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.S. 2005). and it is not considered an animal teratogen or a reproductive toxicant..e. 2006).EPA. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. Thomas et al. 1993. but isomalathion....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.. 2004). 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. Additional information about external exposure (i.. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 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. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al.S.atsdr. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. 2003). a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. Pluth et al.

114(2):260-263. March 2006. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Harley K. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Needham LL. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals .S. Lioy PJ.org/documents/jmpr/jmpmono/v2003pr06. Available at URL: http://www. J Expo Anal Environ Epidemiol 2005. Freeman NC. Szyfter K. Geological Survey (USGS). Arch Environ Contam Toxicol 2000. 4/7/09 Kissel JC. Albertini RJ. Third National Report on Human Exposure to Environmental Chemicals. Eskenazi B.38(4):546-553. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. A longitudinal investigation of selected pesticide metabolites in urine. Toepel K. Environ Health Perspect 2001. Malathion (addendum). Krieger RI. Petitti D. Neutra R. Barr DB. Environ Health Perspect 2006. Rappaport E. Dumoulin MJ. metabolite clearance. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. 2007 [online]. Bravo R. Kedan G. J Expo Anal Environ Epidemiol 1999. Lu C. Grether JK. July 2006. Irish R.gov/circ/2005/1291/. Malathion deposition. Quintana PJ.112(10):1116-1124. and cholinesterase status of date dusters and harvesters in California.15(2):164-171.epa. et al. O’Neill JP. Jaloszynski P.gov/oppsrrd1/REDs/ malathion_red. Hooper K. EPA 738-R06-030. Pesticides in the Nation’s Streams and Ground Water. Giri S. Weltzien E. Gosselin NH.77:1009-1010. EPA). Reregistration eligibility decision (RED) Malathion.445(2):275-283.73(1):182-94. Swan SH. revised February 15. Barr DB. Barr DB. Environ Mol Mutagen 1993. Environmental Protection Agency (U. Genetic toxicity of malathion: a review. Barr DB. Trzeciak A. The Quality of Our Nation’s Waters. 2005. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Harris JA.Organophosphorus Insecticides: Specific Metabolites References Adgate JL.22(1):7-17. Curl CL. Giri A. Toxicol Sci 2003 May. Pluth JM.usgs. Centers for Disease Control and Prevention (CDC). Goldhaber M. Bouchard M. Hammerstrom KA. Mutat Res 1999.S. Samuel O. Fenske RA. Eberly LE. Available at URL: http://www. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues.74(2):following table of contents. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Environ Health Perspect 2004. htm. U. Reproductive outcome in women exposed to malathion. 1992-2001. Hertz-Picciotto I.132(4):794-795. Flessel P. Am J Epidemiol 1990. Dinoff TM. Cancer Res 1996. Bradman A. Sharma GD.S. Prasad SB.inchem. Blasiak J. Mutat Res 2002.56(10):2393-2399. 6/1/09 U. Thomas D. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. et al. Lu C.514(1-2):223231. International Programme on Chemical Safety-INCHEM (IPCS). et al. Jewell NP.109(6):583-590. Griffith W. Am J Public Health 1987. Erratum in: Toxicol Sci 2003 Aug. Nicklas JA. MacIntosh DL. Ryan PB. Available at URL: http://pubs. Carrier G. Atlanta (GA). Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Brunet RC. Clayton CA.pdf.9(5):494-501.

10) 22. 2000).70-3.32-1. Once absorbed.70 (3.0) 3. Many previous registered agricultural uses of methyl parathion have been cancelled (U.61) < LOD 1. was once a restricted-use insecticide with limited applications on certain agricultural crops.20) 5. Methyl parathion has low water solubility.70-6.EPA.60 (4.05) 4. 2006).48) 90th 2.91-3..00) 3. more slowly absorbed through the skin. Ethyl parathion.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .30-3.50) 3.40) 4. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.0) 3. binds tightly to soils resulting in low leachability.44) 2.47) 2.69 (2.40-3.EPA.70 (2.45) 5.90-11. and has a short half-life in soils and on plants.850) < LOD . 2002.60-36.40) 1.790 (<LOD-.298-00-0 Ethyl Parathion CAS No.33 (1.32 (1.90 (1. In the 1990s.49 (1. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.00 (2.70 (2.10-1.11-4.700 (<LOD-. which may vary for some chemicals by year and by individual sample.S.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 149 .70 (<LOD-3.45 (1.0) 2.41-4.60-24. Methyl parathion use is highly restricted.50 (1.0) 3.8 and 0.70) 2.30-16.10 (3.22-3.60) 1.50) 2.860 (<LOD-1.300-.72 (3.80 (2.940 (<LOD-2.62 (1.730 (<LOD-. on cereal grains. with limited applications in agriculture.30 (2.67 (1.0) 3.70-6.28 (1.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . and of the chemical nitrobenzene.50-14. Survey Geometric mean (95% conf. 2003).S.40) 2.37) 2.20-5.10 (3.01-4.50 (1.46 (3.79) 4.36-1.34 (3.910) < LOD < LOD < LOD 1. and aquatic invertebrates.910) < LOD .12) < LOD < LOD 1.32-1.40-4. 2007).33) 2.37-4. ethyl parathion. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.69) 4.50) 1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.15-3.0 (3..40 (1.00 (2. first registered in 1948.0) 3.70-3. 1977).90-9.66 (2.21-1. and oral routes can occur in pesticide and agricultural workers (Muttray et al.57-4.74) 5.16) < LOD 1.10 (<LOD-6. and to a lesser extent. Estimated intakes from diet and drinking water have been below recommended limits.1. Morgan et al.57) 1.89 (2. In animal studies. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50) 3.61) < LOD 1. < LOD means less than the limit of detection.10-11. Methyl Parathion. * 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 5.67) < LOD 1.27) 2.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.28 (1.85 (2.09-1.70) 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 1.0) 4.60-19.32-3. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.50 (1.71 (3.18-3.60-5. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.30 (1.10) 4.37-2.37-4.70 (2.92) 5.80 (1.71 (2.80) 2. and eliminated rapidly from the body after absorption (Kramer et al.50 (1.02-6.13-1. all registered uses were voluntarily cancelled (U.70-6.21 (2.20 (<LOD-2.50-9. population from the National Health and Nutrition Examination Survey.50 (2.28-4. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.50 (2. Methyl parathion is not registered for residential use in the United States.70) 2.910) < LOD < LOD . peak domestic use was as high as 5-6 million pounds per year.S..30-5.20 (2. but by 2003. pulmonary.770 (.19 (.58) 3.01) 695 660 518 679 603 941 Limit of detection (LOD.990-1. Increased risk of exposure via dermal. It had been applied to cotton. Both are toxic to birds.26 (1.11) 2.01) 4. fish.40-4.92-2.80 (2. Given its limited use. methyl parathion was rapidly absorbed after ingestion. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.

850-1.13) 4.73 (1. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS. 1995).1) 2. 2006.840 (.Organophosphorus Insecticides: Specific Metabolites Metabolites”).08-3. 1991).67 (3.55 (<LOD-3.92 (2.37-1.31-3.77-7. Additional information about external exposure (i.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 .41-2. and other metabolites.720-1.94-47..980 (.96 (1. population from the National Health and Nutrition Examination Survey.82) < LOD ..20) . resulting in excess acetylcholine at nerve terminals.44-3.9) 1.00 (1.11) 1.. and producing acute symptoms such as nausea.440 (<LOD-.21) 1.00 (1. Parathion and methyl parathion have high acute toxicity in animal testing.76-14. Jaga and Dharmani.59 (1. 1990. accidental exposure. and seizures. In large doses.01 (.97 (2.72-2.01 (2. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.38-3.01-3.60 (1.90 (1.29) 2. Survey Geometric mean (95% conf.790-1.10 (1..atsdr.970 (.91 (1. 1978. 1995.89 (2.29 (2.09) 2. ethyl parathion. environmental levels) and health effects is available from ATSDR at: http://www.78 (2. gov/toxpro2. paralysis.26) 17.88) 1.33-6. The metabolite.400 (<LOD-..78-2. 2006.14-3.720 (<LOD-. Lores et al.35-3..43) 4. paranitrophenol.880 (.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .730-1.93 (2.html and from U.4 (3. 2004).930 (. 2005. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.310-. Methyl parathion is not considered genotoxic.57-7.71) 1.78-2. gov/pesticides/.10) 90th 2. Methyl Parathion.87 (1. Slotkin et al.S. 2003. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.56-2.80 (1.7) 3. WHO.epa.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . In addition to being a metabolite of methyl and ethyl parathion.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .57-2. methyl parathion. Orsorio et al.870) < LOD . or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS. teratogenic. Karanth and Pope et al.88 (1.e.39) 1. weakness.17-4.39 (1.950) < LOD .540) < LOD . IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.13-12.70) 3.98-7.2) 2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.05) 4. 150 Fourth National Report on Human Exposure to Environmental Chemicals .55) 2.3) 2.89 (2.91) 1. Thus. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S.82 (2.26 (1.15-10.07 (1. but lists ethyl parathion as a possible human carcinogen. 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.15) 3. and unintentional acute or chronic high-level occupational exposure (Hill et al. does not inhibit acetylcholinesterase enzymes.60-2.530) < LOD < LOD < LOD .11-4.940 (<LOD-1.35-3.07) 2.57) 6. cholinergic effects.430 (.08 (1. U.95) 1.2) 2.17) .S.94-4.48-4. At high animal doses of methyl parathion.60) 2. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.23) 1. EPA at: http://www.370 (<LOD-.97-10. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.EPA considers methyl parathion unlikely to be carcinogenic to humans.33-3.21-21.67-2.71 (1.970 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.640) < LOD < LOD 1.500) < LOD < LOD ..cdc.20 (3.690-1.680 (<LOD-1.61) 4. vomiting.86 (2.79 (1.31) < LOD .80 (1.83 (1.84) 3.25 (2.04) 1.04 (2.16-4.20) 3.44-3.97 (<LOD-4.930 (.33-3..800-1.30-1.08) < LOD .29) 1.79) 1.78) 2.790-.830-1.00) 2. 2004).45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.30) 3.25) 1.96 (1. Zurich et al.

Kramer RE. Wellman SE..112(10):1116-1124. 1995).6(2-3):159-173.. References Barr DB. Dharmani C. Moomey CM.9:311-320. Methyl parathion: an organophosphate insecticide not quite forgotten. Morgan DP. Lu C. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.. Pesticide residues in urine of adults living in the United States: reference range concentrations. Hetzler HL. Bradway DE. Chicago area methyl parathion response. Third National Report on Human Exposure to Environmental Chemicals. CDC. Lin LI. Costa LG. 2005. 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. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Environ Health Perspect 2002. Kedan G. Barr DB. Needham LL. Rev Environ Health 2006. Alley CC. and many residents were symptomatic (Barr et al. Environ Health Perspect 2002. 1999). J Biomed Sci 2002.15(2):164-171. population (Olsson et al.. Head SL. Pharmacokinetics of methyl parathion: a comparison following single intravenous. et al.25(5):599-606. Weltzien E. Hryhorczuk DO. Runkle KD. McClure PC. Arch Environ Health 1978. ACGIH recommends a BEI of 0.56(7):449553. Kissel JC. Hill RH Jr. Hill RH Jr.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. McCann KG. Pope C. Bailey SL.21(1):5767.215(3):182-190.5 mg (500 µg)/g creatinine for workers at the end of shift. Cline RE. 2002. Lores EM. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Rubin et al. Head SL. oral or dermal administration. Bradman A. and levels were similar or slightly lower that those in a small convenience sample of the U.. Moseman RF. Karanth S. a range of values several hundred times higher than levels found in the U. Clark JM. Barr DB. Giordano G. 4/7/09 Jaga K.110 Suppl 6:1085-1091.. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. et al. Gregg M.71:99108.S.S. Centers for Disease Control and Prevention (CDC). 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.14(4):213-216. Guizzetti M. In a study of workers who handle parathion. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. DiPietro E. Turner WE. 2005. Rockhold RW. International Programme on Chemical Safety-INCHEM (IPCS). Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine.110 Suppl 6:1075-1078. Role of individual susceptibility in risk assessment of pesticides. Arch Environ Contam Toxicol 1977. Slach EF. Toxicology 2005. Environ Health Perspect 2004. Occup Environ Med 1999. 1995. Lewalter J. et al. McCann et al. general population (CDC. 2005). Laboratory investigation of a poisoning epidemic in Sierra Leone. et al. 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. Baker SE. Baker RC. Jewell NP. Harley K. 2005). Barr DB. Baker S. Atlanta (GA). Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2002). Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. 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. J Expo Anal Environ Epidemiol 2005. Ashley DL. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Leng G. Pesticide workers may have much higher levels following pesticide applications. Hill et al. 2002. Available at URL: http:// www.inchem. et al.. Griffith W. Pathak S. 2005. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al.33(5):270-276.htm. Eskenazi B. Neurotoxicol Teratol 2003. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Environ Res 1995. Parathion-Methyl (addendum). Curl CL.org/documents/jmpr/jmpmono/v95pr14. Barr JR. J Anal Toxicol 1990. Shealy DB. 2004).

Honegger P. Ohio. Environmental Protection Agency (U.gov/oppsrrd1/REDs/factsheets/0155fct. Environ Health Perspect 2002. Dunlop B. Kieszak S.20(4):533-546. Rosenberg J. Ethyl parathion.162(2-3):219-224. Anal Bioanal Chem 2003. Letzel S.Organophosphorus Insecticides: Specific Metabolites Muttray A.pdf. Available at URL: http://www.S. 1995-1996.usgs. Hill G. et al.E. EPA). Toxicol Appl Pharmacol 2004. Nguyen JV. Mengle DC.S. Ames RG.epa. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. 1992-2001. 2007 [online]. External and internal exposure of wine growers spraying methyl parathion. revised February 15.114(10):1542-1546.376(6):808-815. Sadowski MA. Toxicol Lett 2006. Slotkin TA. The Quality of Our Nation’s Waters. Environ Health Perspect 2006. Case No. Levin ED. Olsson AO. 5/19/09 Zurich MG. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Hill RH Jr. pdf. Environmental Protection Agency (U.04/106.epa. 2004. EPA-738-FOO-009.S. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Available at URL: http://www. Available at URL: http://pubs. U. Available at URL: http://www. Esteban E.S.S. Yacovac R.gov/circ/2005/1291/. Investigation of a fatality among parathion applicators in California. 1/14/09 U.110 Suppl 6:1047-1051. Rubin C.who.201(2):97-104. 6/1/09 World Health Organization (WHO). R.D. Jung D. September 2000.pdf. Methyl parathion in drinking water. Costa LG. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. 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. March 2006. Geological Survey (USGS). Ryde IT. Tate CA. gov/oppsrrd1/REDs/methylparathion_ired. WHO/SDE/WSH/03. 0153. 1/12/07 U. Monnet-Tschudi F.int/water_sanitation_health/dwq/chemicals/ methylparathion. Pesticides in the Nation’s Streams and Ground Water. Facts. Barr DB. Schilter B. Am J Ind Med 1991. May 2003. EPA). Seidler FJ. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Backer G. Osorio AM.

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

670 (<LOD-1.2.55) .300-1.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .700-1.250 (<LOD-. 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) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .27) .780 (<LOD-1. Survey Geometric mean (95% conf.470 (.210-1.500 (.740 (. Survey Geometric mean (95% conf.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 .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.700-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .680 (<LOD-.94) .780 (.210-.S.200-. population from the National Health and Nutrition Examination Survey.610 (<LOD-1.840) 669 687 929 Limit of detection (LOD.740-1.210 (<LOD-.64) . 154 Fourth National Report on Human Exposure to Environmental Chemicals .780 (.17 (.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .15) < LOD .00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.21) < LOD .460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .410 (<LOD-1.950) < LOD < LOD 1. which may vary for some chemicals by year and by individual sample.850 (.820) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.760 (<LOD-.S.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.840 (.31) .07) .430 (<LOD-. see Data Analysis section) for Survey year 01-02 is 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th .780 (<LOD-1.580-1.

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

so usage is restricted near water (U. 2002). Certain pyrethroid insecticides (such as permethrin. Adverse effects from large doses are related to the action of pyrethroids on the nervous system. and synergists. by either ester hydrolysis or hydroxylation. pyrethroids are rapidly metabolized. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U.2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. Pyrethroids are not well absorbed through the skin (ATSDR. and are rarely detected in ground waters (USGS. deltamethrin has been used for indoor protection against mosquitoes that carry malaria. They are ranked as having moderate acute oral toxicity. and deltamethrin have been used frequently on cotton. In agriculture. 1997. or carbamate pesticides. 1999. and greenhouses. 2006a. solvent oils. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations. Pyrethroid pesticides have low volatility.. and then eliminated over several days in urine and bile (Kuhn et al. 1992). 2005). Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. EPA. Soderlund et al. 2006b). The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. pyrethroid pesticides have less acute toxicity in animals and people. agricultural fields. such as piperonyl butoxide. cyfluthrin... and sumithrin) are also registered for use in mosquito-control programs in the United States.S. 2002). Woollen et al. 2002. cypermethrin. The table shows the urinary pyrethroid metabolites measured in this Report. This class of pesticides has low toxicity in birds and mammals. After absorption from inhalation or ingestion. in some situations replacing the use of DDT.S.. There are about 30 different pyrethroid pesticides in use..2-Dibromovinyl)-2.2-Dichlorovinyl)-2.. 2003. WHO. which are natural chemicals found in chrysanthemum flowers. Unmetabolized pyrethroids have been measured in breast milk. Soderlund et al. animal facilities. warehouses. but pyrethroids are highly toxic to fish and some aquatic invertebrates. where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals .. They are also applied on livestock to control insects. 2007).Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins. 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.S. Generally. they are not persistent in the environment due to their rapid degradation within days to several months. 1992). but may be poorly transferred across the placenta (ATSDR. bind to soils. Estimated intakes from diet and drinking water are below recommended limits. resmethrin. 2005. Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown.2-Dichlorovinyl)-2. Compared with other classes of insecticides such as organochlorines.EPA. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers. Outside the U.2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. organophosphorus. Woollen et al. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. Leng et al. 2003. followed by conjugation.. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides.

IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Wolff MS. Leng G. Garey J. Int J Hyg Environ Health 2002. Salzgeber SA. motor activity. Hu et al.1/15/09 Aziz MH. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Leng A.. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Miller GW. 2003. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Toxicological profile for pyrethrins and pyrethroids. and striatal dopamine levels in male and female rats. Wang SL.atsdr. Elwan et al. 2002. Kuhn K. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Ray et al. Bernardi MM. Shaw IC. and seizures (ATSDR. Ranft U. Lazarini et al. Regul Toxicol Pharmacol 2002.. J Environ Monit 2006. Biochem Biophys Res Commun 1998.html. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. In developing rodents.8(1):197-202. epa. dopaminergic. 1998. Sunami O. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Kuhn KH.. Go et al. Yamada T. Abell AD. Richardson JR. WHO. Wolff MS. Bull Environ Contam Toxicol 1999. bioallethrin and deltamethrin.300(3):161-165. 2006.gov/toxprofiles/ tp155. and permethrin) in the Hershberger and uterotrophic assays. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Zhao RC. Varoli FM. Cruz-Casallas PE.62:101-108. Moniz AC. Go V.8(1):18-21.. Soderlund et al.. Kunimatsu et al.27(12):1273-1283. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Guillot TS. Elwan MA. Yang J. Lemonica IP.gov/toxpro2.gov/pesticides/ and from ATSDR at: http://www. Neurotoxicol Teratol 2001. Shafer. In California. Kim HS. 2005). Environ Health Perspect 1999. Bernardi MM. Song L. Lazarini CA. Wieseler B. Hu JY. salivation.211(3):188-197. Shukla Y. Agrawal AK. Pogo BG. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. choreoathetosis. Ose K. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Adhami VM.html.205(6):459-472. 2002). et al. 2001.. Chen JH. et al. Additional information about pesticides is available from U. 2003. neurochemical changes in cholinergic. on immature and adult mice: changes in behavioral and muscarinic receptor variables. September 2003. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats.251(3):855-859. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Kang IH. Moniz et al. Idel H. Garey J. et al. et al. 2005). Eriksson and Fredriksson. Levsen K. Kim TS. Sugiri D.23(6):665-673. Seth PK.atsdr. McCarthy AR. Generally. Fourth National Report on Human Exposure to Environmental Chemicals 157 . J Reprod Dev 2004. Toxicol Appl Pharmacol 2006. Thomson BM. Kamita Y. Florio JC. Pauluhn J. fenvalerate. Berger-Preiss E. Lewalter J. EPA at: http://www.S. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. 2000.cdc. 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. 2006. Neurotoxic effects of two different pyrethroids. Okuno Y. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. 1991. Estrogenicity of pyrethroid insecticide metabolites. Eriksson P. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Kunimatsu T.108(1):78-85. 2006).. Leng G. Garey and Wolff. 2003. Kim et al. Available from URL: http://www. cdc. Xenobiotica 1997.27(4):609-614. Neurotoxicol Teratol 2005..50(2):245-255.35(2 Pt 1):227-237. 2001. Leng G. 2005). Kim IY. Fredriksson A. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats.. 2002). Spinosa HS. Shin JH. 2003... McCarthy et al. 1999.107(3):173-177. hypersensitivity. Idel H. 2005)...Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. tremor. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Caudle WM. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Lee SJ. Pyrethroid pesticide-induced alterations in dopamine transporter function. Neurosci Lett 2001. References Agency for Toxic Substances and Disease Registry (ATSDR). 2004. Toxicol Appl Pharmacol 1991.

Lesser JE. Xenobiotica 1992.38:95-101. Shafer TJ.gov/oppsrrd1/REDs/cypermethrin_red. Geological Survey (USGS). 5/26/09 Woollen BH. Revised February 25. Environmental Protection Agency (U. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .S.epa. EPA). Pyrethroid illnesses in California. Marsh JR. Available at URL: http://www.Pyrethroid Pesticides Ray DE. April 2002. 2005. resmethrin. Rev Environ Contam Toxicol 2006.S.gov/ circ/2005/1291/.usgs. EPA). U. Available at URL: http://www. Mullin LS. Environmental Protection Agency (U. 1992–2001. Forshaw PJ. pdf. Reregistration Eligibility Decision for Cypermethrin. Crofton KM.epa. Permethrin. Available at URL: http://whqlibdoc.S.186:57-72.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. sumithrin synthetic pyrethroids for mosquito control.S.epa. World Health Organization (WHO). EPA).S.S. and therapy. Pesticides in the Nation’s Streams and Ground Water. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).171:3-59. Meyer DA.htm. 19962002.113(2):123-136. Spencer J. 5/26/09 U. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. Pyrethroid insecticides: poisoning syndromes.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Available at URL: http://www. Sargent D. Environmental Protection Agency (U. Sheets LP. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Pesticide and Evaluation Scheme.pdf.htm. Toxicology 2002.10. J Toxicol Clin Toxicol 2000. et al. 5/26/09 U. Piccirillo VJ. synergies. Safety of pyrethroids for public health use. Environ Health Perspect 2005. June 2006b. Available at URL: http://pubs. 5/26/09 U.who. Clark JM.S. June 2006a. Soderlund DM. O’Malley M. Laird WJ.22(8):983-991.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. 2007. March 2006.

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

Survey Geometric mean (95% conf. 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. 160 Fourth National Report on Human Exposure to Environmental Chemicals . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2.2 and 0. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.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. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 830 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 700 594 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Fourth National Report on Human Exposure to Environmental Chemicals 161 .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. Survey Geometric mean (95% conf. 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.S.

Sugiri D.209(3):221-233. O’Malley M.209(3):293-299. Int Arch Occup Environ Health 2004. et al.Pyrethroid Pesticides References Baker SE. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.186:57-72. Bernard CE. Heudorf U. 2005. Rev Environ Contam Toxicol 2006. Butte W. Olsson AO. Int J Hyg Environ Health 2006.13(2):112-119. 19962002. Kolossa-Gehring M. Angerer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Heudorf U. Drexler H. Environ Health Perspect 2001. Hoppe HW. Int J Hyg Environ Health 2006. Berger-Preiss E. Ball M. Pyrethroid illnesses in California. Becker K. Spencer J. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Third National Report on Human Exposure to Environmental Chemicals. Arch Environ Contam Toxicol 2004. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Heudorf U. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Angerer J. Angerer J. Seiwert M. Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Atlanta (GA). Centers for Disease Control and Prevention (CDC). 162 Fourth National Report on Human Exposure to Environmental Chemicals . J Expo Anal Environ Epidemiol 2003. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Williams RL. Barr DB. Krieger RI. Leng G. Schulz C. Hadnagy W.109(3):213-217. Ranft U.46(3):281-288. Int J Hyg Environ Health 2003.77(1):67-72. Idel H.206(2):85-92.

2dichlorovinyl)-2.77 (.670-1.440 (.460 (.110-.160 (.220-.920) 1. < LOD means less than the limit of detection.410) .680-3.1.490-1. population from the National Health and Nutrition Examination Survey.54) .28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .155-.340) .180 (.150 (.580) 1.400-.950-2.160 (.770) .630) .630 (.120-.210-. but can also reflect exposure to trans-3(2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.330 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140 (.470 (.120-.680 (.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.600) . which may vary for some chemicals by year and by individual sample.650-1.460-1.900 (.490-..262) * * * < LOD < LOD . Generally.490-. and trans-cyfluthrin.07 (.2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.740-1.32) .08) .550) .530 (.120-.380-.960 (.220-.68) .890 (.370-.630) .580-1.740 (. cis-cypermethrin.200) .710-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. 1985.430-.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. transcypermethrin and trans-cyfluthrin.50) .15) .790-1.250 (.270 (.610) . Survey Geometric mean (95% conf.730 (.53) . In the body.220-.S.510 (. cis-permethrin.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 . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.710) ..380 (.200 (. Biomonitoring Information Urinary levels of cis.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.850 (.700) .240) .330) . 52315-07-8 CAS No.370 (.410) .300-.2dichlorovinyl)-2.380) .1 and 0. trans-cypermethrin.500 (.230) .790 (. ciscypermethrin and cis-cyfluthrin.270 (.11) .610) . 1985.600 (.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis. Similarly.510 (.280-. the presence of trans-3-(2.380-.110-.170 (.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .910-5.780) .490-1.and trans-isomers.35) .350) .380-.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.220) .210) .35) 1.210) 90th .110-.890 (.200-.690) . and ciscyfluthrin.240) .44 (.47 (.300 (.200) < LOD < LOD < LOD .13 (.21) .300-.420-.68359-37-5 Cypermethrin Permethrin CAS No.180) .200-. trans-permethrin.460-.28) 671 680 518 701 591 957 Limit of detection (LOD.200) .340-.2-Dichlorovinyl)-2. The chemical trans-3(2.570-.310) .260 (.770-1.2-dichlorovinyl)-2.200-.68 (.43) . The presence of cis-3-(2. more of the trans-metabolite than Urinary cis-3-(2.740-2.270-. cis-3-(2.12 (.880 (.80) .570 (.470-1.790) .520) .790-1.110 (<LOD-.120-.740) 1.730 (.670 (.600-1.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.670-1.2-dichlorovinyl)2.820 (.160 (<LOD-.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .or trans-3-(2.140 (<LOD-.300 (.670-2.2-dichlorovinyl)-2.640 (. 1999). 1999). Kuhn et al.510 (.220-.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.870) 1.270 (.250-.630-.280 (. Fourth National Report on Human Exposure to Environmental Chemicals 163 .2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.202 (.68) . Cyfluthrin.2-dichlorovinyl)- CAS No. but it can also reflect exposure to cis-3-(2. Kuhn et al.730 (.24) 1.500 (.340) .

104-.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.350 (.11 (.260) .260 (.400-1.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.590) .700-2.640-.130-.640 (.500 (.380 (. 2001.550 (.270 (.710-3.250 (<LOD-.230-. population from the National Health and Nutrition Examination Survey.370-.138 (.810 (.370-.12-2. urinary trans-3-(2.530 (.67) .290) .300) . the median and 95th percentile of urinary levels of cis-3-(2.640) 1.59 (1.03) 1.260 (.150-.2-Dichlorovinyl)-2.440-.680-1. 2005). 2006).300 (. Studies in Germany of 396 children and adolescents (Becker et al.420 (.300 (.540 (.250) .250) 90th .750 (.580-1..S. Lu et al.220) .280-.830) . 2004. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.640-1.880) .840 (.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.270) . 2006.560) 1. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.190) .170 (.470-1.780) 1. 2001) showed urinary levels of cis.270-.37) .230-.11) 1. 2002).700) .400 (.550-1.680-1. median urinary levels of trans-3-(2.180 (.2-dichlorovinyl)-2. urinary levels of cis-3-(2. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al. 2006.03) 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 .250) .260 (.710 (.550-1.250-.182) * * * < LOD < LOD .440-. 2005).and trans-3-(2.and trans-3(2. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.700) .220 (.200 (. In the same residents.380-.49) .440 (.31) .11) .2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.S.390-.640-1.340) .. 2006) and 1177 urban adults and children (Heudorf et al.450 (.580) .. representative NHANES 2001-2002 subsample (CDC.430-1.230-.550) .510-1..200-.380) . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.220 (.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.170 (. 2003).570) .200-.2-dichlorovinyl)-2.33) .530 (...59) .410) .67 (.900 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350) .260-.2dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.240 (<LOD-. In a study of urban residents in Germany (Berger-Preiss et al.80) .370-.550) .780 (.29 (.170) < LOD < LOD < LOD .540 (..360-1.200) .2-dimethylcyclopropane carboxylic acid did not increase.430-. Schettgen et al.450-.140-.160 (<LOD-.150-.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .250-.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.290) .190) ..390-.230 (.210-.2-dichlorovinyl)-2.290 (.560) .440 (.33 (. 164 Fourth National Report on Human Exposure to Environmental Chemicals .840 (.150-..340-.320) .24) .2dichlorovinyl)-2.250-. 2005)..590 (.21) . 2005).890) .180-.800 (.290-.320-. In these volunteers.190 (.. 2004).59) . In a study of volunteers.680 (. post- Urinary cis-3-(2. 2002).270) .890 (.450-1.340) . 2006).750-1.280 (. 2003). interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300-.430 (.300) .390 (.080-.920 (.120 (.11) .12 (.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .2-dichlorovinyl)-2. 2005) In a small group of indoor pest-control operators. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.690-1. Cyfluthrin. Survey Geometric mean (95% conf. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.540) .Pyrethroid Pesticides 2.600 (. Other studies have provided evidence that urinary levels of cis.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.39 (1.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .39-5.2-dichlorovinyl)-2.660) 1.25-3.5) 2.460-.66) 691 680 518 690 595 954 Limit of detection (LOD.49-3.460-.810-1.2-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.920-1.or trans-3-(2.14-2.28 (1.03-1.550 (.55-3.25 (1. population from the National Health and Nutrition Examination Survey.42 (2.520) .800-1.23 (.01 (1.26 (.08) 1.56 (1.710 (.01) 4. 2005).570) 90th 1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.76-3.14-6.68) 2.400-.09 (.670) .730) .41 (1.35) 1.20 (.670) .48) 4.20 (.68) 1. however.95) 3.12-6.820) .85) 4.11-2.17 (.62 (1.54) 4.470 (.780 (.94 (1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .27 (1.420 (<LOD-.68) 1.14) 1.400 (<LOD-.750) .68-3.860) .4 and 0. Finding a measurable amount of cis.03-1.84 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Pyrethroid Pesticides application median urinary levels of summed cis. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.64-4. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.28 (2.410-.07 (1.66) .910-1.560 (.520-.410 (<LOD-.490 (<LOD-.68-2. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.500-.95) 2.680-1.97-11.63) 1.2-Dichlorovinyl)-2.S.77) 1. 2005).13) .50 (1. which may vary for some chemicals by year and by individual sample.41-14.610) 1.560 (.69 (1.17 (.55-5.56 (1.63) 1.42) 1.59 (1.76-4.23) 2.490-1.2-dichlorovinyl)-2.22 (1.580 (.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 .500) .56) 2. trans-Cypermethrin.480-.11-1.49-5.16) 1.08-4.470 (<LOD-.60) 1.37 (1.850-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Fourth National Report on Human Exposure to Environmental Chemicals 165 .760) .910-1. < LOD means less than the limit of detection.19 (2.08-6.940 (.77 (1.440 (<LOD-.56) 2.60-4.17-1.560 (.410-.530) .10) 2.620) < LOD 2.49-3.55-4.and trans-3-(2.69) 1.43) 2.970 (. Survey Geometric mean (95% conf.77) 2.4.2dichlorovinyl)-2. Urinary trans-3-(2. Biomonitoring studies on urinary levels of cisor trans-3-(2.54 (1.20 (.89 (2.87 (1.700-1.90) 1.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .81) 2.60) .840-1.830-1.19) 1.19 (3.7) 2.500 (. The maximum post-application urinary levels.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.410 (<LOD-.40 (1.700) .07-3.91 (1.

31) 1.81 (2.08 (.37 (1.65 (2.850) .07) 2.36 (1.34-4.70 (.87 (1.900 (<LOD-1.15 (1.67 (2.87-3.800-1.20 (1.780) .580 (.16 (1.30-3.33-2.48 (1.40-2.30-6.13) .470 (.80) 1.48-2.570 (.74) .74) 2.33-1.00) 5.35) 1.700 (.12 (.28) 2.55 (2.64 (1.2-Dichlorovinyl)-2. * 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.770) < LOD 2.68) 3.500-.02-1.35 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.800-1.91 (1.13) 1.00-5.880 (.820-2.36) 2.12-1.22-2.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.57 (1.880-1.08 (.670) .780 (<LOD-.22) 1.98 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.60) 2.56-2.730) .19 (1.47 (1.660) .61) 1.89) 2.570-.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.580) .60 (1.60) 2.45-2.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .86 (2.00) 1.15) 3.29) 1.57) 3.470-.640) .15) 2.880 (<LOD-1.39) 1.930-1.41) 1.56 (1.570 (<LOD-.560 (.530 (.15-3.87) 1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.55 (2.07-3.91-11.27-2.610-.27-2.22-1.07-1.19) .410-.44) 2.850-3.47-2. 166 Fourth National Report on Human Exposure to Environmental Chemicals .750) .55 (2.740) .Pyrethroid Pesticides Urinary trans-3-(2.850) 1.31 (. trans-Cypermethrin.56-5.00) 1.31 (2.540) .07-2.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .26 (1.75 (1.65) 1.440-.530 (<LOD-.07) 2.15-3.760 (.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 .700 (.34-3.700-.42) 1.47-2.91) 1.00 (1.87-8.480-.33 (1.780) 90th 1.45 (1.39 (1.720 (<LOD-.520 (<LOD-.20-2.42 (.970 (.3) 2. Survey Geometric mean (95% conf.87) 1.11) .720-1.720-1.S.15-3.

Indoor pyrethroid exposure in homes with woollen textile floor coverings.205(6):459-472.76(7):492-498. Hoppe HW. Angerer J. Leng G. Hadnagy W.206(2):85-92. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. George DA. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Int J Hyg Environ Health 2006. Leng G. Sugiri D. Centers for Disease Control and Prevention (CDC). Butte W. Sugiri D. Angerer J.77(1):67-72. Environ Health Perspect 2006. Ranft U. Schulz C. 2005. Ranft U. Levsen K. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Biological monitoring of workers after the application of insecticidal pyrethroids.62:101-108. Int J Hyg Environ Health 2002. Bravo R. Drexler H.209(3):221-233. Heudorf U. Ball M. Angerer J. Idel H. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Int Arch Occup Environ Health 2004.209(3):293-299. Int J Hyg Environ Health 2003. Angerer J. Bartell S. Wieseler B. Heudorf U. Berger-Preiss E. Angerer J. Int J Hyg Environ Health 2006. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Environ Health Perspect 2001. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Idel H. J AOAC 1985. Schettgen T. Atlanta (GA). Permethrin and its two metabolite residues in seven agricultural crops. Pearson M. Heudorf U. Leng G. Third National Report on Human Exposure to Environmental Chemicals. Bull Environ Contam Toxicol 1999. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Idel H. et al.114(9):14191423.68(6):1160-1163. Int Arch Occup Environ Health 2003. Angerer J. Hardt J.134(1-3):141-145. Barr DB. Lu C. Drexler H. Kolossa-Gehring M.109(3):213-217.Pyrethroid Pesticides References Becker K. Kuhn K. Heudorf U. Berger-Preiss E. Seiwert M.

2-dibromovinyl)-2. Finding a measurable amount of cis-3-(2.2dimethylcyclopropane carboxylic acid formed in the environment.2-dibromovinyl)-2. 1990). Following residential spraying with deltamethrin for malaria protection in Mexico. 168 Fourth National Report on Human Exposure to Environmental Chemicals .... 2005). Biomonitoring Information Urinary levels of cis-3-(2. Baker et al.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.39 µg/L. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Outside the U. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.. (2004) reported a geometric mean concentration of cis-3(2. 2005).2-dibromovinyl)-2. 2004).2-dibromovinyl)-2. 52918-63-5 General Information Cis-3-(2.5 μg/L) than the detection limit (0. in some situations replacing the use of DDT. in detection of cis-3-(2.S. 2001.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population. 2006) and 1177 urban adults and children (Heudorf et al. Deltamethrin can degrade to cis-3(2.2-dibromovinyl)-2.1 μg/L) for the NHANES 2001-2002 subsample (CDC. mean peak urinary levels of cis-3-(2. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.2-dibromovinyl)-2.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. In the NHANES 2001-2002 subsample. 2001) showed that urinary levels of cis-3-(2. Urinary levels for adults and children in these studies were similar (Heudorf et al.Pyrethroid Pesticides Deltamethrin CAS No.2-dibromovinyl)-2.2-dibromovinyl)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. Thus.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. Studies in Germany of 396 children and adolescents (Becker et al.2-dibromovinyl)-2. 2005). urinary levels of cis-3-(2.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.2-dimethylcyclopropane carboxylic acid of 0.. deltamethrin has been used against mosquitoes that carry malaria.3-0.

1. which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 169 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.S.Pyrethroid Pesticides Urinary cis-3-(2. 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. < LOD means less than the limit of detection.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.2-Dibromovinyl)-2.1 and 0. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.

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

Int J Hyg Environ Health 2006. Deltamethrin. Environmental Health Criteria 97. et al. Ball M. Kolossa-Gehring M. Int Arch Occup Environ Health 2004.77(1):67-72. Drexler H. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. et al. Angerer J. toxicokinetics. Available at URL: http://www. Grimaldo M.htm. Hoppe HW. Angerer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.inchem. Atlanta (GA). Heudorf U. Heudorf U. Butte W.org/documents/ehc/ehc/ ehc97. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Batres LE.113(6):782-786. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.Pyrethroid Pesticides References Becker K. Centers for Disease Control and Prevention (CDC). Carranza C. Schulz C. Torres-Dosal A.109(3):213-217. Third National Report on Human Exposure to Environmental Chemicals. Angerer J. Heudorf U. Seiwert M. Lopez-Guzman OD. International Programme On Chemical Safety (IPCS). and genotoxicity in exposed children. 2005. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.209(3):293-299. 5/26/09 Ortiz-Perez MD. Int J Hyg Environ Health 2006. [online] 1990.209(3):221-233. Environ Health Perspect 2001. Angerer J. Environ Health Perspect 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005). A small sample of occupationally unexposed Italian residents had median levels of urinary 3-phenoxybenzoic acid that were about fourfold higher than for adults in the NHANES 2001-2002 subsample (CDC. 2005). CDC. 52645-53-1 Tralomethrin CAS No. mean peak urinary levels of 3-phenoxybenzoic acid in children increased at least sixtyfold over non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (OrtizPerez et al. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. 52918-63-5 use and house dust levels (Lu et al.. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides.52315-07-8 CAS No.. 2005). CDC. In the New York City study. 2005. 2002. 2005). 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. A study of 396 German children (Becker et al.. Thus.. 2005). Becker et al. 2006).. Hardt and Angerer. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. 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. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. representative NHANES 2001-2002 subsample (CDC. Baker et al. 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. In a small group of indoor pest-control operators.. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect..Pyrethroid Pesticides Cyhalothrin CAS No. Saieva et al. 68359-37-5 Cypermethrin Deltamethrin CAS No. (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. In one study of 145 urban residents in 80 private homes in Germany. 39515-41-8 CAS No. 2003. CDC. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. 2004). 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. 2005). Fenpropathrin Permethrin CAS No. 2005). 2005. 2003). 2003. Following residential spraying with deltamethrin for malaria protection in Mexico.. 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 . 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.S. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. 2006. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.

45-5.210-.233-.78) 1.507 (.81 (1.740 (.270) .315 (.240 (.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .340) .65 (1.13) .340) 1.16) 1.311 (.434) .48-2.292 (.440) .345) Selected percentiles ( 95% confidence interval) Sample 95th 4.89-71.353 (.230-.160-.362) .48-2.S.53-3.300 (.12 (.52-4.277-.364) .90) 1.54) 1.1) 3.45 (2.590-.420) .62) 5.76 (1.62-6.230 (.850) .1 and 0.55 (1.34) 8.560-.247-.800) 1.23 (2.610) .240 (. population from the National Health and Nutrition Examination Survey.700 (.1) 3.04) .620-1.328 (.29-1.730 (.320) .12) 4.78) 6.510-.250 (.271-.27-2.25 (2.200-.05) 1.28) 1.430-.830-2.39) 2.246-.520 (.390) .26) 2.800 (.276-.314 (.83-11.190-.41) 3.350-.830) 90th 1.870 (.69) 3.454 (.260 (.300 (.86 (1.35) 2.02-6.32-21.14-6.288 (.41-2.78) 1.560-1.265-.38 (2.990) .820) .570-.26) 2.780) 4.750-1.04-5.352-.355) .190-.227-.320) .297 (.60) .288-.840-1.63-3.25 (2.190-.373) .427) .30) 3.260-.360) .250-.700-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.49 (1.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.670 (.430-.601) .51-6.35) 2.650 (.267 (.250 (.26-2.35 (2.49 (1.253-.314) .387) .210-.33 (2.21 (2. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.25-4.12) .320 (.940) 1.321 (. Deltamethrin. Fourth National Report on Human Exposure to Environmental Chemicals 173 .370) . interval) .62-8.18 (1.52-5.330) . Survey Geometric mean (95% conf.325 (.32 (2.64) 697 680 524 701 603 957 Limit of detection (LOD.93 (1.406) .470-.369) .300) .220-.43) 3.51-3.230-.300 (.53) 1.238-.25-1.340) 75th .13 (.600 (.180-.1.590 (.30 (1.750) .49-2.490-.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 .03 (3.63 (3.550-.298 (.417 (.740 (.530-.820) .374) 99-00 01-02 99-00 01-02 99-00 01-02 .1) 3.41-3.38 (2.260 (.295) .35) 1.273 (.46) .69 (1.850) .8) 3.570-1.260 (.750) .290 (.71 (1.280 (.56-5.72 (1.560-.230 (.640 (.18 (2.680 (.33) .450 (.79) 3.49-2.595) .320) .160-.510-.760 (.490) .78 (1.710 (.32 (1.586) .73) 1.75 (1.428-.30 (.270 (.384) .34 (2.630) .226-.65-2.190-.01 (1.250 (.320) .36) 1.266-.27-11.35 (1.44) 5.92-3.200-.33 (1.46) 2.50 (2.336 (.41 (1.25-7.34-6.05) .530-.710 (.27-2.330) .292-.200-.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .960 (.810) 1.42-2.230-.16-1.

420-.240-.401) .48 (1.677) .320) .210 (.19) 2.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .264 (.21-4.04 (3.91 (2.72 (1.410) .10 (2.280-.321-.200-.840-1.437) .25) 2.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .335-.670) .330) 75th .150-.270) .330 (.270-.423 (.43 (1.490 (.63) 1.240-.00) 1.410-.88-5.90) 3.253) .227 (.640 (.270) .238-. Deltamethrin.60-4.190-.202-.19 (2.60) 1.278) .160-.52 (1.36 (1.80) 4.274-.670) 3.05-3.44 (1.02-1.09) 3.380-.225-. interval) .272 (.630) .510 (.860-1.300-.250) .380 (.328) .16-4.700-1.530-.350) .270 (.67 (1.224-.220 (.190 (.960-1.61-2.37 (1.81 (1.330) 1.49) 3.95) 1.00) 1.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.39) 1.309 (.240-.860 (.27) 1.178-.312 (.25-5.510 (.02 (2.534) .49-2.450 (.330) .550 (.240 (.53 (1.240-.17 (.11 (.440-.440-.21 (1.190-.299-.250 (.400) .41-4.13-1.329) .00) 5.43 (2.62) 1.590-1.378 (.530-.03-1.275 (.510 (.0) 3.480 (.580) .323 (.500) .280 (.309) .40) 2.55) 3.362 (.75-8.810) 1.200-.73-4.230) .52) 2.07) 2.280 (.25-2.35-3.271-.330) .650) .83 (1.310) .272) .229-.280) .67) 1.S.740) .246 (.54 (1.250 (.44) 2.09 (.49) 1. Survey Geometric mean (95% conf.329) .440-.62) .43-64.35 (1.74) 3.280) .210 (.07-5.387) .290) .73) 1.51-7.03 (.590) .200-.41) 1.270 (.570) .460-.36-6.88) 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 .226-.372) .400-.490 (.300-.173-.280 (.610 (.234 (.240 (.96 (1.640 (.365) 99-00 01-02 99-00 01-02 99-00 01-02 .40 (1.274 (.55 (1.13-1.760) .13 (.84 (1.750-1.63-3.390-.17-1.316 (.261 (.460-.730-1.220-.540 (. population from the National Health and Nutrition Examination Survey.550 (.22 (1.290-.240 (.11 (.370-.83) 1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.91) 9.550 (.357) .43) 1.490-.230-.730) .240 (.09-2.32 (2.37) 1.720) 90th 1.930) .480-.35) .86 (1.91-4.860-1.35) 1.930) 1.590) .91) .370 (.261-.730) .350 (.311 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.200-.290) .210-.64-5.590) .19-6.06-3.216-.94 (1.67 (1.230-.04 (.560 (.446) .720 (.09-2.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .580 (.400-.49 (1.15-2.

Fourth National Report on Human Exposure to Environmental Chemicals 175 . Barr DB.76(7):492-498. Atlanta (GA). Seiwert M. Bravo R. Berger-Preiss E.113(6):782-786. Bartell S. 2005. Ortiz-Perez MD. Hoppe HW. Olsson AO. Torres-Dosal A. Angerer J. Godbold J. Idel H. Barr DB. Leng G.114(9):14191423. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Sugiri D. Arch Environ Contam Toxicol 2004. Deych E. Pearson M. Int J Hyg Environ Health 2003. Levsen K. Hadnagy W. Kolossa-Gehring M. Berkowitz GS. Leng G. Exposure to indoor pesticides during pregnancy in a multiethnic. Lapinski R. Int J Hyg Environ Health 2002. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Grimaldo M. Carranza C. Angerer J. Ball M. Biological monitoring of workers after the application of insecticidal pyrethroids. Becker K. Environ Health Perspect 2006. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. et al. Sugiri D. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Berger-Preiss E. Environ Health Perspect 2003.46(3):281-288. and genotoxicity in exposed children. Idel H.209(3):221-233.205(6):459-472. Int J Hyg Environ Health 2006. Lopez-Guzman OD.206(2):85-92. Obel J. Lu C. et al. toxicokinetics. Batres LE. Environ Health Perspect 2005. et al. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Ranft U. urban cohort.111(1):79-84. Liu Z. Hardt J.Pyrethroid Pesticides References Baker SE. Int Arch Occup Environ Health 2003. Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Ranft U. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.

079-.370) .310) .125 (.180) . 176 Fourth National Report on Human Exposure to Environmental Chemicals .108 (.200) .070 (<LOD-.280-.290 (.150) .132 (. solder.110) .112-.120 (.360-.140 (.080-.130 (.260 (.110-.390 (.100-.120-.560) .150 (.144) .120 (.390) . It is also used in paints.070-.120) .490 (.109-.130-.180-. and glass. from air and drinking water.230-.119-.350) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Stibine is a metal hydride form of antimony used in the semiconductor industry.430 (.220) .270 (.132 (.114) .270) . ammunition.230-.220-. 0.300 (.160) .100 (.160-.280 (.320-.130 (.210-.220 (.090 (<LOD-.230-.230) .156-.170-.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 .360 (.350) .210 (.400) . interval) .130 (.250 (.117-.120 (.S.146 (.390) .190 (.360) .120-.220-.154) . and as a fire-retardant in textiles and plastics. respectively.200 (.161) .230) . distribution.140) .470 (.130 (.100) . 01-02.320) .230 (.190) .250-.220-.350) .250-. sheet and pipe metal. enamels. Antimony can exist in one of four valences in its various chemical and physical forms: -3.140) .120-.240-.350 (.160) .136-. Antimony enters the environment from natural sources and from its use in industry.190-.430 (.280 (.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.290-.090 (.240 (.370-.180-.420) .160) .150) 90th .140) .170-.154-.180 (.300 (.100 (.320 (.130 (.170) .260) .120-.130) .350-.123 (.240 (.190) .210) .200-.340 (.500) .115) . storage batteries.240 (.300) . water.200) .200 (.330-.260 (.103) .080) .180-.220-.120-.300) . and pewter.180-.150-.190) .240 (.400-.430 (.220) 95th .330-.150) .207) .250-.190-. and excretion of antimony vary depending on its oxidation state.160 (.330) .210) .110-.164-.115-.460 (.240) .130 (.190) . and refuse incinerators that process or release antimony. +3.330) .250) .128 (.200-.710) .310 (.220) .350 (.178) .180 (.088-.190-. 0.190) .130-. Workplace exposures can occur at smelters.134-.220-.140 (.140) .119) .143 (.087-.460) .300) .190 (.310 (.095 (.120-.150 (.280-.140) .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 .170-. coal-fired plants.160) .230 (.04. castings.320 (.330 (.390-. fireworks.460 (.350-.120-.190 (.126-. Dermal contact with soil.170 (.160 (.440 (.108-.142 (.120 (.160) .390-.070 (<LOD-.137) .300-.390) .280) . metal bearings. < LOD means less than the limit of detection.410-.120) .260) .157) .090-.330 (.04. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.210) .500) .470) .160-.210-.250 (.190 (.350 (.130) . and +5. and 0.130 (.135) * .150-.330 (.130-.360 (.310) .200 (. and 03-04 are 0.250 (.340 (.158 (.190 (.400 (.148-.145 (.260-.300-.130-.184) .330) .133) * .080 (<LOD-.280) .200 (.120) .099 (.140 (.160-.169 (.200 (.470) .160-.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 .230) .270) .131-.130-.180-.110-.160 (.280-.210) .600) .230 (.180 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.170 (.230-. ceramics.128 (.120) .400 (.120-.320-.310 (.190-.330) .320-.176 (.270 (.440) .260 (.093 (.280-.440) .200-.350 (. It is used in metal alloys.Metals Antimony CAS No.300-.270 (.510) .200-.400) .150-.400) .170-.410) .220 (.117-.200) .280) .141-. see Data Analysis section) for Survey years 99-00.197) .290-.150 (.270-.280) .190-.570) .240 (.145) Selected percentiles ( 95% confidence interval) 50th .095-.137) .130) < LOD .180) .170-.110-.240-.260-.122 (.136) * .154) .320-.460 (.180 (.140 (.200 (. 7440-36-0 General Information Antimony is found in ores or other minerals.230-.220) .100-.220-.270 (.250-.130-.160) .280-.130 (.210) .310 (.260) .126 (.180 (.07.140-. The absorption.350-.390) .090) 75th . 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.490) .110 (.130) .390-.410) .120-.340) .320) Total .080) .210 (.098-.530) .175 (. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.360) . People are exposed to antimony primarily through food and.350 (. or other substances containing antimony is another means of exposure.090-.150) .134 (.130-.120 (.105 (.140) . population from the National Health and Nutrition Examination Survey.150-.310-. which may vary for some chemicals by year and by individual sample.180 (.400 (.150-.200) .310-.350) . to a lesser extent.

107-.120 (.253 (.108-.191 (.108-.206-.247) . liver.265 (.203) .183) .109-.444) .277 (.170 (.138-.076-.118 (.321) .100 (.333-.391) .195 (.185 (.357) .280-.068 (.317) .084) .259 (.115 (.471) .123 (.129 (.149-.187) .167 (.130 (.130) .380 (.164-.233-.140) < LOD .320-.080 (.179-. Histopathologic inflammatory and degenerative changes in the lung.182 (. Inorganic antimony salts irritate the mucous membranes.500) .239-.069-.124-.224 (. and route of exposure (Elinder and Friberg.181) .132) .338) .113) .Metals than for trivalent compounds (Elinder and Friberg.417) .200) .186) .129) * .233 (.117-.308-.238) .143) .103-.471 (.121) .185 (.364 (.154-. interval) .120 (..092) .102-.149) . 1995).30) .124 (.120 (. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.276 (.338 (.S.153-.127 (.217 (.269 (. 1944).087) .109 (.068-.228 (.196 (.111 (.137 (.438) .115-.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.333 (.250-.150-.226 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.203) . and gastrointestinal symptoms such as vomiting.078 (.112 (.147) .278) .077) .105-.122 (.211) .333) .146-.131) . population from the National Health and Nutrition Examination Survey.076-.263 (.116 (. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.117-.103-. 1958) and occupational exposures (Briegner et al.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 .163 (.267-.333-1.143) Selected percentiles ( 95% confidence interval) 50th . The toxicity of stibine after acute inhalational exposure is similar to that of arsine.108-.146-.114 (.172-.250-.113-.222 (.079 (<LOD-. diarrhea.069-.127) .300 (.250 (.127) .173) .147-.320) . skin. 1953).139 (.429 (. abdominal pain.263-.082) .153 (.120 (.257) .228-.352) .338 (.310) .167 (.391) .248-.236 (.156-.248) .082) .095-. 1962).181) .209) .148-.143) 90th .143) . 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.318-.108 (.121 (.096-.241-.114 (.161) .189 (.261) .148-.244-.200-.294) Total .265-.119-.188) .205-.175 (.200-.116-.308) .118 (.267 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130) .241-.167-.102-.242-.300) .107-.250) . and kidney have been demonstrated in high dose animal studies depending on the dose.235-.741 (.130) . 1986).161) .238) ..250-.213 (.193 (.135) .371 (.109 (. 1986).145) .272) .086) 75th .255-.198) .117-. and eyes.268) .333-.132 (.194-.126-. 1954).152) .135) .107-.159-.214) .195-.229-.421) .444) . 1988.320 (.185-.135 (.417) .115) .181) .192) .061-.115-.373) . resulting in hemolysis with abdominal and back pain (Dernehl et al.200-.208-.727) . species.266 (.192-.176 (.209-.320-.317) . myocardium. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.136) .288 (.143 (.146) .148) * .104-.080 (<LOD-.230) 95th . and ulcers (Werrin.106-.156 (.159-.138-.310) .119-.098-.230-.209 (.127) .085) .209) .320 (.082 (<LOD-.106-.098) .128-.176-.121 (.099-.160 (.315) .162-.278 (.115 (.225 (.099-.095-.228 (.741) .144-.131-.131 (.115 (.357-.138) * . 1973).151) .271-. Fourth National Report on Human Exposure to Environmental Chemicals 177 .171) .112-.167 (.364 (.480) .298 (.075 (.238 (.250-.245) .227-.173 (.125-.208 (.429) .129) .123) .250 (.164) .295 (.139 (.163 (.071-.124-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.086 (.280 (.233) .188-.333-.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 .097-.333 (.485) .405) .122 (.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 .140) .256 (.178-.159-.267) .352 (.112 (.113-.310 (.138 (.081 (<LOD-. Ming-Hsin et al.125 (.111-.447 (.318-.119 (.204-.075 (.164 (.104-.126 (.178 (.193) .255) .173-.081) .146-.. Acute antimony poisoning may cause a metallic taste.385 (.089) .199-.300) .126) .220) .176 (.152) .313-.430) .127) .173 (.281-.343 (.414) ..135 (.207) .253-.317) .195-.133) .098-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.400 (.333 (.150-.225) .124) .135) .134) .286 (.114 (.192 (.092-.074 (.129 (..425) .

.. Piatnek DA.html. which may be due to methodologic. Biomonitoring Information Levels of urinary antimony reflect recent exposure. 20012002. Centers for Disease Control and Prevention (CDC). 2002. Information about external exposure (i. Arch Dis Child 1997.. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Third National Report on Human Exposure to Environmental Chemicals. Ho C-K. Mayne P. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Pietra R.16: 33-39. 1994) have reported values slightly higher than those in this Report. Apostoli P. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. 1986. Dunkelberg. Leinemann M. Buchet JP. gallium.10(3):560-586. Dezateux et al. Gebel TW. Wu M-T. et al. stibine. Industrial Medicine and Surgery (Dec. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. 1995.106:33-39.)1954. Yu H-S. Paschal et al. 1990. Stasney J. Gallorini M. J Clin Pathol 1998. 1991. 2005. Int Arch Occup Environ Health 1995. Review of elements in blood. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Kuo-Juie Y. Schaller KH.. New York: Elsevier. Stocks J. References Berman JD. Pozzoli L. arsenic. J Trace Elem Med Biol 2002.. Mayer P. Lenert G. Industrial antimony poisoning. EPA. Handbook on the toxicology of metals. Chemotherapy for leishmaniasis: Biochemical mechanisms. Shao-Chi C. Bailly R. and a drinking water standard has been established by the U. Skulsukai G. VI. Kiberd B.59:469-474. and hydrogen sulfide.51:238-240. J Occup Environ Med 2004. Stead FM. Yang C-Y. Hamilton EI. In: Friberg L. Roland H. environmental levels) and health effects is available from ATSDR at: http://www. Liao Y-H et al. Antimony. Chia-Yu H. pp. and future strategies. Nau CA. Van der Venne MT. Briegner H. Urinary antimony in infancy. Pulmonary edema of environmental origin. Ludersdorf et al. 2004. Mahieu P.. Vouk VB. Lauwerys R. Suchenwirth R. Int Arch Occup Environ Health 1987.. 1998. Carelli G. clinical efficacy. Rev Infect Dis 1988.atsdr. Petrucci F.521-523. Antimony trioxide is rated by IARC as a possible human carcinogen. or exposure differences. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. gov/toxpro2. Iavicoli I. and antimony in optoelectronic industry workers. Chin Med J 1958. Alimonti A.46:931-936. Arsine. Weltle D. Caroli S. Luedersdorf R. Br J Ind Med 1991. Elinder CG. Iavicoli et al. Delves HT.76:432436..cdc. Biological monitoring of exposures to aluminum.. Pilgrim L.48:93-97. Konings J. Minoia C. External and internal antimony exposure in starter battery production. Sci Total Environ 1994. 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.Metals to antimony have been established by OSHA and ACGIH. Delves HT. O’Regan M. Cullen A. 26-42. and 2003-2004. 1998) or compiled reference ranges (Hamilton et al. 1997).. Cordasco EM. even when exposure levels were below workplace air standards (Bailly et al. plasma and urine and a critical evaluation of reference values for the United Kingdom population.. Schacke G. Trace element reference values in tissues from inhabitants of the European community I. Sabbioni E. Sabbioni E. Ju-Sun P. Atlanta (GA).76(2):103-115. Costeloe K. 2nd ed. et al. Dezateux C. 1987). Earlier measurements in general populations (Minoia et al. respectively.13:361-362. Industrial Medicine 1944. 1998). Environ Health Perspect 1998. Kentner et al. Cheng-Wei L. Bolten C. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Biomonitoring of a worker population exposed to low antimony trioxide levels.64(2):182-185. Antimony in blood and urine of infants. Stone FD. Matthews T.e. Biological assessment of exposure to antimony and lead in the glass-producing industry. eds.. Fuchs A. Ming-Hsin H. Wade A. indium. HH. population.67:119-123. Element reference values in tissues from inhabitants of the European community. Liao Y-H. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect.158:165-190. Friberg L. Kentner M. Chen J-R. Chest 1973. Dernehl CU. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Nordberg GF.S. Semisch CW. et al.

Antimony poisoning in industry. Morrow JC. Chemical food poisoning. Trace metals in urine of United States residents: reference range concentrations. Ting BG. Industrial Hygiene and Occupational Medicine 1953. blood. 27:38-45. Quarterly Bulletin of the Association of Food and Drug Officials 1962. et al.76(1):53-59. Werrin M. Renes LE. Sampson EJ. Pirkle JL.99-108.Metals in urine. Paschal DC. Sci Total Environ 1990. Environ Res 1998. Fourth National Report on Human Exposure to Environmental Chemicals 179 .95:89-105. and serum of Italian subjects. Jackson RJ.

8) 17. semiconductors. Although it is still widely used in the United States.9-46. aluminum. grain.66-8.3-19.1) 1281 1276 03-04 03-04 03-04 9.0 (14. and.8 (48.30) 17.13-8. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.5 (34.5 (36.2 (41.7) 24.6 (9.7) 90th 37. or rarely as elemental metalloids (yellow. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.84) 8. arsenocholine. such as arsenopyrite (FeAsS) and realgar (As4S4).90 (7. the smelting of copper. and in lead-acid storage battery grids.2-20.000 metric tons annually.6 (13.1-18.3) 10.1) 15. Arsenic and its compounds have had many uses in the past and present as medicines. from coal burning.2-61. 180 Fourth National Report on Human Exposure to Environmental Chemicals . trimethylarsine oxide.5) 95th 65.19-9.Metals Arsenic CAS No. to a lesser extent.27) 9.1-40. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.6) 618 722 1074 Limit of detection (LOD.74.29 (8.5 (40. referred to as inorganic arsenic compounds.70 (6.80-9.40) 7.10-7. Arsine (AsH3) is a reactive. +3 and +5).57) Selected percentiles ( 95% confidence interval) 50th 7.1 (38.90) 75th 16.4 (24. In the last century.4 (48. were used as treatments for syphilis. and gray forms).4) 60.0 (43.2 (13. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.1) 290 725 1542 03-04 03-04 9.08 (5.8) 34.0 (15.00-9.30 (7.70) 8. lead hydrogen arsenate.0 (22.2-17.2 (12. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. arsenic as elemental metalloids may be used in some ammunition.8) 33.2) 46.10-10.6-35.90-11. cacodylic acid.5-52. gaseous hydride manufactured in small quantities for use in the semiconductor industry. and produce. solders.7 (11. In nature.9) 21.5-178) 46. and as homicidal poisons. interval) 8. retaining walls. and as a cosmetic to lighten complexion.5) 43.70-9.5 (14.2 (51. sodium arsenite.77) 6.97) 8.80) 6. meats. though in some locations arsenite may be prevalent (WHO.7) 65. Survey years 03-04 Geometric mean (95% conf.80 (5.90-8. Various arsenic compounds were used in paint pigments and for tanning animal hides. Since the 1940s.5) 41.3-111) 78.34-9.50-14.8-77. to a lesser extent. Gallium. Before the 20th century. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. mental disorders.9-62. Arsenic trioxide (As2O3.8-61.10 (6.4 (31. psoriasis.1) 7.84) 8.5-19. Arsenic trioxide is approved to treat acute promyelocytic leukemia.2) 15.6 (15. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. Also.8) 30.20 (8.25-9.2-93. arsenites. and play sets.9-34. and indium arsenides are used in the semiconductor industry. as alloy in metal bearings.90-8.5) 66.90-14.90 (5. alloys.4) 40.50 (8. pesticides. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2005).3-15. population from the National Health and Nutrition Examination Survey. ocean and fresh waters.6) 11. lead.6 (32.0 (11.00 (6.9) 68.4 (26. mostly for use in wood preservation (ATSDR. and arsenosugars.4-65.3) 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 7.34-10. cancers.9 (17.7-83. particularly arsenic trioxide.30 (6.55 (7.6-43.10) 10.90) 16. black.6-141) 53. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. and foods.12-10. it is found in over 200 crystalline or mineral forms.8) 7. and other metals.8) 7.S.1 (32.5-41.02-8. 2001).8) 29.90 (7.12 (6.90-7. General population exposure to inorganic arsenic can occur through consumption of drinking water and. and arsenates (oxidation states of -3. arsenic compounds. Arsenic is measurable in most soils. The United States no longer produces arsenic from mining but imports about 22.9 (8.41 (7. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.4 (7.7-95. see Data Analysis section) for Survey year 03-04 is 0. copper arsenates. Water sources contain mostly inorganic arsenate.5 (23.0-60.0-19.4) 13.

0) 1281 1276 03-04 03-04 03-04 8.66 (7.18 (5.7) 95th 50.S. U. interval) 8.1 (14.5-17.7) 28.3) 6.2) 40. age. EPA’s maximum contaminant level (Hughes. organic arsenic can be converted back to methylated and inorganic arsenic.5 (9.7-18. 2001). Smoking tobacco is also a source of inorganic arsenic. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.3-41. 2001. NRC.. 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. inorganic arsenic is widely distributed within the body.8) 27.. arsenic does not show biomagnification in the food chain (WHO.0-26.0-38.0 (31. 1988).88) 7.2-15.9) 53.3-64.40) 8.6-17.7 (25.4) 54. 2001. Direct exposure to DMA and MMA may result from use of the two pesticides.00 (6.8 (12. Survey years 03-04 Geometric mean (95% conf. 2006. EPA.47 (7.86-17.20-9.1) 24.7-35.4 (24.41) 6.9) 13.35) 7.32 (5. selenium. 2003.7 (11. dust.25-9. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.6) 45. as observed in Bangladesh where millions of people have been exposed.51) 75th 14.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. shellfish.50 (6.38-10. In aquatic sediments.01) 7.76 (6.4) 32.58-10. are used in enclosed ultraclean operations within the semiconductor industry.g.1) 6.93-9..8 (11.0) 42.66-8. and contact with CCA-preserved wood structures.4 (40. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.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 8.6 (17.64 (7.0) 26.0) 12.2 (12. 2001).8-62.2-46.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.13) 8.5) 290 725 1542 03-04 03-04 8. Tseng..66-8.3 (24. 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.45) 5.75 (5.0 (17.0) 33.5-120) 40.3 (27.8) 22.59) Selected percentiles ( 95% confidence interval) 50th 7. 2001). population from the National Health and Nutrition Examination Survey.8-75.61 (7. 2001). arsenocholine. though some reduction may occur in the gut prior to absorption.96) 12.75) 13. WHO. trimethylarsine oxide (TMAO).07-9. so exposure to the general population is extremely limited. 2001).8-32.1) 7. and folate status (Chen et al.4 (12.31 (6. 2007. The semiconductor dopants.1) 8.0-18. After absorption.1) 58.93-8. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.28-7.04) 7.88 (5.47-6.9-56.24 (7.7-34.12-10. 2001).10-16.8 (27. gallium arsenide and indium arsenide. and some other seafood can contain organic forms of arsenic including arsenobetaine. In aquatic organisms.0) 14. have caused clinical arsenic poisoning.6 (35.9 (45. Though modest bioconcentration occurs in some aquatic life. 2007.4 (42. Chowdhury et al.33 (6.23-7. 2007.2) 15. and arsenosugars.06 (4.04 (5.47 (6.7-17.8 (20.33-10. 2001).81-9.44) 6. Extremely high groundwater arsenic levels.10-8.01) 11.3) 9. Arsenate is reduced in the body to arsenite (oxidation state +3).1-36.25 (6. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.30-9.. dose level. mine tailings).1 (11. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.4 (11. Children may have additional exposures from ingestion of contaminated soils (e. Steinmaus et al.6 (10. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.7 (9.3-62.5) 17.11 (5. cacodylic acid and monosodium methyl arsenate.8 (21.3-53.0-69. WHO.S.4 (26. 2006. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. Inorganic forms of arsenic demonstrate high acute toxicity.2) 90th 30. Fish. kelp.99-9.44-11. 2001). but is poorly absorbed dermally (WHO.4-64.S.. Gamble et al.7-188) 27.

Chronic human intake of arsenic at less than acutely toxic doses.10 (<LOD-1. WHO.. cytotoxicity.20 (<LOD-1. 2001. including drinking water sources with elevated arsenic levels (e. 2004. 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.10 (<LOD-1. and production of glutathione may be affected as well.60) 1. The U. and altered gene expression.10 (<LOD-1. Such actions may lead to decreased energy production. and diarrhea. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. peripheral vascular disease. which may vary for some chemicals by year and by individual sample. noncirrhotic portal hypertension. and bladder cancer (IARC. apoptosis. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and endothelial injury (Kumagai and Sumi. respectively. Arsenic has many actions demonstrated in cellular studies. hematocytopenias.S. WHO. see Data Analysis section) for Survey year 03-04 is 1.S. 2006. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. 2006. including inhibition of numerous enzymes. 2006. leading to a decrease in adenosine triphosphate energy production. Acutely. gluconeogenesis. The organic forms of arsenic occurring in seafood have little known toxicity. renal failure..50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. interference in signal transduction pathways. Chile). 1998. Raml et al. hepatotoxicity. can cause peripheral sensorimotor neuropathies. 2001.80) 1. which can lead to dehydration and shock. 2001).30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Cohen et al. and it also will inhibit succinate dehydrogenase. 2000. Cellular glucose uptake. With chronic exposure..0. 182 Fourth National Report on Human Exposure to Environmental Chemicals .20 (<LOD-1. hypertension.10 (<LOD-1. Chronic elevated arsenic intakes have been associated with diabetes.g. lung.S. NRC. substitution in phosphate metabolism.. increased oxidative stress. hyperkeratosis.. but additional or confirmatory research is needed (Kapaj et al. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. Chronic arsenic exposure in humans is considered to be a cause of skin. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. 2007. 2001)..20 (<LOD-1.30) 1.EPA has established drinking water.. 2006) or when exposure occurs in smokers (Chen et al. 2007).50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Although arsenate is reduced in the body to arsenite. cell transformations. Survey years 03-04 Geometric mean (95% conf. Taiwan. 2004). 2001). and by uncoupling oxidative phosphorylation (NRC. drinking water have not been associated with increased cancer rates (Schoen et al. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways.S.. food residue.20 (<LOD-1. vomiting. 2001). WHO.g. 2001)... Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. Studies of arsenic at levels typical of U. < LOD means less than the limit of detection. some of these effects may take years to develop. Cardiac arrhythmias. 2004).. U. and DNA repair inhibition (Cohen et al. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 1. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. fatty acid oxidation. 2007.10 (<LOD-1. Bangladesh. NRC.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al.50) 1. Bredfeldt et al. WHO. population from the National Health and Nutrition Examination Survey. and childhood neurodevelopmental effects in observational human studies. 2001)..EPA.60) 1. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. and hyperpigmentation of the skin (NRC.50) 621 725 1078 Limit of detection (LOD. arsenic trioxide) includes hemorrhagic gastritis with nausea.

Caldwell et al. 2008). Fourth National Report on Human Exposure to Environmental Chemicals 183 . Pellizzari and Clayton. Levels of total urinary arsenic in the U. population in NHANES 2003–2004 (Schulz et al.. 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.. Meza et al. 2006.. 1992. Consequently. 1986). Shalat et al..50) 1.cdc. 2007. 2008). median urinary total arsenic levels in 4052 adults varied with seafood intake. Compared with this Report.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2.61 (<LOD-3.. 2006)..e. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al.04 (<LOD-3.75 (<LOD-2. 2001). 2000. Valenzuela et al. Offergelt et al. 2008.. 2000).html... 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. but generally only at maternally toxic doses (WHO.41) 3. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. gov/toxpro2. and the FDA has established a bottled drinking water standard. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (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.. had decreased since the prior 1990– 1992 survey.Metals compounds. Josyula et al..atsdr. 1999.. Pellizzari and Clayton 2006). Additional information about external exposure (i.19) 3. Survey years 03-04 Geometric mean (95% conf.S. 1999). environmental levels) and health effects is available from ATSDR at: http://www. 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.S.18 (<LOD-3.. 2001). 2003. WHO. In animal studies. Caldwell et al.18) 3. Vahter et al.S.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. In a Nevada town where groundwater levels were naturally elevated. 2006).50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. and were about two-fold lower than those for the U. although urinary arsenic levels were not associated with CCA contact (Shalat et al.. population from the National Health and Nutrition Examination Survey.S. 1998. 2007..33 (<LOD-3.33 (<LOD-3. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. 2006). 2006).80 (<LOD-4. 2004. 2006.. 2001).69 (<LOD-3.75 (<LOD-2. DMA produced bladder cancer in some chronic rat studies (Cohen et al.. Pellizzari and Clayton.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In the German Environmental Survey III of 1998. Calderon et al. 2006.. Shalat et al. 2004. 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. 1999. 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.. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. arsenic has been fetotoxic and teratogenic. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. population (Rubin et al..00) 1.

9-23.4-35. MMA.8.20) 18.3 (21. Caceres et al.500-1.93) 1.. Blom et al.20 (2.48-2. population (Ahsan et al. 2005.17-1.5 (14.43-1.5) 292 728 1548 03-04 03-04 1. Chowdhury et al. 2007) with higher levels of arsenic in the drinking water. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.9 (7. and TMAO were detected in only 7.8-50. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.00) 3.50) . Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Arsenate.3% of a representative sample of the U.S.8 (12. 2001.1) 45.70 (3.6 (25.1-25.4..40-6. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.3 (9.S.9) 13.80 (4.7-22.S.6 (11. For residents of Inner Mongolia. 2000.S.10) 8.600 (.20-3.1) 18.05) < LOD .900 (.5) 621 725 1078 Limit of detection (LOD.Metals other areas of the world (Ahsan et al.80 (. 4.3-39.700-1. and two methylated metabolic products... 2008. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.45 (1.70-21. population (Sun et al. Also. arsenite.80 (3.4 (16.40) 5.3) 35. Measurable organic arsenic species in this Report are three biologically generated environmental forms. Survey years 03-04 Geometric mean (95% conf. The higher percentiles of total urinary arsenic levels in the U. arsenocholine.55 (1.400-.8-40.20) 3.4) 23.00-4. 1996.. DMA and MMA.20-25..31-1.800 (. WHO. in NHEXAS 1995–1996.5) 29. interval) 1. 2007).20 (4.0 (27..0) 29..4) 31.2 (6. 1985. arsenobetaine.11-1.20) 7.8) 35. 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.70 (5.90-29.871-1.40-7. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and..20 (...7 (13. 2008).00-1.00 (.80-5. 2008). median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.60) 1. and 0. 2008).2-35. Caldwell et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and duration of exposure are also considered important. In the residents of a Chilean town who consumed water with high levels of arsenic.1-94. vasospasm.5) 32. After recent seafood ingestion. Aposhian et al.10) 4.800 (. arsenite.50-6. 1.3) 1284 1284 03-04 03-04 03-04 1.0-23. 1990. 2001).30) 10. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.19 (. 2005. and TMAO. which may vary for some chemicals by year and by individual sample.62) 2.8 (17.800-1. 2008.700-1.30 (1. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.68) .70-21. In most human studies.6. In the late 1980s.. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. see Data Analysis section) for Survey year 03-04 is 0.70) 6. 2000.6) 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. arsenocholine.00 (1..g.30 (2.900-1.0) 4. and other factors such as nutrition.66 (1.7) 15.5 (26. Pellizzari and Clayton.29 (1.30) 2..80) 1. 2006)...90-7.00-6.50) . DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. Sun et al. Some noncancer effects of arsenic (e. population showed a higher contribution of arsenobetaine (Caldwell et al.60-3. methylation capacity.7 (21.3) 95th 35. with DMA.. 2005.20-190) 31.2-38.6-44.7) 13.10 (4. Tseng et al.50) 90th 16. Individually measurable species resulting from inorganic arsenic exposure are arsenate. Caldwell et al.1-51..e.28) 1..00-12. dermal keratosis. geometric mean levels were about 70-fold higher than for the U. 2000.37 (1. population from the National Health and Nutrition Examination Survey.9 (6. 2003).0 (26.20 (1.74 (1.40) 75th 5. < LOD means less than the limit of detection.6 (13.S. when seafood organic arsenic is subtracted).800) 1.. When seafood intake is avoided.6. China. 2008). Total arsenic measured in the urine includes all species of inorganic and organic arsenic. Caldwell et al. population in the NHANES 2003–2004 subsample. These associations are stronger at higher urinary levels. Valenzuela et al.83) Selected percentiles ( 95% confidence interval) 50th 1.800-4. respectively. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. 184 Fourth National Report on Human Exposure to Environmental Chemicals . a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.

959-1..78-5.70) 5.3) 95th 29.37-2.67) 1.6-32.91 (4. population from the National Health and Nutrition Examination Survey.2 (13.05 (. 2007).9 (25.43) 75th 5.6 (6.612-1..4 (24. 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.58 (3.9) 14.6) 19.28) 1.36) 2. Offergelt et al..833-1.00 (3.9 μg/L.16 (.9 (13. Vahter et al. Sun et al.4) 13.7) 9.47 (1.88) 2.68 (1. Information about the biological exposure indices is provided here for comparison.4) 292 728 1548 03-04 03-04 1.83) 2.39-3. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.. 2003.47 (2.8) 29.64-29.1-36. 1986.400-. 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.9-18.7) 17.4) 32.19-2.76-27.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.11 (.80) . 2008). Fourth National Report on Human Exposure to Environmental Chemicals 185 .61-6. Caldwell et al.30) 1. 2001). 2008). 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.786-1.6-29.4-28.79 (1.3 (10.91) 90th 16.3-24.83) 8.Metals as with DMA.1-18.6 (9.00 (1. WHO.909-1.531 (.53 (.0-36.40) 1.15-1. 1998.4) 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 * * 1.25-7.25 (.29 (4.62-6.938-1.2 (12. Survey years 03-04 Geometric mean (95% conf.9) 32. interval) 1.4 (11. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. 1992.78 (3.32-7.45) 1.5 (18.50-7.10 (.65 (1.81 (4.2 (4.S. population for the sum of inorganic related species was 18.51) 5..3) 1284 1284 03-04 03-04 03-04 1.15-4.51-2.5) 17..1) 26.82) Selected percentiles ( 95% confidence interval) 50th 1.901-2.55) 1.43) 14.3 (10.50-15.1 (26. 2006.S.29-14.5) 26.72) 12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40 (1.21) 5.0 (9.6-46.4-82.05) 1.80-153) 17.18-1..5 (18. In recent years. 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. not to imply a safety level for general population exposure.44 (1.13-39.7) 30.82) 4. which is below the ACGIH BEI (Caldwell et al.638) 1. 2001).877 (.93 (1.2 (12.88 (5.67) 4.73-6.4-21. The 95th percentile of the U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.30-1.15-1.14 (1.54 (1. 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. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.12) < LOD .5-20.

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

08 (<LOD-4. Fourth National Report on Human Exposure to Environmental Chemicals 187 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 1. population from the National Health and Nutrition Examination Survey.20 (<LOD-1.95 (<LOD-2.80) < LOD 621 725 1078 Limit of detection (LOD.44) 2. Survey years 03-04 Geometric mean (95% conf.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. 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. < LOD means less than the limit of detection. 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. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.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. see Data Analysis section) for Survey year 03-04 is 1. which may vary for some chemicals by year and by individual sample. Survey years 03-04 Geometric mean (95% conf.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.00 (<LOD-2.S.00 (<LOD-3.40 (<LOD-1. * 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.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2.

00-22.1-15.29-4.16 (4.00-12.00 (5.95-6.67) 8.8) 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 3.00-8.34 (3.7) 12.12-4. see Data Analysis section) for Survey year 03-04 is 1.38 (3.25 (4.0-16.8) 7.79 (3.80 (4.00 (3.S.18 (6.00) 6.0 (14.9) 13.46 (4.15) 4.72 (4.0) 11.0) 9.6 (9.82-9.10) 3.11 (3.48 (2.00) 90th 11.0) 9.31-4.69 (3.20-12.0 (9.22) 4.00 (3.3 (7.00-15.90) 2.00) 6.92) 3.0 (8.0-18.00 (4.00-13. population from the National Health and Nutrition Examination Survey.80-3.00 (6.95 (4.70 (3.11) 4.44 (2.5) 12.55 (2.0) 292 728 1548 03-04 03-04 4.34-4.67) 9.0-19.60-7.33-4.0) 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 4.82) 3.00-3.00) 6.0 (10.71) 3.12 (3.48 (3.00 (3.70-4.49-4.08 (2.1-22.31) 4.0-25.00-4.0) 621 725 1078 Limit of detection (LOD.17-6.89 (3.0) 13.49) 10.88 (4.0-16.62) 4.32 (8.00) 7.9) 11.71 (3.30) 3.00) 3. Survey years 03-04 Geometric mean (95% conf.00 (6.14) Selected percentiles ( 95% confidence interval) 50th 3.20) 11.80-6.39-3.20-4.90) 5.34 (3.60-6.73) 6.00 (7.00 (5.0) 17.50-15.9) 12.00-11.16-11.74) 90th 9.95-4.78) 4.81 (5.00 (3.45) 8.00-7.0) 16. population from the National Health and Nutrition Examination Survey.03 (3.06) 5.74 (2.95-3.00 (3.0 (9.73 (3.80) 2.09 (7.70-12.17-4.0) 10.34) 3.86 (2.32-10.90 (3.34-4.0) 17.1-18.0 (13.00 (5.7) 1284 1284 03-04 03-04 03-04 4.17 (2.0 (10.00-12.00-4.77 (3.00) 5.00-4.80-5.92-12.70-3.00-7.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .6) 292 728 1548 03-04 03-04 3.00) 4.6) 1284 1284 03-04 03-04 03-04 4.57 (3.61-16.0) 12.00) 3.4 (7.8) 7.0) 14. interval) 3.7-16.60-4.84-18.0 (10.2) 10.59 (6.00) 6.S.32 (4.10) 6.00) 12.30 (7.33) 3.7.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80) 7.0 (10.1 (8.14) 3.05) 3.86-21.45) 3.16 (2.00-4.24-4.13-4.00-3. Survey years 03-04 Geometric mean (95% conf.24) 3.0-17.5 (11. interval) 3.82-5.71-4.00-11.69-6.7) 13.00 (7.00) 4.0 (8.0) 13.69 (3.84-8.0) 9.05) 10.3 (8.85 (3.7 (10.0 (13.00) 75th 6.50 (4.9) 5.0 (12.0) 95th 16.98) 4.00-15.50-5.9 (7. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.45 (8.65-8.0) 11.94-3.00 (5.00-9.60-3.52) 3.78 (4.00-15.00 (5.61-11.70) 5.6-18.00-5.00-10.27-5.00-7.69-3.5) 95th 13.71 (4.57-5.37 (2.03-6.91) 75th 5.3 (8.19) Selected percentiles ( 95% confidence interval) 50th 3.0 (11.00-4.05) 5.27 (3.27-2.0 (9.42) 3.0 (12.86-7.9 (11.0-12.27 (2.00 (3.97-3.94) 3.0) 16.00-7.65-6.00) 9.28) 2.00 (6.44) 5.0-17.00-11.00-4.37 (3.

30) 2.90 (1.40 (1.40-2. Survey years 03-04 Geometric mean (95% conf.60) 2.20 (1.82-2.28 (1. < LOD means less than the limit of detection.07-3.00 (<LOD-1.80 (1.10 (1.88 (1.35-3.37 (1.50-2.60-2.71-2.07 (1.00 (1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.60) 1.9.93) . see Data Analysis section) for Survey year 03-04 is 0.86) 3.07) 2.30) 90th 1.85) 1.985) 1.S.10 (.53 (1.60) 2.853-1.70-2.80-2.20-3.00-2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .50) 1.00) 2.90) 1.50 (<LOD-1.90) 2.20 (1.31 (1.40-3.90 (2.61-3.10 (1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.30 (1.86) 2.30-2.79) 2.82-2.31-3.30 (1.80) 1.80 (1.88-2.30) 1.10-3.20 (1.00-1.20 (1.50 (1.S.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.43-3.77) 1.00) 1.30 (2.40-3. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.60 (2.30 (1.90) 2.900-1.40) 2.00-4.20 (1.30-1.70-3.23) 1.50 (1.16 (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 1.00 (<LOD-1.00) 1.36 (1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00 (2. * 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.73-2.00) 2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.20-1.86 (2.00 (2.14-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80 (1.28 (1.60 (1.33 (1.18-1.63 (<LOD-1.62) 2.52 (2.84-3.30-1.10-1.18-1.10) 2.80 (1.70-2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00-1.53-2.96-2. population from the National Health and Nutrition Examination Survey.10) 95th 2.50) 621 725 1077 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.20 (1.45) 3.85) 2.40) 1.40-2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.34) 2.70) 2.36) 1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.54) 90th 2.11-1.10 (<LOD-1.40) 1.70-2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1. Survey years 03-04 Geometric mean (95% conf.61) 2.22) 3.00-2.46-2.05-1.10-1.22 (1.86 (2.80-2.816 (<LOD-.80 (2.33 (1.81) 1.10 (.70-2.15-1.20) 2.46 (1.00) 1.57) 95th 2.30) 1.58) 2.17) 2.50 (2.88 (1.40 (2.80) 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 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. 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. population from the National Health and Nutrition Examination Survey.0. Survey years 03-04 Geometric mean (95% conf. 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.Metals Urinary Trimethylarsine oxide Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.S. 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. 190 Fourth National Report on Human Exposure to Environmental Chemicals . Survey years 03-04 Geometric mean (95% conf. Urinary Trimethylarsine oxide (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. < LOD means less than the limit of detection.

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50-1.20-8.1) 9.00) 1.06-1.62) 1.72) 1.55-3.71) 2.20-5.26) 5.24 (4.48-4.70-3.20-8.65-1.57-7.62) 1.50 (2.47) 4.10-4.48) 1.61 (3.50) 1.49) 11.78) 1.00-8.80-2.9) 5.64-3.43) 6.18-1.60) 3.10) 3.93-2.47-1.37) 1.50 (4.15 (6.49-1.60) 1.40-13.30 (1.50 (4.32) 8.60-10.21 (1.30 (3.60 (1.50) 4.90) 4.15-1. are high in barium (Genter. 01-02.50-6.19) 2.56 (6.40 (1.63) 1.87-3.35 (2. respectively.87 (5.61 (1.54) 1.50-6.49 (1.11 (2.15) 5.27) 2.51) 1.70-5.90 (6.50 (1. tiles.00) 6.73-5.87-9.11-1. 0.20 (3.11 (3.04-2.54) 1.84) 5.35-1.61 (1.76-3.63) 1. Barium compounds are used by the oil and gas industries to make drilling muds.20 (4.80 (2.60) 4.30) 5.00) 4.54 (6.Metals Barium CAS No.33 (1.76 (3.38) 8.77-3.50 (4.34 (1. interval) 1.29-1.30-5.15-11.70 (1.30 (5.30-1.70) 3.07 (2.21-2.63 (5.95 (4.S.88) 1.40 (5.20 (1.05-2.78-2.37-8.71 (2.78) 1.86-5.87 (6.30) 2. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.85) 1.18) 3.73) 1.38) 2.40 (4.39-1.63 (2.97 (1.41-3.91) 2.70-2.65 (5.18 (6.67) 6.25-1.06-2.36 (4.57) 3.85 (2.19-1.98) 1.24-1.70) 1.99-5.66) Selected percentiles ( 95% confidence interval) 50th 1. Certain foods.88) 4.8 (6.74-2.09 (1.60-2.76-2.30) 4.50 (1.86-4.8) 9.56) 1.80) 6.94-6.26) 2.72) 75th 3.76) 1.34 (2. depilatories.50) 2.63) Total 1.70-2.63 (8.31 (2.90 (1. 7440-39-3 Medically.51) 2.43) 2.92) 2.39 (1.40 (5.20-1.20-8.53) 2.70) 7. glass.27 (1.75-3.39 (1. see Data Analysis section) for Survey years 99-00.52 (1.01-7.29-5. In nature.78-3.00 (1.56) 4.69 (1.74-3.30) 5.62 (1.08-8.25 (1. Fourth National Report on Human Exposure to Environmental Chemicals 193 . Barium compounds are also used commercially in paint.30-2.15-1.42 (1.70-8.39) 1.22-1.80 (1.44-2. barium sulfate and barium carbonate).82-6.30-1.38 (1.60-6.93 (4.43 (1.87-7.36 (1.54) 2.35-4.08 (6.77) 1.10 (4.54-1.56 (2.43) 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. bricks.37 (4.4) 7.40) 7.48 (6.30 (5.10-5.30) 8.50-1.86 (4.81-3.35 (3.54-1.34 (1.21-8.01 (4.26-1. and 03-04 are 0.24-1.96-2.35 (1. fireworks. In single dose animal studies.57 (5.75) 2.63 (1.81-2.50 (1.41-1.46-1.17-1.65) 1.59) 3.73) 3.00-76.10 (2.65-5.52 (4. Workers employed by industries that make or use barium compounds can be exposed to barium dust.59-11.14 (6. it combines with other chemicals such as sulfur or carbon and oxygen.90) 2.60) 1..20) 2.14-6.80-5.48) 1.47-1.44 (1.90-2.12 (2.99 (4.31-2.70 (5.48-4.35-1.35) 5.95-6.85) 1.80-7.03 (1.40) 7.70-6.16 (1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.02 (7.21 (1.04-6.49) 4.12.62 (1.50 (3.40 (1.80 (1.36) 5.49) 8.64 (1.50) 2.71-9.15 (2.82) 2.80) 7. and ceramics.45) 7.72) 4.12 (2.90-9. Small amounts of barium can be released into the air during mining and other industrial processes.80-3.20-1.14-1.91) 6.25-11.22-1.36-1.30 (2.44-5.50 (1.28) 90th 5.49-9.80 (1.56 (1.39) 4. Barium salts have also been available as rodenticides.60-3.90 (4.40) 3. The general population can be exposed to low amounts of barium in air.53-5.4) 9.32-7.66 (4.38 (1.51 (1.70) 4.88 (5.22) 6.87-14.26-7.20-6.8) 5.29) 5.61-8.86) 6.28-1.54 (2.80 (5.09 (2.86 (4.10 (3. and food.37-1. and 0.2) 6.50 (1.90) 2.30) 3. 2001).10) 5.71) 95th 6.27 (1.90-13.80) 1.16) 5.73 (5.43 (1.41) 1.30-2.81-2.49) 2.70) 5.73 (6.00-3.60-6. water.53) 1.56 (1. rubber.87) 7.88) 7.51) 7.4) 6.65-8.68 (1. such as barium chloride.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.40 (5.32-1.00 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.15 (1. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).65) 1.12-1. such as brazil nuts.g.00) 1.37) 5.12) 6.70) 1.80 (2.45 (1.43 (5.91 (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 2.05% of the earth’s crust.30) 5.90) 1.65) 3.12) 7.31.54-8. population from the National Health and Nutrition Examination Survey.34) 2.77 (3.30-3. whereas others are practically insoluble (e.36-1.20-1.61 (5.40 (1.71) 1.93-8.60 (2.74) 3.46) 1.10) 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. Some barium salts are freely soluble in water.76-7. soluble forms of barium.46) 1.61 (2.11 (3.50 (6.12.55-7.50 (5.82) 1.20-1.

59) 2.14-2.04) 1. and route of exposure.03-1.34-1.15-4.73-2.34) 1.57-7.97-4.26-1.80-6.65 (2.84 (3.22-2. Perry et al. vomiting.41 (1.29-1.00) 4.5) 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 1.39-1.10) 3.28-6.37) 2.10-2.33-4.37 (1.46 (2.76) 1.0) 6.76 (4.76-3.74) 1.55 (5.53 (2.963 (.4 (5.10) 6.52 (3.34 (1.80) 3.96-6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.26) 4.64 (1.3) 6.65 (5.39 (2.96 (4.27) 7. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.45-6.26-1.48-1.96) 4.39 (2.69-9.60 (2.38 (4.98 (2.20) 4.77) 1.48 (1.44-2.08-1.91 (3.2) 5.97 (5.49-1.60 (1.50 (4. 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.85-5.42) 1.4) 5.47) 4.38-5..38-7.59-7.96) 4.00 (3.91-2.32 (1.33) 6.58 (4. 1989).36 (1.33 (5.44 (1.77) 1.16 (1.27) 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 .28 (1.59 (1.34-5.74) 1.51 (3.04) 5.55-5.68) 3.05-1.30) 2.73-4.77-5.905 (.84) 2.90-2.54 (2.62 (1.52) 7. Following intravenous injection in animals.2 (3.64 (1.40 (1. Barium is not rated for human carcinogenicity.70) 4..Metals was eliminated primarily in feces and to a lesser extent.56-3.38) 1.58) 75th 2.00) 1.40-1.29-7.24-11.33) 1.20 (1.28) 5.36-2.36 (3.00-7.35-1.39-1.880-1.55 (1.99 (2.52-4.70) 10.47 (5.31-1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Wones et al.00) 6.16-1.45 (1.33-1. weakness.777-1.48-3.29) 1.29-3. 1986).29-4.88 (6.31) 5.13-3.54) 2.84-5.91 (3.72) 4.47-8.77) Total 1. chemical form.08-2.24-6.96 (4.38 (1.75) 1.25-11. Toxicity from soluble barium salts is rare. The health effects of exposure to barium compounds depend on the dose.99 (4.26-4.82) 1.24 (5.47) 10.34-3.36 (5.55) .31-1.12) 2.41 (2.64) 7.00 (2.39) 4.80) 4.61) 2.29 (1.21 (1.48 (1.45-1.78 (2.0) 5.52) 1.76) 2.62 (4.25 (1.47 (2.13-2.54 (1.53) .35-3.04 (2.72) 6.68-3.51-3.37 (1. NTP.00 (3.19-1.43-6.86-7. Symptoms following acute high dose include perioral paresthesias. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.921 (. 1984.28-1.24-3.10 (6.29 (3.49 (1.46-22.72 (2.87) 1.56 (1.55 (4. population from the National Health and Nutrition Examination Survey.64) 7.96) 7.81-6.8) 4.S.53-21.91) 2.02) 4.0) 7.32 (2.81-7.97-3.42 (4.51 (1.20-2.41 (1.30 (1.49-1.27 (2.00 (5.18 (1. 1985.32) 2.86 (2.48-5.22-1.40 (1.31 (1.37-1.45-1.22-4.66 (1.68) 1.03) 3.3 (6.70) 1.76 (3.2) 6.75) 2.92 (4.97) 1.24) 3. diarrhea.59) 1.46) 2.18 (1. 2001).81-6.36-1.11) .47) 1.48 (1.75-3.86) 5. 1990).76) 2.96) 4.24 (3.51 (1.38 (1.50) 1.38) 1.88 (2.39-10.03) 1.57-10.77) 5.40 (1.46) 3.41) 5.25) 4.79) 1.71 (5.10-1.68-3.38 (4.11-2.51) 4.09) 6.50) 1.84-2.89) 90th 4.68 (3..39 (3.24-1.62 (2.97 (4.832-1.60 (5.92) 2.06) 2. Insoluble barium salts.64 (1.52) 2. are not absorbed when administered.38-1.19-1. water solubility.02) .49-1.19-1.881 (.77) 1. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.38) 4.58) 1.68 (2.32 (1.39 (2.60 (2.63) 1.28-7.31 (4.16) 11. and cardiac dysrhythmias. paralysis.36 (1.59) 1.76 (2.35-1.36-1.58 (2. in urine.01 (5.20-1.26-1. hypertension.02-5.55-6.26-1.58) 4.45 (3.32) 2.23-5.42) 1.44-2.45-8.57) 2.11) .60 (1. such as those used in medical radiographic procedures.61 (4.33 (1.67-6.64 (1.56 (1.54) 1.74 (5.82) 1. a benign condition that may occur among barite ore miners.24-1.00-1.48) 2.99) 1.75) 1.89 (2.27-1.23-1.45) 95th 6.52-10.06) .33 (1. interval) 1.57 (6.703-1.31-1.27-3.59 (1.24-6.915 (.20-8.79-5.19-2.46) 1.30 (1.75) 2.58-6.51) 4.45) 1.68 (3.69 (5.28-11.47) 1.891 (.23-2.56) Selected percentiles ( 95% confidence interval) 50th 1.43) 1. 1994.51) 6.00) 4.39-5.50) 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 1.75-22.01) 1.41) 4.50) 2.03) 2.62) 2.36 (3. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.83) 2.01 (4.29-4.56) 4.57-5.02 (3.73) 2.22-1.63-4. Chronic high doses in animals resulted in kidney damage (McCauley et al.754-1.03-1.83) 3.710-1.37-2. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.49 (1.55 (1.60) Sample size 2180 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.

Trace element reference values in tissues from inhabitants of the European community I. 1984.95:89-105. Levy. Magnesium. Pirkle JL.296(1-2):71-90. et al. 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. Handbook on the Toxicology of Metals. the welders had no obvious adverse clinical effects (Zschiesche et al. Douglas BH. 1989. Ting BG.76(1):53-59. 2001-2002. Pozzoli L..28(3):373-388. Perry EF.. Environ Health Perspect 1990. In Friberg L. and 2003-2004 (CDC. In: Inorganics in drinking water and cardiovascular disease. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies).. Princeton (NJ): Princeton Scientific Publications. 1986. Princeton NJ: Princeton Scientific Publications. Third National Report on Human Exposure to Environmental Chemicals. strontium. Sci Total Environ 1990. Advances in modern toxicology. Exposure to soluble barium compounds: an interventional study in arc welders.e. Sampson EJ. Pietra R..atsdr. 231-249. blood. eds. and radium In: Bingham A. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005. Schaller KH.85:355-359. Vol 2: Specific Metals. NTP. 2000) to levels in NHANES 1999-2000 and 2001-2002. Centers for Disease Control and Prevention (CDC). 1998). technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. Epidemiological study of barium in Illinois drinking water supplies. Kopp SJ. 2nd Ed. et al. and a drinking water standard has been established by U. Lack of effect of drinking water barium on cardiovascular risk factor. Sabbioni E.nih. Int Arch Occup Environ Health 1992. Reeves AL. EPA.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. 4/8/09 Paschal DC. Minoia C. National Toxicology Program (NTP).. Jackson RJ. Paschal et al. LA. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Gallorini M.. Comparison of representative ranges based on U. Vouk VB.. Howerton K. Available at URL: http://ntp. 1985.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en.. eds. Morrow JC. Cohressen B. Perry HM. J Toxicol Environ Health.niehs. 1992). barium. Powell C. p. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report.S. patient population and literature reference intervals for urinary trace elements. Weltle D. pp. environmental levels) and health effects is available from ATSDR at: http://www. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. Barium. Inc. Nordberg GF.nih. et al. Environ Res 1998. Apostoli P. ed. Jr. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report.html?charset=iso-88591&url=http%3A//ntp. PS. 84-94. ed. [online]. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Fourth National Report on Human Exposure to Environmental Chemicals 195 . and serum of Italian subjects. Frohman. New York: Elsevier. Atlanta (GA). Costa R. A study of 46 elements in urine.gov:8080/cs. Laurie RD.S.html. Investigations into the effect of drinking water barium on rats.64(1):13-23. 1990. p.197210. Stadler BL. In: Calabrese EJ. 221-252 Komaromy-Hiller G. p. Biomonitoring Information Levels of urinary barium reflect recent exposure.. 2001. et al. 5th ed. New York: John Wiley & Sons.cdc. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. McCauley PT. 1994. calcium. Genter MB. Wones RG. Zschiesche W. References Brenniman GR.gov/toxpro2. 2005. Patty’s toxicology.gov/ntp/htdocs/LT_rpts/tr432. Calabrese EJ. Ash KO. Minoia et al. Trace metals in urine of United States residents: reference range concentrations. Information about external exposure (i. Clin Chim Acta 2000.niehs.

13. beryllium is used in instruments. aircraft. electrical. and dental bridges. eating food. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. and refined beryllium is used in mirrors and special metal alloys for the automobile. Two types of minerals. soil. In medicine. see Data Analysis section) for Survey years 99-00. or drinking water containing the metal. and can be found in mineral rocks. Low-level beryllium exposure in the general population can occur through breathing air. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 0. respectively. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. In studies of laboratory animals.130 (<LOD-. 7440-41-7 General Information Pure beryllium is a hard gray metal. and volcanic dust. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. coal. 01-02. which may vary for some chemicals by year and by individual sample. nuclear. and machine-parts industries. 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 . Survey years 99-00 01-02 03-04 Geometric mean (95% conf. computer.S.13. are mined for commercial recovery of beryllium.Metals Beryllium CAS No. Exposure to beryllium occurs mostly in the workplace. 196 Fourth National Report on Human Exposure to Environmental Chemicals . near some hazardous waste sites.13.130 (<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 . and 03-04 are 0. the lightest of all metals. and from breathing tobacco smoke. and 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 . bertrandite and beryl. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. Beryllium compounds are commercially mined. x-ray machines.140 (<LOD-. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes.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.

respectively.281 (<LOD-.231 (<LOD-. Maier. NTP considers beryllium to be a known human carcinogen. or berylliosis. based upon excess lung and central nervous system cancers in studies of workers. 2003. 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. population from the National Health and Nutrition Examination Survey. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. IARC has classified beryllium as a human carcinogen. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. 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 .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 . Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Fourth National Report on Human Exposure to Environmental Chemicals 197 . 1990). EPA. Skin exposure can result in delayed hypersensitivity reactions. S..S. 2002). Chronic beryllium disease.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. and drinking water and environmental standards have been established by U. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. including contact dermatitis and subcutaneous nodules. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. which produces pneumonitis. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .346 (<LOD-.

296(1-2):71-90.e. et al. Sabbioni E..html.cdc.e.. Int Arch Occup Environ Health 2001. Sabbioni E. Ting BG. which approximate this Report’s limit of detection... Jackson RJ. Morrow JC. Environ Res 1998. Pirkle JL. Sci Total Environ 1994. blood.23:827-839. Schaller KH. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. and 2003-2004. Genetic and exposure risks for chronic beryllium disease. Minoia C.S.12 to 0. Comparison of representative ranges based on U. et al.95:89-105. McCanlies EC. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Paschal DC. Howerton K. population were generally undetectable in NHANES 1999-2000. Clin Chest Med 2002. patient population and literature reference intervals for urinary trace elements. 1998).S.1 μg/L). Van der Venne MT. and the fact that most NHANES participant levels were undetectable. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure.inchem. Kriess K. Apostoli P. Sampson EJ. Element reference values in tissues from inhabitants of the European community.157:388-398. Given these results. Atlanta (GA) 2005.13 μg/L. 1990. Ash KO. Weston A. less than 0. Minoia et al. Clin Chim Acta 2000. it is likely that urinary beryllium levels in the U.atsdr. environmental levels) and health effects is available from ATSDR at: http://www. Hamilton et al. References Apostoli P. VI. Review of elements in blood. 0. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Trace metals in urine of United States residents: reference range concentrations.76(1):53-59. Pietra R.Metals (i. 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. HLA-DPB1 and chronic beryllium disease: a HuGE review.. 2000.gov/toxpro2. Centers for Disease Control and Prevention (CDC). Am J Epidemiol 2003. and serum of Italian subjects. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. In other studies. 3/27/08 Komaromy-Hiller G. 106. 1990. Third National Report on Human Exposure to Environmental Chemicals. They reported urinary beryllium levels ranging from 0. Available at URL: http://www. Trace element reference values in tissues from inhabitants of the European community I. 20012002. Sci Total Environ 1990. Pozzoli L. population are lower than levels in workers.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Levels of beryllium in urine for the U.158:165-190. Costa R.org/documents/ehc/ehc/ ehc106.htm. Andrew M. Gallorini M. 2001). International Programme on Chemical Safety (IPCS). A study of 46 elements in urine. Paschal et al. Beryllium [online]. Environmental Health Criteria. Maier L. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure.74:162-166. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Hamilton EI. and the 95th percentile for males in NHANES 2001-2002.

10 (1.500-.700) 1.500 (.367-. Fourth National Report on Human Exposure to Environmental Chemicals 199 .300) .200 (<LOD-.500 (.300-.500-.20) .700) .468 (.600 (.470) * .400 (.20) 1.200-.600) .60 (1.403) .600 (.600) .00 (. during refining of lead and copper from sulfide ore.600) .600) .500-.900 (.900-1.900-1.400 (.500-. see Data Analysis section) for Survey years 99-00. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.300-.382 (.500-.300-.304 (.10) 1.400 (.80) 1.376-.20) .20 (1.266-. The predominant commercial use of cadmium is in battery manufacturing.200-.500 (.400-.600 (.400-.300) .300) .600-.700) .50-1.20) 1.20-1.500) .30-1.300 (<LOD-.300 (.30-1.304 (.40-1.309-.70) 1.20) 1.600 (.500) .600 (.441) * .378-.40 (1.500) .300) 75th .400) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40 (1.30) 1.30-1.70) 1.600 (.70) 1. and 0.60) Total * .00 (.S. malleable.600) 90th 1.300 (.30-1.10 (1.20-1.395 (.50-1.300 (.10) 1.600-.300 (.400 (.40 (1.300-.500 (. 01-02.400-.600) .50) 1.00 (. respectively.452) .50) 1.300 (<LOD-.00 (.60-1.300) .400) .00 (.700-1.300) 1.500-.80) 1.300 (.600 (.400) .40 (1.400) .00 (.800-1.500-.300-.60) 1. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.30 (1.90) 1.424) * .20) 95th 1.400) . and nonferrous alloys.359-.800) 1.20 (.300 (.500-.420 (.400) .60 (1.331) .00 (1.00-1.400-.70) 1.500) .300-.500 (.00 (1.700) .10 (1.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .20) 1.50-1. cadmium use has declined in response to environmental concerns (http:// minerals.600) .S.00-1.400) .600) .300-. Other uses include pigment production.10) 1.300 (.40-1.200-.600 (.50 (1.30) 1.400 (.427) * .50) 1.14.300) .398) < LOD < LOD < LOD < LOD < LOD < LOD .20) 1.200-.400) .700-1.255) .00-1.20) 1.10) 1.600 (. U.300) .200-.20-1.00) .400 (.800) .400 (.300-.400) .378 (.300-.10 (1.400) .400 (.30) 1. lead.00-1.40) 1.00) . as zinc sulfide) and to a lesser extent.600-1.400 (. coatings and plating.300) .00-1.500-.50-1.300 (.800 (.513) .500-.403 (.60) 1.500 (.300-.20) 1.600) .500) . Since 2001.296-.900-1. and 03-04 are 0.400) .10 (1.300) .400-.426-.60 (1.326 (.333 (.400 (.300 (.500 (.362-.425 (.00-1.500-.200) .368-.200 (.300 (.300-.30-1.400) .400 (.300-.usgs.10) 1.600 (.386-.400-.60 (1.10 (1.275-.300 (<LOD-.313 (.00-1.20-1.300-. Cadmium also may be emitted into the air from zinc.40 (1.600) 1.500-.700) .300) .3.700) .00-1.400) < LOD . 7440-43-9 General Information Cadmium is a soft.600 (.500-.361-.300-.500-.500) .900-1.600 (.00 (.00 (.10 (.10) 1.300-.300-.80 (1.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.gov/minerals/pubs/commodity/cadmium).300-.50 (1.200 (.20-1.700) .800) . which may vary for some chemicals by year and by individual sample. EPA.400 (. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.500-.3.00 (.900-1.500-.900-1.20) 1.500) .60 (1. plastic stabilizers.300-.10) 1.200 (<LOD-.289-.300-.700-1.400 (.600) .900-1.00 (.900 (.337) .400-.30) .20-1.400-.400 (.400) < LOD < LOD < LOD . interval) .900-1.400 (.400 (.700 (.300) .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 .300 (.50 (1.300-.400) < LOD .460) .400-.50 (1.10 (1.S.304-. < LOD means less than the limit of detection.344) .400) .216-.40) 1.400) < LOD .Metals Cadmium CAS No. or copper smelters (U.900-1.00-1.300 (.300) .70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 . 0.300-.421 (.300 (.800 (.400) .300 (.449) Selected percentiles ( 95% confidence interval) 50th .60) 1.300) .900-1.300 (<LOD-.600 (.40 (1.393 (.10) 1.800-1.200) .600 (.366) * * . and incineration of municipal waste materials.400 (.200 (.300) .400-.600-.500 (.300-.20-1.700) .400-.283 (.412 (.235 (.500-.40 (1. population from the National Health and Nutrition Examination Survey.500 (.500-. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.700) .

390 (.090) .510-.426 (.209 (.284) .221) .17 (.820 (.181 (.157-.455 (. 1999.493-.061 (<LOD-.48 (1.210 (.498-.109 (.04 (. copper) and protein.219 (.20 (1.972 (.206 (.220 (.25 (1.273 (.458 (.200 (.741-1.26) 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.219 (.476-.886) .183-.980-1.160) .366-.222) .855-1.387) .843-1.272-.233) ..393-.195-. 2001).875 (.281 (.990) ..100-.329 (.289-.989-1.680 (.135 (.178-.220-.875) .170 (. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.203 (.134) .400-.233) . ingestion through food is the largest source of exposure.277 (.128 (.326) .. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.265 (.249-.28 (1.313) . zinc.153-. respectively.753-.848 (.229) .175 (.980) .241) .800-.114-.22 (.299) ..107-.500) 90th .306 (.** Survey Geometric mean (95% conf.295) .200-.230 (.475 (.817 (.447 (.918-1.433-.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 .470-.507) .210) .165-.388-.192-.596) .362) .061-.135-. Diamond et al.980 (.Metals 2000).36) 1.092) .246) .160) .270 (. 200 Fourth National Report on Human Exposure to Environmental Chemicals .302 (.234 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .38) .820) 1.262) .060-. see Data Analysis section) for Survey years 99-00.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .366) .892-1.167-.960) 1.140 (.800 (.211-.41 (.450 (.06.081) .450 (.200 (.270 (.19) 1.03) . For nonsmokers who are not exposed to cadmium in the workplace.235) . wheat.452 (.285-.327 (.220) .481) . and 0.482) .336) .06.10 (1.04 (.320) .249) .559 (.551 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.17 (.354) . 01-02.510) .092 (.390-.836-1.247) .121 (.253-.S.440-.199 (.157) .17) .148) .237-.550 (. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.545 (.360) .351-.940-1.519) ..01-1.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .20-1.261-.13) .308) .169-. drinking water is a source for cadmium intake.255) .43) 1..700-. and 03-04 are 0.37) 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 .196-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.257-.817 (.219 (.191-.229) .173) .960 (.07-1.067-.381-.077 (.160 (.238-.919) . 2003).210 (.372) .980) .077 (.190-.858 (.818 (.316 (.466 (.539) .766 (. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.763-.28-1.09-1. 2004a.136) .890 (.700-.109-.193 (.440 (.440 (.191 (.730-.717-.283 (.860) 1.080 (.790 (.15 (.13 (.201 (.210 (.189-.633-1.260-.260 (. and various seeds.112-.456-.74) 1.251) .530 (.551) .394-.148-.366-.17 (.530) .12 (.51 (1.190-.640) . Renal tubular and glomerular damage.713) .260-.01 (.580) .170-.202 (.02-1.141 (.198) .240-.820-1.208-. The kidney is a critical target and shows the earliest sign of cadmium toxicity.06. 2003.430-.38) 1. With chronic exposure.282 (.810-1.207-.01) .430) .13-1.892 (.115-.211 (.462 (.47) 1.189) .490) 1.189-.886-1.06) . 2003).192-.265) .190-.733-.239 (.226) .065-.067-.963-1. an inducible metal binding protein.179-.30-1.28) 1.202-.230) .790 (. 1994).748-1.520-. Cadmium absorption may be increased with iron deficiency (Berglund et al.221 (.390-.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.38) .977) .890-1.310) .210 (. however.206) .32 (1.231) .479) .310 (.200-.492 (.633 (.171-.15) 1.177-.232 (.880) .223 (.150) .203) .813 (.193-.180 (.20 (1.72) 1.322 (.623) . To a lesser extent.412) .238) .806) .980-1.490) .175 (. including many food crops such as cereal grains.607) .078 (.240) .705-.15) . 0. whose body burdens of cadmium can be approximately twice that of nonsmokers.06-1.38) 1.255) .230) 75th .339) .12-1. **All results are corrected for molybdenum oxide interference in the ICP-MS method.57) 1.400-. Inhalation of cigarette smoke is a predominant source of exposure in smokers. 2003).290-.257) .480) .24) 1.090) . Horiguchi et al.839 (.25) 1.214-.130 (.243-.20) 1. interval) .714-1.170-.150-.120 (.087-.20 (1.423-.330-.686-.220-.255) .210 (.151-.232) . calcium.229-.445 (.261-.216 (.191-. Kikuchi et al.227 (.589 (.436-.350 (. Cadmium is absorbed via inhalation and ingestion.540) .34) 1.101) .733) .445 (.610) .519) . potatoes.82) 1.83) 1.300 (. population from the National Health and Nutrition Examination Survey. rice.184-.279 (.500) .110-.700-.280 (.263) .160-.204 (.126) .187 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.210) .06-1.22 (1.870) .52 (1. Cadmium in soil is absorbed by plants.194-.

631) .182) .208 (.668-.472) .559-.818) .270 (.813-1.321) .143) .873 (.336-.288) .170 (.687 (.156 (.479 (.818) .100 (.094) . Fourth National Report on Human Exposure to Environmental Chemicals 201 .917 (.227-.140-.051-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.678-.352) .906) .607) .767 (.826-1.181-.438-.184-.667) .090 (.481 (.630-.281) .02 (.338 (.722-.202 (.404 (. Olsson et al.500-. most often a result of occupational exposure (Roels et al.13) .210) .700) .101) .398-. can result from high dose chronic exposure.281) .232) .297) .438) 90th .223) .708-1.00 (.653) .219 (. population from the National Health and Nutrition Examination Survey.941 (.136-.163) .38) .220 (..830) .931 (.238-.516-.418-..421 (.303) .234) .17) .S.335 (.268 (.187) .211 (.909-1.168-.850) . Noonan et al.343-. 2000.423-.05) 1.085 (.071 (.157-.250) .518) .181 (. 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.308) .183) .204-.240) .490 (.267 (.998) .157-.645-.221-.856) .431) .449) .541) .112) . 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. Staessen et al.767) .171-.536 (.16) ..278) .111-.12) 1.216-.538) .190 (.086 (.423 (.691-.148 (.191 (.182) .229) ..280 (.091 (.716) .678 (.096) .686 (.154 (.063-.122 (..273 (.078-. 1999).226) 75th .874-1.263 (.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 .240) .827) .104) . Jarup et al.828) .16) 1.147-.381-.184) .130-.178) .158-.210 (.387-.690 (.754) .444-.985 (.591 (.292) .533) .215 (.162 (. 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.205 (.929) .617 (.940 (.147-.218) .190 (.225) .470) .154-.255-.147 (.446) .07 (.311) .792 (.783 (.185) .239-.191-..283 (.940-1.318 (.200 (.614) .08) .104) .131-.192) .236-.263-.247-.123-.434 (..537-.168 (.247-.** Survey Geometric mean (95% conf. 1999).470) .507-.106) .850) .173 (.161-.830-1. **All results are corrected for molybdenum oxide interference in the ICP-MS method.700 (. Horiguchi et al.418) .865 (. 2002.245 (.135) .304-.266-. However.191) .209) Selected percentiles ( 95% confidence interval) Sample 95th .126 (.917) .175 (.562-.388-.166 (. 1999).440) .826-1.414-.199-.856 (..084-.261 (.350) .146-.225) .757) .687-..531 (.156) .441-.484 (.10) 1.091) .364) . 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.716-.212 (.289) .201-.075-.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.979 (.00 (.209) .233 (.181 (.091 (.296 (.242) .769 (.784) .412 (.143-.487 (.176 (.137-.247-. 2003.234-.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 .382) .093 (.316 (.198) .501 (. 1996.176 (.235) .207) .325 (.740 (.224 (. 2002.174-.144-. interval) .789 (.206-.253) .433-.688-.674-1.182) .261-. At lower environmental exposures.693 (. 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.163 (.391-.197-.308 (.199 (.067-.181) .238) .316) .09 (.622 (.159 (.266) .189-.884) .183 (.729 (.075 (<LOD-.084 (.757 (.962) .143-.300-.097) .140-.085-.696-.083-.185 (..473 (.426-.725-1.078 (.210 (.168-.175 (.159 (.712 (.545) .074-.177) .282 (.274) 1.476) .123-.950) .329 (.221 (.267 (.219 (.184-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.170-.187-.234 (.647-.07) .432 (.252 (.795) 1.927-1.06 (.107) .04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .175-.690-.415) .690-.156-.178-.876-1. During the 1950’s and 1960’s.194-.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.839) .288 (. 2004b). 2002.491-.173-.331 (.241) .663 (.833-1.666-.560-.340) .219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .650-.387 (.802 (.304) .253 (.288-.551) .806-1.919 (.136-.377-.256-.222-.077-.261) .289) .208-.113-.414 (.150-.098) . 2004).783) .404) .196 (.779 (.293-.382-.813-.440) .228-.719 (.207-.137 (.232) .727-.718 (.

potentially fatal pneumonitis (Fernandez et al. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. 2003). 2000. has resulted in severe.. 2006. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . 2002. 1999).. Becker et al. In postmenopausal women. 2006). In the typical environmental exposure. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1.26 and 3. Women had higher blood and urine cadmium levels compared to men of similar ages. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. 2004b.. 2004. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Jarup et al.cdc.. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. 2006. 2003. environmental levels) and health effects is available from ATSDR at: http://www. 2002).. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. 2003. 2005. 1996). Ezaki et al.. 1996. 2000)..e. 2003. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. 1988). 2004). 2002. 2002).. 2005. 2002. Olsson et al. 2002.gov/ toxpro2. Staessen et al. Moriguchi et al. 2002).. intermediate in former smokers and lower in never-smokers (Becker et al. EPA. 2003.. For NHANES 19992000..46 mg/gram of creatinine) (Ezaki et al.S.. Animal studies have demonstrated reproductive and teratogenic effects. respectively. 2004. 2004. 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.. Olsson et al. Wilhelm et al. Becker et al.atsdr. approached these values associated with subclinical changes in renal function and bone mineral density. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC.. Suwazono et al. maternal blood or maternal urine and birth weight (Nishijo et al.. 2004b). Staessen et al. 2003. 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. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. In adults aged 60 years and older. Occupational standards are provided here for comparison only. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. 2002. Ezaki et al. Information about external exposure (i. 1999. 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). Acute and heavy exposure to airborne dusts and fumes. 2002).. not to imply a safety level for general population exposure... Friedman et al. Mannino et al...Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. and drinking water and environmental standards have been established by U... 2005.... respectively. 2000. 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. CDC. Wennberg et al.. Zhang et al.. Creatinine-corrected urine cadmium values in U. Wennberg et al. 2002. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.. However.... 2002). Horiguchi et al. Horiguchi et al. with peak values observed in the fifth to sixth decades (CDC. Noonan et al. Cadmium can produce lung.. Becker et al. 1999).. 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. Jarup et al. 2005). Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. 2004. 2002) and length at birth (Nishijo et al.. Jin et al. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. data (CDC. Komaromy-Hiller et al. Staessen et al. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. Both IARC and NTP consider cadmium a human carcinogen.html.. 2005. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. Olsson et al. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity.. 2006).S... 2003.... Further research is needed to address the public health consequences of such exposure in the United States..S.1 mg/L (Alfven et al. 2000. as may occur from welding cadmium-alloyed metals. Salpietro et al.

Kikuchi Y. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Akesson A.atsdr. Okamoto S.296(1-2):71-90. Savage-Brown A.59:194-8. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Atlanta (GA).46:372-374.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. Kaus S. Agency for Toxic Substances and Disease Registry (ATSDR). Kundiev YT. Bernard A. Kumagai N. Ukai H. environmental. Serra J. 4/8/09 Alfven T. Consonni D. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Lukyanova EM. Tsukahara T. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Thorax 2004. Zhu G. Mannino DM. Thayer WC. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. ShkiryakNizhnyk AZ. Bo M. Oguma E. Gadea E. Clin Chim Acta 2000. Ezaki T. Krause C. Sasaki S. Environ Res 2006.1(8587):663-667. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake.66(Pt A):2141-2164. Miyamoto K. Centers for Disease Control and Prevention (CDC). J Occup Health 2003. J Toxicol Environ Health 2003.gov/toxprofiles/tp5. Greves HM. Uemura T. et al. Nomiyama T.205:297-308. Furuki K. Bellerup P. Lundh T. Toxicological profile for cadmium update. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Furuki K. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. 1999 [online]. Fatal chemical pneumonitis due to cadmium fumes.102:83-89. Komaromy-Hiller G. Lauwerys R. Fukui Y. Taylor AJ. et al. population. Chiappino G. Sasaki S. Bregante G. Lancet 1999. Howerton K. Nermell B. Ezaki T. Jones RL. Horiguchi H. 2005. Friedman LS. Int J Hyg Environ Health 2003. Carlsson MD. Ikeda Y. Tsukahara T.html. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Environ Res 2004.148(1-2):11-20. Pickering CA.24:717-724.45:43-52. Chislovska NV. 206:15-24. Comprehensive study of the effects of age. Anthropometric.57:668-672.cdc. Choudhury H. Schulz C. Mucha A. Miyamoto K. Toxicol Lett 2004. Palomar M. Alfven T. et al. Wang H. Lancet 1988. Comparison of representative ranges based on U. Int J Hyg Environ Health 2002. Machida M. Vahter M. et al. Fourth National Report on Human Exposure to Environmental Chemicals 203 . and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group.59:497]. Occup Environ Med 2000. Toxicol Appl Pharmacol 2004a. Fayers PM. Lidfeldt J. 196:114-123. Dekio F. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Persson B. Hotz P. Lepom P. et al. Hellstrom L. Environ Health Perspect 2002. Nordberg G. et al. Sanz P. Seifert B. Moriguchi J. et al. Oguma E. et al. Diamond GL. patient population and literature reference intervals for urinary trace elements. Seiwert M. Fernandez MA. 102:10581066. References Akesson A. Schulz C. Third National Report on Human Exposure to Environmental Chemicals. Costa R. diabetes mellitus. Buchet JP. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Machida M. Takebayashi T.110:699-702. Horiguchi H. Cadmium fume inhalation and emphysema. Holguin F. Environ Res 2004b. Stock AL. Fukui Y. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Ikeda Y. Elinder CG.000 women in the Japanese general population: a nationwide large-scale survey. Available at URL: http://www. Olfactory function in workers exposed to moderate airborne cadmium levels. Becker K. Berglund M. Davison AG. Jarup L. Darbyshire J.96:353-359. Jarup L.13(11):1627-1631. Neurotoxicology 2003. Grubb A.S. iron deficiency. Vahter M. Becker K. possibly better than b2microglobulin. Venables KM. Seiwert M. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Nerbrand C. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Environ Health Perspect 2005. Moriguchi J. Lison D. Toffoletto F. et al. et al. et al. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Environ Health Perspect 1994.76:186-196.95:20–31.S. Ash KO.354:1508– 1513. Mascagni P. Jin T. Kaus S. Int Arch Occup Environ Health 2003. Occup Med 1996. Ye T.

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

40) 5.3 (8.90 (6.60-6.87 (4.1-13. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.00-10.52-9.9) 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. and clay. and cardiac arrhythmia (ATSDR.23-4.7-14.10 (6.03 (4.62 (5.96 (6.4 (9.87 (4. and high-power gas-ion devices.76-6. nausea.62 (5. 2004).3) 10.1-12.24) 4.74-5.86-11.20-4.7 (8.45-8.9) 8.36) 3.89) 4. although cesium was generally of low toxicity when given to animals.00) 7.90-12.43-8. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.9 (10.63 (4.80-10.95) 5.30) 5.55 (4. diarrhea.32-5.0) 10. the body half-life is estimated to be 70-109 days based on 137Cs exposures.10 (8.6 (9.7) 10.94 (4.05-5. photographic emulsions.43 (5.8 (10.80 (4.33 (6.5 (10.73-11.33-5.01-8.10 (8.20) 8.4) 10.72-7.9 (11.80 (4.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 01-02.09-5.39) 7.1-12.84-9.22 (4.07) 4.25 (3.2-14.25) 4.60-5.40) 5.64 (4.90-10.37) 5.3) 10.05-5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30 (6.35-5.1 (11.86 (7.4) 12.6) 11.90-12.84-5.56 (4.89-5.54) 4.80) 7.8) 12.50) 5.23) 9.8) 11.17 (6. and 03-04 are 0.60-7.1) 9.70) 5.81) 4.86-12.90-10.59-5.13-8.59-5.3) 10.87 (4.94) 4.14.50 (4.40-5.40-5.40-5.33 (5.08) 7.80-10.37) 7.20-5.90-10.01-6.6 (9.49 (4.49 (5. population from the National Health and Nutrition Examination Survey. soil.6 (11.20) 4.36 (6.69-6.55 (7.42-7.71) 4.03-4.0) 11.16-6.56) 5.29) 4.0) 11.50) 9.39-4.80 (8.16-6.05) 5.71 (8.50-7.70-8.4) 12.07-11.17) 4.13 (7. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.60) 5.20 (6.7 (9.12) 5.97) 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 4.70 (8.9) Total 4.77 (9.62) 4.59-5.59) 7.52) 7.32) 4.7) 11.67 (4. For absorbed cesium salts.5-16.93 (4.2-13.20) 5.42) 7.17-6.71-9.47-4.00-4.60-12. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S.20 (4.83-4.03 (4.70 (9.84 (4.9 (10.30-10.50 (6.53 (6.2 (9.60 (8.4 (10.1 (9.64-10.81) 9.60) 7.2 (9. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70 (4.21) 90th 9. and as polymerization catalysts.6) 10.68) 9.08 (6.12-11.98 (7.63) 6.4) 10.0-15.70-5.8 (11.4 (9.30-5.87) 5.50 (4.7 (9.95-4.40-11.3-15.2-13. However.10-9.90) 5.3-13.42) 6.0-13.7 (10.9) 11.80-6.12 (4.64) 5.56 (4.32 (3.9 (11.44 (8.61-6.98 (7.8) 9. 0.81 (4.59 (5.20-8. and 0.94-4.0) 12.08 (7.84) 8.7) 11.40-7. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.22-4. Radioactive 137Cs has been used medically to treat cancer.63-4.04 (4. semiconductors.60) 7.5) 9.81) 4.00-8.2-12.10-5.70 (5.31-8. respectively.3 (8. Most human exposure to cesium occurs through the diet.36 (3.27 (7.55-11.26) 4.83) 6.35 (4.00-8.97-7.70) 7.99-6.15-8.60 (7.27) 4.29 (4.2) 11.97 (7. cesium hydroxide is corrosive and irritating at high concentrations.8) 9.5-14.49) 75th 7.5-14.04) 7.60-6.1) 11.54-11.89) 5.0) 12.2-13.27-5.60-7.1) 9.99) 9.71-8.64) 4.7) 10.66 (7.64-5.95 (3.90) 5.70 (6.7 (10.1) 10.00) 6.Metals Cesium CAS No.4-13.7 (10.70 (6.99) 7.90) 9.00-9. scintillation counters.6 (9.64) 5.77-8.01) 7.90-8.02 (4.00) 4.4) 11.87-7.2.72) 4.8) 11.26-11.5-13.14.08-5.34) 9.0 (10.35 (4.46) 7.13 (8.13 (5.30 (6.6 (11.74) Selected percentiles ( 95% confidence interval) 50th 4.0) 9.26) 7.38) 5.53-11.14 (4.1 (10.10-8.20-7.05) 5.88 (8.40 (4.77 (4.81-14.40-5.80-11.90) 4. see Data Analysis section) for Survey years 99-00.0 (9.3) 10.3) 12.25-5. interval) 4.82-4.80 (8.8) 12. Whether cesium compounds are carcinogenic is unknown.56-11.70) 5.10 (6.4) 95th 11.6 (9.09) 5.9 (11.12-5. Fourth National Report on Human Exposure to Environmental Chemicals 205 .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 4.7 (9.92-13.97) 4.74 (4.73-5.26 (3.80 (4.7 (11.8) 12.49) 4.71-5.8 (10.50 (4.5) 10.2) 12.9) 12.3) 9.91-8.57-5.99-11.80-13.84) 5. infrared lamps.21 (4.99-11.5 (8.45-5.50 (7. Little is known about the health effects of this metal.8-13.68 (7.77 (9.91 (7.47-8.34 (4.61) 7.00 (7.71 (4.0) 12.80 (8.10-7.4) 9.80-10.1) 11.40-11.40) 7.30) 7.70 (8.79 (4.3-13.08-5.9 (11.90 (4.5) 12.90) 7.82) 5.94 (4.20) 7.

17 (6.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.72) 4.99-4.26 (3.72-5. 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.64) 4.56-10.59-8.29) 5.35-7.91-7.27-6.71) 6.44 (4.42 (5.95) 8.44-9.10 (5.08-7.10 (3.64 (8.06) 4.85) 5.68) 4.84-9.98) 5.50) 4.7-12.94) 7.47) 6.78 (3.2) 11.00-8.63 (7. and were also roughly similar to those in this Report.16) 5.26-6.17) 4.76-9.01-8.48) 7.15) 95th 8.99 (3.29-3.03) 6.3) 11. Komaromy-Hiller et al.00-10.64) 9.96-4.16-8.52-5.90-8.96-4.18 (7.68-11.6 (9.30-4.63-6.28 (4.41 (5.79) 9.39 (5.00-5.85) 4.63) 6.05-3.62-8.39) 8.98 (7.73 (3.05) 6.5 (9. 2004).79 (5.02 (5.0 (7.10-4.68) 6.00-9.47) 4.10) 7.30 (3.42-4.26 (4.33 (5.78) 4.68 (4.43 (4.97) 8.19-3.82-4.44) 3.20-4.61 (7.29-3.76-6.91-6.12-6.0) 7.55-5.65 (6.17) 9.41) 4.05-3.41 (4.77) 4.99-9.99) 4.4) 10.50 (5.75 (6.39) 5.54 (3.43-11.2 (8.73-4.7) 10.0) Total 4.08) 4.91) 5. Using clinically submitted specimens.24-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.67 (6.83) 8.58-5.06) 5.9 (9.14) 4.36-10.07) 8.28) 7.3-15.09) 8.00 (8..56) 3.48) 90th 7.43 (8.54 (4.56) 4.99-9. population from the National Health and Nutrition Examination Survey.5) 7.7) 10.30) 10.60 (5.66 (5.28) 8.31-6.00-5.3) 9.95-12.58 (6.93-9.50) 4.54 (5.31 (4.30 (7.5) 9.02-4.43 (3.29) 4.04) 6.00) 6.21-3.46 (7.68) 3.46) 6.08) 4.51 (4.8 (9.95-6.98) 5.50 (7.25) Selected percentiles ( 95% confidence interval) 50th 4.11 (5.27 (8.15-4.50) 4.88-10. Minoia et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.12) 3.30-4.38 (3.08 (6.77 (6.85-4.91) 4.08-3.64-6.17-4.75-11.43-6.55) 4.03-5.59) 4.44 (8.20-4.88-4.51) 4.13-9.3) 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 3.38-12. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.31 (4.30) 10.77-5.56 (4.63 (6.1) 11.41 (8.72 (4.94 (5.14) 4.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.47) 7..07-4.08 (5.24-10.65-4.40) 7.45 (4.91-9.91 (5.3 (10.74-11.9 (10.66-6. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.00-4. (2000) found urinary cesium levels that were slightly lower than those reported for the U.51 (3.15-11.31-4.89-4.67) 5. 2005. Two small studies of European populations reported urinary cesium levels similar to U.9) 10.58 (4.20-8.08) 3.95) 4.83-7..53) 6.11 (5.90-8.05) 3.03-6.55 (3.70) 7.13-9.97-5.62) 5.42 (4.84-9.24 (3.04-5.82) 7.87-4.51 (3.8) 6.96) 4.19-6.38-7.71 (7.16-8.67 (5.64) 5.13 (3.90 (7.S.20-4.63-6.77 (4.79) 6.79-5.74 (4.49) 3.38) 10.6 (9.22) 6.41) 9.87) 5.35-11.74) 75th 5.46 (8.96 (4.46-4.35 (3.43 (4.33 (5.06 (3.53) 3.36-3.07) 8.34 (5.42-4.23 (7.60) 3.10 (3.47 (4.79) 4.28 (5.92 (5.64 (4. population results shown in this Report (Alimonti et al.74) 3.78 (3.51 (7.21-4.86 (4.5) 9.37-3.04) 5.18) 8.93-7.35 (4.43) 8.47 (7.48-6.16-5.07 (5.80) 6.14-6.30 (4.04-11.37) 4.06 (5.44-5.74 (5.58) 3.95 (3.21-5.36-6.61-3.91) 5.84-7.29) 4.2 (8.14-7.70) 6.51 (4.09) 4.65-3.8) 5.20) 5.96) 4.54 (4.97-4.12 (3.77 (7.53 (6.90-3.41-4.60 (3.60-10.66 (5.91 (5.22 (3.66 (6.60-20.83-6.95 (5.84-7.27 (6.2) 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 3.08 (3.98 (6.40-5.S.92) 3.78) 4.57) 3.14 (6.70 (7.8) 10.21 (2.22-11.38 (3.33-3.0) 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 .05-4.18-6.75 (7.50-5.56) 4.81 (4.27 (6.27) 4.87 (5.40) 6.27-4.46-8.03) 5.50) 8.84-11.33-8.14-4. interval) 4.15 (7. population.3 (9.50 (6.05 (4.41-7. 1990).25) 4.13) 7.63 (4.42-6.09 (4.3 (8.S.58) 8.6) 6.95) 10.53 (4.45-6.47) 6.81 (4.18-7.35) 3.

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

07-1.540-.360-.75 (1.460 (.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 .950) .690-.399) .370-.440-.16) 1.16 (1.04 (.454 (.740 (.47 (1.350-.308-.48) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.760 (.470 (.388-.370-. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.570-.333-.670-.590) .520 (.510) 1. The cobalt used in U.820 (.700) .26-1.390 (. interval) . Usual human exposure is from food sources.03) 1.700) .590 (.850-1.430) .343 (.60 (1.28 (1.840) . It is also a component of porcelain enamel applied to steel bathroom fixtures.404) .930-1.68 (1.73) 1.03) 1.32-2.25-1.316-.07.790 (.560 (.65) 1.480-.620) .710 (.360-.380 (.540) 1.81) 1.03-1.860 (.630 (.370-. respectively.414) .26-2.09) .400-.910-1.620-.07-1.930) .810) .16) 1.92) 1.03 (.680 (.430 (.940-1.08) .660) .81) 1.22 (1.450) .300 (.900-1.19) .900-1.680) .386) . and 03-04 are 0.375 (.369 (.04) 1.33-1.427-.380 (.04-1.640) .610) .339 (.980) .46 (1.45 (1.17 (1.890) . automobile airbags.16 (1.05) 1.270-.430 (.310-.920) 1.42) 1.359 (.500 (.390-.331-.420 (.28 (1.460) .770) .850) 1.850-1.327-.22) 1.291-.435 (.352 (.480 (.519 (.380-.350 (.340) .47) 1. see Data Analysis section) for Survey years 99-00.300-.380 (.450) .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 .530-.52 (1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.410-.520) . blue-colored pigments.32 (1.20 (1.99) 1.419) Selected percentiles ( 95% confidence interval) 50th .461 (. and soil.600 (.520 (.550) 90th .690 (.950 (.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.620-.04-1.465) .50) 1.370) .24 (.810) . It is emitted into the environment from burning coal and oil and car and truck exhaust.53) 1. and 0.270-.405-. hard metal (alloys of cobalt and tungsten carbide).570 (.520-.47 (1. hard metal or in combination with other elements.28 (1. and fertilizers.800-.460) .17 (.900) .334) .32) 1.570) .416) .364-.336-.650 (.270-.01 (.740-. industry is imported or obtained by recycling scrap metal that contains cobalt.56) 1. Cobalt is used as a drying agent in paints.03 (.08.580 (.348-.830-1.487) .590-.32) 1. and inks.410 (.285 (.64) 1.59 (1.550-.379 (.890) 95th 1.393-.540-.580 (.590-.434 (.520-.S.452 (.390) .800-.07.390 (.340-.36) 1.05 (.880-1.750 (.398 (.550 (.23-2.690-.900) .499 (.29 (1. large appliances.360-.394) .530) .16-1.398) .750-.03) .640) .450) .44) 1.S.21) 1.377-.540-.502) .14) . seawater.450) .14-1.430) .417) .790) .06-1.610-.496) .410 (.330 (.47) 1.850) .515 (.01 (.17 (1.430 (.490-.670 (.790-.570-.820 (.650 (. Cobalt occurs naturally in airborne dust.22-1.523) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.710) .450-.420) .460) .410) .530 (.01-2.463-.950 (.520-.450-.13) 1.520 (.373-.301 (.259-.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 .290-.630 (.26) Total .319) .350-.350) 75th .543) .431) .24 (1. 0. 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.320 (.33 (1.06 (.610 (.316 (.390 (. and magnetic recording media. and kitchenware.07 (.930 (.333-.460-. population from the National Health and Nutrition Examination Survey.750 (.730) 1. 208 Fourth National Report on Human Exposure to Environmental Chemicals .890-1.Metals Cobalt CAS No.564) .900) .410-. and in synthesizing polyester and other materials.950-1.410 (.23) .17-1.940-1. steel-belted radial tires. varnishes.880 (.428-.372) .870 (.940 (.48) 1.670 (.431) . diamond-polishing wheels. Cobalt compounds are also used in manufacturing battery electrodes.490-.05 (.410 (.583) .09 (.580 (.750 (.581) .340-.420) .950-1.06 (.374 (.350-.469-.67) 1.424) .890-1.540-.39) 1.305-.660-.380-. shiny.480 (.470) .340) .367 (.630-.740-.890-1.960-1.620-.520-.710) 1.660) .670 (.330-.410-.640) .379 (.16-1.500) .810-.02-1.09 (.600-.800) . 01-02.870 (.370 (.15 (1.520 (.373) .310 (.418 (.313) .15-1.680) .348-.37-1.12) 1.670-.460 (.371 (.570) .294 (.28-2.870-1.50 (1.410 (.16 (.650-.32 (1.00) .820 (.600) .12) 1.920-1.410) .980-1.355-.610) .01-1.26) 1.520) .430-.330) .280-.680 (.08-1.760) .340 (. Cobalt compounds are used as catalysts in producing oil and gas.04-1.338-.

786-.669) .471-.11-1.10-1.700 (.346 (.905) .591 (.275-.781) 95th 1.329 (..804) 1.537 (.848 (.337 (.554 (.04-1.394) . using hard metal cutting tools. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.505) .626-.736-.872 (.362-.24) .434-.83) 1.314 (.378-.348) . interval) .294-.407) .313-.728) . 1972).303-.393 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.361-.35) .391 (.829) .259-.562) .938-1. population from the National Health and Nutrition Examination Survey. refining or processing alloys.469-. respectively.488) .335 (.00-1.425-.378 (.361 (.342-.495 (.313 (. A portion of cobalt retained for long periods is concentrated in the liver.409) .282 (.296-.691 (.428-.615) .455 (.333-.277-.976 (.554 (.792 (.297-.27) 1.426 (.898 (.290 (.508-.327 (.523 (.593) .513 (.396) .757-1.290 (.10) Total . A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.660-.529 (.278-.02 (.838 (.481) 90th .673-.57) 1.268 (.273 (.457-.03 (.73) 1.963) .33) 1.248-.388 (.313-.333-.29 (1.471 (.378-.429) 1.550-.368 (.256-.247 (.487-.435-.704-.662) .449) .462) .542 (.44 (.900-1.479-.316 (.777-. Cobalt is absorbed by oral and pulmonary routes.515 (.352) .911-1.355) .282-.733-1.239-.833-1.28) 1.29) 1.694) .561) .679-.647) .703-.983) .12-1. Smith et al.243-.274-. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.04 (.689 (.301-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.850 (.391) Selected percentiles ( 95% confidence interval) 50th .824 (.598 (.463-.595) .298 (.585) .417) .368) .361 (.237-.296) .12 (.60) 1. Once absorbed and distributed in the body.25 (.328 (.753) 1.738 (.534-.548 (.774 (.343-.306) 75th .442-.00) .560-..360) .257 (.290 (.326-.302-.847) .289) .975 (.500 (.594) .54) 1.616-.10 (.365-.792-1.00 (.352 (. and to a lesser extent. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.304-.368) .861-1.417 (.353-.635 (.842) .667-1.640) ..433) .327-.00 (. Exposure in the workplace may come from electroplating.16) .60) 1.611) .331-.304) .06 (.259) .683-.275-.384) .500-.278 (.333-.630-.386 (.600-.329-.328 (.609) .407 (.313-.293 (.990) .479) . but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.29 (1.16 (1.279 (.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 .250) .750-.421) .895-1.363) .738 (.297) .963) .381) .S.30 (1.990-1.286) .361-.50) 1.439) .309) .251-.533 (.387) .523 (.55) .513) .11-1.829-1.324-. 1994.404-.323) .319-.339-.17) .324) .744) 1.552 (.756 (.467-. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin). or using diamond-polishing wheels that contain cobalt metal.634-.821 (.821-3. 1994).380-.917) .753-.964 (.638-1.826-1.419) .09) 1.16 (.35) 1.376 (.00 (.400 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.402 (.932-1.382-.963-1.372) .830 (.33) .313-.547 (.851 (.29) .301) .00) .707) .349) .760-1.10) .879-1.15 (.50) 1..362) .582-.362 (.461) . 2003).300) .365) .457 (.334) .257-.850-1.328) .476-.500-.15) 1.563-.599) .388 (.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 .435 (.50 (1.468) .632-.393-.844 (.396) .291 (. 1972).14 (.895-1. an essential human nutrient.857-1.960 (.938) .352 (.740-1.611) .983-1.457) .727 (.27) 1.279) .513-. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.03-1.358 (. 1979)..471-.313-.562) .408 (.248-.708) .425) .333 (.444 (.581) .929) .487-.452-.963-1.272-.723 (.271 (.392 (.438) .606 (.280-.574-.937 (.234 (.29 (1.781-1.750) .955) . cobalt is excreted predominantly in the urine. in the feces.534 (.Metals fabricated from cobalt alloys (Lhotka et al.644 (.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 .343 (.259 (.00 (.215-.543) .36) 1.700 (.353 (.955) .310) ..337) .667-1.281) .737 (.378-.317 (.449-.728 (.952 (.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 .503-.19) .344-.369 (.949) .49) 1.630-.522) .861 (.23 (1.16 (.36) 1.475 (.785) . Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.608 (.25 (.306 (.

Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al. 1997. 1988). A 1982-1992 surveillance programme on Danish pottery painters. 1994. Roycroft JR.. 2001). “Hard metal” disease.atsdr.53:395417.50(13):95-104. Atlanta (GA). Available at URL: http://www. 2005. Third National Report on Human Exposure to Environmental Chemicals. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al.. has been associated with exposure to dusts that contain cobalt. 1988).. 210 2006. Perkins DG. 2005 [online]. 1955). 2001. Cugell DW. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans.. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. population (CDC.. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. Arch Environ Health 1988. 1993). Sci Total Environ 1994. with mean levels that were about 15-20 times higher than in the general U. Dunstan et al. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al.. Toxicol Sci 1999. Information about external exposure (i. Lisi. 2005.. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen..Metals Toxic effects of cobalt have been encountered in workplace settings. A clinical and pathological study of twenty-eight cases. Cobalt was once added as a foaming agent to beer. 1994). 2001. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al.. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. Bucher JR. 4/3/08 Christensen JM.. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. 1999).. 1997).43(4):299-303. 2001. Rubin A.html.S. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. Linnainmaa and Kiilunen.. 1972)..gov/ exposurereport/. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals ..49:56-67. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al. 1998). White and Sabbioni. 1989). Daniel et al. Krause et al. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect.e.. MacDonald et al.. 1998). For workers exposed to cobalt in the air. Grumbein SL. Centers for Disease Control and Prevention (CDC). Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. Thomassen et al. Urinary measurements mainly reflect recent exposure.cdc. 1992).. Haseman JK. 2003. Iavicoli et al. 2006.. 2003.. Cobalt-beer cardiomyopathy.. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L.gov/toxpro2. usually in combination with tungsten carbide (Cugell et al. References Alexander CS.. Morgan WKC.. Alexandersson R. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. et al. Swennen et al. Lauwerys and Hoet. population results in this Report (Kristiansen et al. Shirakawa et al. not to imply that the BEI is a safe level for general population exposure. Information about the BEI is provided here for comparison. 2003). Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lison et al. 1985. 1990). 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. Poulsen OM... Blood and urinary concentrations as estimators of cobalt exposure. although substantial occupational exposures have produced elevated urinary levels for many weeks. Am J Med 1972. Sills RC. 1993).cdc.. Hailey JR. environmental levels) and health effects is available from ATSDR at: http://www. 1994.S.

Moulin JJ. Gross RT.34:620-626. Arch Intern Med 1990. Kato M. The release of metals from metal-onmetal surface arthroplasty of the hip. DeSantis V. Edmonds CJ. oxides. Molders J. Int Arch Occup Environ Health. Bunn HF. Hoet P. Lison D. Occup Environ Med 1994. HoffmannB. Cleland D.69(3):193-200. Robinson C.157:117121. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Co-sensitivity between cobalt and other transition metals.(1-3):133-139. Science 1988. Vitali MT. Dunstan E. Lauwerys RB. Buchet JP. Laippala P. Health Phys 1979. Lhotka C. Zweymuller K. Iavicoli I.44:124-132. J Occup Med 1992. 1985. J Bone Joint Surg Br 2005. McMinn DJ. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Bacis M. a study of 13 elements in blood and urine of a United Kingdom population. White MA. Health Phys 1972. Schank M. Cresti R.216:253-270. Tilley S. et al. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Cobalt cardiomyopathy.533:135-152. X. and cobalt metals. Ghat IS. Sci Total Environ 1997. J Rheumatol 2001. Alessandrelli M. salt.148:241-248. Meyer zum Buschenfelde K-H. cobalt salts. Pisati G. Respiratory health of cobalt production workers. Mutat Res 2003. Ichikawa Y. Br J Ind Med 1993. Falcone G. Sci Total Environ 1994. Dickel H. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Shirakawa T. Zhuber K. J Trace Elem Med Biol 2006. Trace element reference values in tissues from inhabitants of the European Union. Epidemiological survey of workers exposed to cobalt oxides. Sabbioni E. Sci Total Environ 1998. Smith T. Am J Epidemiol 1998. Fujimura N. Sabbioni E. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine.58(10):631-634. Szekeres T. Kiilunen M. Cannon SR. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Schaller KH.45:246-247.” Contact Dermatitis 2001. MacDonald SJ. J Bone Joint Surg Br 2006. Meier R. Christensen JM. Thabe H. Roto P. Daniel J. Kristiansen J. Goto S. Outcome of occupational asthma due to cobalt hypersensitivity.95:29-37. Lauwerys R. Goto S. Steffan I. Sci Total Environ 1994.150. Uitti J. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. J Orthop Res 2003. Lisi P. Int Arch Occup Environ Health 1997.36:732-734. Unwin P. Lung cancer risk in hard-metal workers. Thomassen H. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Radulescu M. et al. Mosconi G. 3rd ed.87(5):628-631. Hoher T. Lison D.Metals effects of cobalt. Salvatori S. Contact Dermatitis 2003. Leghissa P. Sabbioni E. Heki S. Rorabeck CH. et al. Kriss JP. Goldberg MA. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Boca Raton (FL): Lewis Publishers. et al.88(4):443448. Chest 1989. Angerer J.20(1):25-31.28(5):1121-1128.150:177-183. and hard metal dust. Kraus T. Zedda S.55(4):269-276. McCalden RW. Ziaee H. Lison D. De Boeck M. Absorption and retention of cobalt in man by whole-body counting. Kirsch-Volders M.21(2):189-195.204:147-160. Salama A. Barnaby CF. Kusaka Y. Lasfargues G. Palmroos P. Weyher I. Long-term clearance of inhaled 60Co. Kuska Y. Chess DG. Schramel P. Occup Environ Med 2001. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Carnes WH. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Hedge AG. Occupationallyinduced “isolated cobalt sensitization.51(7):447450. Weber A. Stanescu D. Cobalt and antimony: genotoxicity and carcinogenicity.22:359367. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Linnainmaa M. A report of two cases from mineral assay laboratories and a review of the literature. et al. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Lauwerys R. Swennen B. Bozec C.50(9):835-842.242:1412-1415. Linna A. Thakker DM.48:172-173. Sanghrajka AP.150(1-3):167-171. Wild P. 2001. Am J Ind Med 2003. Romazini S. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Swennen B. Oksa P. Iversen BS.406:282-296. Hammon E. Dunning SP. Bourne RB. Jarvis JQ. Peltier A. Zobelein P. Blunn G. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Pradhan C. Biological monitoring of workers exposed to cobalt metal. et al. Clin Orthop Relat Res 2003. Diepgen TL. Buchet JP.

20 (1. 0.50 (1.50) 1.40 (1.50-6.00-4.20-1.32-1.60) 1.80) 1.70-6.80 (1.70 (3.32-1.80 (2.70-1.62 (1.69 (1.60 (2.80 (5. the main source of lead exposure for the general U.30-2. such as lead phosphate and tetraethyl lead.70) 4.95) 1. 7439-92-1 General Information Elemental lead is a soft.60-6.10) 1.50-3.60 (2.90-2.20-2.39) 1.40-3.55 (1.60) 5.90 (3.50-2.90-4.80) 3.70 (2.30 (1.83 (1.60) 4.20) 4.60-2. Before the 1980’s.30 (4.10 (4.10-8.14-1.10-2.43) 1.60-3.50 (2. dense.10) 4.80-4.66) 1.90 (3.43) 1.00) .69) 1.00) 5.00 (1.10-2.60 (1.60 (4.40-3.20-6.40 (1.70) 4. and 03-04 are 0.80 (2.60 (2.52-1.40-6.50-5.20 (3.53) 1.10-3. 212 Fourth National Report on Human Exposure to Environmental Chemicals .00 (2.36-1.60) 2.80-3.90) 2.40 (4.900-1.70) 1.70 (1.00) 3.70) 1.20 (3.10-3.50) 2.80 (1.10-2. see Data Analysis section) for Survey years 99-00. 01-02.10 (1.60 (3.30 (2.87) 1.10) 2.40-2.80) 2.50-2.70 (1.899-.00 (1.50) 4.90-4.10) 1.40) 4.50 (2.70) 1.10) 1.20 (2. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.900 (.36) 1.30-2.10) 3.60) 5.40-2.93-2.40) 1. bronze). ammunition.80-5.75) 1.90 (3.40-2.23 (1.96-2.g.50-1.80) 2.80 (5.45 (1.40-1.10) 2.31) 1.986) .86) 1.40 (1.40) 2.80-3.51) 1.70 (5.50-1.40) 2.50) 1.90 (1.30 (4.20 (1.00) 4.30 (2.50 (2.00) 1.900 (. population from the National Health and Nutrition Examination Survey.00 (6.20) 3. Lead is most often mined from ores or recycled from scrap metal or batteries.65 (1.28.90) 3. malleable.80 (1. and 0.60 (3.14-1.60) 4.3.50) 75th 2.70-2.60) 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 2.69 (1.50-1.20 (3.50-2.81) 1.10-3.70) 4.30 (1.40-6.40-1.00-1.09) 1.20-2. respectively.40) 2.60) 3.90 (3.80-2.10-1.70) 1.90) 2.80 (2.50) 1.90-6.70 (2.30-2.50) 5.01 (1.60-1.70 (1.75-2.00) 1.3.30 (2. population was aerosolized lead emitted from combustion engines that used leaded gasoline.40-3.91) 1.80-4.50) 3.50-2.30 (1.60-1. interval) 1.70) 3.50-5.50-1.22 (1.50 (2.S.90 (1.10 (2.90) 2.60 (1.90) 2.40) 1.14-1.20-3.49-1.20 (3.20 (2.40) 2.10 (3.60 (1.30-1.43 (1.70 (3.00 (5.70) 3.90-4.60 (1.50-3.80-3.800-1.80-3.43-1.19 (1.10-3.60 (3.80) 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. blue-gray metal that occurs naturally in soils and rocks.70-4.12-1.60 (1.50) 1.30 (2.20 (4.50 (1.70-5.80 (1.70-3.60) 1.00 (4.50 (4.80-4.00) 3.00-4.80) 2.40) 3.70 (1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.40) 1.00) 2.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. brass.60) 1.25 (1.60) 4.30-1.30) 2.20-3.90) 1.30 (2.60) 1.60-4.90 (4.60-4.50 (4.60 (1.60-1.10-6. leaded glass.20) . In the past.70-1. Lead was used in plumbing for centuries and may still be present.40 (5.60) 2.30) 95th 5.50) 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 2.50-1.60-2.Metals Lead CAS No.90) 5.10-1.30-1.39-1.60) 3.00) 4.10 (2.50) 2.90-4.00-6.00) 2.30) 2.10) 3.00) 2.20 (1.00) 1.70-1. and for radiation shielding.30-1.90-3.80 (1.87 (1.50 (1.30-2.80) 1. plastics.90 (2.70) 3.60) 3.90-2.60) 2.71-1.60 (2.20) 1.36-1.00-2.62) 1.30) 5.90 (3.20-1. Lead has a variety of uses in manufacturing: storage batteries. Elemental lead can be combined with other elements to form inorganic and organic compounds.30-1.946 (.20 (1.52 (1.70) 1.30-5.00-4.20 (3.50 (3.60 (2.89) 1.80) 1.40) Total 1.60 (3.90-2.55-1.60 (2.60-1.43 (1.50-4.20) 3.10-2.45-1.75-1.80 (3.50) 7.20-3.50) 5.25 (1.70-2.70 (2.10) 5.25) 1.00) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80) 1.20 (3.10-2.50 (1.90) 3.80) 1.20) 90th 3.10 (1. solders.17) .52-1.00 (4.37 (1.20-3.00) 6.80 (1.10-1.90) 1.40-1.50 (3.68-1.40-5.30) 1.34-1.80) 2.20) 5.50 (2.40 (1.00) 2.10-4.90 (2.75 (1.69) 1.00 (3.S.50-4.78 (1.20) 4.10 (1.70-2.30 (2.10-6.48) 1.40 (3.40) 5.80 (4.60) 3. Since lead has been eliminated from gasoline.878-1.30 (2.20) 3.00-5.50) 4.20) 3.90) 2.90) 1.40-4.46 (1.40 (2.20) 2.30) 2.70) 4.40-1.30 (3.40 (2.30-1.20 (1.00) 1. metal alloys (e.60 (1.10-4.40-1. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.20-4.40-1.72) Selected percentiles ( 95% confidence interval) 50th 1.942 (.10 (2.90-2.51 (1. antique-molded or cast ornaments.60) 1.30 (1.10-2.00-1.30-4.77 (1.30-6. ceramic glazes.55-1.70) 2.66 (1.02) 1.62-1.60) 4.20 (3.04-1.37 (1.37-1.10) 3.30 (4.60) 2.80 (4.60) 2.56 (1.

553-.641-.75) 4.20) .700) 1.72) 1. 01-02.900-1.20-2.30) 1.688 (.20 (1.640-.20 (1.14-1.604 (.10-3.80-2.21 (2.900-1.800 (.40-1.40) 3.10-1.40 (1.30-3. see Data Analysis section) for Survey years 99-00.986) .10) 2.80) 1.900) .02) 1.90) 2.30) 1.560-.900-1. interval) .40) 1. imported children’s trinkets and toys. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.480-.900) .40) 2.00-2.00) . 0.600-.80-3.52 (1.S.990) 1. stained glass framing.00 (2.700-.785) .20-1.35 (.30) 1.800-1.10-1.04 (.40 (1..900 (.80 (1.710-1. CDC.572-.04) 2.600 (. or water contaminated by mining or smelting operations.766 (.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 1.10-1.10 (1.20 (2.70) 1.31 (1.800) .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 1.00 (1.80) 1.64) 2. population from the National Health and Nutrition Examination Survey.710-. Fourth National Report on Human Exposure to Environmental Chemicals 213 .80) 2.70) 1.900-1.00) 1.27) 1.920 (.82 (1.822-1.990) 2.690) 75th 1. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.75) 3.59) 1.90 (2.600-.650) 1.1.00 (1.620) 1.10 (1.80) 2.90 (2.80) 3.10 (1.674) 1.50) 1.62-4.50) 2.80) 3.00 (1.60 (1. dust.80 (2.90-3.752 (.Metals occupational (e.579-.20) 1.795 (.10 (..800-.40-1.815 (.12) 90th 2.30) 1.616) .840 (.10) .40-5.70 (2.833 (.13) .960-1.757-.636 (.940 (.800-1.44-2.90-2.52-1.564 (.900) .640 (.628) 1.30) 2.20) 1.59-2.27 (1.500-.30) 2.30) 2.50-3.09) 1.915-1. In the blood. or after soluble lead compounds are ingested.50) 1.40 (2.50-2.86-2.30) 1.03-2.900 (.90) 1.800 (.695 (.30-2.920 (.60 (2.900 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.29 (2.60-2.20-2.50 (2.50-2.19 (1. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.g.70) 1.04 (.790 (.960-1.708-.637-.718) .605) .651) .970-1.20 (2.50) 2.91) 2.955-1.40-1.90-3. lead-contaminated dust in indoor firing ranges.30-1.70 (2.40) 2.540 (.06) .20 (2.20 (1.03 (1.49 (1.600-.40 (2.60 (1.800) .700-.745-.20) .90) 2.20) .20-1.80-2.591 (.14 (1.625 (.613) .659 (.90 (1.20 (3.07 (. and 03-04 are 0.90-2.22) 1.00) .700 (.600-.80 (1.731 (.40-3.625-.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 .11) 2.90 (2. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.80) 2.610 (.526-.50) 3.941) .700 (.10 (.30-1.850 (.600) .11 (1.818) .661-.50 (2.00 (1.680) .00) . older plumbing systems with leaded pipes or lead soldered connections. and contact with soil.30 (2.40) 2. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10-3.50-2.90 (1.671-. 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.580-.848 (.862) .73 (1.00) 2.808 (.800) .60-3. bullet fragments retained in human tissue.680-.40) 2.40) 1.931) .753 (.935) 1.800-. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.677 (.50 (1.910-.680-.50) 1.800) .700 (.90-2. and 0.66 (2.700-.570-.00) .900) .620 (.10 (1. 1991).60 (1. lead-containing folk remedies and cosmetics.600-.10-1.14 (1. 2007.20-1.33-2.738) . Approximately half of the absorbed lead may be incorporated into bone.30 (1.506-.800 (.04) .40 (2.40 (2.02 (.40) 1.691-.923 (.40) 1.810-1.00 (.10) 2.540-.558 (.700-1.90) 2.07-1.600 (.730 (.10) 1.700-.60-1.00-2. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.90-2.40 (1.660) .00-1.900) .90 (1.04-2.10) .535-.30-1.24-1.70 (2.00-1.41) 2.60-3.857) .00-2.70-3.595-.40 (1.700) .833-1.30-1.40-2.80) 1.13-3.828) Selected percentiles ( 95% confidence interval) 50th .10-1.60) 2.800 (.10-3.630 (.556-.97) 4.20) .960 (.89) 2.18-1.17 (1.86) 1.729-.800) .20 (1.50 (1.20 (1.700-.78-2.70 (2.00) 2.590 (.20) 1.773) .80) 2.66 (2.642 (.70-2.30-5.10-5.30 (3.70) 2.40 (1.00-1.10 (.23) .579-.32 (1. respectively.820-1.80) 2.60 (1.90-4.70) 3. battery and radiator manufacturing) and recreational sources.82 (2.700 (.33.78-2.62) Total .50-1. pewter utensils and drinking vessels.23-4.700 (.78-2. lead-based painted surfaces undergoing renovation or demolition.749) .70 (1.40-1.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.589-.52-1.50 (2.40) 1.86 (1. 2000).31-3.701) .70) 3.900) .30) .573 (.1.20 (1. However.60-2.700 (.33 (2.86) 95th 2.600) .29) 2.

702-. In 1991.933) .09-1.992-1.15-2.55 (1.97) 1.12) 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 .70 (1.79 (1.693 (.72) .64 (1.641 (.22) 1.571-.38 (2. 1995).45 (1.08) .62-2.06 (1.781-1.51 (1.03) 1.03-2.988-1.78 (2.702) .83 (2.02) 1. hair.72-2.671 (.05 (.55 (1.510-.639 (.79) 1.26) Total .696 (.655) 75th 1.14 (1. Large amounts of lead in the body can cause anemia.94-2.53) 1.22-2.10) 1.73) 2.882-1.01 (.88-2.82) 1.739) .541-.61) 3. 1995.50 (1.893) .853-1.722 (.593 (.615 (.644) .720 (.33 (1.408-.92) 2.09-1.85 (1.617-.40-1.83) 1.639 (.03) .529-.638 (.65 (1.74 (1.41-1.07 (.645-.50-2.33) 1.649 (.828) .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 .47) 1.683-.56-2. scant amounts are lost through sweat.963-1.914 (.44) 1.79) 2.03 (.11 (.66 (1.946-1.64) 2.900 (.979 (.655) .47 (2.603-.436) . abdominal pain.668-.400) .703) .404 (.18 (1.33-1.938 (.71 (1.86 (1.03) 2.18) 1.41) .28-1.622 (.609 (.708 (. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.11 (1.876-1.31 (1.61) 1.31 (1. Approximately 70% of lead excretion occurs via the urine.39-1.730) 1.701 (.18) .S.592-.11 (. based on prospective population studies.608-.97-18.662) 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 1.61) 1.988 (. Schwartz.731-.43) 1.89-5.26) 2.43-1.48 (1.04) 2.07) .992-1.53-1. and paralysis.862-.679) 1.89-2.887 (.37-1.20) .810 (.635 (. and through binding to ion channels and regulatory proteins. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.681-.559-.659-.31 (2.02-1.469 (.914-1.633 (.698) .618 (.46 (1.632 (.63) 4. population from the National Health and Nutrition Examination Survey.725) .06) 1.828-1.09-1.615 (. zinc.670) 1.718) .686) .926 (.841-1.796-1. Lead can cross the placenta and enter the developing fetal brain.50-2. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.44 (1.851) . 1996).36-2.673) .648 (.00 (. BLLs and associated toxic effects differ in children and adults.25-1.66 (1.914 (.603 (.56) 3.97) 1.682) . with lesser amounts eliminated via the feces.639) .56-3.667-.380-.73-2.725) .579-. The skeleton acts as a storage depot.940 (.722 (.18) 1.67-4.24 (1.383-.569 (.588-.621 (.375 (. encephalopathy.85) 1.75 (2.03) 2. The toxic effects of lead result from its interference with the physiologic actions of calcium.746) .11) 1. O’Flaherty.03) 90th 1.43) 2.15) 1.23 (1.0) 3.707 (.28) .758) .655-.654) .19-5.20) .61) 1.793-1.00) .742) .88) 1.58) 1. 2007).62-3.981-1.652 (.700-.38 (2.00 (1.667) .33) 2.721 (.962 (.734) .432 (.753) .838) .677 (.918 (.938-1.88) 2. CDC.551-.997-1.571-.29 (1.22) 1.44 (1.11) .27 (1..667-.623 (.98 (1.718) 1.06) .977) 1.957-1.22-1.01) .97 (1.765) .583-.657) 1.755 (.88 (1.49 (1.586-.461) .62-1.06 (.14) 1. through the inhibition of certain enzymes.812-1.04-3.990 (.606-. 1993).03) .59-3.31) 1.85-2.709 (.404-.94 (1.870 (.607-.00 (1.917-1.37-1.720 (.496 (.710) .676) .50) 1.342-.677-.561-.933-1.15) 1.22) .625 (.17 (.08-2.87) 1.47 (1.51) 1.03 (. Staessen et al.18) 2.645-.56 (1.10 (1.12-1.587-.763) .605-.20-3.31) 1.75-2.77) 2.971 (.800-.10 (. 2003.78-4.19) 1.601-.774 (.05 (1. and nails (Leggett.62) 2.688) ..88) 2.712 (.588-.85-2.918-1.25-1.00 (1.03 (. For instance.69 (1.08) .64) 95th 2.07-1.65-2.52 (1.Metals 90% of the body lead burden in most adults.03) 1.460-.15-3.15-2.920-1. 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.898) .05-1.98) 2.46 (2.09) 1.612-.41 (1.492-. Nash et al.64-2.03 (1.639 (.535) .404 (.34-1. 1993.742) Selected percentiles ( 95% confidence interval) 50th .594-. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.677) .702) .61) 1.623 (. and iron.63) 1.71-2.05-1.594-. 1991. interval) .658 (.68 (1.20) 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 .604-.701) .644 (.. kidney injury.66) 2.50-1. seizures.96 (1.603-.428) .508) .11 (1.35) 2.72-2.50-2.698) .17-1.52) 1.98-2.43 (1.11-1.608 (. 2004.681-.790) .38 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.679-.43 (2. with a half-life of years to decades.28) 2.975-1.

Data submitted through state public health programs from 2006 showed that 1.. adults in the 19992000 NHANES sample (Apostoli et al. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.75 µg/dL in U. IARC considers inorganic lead compounds probable human carcinogens.. seizures.. 2007). the prevalence rate has declined annually since 1994 (CDC.5 per 100.S.. Borja-Aburto et al.6%) were lower than those from NHANES 1991-1994. both the geometric mean (1. EPA. adult residents. Both drinking water and ambient air standards for lead have been established by the U. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al... when the geometric mean BLL was 2. 2006). 2001).6% in NHANES 1988-1991 to 1. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. 1987. Payton et al.Metals µg/dL or higher as the level of concern in children.. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. 2002). Overall. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC.S. which is an 84% decline. 2005a). environmental levels) and health effects is available from ATSDR at: http://www. 1994). residing in housing built before the 1950’s. Muntner et al.. 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.0 µg/dL in females (Soldin et al. lead in women may be associated with hypertension during pregnancy.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 2005b. 2000). Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. Jones et al.. However.4% in NHANES 1999-2004.html.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. Lanphear et al.S. usually with BLLs greater than 40 mg/dL.. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. Telisman et al. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.S. Schwartz.. In NHANES 1999-2002 in children 1-5 years old. 2006). 1999). the geometric mean BLL was 3. with overt encephalopathy. Bellinger 2005. almost double the geometric mean of 1.. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC.. particularly in the skeleton.g. 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. 2005b). 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al.e.cdc. approximately 11.07 µg/dL (Becker et al. may alter sperm morphology. 1996.21% of approximately 3. 1996. Korrick et al. and decrease fertility (Alexander et al. 2002a).. BLLs reflect both recent intake and equilibration with stored lead in other tissues.. 2002..S. and spontaneous abortion (Baghurst et al.S. 2003)..cdc.. Fourth National Report on Human Exposure to Environmental Chemicals 215 . Surveillance data reported by U.. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. The U. and low family income (CDC.. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U.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. Urine levels may reflect recently absorbed lead. urban residence. Pirkle et al.xls). including minority race or ethnicity.. and peripheral neuropathy generally occurring at much higher levels (e. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. 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. higher than 100-200 µg/dL). 1991. High dose occupational lead exposure. 1984. reduce sperm count.. though there is greater individual variation in urine lead than in blood and greater potential for contamination. adults in the 1999-2000 NHANES sample. 1996. For example. 2000).4% of children had BLLs of 10µg/dL or higher (CDC. 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. In occupationally exposed adults.2 µg/dL in males and 3.7 µg/dL and 4. and organic lead compounds not classifiable with respect to human carcinogenicity. 2009).000 adults.atsdr. 1998). subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al.. 2003. 2003. Staessen et al. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. Schwartz et al. More recently. Information about external exposure (i. respectively. 1999). 2003. At low environmental exposures.3 million children tested had BLLs of 10 mg/dL or higher (http://www.gov/toxpro2. 1995. CDC. premature delivery.

Hertz-Picciotto I. Bavazzano P. MMWR Morb Mortal Wkly Rep 2005a. Ganzi A.101(7):598-616. Caldwell KL. MMWR Morb Mortal Wkly Rep 2006. Farias P.53:411-416. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Mantere P. Lanphear BP.10:43-50. Rotnitzky A.205:297-308. Hänninen H.287:1-11. Rotnitzky A. Sparrow D. Hu H. Henderson CR. Leggett RW.htm. 4/14/09 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. Ga. Lanphear BP.gov/toxprofiles/tp13.275(15):1171-1176. van Netten C. Centers for Disease Control and Prevention (CDC). et al.gov/mmwr/preview/mmwrhtml/ mm5532a2. Managing Elevated Blood Lead Levels Among Young Children. Dietrich K. Hernberg S.348:15171526. IARC Monogr Eval Carcinog Risks Hum 2006. Blanco J. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.89:330-335.54(20):513-516. Payton M. Wager C. Kaufman JD. 2005b. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Kim R. Krause C.htm. Ewers TG. Jacobson SW. Manton WI.cdc. Third National Report on Human Exposure to Environmental Chemicals.cdc. Available at URL: http://www. Blood lead levels—United States. Checkoway H. et al.275:1177-1181. Environ Health Perspect 1993. Muntner P.150(6):590-597. Korrick S.gov/nceh/lead/publications/ books/plpyc/contents. 2003-2004. et al. Hunter DJ. Am J Public Health 1999. Adult blood lead epidemiology and surveillance—United States. Neurodevelopmental effects of postnatal lead exposure at very low levels. Kuehnemann TJ. 2002 [online]. Hu H. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Jacobson JL. Environ Res 2000. Sci Total Environ 2002. Borja-Aburto VH. Blood lead reference values: the results of an Italian polycentric study. Atlanta (GA). Cox C. Atlanta (GA). Am J Epidemiol 1999. Bellinger D. Homa DM. Jones RL. 1988-2004.87:1-471. McMichael AJ. Muller CH. Reese YR. 4/14/09 Centers for Disease Control and Prevention (CDC). Teratogen update: lead and pregnancy.htm. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Birth Defects Research (Part A). Meyer PA. Schulz C. N Engl J Med 2003. Roberts RR. Available from URL: http://www. Hu H. Canfield RL. Bellinger D. Wigg NR. References Agency for Toxic Substances and Disease Registry (ATSDR). Inorganic and Organic Lead Compounds.82:60-80. Batuman V. Jusko TA. Preventing Lead Poisoning in Young Children. Brody DJ.cdc. Available at URL: http://www. et al. Aug 2007 [online]. gov/mmwr/preview/mmwrhtml/mm5420a5. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Baghurst PA. Rios C. et al. Acquisition and retention of lead by young children.8(3):395-401. Rojas LM. Int J Hyg Environ Health 2002. Toxicological profile for lead. The relationship of bone and blood lead to hypertension.atsdr. Occup Environ Med 1996. Atlanta. Becker K. Lead and hypertension in a sample of middle-aged women. JAMA 1996. Pediatrics 2004.113(4):1016-1022. Vupputyuri S. Luukkonen R. Scand J Work Environ Health 1984. Available at URL: http://www.26:359-371. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Age-specific kinetic model of lead metal in humans. Seiwert M. Chiodo LM. 1999-2002. Blood lead levels measured prospectively and risk of spontaneous abortion. Baj A. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development.55(32):876-879.cdc. Pediatrics 2009. CDC. Coresh J. Korrick SA. Cox C. Semen quality of men employed at a lead smelter. Neurotoxicol 1987. Auinger P. Apostoli P. 4/14/09 Alexander BH. 4/14/09 Centers for Disease Control and Prevention (CDC). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Robertson EF.gov/nceh/lead/ CaseManagement/caseManage_main. Weiss ST. Lead. Aro A. Public Health Rep 2000. Stanek KL. Neri A. 4/14/09 Centers for Disease Control and Prevention (CDC). Ronchi L. doi:10.1542/peds:2007-3608. 1991 [online].htm. 2005. Angle CR. Available at URL: http://www. Pirkle JL.123:e376-e385. Cory-Slechta DA. Sparrow D. Vimpani FB. JAMA 1996. Kaus S. A prospective follow-up study on psychological effects in workers exposed to low levels of lead.cdc. Lepom P. Speizer FE.html.115:521-529.73:409-420. Neurotoxicol Teratol 2004. Weiss ST.

and tibia lead with neurobehavioral test scores in South Korean lead workers. J Hum Hypertens 1995.108(1):45-53.9:303-327. Environ Health Perspect 2000. and hypertension in perimenopausal and postmenopausal women. Lauwerys RR. Payton M. Clin Chim Acta 2003. Weiss ST.153(5):453464. IV. JAMA 2003. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Osterloh JD. Magder L. O’Flaherty EJ. et al. Schwartz J. blood pressure. Blood lead. Soldin OP. Kidney Int 2003. Kinetics of lead disposition in humans. Rubin R.289(12):1523-1531. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Schwenk M. Environ Health Perspect 1996. Flegal AR. Revised and new reference values for arsenic.Metals results from NHANES III. stable lead isotopes to determine release of lead from the skeleton. Pizent A. Lead. Lee SS. blood pressure and cardiovascular disease in men. Use of endogenous. Toxicol Appl Pharmacol 1993. Schulz D. Low-level lead exposure and blood pressure. Rocic B. Gunter EW. Roels H.106:745-750. lead. Physiologically based models for bone-seeking elements. Kaufmann RB.209:301305.S. Brody DJ.63:1044-1050. Arch Environ Health 1995. Association of blood lead. Gavella M. cadmium. Nash D. Wilhelm M. Pirkle JL. 50:31-37. Hwang KY. Lustberg M. Cvitkovic P. Staessen JA.327:109-113. Paschal DC. Hickman T. Smith DR. Lee GS.104(1):60-66. dimercaptosuccinic acidchelatable lead.118:16-29. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Environ Health Perspect 1998. Blood lead concentrations in children: new ranges. Schwartz BS. Sherwin R. Sparrow D. Hu H. Soldin SJ. Lee BK. Jurasovic J. Am J Epidemiol 2001. Am J Epidemiol 1994. Kaufmann R. cadmium. zinc. Low-level lead exposure and renal function in the Normative Aging Study.140:821-829. Telisman S. et al. and copper in men. Exposure of the U. Hanak B. population to lead: 1991-1994. Amery A. Int J Hyg Environ Health 2006. Stewar WF.

80) 4.60) 1.00-1.797 (.S. population from the National Health and Nutrition Examination Survey.60-6.500) . have often required public health intervention (Zeitz et al.814 (.00-5. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.00 (.30) 4132 4241 03-04 03-04 03-04 .860-1.700) . Kingman et al.781 (.700 (. which create an episodic potential for volatization and inhalation of mercury vapor. 1993).979 (. which can bioaccumulate in aquatic and terrestrial food chains.Metals Mercury CAS No. thermometers. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.50) 1. Also. synthetic organomercury compounds were once used in pharmaceutical applications.700-. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury. predominantly from fish and other seafood.00) 1. may contain inorganic mercury. see Data Analysis section) for Survey year 03-04 is 0. Apart from methyl mercury. mercuric chloride).285-. Other major uses include electrical equipment (e.30) 1.90-3.2. constitutes the main source of dietary mercury exposure in the general population.00 (2.50-1.90) 90th 3. interval) .484) .. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.90 (1.80 (1.363-. Woods et al.700-.90) 3. solid-waste incineration. In addition.714-.00) 4.655-.80 (1.g.10) .30 (2.689-. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).326 (. and mining and smelting.g. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.g.886) . silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.30 (1. merbromin).00 (2.70-2..80 (3.776 (. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. Poorly absorbed from the gastrointestinal tract. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).900) 1.903) Selected percentiles ( 95% confidence interval) 50th ..700) .900 (.800 (.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 . thermostats and switches).50) 5.60 (1.30) 1.40-1. to form inorganic mercury compounds or salts.372) .300) . phenylmercuric acetate) or topical antiseptics (e.753-1.40-2.02) . The ingestion of methyl mercury.00 (. Survey years 03-04 Geometric mean (95% conf..500-.20) 2.919) .400-.490 (.20 (2.563 (.00 (1.800-1.20-3. Hursh et al.70 (4... with the highest concentrations occurring in the kidneys (Barregard et al. and dental amalgam.30) 5.80 (1. 1980. Accidental spills of elemental mercury.900) 1.472-.30) 3.800 (.70 (3.300 (.g.900) 75th 1.70 (1. 2002).40-3.500 (. sulfur.80) 1. and organic forms.00 (. electrical lamps.700-.600) 1.00 (.40 (3. and mercury compounds are still used as preservatives (e.400-.60) 1.S. 218 Fourth National Report on Human Exposure to Environmental Chemicals .800 (.40 (3.60 (1. Some cosmetic skin creams from countries other than the U.800-1. Elemental mercury is a shiny.800-1.40 (4. thimerosal.418-.927) . IARC.40-1..12) .50) 2.703-.80) 3.30-6.00) .60-2. an organic form of mercury.600 (.. 1994.400 (.30-2.60-6.60-5.30-5.800 (.900) .00) 3.419 (. After elemental mercury is absorbed.700-.00) 1.50-2.90) 95th 4. such as chlorine (e.40) 1.60 (2.900) 1.877 (.500-.70 (1.700-.70) 911 856 2081 4525 03-04 03-04 .300-.60) 2085 2293 3478 Limit of detection (LOD. elemental mercury is absorbed mainly by inhaling volatilized vapor.500 (.90 (4.90 (1.40-2.00 (2. 2007). 1999 .60-3.800-1. Atmospheric elemental mercury can be deposited on land and water.20-4.574) .40 (4. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. sphygmomanometers and barometers.50-3.50) 4. The kinetics of the different forms of mercury vary considerably.30-4.800-1. or oxygen. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.40) 3..672) .10-3. 1998.30) 3. inorganic.20-4. and is distributed to most tissues.

300) .820 (.90 (4.60 (2. 1975.0) 4. Fourth National Report on Human Exposure to Environmental Chemicals 219 .00) 2. Smith and Farris.90) 90th 1.00-2.01) .. Sandborgh-Englund et al.944 (. Myers et al.35 (1.40) 5. 2003).30 (1..50) 2. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.S.50) 3.90) 2.00) .00-2.200-.00 (3.200-..300) .30-6.00) 7. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.343 (. 1969. 1998).06 (.30 (.50-2. McDowell et al.800) 75th .600) . The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.20-3.40-1. 1993). 1990). 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .833 (.10 (.20 (2.80) 1.800) 1. 2003). 1992 and 1999.60) 3.40-2....940) Race/ethnicity (females. Excretion occurs by renal and fecal routes.307 (.265-.70 (1.23) ..10) .200 (.800 (.00-2.60 (1.700 (.50 (1.10-3.374) .297-. Vahter et al. population.300 (.30-6.7) 4. 1994).700 (.70-3.50) 1.. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury..10) .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 .50-3. 2004.475) .60) 1. 2005).20-3.27) .70 (1. Smith et al. 1995.90) 5.700) 2.00-6. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.02 (.80 (3.Metals the tissues to mercurous and mercuric inorganic forms.30-6.500 (.500-.600) .20-3.900-1.824) 1..300 (. Methyl mercury enters the brain and other tissues (Vahter et al..268-.600 (.70) 1.. 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.10 (1.00 (1.00 (2.20-2.70) 4.90 (4.500-.60) 1.70-3. for both acute and chronic exposures.299-.70-5.10 (1.90 (3. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.40-2..697-.10 (1.395) .50-12. 1994.00) 4. National Health and Nutrition Examination Survey.400-.369) 1.20) .329 (.20 (.00) 1.200-.30-5.919) .700-.90 (1.30) 1.726-1.900 (. 1998). and a useful marker of exposure in epidemiologic studies (Grandjean et al.200-.60 (1.700 (..300 (.200-.80 (1. 1973).. and the newborn’s levels decline gradually over several weeks (Bjornberg et al. Miettinen et al.40 (1. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.500-.00-3.20-11.20) 1.500-1.10-1.70) 4.500 (.900 (. 1991.06-1.10 (5.800) 1.80-3.60 (3.300) .14 and 0.30) 1. interval) Selected percentiles (95% confidence interval) 50th .29) .318 (.800-1.40) 1. a measure of accumulated dose (Cernichiari et al.700-.317 (.407) .256-.900 (.70-6.30-3. Suzuki et al.664-1.90 (1.800 (.14. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days. After exposure to elemental mercury. Methyl mercury is incorporated into growing hair. thereafter. 1994) and then undergoes slow dealkylation to inorganic mercury.30) 3.300) .00) 6.. with most elimination occurring through in the feces (Sherlock et al. Jonsson et al.300 (.73) 1. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al. 1984..10 (. 1971).800) .40 (1.377) .20) .800-1.541-.800 (. 1996).800) ..738-.00 (2.30-4..700-1. 1999).300) .700-1.200-.60 (1.667 (. 1992). see Data Analysis section) for Survey years 99-00 and 01-02 are 0.269-. 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..60 (3.10 (3.90) 3. 1992.30-11.70-5.30-2.00 (2.00) 1.800-1.. Vimy et al. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.500-.30 (1.871-1.30-4.50) 95th 2.377 (.500-.60) 2. Geometric mean Survey years (95% conf.30 (1.50) 1.825-1.200 (.40) 2.900-1.70 (1.300) .10) 1. 1999-2002.80) 579 527 370 436 588 806 Limit of detection (LOD. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.50 (2. 1996.3) 4. 1993).700 (.90) 2.00-1..

600) .600) .500-. 2004). Acute.600-. maculopapular rash. 1996). depression. Salonen et al. The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure. Factor-Litvak et al. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. 1995. The constellation of findings may include anorexia. 2006. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. 2002. 1983). Stern 2005.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .. dysarthria. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.600) .600 (.600 (.600 (..500-. Smith et al.500 (<LOD-.700-. fatigue. Survey Geometric mean (95% conf. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. insomnia. and sleep disturbance (Bidstrup 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 . irritability. 1995. Inorganic mercury exposure usually occurs by ingestion.500-. 2004). 2004. Sakamoto et al.500-. 2000....500-.600) .700 (. 1951. overt signs and symptoms of chronic inhalation may include tremor.600 (.600) .500-. dysarthria. Once absorbed. Vupputuri et al.700-. Bellinger et al. Drexler and Schaller.600-. 1987).800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . 220 Fourth National Report on Human Exposure to Environmental Chemicals . 2000). Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.600-. sensory impairments. short-term memory loss.600) .. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. population from the National Health and Nutrition Examination Survey.Metals may be more efficient for inorganic mercury (Grandjean et al. 2006. 2000. 2004. particularly irritability. limb deformities.500-.600) . Oskarsson et al. altered physical growth. and cerebral palsy (NRC. gingivitis.700) 2007 2240 3406 Limit of detection (LOD. cerebellar ataxia. 1998. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. 2005).600-.. 1970. hypertension. 1963). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. the existence of a causal relation is unresolved (Chan and Egeland.700 (.600 (. Sakamoto et al.500 (. DeRouen et al. 2003). and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.700 (.600) .500 (<LOD-. pain in the extremities...S. At levels below those that cause acute lung injury. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. 2005.. anorexia.500-.. see Data Analysis section) for Survey year 03-04 is 0.600 (. Rissanen et al. and pinkish discoloration of the hands and feet (Tunnessen et al. 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. and progressive constriction of the visual fields.600 (. Overt poisoning from methyl mercury primarily affects the central nervous system...700 (. 1993). causing parasthesias..800) . hearing impairment. Smith et al. and neurocognitive and behavioral disturbances.700) . Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.500-. < LOD means less than the limit of detection.600) ...600 (. typically after a latent period of weeks to months. Rice. In recent epidemiologic studies.500 (..700 (. ataxia.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .500) . which may vary for some chemicals by year and by individual sample..700-.42.700 (.

330-.00 (.26 (1. Sanzo et al.570) ..330 (.360 (.08 (1.160-.01 (. et al..78 µg/L for adults and 0.78-2.S.67-3. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females. range 40 years to 78 years) had an average total blood mercury concentration of 2. However.S.00) 1.16 (.14.416 (.gov/mercury and from ATSDR at: http:// www.61) 1.530) . 2001.770-1.460) .30) 3.03-4.442-.19 (1.atsdr..413-. Over the NHANES 1999-2006 survey periods.24) 1. In NHANES 19992002. 2003)..52) 2. Benes et al. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.28) 1. Grandjean et al.08 (1.430 (..39-3.20 (1. 2004.S.93 (1. A cohort of 1127 U.960 (. Survey years 03-04 Geometric mean (95% conf. total blood mercury increased with age.280-.05) 3. and the age-related changes differed across the groups (Caldwell et al.406-. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC. 1997. the total blood mercury concentration is due mostly to the dietary intake of organic forms.63-2.42) 95th 3.495 (.254 (. interval) .447 (.34-3.19 (2. average age 9. These distinctions can help interpret mercury blood levels in people.358 (.460 (.76-3. population from the National Health and Nutrition Examination Survey. Among the three racial/ethnic groups.410-.476 (.46 µg/L for children.509) .31) 1266 1272 03-04 03-04 03-04 .90) 2.304) .cdc. EPA at: http://www. 1995. 1998). military veterans (mean age 52.S. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.396-. environmental levels) and health effects is available from the U. During the same survey periods.360-.54 (2.290-. In Germany the geometric mean for blood mercury was 0. adult women in several ethnic subgroups (Hightower et al.200 (.408) . total blood mercury geometric mean levels in females aged 16-49 years did not change.530-. 1998).23) 2.13-2.440 (.509) .840) 1.420 (. see Data Analysis section) for Survey year 03-04 is 0.97) 2.55) 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 .890 (..480 (.360-. slightly higher total blood mercury levels were found in U. who participated in a 1998 representative population survey (Becker et al. 2009)..441 (. 2000).870-1.96 (1.940 (.340-.31) 2.76-3. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.24 (2. the median concentration of blood mercury was 0.16 (1.530) .520) .14) 90th 2. 2006).250) .9 years).18) 2. From 1996 through 1998.29) 1.549) .Metals standard for inorganic mercury has been established by U. particularly methyl mercury. 758 children.60) 619 713 1066 Limit of detection (LOD.. Biomonitoring Information In the general population.67-2. Schober et al.610-1. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.313-. Fourth National Report on Human Exposure to Environmental Chemicals 221 .700-1.epa. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.12 (.382-. Kingman et al.350-.430 (. Total blood mercury levels increase with greater fish consumption (Dewailly et al.88) 287 722 1529 03-04 03-04 . Mahaffey et al. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.870-1.420 (..07 (..534) .840-1.330-.555) .492) Selected percentiles ( 95% confidence interval) 50th ..213-. Information about external exposure (i.. average age 33 years.58 µg/L for 4645 adults.46) 3.gov/toxprofiles.463) .85-2.400 (.60 (1. 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.66) 3. 2009). and increased slightly in non-Hispanic white children (Caldwell.8 years. aged 18 to 69 years.60-2.65) 1.99-6.33 (2.S.e. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.05) 1. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.76-4. 2003). 2001. EPA.840-1.88 (1.580) .370) .430) .89) 3.433 (.68 (2.55 µg/L.700 (.23) .09 (2.14-2.330-.96 (1.930-1..405-.77-2.88-3.480) 75th 1. 2002)..

.276 (.498) 75th .486) Selected percentiles ( 95% confidence interval) 50th . 2009).667-1. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.333-.619-.76 (1. 2005).275) .S..13 (1.384 (. 1998).417) .00 (.56) 1266 1271 03-04 03-04 03-04 .620-.87 (1.51-2.16) 1.535) 1. the urine mercury increased by approximately 0. Survey years 03-04 Geometric mean (95% conf.599) .714-1.00) 286 722 1529 03-04 03-04 . et al..87) 2.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .. Langworth et al. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect. In the study of U.41-2.525 (.265-.S.1 µg/L.455) .347) .61) 1.964-1. 2009).522-.. women of childbearing age have generally been much lower than these levels (CDC.18-1.255 (.88-2. 2006). representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell. mean urinary mercury was 3.587 (.31 (1.35 (1.196-.545 (. Levels in U.480) .09) 1.32-2.588) .400) .S.392-. and Italian (Apostoli et al.463 (.06 (. reversible increase in urinary N-acetyl-glucosaminidase.508 (.280-. 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.67 (1. and on average.06 (.78-4. An expert-panel report recently prepared for the U.307-. et al.217 (.13-2.970 (.532 (. not to imply a safety level for general population exposure.289) .225-.687) . a biomarker of perturbation in renal tubular function.696 (.23-2.990) .. interval) .77 (2.800-1.S.208-.768 (.30) 1.40 (1..62 (1.309-.21) 1.11) 2.784) 1.88-2.362 (.79) 1. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.46-2.969-1. population from the National Health and Nutrition Examination Survey.368) .297 (. military veterans with dental amalgams. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.376-.44) 1..28 (.447 (.25 (.65 (1.566) .246-.343 (.04-3.12-3.443 (. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 µg/L for each surface with a dental amalgam (Kingman et al.365 (.64-2.306 (.86) 95th 2.32 (1. 2003).79 (1.785-1.455-.40-1.07) 1. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.909 (.67 (1.11) 1. Urinary mercury levels in recent German (Becker et al.472-.537) . 1992).385-.01) 2. Department of Health and Human Services noted that several studies have observed a modest. 2002) adult population surveys were similar to those in a U.88 (1.616) .447-.875-1. 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.00) 90th 1.630) .. Information about the biological exposure indices is provided here for comparison.455-.365 (.391-. DeRouen et al..391) .301-.S. 2006.63) 1.03) 2.400-.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 .485 (.358) .464 (.39) 1.476 (. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.404-.Metals 2000).54 (2.11-2.652) . Czech (Benes et al. Urine mercury and the number of dental amalgams were correlated.30) 2. 1988. 2002).

24-1.706 (.909-1.45-2.55) 90th 3.560 (.664) .50-4.32 (1.85) 4.14.810) .27 (2.92) 2.Metals Urinary Mercury−Females Aged 16-49 Years Old.892) .50 (1.655 (.475-.97 (1.508-.94) 1.13 (2.740 (.03-2.47) 1.450-.97) 2.582-.592 (.61-6. interval) Selected percentiles (95% confidence interval) Survey years 50th .910) .516 (.578-.833) .07) 1.45) 95th 3.30 (1.79) 1.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .47) 1.21 (2.10-4.565 (.41-6.04-1.30 (2.632 (.46) 3.84 (2.42) 90th 2.99-2.799) .742-1.51 (3.46-4.553-.91 (2.45-3.42-3.97) 2.03 (. interval) Selected percentiles (95% confidence interval) 50th .22-3.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.540 (.59-5.95 (2.46 (1.92) 3.14) 3.53-3.44) 3.09-1.30-2.420-. Geometric mean Survey years (95% conf.62 (4.760 (.21-3.51) .23-1.37) 1.596 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.55-3.27-1.710) 1.656-.76-5. 16-49 years) 99-00 01-02 .724 (.699) 1.18 (3.03 (.98 (5.99 (2.16) 5.809) .557-.622-.99 (3.502-.42) 2.57-4.65-4.72) 1.77) 1.637) .28 (1.606 (.772 (.65) 1.670) 75th 1.76) 2.00) 2.426-.69-3.658 (.21 (1.68 (3.691) .32) 2.68) 3.56) 4.23-1.77) 2.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.97) 2.685 (.81 (3.966) .69 (1.79) 3.620 (. 16-49 years) 99-00 01-02 .05 (2.41 (1.14-1.723 (.48 (2. Geometric mean (95% conf. population.831) .41 (2.870) .744) 1.38) 4.657 (.07-2.639 (.31 (1.774) .43-1.S.15 (2.522 (.709) . National Health and Nutrition Examination Survey.76 (1.16-5.610-.569-.45) 2.850-1.00 (3.526-. population.14-2.636-.790) .68-3.846) .54) 595 531 381 442 594 826 Limit of detection (LOD.07-5.56) 3.09-1.650 (.387-.615 (.83-3.650) 1.631-.62 (3.616-.930) .61) 1.579-.710 (.04-10.87-4.41 (1.05 (3.35) .81-6.520-.84 (2.710 (.70 (2.50 (2.00 (2.709) 75th 1.560-.686) .31-1.832-1. 1999-2002.580 (.03) 1.45) 2.92) 4.32-3.99) 1.721 (.824) .85-3.15-1.719 (.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 . 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.605-.24) 6.650 (. 1999-2002.25) 2.540-.89 (2.600 (.06 (.624-.501-.806) .831) .22 (.14 and 0.665) .52) 3.27 (1.520-.45 (1.3) 5.91-7.35 (1.39-3.S.10-2.37 (1.18) 3.410-.580-.13-4.17) 95th 5. 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.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .30 (2. National Health and Nutrition Examination Survey.56 (1.500-.62 (1.

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79:786789. Suzuki T. 1993-1998. Allen PV. et al. Amurrio A. Environ Health Perspect 2007. Smith RG. 1999-2000. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury.31:687-700. Lorscheider FL. Turner MD.4(5):981-988. Bolger PM. Effects of exposure to mercury in the manufacture of chlorine. The hair-organ relationship in mercury concentration in contemporary Japanese. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Most B. Imai H. Orr MF.258(4 Pt 2):R939-945. Stern AH. Am Ind Hyg Assoc J 1970. Mottet NK. Smith JC. Woods JS. Hum Toxicol 1984. Arch Environ Health 1993. Matsuo N. Public Health Nutr 2001. McDowell M. Vupputuri S. Hall LL. Br J Ind Med 1983. Environ Res 2005. Leroux BG. Goldberg J. Zeitz P. Yoshinaga J. Langolf GD. Tunnessen WW. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Baser M. Newton G. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. JAMA 2003. Schober SE. Amiano P. Toxicol Appl Pharmacol 1994. Aguinagalde FX. Longnecker MP. Patil LS. Friberg L. Vahter M. Farris FF.124:221-229. Shen DD. Fisher HL. Burbacher T. Bernardo MF.40:413-419. Acrodynia: exposure to mercury from fluorescent light bulbs. Hislop D.48(4):221229. Martin MD. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Toxicol Appl Pharmacol 1994.128(2):25125-25126. Am J Physiol 1990. Jones RL. Whittle K. The contribution of dental amalgam to urinary mercury excretion in children. Dorronsoro M.289(13):1667-1674.97(2):195-200. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Smith JC. Vimy MJ. Nakazawa M. The kinetics of intravenously administered methyl mercury in man. Sandler DP. Azpiri MA.115(10):1527-1531.111(12):1465-1470. Sherlock J.Metals Sanzo JM. Smith AE. Pediatrics 1987. Kaye WE.98(1):133-142. McMahon KJ. Environ Res 2005. Sinks TH. et al. Methyl mercury pharmacokinetics in man: a reevaluation.110:129-132. Mooney TF. DeRouen TA.2:117-131.37:245-252. Topping G. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Leitao JG. Guo S. Blood mercury levels in US children and women of childbearing age. Smith PJ. Lind B. Effects of occupational exposure to elemental mercury on short term memory. Stern AH. Takahashi Y. Daniels JL. Osterloh J. et al. Hongo T. Environ Health Perspect 2002. Vorwald AJ. Toxicol Appl Pharmacol 1996. Environ Health Perspect 2003. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment.

and xanthine oxidase (Kisker et al. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.9-82.2 (49.3 (64.3) 41.0) 97.7 (50. interval) 45.1-51.2-53.7-41.6 (73.6 (52.9 (78. 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.2) 53. urinary excretion over six days CAS No.7) 57. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.3-47. semiconductor and battery industries have begun to use molybdenum.9 (52.2 (69.0 (46.7) 86.2) 52.2) 48.0-53.6-82.8 (67.0 (48.7 (37.8) 39. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.7) 75th 84.3 (37.7-50.Metals Molybdenum or ore deposits.0) 60.8-106) 88.1-44.3) 37.3-91.7-73.3 (79.9-55.8-46. which exert homeostatic regulation over molybdenum balance.3 (55.0 (43.6) 71.6 (55.7 (73.8 (42.6) 51.1-88.4 (79.7-39. At a daily oral molybdenum dose of 24 µg.6) 71. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.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 (99.9-85.2) 79.5-124) 108 (92.4) 42.1-55.5-66. Compounds of molybdenum are also used as corrosion inhibitors.0-71.3-75.2 (56.8) 40.7-91.7-51. chemical reagents in hospital laboratories.7 (45.5 (74.0-100) 63.7) 78.1-63.2 (83.S.9 (34.7 (36.1-52.1 (71.9 (44.8-49. inks.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) 41.6-46.4 (48.9 (40.8) 75.7-122) 93.1) 126 (106-147) 109 (94.3 (47. 7439-98-7 General Information Elemental molybdenum is a silver-white.5 (49.6-55.6 (55.3) 85.5) 85.1 (38.3-115) 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.1-48.1-59. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7) 46.5) 47.4) 76.5 (43.0 (76.0 (41.2) 40. WHO.3) 83.2 (40.3 (53.0 (81.9 (73.2) 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 (98.6) 53.7-84.2 (55.4-75.0-110) 90. 01-02.7 (58.7) 45.1 (34.6-62.2-79.0) 84. and in pigments for ceramics.3 (55. hydrogenation catalysts.8.1) 46.8 (82. 1997). 2001).0) 62.4-61.8) 46.9 (37.1-52.8-108) 87.8-90.1) 82.0 (42.2-42.8) 44.5 (41.9-55.7-105) 69.0) 45.2) 37.5) 80.3 (84.7 (44.3 (38.4 (72.6-96.0) 39.2-59.9-83.7) 51.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.0) 54. 0.0-62.5-68.9) 34. population from the National Health and Nutrition Examination survey.2) 41.8-94. respectively.6 (40.0-65.9) 62.4 (48. and 1.9 (33. Fourth National Report on Human Exposure to Environmental Chemicals 227 . lubricants.5.5) 80.4) 52.4-82.0) 55.9-56.5-91.1) 35.2-91. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.2-70.5 (81.1) 57.6 (40.1 (91.8.3 (71.0-101) 82.3 (73.0-38. 1996).1) 60.3 (46.6-42.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.1) 59.3) 47.4) 56.4-52. see Data Analysis section) for survey years 99-00.0-77.5) 60.4 (80.5-46.7 (51.9) 67.5 (67.7-96. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.5 (37.9 (32.5 (48.3) 65.4) 49.8) 48.2-37.4 (34.0-85.6-72.6) 93. and 03-04 are 0.5 (41.6-111) 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 52.7-92.2-59.6) Selected percentiles ( 95% confidence interval) 50th 50.. and paints.7) 78. 2001.5-41.5-52.0 (42.3-108) 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 47.9-109) 97.6-58.2 (49. In humans.3-44.2 (61.4) 45.5-65.3) 54.7 (71.7) 77.7-47. More recently. Excretion occurs predominantly via the kidneys.6 (43.5-52.2 (38.7-60.0-56. aldehyde dehydrogenase.8 (85.5) 44.2 (63.7-68.

7) 53.8-65.3) 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 85.5 (38. and clinical or epidemiologic evidence of adverse effects is limited.1) 56.9) 31. 1995).4-39.2) 39.1-81.5 (78.4) 58.2) 38.2-40.6-88.2) 39. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.6 (42.7-137) 129 (109-155) 112 (97.5) 60.3 (36.0 (58.1 (44.1 (38.2 (50.0) 62.2 (37.3 (71.5 (54.1 (49.8) 38.5 (35.0 (74.4-66.1-38.2) 42.6-41.2 (33.3 (37.7-43.7-44.4 (53.9 (36.7 (30.4) 40.7 (75.0) 72.3-43.4) 44..2 (36.1-67.4-120) 101 (84.1-43.7-100) 77.1-79.2 (40.3 (36. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.S.5 (37.3) 43.0-133) 119 (88. and molybdenum has not been systematically evaluated for carcinogenicity by IARC. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.7) 42.1-39.0-120) 85.1 (33. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.3 (55.2 (40.2) 37.3) 40.3) 41.5) 90th 108 (97.7 (77.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.9-40.6) Selected percentiles ( 95% confidence interval) 50th 41.3 (37.6-45.S.2-96.2 (43. Based on studies finding adverse reproductive effects in rats and mice.5) 71.9-68. 1999).3) 64.7-120) 87.6 (59.1-109) 89.4) 116 (101-126) 104 (88.9 (35.9 (73.5 (37.4) 89.8) 45.6) 39.2-41.5-119) 90.4) 47.1-127) 90.0 (35.9 (79.3 (83.3-46.4-106) 85.5 (65.9-118) 91.8-46. at daily oral doses of 95 µg and 428 µg.7-38.3-52.2-49.6-76.3) 57.6-63.4-107) 85.5 (40.5 (65. U.3-44.5 (41.Metals was 18% of the ingested dose.3-68.8 (75.4-42.0-38.6) 39.0 (80.9-45.7) 41.7-40.0) 36.4) 61.1-112) 78.7-93.1) 37.2) 43.3-102) 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 40.9-41.4) 48.0-41.1-100) 86.5-50.9) 92.9-87.7) 62. and urinary levels reflect intake from all sources.2-65.8 (56.6 (36.5) 63.5-44.9 (39.1) 101 (83.5-45.1 (38.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.0) 88.1 (82.0) 44.2 (73.2) 55.5-97..2 (52.5-35.3-141) 109 (81.8-67.3 (51. respectively.9) 40.7) 112 (95.8) 79.8 (90.7) 57.5 (80.5 (59.4 (67.0) 33.7-52.2 (57.5-70.7) 115 (93.4-185) 106 (94.5-69.1 (54.9 (64.3-56.7) 75th 63.6-78.2-96.9-71.5) 72.8) 37.6-61.3) 61.5 (39. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 (40.0-56.0) 39.9 (64. population from the National Health and Nutrition Examination survey.8) 39.8) 38..9-117) 57.9-96.5 (39.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.6-61.5 (79.3 (53.5 (36.9) 41.8 (57.3-59.2) 58.9 (40.8 (37.4) 60.5-48.8) 61.9 (49.2-80.4 (56.6) 36.0-46.5 (50.4-118) 172 (131-195) 138 (120-163) 118 (106-134) 780 682 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites 228 Fourth National Report on Human Exposure to Environmental Chemicals .2) 37.2 (69.5 (41.7-62.4 (59.5 (40.0) 53.3-45. 1993).1) 37. urinary excretion over six days rose to 50% and 67%.0-46.5-60.5) 73.5-46.5-99.3) 56.8-84.7 (66.4) 77.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.1 (39.5 (83.1 (37.3) 37.5-92.6 (57. EPA.4 (40.8) 71.1-45.4 (78. 1961.5 (35.8-52. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.9 (39.1-34.9) 44.7) 45.2-46.4 (37.6 (38. interval) 43. In industry.6 (71.4) 122 (107-133) 109 (99. but available epidemiologic data are scant.6 (36. of the ingested dose (Turnlund et al.9) 79.4-76.2-121) 107 (92.9 mg/kg/day and established a tolerable upper intake level of 0.8-47. Biomonitoring Information Molybdenum is an essential element for health.4 (55.1-43.9-45. 1997).1-39.9-42.6-63.5 (34.3 (71. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.3) 44.1-41.0) 38.0) 39.2) 42.8-47.3-115) 98.9-61.1 (30.1 (42.6) 43.2-47. 2001).4-41.5-62.1-40.8 (36.8-118) 81.8-42.3 (58.03 mg/kg/day in humans (IOM. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1) 65.0-103) 103 (90. Molybdenum is generally considered to be of low human toxicity.1) 43.8) 62.1) 40.4 (44.6) 48.8-66.2 (40.

nickel. Kristiansen J.niehs. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Turnlund JR. U. National Toxicology Program (NTP). Schleyerbach U. Molybdenum-cofactorcontaining enzymes: structure and mechanism. vanadium. Washington.22(3):179-191. pp. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Sci Total Environ 1998. Molybdenum absorption. excretion. Kisker C. Environmental Protection Agency (U. 4/14/09 Sievers E. edu/openbook. Third National Report on Human Exposure to Environmental Chemicals.. X. 16:1313-1319. Sciarra G. Occupational risk factors of lung cancer: a hospital based case-control study. Christensen JM. 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. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Minoia et al.15(2-3):149-154. Aprea C. Gatti A. arsenic. Vermeire PA. et al. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. Molybdenum. Keyes WR.62(4):790-796. Rees DC. chromium.123(1):81-85. molybdenum. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. pp.216:253-270. iodine. Ronchi A. Analyst 1998. 2005). TR-462. Available at URL: http://www.S. White MA.. manganese. 1996. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Available at URL: http://books. Minoia C. Sabbioni E. Occup Environ Med 1999. Ann Rev Biochem 1997.php?record_id=10026&page=420. World Health Organization (WHO). 2005. Shmavonyan DM.gov/index.htm. 1998). Molybdenum in infancy: methodical investigation of urinary excretion. Koval’skiy GA. Food and Nutrition Board. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al.epa. Institute of Medicine (IOM). 1998. Schaub J. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. White and Sabbioni. J Trace Elem Med Biol 2001.Metals in urine for the U. vitamin K. References Centers for Disease Control and Prevention (CDC). Dietary reference intakes for vitamin A. Yarovaya GA. Trace element reference values in tissues from inhabitants of the European Union. Zhurnal Obshchey Biologii 1961. 144-154. Molybdenum 1993 [online]. Am J Clin Nutr 1995.66:233-267. A study of 13 elements in blood and urine of a United Kingdom population.nap. Schindelin H. Menne C. Turci R. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online].S. van Sprundel MP. silicon. 56:322-327. 2001. iron. Weyler JJ.gov/iris/ subst/0425. 2002.nih. copper.S. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. Geneva: WHO. 2001). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Sabbioni E. Droste JHJ. (DC): National Academy Press. 420-441. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Available at URL: http://ntp. boron. EPA). Peiffer GL. 4/14/09 White MA. Atlanta (GA). Rapid Comm Mass Spectrom 2002. 4/14/09 Iversen BS.. and zinc: a report of the Panel on Micronutrients. In: Trace elements in human nutrition and health. Van Meerbeeck JP.

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

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

5th ed. et al. In: Bingham E. Int Arch Occup Environ Health 1997. Platinum concentrations in urban road dust and soil. Carelli G.S. Influences on human internal exposure to environmental platinum.inchem.56(3):283-286. Fries HG. osmium. Gieler U. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. 1998).13(1):24-30. Arch Environ Health:1969. Schulz C. Gromiec JP. Saindelle A. pp. Turfeld M.. 2003.04 µg/L) in this Report. and in blood and urine in the United Kingdom. Urinary excretion of platinum from platinum-industry workers. Available at URL: http://www. Schierl et al.19:685-691.70(3):205-208. Hauff K. Farago ME.207(1):69-73. Schierl R. Ruff F: Platinum and platinosis. and platinum.htm. Ruff F: Histamine release by sodium cholorplatinate.inchem. et al. Petrucci F. Boos KS. 206:15-24.htm. Grimm CH. Angerer J.. Pethran A. 2000.55(2):138-140. Neuendorf J. Pethran et al. Biomonitoring Information Urinary platinum levels reflect recent exposure. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Uptake of antineoplastic agents in pharmacy and hospital personnel. Kavanagh P. Arch Environ Health 2001. Kaus S. International Journal of Hygiene and Environmental Health 2003. Ewers U.. Herr et al. Wilhelm M. International Programme on Chemical Safety (IPCS). Fruhmann G. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Powell CH. Platinum. Urinary platinum levels associated with dental gold alloys. Rommelt H.Metals the International Programme on Chemical Safety at http:// www. Iavicoli I. Analyst 1998. et al.61(7):636-9. Schierl. 1999. Raab W. Jankofsky M. Hebert R. Hysell D. Alimonti A. Pethran A. Hall L. Ensslin AS. Seifert B... Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies.9:152-158. Environmental Health Criteria 125. Begerow J. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Herr et al. J Expo Anal Environ Epidemiol 2003. 2004) or less than 0.. Cohrssen B.10:63-71. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Int Arch Occup Environ Health 2003. Bocca B. 2001). Blanks R. Kulka U. population were below the limit of detection (0. Saindelle A. Moore W Jr. Kuster W. 2004.. Kelly J. Kazantzis G.. Seiwert M. et al. Czerczak S.4(1):27-36. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Wilhelm et al. Several studies have shown that background concentrations in general populations were usually less than 0. palladium. which elevate urinary platinum by five to twelve-fold (Begerow et al.org/documents/ehc/ehc/ehc125. 232 Fourth National Report on Human Exposure to Environmental Chemicals . 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. Levels of platinum in urine for the U.01 µg/L (Becker et al.. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. 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.35:313-321. rhodium.org/documents/ehc/ehc/ ehc125. 1991 [online]. 289-380. Schulz C. Part 1: monitoring of urinary concentrations.76(1):5-10. Br J Pharmacol 1969. Occup Environ Med 1998. Int J Hyg Environ Health 2004. 2003. Biomonitoring of traffic police officers exposed to airborne platinum. Environ Health Perspect 1975b. Environ Res 1975a. Senofonte O. Schierl R. van de Weyer C. Stilianakis NI.005 µg/L (Iavicoli et al. Schierl R. 2004). Crocker W.. and gold excretion of patients after insertion of noble-metal dental alloys. Biomarkers 1999. Schierl R. Parrot JL. eds. Campbell K. References Becker K. 3/31/08 Moore W Jr. palladium. Patty’s Toxicology. Allergy and histamine release due to some platinum salts. Hysell D. New York: John Wiley & Sons. Herr CE.123(3):451-454. 2003).. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Huber R. Nowak D. 1997. 2003. Occup Environ Med 2004. ruthenium. Nickel. Duneman L:Long-term urinary platinum. 1998). Thornton I.

243) .290 (.370-.360) .280 (.137-.165 (.140-.183) .380 (.370 (.160-.360 (.150-.420) .430) .240) .220 (.250-.410-.200) .400-.430 (.156) .430) .340-.200 (.200 (.370 (.220-.360-.200 (.370) .270-.340) .440) .340) .145 (.270 (.180 (.350 (.490) .172 (.250-.420) .410-.350-.230) .250-.400) .420) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.160-.134-.159 (.480) . thallium was obtained as a by-product of smelting other metals.160-.133-.300 (.192) Selected percentiles ( 95% confidence interval) 50th .410-.490 (.640) .330-.370-.202 (.135-.370 (.160 (.160 (.480) .260-.239) .480) .350) . respectively.170-.190 (.145-.300 (.202 (.270) .185-.360-.159 (.250-.200 (.450 (.460 (.170-.217) .520) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.360 (.173) .200) .200 (.410-.270 (.330-.380-.350-.390-.160 (.200-.400 (.290 (.360 (.350-.510 (.260-. 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.240-.400-.420-.340-. 2005).420) .330-.360 (.290 (.330) .410 (.210) .154-.500) .400 (.500) .150-.330-.410) .310 (.156) .330-.170) .159 (.240) .157-.170-.370-. Fourth National Report on Human Exposure to Environmental Chemicals 233 . population from the National Health and Nutrition Examination Survey.160-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.340-.215) .167-.360-.02.290-.400) 95th .170 (.158) .187-.410-.270-.147-.500) . 01-02.225) .260-.480) .179-.163) .420-.206) .320) .450 (.470) .218) .280 (..230) .220 (.260) .220) .290 (.290) .310) .250-.180-.200-.S.370-.270) .145-.420-. Thallium disappears from the blood with a half-life of several days.220 (.260-.180 (.310 (. 0.450 (.196) .320) .490) .430 (.220) .390) .147-.420) .400 (.400) .300) .290) .330) .250-.330) .190 (.150-.440-.290) .430-.450 (.390-.156-.220 (.320-.350) .310 (.590) .155 (.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 .167 (.430-.220 (.390-.450 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.178) .370 (.380-.240-.420 (.180-.290 (.330) .160 (.230) .410 (.185 (.430 (.410 (.146 (.218) .520) .520 (.200-.300) .260-.170-.149 (. however.230) .380) .290-.150-.184 (.360-.350-.162-.02.153-.190 (.400) .450 (.370) .150-.167-.270 (.250-.147-.310-.200) .440) .190-. see Data Analysis section) for Survey years 99-00.173-.520) .490) .270 (.470 (. it has not been specifically mined or refined in the United States since 1984.350 (.180 (.480) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.280-.171 (.400-.420-.400) .180) .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 .500 (.210 (.180) 75th .180-.197 (.490) Total .220) .380 (.176 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.170) .175) .360-.280-.390) . In the United States.250) .173) .550 (.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 .230-.400-.182-.250 (.144 (.170-.410 (.430 (.400-.183) .190 (.240) .Metals Thallium depilatory cosmetics.430-.440 (.300-.420) .440 (.172) .201 (.260 (.280 (.270-.410 (.440) .390-.260 (.230-.280) .180-.470) .202) .201 (.160-.220) .340 (.320) .470) .181-.400 (. the latter being the current major industrial consumer of thallium in this country. In the past.560) . Human health effects from thallium at low environmental CAS No.210-.460-.150-. and 0.260 (.170-.148-.210 (.390) .410-. representing distribution into other tissues.340-. thallium readily crosses the placenta and also distributes into breast milk.230 (.217 (.400 (.290) 90th .350-.450 (.188) .250 (.440 (.160 (.220) .350-.420) .450) .630) .190 (.410 (.200) .197-.170 (.330-.270 (. From these and other sources.170) . and 03-04 are 0.330-.470 (. interval) .196) .191 (.320 (.510) .200) .250-.230-.177) .02.390 (.300) .200-.200) .370 (.590) .290) .172 (.300 (.170-.690) .200 (.170 (.240-.450 (.460) .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.370 (.280) .390) .300) .220) . In addition.390 (.190 (.280) .450 (.290 (.370 (.440 (.

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

Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. et al. Paschal et al. Valentin H.48(4):375-389. 1998. et al. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Sci Total Environ 1998. Toxicological profile for thallium.S. Sabbioni E. Gallorini M. Centers for Disease Control and Prevention.html.gov/toxprofiles/tp54. Trace metals in urine of United States residents: reference range concentrations. Trace element reference values in tissues from inhabitants of the European community I. Raithel HJ. 2005) and are shown with results from NHANES 2003-2004 in this Report. White MA. References Agency for Toxic Substances and Disease Registry (ATSDR). Schaller KH. Cassot G. (1981) studied 1. Challeton-de Vathaire C. 1980. et al. Buhlmeyer G.1 mg/m3 (Marcus. Available at URL: http://www. Investigations of thallium-exposed workers in cement factories. Boisson P. X. A study of 13 elements in blood and urine of a United Kingdom population. Brockhaus et al.. Atlanta (GA). Brockhaus A. Manke G.5 μg/L. 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. Sampson EJ. Martin J-C. 2005.216:253-270. 1992 [online]. Pietra R.cdc. Minoia C. Ting BG. Int Arch Occup Environ Health 1980. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. blood. Schmidt M.113(1):47-53.47(3):223-231. White and Sabbioni. 1985). and serum of Italian subjects.95:89-105. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Schaller et al. Environ Res 1998. 1990.atsdr. 7/15/09 Blanchardon E. Radiat Prot Dosim. 1981.. Jackson RJ. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Sabbioni E. Paschal DC. J Soc Occup Med 1985. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Sci Total Environ 1990. Wiegand H.Metals (CDC.76(1):53-59. Investigation of a working population exposed to thallium.265 people living near a thallium-emitting cement plant in Germany. Pozzoli L. 2005. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Ewers U. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Soddemann H.35(1):4-9.. 1998). with concentrations ranging up to 76. Minoia et al. Celier D. Int Arch Occup Environ Health 1981. A study of 46 elements in urine. Kramer U. Biomonitoring studies on levels of thallium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of thallium than are found in the general population. Trace element reference values in tissues from inhabitants of the European Union. Marcus RL.. Third National Report on Human Exposure to Environmental Chemicals. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Pirkle JL. Dolger R. Morrow JC. Apostoli P.

400 (.450-.320 (.230) .081 (.310 (.120) . filaments for incandescent lamps.130 (.090-.120 (.380-.073-.080 (.350-1.510-1.092 (.270-.210-.270-.370 (.105 (.100) .430 (.113 (.070 (.090 (.160) .220) .340) .180-.080-.120) .093) .070-.260-.250) .060-.060 (.100 (.060 (.210 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .056-.230-.530 (.100) Selected percentiles ( 95% confidence interval) 50th .400-.330-.250-.120-.082) .310-.370) .560) .390 (.070) .230-.490 (.280 (.110 (.122) .170) .090 (.082 (.270 (.380 (.470) .210) .110 (.500 (.110) .290-.070) .470) .069) .090-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water. population from the National Health and Nutrition Examination Survey.104) .070) .350) .470-.290-.310-.300) .260) .520) .560) .410-.380-.270-.086 (.150 (.050-.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.080) .200) .170 (.320-.420-.210 (.630) .056-.330) .560) .065 (.400) .190-.123-.070 (.062 (.101 (.280-.110 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.250) .088 (.113 (.084) .350) . Occupational exposure is from dusts released during grinding or drilling of hard metals.096 (.270 (.060 (.190-.250) .560) .050-. 0.220 (.068) .210 (.090) .140 (.060-.340-.140) 90th .060-.320 (.180-.070 (.101-.360-.170) .500 (.340-.073 (.130) .250-.190-. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.310-.110-.790) .580) .058-.04.160 (.440) .064-.090-.250) .180) .490) .070) . which is used in the steel industry.180 (.091) .290) .430 (.130-.120) .090) .060-.190 (.095-.133) .400 (.160 (.450 (.290-.077-.620) . and for producing ferrotungsten.090-.084 (.092) .300-. and 03-04 are 0.120-.370-.350) .100 (.380-.082 (. bronzes in pigments.590) .410 (.087-.230) .100 (.100-.140-.510-.120-.300 (.620) .830) .04.230-.090-.204) .460 (.180 (.150 (.53) .120-.160 (.430) .360-.090) .510 (.460 (.080) .130) .116) .800) .100-.430 (.180) .640 (.160-.400 (.200 (.080 (.096-.650) .160) .092 (.170-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.310-.430-.260-.140 (.113 (.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 .04.060 (.220) .130) .470 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.151) .097-.105) .430-.080-.132) .360 (.320) .220-.620 (.100-.460) .100 (.230 (.073-.200-.270-.570 (. and 0.110 (.087) .080-.090-.400 (.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 .100) .090 (.360) .260-.109) .060-.470 (.00) .110) .078-.240-.060 (. Little information is available on the toxicity of tungsten.082-.120) .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) . Tungsten compounds are used as lubricating agents.080) .090-.350 (.420-.060-.220) .390) . which are used in rock drills and metal-cutting tools.120-.310-.066-.069-.111-.210 (.300 (.080 (.062 (.076 (. and as catalysts in the petroleum industry.370 (.180) .550 (.110 (.380) .570 (.530 (.180-.074-.088) .500) .370 (.170 (.520) .250) .530 (.135) .070-.270 (.080 (.071-.370-.071 (.158 (.080 (.113 (. see Data Analysis section) for Survey years 99-00.095-.360 (.560 (.073) .670) .110-.330-.690) .090-. Tungsten is used mainly for producing hard metals.290 (.230-.480) Total .160 (.084-.107 (.250) .126) .130-.130-.770 (.150-.093 (.190) .050-.140 (.340-.380-.800) .120-.550) .100) .280 (.190-.170) .150 (.290) . 01-02.170) .060 (.100) .120) .S.300) 95th .140 (.100) .360 (. respectively.050-.260 (.110-.090) .Metals Tungsten CAS No. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.950) .320-.137 (.330) .550) .180) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).520) .210 (.065-.300 (.380 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.130 (.130) .070-.076 (.093-.150) .130) .160-. interval) .160-. Evidence is lacking for the carcinogenicity of tungsten.070-.180-.120) .130-.330 (.240 (.160 (. mainly as scheelite (CaWO4).160-.080) 75th .190 (.550) .260 (.140-.460 (.310) .810) .070-.

122 (. 2003. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.139) .136-.300-.063-.069 (.739) .333-.079) .143-.333 (.060-.122-.667) .151 (.181 (. 2001).279 (.084 (.077) .119 (.119-.253) 95th .069-.500) .538) .301) ..070 (.158) .203-.106 (.059 (.168 (.071) .138) .125) .359 (.339 (.077-.386) .085 (.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 .200-.317) .287) .278-.333 (.077-.078-.208-.080-. and 2003-2004 (Paschal et al.308) .143 (.S.275 (.198-.079) .174) .293 (.186 (.217-.122-.083 (.333-.086) .090-.497 (.436) .634 (.823) .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.084 (.105 (.333 (.071 (.439) Total .200-.605) .187) .098-.120) .302-.089) .077) .S.136-.103-.158 (.116) .146 (.197 (.431) .426) .197) .060 (.085-.358) .061-.088) .484) .233-.116 (.078) .075 (.083-.105 (.063-.091) .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 .184 (. measure urinary tungsten.331-.344-.340 (.211 (.205-.070 (.073 (.100) .063-.059-.146) .161) .197) .158) .091 (.075) .215 (.145 (..245-.265 (.084) .075 (.216 (.090-.267-.253-.301) .081 (.201) .555 (.392) . Nicolaou et al.250 (.379 (.201 (.258 (.385 (.068-.199 (.214) . population from the National Health and Nutrition Examination Survey.412 (.237) .071 (.381) .360 (.667 (.165) .139 (.072-.198) .104-.121 (.057-.079) . Patients with medically-inserted tungsten found at increased levels in drinking water. population (CDC.329 (.058-.065-.329-.170-.431) . similar to those in this Report (Schramel et al.067-.253 (.258-.797) .148) .120) .108-.302-.053-.100 (.074-. or exposure that a control group of non-metal workers had mean levels differences.079 (.074 (.285) .167-.284) .080 (.108) .333) .231-.060-.169) .169 (.317-.279 (.167) .125 (.216 (.073 (.164 (.107-.062 (.083) .100) .078) .179-.465) .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 .283) .383 (.091) .136-.069 (.117 (.065) .216-.231 (.059-..222) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.426) .055-.082) .078 (.154) .439 (.064-.359 (.261-.078 (.095-.061-.436-1.063-.339 (.098) .28) .237-.179-.130-.279 (.124-.S.084) .065-. (1987) found possibly due to methodologic.133) .299 (. 2001-2002.126-. 1997).347 (.091) .459) .074) .306) .111 (.064-.214-.333) .130 (.217-.067 (.066 (.131-.180-.071 (.157) . population.167-.272-.(Kraus et al.353 (.206-.098-.144 (.067 (.075-.082) .255-.315-.727) .092) .880) .354-.224) .158) .216-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.065 (.063 (.146 (.255 (.176-.218 (.121-.255 (.080 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.091 (.431) .071) .117) .410-.136 (.209-.081 (.087 (.065-.073 (.082 (.056-.250 (.086) .054-.216-.270 (.072 (. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.061-.087) .081) .582) .136-.079 (.074-.286-.341 (.300 (.222-.215) .091) .075-.083 (.099-.300-.063 (.452-.154) .095) Selected percentiles ( 95% confidence interval) 50th .439 (.333 (.462) .150-.109 (.300) .317 (.150-.364 (.482 (.414) .176-.071-.150 (.153-.237) .152-.155-. 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.554) .083) .250-.326) .071) .075) .197-.085) .188-.086) .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 .096) .056-.353 (.073 (.301) .074) 75th .072-.088) .093) .375) .190) .093-. 2005).080-.174 (.465) .094-.133) 90th . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.059-.139-.079) .148 (. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.124 (.453) .138 (.109-.094) .098-.086-.308) .065 (.068 (.057-. Using neutron activation analysis to 2000.049-.167) .354) .054-. 1998).089 (.240-.081-.066 (. interval) .153) .138 (.144-.098 (.094) .484 (.133) .116-.294 (.267) .199 (.

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

008 (.046-.027 (.029-.009) .064 (.005-. and 0.017-.014 (.011) .033-.035-.022-.012) .007 (.040) .008 (.009) .016-.012) .012) .014 (.007-.009) .006-.009-.006 (.012) .065) .011 (.039) 1227 1335 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .009) .008 (.056) .023-.020-.007) .023-.009-. Variable concentrations of uranium occur naturally in drinking water sources.127) .010) .030 (.009) .024-.007 (.008-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.010-.008 (.012 (.039-.031-.009) .015-.013 (.004.036-.018) . including nuclear weapons.009) .020-.011 (.023 (.008 (.050) .018-.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.016) .054) .010) .023-.017 (.041 (.021) .005-.040 (.015 (.055 (.026) .011) .037) Total .007-.014 (.012-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.010) .006-.008 (.008 (.037 (.034-. or processing.006-. interval) .020) .008 (.027 (.036) .023-.012 (.013 (.033 (.020-.072) .010) .007) .073) .015 (.008-.027-.028 (.041 (.028 (.040 (.022-.019 (. 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.040) .011) .046 (.009 (.014 (.013-.009) .013 (.026) 95th .006-.031 (.015 (.004. 235U (about 0.009 (.049) . and 03-04 are 0.027 (.010 (.009) .010 (.006-.011) .006-.027) .028 (.007 (. Thus.010) .035) .008-.043 (.030) .005-. and as an aid in electron microscopy and photography.010-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.008 (.007 (.027 (.009) .007-.035) .011) .010-.039) .019-.020 (.008) .009-.008) .009 (.024 (.032 (.023) .008) .013 (.045) .023 (.050) .018 (.026-.010) . Uranium has many commercial uses. 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.009-.023) .034-.007 (.027) .053 (.063) .007-.016) .037) .012 (.017-.009 (.012 (.009 (.036-.033 (.016-.011-.007-.031 (.013 (.021 (.011-.088) .016) .006-.010) * .158) .011-.013 (.020-.006-.017) .009) * .051) .031 (.007-.018) . in some ceramics.006-.009-.012-.009-.013-.009) Selected percentiles ( 95% confidence interval) 50th .042 (.005-.021 (.018) .018 (.036 (.006-.025-.009 (.007-.022-.009 (.021) .017-.008-.007-.009-.020-.009-.026 (.011-.008 (.017) .007-. human exposure occurs primarily by inhaling dust and other small particles.012 (.008 (.013-.007-.007-.008-.007-.010-.030 (.006 (.040-.026-.009 (.039) .007 (.019-.010 (.023 (.037) .007 (.042) .031 (.034) .007-.007-.008-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).062) .049) .72%).048) .008) .010 (.011-.006 (.009) .053) .007-.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 .011) .007 (.036) .030 (.012-.020) .S.006 (.015 (.048 (.021 (.067) .027) .017 (.010) .024-.016) .026 (.046) . and 234U.023) .038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .010-.279) .019-.012-. 01-02.007-.014 (.019-.013) 90th .016) .037) .016) .054-.010 (.009 (.038) .008 (.029-.065) .009-.005.011) . nuclear fuel. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.040-.046 (.007) .006-.006-.054) .021) .045) .010-.008 (.047 (.007-.008-. In workplaces that involve uranium mining.010) * .028-.005-.044 (.029 (.021-.027-.017-.010) .031 (. population from the National Health and Nutrition Examination Survey.015) .036 (.026) .024-.114 (.013 (.008 (.016 (.022 (.012-.008 (.014 (.069) .017-.007-.027) .013) .007) 75th .011-.017) .066) .046 (.009 (.022) . Since the 1990’s.017) .007 (. see Data Analysis section) for Survey years 99-00.009) .016-.067) .007) .009-.046 (.056) .008-.026 (.017-.017) . Fourth National Report on Human Exposure to Environmental Chemicals 239 .008) .009) .015) .021-.008 (.043) .038 (.007) .037-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.006-. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.012-.060 (.Metals Uranium CAS No.012 (. respectively. milling.027-.011-.008 (.030-.028-.033) .007 (.018) .007 (.052 (. 0.

031 (.035 (. 0.011 (.015) .020-.010) .008) .021-.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 .012-.008 (.007 (.022 (.008-.006-.011-.006 (.009 (.029 (.024) .051) .015) .039) .011-.015-.051 (.S.033) . 2005).016) .025-.058) .019-.018) .008) .006-.021 (.014) .009) .034-.008-.032) .146) .020) .006) .027) .007 (.017-.013 (.009-.1%-6% of an ingested dose may be absorbed.020-.029 (.014-.006-.030-. population from the National Health and Nutrition Examination Survey.027) .007-.024) .007 (. After long term or repeated exposure.008) 75th .033 (.033 (.006-.010) .Metals impact.016-.080) .015) .010-.058) .008) .014) .014) 90th .009 (.020-.005-.029) .005-.007 (.019) .013 (.008) .028) ..008 (.026 (.007-. Studies of persons with chronic exposure to soluble uranium salts in drinking water have not shown kidney Urinary Uranium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.007 (.008) .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.007 (. 2003).027-. where limited absorption occurs (less than 5%).008) .074) .006 (.010) .020 (.021 (.039) .050 (.009) .007) .007 (. Radiation risks from exposure to natural uranium are very low.020 (.006-.019 (.010 (. liver.010 (.006-.015 (.034) .014-.013) .008 (.039) .033 (.007-. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al. Inhaled uranium-containing particles are retained in the lungs.011-.024) .012 (.005-. In cases of retained DU shrapnel.013-.007-.008-.014) .010-.039) Total . Depending upon the specific compound and solubility.007 (.009-.011) * .009) .045 (.007 (.013 (.007) .021 (.019-.009) .022) .025) 95th .010 (.004-.007 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.006-.009 (.015-.018-.019-.026 (.063) .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 .006-. which represents distribution and excretion.008 (.031-.007 (.024-.006-.009) .007 (.029) .011-.007 (.010 (.059 (.006-.022 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.028) .015-.006-.034 (.015-.018-.034 (.024-. After exposure to soluble uranium salts.010 (.006) .009) .026) .013 (.005-.006) .008) .012) .011-.050) .020 (.006-.033 (.027 (.025 (.027-.067) .100 (.061) .006-.005 (.010-.011-.005 (.004-.009) .005 (.015) .008 (.012 (.019 (.018-.006-.077) .008 (.014 (.013) .006-.009) .011) .017-.007-.022-.027-.006-.030-.028 (.009 (.008) .007 (.009) Selected percentiles ( 95% confidence interval) 50th .037 (.011 (.012 (.008) .007 (.019 (.015 (.027 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.011-.012 (.025-.006-.025-.006-.025 (.016) .030 (.008-.010-.018-.051) .008 (.010) .016-.009) * .007 (.042-.005-.006 (.010) * .034-. with much slower elimination from bone.013) .050) .017 (.009-.005-.007) .010) .006 (.007 (.048) .016-.007 (.042) .014 (.043 (. which can occur occasionally from high occupational exposure.040 (.034 (.006 (..006-.007 (.035 (.026-.010) .053) .013 (.024 (.007-.012 (.016) .013 (. After inhalation.016) .029 (.006) .021 (.012-.007-. Health effects from uranium exposure result from chemical toxicity to the kidney.017-. 1992).009 (.010-.012) . low level exposure.016) . about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.026 (.006-.027 (.012) .028-.007 (.016) .053) .054) .024-.009-.024) .009) .017 (.016) .006-. 240 Fourth National Report on Human Exposure to Environmental Chemicals .017-.270) .029) .022-..024 (.005-.030) .022 (.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 .010-.021) .015 (.010-.041) .006-.015-.030 (.015 (. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.034 (.024) .016) .016-.056) .028) .006-.030 (.013 (.029) .028) .051) .025-.044) .007-.017) .030) .018-.020-.008 (.010-.008-.019-.005 (.011-.017) .022-. the shrapnel acts as a source of chronic.011) .034 (.007 (.008) .006-.007-.017) .011-.012 (.009-.014-.009-.006 (.009) .042) .010-.011) . kidneys.012 (.019) .009) . Uranium is eliminated in feces and urine.019-. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.006) .013 (.010-.023-.016 (.048) .024 (.008) .007-.027-.013 (.013 (.047) .008 (.032) .008-.018 (. interval) .008 (.028 (.

2005. Atlanta (GA). NRC. had a mean urinary uranium concentration of 0. Boyd P. Tolmachev et al. Radiation protection dosimetry. McDiarmid et al. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population.066 μg/g creatinine (Gwiazda et al. eds.61 μg/g creatinine. Breitenstein BD. the median urinary uranium concentration was 2. the geometric mean urinary uranium concentration was 0. and 2003-2004 (Dang et al. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.. urinary levels of uranium were as high as 9. Thomas RG.. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U.S. Sci Total Environ 1991. 1994.S. soldiers evaluated before. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. In a study of 105 persons exposed to natural uranium in well water.. Stradling GN. Metivier H. population..110 to 45 μg/L (Ejnik et al. 28 soldiers who may have been exposed to DU by inhalation. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. 1991.. In: Gerber GB. respectively. McDiarmid M.1996. Health Phys 2000. Dang HS. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Hamilton MM..atsdr. Kent (England): Nuclear Technology Publishing.S. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. environmental levels) and health effects is available from ATSDR at: http://www. Six workers in a depleted uranium program showed concentrations of 0. Dietz LA..011 μg/L (McDiarmid et al.1992. 2001-2002. Volf V..55 μg/L (median 0.62:562-566. 41 (1). Muggenburg BA. In 17 U. with emphasis on quality control. 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. Hamilton et al. In the same study. 2000). (May et al. Third National Report on Human Exposure to Environmental Chemicals. ingestion. Pullat VR. 2002. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. The U.65 μg/L). Zimmerman I.Metals injury associated with elevated urinary uranium levels (Kurttio et al. Squibb K. the median urinary concentration was 0. but in whom no shrapnel was embedded. 1978). IARC and NTP have no ratings for uranium human carcinogenicity. Benedik L. Fourth National Report on Human Exposure to Environmental Chemicals 241 .78:143-146. 1-49. Pillai KC. EPA. Karpas et al. 2000)..107:143-157.168(8):600-605. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Vol. Byrne AR. in that the levels were below their respective detection limits (Byrne et al. Durakovic A. 2004). Ejnik JW. Drinking water and other environmental standards have been established by U. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. References Bhattacharyya MH.e. Carmichael AJ. 2002). or wound contamination..162 μg/L) (Orloff et al. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. In two studies of a Finnish population with high natural uranium concentrations in their drinking water.. Uranium content of blood.. 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. 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. Mil Med 2003. 2004).S. during. 2004)... 2006). Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. 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.078 μg/L (ranging up to 5. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2003. 1992. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Health Phys 1992. 2006). Information about external exposure (i. pp. 2006.cdc.S.gov/ toxpro2. 2006). A cohort of 46 U. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts.. Centers for Disease Control and Prevention (CDC). Horan P. (Kurttio et al. 2004)... et al. and no consistent effects on multiple endpoints of kidney function were found.. although slightly increased during and after deployment. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.S.html. 2006). Komaromy-Hiller et al. Galletti.

Sci Total Environ 1994. et al. Human exposure to uranium in groundwater. Oeh U. Auvinen A.67(8-10):697-714. Salonen L. Health Phys 1996. Health Phys 2006. Cremisini C. concentration and daily excretion of uranium in urine of Japanese. Health Phys 2004. Howerton K. Biologic monitoring for urinary uranium in Gulf War I veterans. Health Phys 2003. VI.44:29-40. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Englehardt SA. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Li WB. Karpas Z. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Environ Health Perspect 2002.S. Clin Chim Acta 2000. Oberbroekling KJ. Ejnik J. Roiz J.79(1):11-21. Hollriegl V. Salonen L.158:165-190. Makelainen I. Environ Res 1999. Paretzke HG. Sampson EJ. Wahl W.82(4): 527-532.94:319-326. Jackson RJ. McDiarmid M. Halicz L. Noguchi H. Tolmachev S. Ash KO. Review of elements in blood.296(1-2):71-90. Uranium and thorium in urine of United States residents: reference range concentrations. May LM. Radiat Environ Biophys 2005. Sabbioni E. NRC). Gwiazda RH. July 1978. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Van der Venne MT. et al. Pinto V. Heller J. Lewis BM.85:228-235. Wilson PD. Washington (DC): NRC. Kurttio P. D’Annibale L. et al.22–Bioassay at uranium mills. U. Health Phys 2004. Scott K. Squibb K. Nuclear Regulatory Commission (NRC) Guide 8.S. U. Inductively coupled plasma mass spectrometry as a simple. Metcalf S.S. Karpas Z. patient population and literature reference intervals for urinary trace elements.81:45-51. Am J Kidney Dis 2006.110(4):337-342. et al. Engelhardt SM. Komulainen H. Hamilton EI.91(2):144-153. Mistry K.S. Auvinen A. Saha H. Hancock RG. Ting BG. Element reference values in tissues from inhabitants of the European community. Orloff KG.87:51-56. Health Phys 2002.Metals Galletti M. Cordero S. Roth P. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Harmionen A. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Squibb K. Biokinetic modeling of uranium in man after injection and ingestion. Paschal DC. Gucer P. Shelly T. Nuclear Regulatory Commission (U. Kalinsky V. J Toxicol Environ Health A 2004. Marko R. Kuwabara J. Smith D. Kurttio P. Charp P. Pekkanen J. Lorber A. Komaromy-Hiller G. Costa R.71(6):879-85.86:12-18. Oliver M. Kidney toxicity of ingested uranium from drinking water. McDiarmid MA.47(6):972-982. Bennett LG. Andrews WS. Comparison of representative ranges based on U. Saha H. rapid. Pirkle JL. Int Arch Occup Environ Health 2006. Renal effects of uranium in drinking water. Environ Res 2004. Marino R. Uranium daily intake and urinary excretion: a preliminary study in Italy. Katorza E. Kane R. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. McDiarmid MA. Jarrett JM. Ough EA. et al. et al.

40 (4.00-6.40) 3.0 (11.10) 3.50 (3.40-13.70-5.50 (8.0) 11.40 (5.30 (5.09) 3.0) 12.0) 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 3.90-3.20-3.20 (8.02 (3.00) 5.30) 6.45-4.40 (3.88) 3.50) 3.10-12.35 (3.70 (3.0 (11.0 (9.20 (4.01 (2.50-4.20-12.90 (5.0 (8. matches.0-17. but has strong oxidant properties in the presence of concentrated acids.90 (4.10 (6.30 (5.19-4.S.0 (11. 2002).56) 3.0 (12.90-11.68) 4. 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.90-11.75-3.0-15.0 (8.0) 13. fabric dyeing.0 (11.0-17.10-4.03) 3.51 (3.0-14. milk.0) 9.0) 13.0 (8.0) 95th 14.84) 14.31) 2.40 (8.29-3. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.0) 13.80 (6.0-23. 2005).20 (4.40) 6.0-20.40-4.0 (12.10-11.11) 4.30-19.76) 4.70-6.0 (9.20 (6.50 (5. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.0 (13. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.0) 11.90) 5.0) 8.0) 13.93-4.10 (5.16) 3.60) 8.81-16.20-4.46) 3. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0) 9.47-4.0 (11.0 (9.90-9.60) 5.0) 10.40-7.90 (5.0 (11. certain catalytic metals.0) 9.90-9.80-12.79 (2.0 (11.74-3.12) 3. lettuce) can be the main sources of intake for humans (FDA. 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 (9.0) 9.39-4.49-3.80-6.50-11.0) 14.60) 3.50) 6.20 (7.93-3. population from the National Health and Nutrition Examination Survey.90-3.0-17.0) 14.S.0-18.80 (3.40 (3.0) 13.96 (3.40) 3.0) 19.0-17. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.44-4.60-7. It is normally found and produced as the anion of a sodium.70-3.S.EPA.20) 7. and limited applications in pharmaceutics.05 and 0.00-6.90 (3.08-3.70-7.60 (4.93 (4.11) 3.0) 10.60 (7.0) 708 617 681 652 1228 1092 Limit of detection (LOD.70-9.. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.70-11.00) 3. and reducing agents.00) 4.54 (3.0-29.40 (5.20) 3.0) 15.80 (7.40-11.65) 3.0) 13.22 (2.80-15.40) 90th 10.0-18.5 hours and has a small estimated volume of distribution (Crump and Gibbs.40-6.05.80 (3.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.80) 12.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.70-12. Perchlorate is stable under most environmental and physiological conditions.50) 5.62 (3.81) Selected percentiles ( 95% confidence interval) 50th 3.0-17.10) 3. laboratory analysis.70 (3. Survey years 01-02 03-04 Geometric mean (95% conf.50) 11.40 (5. 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.30-7.50) 5.20 (5.0 (11.0 (8.66) 3.51 (3. Perchlorate was added to the U.0 (8.30-7.20) 4.Perchlorate Perchlorate (Urbansky.20 (2.32 (3.50-7.10 (7. leather tanning.19 (3.10 (6.0) 13.38) 5.40) 3.50-4.07-4.80) 75th 6.80) 3.40-5.30 (2.05 (2. 2007).40) 4. potassium.70) 3.20 (2.10-7.75 (3.67-5.76 (3.0) 11. Drinking water.80-8.10 (2.0 (10.0) 10.0) 16.90 (5.90) 6.22-5.10-11. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .0-15.80-4.60 (4.50-3.10) 12.0 (12.89-3.40 (4.0) 9.10) 5.70-3.00) 7. and certain plants with high water content (e.g.0) 9.20-11.40-4. 1998).0-17.21 (2.20-4.80) 7.70 (3.0 (9.60-6.0) 8.90-6.0) 13.0 (9.18-3.80-4.0-19. Other manufactured uses include fireworks.0 (11.26 (2.0 (9.30 (2.0) 15.0 (12.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.00-5.90-10.30-6.10) 5.0-18.90 (2.30) 6.40) 2.. 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.00) 3.90-12.0) 14.0 (11. interval) 3. 2005). Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.87-3.30-17. and electroplating. or ammonium salt. In addition.

S. menopausal status.19-10.10) 3.0-44.30) 5. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.90 (7.89 (2.87) 2. although iodine intake was higher than U.24-2.61-10.87 (7.30) 90th 9.60-15. NAS.76 (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.60) 3.10) 13.10) 6..44-6.0) 6.20-4.37 (4.g.50-5.29) 2. population from the National Health and Nutrition Examination Survey. levels.00) 9.60-11.50) 5. 2006.80-3.30-5.0 (11.18-3.22-6.80 (7.14 (2.35 (4. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.50-9. 2003.0) 7.73) 3.77 (3.0-19.00-3.20 (2.32) 5.82 (5. 2005).40) 5.60-6.90 (4.60-11..30 (5.0) 13..60-8.1) 8.35) 3.87-3.50) 2.08) 3. 2005).50 (6.99 (5. Greer et al.61 (5.43) 6.S.24 (4.60-3.3-14.90) 5.20-9.5 (13.10) 4.93-8.93-7.60-5. Lawrence et al. nitrate.86) 4.70-4.5) 8.30-5.07 (2.6) 20.64-3.00) 3.0 (10.64) 5.EPA.03 (2.00) 4. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al. up to 68% RUI has been demonstrated. 2001..30-10.0 (9.30 (3.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.10 (6.39 (3.93-5.29-6.50) 2.25 (3.80-3.0) 9.40-10. medications).30) 75th 5. altered thyroid function was not found in Chilean pregnant women or their newborns with mean urinary perchlorate levels about 40-fold higher than average U.90-3.26 (3.67) 5.70) 2.39-4.2) 8. age.84) 2. 2005.09) 3.90 (2.00 (2.60) 8. 2002. chronicity of exposure.35 (2.80 (7.90-2.96) 2.0 (8. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.20-10.1 (11.51-4.10 (4. gender.4) 13. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.0 (9.45) 3. Many factors may be important in consideration of perchlorate action on the thyroid: dose.10 (1.0) 10.4 (11.10 (4.80) Selected percentiles ( 95% confidence interval) 50th 3.30) 3.75) 3.72 (3.93-5. U.8 (11.20) 3.S.S.Perchlorate inhibition (RUI).02-4.05 (4.EPA.46 (3.40) 17. 1999. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.40 (3.50-3. Steinmaus et al.0 (11.7 (11..22 (2.S.40) 3.36 (8.0) 14.93) 3.00 (4.90-15.25) 5.70-15.74) 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 .26) 4.1-16.70 (4.58) 2.4-16.0-14.0) 4. 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.71 (5.0) 11..33-12.0) 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. During gestation and infancy. perchlorate is negative in most genotoxic assays (U.39) 2. 2002).70 (2.0 (8. thiocyanate.33 (7.0) 12.20 (6.1-22.56-3.0 (9.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.6-17.60-8.4 (10. in a representative sample of U.90-20.0 (11.98) 3.10-7.54 (2.20 (3. interval) 3.1-13.66) 3.25) 5.70-3.3) 11. 2007).16-3. 2000).22-4.42 (3.87 (5.60 (3.20-3.00-2.70) 10.50 (3.04-3.60-5. In the U.50) 9..15-12.02) 3.87) 7.0) 13.99-3.40 (4..2) 8.83 (5.4) 8.97-5.45-2.90-11.20 (4.19-6.00-11. Survey years 01-02 03-04 Geometric mean (95% conf.70 (2.0-14.20-3.09 (7.76-3.3 (10.20 (7.3) 8. Also.0) 12.21 (2.95 (2.56 (3. women with urinary levels of iodine less than 100 micrograms per day.46-13. However.40 (7.30 (6.89-3.90 (2.0-17.12 (6. Li et al.25) 5.6) 12.59) 3. levels and sufficient in most participants (Tellez et al.41-9. 2002.22-4.08 (3.3) 12.50) 6.50) 95th 12.10-3.1-14. 2005).33-6.44) 3.60) 10.40 (3.10 (2.53 (2. 2005.S.52 (8. dietary iodine intake. and the presence of other substances known to affect thyroid function (e.4 (11.0) 9.80 (4. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.54 (3.0) 12..46-4.00 (6.4 (8.1 (8.37-13. 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.61-5.51 (3.47) 2.52-9.12-2.90-9. Lamm and Doemland.81-3.34-3.0) 12.91) 4.S.20) 8.04-3.70-5.

Li Z. He X. Kelsh MA. Health Implications of Perchlorate Ingestion.gov/safewater/ccl/perchlorate/perchlorate. 6/2/09 Greer MA. Analysis of relative source contributions to the food chain. The effect of perchlorate. Benchmark calculations for perchlorate from three human cohorts. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Pirkle JL. Landingham CB.10(8):659-663. J Clin Endocrinol Metab 2005.htm.S. Buffler PA. Rutherford GW. Thyroid 2001. population.46(5):509.. Erratum in: J Occup Environ Med 2004. Environ Health Perspect 2007. Howd R. Environ Sci Technol 2006. Caldwell KL. thiocyanate.S. Perchlorate in the United States. et al. Environ Health Perspect 2002. Additional information about exposure and health effects is available from the U. National Academy of Sciences (NAS). Sesser DE. 2005). Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.17(4):400-407. Lawrence JE. and nitrate on thyroid function in workers exposed to perchlorate long-term. and environmental perchlorate exposure among residents of a Southern California community. Crump KS. Richman K. 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. Goodman G.114(12):1865-1871. Pirkle JL. Erratum in: Environ Health Perspect 2005. Low dose perchlorate (3 mg daily) and thyroid function. epa. Abarca CR. Lawrence J. Environ Health Perspect 2005. Lamm SH. J Expo Sci Environ Epidemiol 2007. Steinmaus C. Blount BC. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 .gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Kirk AB. J Occup Environ Med 2003. Gibbs JP. Mauldin JP.html and from ATSDR at: http://www. 2005.. 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. Cross M.atsdr. Blount BC. Dyke JV. Magnani B. Food and Drug Administration (FDA). Valentin-Blasini L. et al. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Pleus RC. Also. J Occup Environ Med 2000. 2001-2002. Doemland M.110(9):927-937. (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. Osterloh JD. Daaboul JJ. Jackson WA. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Pino S.41(5):409-411. Thyroid 2000. Blount et al. Neonatal thyroxine level and perchlorate in drinking water. National Research Council of the National Academies. Perchlorate Exposure of the US Population.fda. 2007).cdc. Environ Health Perspect 2006. Byrd D.html. Dasgupta PK.115(9):1333-1338. Crump KS. Li FX. Lamm SH.40(21):6608-6614. CFSAN/Office of Plant & Dairy Foods. Braverman LE. most of the population is considered to be below the U.gov/toxpro2. Lamm S. 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. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Chacon PM. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. et al. Barnard JC. Washington (DC): National Academy Press.42(2):200-205.EPA at: http://www. Skeels MR.113(8):10011008. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. May 2007. Braverman LE.. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Pino S. 2005). Primary congenital hypothyroidism. Lamm SH.11(3):295. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Braverman LE. Osterloh JD. Available at URL: http://www. newborn thyroid function. Greer SE. Valentin-Blasini L.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Lau EC. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Deyhle GM. et al.S. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. EPA reference dose (Blount et al. References Blount BC.113(11):A732. Miller MD.90(2):700-706.45(10):1116-1127. Tellez RT.

EPA). Available from URL: http://cfpub. Revised 2/11/05. U. Doc. Environmental Protection Agency (U.S.S. Perchlorate as an environmental contaminant.1/15/06 U. 246 Fourth National Report on Human Exposure to Environmental Chemicals . Perchlorate.S.S. Environmental Protection Agency (U. Urbansky TF.9(3):187-192. 1988. cfm?substance_nmbr=1007. EPA). Environ Sci Pollut Res Int 2002. No.Perchlorate pregnancy and the neonatal period.gov/iris/quickview. Integrated Risk Information System (IRIS). Drinking Water Contaminant Candidate List. Thyroid 2005.15(9):963-975. EPA/600/F-98/002 Washington (DC).epa.

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

2003). 2004. The PFCs often measured in human serum are listed in the table. PFOA is mostly excreted in the urine in animal studies.. 2004. environmental fate. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al.. approximately 4.. C6. 1990). and in offspring. may metabolize or degrade to PFOA (Dinglasan et al. 2002.S. 2005).. the 8-2 telomer. 2003). heptadecafluoro-1-decanol. 2004. Survey Geometric mean (95% conf. peroxisomal proliferation. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al.S...... 2007a).8 years (Olsen et al. Lau et al. Unlike many organohalogen contaminant chemicals.. in a wide variety of marine and land animals (Kannan et al. Olsen et al. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins.. Lau et al. and in human blood and semen (Calafat et al. PFOA has been reported to cause liver. endocrine and immune effects. The elimination half-life of PFOA in humans is roughly estimated to be 3... Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Some of the effects in animals may be mediated through peroxisomal proliferation. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. Vanden Heuvel et al. but probably include dietary sources (Kannan et al. 2006a. 2003. Serum Perfluorobutane sulfonic acid (PFBuS) 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... 2005. All sources of human exposure are uncertain. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. U. For instance.4.5 years and for PFOS.. 2004).. Excepting PFOS and PFOA. 2004. 2005). C7). growth retardation and delayed sexual maturation (Kennedy et al. 2005. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. 2004). Tittlemier et al. 2000. there is limited information on the sources. Guruge et al. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. Keller et al. Kannan et al. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. 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.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). but still can have long residence times in the body. In some cases... PFCs have been identified in surface coastal and ocean waters (Yamashita et al. 2005. in part. Bookstaff et al. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al.. 2003a and 2004a). human toxicokinetics. Taniyasu et al. 2006. and β-oxidation of lipids (Kudo et al. C5. EPA.. 1995. which may vary for some chemicals by year and by individual sample.. including immunologic effects and tumor induction. kidney.. It is unclear if environmentally degraded telomer products are a major source of other PFCs. < LOD means less than the limit of detection.e. pancreas. by high protein binding in plasma and other proteins. 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. or effects of other PFCs. 248 Fourth National Report on Human Exposure to Environmental Chemicals . Prevedouros et al... 1993). 2005). population from the National Health and Nutrition Examination Survey. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. hepatotoxicity. 2007). thymus and spleen.

800 (. U. 2003a.3. 2007b). population from the National Health and Nutrition Examination Survey...00 (.700) .. 2003a.500-1. 2003. population. Olsen et al. and there was no clear evidence of excess all-cause or diseasespecific mortality.500 (<LOD-1. 2007..900 (.. 1999.300 (<LOD-.300-1..400) . hepatotoxicity.500-3. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. Olsen et al.10) . 2001.500) .800) 1. reproductive. and changes in thyroid hormone concentrations (Grasty et al. monkeys.50) . 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.108 times higher than background serum levels in humans (Butenoff et al.400 (<LOD-. 2004).. 2003). possibly related to lung immaturity (Lau et al.. PFOS. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. Fei et al. 2007a..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 . the potential to estimate risks to humans from animal doses is uncertain. 2003.800) 1.80) 485 538 962 Limit of detection (LOD. 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.80) 640 1454 03-04 03-04 * * < LOD < LOD .500-1. see Data Analysis section) for Survey year 03-04 is 0. In comparing three separate reports on adults.. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years.800 (.400-1. development in offspring was stunted and hypothyroxinemia was observed. 2007a.00) . and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. Cook et al. In such studies..500) .600 (. Lau et al. and humans.. At high but non-toxic maternal doses of PFOS. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality..400-1. Thibodeaux et al. 2003a).800 (. 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. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U..S. 2007b.700 (. 2007). A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. However.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. perfluorohexanesulfonate (PFHxS).600-2.. developmental and teratogenic effects were demonstrated in offspring.. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.400 (<LOD-.400-1. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al.500 (. Kennedy et al.10) * 03-04 03-04 * * < LOD < LOD < LOD . PFOA. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400-1.500-1. PFOS. 2005). At doses causing maternal toxicity.20) .40) .00) . 2005).. or increased cancer rates (Alexander et al.400 (<LOD-. 2003a)..600 (. 1992. thyroidal).900 (. 2003). 2003. Animal studies of PFOS have demonstrated weight loss. Survey Geometric mean (95% conf. 2004. Olsen et al.800 (. EPA.500-1.400-1.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . EPA.500) 90th . Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.500) . animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.10) . 2004b). 2003a. 2004). PFOA. Harada et al.900 (. 2003).S.S. 2004a.500) . U.400-. which may vary for some chemicals by year and by individual sample.300 (<LOD-.300 (<LOD-.500-.S. Fourth National Report on Human Exposure to Environmental Chemicals 249 ..400-. 2004. interval) Selected percentiles ( 95% confidence interval) Sample 95th .10 (.600 (..00) .500 (. elderly and children. < LOD means less than the limit of detection.

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

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. < LOD means less than the limit of detection.300-.S. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0.500) 485 538 962 Limit of detection (LOD.300 (<LOD-.400 (<LOD-. 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 year 03-04 is 1. Fourth National Report on Human Exposure to Environmental Chemicals 251 .Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400 (<LOD-. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500-. population from the National Health and Nutrition Examination Survey.300 (<LOD-.500 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.3.600) < LOD .900) < LOD . which may vary for some chemicals by year and by individual sample.400) .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 . interval) Selected percentiles ( 95% confidence interval) Sample 95th .0.400 (. population from the National Health and Nutrition Examination Survey.600 (. < LOD means less than the limit of detection.

50 (2.03) 1.70-2.70-7.20-3.30 (2.900 (.900-1.40-1.60) 9.30 (1.3.08) 2.90) 90th 5.30) 3. see Data Analysis section) for Survey year 03-04 is 0. interval) .60 (1.90) 8.86 (1.809) 1.50 (4.77-2.984 (.963 (.00) 2.90) 1.70 (2.835-1.70-5.80-7.900-1.20 (6.50) 6.00-7.900-1.5) 8.20 (1.87-2.90 (1.10) 4.900) 1.67-2.50-10.10) 1053 1041 03-04 03-04 03-04 .Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.30 (7.72 (1.80) 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 1.912-1.S.80-3. population from the National Health and Nutrition Examination Survey.00) 1.20) 2.20-1.90 (1.00) 1.10) 6.90) 1.50 (6.30 (3. 252 Fourth National Report on Human Exposure to Environmental Chemicals .50-6.10) 8.834-1.20-1.50-6.50 (1.40-1.30-12.00 (2.30-2.00 (1.861 (.S.50 (4.60-2.586-.90-2.54) .16) .10) 4.10) 75th 3.60-4.80-8.00 (.70) 1. Survey Geometric mean (95% conf.80-12.10-9.40 (1.80 (4.10) 1.900-1. Survey Geometric mean (95% conf.90) 3.90-19.70 (1.20) 03-04 03-04 2.80 (1.44 (2.700-1.17 (1.60-3.60-3.40) 640 1454 03-04 03-04 1.40) 4.00 (1.40 (2.90 (1.50 (6.80) 90th 2.30 (2.50) 2.40 (1.90 (4.70) 1.91) 2.40) 640 1454 03-04 03-04 2.20 (1.42 (1.00) 3.20 (6.04) .10) 5.20) 485 538 962 Limit of detection (LOD.600-.26) 2.900-1.30 (1.20 (1.60-4.30 (6.14 (.70-6.3 (9.00 (5.1) 485 538 962 Limit of detection (LOD.697-1.10-9.20) 1.0) 8.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.70) 2.05-2.90 (2.816-1.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.60) 3.40) .80) 5.900 (.80-4.00 (1.80-4.70-10.10) 1.80-4.20-1.10) 75th 1.20 (1.27) 1.20) 1.92 (1.80) 4.50) 2.60 (1.40 (1.826-1.00 (.80-8.966 (.70) 2.700 (.20) .50 (1.30 (1.10 (1.72) 1.70) 13.80-2.10 (4.10 (.6) 7.721-1.5) 5.01 (1.90 (1.80) 3.800 (.80-7.60) 2.30) 3.93 (1.80 (1. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50 (1.00-8.50-3.51) 1.0) 1053 1041 03-04 03-04 03-04 1.60-8.20-2.60) 1.90) 1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.00-6.20-1.800-1.852 (.30) .56-1.900-1.70-2.10 (.00 (1.10 (4.40-3.90-10.10) 6.17-1.30-6. population from the National Health and Nutrition Examination Survey.60-7.1.60-2.40 (1.60 (6.30) 3.40) 1.40) 1.40) 2.09 (.70) 3.80-3.30 (1.80-6.60 (1. see Data Analysis section) for Survey year 03-04 is 0.30-9. interval) 1.60-2.00-1.689 (.10 (.10-5.62-2.30) 03-04 03-04 .12) .73-2.90 (4.00-1.50 (1.

30-6.6) 21.5-33.5) 57.1) 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 4.8 (34.80-4.3-61.60-13.30-8.6 (44.65-4. see Data Analysis section) for Survey year 03-04 is 0.4 (17.0 (27.6) 42.7 (43.5) 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 21.6-50.3) 42.5 (28.07-4. see Data Analysis section) for Survey year 03-04 is 0.50 (4.4) 75th 30.4) 21.9-38.8) 27.60) 8.40) 75th 5.30 (3.5) 19.7-23.0) 36.40-14.0-70.60 (3.9 (22.3 (44.7-69.50 (3.0) 21.80 (7.2-57.00 (5.4) 56.0) 23.5) 18.8-22.90 (7.7 (19.8-35.3) 41.1-35.90 (7.40-6.40-17.50) 4.6 (35.5 (28.7 (35.6) 35.40 (6. Survey Geometric mean (95% conf. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20-4.3 (17.70-7.70 (5.80 (6.99-3.10 (6.90) 6.1-24.60-14.80-9.7 (7.10) 5.20-5.4 (28.70-5. interval) 20.50-13.6) 62.00) 3.2-22.20) 10.96 (3.4) 20.2 (28.3 (28. population from the National Health and Nutrition Examination Survey.70) 4.8) 46.60 (5.6-45.90 (7.4-42.80-12.70 (5.9) 22.11 (2.9 (19.4) 640 1454 03-04 03-04 23.60 (6.7-33.91) 3.7-49.30 (5.20) 7. interval) 3.5) 8.6 (19.4 (23.5) 9.5) 32.5-23.50-6.2 (21.30) 6.0-16.53) 3.60) 03-04 03-04 3.20) 4.1.8-81.70-10.10 (3.6) 9.67-4.8-78.60 (7.60 (4.20) 5.8-30.9) 9.3) 485 538 962 Limit of detection (LOD.3) 28.7) 39.20) 5.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.40) 3.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.00 (3.79) 4. Fourth National Report on Human Exposure to Environmental Chemicals 253 .30) 7.90 (5.6) 18.20 (4.1) 57.4-25.95 (3.1) 15.4.40-10.9) 27.0) 43.0) 03-04 03-04 19.1 (19.80 (6.8 (45.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.0) 485 538 962 Limit of detection (LOD.84-3.50) 7.40-6.8 (37.1 (24.80 (5.30 (3.50-4.70) 3.85-4.4 (19.0-66.90-4.20 (4.1-25.82) 4.6) 7.0 (20.2 (16.2 (19.3 (35.6-24.20-9.2 (18.5-62.10-3.S.10 (3.9 (13.2) 30.1-33.18 (3.21-3. population from the National Health and Nutrition Examination Survey.0-20.7 (43.8-22.60 (6.35) 3.70) 6.40) 5.70 (3.6) 1053 1041 03-04 03-04 03-04 3.2) 640 1454 03-04 03-04 4.2) 45.9-19.00 (5.0) 21.9-23.70-7.5) 1053 1041 03-04 03-04 03-04 14.70-9.4-17.40) 90th 7.8) 32.2 (27. Survey Geometric mean (95% conf.60-9.3-22.47-4.0) 90th 41.1-36.8-22.89 (3.6 (42.90-12.90-4.3 (35.40 (4.S.27) 4.9) 22.1-52.30-5.80) 8.30-11.20) 7.7-53.7 (13.4 (19.1 (23.60-6.5) 7.7 (35.7-30.2) 30.5-21.30-3.47 (4.9 (17.37 (2.

300-.300 (.300) .200 (<LOD-.300 (.500) 485 538 962 Limit of detection (LOD.300) . < LOD means less than the limit of detection.500) < LOD 485 538 962 Limit of detection (LOD.300-.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .300) .200-.300 (. which may vary for some chemicals by year and by individual sample.300) . population from the National Health and Nutrition Examination Survey.200-.400 (<LOD-.300-.300-.300) .Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (.300 (.200-.200-.S.200-.300 (.200-.500) .200-.300 (. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. see Data Analysis section) for Survey year 03-04 is 0.300 (. 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. Survey Geometric mean (95% conf.500) .200-.300 (.200-.200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 254 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample.300 (.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300) .500) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2.300 (. see Data Analysis section) for Survey year 03-04 is 0.400) 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 .300 (.300 (.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.300) .

10) 1.600 (<LOD-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 .30) .00) < LOD .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 .30) 1. see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey.40) 1.50 (1.700 (<LOD-.40) < LOD < LOD .3.600) . see Data Analysis section) for Survey year 03-04 is 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (<LOD-.10) 1.90) . population from the National Health and Nutrition Examination Survey. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20) 1.10-1.300 (<LOD-1.S.600 (<LOD-1.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.300 (<LOD-.700 (<LOD-.700 (<LOD-.700) 1.900) 1.10-1.400 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700) 90th 1.30 (1.10) .6. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.20 (1.10-1.00 (.00 (.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 255 .900-1.50 (1.20-1.900-1. which may vary for some chemicals by year and by individual sample.900) .800) .700 (<LOD-2.60) 485 538 962 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (1.00 (.900 (<LOD-1.30 (1.10) * 03-04 03-04 * * < LOD < LOD .30 (1.800) .10 (.00 (. Survey Geometric mean (95% conf.600 (<LOD-.900-1.900-1.600 (<LOD-1. < LOD means less than the limit of detection.70) 1.700) .80) 1.700 (<LOD-.10-1.900-1.900-1. < LOD means less than the limit of detection.10 (.10) .300-2.700 (<LOD-.800 (<LOD-.S.10 (.900 (.00-1.10-1.900) 485 538 962 Limit of detection (LOD.400 (<LOD-1.900-1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .30) 1.60) 640 1454 03-04 03-04 * * < LOD < LOD . which may vary for some chemicals by year and by individual sample.500 (<LOD-. Survey Geometric mean (95% conf.80) 1.700) 1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .

115(11):1670-1676. Edwards EA. Moore JA. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Environ Health Perspect. Murray SM. Perkins RG. Caudill SP. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Inoue K. Seacat AM. Mandel JH.60(1):44-55. Chem Biol Interact 2000.113(2):209-217. Kuklenyik Z. Environ Sci Technol 2006a. Jarnberg U.39(3):363-380. Moore RW. Environ Sci Technol 2004. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Saito N. Environ Sci Technol 2004. Reidy JA. et al. Kawashima Y. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Rodricks J.7(4):371-377. Polyfluoroalkyl chemicals in the U. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Keller JM. Kannan K. Environ Sci Technol 2005. Kuklenyik Z. Bookstaff RC. Halden RU. Frame SR. Toxicol Appl Pharmacol 1995. Frame SR. Biegel LB. et al. Falandysz J. and ex vivo studies. Calafat AM. Morikawa A. Kuklenyik Z.1968--2003. Harada K. Crit Rev Toxicol 2004.124(2):119-132. Evans TJ. Environmental and toxicity effects of perfluoroalkylated substances.34(4):351-384. Biegel LB.39(23):9057-9063. Katakura M. Reidy JA. Gaylor DW.99(2):253-261. Olsen J. Laane RW.115(11):1596-1602. et al. Hurtt ME. Hurtt ME. Kannan K. Mohotti KM. Environ Res 2005. Hurtt ME. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. et al. Yoshinaga T.S. O’Connor JC. Seneviratne HR. Toxicol Appl Pharmacol 1990. 256 Fourth National Report on Human Exposure to Environmental Chemicals .38(17):4489-4495. Caudill SP. Environ Sci Technol 2007a. Inoue K. Peterson RE. Kuklenyik Z. Grasty RC. J Occup Health 2004.60(10):722729.39(23):9101-9108. Aguilar-Villalobos M. Chlorinated. Calafat AM. Kennedy GL Jr.39(1):80-84. Mabury SA. Saito N. Burris JM. 2007b. Olsen GW. Toxicol Appl Pharmacol 1992. Witter FR. Reidy JA. Dinglasan MJ.68(6):465-471.S. Environ Sci Technol 2005. Characterization of risk for general population exposure to perfluorooctanoate. Calafat AM. Tully JS. Herbstman JB. Day RD. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Mandel JS. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat.41:2237-2242. Arendt MD. Rev Environ Contam Toxicol 2003. Liu RC. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Ingall GB. Bandai N. Tarone RE.38(10):2857-2864. Kannan K. McLaughlin JK. brominated. Harada K. Environ Health Perspect 2007. The toxicology of perfluorooctanoate. Needham LL. Holmstrom KE. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Suzuki E. in vivo. Kamiyama S. Guruge KS. and perfluorinated contaminants in livers of polar bears from Alaska. Olsen GW. Fillmann G. Perfluorinated chemicals in selected residents of the American continent. Apelberg BJ. Cook JC. Yamashita N. Fei C. Wong LY. O’Connor JC. Koizumi A. Kudo N. Yun SH. Calafat AM. Sasaki S. Environ Health Perspect 2007. Reidy JA. Occup Environ Med 2003.46(2):141-147. J Environ Monit 2005. et al. Needham LL. Olsen GW. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Yoshinaga T.179:99-121. Bignert A. Wijeratna S. Kumar KS.115(11):1677-1682.63:490496. Corsolini S. de Voogt P.134(1):18-25. Needham LL.40:21282134. Grey BE. Cook JC. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Watanabe T. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Mandel JH.104(2):322-333. Taniyasu S. Hekster FM. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Cook JC. Chemosphere 2006b. et al. Regul Toxicol Pharmacol 2004. et al. Fluorotelomer alcohol biodegradation yields poly. Environ Sci Technol 2005. Birth Defects Res B Dev Reprod Toxicol 2003. Lau CS. Taniyasu S. Calafat AM. Toxicol Sci 2001. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility.Perfluorochemicals References Alexander BH. Ye Y. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Tully JS.Koizumi A. The influence of time. Butenhoff JL.and perfluorinated acids. Loganathan BG. Rogers JM. Yamashita N. Butenhoff JL. Needham LL.

Rogers JM. and perfluorooctanoate in retired fluorochemical production workers. Prevedouros K. Burris JM. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Zobel LR.111(16):1900) Olsen GW. fast foods. A global survey of perfluorinated acids in oceans. Burris JM. Hansen KJ. Lundberg JK.74(2):382-392. Olsen GW. fate and transport of perfluorocarboxylates.epa.1177(2):183-190. 2007a. Froehlich JW. Toxicol Appl Pharmacol 2004. Mandel JH.115(9):1298-1305. U. fish. and humans from Japan.74(2):369-381.) Tittlemier SA. Miller JP. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Mandel JH. II: postnatal evaluation. Sources. Environmental Protection Agency (U. Historical comparison of perfluorooctanesulfonate. Lau C. et al. The developmental toxicity of perfluoroalkyl acids and their derivatives. Hansen KJ. Grey BE. Seymour C. Hansen KJ. Sterchele PF. van Belle G. Butenhoff JL. Olsen GW. Burris JM.S. Mandel JH. Reagen WK.111(16):1892-1901.41(9):799-806. Yamashita N. Olsen GW. Available from URL: http://www. Yamashita N. Horii Y. Environ Sci Technol 2006. 2003. Rogers JM.2(1):53-76. Church TR. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Barbee BD. Hanson RG. Toxicol Sci 2002. Environ Health Perspect 2003a. Bronson R. et al.82(1):359. Toxicol Sci 2003. Thibodeaux JR. Ehresman DJ. Olsen GW.55:3203-3210.37(12):2634-2639.. Butenhoff JL. Hansen KJ. Rogers JM.Perfluorochemicals Kudo N. Cousins IT. Horii Y. perfluorooctanoate andother fluorochemicals in human blood. Church TR. Biochim Biophys Acta 1993. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Richards JH. Peterson RE. Chemosphere 2004a. Butenhoff JL.45(3):260-270. Thibodeaux JR. J Ag Food Chem 2007. Environ Health Perspect. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Lau C. Stanton ME. Nesbit DJ. EPA). Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Cao XL et al.54(11):1599-1611.40(1):32-44. Kannan K. Ellefson ME. Lundberg JK. et al. Taniyasu S. Petrick G. Gamo T. Environ Health Perspect 2005. (Erratum in: Environ Health Perspect. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Burris JM. J Occup Environ Med 2003b. Kannan K. Burlew MM. Olsen GW. Moisey J. Church TR. Huang HY. Washington. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. J Occup Environ Med 1999. Grey BE. Hansen KJ. Seacat AM.26(1):47-51. Thomford PJ. 2003a. Kawashima Y. Biol Pharm Bull 2003. Seacat AM. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Chemosphere 2007b. (Erratum in: Toxicol Sci 2004. Case MT. Mair DC.68(1):249-264. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Butenhoff JL.gov/opptintr/pfoa/pfoara. Olsen GW. Burris JM. birds. I: maternal and prenatal evaluations. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Half-life of serum elimination of perfluoroo ctanesulfonate. Hanari N. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. et al. Mar Pollut Bull 2005. Environ Sci Technol 2003.S. and food items prepared in their packaging. Korzeniowski SH. Olsen GW. Ehresman DJ.198(2):231-241. Olsen GW. Hanson RG.68:105–111. Toxicol Sci 2003.perfluorohexanesulfonate. fish.113(5):539-545. et al. htm. Butenhoff JL. Helzlsouer KJ. Larson EB. J Children’s Health 2004b. 1/15/06 Vanden Heuvel JP. Butenhoff JL. Mandel JH. et al. Taniyasu S. Pepper K. Buck RC. Coordinate induction of acyl-CoA binding protein.51(8-12):658-668.

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

Assessment of critical exposure pathways.. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Herbert AR. 2005. In Staples CA (ed). dibutyl phthalate (DBP). at very high levels. ovarian abnormalities in the female animals (Jarfelt et al. Vol.. Springall C. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al.gov/ reports/index. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.45:19-25. Schroeder JL. and Sertoli cell abnormalities in the male animals and. 2000a. In animals. which may be a pathway to the development of liver toxicity and cancers in these animals.. 2004. 2000c. 2004. Anderson WA.Phthalates and metabolites have been tested. Also. J Chromatogr B 2004. Massey RC. testicular atrophy. Clark K.. efficiency of intestinal absorption. variation also occurs in the same person during repetitive monitoring (Fromme et al. Springer. However. The Handbook of Environmental Chemistry. and extent of metabolite conjugation to glucuronide (Albro et al. Mackay D. Needham LL.cdc. 2001).. 1982. at higher doses. Hoppin et al. The monoester metabolites are thought to mediate toxic effects for some of the phthalates.atsdr. reducing estrogen production. Matthews HB. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. Slakman AR. atsdr. 2004. Part Q: Phthalate Esters.html. Sauer MJ. Lovekamp-Swan and Davis. These differences may contribute to species-specific differences in toxicity (ATSDR. 2002). environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. Cousins IT.... and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. Connor C. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. 2002. McKee et al. 2003.805:49-56.html).. 2001. Silva MJ.gov/toxprofiles/ tp135. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites.html..18(12):10681074. Hauser et al.gov/ toxprofiles/tp9. 2003. Hauser et al. 227-262. van der Broek PH. Available at URL: http://www.. phthalates have been shown to induce peroxisomal proliferation in rodents. 2007. Jongeneelen FJ. 2001. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . Albro PW and Lavenhar SR. Evaluation of a recombinant yeast cell estrogen screening assay. Dirven HA.e. Information about external exposure (i. Available at URL: http://www. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. 2007). Population estimates of concentrations of specific phthalate metabolites may differ by age. 2006). Castle L.21:13-34.niehs.. Coldham NG. 2006).gov/toxpro2. 1986). effects that may be mediated by inhibiting testicular and ovarian steroidogenesis.. NTP-CERHR. Jordan S. Kessler et al. Corbett JT. High doses of di2-ethylhexyl phthalate (DEHP). 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.3. pp. 1985. 2004.atsdr. 2002). but there are known species-related differences in the hydrolysis of diester phthalates. Calafat AM. 2005). Metabolism of di(2-ethylhexyl) phthalate. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. gender.html. 2000b. 2004). 4/20/09 Albro PW. Food Addit Contam 2001.. 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.New York. Environ Health Perspect 1982. and race/ethnicity (Silva et al. Environ Health Perspect 1997. Toxicological profile for di-n-butyl phthalate update [online]. Dave M. 1982). Scotter MJ. Silvapathasundaram S.cdc. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.. 105:734-742. Peck and Albro.nih. Drug Metab Rev 1989. phthalates produced anti-androgenic effects by reducing testosterone production and. Rhodes et al. McDonnell DP.cdc.. interactions with macromolecules and species differences in metabolism of DEHP. 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. Pharmacokinetics.

White R. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Drexler H. Research Triangle Park (NC). 6/2/09 NTP-CERHR. Park S. Lovekamp-Swan T. Butala JH. McKee RH. Available at URL: http://cerhr. Ladefoged O. Research Triangle Park (NC). Baird DD.11(5):381-387. Available at URL: http://cerhr. Hum Reprod 2007. Parker MG. Akesson B. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Sumpter JP. Hass U.22(3):688-695. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Zhang S. Giwercman A. Dalgaard M.html. Hauser R. Andersson A-M. Hartle RW.106(1):23-26. Stringer WT. Henttu P. Davis BJ.gov/chemicals/ phthalates/dbp/dbp-eval. Suzuki T. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro.19(4):505-515.46(11):643-647. Kalita JC. Grote K. Liss GM.nih. Ryan L. Environ Health Perspect 2003.nih. Balasubramanian AV. Environ Health Perspect 1998. Singh NP. David RM. Jarfelt K. Hauser R. 6/2/09 Okubo T. 6/2/09 NTP-CERHR. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Tsukino H. Gans G. Available at URL: http://cerhr. Ryan L. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Biol Pharm Bull 2003. Epidemiol 2005. Brock JW. Reproducibility of urinary phthalate metabolites in first morning urine samples.382:10841092. Environ Health Perspect 1995. Leffers H. 2000b [online]. Yoshimura M. Skakkebaek NE. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].25(2):293-302. Richthoff J. Reynolds T. Jobling S. Urinary phthalate metabolites and biomarkers of reproductive function in young men. The estrogenic activity of phthalate esters in vitro. Rylander L. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Borch J. Hanaoka T. Reprod Toxicol 2004. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.html. Jonsson BAG.16(4):487-493. Yokoyama Y.nih. Environ Health Perspect 1997. Sumpter JP.niehs. 2000c [online]. et al.105:802-811.210:21-33. Calafat AM.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Scand J Work Environ Health 1985. Silva MJ.html.112(17):1734-1740. Reprod Toxicol 2005. Park MG.niehs. Harris CA. Duty SM. Determination of phthalate monoesters in human milk. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. 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 . et al. Csanády G. Jacobsen H. Meeker JD. Silva MJ.gov/chemicals/dehp/dehp-eval. Toxicol Appl Pharmacol 2004. Calafat AM. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Research Triangle Park (NC).111(2):139-145. Wang P. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic.nih. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Mortensen GK.195:142-153. Available at URL: http://cerhr. Albro PW. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). consumer milk. Meeker JD. Hoppin JA. 6/2/09 NTP-CERHR. Hagmar L. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP).26(8):1219-24.110(5):515-518. Kano K. Angerer J. Am Ind Hyg Assoc J 1985. NTP-CERHR. Davis BJ. Numtip W. Nielsen J. and infant formula by tandem mass spectrometry (LC-MS-MS). Environ Health Perspect 2002. Kano I. Bolte G.103:582-587. Fromme H. et al. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Boehmer S. Mechanisms of phthalate ester toxicity in the female reproductive system. Brock JW. Main KM. Pan G. Kessler W. Int J Hyg Environ Health 2007. Chahoud I.html. Research Triangle Park (NC). Filser J.112(17):1740]. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.18(1):122. Environ Health Perspect 2004. Anal Bioanal Chem 2005. Chen Z. Duty S. Int Arch Occup Environ Health 1993. Skerfving S. 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Meek MD. Environ Health Perspect 1982.46:282-293. Peck CC. Wu ZF.65:299-308. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Clemons JH.112(3):331-338. Abbott BD. Batten PL. Environ Health Perspect 1986. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Cunningham ML. 112(5):A270]. Crit Rev Toxicol 2006. Orton TC. Klinefelter GR. Environ Health Perspect 2006. Bratt H.S. Fielden MR. Caudill SP. Malek NA. et al. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Environ Health Perspect 2004. Ostby JS. Toxicol Sci 1998. Urinary levels of seven phthalate metabolites in the U. Parks LG. Silva MJ. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man.45:11-17. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Hodge CC. Lambright CR. et al. Barr DB.114(11):1643-1648. Rusyn I. Barlow NJ. Peters JM.58:339349. Matthews JB. Albro PW. Zacharewski TR. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Fourth National Report on Human Exposure to Environmental Chemicals 261 .Phthalates phthalate (DEHP): a cross-sectional study in China. et al.36:459-479. Jackson SJ. Pratt IA. Toxicol Sci 2000. Reidy JA. Rhodes C.

9-16.3 (30.2-33.8 (80.2-19.8 (28.7-16.5-25.8-18.0-26.6-92.. can produce developmental and reproductive toxicity in rodents.8.0 (20.8 (38.7) 38.7-58.3 (29. IARC considers BzBP not classifiable with respect to human carcinogenicity.8) 14.9-49.6) 95th 103 (94.1) 12.9) 12.8-13.4 (53.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.1-18.6-39..6 (41.0 (43.2) 78.0 (33.9-62.6-38.9 (16.6-43.6-18.7-82.0-106) 58.0) 16.1-43.2-116) 122 (102-143) 101 (84.1 (14.8-35. 2000).1 (20.S.9 (28.8 (10.9) 11.8 (86.2) 13.1 (13. vinyl tile.2) 22.8) 28.2) 12.3 (33.5) 55.5) 65.2 (14.6-17.2-38.4) 38.1-61.4-16.7 (82.0) 20.7-17.6-132) 103 (84.3 (44.2-183) 101 (78.9) 18. car care products.0 (11.8-98.9 (70.1-35.3) 23.4) 98.5-97.9-47.6) 29.1 (55.9 (39.3-74.6-72. because it is not bound to products in which it is incorporated.5 (55.4) 71. residents (Blount et al.4) 129 (98. 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.0) 90th 67.5 (61.1 (19.6) 50.4-92. it can be released into the ambient air during use or disposal of the products.3) 15.6) 25.9-30.7-170) 169 (134-198) 152 (99.2 (43.1-15.2-40.5) 30.8 (30.9 (22.3-34.6-92.6 (12.3-161) 99.4) 12.3) 13. High dose BzBP and its monoester metabolites.6) 67.4) 51.5-35.8-121) 79.6) 13. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (30. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives. 2004.1 (10.1-116) 122 (93.6) 37.5) 82.2) 33.3-125) Total 15.0 (15.2 (47.5-14.6-79.4) 65.9-27. and 0.4-24.1.2) 14.5) 15.4) 49.5 (66.1-39.4) 35.8-14.8) 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 16.8 (53.1) 31.6) 35.6 (66.9-28.0) 24.9 (11.3.2-155) 91.3 (13.2 (10. respectively.0) 70.4) 14.4) 81.3-43.7 (15.8 (12.8 (71.0 (34.5-41.3 (22.8-17.8 (21.3) 54.5 (26.3-75.8-17.5-33.1-38.4-120) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 13.0) 32.2-39.7-35. including MBzP.3 (12.4 (48.0 (30.4 (29.4 (59.0 (26.5) 16. BzBP can be released into the environment during its production and.5) 27.6 (21.6 (13.5-36.5) 15.1) Selected percentiles ( 95% confidence interval) 50th 17.2) 17.6) 63.6 (53.S.7-14.9) 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 39.5 (13.3-130) 122 (88.0-85. NTPCERHR.5-40.2-31.8-133) 89.1) 13.8-41.8-16.1) 67.8-16.6) 14.7-15.9-14.8 (50.3-27.4) 80.8) 63.8-72.4-15.5 (27.1) 29.1) 76.3-82.6-116) 122 (102-142) 101 (85.6 (13.6) 35.1-16. 2000).3) 37.6 (32. 262 Fourth National Report on Human Exposure to Environmental Chemicals .7-25.1) 32. and to a lesser extent.7-119) 99. and diet is the major source for general population exposure.4 (13.4 (68.0 (55.4 (31. sealants. some personal care products.4-127) 80.3 (12. and 03-04 are 0.6) 24.4 (32.Phthalates Benzylbutyl Phthalate CAS No.9-190) 86.0) 23.1 (58.2) 69. and 2003-2004 were generally similar those reported in U.2-16.1) 14.8-76.3) 94.2-115) 113 (91.2 (19.5-145) 138 (106-241) 143 (127-179) 120 (99.4 (10.1-16. interval) 15.3-91.6) 13.8) 33.7 (51.7 (53.4 (32.3 (29.3-18.4 (53.6-29.7 (13.0 (27.5-18.8-48.9 (12.3) 13.3-88.6 (13.2 (19.6) 15.4) 108 (96.5-36.8-64.7-172) 103 (74.1 (32.7) 23.1 (13.2) 15.9) 14.4) 33.5-62.5-84.5 (76.3-21. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.9) 13.4 (63.4) 35.4-25.7 (80. 01-02.3 (12.6) 14.4-62.9 (21. 0.3-12.6) 16.1-15.9) 15.9) 43.1 (14.1-120) 52.2) 32.2) 66.4 (27.9) 14. Food crops take up BzBP.4 (10. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.3) 63.8-14.1-90.6-150) 94. see Data Analysis section) for Survey years 99-00.8 (14.0-55.3-18.5 (67.7 (12.1) 68.9 (12.6 (13.2-17.2-16. 2001-2002. particularly male animals (McKee et al.7-16.7-16.9 (13.8) 24.7 (11.0 (12.0) 33.2) 14.1-214) 166 (116-191) 145 (110-213) 88.2-20.5) 23.4) 75th 35.7-13.2 (25.9-87.7 (70.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7) 40. population from the National Health and Nutrition Examination Survey.5-94.0 (23.9) 49.0 (14.0-130) 101 (86.8 (71.5 (57.0 (15.2 (11.5 (47.0) 34.3 (54.

DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.2-13.6-86.4-42.9-69.8) 16.0) 60.9) 52.9) 12.1-35.7 (59.7-20.0 (13. 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.2-57.4) 14. and in a small sample of German residents (Koch et al.7 (55.7 (12.8-42.9) 64..9 (24.0-109) 65.5-16.5-13.5 (10.7-14.0 (67.1) 142 (99.2-51.4) 104 (89.8 (69.6-99.8-13.1-79.4) 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. in men attending a Boston infertility clinic (Duty et al.9 (12.1 (21.8-69.5-26.9-83.7-123) 77. A small study of African-American women in Washington.4-99.4) 51.9) 24. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.4 (12.4) 25.1-12.1-27.7 (13.6) 30.0 (12.3) 18.4) 12..9 (10.0 (10.2) 15.69-11.6 (36.8-60.9-104) 62.1-14.6 (14.8-15.7 (13.8) 108 (75.0) 24.3-64.2) 67.6-13. Weuve et al. 2004.8) 33.0-48.9 (43.3) 13. 2003).6) 13.5-79. 2006).4) 60.0) Selected percentiles ( 95% confidence interval) 50th 13.7 (11.3) 16.4-93.2-15.3 (38.5) 78.2) 26.6-40.7 (18.3-11.6-116) 74.1 (34.7 (19.3) 14.8-34.7) 19.4-102) 70.3) 14.9 (51.5) 10.0 (62.1 (43. Hauser et al.9 (12.Phthalates York City (Adibi et al. 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.5 (42.4 (34.3) 29.8) 11.0 (41.4 (69.4) 21.2-15.7 (38.8 (11.5 (56.8 (30.9-28.9 (22.4 (10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2002).3) 13.9-16..3) 37. interval) 14.6 (11.1 (21.1 (14.6-15.8-27.4-116) 73.6) 53.7) 25. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.7-31.4) 15.0 (33.4-17.0-53.4-15.4-142) 134 (116-176) 136 (85.4 (46.3 (15..9 (54.3) 13.6-20.4 (74.8) 34.6 (30.6) 12.2-78.4 (26.6-81.5) 17.8-80.3) 21.7-15.1) 39.8-64..0) 24.8 (64.3 (24.8) 71.2 (27.1) 17.5-42.3) 73.5 (12.4) 13.0) 13.8 (49.0 (12.4 (11.5) 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 .4 (11.4-27.8-15.8) 15.8 (50.1 (21.5-26.9-40.0 (38.5) 95th 77. adolescents compared with adults.1) 80.9-115) 57.4-60. and females compared to males (Silva et al.8-14.S.5 (48.8) 13.8-14.5 (35.1) 23.9 (15.9) 42.0 (41.2 (69.3) 36.6 (11.8) 56.6) 38. In an annual sample of German university students.1 (13.2 (41.2 (40.8) 80.0-15.8 (12.9 (9.4 (25..4-14.6 (15.1-29.5 (9.0-90.7) 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 40.3-16.8) 68.6 (30.0-51.6-47.9-62.0) 12. Hoppin et al.8) 46.6 (57.6) 73.3 (12.7-69.8) 26.2-13.4) 17.3 (39.2-21.5) 23.5-99.4) 50.1-120) 77.3 (13.2-117) 95.6 (11.9) 12..5-76.1 (53.3) 89.5) 20.1 (15.3 (35.9-23.1 (41.4 (13.7-61.6 (19..1) 24.1-125) 86. 2007).9 (24. 2007). 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.73-12. 2003).6) 12. 2002.8-173) 195 (121-305) 229 (99.5-61.7-12.5-38.8 (57.7 (21.4 (21.4-23.0-26.7-14.3 (23.8 (10.9) 11.7-397) 70.6-12.1 (19.9 (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.4-14.1 (18.9) 11.4-79.1) 35.1 (25.2 (56.0) 15.8-48.6-26.7-29.0 (11.5-58.2-49. in young Swedish men (Jonsson et al..7 (23.7-19.1 (13.0) 49.7 (11.8-13.1 (21. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.3-38.9 (29.6) 58.1 (46.9) 100 (80.8-39.3) 90.0 (49.1 (9.8-16.7) 46.5-23.8) 53. In NHANES 1999-2000.2-12.9) Total 14.6 (22.6 (51.0-27.8-85.1 (23.3-34.2) 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 12.2-26.1) 24.95-14.4) 28.4) 13.7) 56.6 (24.4 (33. 2005.5) 13.3 (60.5) 46.9 (55.7) 38.4 (11.7 (54.8 (46.5-31.2) 12.1-58.2) 32.7-15.7 (14.8 (13.8) 24.6) 25.5) 14.7-20.9 (39..4) 44.2) 11.5-58.5) 16.4-90.1 (11.6 (34.0) 11.8) 53.4 (63.5 (10.3-73.4-18.7-90.4 (60.4) 90th 50.3) 12. population from the National Health and Nutrition Examination Survey.5-213) 49.6) 75th 25. 2005).2) 11.5-29.7-56. 2004).5) 41.4-19.3) 67.3) 55.5 (11.9) 12.9-14.8-13.7-19.1) 27.9-13.5 (49.5-57.8) 54.9 (15.8) 33.1) 12.2) 11.9-13.7) 11.7 (11.2-17.1-12.

Epidemiol 2005. David RM. Jacek R. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. 2000 [online]. Drexler H. Ryan L. Phthalate monoesters levels in the urine of young children. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Schettler T.114(9):1424-1431. Pirkle JL. J Androl 2004. Urinary levels of seven phthalate metabolites in the U. Available at URL: http://cerhr. Caudill SP. Eckard R. Silva MJ. Hoppin JA. Third National Report on Human Exposure to Environmental Chemicals. Environ Res 2003.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. et al. Wittassek M. Environ Health Perspect 2006. 4/20/09 Silva MJ. Angerer J. Int J Hyg Environ Health 2007. Prenatal exposures to phthalates among women in New York City and Krakow.25(2):293-302. Blount BC. Research Triangle Park (NC).108(10):979-982.112(3):331-338. Centers for Disease Control and Prevention (CDC). Meeker JD. Barr D. Dobler L. Brock JW. Reproducibility of urinary phthalate metabolites in first morning urine samples. Helm D. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Jedrychowski W. Chen Z. Caudill SP. et al.111(14):1719-1722. Butala JH. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. 2005.Phthalates References Adibi JJ.210(3-4):319-333. Silva MJ. Calafat AM. Hilborn ED. Atlanta (GA).nih. Poland. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Baird DD.16(4):487-493. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. NTP-CERHR.68:309-314.S. Gans G. Brock JW.22(3):688-695. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Levels of seven urinary phthalate metabolites in a human reference population. Duty S. Needham LL. Sanchez GN. Environ Health Perspect 2002. Hu H. Duty SM. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Green RA. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. et al.110(5):515-518. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Richthoff J. et al. Hodge CC. Environ Health Perspect 2004. Silva MJ. Bull Environ Contam Toxicol 2002. Sampson EJ. Reidy JA. Hum Reprod 2007. Ryan L. Camann DE.18(1):122. Environ Health Perspect 2000. Wiesmuller GA.html.niehs. McKee RH. Weuve J. Davis BJ. Koch HM. Malek NA. 112(5):A270]. Reprod Toxicol 2004. Singh NP. Koch HM. Environ Health Perspect 2003. Caudill SP. Perera FP. Silva MJ. Calafat AM. Rylander L. et al. Rossbach B. Giwercman A. Hauser R. et al. Jonsson BAG.93:177-185. Hagmar L. Needham LL. Barr DB. Brock JW. et al.

30 (3.43) 6.91) 4.6 (9.60 (2.10 (4.50-4.30 (4.10-2. Survey Geometric mean (95% conf.1-17.26 (2.6 (14. OSHA has established a workplace air standard for external exposure to DBP.70 (5. interval) 2.00-11.3 (13.10) 8.3-19.5 (17.7-18.20 (3. NTP-CERHR.6-26.4-27. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.5) 19.7 (17. 2005).6) 26.1) 22.30-3.11-3.90 (4.7 (17.55 (3.6) 16.10) 9.2 (8.2-14.3 (13..1) 16.9) 10..40 (6.3) 18.3-24..40-3.5 (10.97-7.1-12.59) 3.30-7.56) 3.0) 13.1-20.30) 10. When total DBP metabolites have been measured. and insecticides.00 (7. 2000.4 (20.10) 3.30-6.40 (3.63) 3.4) 22.S.46-5. 2000).80 (2.46) 2.67 (5.40 (2.90-7.10 (4.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.00) 7.85-6..9 (16. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U. about 65% to 80% of a dose is eliminated in urine within 24 hours.96) 3.6-18.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3. 2004.80 (5.4) 12.10-9.46 (2.60 (5. 2005).5) 18.97) 4.6 (29.10) 11. Hauser et al.40-3.00-6.6-20.56 (5.6 (10.50 (6.30-2.7) 15.20-9.20-6.5-24.20-2.0-14.00) 4.80 (5. pharmaceutical coatings.30) 2.Phthalates Di-n-butyl Phthalate CAS No. Studies of children found age-related differences in urine MBP levels. population from the National Health and Nutrition Examination Survey.00-6.6-14.2 (11. 84-74-2 Di-isobutyl Phthalate CAS No.30) 6.20) 7.68 (2.90-4.3 (11.0 (11.19-3.40) 5.7) 14. Koch et al. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.50) 18.50) 2. they have been referred to as monobutyl phthalate (MBP).3-48.0) 24.30 (1. 2004.0-38.00 (5.8) 677 652 703 699 1216 1088 Limit of detection (LOD.07 (3.6 (13.5 (27. 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.0 and 0.28-5.46 (3.8) 21.7-20.90) 12.50-2.20-12.30-13.8) 40.7 (9.7) 7.50) 8. 2001).0) 12.3 (19. and in a small sample of Japanese adults (Itoh et al.90 (6.0 (13.4 (14.0) 9.6) 16. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.0 (13.7 (7.8 (9.5) 23.10-9.97) 2.22) 3.00) 4.3-43.00) 6.17) 4. 2005).7 (18.5-29. Fourth National Report on Human Exposure to Environmental Chemicals 265 .73-5.5 (11.10 (3.72-3.50) 7.00) 10.6) 10..40-12.1 (13. 2005.6 (11.80-5.30-11.60 (8.5 (20.60) 3. 2007).30) 5. residents (Blount et al.30-6.3) 33. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.90-4. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.30) 10.2) 5..56 (3.40 (7.0-18.20-12.6) 17.2-22.70-8.7-31.7) 4.70 (2.0-25. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.40-17.0) 20.3-18. in men attending a Boston infertility clinic (Duty et al.7 (16. CDC.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.40 (2.3 (16.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2. and also in some printing inks.S.3) 3.50) 5.56-4.44-2.5) 25.70) 3.20 (6.50-10.6 (13.5-16.49-2.9-23.40-5.40-4.02) 4.70-4. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.4) 5.20) 4. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics. DBP can produce reproductive toxicity in male rodents (McKee et al.40-4.33 (2.80) 75th 5.40-9.81 (3.00-9.90 (3.3 (18..9-14.22 (3.9) 15.90-2.55) 2.20 (7.1 (8.6-34.80-5.. Following oral administration of DBP to humans.10) 2.37) 6.1-25.90 (4. mostly as MnBP (Anderson et al.5) 18.7) 18.6 (10.4-12.71 (2. in a small sample of pregnant women in New York City (Adibi et al.2-33.66) 2.5) 12. Biomonitoring Information Median concentrations reported in the NHANES 19992000.17 (2.73 (2. In addition. 2003).80 (3.24-8. 2003).50 (3.60-6.6) 17.6) 12. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.7-31.6 (14.5-16.70) 5.3-20..80 (2.1) 25.2 (12.9 (16.48 (2.70-4.82-3.60 (4.5) 14.50-6.3-30.3 (16.0) 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 2.00-4. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.0 (19.5) 22.3.84) 4.50) 90th 12.

94) 6.61-3.11-2.98 (2.3 (13.20 (7.6-19.69 (2.1-12.3) 13.32 (7.18-10.9-16.09-2.6 (9.38-10.56-4.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .8 (8.3) 18.5) 15.17 (2.97-2.1) 7.68) 3.32 (3.4 (12.2) 8.47 (3. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.2-13.2 (11. 2005).20-2.17) 90th 8.1) 13. 2002.7) 11.6 (10.33) 3.8 (9.94 (5.83 (2.53-3.6 (8.81 (3.04) 3. 2007).80 (3.42) 2.0 (8.30) 2.1) 15.7) 3.24) 3.76 (3.20 (2.55-6. Between 1998 and 2003.33 (3.75 (6.1-25.18) 3.57 (3.43) 3.7 (21.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.52) 3.0 (12.69) 4.0) 11.7 (11.02 (7.13 (2.0) 7.10-5.65-11.00-3.0 (10.9 (11.15-4.74-3. up to four and 13 fold.9-26.6) 13.66) 10.31 (7.43) 3.39) 5.4) 15.6) 11.4) 7.25) 5.89) 6.1-24.04-5.88 (2.47-12.9 (9.6 (15.35) 3. 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.30 (6. samples from German university students had consistently higher median urine levels of MnBP and MiBP.95) 2.93-6.76-3. ranging from more than one-tenth the NHANES median (Itoh et al.81) 9..31 (2. 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.79-6.82 (4.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.92 (7.58-4.84 (4.45) 3.S.14 (4.31) 2.86) 6.57-4.80-3.8-36.9-40.51) 2. while MnBP declined (Wittassek et al.81 (6.08-2..8-18.2 (10.8 (10.18 (4.2) 24.56) 2.43) 3.6-19. 2007).22 (2.08) 75th 4.5-19.54) 2.52-3.8) 10.52 (2.5) 13.02-10. Weuve et al.18-4.28 (4.46 (2.62-12.51) 5.72) 5.03-7.7) 10.29-8.29-3.99-4.9) 12.57 (3.73 (5.01-2.31) 2..36-7.79-8.and gender. 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.81) 4.3) 16.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.7 (9.89 (3.85 (2.27-12.05) 2.38 (6.56-15.64-10.78-8. respectively. In an analysis of NHANES 1999-2000. An analysis of NHANES 2001-2002 showed similar age.66 (8.7-28.03 (5.53-5.65 (4.8-18.54 (2.68) 5. to about two to fourfold higher (Fromme et al.53-4.44 (3.51) 15.64-7.76-3.26-2.17-12.6 (12.74 (4. 2004).52-20.1) 4.11) 5.68 (2.00-3.75 (4.69) 6. than adults in NHANES subsamples during the same time period.03-11.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.99) 7.5 (9..21) 10. Survey Geometric mean (95% conf.56) 5.20 (2.46) 3.37) 3.15) 3.04) 7.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.0-18. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.00 (3.13-6.2) 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.66) 4.2-15.4-16.79 (4.3) 28..0) 3.94-12.19 (2.84 (8.0) 15.20-3.7 (13.4) 23.1 (10.9 (15.26 (2.46-11.65-4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.32) 7.64-7.54 (4.18) 4. 2005).95-3.72-7.6) 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 2.1-15..11 (5.21 (5.36-2.66) 2.39-3.28-13.1) 10. Over this time.00-7.07-5. 2004).78) 9.76-15.3 (17.67-5.89-5.41 (2.58-3.91-6.5 (11.33 (2.95) 10.78) 8.00) 01-02 03-04 01-02 03-04 01-02 03-04 4..18 (1. the students’ median values for MiBP levels remained relatively unchanged. interval) 2.86-4.07 (2.80) 7.62 (6.96 (3.59 (4.82) 4.1) 11. population from the National Health and Nutrition Examination Survey.8-13.34 (3.69-7. 2006).6 (8.1 (11.20-4.7) 19.47-5.33-9.3) 13.

3 (56.8) 23.0 (36.6) 39.3 (37.3) 24.5-44.7 (38.3 (17.8-42.4 (35.1) 19.0-24.1-20.8) 58.1 (19.2 (58. and 03-04 are 0.2) 62.7-106) 69.7-26.9-22.5) 36.7-121) 97.3 (60.1) 17.0) 27.9) 29.5) 24.1-24.2-21.5-53.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.7 (18.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89. Fourth National Report on Human Exposure to Environmental Chemicals 267 .2) 68.2) 90th 98.3 (51.3) 18.2) 20.7 (70.6-33.0 (17. 1.4-44.9 (79.6 (22.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.1 (51.0) 117 (104-131) 112 (84.3-79.5) 20.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.6-40.1. *In the 1999-2000 survey period.2 (75.1-29.2 (21.2-159) 92.1-80.1 (54.8-25.0-51.1) 25.5-43.6-44.8) 19.7-34.8) 43.1 (31.3) 26.5-42.9.4-31.7 (43.3 (30.1) 30.4-26.7-92.8) 75th 51.9 (17.7 (64.2) 26.2-33.1-51.6-113) 108 (90.1) 20.8-111) 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 23.0-73.5) 34.1 (19.2 (17.3-60.0) 84.4 (21.5 (74.1 (58.6-20.4 (23. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.5-60.3 (23.0-19.8-119) 90.1-92.2 (21.2-93.5) 40.7 (22.4) 20.6-48.4.3-96.6 (26. 01-02.7-116) 95.2-22.2 (25.2-56.2) 38. respectively.7 (18.6-29.6-49.0-32.0-26.2 (79.3-85.0 (30.5) 17.7-42.7) 42. interval) 24.1) 23.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.5-121) 106 (94.3 (36.0 (45.8 (19.0-21.1 (28.9-22.5 (29.0) 21.1-75.7-124) 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 (55.5 (59.4 (19.6) 38.0) 30.9-28.0-24.6-37.3 (30.1 (41.1 (16.6 (65.7) 124 (98.7-117) 118 (108-143) 93.1 (21.5-117) 95.8 (57.5) 78.0) 38.4 (35.2-63.0 (25.6) 80.S.6 (19.3 (23.1 (62.6-31.0 (15.6 (44.6 (32.0) 20.9-33.9-92.4) 64.6) 21.6) 71.8) 62.9) 26.8-132) 95.5) 37.9) 21.9-42.3-136) 137 (107-162) 119 (90.1 (36.9-79.4 (35.7 (19.9) 71.6) 35.4 (84.7) 52.0 (18. referred to as monobutyl phthalate (MBP).6 (16.5 (59.3) 23.0) 120 (98.7) 74.9) 46.1 (19.4 (25.6 (61.6-29.9-87.1) 23.4) 22.5 (30.6) 46.0 (78.8-29.4-20.1) 23.5) 36.3-40.7 (33.5 (28.6 (48.7 (16.3) 40.7 (24.9 (17.2 (59.5) 47.3-24.1 (18.7) 28.2) 42.1) 36.7 (28.0) 31.1) 47.4 (71.7-127) 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 22.2 (18.5) 19. see Data Analysis section) for survey years 99-00.2 (19.1 (19.1 (17.5) 31.9-53.3) 19.9 (79.7-91.2-87.7-111) 64.7-53.1) 46.6-36.4 (35.9-114) 116 (97.0 (20.5-27.9) 75.4) 59.7-20.0 (72. and 0.0 (23.6-143) 127 (99.8-22.3-67.2-23.5) 26.4-60.2-49.2-32. population from the National Health and Nutrition Examination Survey.0-58.1-82.3-145) 85.9) 18.0-19.1 (34.7-34.3-76.9 (20.4-42.2 (78.1-22.2-24.3 (42.6) 17.8) 48.4 (38.4-159) 107 (84.3-21.1 (26.4-18.6 (90.6-24.3) 21.5-47.7-24.5-47.1-27.2 (20.4-25.5) 85.2 (74.0 (31.2-114) 73.3) 36.6) 20.9-101) 77.2) 32.6-69.5) 65.7-42.5) 21.1) 31.7 (51.7) 92. Survey Geometric mean (95% conf.4 (72.5) 95.9) 36.4) 52.8-123) 101 (90.4 (36.

9) 24.4) 20.9 (16.7 (16.5 (14.6-27.8) 13.1) 22.7) 36.3) 19.6 (61.3 (71.0) 29.6 (19.6) 64.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.3-40.1-32.7-19.0) 81.9 (35.9 (64. interval) 22.0 (71.9 (35.2 (83.2 (19.3 (52.4-34.6 (27.9) 62.6 (17.1-99.4 (50.5) 60.6-44.6-24.0 (20.8) 34.3 (69.0) 75.0) 59.4) 16.8) 34.6) 18.8 (18.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.7 (54.0 (34.6 (57.2) 31.0-41.5-15.7 (12.1 (46. 268 Fourth National Report on Human Exposure to Environmental Chemicals .8) 23.2 (19.9-14.6) 34.5 (81.0) 55.3 (55.0 (70.5-23.6-16.9 (30.3-81.8 (16.6) 31.0) 35.9-34.2-61.3-18.9) 52.0 (61.8 (33.3-78.5-16.6-128) 96.2 (35.1 (21.0) 19.5-64.3-106) 74.3-23.5) 39.5) 91.5 (18.2-106) 64.4 (37.4 (31.1) 21.1) 44.7 (60.0) 28.6) 38.9 (30.3 (16.4 (68.1-23.6 (29.9) 19.6-50.1-62.0 (26.0) 94.4 (31.7 (28.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.0) 25.8) 22.5-76.5 (15.3-38.2-21.2-18.4 (13.8-24.4 (17.6-23.3-32.0) 41.7 (27.3) 33.9 (37.8) 17.4 (31.2-48.3 (24.5 (18.3 (17.0-47.7-19.0-17.6 (41.3-26.7-28.5-142) 81.6-42.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.4) 51.0) 26.0-113) 104 (83.8) 35.2-85.6) 37.8-24.9 (21.1) 53.4-24.1 (61.3-21.3) 21.4 (17.8) 75th 38.7-21.4) 21.6) 65.1) 37.8) 17.4 (16.6-119) 63.8 (18.9) 39.2-73.9) 49.4) 62.0 (19.6) 14.2 (16.3) 18.8) 17.2) 159 (102-263) 147 (93.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.6) 23.5) 21.1-99.5-142) 89.4) 15.0 (50.5 (30.8) 20. population from the National Health and Nutrition Examination Survey.0-19.8 (13.4-103) 117 (83.7) 19.6-53.5) 17.5-41.8-43.5-37.8 (65.8-23.4) 19.7) 20.3) 33.2) 21.7 (60.1) 20.3-21.2-22.9-84.7 (43.1 (34.0-75.7-39.9-68.2-27.2) 74.4-131) 81.4 (50.9 (19.1) 17.5-18.3 (17.6-23.0) 70.7-23.5 (64.9) 14.8-32.1-18.6) 39.1-83.1) 20.7 (19.9-56.6) 24.3 (28.9 (58.6-43.6) 24.9 (73.3 (46.4-76.9-26.6 (74.4-72.8 (25.2-16.3 (19.9 (20.0-60.3-20.4 (45.6-92.3) 59.4-47.9) 20.3 (76.1 (15.6-32.2) 65.1-128) 97.5) 90th 68.4) 53.9 (30.4-61.9-38.6 (72.1) 42.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) 17.1 (56.5-21.8) 30.4) 15.8 (50.4 (20.0 (43.S.3 (42.9-68.8) 19.6-26.9 (56.7 (20.7 (73.6-28.4 (47.9) 91.3) 52.7-51.4 (56.9) 28.4 (33.1) 35.2 (38.6-19.8) 40.5) 134 (93.1 (32.0-90.2-28.1) 50.9-105) 85.8) 28.9) 30.5) 84.3) 19.3-39.9 (39.7-26.5-30.7-80.3) 35.1) 61.6 (25.5) 82.0) 108 (71.8 (18.3-49.7-37.2) 59.2-179) 84.3-71. Survey Geometric mean (95% conf.6) 25.2-22.0 (69.6-74.3 (52.8-235) 137 (108-198) 88.4 (18.3 (48.4 (19.6-22.4 (16.6-44.0 (18.0) 53.5-70.0 (52.7-78.6-24.9-70.0 (15.9-36.6 (25.3 (21.0-38.7-42.4-135) 71.0-92.4-164) 96.2-86.6) 83.9-100) 86.7-20.7 (81.7 (14.2-22.4 (53.3 (60.0 (18.3) 67.6 (31.7 (57.3-114) 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 17.1 (29.7) 42.8) 20.4 (23.0 (27.3) 20.6-155) 91.8 (17.2) 16.3 (17.3-17.8 (22.0 (16.5-22.9-49.8) 63.4-65.1-21.

Atlanta (GA). Fourth National Report on Human Exposure to Environmental Chemicals 269 . Springall C. Sampson EJ. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Needham LL. Angerer J. Hum Reprod 2007. Third National Report on Human Exposure to Environmental Chemicals. Itoh H. Bull Environ Contam Toxicol 2002. 112(5):A270]. Environ Res 2003. Camann DE. Ryan L. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Rossbach B. Reprod Toxicol 2004. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Eckard R. Centers for Disease Control and Prevention (CDC). Anderson WA.Phthalates References Adibi JJ. Epidemiol 2005.68:309-314. Jedrychowski W. Giwercman A. Int J Hyg Environ Health 2007.18(12):10681074. Wiesmuller GA. Duty SM.208:237-245. et al. Wittassek M. Needham LL. Koch HM. Duty S. Silva MJ. et al. Meeker JD. Pirkle JL. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Environ Health Perspect 2000.210(3-4):319-33. Green RA. Ryan L. Boehmer S. NTP-CERHR. Hodge CC. Schettler T. Drexler H. Helm D. Brock JW. Weuve J. et al. McKee RH. et al. Chen Z. Environ Health Perspect 2003. Rylander L.S. Research Triangle Park (NC). et al. David RM.210:21-33. Food Addit Contam 2001. Silva MJ. Calafat AM.gov/chemicals/ phthalates/dbp/dbp-eval. Available at URL: http://cerhr. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Caudill SP. Perera FP.niehs. Dobler L. Poland. et al.nih. Fromme H. Occurrence and daily variation of phthalate metabolites in the urine of an adult population.114(9):1424-1431. Phthalate monoesters levels in the urine of young children. Gans G. Hagmar L.111(14):1719-1722.html. Koch HM.108(10)979-982. Angerer J. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. et al. Jonsson BAG.22(3):688-695. Caudill SP.25(2):293-302. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Reidy JA.93:177-185. Hilborn ED. Koch HM. Singh NP. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Masunaga S. 2005. Environ Health Perspect 2004. J Androl 2004. Prenatal exposures to phthalates among women in New York City and Krakow. Malek NA. Richthoff J.18(1):122. Silva MJ. Environ Health Perspect 2006. 2000 [online]. Bolte G.16(4):487-493. 4/20/09 Silva MJ. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Barr D. Scotter MJ. Levels of seven urinary phthalate metabolites in a human reference population. Int J Hyg Environ Health 2007. Calafat AM.112(3):331-338. Massey RC. et al. Int J Hyg Environ Health 2005. Yoshida K. Drexler H. Butala JH. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Silva MJ. Blount BC. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Barr DB. Hu H. Brock JW. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Castle L. Sanchez GN. Caudill SP. Jacek R. Hauser R. Urinary levels of seven phthalate metabolites in the U.

only levels at or above the 90th percentile could be characterized. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300) < LOD .300 (.300-.200-.200-.600) .400 (.500) 1. 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.500) < LOD 1.600) . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.400 (.300-.600) .300 (. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.400-.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400-.3.200-.300 (<LOD-.400) < LOD < LOD . 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 (. population from the National Health and Nutrition Examination Survey.600) .500) < LOD < LOD . 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.400 (<LOD-.500) . and polymers.400-.10 (<LOD-2.500) < LOD < LOD .00 (<LOD-1.500 (.300-.300-.500 (.400 (.00) .200-.500) .300-.700) . 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.200-. polyvinyl acetate.400 (<LOD-.50) .700) . respectively.00-3.90) .600 (.70 (1.10 (.00 (<LOD-1. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine. 01-02.S.300 (.300-.400-. and 0.00-2.500) 1. Survey Geometric mean (95% conf.10 (<LOD-1. In this Report.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .200 (<LOD-.00 (<LOD-1.600) .400 (<LOD-. and 03-04 are 0.500-. resins.500 (.300-.400 (.300-. 270 Fourth National Report on Human Exposure to Environmental Chemicals .500 (.70) .80) .70 (1.500) .10) .500 (.400-. < LOD means less than the limit of detection.70) .700) .50) .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) .400-.20) .10 (<LOD-1.500 (. including nitrocellulose.300) < 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 .600) < LOD .400) < LOD 1.500) < 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 (<LOD-.400) 1.400 (. see Data Analysis section) for Survey years 99-00.400) 1.300 (.500 (.Phthalates Dicyclohexyl Phthalate CAS No.500 (. which may vary for some chemicals by year and by individual sample.900-1. 0.300 (.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9.300-. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.300-.500) 1.400 (.400 (.2.400-. and polyvinyl chloride.200-.300 (.

530-.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 1.660) < LOD < LOD .670 (<LOD-.170-.54-6.330 (.830) 1.54 (<LOD-2.330 (.53) .16 (<LOD-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.410 (.910 (.420-.11) .770-1.00) .500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .420-.590 (<LOD-.18) .590 (.530 (.950 (.14 (<LOD-3.500) 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 .310) < LOD .800-1.450 (.370 (<LOD-.06) .690) < LOD < LOD .710) .630 (<LOD-.500-.S.510-. Survey Geometric mean (95% conf.940 (.770 (.290-.16) .560) 1.360-.770-1.380 (.270) < LOD .250 (.33) .310-.12-1.910 (.10) .54) .220 (<LOD-.380-.480 (.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.530) 1.400-.240-.05) .17) .740) .690) < LOD 2.660) . Fourth National Report on Human Exposure to Environmental Chemicals 271 .82 (1.260-.770) < LOD 2.490) .510 (.74) .620) < LOD .67 (1.770-1.880 (.690 (.630 (<LOD-.470 (.530-1.43 (1.36-1.690-1.610 (.82) .450 (. population from the National Health and Nutrition Examination Survey.470) 3.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .790-1.910 (.34) .33 (<LOD-3.400-.500) 3.390 (.53) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.670-1.500 (.44) .910 (.420-.00 (<LOD-3.22 (<LOD-1.350-.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.06) .740) < LOD < LOD .

deodorants.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75.3 (82. shampoos. respectively. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 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. and 0. 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. 2007).3 (74.4 (62. population from the National Health and Nutrition Examination Survey. Products that may contain DEP include perfumes.Phthalates Diethyl Phthalate CAS No.9 (61. DC (Hoppin et al.. In contrast. 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 0.1 (71. 272 Fourth National Report on Human Exposure to Environmental Chemicals . Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.7) 71.7 (70.3-103) 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