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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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4.5.2'.1. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.6'-Hexabromodiphenyl ether (BDE 154) 2.What’s New in this Report What’s New in this Report In this Fourth Report.3'.4.2'.5'-Hexabromodiphenyl ether (BDE 153) 2.2'.4. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.6.2.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.2-Dichloropropane 2.2'4. The process for selection is described at http://www.5’.2-Dichlorobenzene (o-Dichlorobenzene) 1.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2’.6-Heptabromodiphenyl ether (BDE 183) 2.5'-Tetrachlorobiphenyl (PCB 44) 2.4'-Tetrabromodiphenyl ether (BDE 66) 2.3-Dichlorobenzene (m-Dichlorobenzene) 1. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.gov/exposurereport/chemical_selection.2-Dichloroethene trans-1.3’. Table 1.2'.4'-Tetrabromodiphenyl ether (BDE 47) 2.1.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.4’.2'.4'.4-Tribromodiphenyl ether (BDE 17) 2.4.3.2'.5-Pentabromodiphenyl ether (BDE 99) 2.4’.4-Dichlorobenzene (p-Dichlorobenzene.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.4.2'.4.4.3-Tetramethylbutyl] phenol) Triclosan (2.4'.4.1-Dichloroethane 1.4'.5'.html.2'3.4.4'.5.1-Dichloroethene (Vinylidene chloride) cis-1.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.4'.2'.2-Trichloroethane Trichloroethene (Trichloroethylene) m.4.2'.4.3.3.4. Paradichlorobenzene) 1.5.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.1-Trichloroethane (Methyl chloroform) 1.3.1.cdc.5.4'-Tribromodiphenyl ether (BDE 28) 2.5'-Tetrachlorobiphenyl (PCB 49) 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.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.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .2-Dichloroethene Dichloromethane (Methylene chloride) 1.2-Dichloroethane (Ethylene dichloride) 1.4'-Pentabromodiphenyl ether (BDE 85) 2.6-Pentabromodiphenyl ether (BDE 100) 2.1.

Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period.5-dichlorophenol for the 1999-2002 survey periods.. Details of this procedure are provided in Appendix A.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. and these data will be included in the next release of the Report. Explanations for each change are provided in Appendix B. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available.. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report. Only slight differences should be noted when one compares the recomputations to previous releases of the Report.g.4-dichlorophenol and 2. Percentiles for all three NHANES survey periods (1999-2000. 2001-2002. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. Data for other pesticides are included only for 1999-2000 and 2001-2002. Fourth National Report on Human Exposure to Environmental Chemicals 3 .g. five results that all have the value 90.1). urinary 2. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. 2003-2004) have been re-computed by use of this improved procedure. the presence of an interference) that produced results of inadequate quality.

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

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

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

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

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

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

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

7) 58.5 (79.9-52. and cosmetics (NTP-CERHR.. 1994).2-59. see Data Analysis section) for Survey year 03-04 is 3.1 (88. and from dermal contact with products that contain residual acrylamide.0 μg/kg for adults (FAO/ WHO.3 (53.8 (81. Elimination occurs mainly in the urine as mercapturic acid conjugates.1) 62. ocular and dermal irritation from direct contact with acrylamide containing materials. Survey Geometric mean (95% conf.4-60.4 (54.9 (54.5) 58.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.4-83. Since acrylamide has limited volatility and high water solubility. and well below doses known to cause nerve damage or carcinogenicity in animals.3-2.7) 54.7 (63. 2006.2 μg/kg/day (U.9) 58.2-93. 1990. 2002).S. (NTP-CERHR..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 54.1 (47.5-85. 2005.6) 71. population from the National Health and Nutrition Examination Survey. drinking water.2-114) 163 (147-191) 96.8-57. Fourth National Report on Human Exposure to Environmental Chemicals 11 .6-65.6-108) 61.S.6) 50.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.7) 73. These estimated intakes are hundreds of times lower than occupational exposures.1 (52. it was discovered that acrylamide is formed when starch-rich foods. Animal studies indicate that acrylamide is well absorbed. 2005).1) 53. in some sealing grouts. and in the synthesis or compounding of dye materials.2 (75.6 (51. EPA.9) 75.6-61..S. gels. but can covalently bind to form adducts with proteins.0-49.7) 75th 79. In 1997.5 (52. 2005).7-64. 2004.2-70. EPA.5) 66. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.8 (57.2) 57.3) 63. in permanent press fabrics.8 (91. widely distributed in tissues. Commercially. Recently.1) 46.1 (83.9 (69.S. People may be exposed to acrylamide from foods.6-104) 82.0 (67.7 (58.4) 57. Tareke et al.1) 101 (95.0) 85. In the general population.1-64.1) 55.4) 57.3 (55. and binding agents.4-60. 2006).1-61.0-66. and an average daily intake is estimated as 0.2 (62.4 (51. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. 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. Polyacrylamides are useful water-compatible polymers used in water treatment.2-77.8 (52.0 (53. are heated at temperatures used for frying and baking. smoking. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.0 (69.4 (53. mineral processing. and is either metabolized to the reactive epoxide.9 (60. as an absorbent in disposable diapers.1-57.2) 57.5 (44.6) 73. Estimated intakes in children are about twice that of adults (DiNovi and Howard.6-75. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.1-64.7) 96. 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 61.5-80.7 (65.4) 100 (89. Natural substances in the food are converted to acrylamide.2-118) 98. 2005). interval) 61.9-61.2 (58. 2005).4-89. such as potatoes and some grains.7-60.6 (56.6 (81. but are generally above the U.6) 90. and in some cosmetics. the main source of exposure is from the diet. 2005). soil conditioners. In humans. or to glutathione conjugates (Calleman et al. pulp and paper production.0-58.2-67. acrylamide has produced upper airway irritation following inhalation of high levels.5 (74. 217 million pounds of acrylamide were produced commercially in the U.7 (55.3) 70. acrylamide is synthesized and used in the production of polyacrylamide polymer.0.4 (54.7-64.0 (57.2-91.9-105) 86.Acrylamide Acrylamide CAS No. Fennell et al.3-71. Acrylamide is not thought to accumulate in the body at environmental doses.0) 57. FAO/WHO.3) 86.4-76.9) 57.9) 63.8-55. glycidamide.S. FDA. EPA reference dose of 0.1 (73.4 (59.0-108) 152 (139-175) 126 (111-142) 108 (86.6-66.

.. EPA at: http://www. 2005) and sperm DNA adducts (Xie et al. U. 2002.1) 56.epa.6 (66.int/ ipcs/food/jecfa/summaries/summary_report_64_final. although different analytic methods can affect results. thyroid.9-78.. Schettgen et al.. 2005..5-94. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.4 (51.8 (51. IARC classifies acrylamide as probably carcinogenic to humans. altered gene expression in testicular tissues (Yang et al.4 (90.8-49. uterine.8-48. 2005). 2005. Axonal degeneration.3) 59.7) 60. 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. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.1 (70.4-59. Puppel et al.7) 74.2) 55. reproductive effects (reduced litter size.7-64.1 (66.6 (90.2-91. interval) 59. After exposure ceases. and cancer (mammary. 1997.3) 59.6-90. Mucci et al.4) 46. 1997. and other sites) (FAO/WHO. dominant lethality). population from the National Health and Nutrition Examination Survey. In addition.. 2005.9-62. Vesper et al.S. male germinal cell injury.0 (70. 2005.9 (58.1 (56.5) 87. 2002.2) 87. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.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.7 (84. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. 2005.2-68. and neuronal DNA reactivity (Doerge et al..8 (44.S.Acrylamide occupational exposures.7-62. 2005. Puppel et al. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA...1 (82. NTP-CERHR.1-62. AHA levels have been shown to increase with dietary intake (Hagmar et al.8) 60.. Vesper 2005) and smoking (Bergmark. presynaptic nerve terminal binding (LoPachin..1-56.7 (87. 2005).7) 90.5 (56.4) 53.9 (81. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. Rice.0 (52.0-93. Additional information is available from U.. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al. 2005. Survey Geometric mean (95% conf. fetal death. 2005). 2005) have been demonstrated in animals.1 (57.7-86. most non-smokers had levels less than about 100 pmol/gram hemoglobin.1) 62..9) 87..4) 83. scrotal. 2005..9 (57. 2006..pdf.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 64.0) 94.0-62.3) 59.5-92.9-64. Glycidamide has been shown to react with DNA (Doerge et al. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.3) 85.0 (80.5 (59. EPA. 2008).9-77.3-78.4-103) 79. glycidamide (NTP-CERHR. 2003.5 (83.1) 60.1-70. 2001).4-65. respectively) are markers of integrated acrylamide exposure over the preceding few months.8) 45.5-64.7 (57.4 (57.6-64.6-62.1-60. Schettgen et al..5) 75th 85.5 (42. 2006).4 (81. 2004.2-90.. Hagmar et al.4 (56.2 (63.4 (61. 2006) have been demonstrated after acrylamide dosing.9-138) 143 (130-159) 96.7 (61. EPA.. Klaunig et al.3 (56. 2008). probably through its epoxide metabolite. adrenal.0.9) 59.5-66.8-61. 2004). 2009).5) 71. 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. 12 Fourth National Report on Human Exposure to Environmental Chemicals .who. 2006).4-98. Maniere et al.2 (72.1) 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 59.9) 75. 2005. 2005).2 (56. 2005. 2005.9-76..7) 61.0) 118 (103-126) 121 (112-134) 113 (94. Acrylamide is clastogenic and can produce dominant lethal mutations.S. see Data Analysis section) for Survey year 03-04 is 4.2) 65.9) 65.0 (75.S.3-101) 95. U. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.

Magnusson AL. 054472. NIH Publication No. Becher G. Axmon A. Tian G. Perez et al. Available at URL: http://www. April 13-15. Bjellaas T. 2005. and Research Strategies. 2001). DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide.fda.cfsan. Granath F. Bergmark E. Mutat Res 2005. Toxicol 2005. Italy.561:49-62. Laurentie M. References Bergmark E. gov/~dms/acrydata. Mutat Res 2005. Yang JS.nih. Bruze M. Bergmark E. LoPachin RM. Mucci LA.10(1):78-84. Metabolism and hemoglobin adduct formation of acrylamide in humans.gov/chemicals/ acrylamide/Acrylamide_Monograph. et al. 6013-6019. Rosen I. Mechanisms of acrylamide induced rodent carcinogenesis...3:406-412.. smokers and nonsmokers. Food and Drug Administration (FDA). 1999). et al. Churchwell MI. CFSAN/Office of Plant and Dairy Foods. Tornqvist M. Costa LG. Aprea P. 64th Meeting: Summary and Conclusions (FAO/WHO).580(1-2):157-165.html#u1004. Human exposure and internal dose assessments of acrylamide in food. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. J Agric Food Chem 2008. Haugen M. 2/3/09 Klaunig JE. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Hagmar L. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). DNA adducts derived from administration of acrylamide and glycidamide to mice and rats.Acrylamide In occupational settings. Bergmark E. Wu Y. Guffroy M. Calleman CJ. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Acrylamide neurotoxicity: neurological. Acrylamide intake through diet and human cancer risk. Fennell TR. 1994). Godard T. Joint FAO/WHO Expert Committee on Food Additives. 1993. Calleman CJ.. Cheong HK. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. National Toxicology Program. Chicago. He F.120(1):45-54. morphological and molecular endpoints in animal models. In another study. Toxicol Appl Pharmacol 1993. Malmberg B. Churchwell MI.43:365–410. Twaddle NC. 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. smoking habits and gender. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. 2/3/09 Perez HL. Survey data on acrylamide in food: individual food products. Beland FA. Doerge DR. et al. Toxicol Sci. 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. Adv Exp Med Biol 2005. Illinois. Kamendulis LM. Andersen M. Mutat Res 2005. Hagmar et al. Uncertainties.niehs. Alexander J. Burgess J. Wirfalt E. Costa LG. Nordander C. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide.126(2):361-371. Summer SCJ. Calleman CJ. Spicer R. The Updated Exposure Assessment for Acrylamide. et al. 2001. DiNovi M and Howard D. McDaniel LP. 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. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide.who. Chem Res Toxicol 1997 Jan. 2004. 8-17 February 2005. Maniere I. Tornqvist M.580(1-2):131-141. July. 2009 Jan 8. Farmer PB. Osterman-Golkar S. Toxicol Sci 2005.pdf.561:21-37. He F. Scand J Work Environ Health 2001. Rome.27(4):219-226.Toxicol Appl Pharmacol 1994. Food Chem.580(1-2):119-129. 2/3/09 Hagmar L. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Adv Exp Med Biol 2005.56.. Paulsson B. Available at URL: http://cerhr. Kautiainen A. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . et al.85:447-459.pdf. Paulsen JE. Wilson KM. Doerge DR. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. da Costa GG. Available at URL: http://www. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Fennell TR. [Epub ahead of print] Dybing E. February. Zhang S. Duale N. Chem Res Toxicol 1990. 2006. Snyder RW. Bridson WE.

Schettgen T. Rice JM. September. Tjaden Z.206(1):9-14. propylene oxide. Sun H. Reprod Toxicol 2005. Letzel S. et al.htm. Environmental Protection Agency (U. Rossbach B. Int J Hyg Environ Health 2003. Drexler H. Toxicol Lett 2002.epa. Weiss T. Jin Y. Fu D. Han DU. Liu K. Available at URL: http://www. Benetou V. Tjønneland A. Acrylamide. U. Kutting B. EPA). J Agric Food Chem 2002. Vesper HW. Agudo A. Licea-Perez H. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Smith A.txt. Int J Hyg Environ Health 2004. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Han CH. Hemoglobin adducts of ethylene oxide. Tareke E. Hallmans G. Analysis of acrylamide.207(6):531-9. Anal Biochem 1999. Mutat Res 2005 Feb 7. Ding X. Slimani N. J Agric Food Chem 2008. Toxicol Lett 2006. 2/3/09 Vesper HW. Chae C.56(15):6046-53. U. Liu Y. revised 1/3/06. Office of Pollution Prevention and Toxics. Yang HJ. Angerer J.134(1-3):65-70. Eriksson S.S. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Karlsson P. Marko D. Schettgen T. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Meyers T. Integrated Risk Information System (IRIS).S. Adv Exp Med Biol 2005.163(2):101-8.epa. Vesper HW. Angerer J.580(1-2):3-20. Toxicological effects of acrylamide on rat testicular gene expression profile. EPA). Rapid Commun Mass Spectrom 2006. Ingham L. Tornqvist M.Acrylamide glycidamide by gas chromatography-mass spectrometry.20(6):959-64. Environmental Protection Agency (U. Schettgen T. Mutat Res 2005. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry.50(17):4998-5006. Rydberg P. The carcinogenicity of acrylamide. Drexler H.19(4):527-34. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Lee SH.gov/iris/subst/0286. Myers GL.274(1):59-68.561:89-96. Washington (DC). DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Xie Q. Chemical Summary for Acrylamide.gov/chemfact/s_acryla.S. Fueller F. Puppel N.S. Broding HC.580(1-2):71-80. et al. Angerer J. Available at URL: http://www. Drexler H. 2/3/09. Ospina M. Gray JG. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. a carcinogen formed in heated foodstuffs. Meyers T. Choi JH. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Lee MH. 1994. Ospina M.

066-.120 (.950 (. maternal exposure during pregnancy can result in lower birth weight.860 (.33-2.310) .201) .12-4.068) .49) 1.193) .580 (.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .084) .S.70) 2.53-4.030-.310-1.148-.040-. and various other disorders (U.070 (<LOD-.086 (.05.187) .430-1.87-3. ** In the 2001-2002 survey period. Children exposed to ETS are at increased risk for sudden infant death syndrome.047-.060 (<LOD-.65 (1.164 (.050 (<LOD-.198) * .540-.087) < LOD < LOD .09-3. 2006).77 (2.163) .050 (<LOD-.230) .95) 1.670) .040 (.280 (.81-2.350-.820) .990 (.131 (.800 (.142-.480-1.071) . 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.047-.930 (.052 (<LOD-.050 (<LOD-.770-1.38-2.090-.043-.89) 1. and 17% had an LOD of 0.49) 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.052 (<LOD-.188) .570-1.01) 3.600-1.060 (.05 ng/mL.087-.110 (.45) 1.840) 3.30) 2. and 03-04 are 0.164 (.23-2.506 (.060 (.34 (1.180) .130) .115-.260-1.55 (1.400-.50-1.77 (1.180) .059-.630 (.48-2.02 (.054 (.077) .160) .110-.120 (.130 (.19) 1.120 (.180 (.93) .080-.059-.47-3. 2004).197) .080-.216 (.960-1.14) .087 (.68 (1.997-3.360) .030-.077) .470-.18-3.110) .12) 1.080-.145) .200) 1.63-2.094) . population from the National Health and Nutrition Examination Survey.96-4.12 (2.23 (.32-2.21-1.120 (.20) 1.54) 1.520 (.76 (1. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.220) .210 (. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.28-1.120) .040 (.060 (<LOD-.26-1. Survey Geometric mean (95% conf.50 (1.167 (.540 (.94) 1. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.139) * .20) .070) .110-.32-2.061) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.88 (1.12 (1.260) 1.070-.110 (.500 (.44) 2.480-.570 (.060) .79) 3.320) .080) < LOD .42 (1.450-.080-. acute respiratory infections.150) .154-. see Data Analysis section) for Survey years 99-00.175 (.120 (.620 (.110 (.160 (.230 (.126) .39) 3.075 (.83-2.5% nicotine by weight (Kozlowski et al.410) . < LOD means less than the limit of detection.730 (.030 (.089) Age group 3-11 years 99-00 01-02** 03-04 .190-.S.088-.300) .900-1. respectively.090-.090-.350 (.910-1.050-.17) .23 (2.88 (.080 (.54 (1.106-.660) .220-.01 (1.580-1.137 (. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.84-3.66) 1.16) .30) * .950-1.053 (<LOD-.28) .124 (.580) .85 (1.190-.68) 2.990) .49) 1.062 (.070) .66-3.015.42-4.00) 1.09-2.02) 1.020-.060-.53 (1.726) .066 (.78) 2.428-.77 (1.770) .63 (2.071 (.20-2.44) 2. DHHS.00) .160-.015 ng/mL.080) < LOD < LOD .05) 1.144 (.050) .040-. cardiovascular disease.32) 1.110-. emphysema.21-1.510 (.110 (.620-1.140 (.140-.790) . stroke.43 (1.110 (.92 (1.076-.120-.S.54 (1.057-.04 (1.058 (.09-3.22) 2.310) 90th 1.160) .073) < LOD .140-.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 .50) 3.190-.040 (. DHHS.180) .96 (1.350-.050-.137-.920 (.310-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.62) 2.44 (1.96) 2.120-.180) .625) .153-.02) 1.15 (2.150) .066) .50-4. acute respiratory illness.30) 2.060-. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.160 (.19-2.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .740-1.505 (.621-1.111-.20 (. 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.68) .312) .080 (. 83% of measurements had an LOD of 0.17 (1.063) .60-2.070) 75th .050 (.050 (<LOD-.21 (.55-2.19) .99) 2.14-1. ear problems.213) .23 (1.220) . and exacerbated asthma (U.370-.180 (.308 (.710 (..14) .533-.35 (2.630 (. Cigarettes contain about 1.163 (.40) .108) * .180) . 2004).100-.15) 2.030-.66 (1.240 (.068) .11) .234) .690 (.48-3.99) 2. 1998).44 (2.104-.57) 2.70-2. and 0.850 (.302) .17 (.770) .39 (1. Fourth National Report on Human Exposure to Environmental Chemicals 15 .160 (.630 (. which may vary for some chemicals by year and by individual sample.740-1.110) .060-.050) .Cotinine Cotinine CAS No.75) 1.62 (2.140 (.20 (1.

2004). a process involved in the development of addiction. Biomonitoring studies of serum cotinine will help physicians Fourth National Report on Human Exposure to Environmental Chemicals . Nicotine is also used commercially as an insecticide in its sulfate and alkaloid forms. 2005.. which include potatoes. Cotinine can be measured in serum. 1999)... Over the previous decade. or chewing gum. 2005).Cotinine 1994.3 to 30 µg/m3. nausea.. vomiting. NIOSH guidelines consider ETS to be a potential occupational carcinogen and recommend that exposure be reduced to the lowest feasible concentration. 2006)... 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. 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. 2006. The Federal Aviation Administration has banned the smoking of tobacco products on both domestic and foreign air carrier flights in the United States. Nicotiana tabacum. and hair.gov/researchreports/nicotine/nicotine.. Nicotine can also be absorbed from the gastrointestinal tract and skin by using snuff.. diaphoresis. 1998). nicotine has a half-life in blood plasma of several hours (Benowitz. the primary metabolite of nicotine. with higher levels measured in restaurants and bars. mean air concentrations typically range from 2 to 14 µg/m3 (NTP. 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. Nonsmokers exposed to typical levels of ETS have serum cotinine levels of less than 1 ng/mL. 1996). 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. Inhaling tobacco smoke from either active or passive (ETS) smoking is the main source of nicotine exposure for the general population. and increased appetite. 2005). Soliman et al. eggplants. 2005). cognitive and sleep disturbances.. chewing tobacco. nasal sprays. Nicotine also indirectly causes a release of dopamine in the brain regions that control pleasure and motivation. Wilson et al. tomatoes. Children are primarily exposed to ETS by parents and caregivers who smoke. saliva... The tobacco plant. (CDC. Biomonitoring Information Serum cotinine levels reflect recent exposure to nicotine in tobacco smoke. However. 1996). Cotinine. Higher levels of cotinine have previously been reported for non-Hispanic black smokers (Caraballo et al. During each previous NHANES survey. 2005. 1999. with heavy exposure to ETS producing levels in the 1–10 ng/mL range. In homes with one or more smokers. 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. urine. the primary sources for ETS exposure are in a workplace where smoking occurs and in a residence shared with one or more smokers. Once absorbed. seizures. or skin patches that contain nicotine. diarrhea. contains nicotine in larger amounts than other nicotine-containing plants. 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. Perez-Stable et al. Nicotine stimulates preganglionic cholinergic receptors within peripheral sympathetic autonomic ganglia and at cholinergic sites within the central nervous system. NCI. 2006). 2004). 1999. 1991). 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. More information about the effects of smoking and nicotine can be found at: http://www. Serum cotinine has been measured in many studies of nonsmoking populations. Symptoms of 16 nicotine withdrawal include irritability.nida. Acute tobacco or nicotine intoxication can produce dizziness.. is currently regarded as the best biomarker in active smokers and in nonsmokers exposed to ETS. Up to 90% of the nicotine delivered in tobacco smoke is absorbed rapidly from the lungs into the blood stream (Armitage et al. Hukkanen et al. salivation. 1998). For an adult. Hukkanen et al. The IARC and the NTP consider tobacco smoke to be a human carcinogen. Non-Hispanic blacks had higher serum cotinine concentrations compared with either non-Hispanic whites or Mexican-Americans. Pirkle et al. 1994)..nih. with levels showing similar or slightly higher results (depending on the degree of ETS exposure) than those reported in the previous NHANES (CDC 2005.. non-Hispanic blacks metabolize cotinine more slowly than do non-Hispanic whites (Benowitz et al. the adjusted geometric mean serum cotinine was higher in children (aged 4–11 years) than in adults among both non-Hispanic blacks and non-Hispanic whites (Pirkle et al. Nonsmoking is usually defined as a serum cotinine level of less than or equal to 10 ng/mL (Pirkle et al.. html. and peppers. craving. Mean air concentrations of nicotine in public spaces where smoking is allowed range from 0. Iwase et al. and death.

Am J Public Health 2004.niehs.57(1):79115. Pechacek TF. Benowitz NL.gov/tcrb/monographs/10/. Centers for Disease Control and Prevention. Epidemiol Rev 1996. Metabolism and disposition kinetics of nicotine. 1999-2002.php. Kozlowski LT. Summary of Data Reported and Evaluation [online] 1986.18:188-204.gov/ntp/roc/eleventh/profiles/ s176toba. Mowery PD. Benowitz NL.56:483-493. Racial/ethnic differences in serum cotinine levels among adult U. Available at URL: http:// cancercontrol. Bernert JT. Benowitz NL.S. Available at URL: http://monographs. Available at URL: http://ntp. Benowitz NL. 4/13/09 Perez-Stable EJ.php. IARC Monogr Eval Carcinog Risks Hum. Centers for Disease Control. Strauss WJ. et al. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Tobacco Smoke and Involuntary Smoking. National Center for Chronic Disease Prevention and Health Promotion.S. Coordinating Center for Health Promotion. Benowitz NL. 2004. 4/13/09 Iwase A. Vol 38.63:139-43.nih. DHHS). Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Dollery CT. cigarette smokers: the Third National Health and Nutrition Examination Survey. Brody DJ. available at URL: http://mtn. JAMA 1998. U.gov/eid/rmca/critdocs/ criteriadoc/33. the United Kingdom. Department of Heath and Human Services. Caraballo R. Jacob P III. Vogler GP. Available at URL: http://www.niosh. Summary of Data Reported and Evaluation [online] 2004. 1988-1991. BMJ 1975. Pharmacol Rev 2005. Pickett MA. Available at URL: http://monographs.280:135-140. Houseman TH. Kira S. Jacob P. Flegal KM. Clin Pharmacol Ther 1994. 1988-1991. Herrera B. Tobacco Smoke. International Agency for Research on Cancer. 4/13/09 International Agency for Research on Cancer.cancer. Schwartz SS.pdf. Atlanta (GA): 2005.7:369-375. iarc. Aiba M. Office on Smoking and Health [online] 2006. Herrera B. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Tobacco related exposures. U. National Institute for Occupational Safety and Hygiene (NIOSH). Coordinating Center for Health Promotion. George CF. Soliman S. JAMA 1998.S.fr/ENG/Monographs/ allmonos90.surgeongeneral. In Report on Carcinogens. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults.94(2):314-320. Third National Report on Human Exposure to Environmental Chemicals. Hukkanen J. Pirkle JL.S. Fong I. National Toxicology Program (NTP). Exposure of the U. Vol 83. Centers for Disease Control and Prevention. Perez-Stable EJ. Mehta NY.S Department of Health and Human Services (U.S. et al. 4/13/09 Centers for Disease Control and Prevention (CDC). Warner K.pdf. Trends in the exposure of nonsmokers in the U. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Jarvis MJ.iarc. Nicotine metabolism and intake in black and white smokers. Curtin LR. Jacob P III.15:302-307. JAMA 1996. IARC Monogr Eval Carcinog Risks Hum. and the United States.280:152-156. Giovino G. Int Arch Occup Environ Health 1991. Department of Heath and Human Services. Absorption and metabolism of nicotine from cigarettes. Metabolism of nicotine to cotinine studied by a dual stable isotope method.cdc. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Modin G. DHHS). Sweeney CT. Cotinine as a biomarker of environmental tobacco smoke exposure. Pirkle JL. June. Tob Control 2006. Smoking and Tobacco Control Monograph 10 [online]. Lewis PJ. Bernert JT. References Armitage AK. population to secondhand smoke: 1988-2002.gov/library/ secondhandsmoke/. Pechacek TF. Caudill SP. 4/13/09 National Cancer Institute (NCI).S. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. 1999. Pollack HA.4:313-316. Brody DJ. 1991. [online]. Ethnic differences in N-glucuronidation of nicotine and cotinine. Tob Control 1998. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.291(3):1196-1203.275:1233-1240. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Richter PA. Maurer KR. Turner DM. Sosnoff CS. Respiratory nicotine absorption in non-smoking females during passive smoking.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. 11th ed.fr/ENG/Monographs/allmonos90. U.S.S Department of Health and Human Services (U. 4/13/09 U. Jacob III P. Environ Health Perspect 2006. Schober SE. Giovino GA. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. J Pharmacol Exp Ther 1999.114(6):853-858. Etzel RA.

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

100-.130-.gov/pesticides/. There are over 225 insect repellents brands containing DEET.S.140) < LOD .140-. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.N-Diethyl-meta-toluamide (DEET) N.170 (.120-. 2005). including seizures and encephalopathy.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.110-.EPA at: http://www.130-. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.130 (. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. have been reported as result of self-poisoning by ingestion or excessive dermal application.110 (. 134-62-3 General Information N. DEET is not a developmental or reproductive toxicant in animals (U.N..180) < LOD . Its use is recommended for prevention of several vector-borne diseases. Survey Geometric mean (95% conf. 1998).110 (. Fourth National Report on Human Exposure to Environmental Chemicals 19 .140 (.270) 688 678 518 700 598 956 Limit of detection (LOD.130) < LOD .100-. After absorption. (Kolpin et al.S.180 (.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .170 (. population from the National Health and Nutrition Examination Survey. DEET is not registered for use on agricultural commodities. 2002).100-.190) < LOD .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 .140) < LOD .110 (<LOD-. 1995.110 (. 2003). 1998).150) < LOD .epa. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .210 (. DEET is also used in combination with dermal sun screens (U. (U.S. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.1. < LOD means less than the limit of detection. DEET is not genotoxic. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Additional information is available from U.N-Diethyl-meta-toluamide (DEET) CAS No. 2003).S. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.100-. Urinary N. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. which may vary for some chemicals by year and by individual sample.130-.130 (.S. About 3-8% of dermally applied DEET is absorbed.140) < LOD .449 and 0..110-. One survey detected DEET in 74% of sampled streams in the U. EPA.S.160) < LOD .220 (. Sudakin and Trevathan. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .100 (<LOD-.110 (<LOD-.560) < LOD .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 .180 (.120-. 2002). and it has not been rated by IARC or NTP with respect to human carcinogenicity..180 (. and they range in concentration from 4% to 100%.130-. DEET can be applied to clothing and the skin to repel biting insects. DEET has low acute toxicity.130) < LOD .100-.130 (.250) < LOD .520) < LOD .100-. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.EPA.EPA. Neurological effects in humans.110 (.240) < LOD .

150-. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.230-.190 (<LOD-.500) size 1977 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .630) < LOD .550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2007).N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.170-.270-. Urinary DEET levels as high as 5.130 (<LOD-.280-1.490) < LOD . 20 Fourth National Report on Human Exposure to Environmental Chemicals .200 (. Urinary N.640 (.440) < LOD .350-.250-.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.370-.230-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.390-. 1992). DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.330 (.250 (.320 (.240) < 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 .140-.410 (.410 (.500 (.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .240-. In this survey period.250) < LOD .270) < LOD .S.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.480 (. population from the National Health and Nutrition Examination Survey.410-.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .190 (..320) < LOD .290-.300 (. 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. 2005).350) < LOD .190-. representative subsamples from NHANES 2001-2002.190 (.330 (.270 (.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 .93) < LOD .280 (.150) < LOD .N.350) < LOD .270 (<LOD-.230) < LOD .. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.370) < LOD .

J Toxicol Clin Toxicol 2003.S. pp. Meyer MT.S.S. 1-118.41(6):831-839. 4/9/09 U. 2005.EPA).gov/oppsrrd1/REDs/0002red. Pharmaceuticals. Osimitz TG.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. U.N. Centers for Disease Control and Prevention (CDC). September 1998. Gabriel KL. Washington (DC): U. Int J Toxicol 2002. Quandt SA. streams. Chen H. Tapia J. hormones. Environmental Protection Agency (U.N-Diethyl-meta-toluamide (DEET) References Arcury TA. and excretion of N. Selim S. Environ Sci Technol 2002.EPA. 1999-2000: a national reconnaissance. Available at URL: http://www. Hartnagel RE Jr.115(8):1254-1260. Grzywacz JG. Toxicity and Exposure Assessment in Children’s Health. DeBord KE. 2005 Kolpin DW. Available at URL: http://www.S. Barber LB. Thurman EM. pdf. Trevathan WR. Barr DB.25:95-100. metabolism. Bell JW.EPA).pdf. Page BC. Environ Health Perspect 2007. Smallwood AW.36(6):1202-1211. et al. J Anal Toxicol 1992.S. Absorption. DEET: a review and update of safety and risk in the general population.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers. Lowry LK. EPA 738-R98-010. Diethyltoluamide (DEET). Atlanta (GA).16(1):10-13. Veltri JC. and other organic wastewater contaminants in U. Third National Report on Human Exposure to Environmental Chemicals. Human exposures to N.gov/teach/chem_summ/ DEET_summary. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Reregistration Eligibility Decision (RED): DEET. Sudakin DL. Furlong ET. Zaugg SD. Fundam Appl Toxicol 1995. N. Schoenig GP. Environmental Protection Agency (U.epa.S.2:341352. Chemical Summary.S. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.epa.N-diethyl-mtoluamide following dermal application to human volunteers. 1993-1997. U. EPA.

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

eu/ health/ph_risk/committees/sct/documents/out156_en. Zaugg SD. Caudill SP. Gray GM. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Ispra. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Fujii S. Imai H. vom Saal FS. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Lynch BS. Doull J. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR).jrc.145:592-603.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Available at URL: http://cerhr. Available at URL: http://ecb. Calafat AM. Toxicol Sci 2002. Yoshinaga J. Department of Health and Human Services. T.S. Tyl RW. Occup Environ Med 2002. Serizawa S. Ekong J. Twomey K.. Howdeshell KL.780(2):365-370.. MacLusky.59(4):403-408.niehs. Klinefelter GR.68(1):121-146.312(2):441-448. Hlywka JJ. DirectorateGeneral Health and Consumer Protection. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Hara K.10:875-921. Bisphenol A.nih. et al.nih. Chem Res Toxicol 2001.pdf . November 26. J Chromatogr B Analyt Technol Biomed Life Sci 2002.gov/chemicals/bisphenol/BPAFinalEPVF112607. Kim CS. Thurman EM. Environ Sci Technol 2002.102(19):7014-7019.35(2 Pt 1):238-254. et al. Reprod Toxicol 2001. with estrogen receptors alpha and beta. K. Needham LL. Wong LY. 2008. Environ Health Perspect 2008. Kim JC. and other organic wastewater contaminants in U. Ye X. Kroes R. C.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Barber LB. Furlong ET. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Cohen JT. Nippon Eiseigaku Zasshi 2004. Rhomberg et al. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. August 2001. Research Triangle Park. 4. Brine DR. Cha SW. bisphenol A glucuronide.gov/chemicals/bisphenol/bisphenol. Ikka T. et al. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. niehs.pdf. and Hajszan. Kim YH. Belgium. Joint Research Centre Institute of Health and Consumer Protection. Needham LL. Thomas BF. Italy. Park S. Kiguchi M.149:988-994. Biochem Biophys Res Commun 2003. Han SY. N. 1999-2000: a national reconnaissance. Human Health. National Toxicology Program. Endocrinology 2008.pdf.Scientific Committee on Toxicity. Arakawa C. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Calafat AM. Rat two-generation reproductive toxicity study of bisphenol A.europa.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt.Environmental Phenols References Akingbemi BT. Watanabe C. Kolpin DW. Pharmaceuticals. Keimowitz AR. Reidy JA. Harazono A. An evaluation of the possible carcinogenicity of bisphenol A to humans. European Commission. streams. Exposure of the U. May 22. Zacharewski TR. Gender differences in the levels of bisphenol A metabolites in urine.. Timms BG. Chung MK. Furukawa M. Regul Toxicol Pharmacol 2002. Han SS. 2003.14(2):149-157.137(3):353-362. Sottas CM. Life Sci 2001. Hanaoka T.69(22):2611-2625. NC. Tsugane S. Ecotoxicity and the Environment (CSTEE). Ema M. Meyer MT. Proc Natl Acad Sci USA 2005. and Hardy MP.59(9):625-628. Kuklenyik Z. Bradley S. Joskow R.S. U. Cunha G. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Yang M. Leranth.pdf .nih. Richter CA. J Am Dent Assoc 2006. Available at URL: http://ec. Haighton LA. 2/4/09 European Commission. Barr DB. Koh WS. Koulova AI. Available at URL: http://cerhr. Matthews JB. 5: 505-523. Calafat AM. Hughes C.J.S. September. Brussels. Rubin C.pdf.116(1):39-44. Szigeti-Buck. McConnell EE. Hum Ecol Risk Assess 2004. National Institutes of Health. Reidy JA. niehs. Barton L. In vitro and in vivo interactions of bisphenol A and its metabolite. National Institute of Environmental Health Sciences. Environ Health Perspect 2005. Myers CB. Watanabe S. 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. Marr MC. Shin HC. 2002. Kawamura N. Barr JR. Needham LL.113(4):391-395. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. hormones. Pyo MY. Available at URL: http://ntp. 2/4/09 Ouchi K. Endocrinology 2004.36(6):1202-1211. Munro IC. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. 2007. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). 2/4/09 Fujimaki K. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra.

Kawamoto T. vom Saal FS. III. Dekant W. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Kim SY. Jang JY. Lordo RA. bisphenol-A. et al. and nonylphenol at home and daycare. Chang SS. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Vom Saal FS. An observational study of the potential exposures of preschool children to pentachlorophenol. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Witorsch RJ. Endocrinology 2006.40(7):905-12. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Environ Health Perspect 2005. Large effects from small exposures. Csanady GA. Colnot T. Biological monitoring of bisphenol a in a Korean population. Morgan MK. Arch Environ Contam Toxicol 2003.103(1):9-20. Food Chem Toxicol 2002. Sheldon LS.44(4):546-51. Wilson NK. Chem Res Toxicol 2002.147(6 Suppl):S56-69.113(8):926-33. Welshons WV.Environmental Phenols Volkel W. Chuang JC. Environ Res 2007. Lee SM. Filser JG. Hughes C. Nagel SC.15:12811287. Yang M. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment.

.400) 1. 1997.700-1. and to alkylphenoxycarboxylates.900 (. 2002).000 tons of alkylphenol ethoxylates were produced annually worldwide. which may vary for some chemicals by year and by individual sample.600-1.. industrial cleaners. which are anionic surfactants used in detergents.70 (1. and the polyethoxy chain may consist of up to 50 ethoxy units. 1996). Survey Geometric mean (95% conf. did not bioaccumulate.800-1. fish) and drinking water. Disposition in humans has not been studied sufficiently.. < LOD means less than the limit of detection.60) 1.500-1.00 (.10 (.S. to shorter chain alkylphenol ethoxylates. 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.20-2.g. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.300-. In the 1990s. Indoor and to a lesser extent. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.507) * < LOD . Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates. the various alkylphenols have also been used as emulsifiers and modifiers in paints.357 (. testicular atrophy.60-3.497) * .500) .10) 1.900 (. through sewage.900 (.30 (.00) 1229 1288 03-04 03-04 03-04 * . Laws et al.900 (.900 (. and some personal care products. 34 Fourth National Report on Human Exposure to Environmental Chemicals .50-3. Less frequently. 2000.60-3. 2003.300 (<LOD-. 1995.40) 1.20) 1. The alkylphenol ethoxylates enter the environment through human use of products containing them.30) 90th 1..600-1.60-3.70 (1. over 500. 2002).389 (. leading to inhalation as another potential exposure route (Rudel et al. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.40) 2.20-2.369 (.500) 75th .. In rats.274-.90) 2.2.400 (. and impaired spermatogenesis (e. altered neonatal sexual development.90) 2.1.3.200-.300 (<LOD-.40) 1. Ying et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.50) ..30) 1. have demonstrated estrogenic effects particularly when injected at high doses in animals.300 (<LOD-.30-2.50) 1.20) 2.. Several alkylphenols.70 (1.600) .600-1.60) 613 652 1092 Limit of detection (LOD. is used to manufacture alkylphenol ethoxylates.20-2.60-3.400 (.500) ..S.10 (. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).300 (<LOD-. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. 4-octylphenol monoethoxylate was detected in 43. altered estrus cycles and reproductive outcomes.400 (.20-2. Blake and Boockfor. and from contact with some personal care products and detergents. 2000.5% of 139 U. including 4-tert-octylphenol.60) .40 (1. 2006. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-. textiles.600-1. The alkylphenols can bioaccumulate in some fish.477) .80 (1..10-2.00 (.20 (1.70 (1.30 (1.10) 2. During the 1980s and 1990s.30 (1.30 (1. Bian et al.268-. 140-66-9 General Information 4-tert-Octyphenol.500) .20-2.80 (1. Katsuda et al. and some of their degradation products are toxic to aquatic life. population from the National Health and Nutrition Examination Survey.40) 2.30 (1. an alkylphenol. pesticides. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. and emulsifiers. and through manufacturing waste streams (Warhurst.50) 1.600) .500 (.50-2. Saito et al.10 (1.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. orally administered 4-tert-octylphenol was well absorbed.Environmental Phenols 4-tert-Octylphenol CAS No.g.50) 1.300-.500-1.00 (1. see Data Analysis section) for Survey year 03-04 is 0.60-3.300 (<LOD-. In 1999-2000. streams in 30 states (Kolpin et al.50) . several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.60-3. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.50 (1.20) 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 . Urinary 4-tert-Octylphenol (4-[1.40) * 03-04 03-04 03-04 .30) 2.299-. and was quickly eliminated from the blood (Certa et al.80) 2.600-1.600-1.600) 1..600) .20) 314 715 1488 03-04 03-04 * * . 2004). impaired steroidogenesis.80 (1.20-2.

50 (2. 2004).460 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. representative subsample of NHANES 2003-2004.08) 1.11) 2.31 (1.06 (2.14) 314 713 1487 03-04 03-04 * * .00 (.199-.620-1. Urinary 4-tert-Octylphenol (4-[1. 2001). Sweeney et al. 4-tert-Octylphenol is not considered directly genotoxic.630-1. or their corresponding ethoxylates with respect to human carcinogenicity.33) 3.269 (..610) .380 (<LOD-.300 (<LOD-.41) .05-2..76 (2. It is unclear if estrogenic or other effects occur in animals through oral dosing.S. Tyl et al.68) 2.29) 2.730-1..00) 2.36-3.78) 3.85 (1.53-3.54) * 03-04 03-04 03-04 .40-4.00 (.59 (1.Environmental Phenols Myllymaki et al. 2003.470-1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.207-. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.62 (1.78 (1.1. IARC and NTP have not rated octylphenol.40 (1. Survey Geometric mean (95% conf.S.64 (.320 (<LOD-.435 (.640-1.410 (.60 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.68-2.450) .03 (1.470) 75th .11) 1. population from the National Health and Nutrition Examination Survey.276 (.170-.25-2.540-1.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 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.270 (.00) 1.25) 2.31-2.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.740 (. at lower or environmentally relevant doses (Blake et al.400) .337-.620) .96-4.384) * .270-.17 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..65-3. 2000.280-.73) 2.22) .450) 1.420) .59) 1.78) 1228 1286 03-04 03-04 03-04 * .270 (.740 (.370 (<LOD-.62) .02-4.25) 90th 1.890-2.15) 1.260 (<LOD-.570) ..20 (1.67-2.00) 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 .860 (.910 (. Kawaguchi et al.71) 2.349) * < LOD .500-1.03-6.3. 2005.43) 1.33 (2. 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.11-2. Fourth National Report on Human Exposure to Environmental Chemicals 35 .560) .470-1.81 (1.160-. Calafat et al.18-4. In a small number of adult Japanese volunteers.770 (.550-1.62 (1. 2004. Nagao et al. Yoshida et al.43) 1. 2001..10-2. nonylphenol.00) 2.03 (1.850 (. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.530) .43-3. 1999).

Laws SC. Brooks AN. 2/4/09 Ying GG. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Brody JG. Blake CA. prolactin. 1995. Warhurst AM. Wong LY. and other endocrine-disrupting compounds in indoor air and dust. Korn LR. testis size. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone.207(1):59-68. Regul Toxicol Pharmacol 1999. Environ Sci Technol 2003.14(5):325-332. streams. Sweeney T. Toppari J. Kookana R. Millette CF. Kawaguchi M.36(6):1202-1211. Saito I. Wiegand HJ. Pharmaceuticals. polybrominated diphenyl ethers. Ye X. Nagao T. Reprod Toxicol 2004. Xu L. Takai N. Endocrinology 2000. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats.57(2):255-266. Bodman GJ. Thurman EM. Seely JC. Certa H.folliclestimulating hormone.54(1):154-167. Myers CB.foe. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Inoue K. Song L.S. Makino T. Katsuda S. Carey SA. Taya K.Environmental Phenols References Bian Q. Haavisto TE. Calafat AM. Nair-Menon JU. Brine DR. Boockfor FR. Anal Chim Acta 486:41-50. Sakui N. Meyer MT. Toxicol Lett 2001. Ito R. Two-generation reproduction study with para-tert-octylphenol in rats.28(3):215-226.165(3):217-226. Usumi K. Tyl RW. Okada F. Raychoudhury SS.37(20):4543-53. 1999-2000: a national reconnaissance. Qian J.799(1):119-125.30(2 Pt 1):81-95. Indoor Air 2004. nonylphenol. Environ Sci Technol 2002. Furlong ET. Watanabe G. Barber LB. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Spengler JD.co.121(1):21-33. alkylphenols. Muller AM. Exposure of the U. Karjalainen M. Ferrell JM. and sertoli cell number. Needham LL. Yoshida M. Myllymaki SA. et al. Yoshida M. and testosterone. Horie M. Seto H. Onuki A. Environ Int 2002. Toxicol Sci 2000. Bolt HM. Toxicol Appl Pharmacol 2005. Arch Toxicol 1996. An environmental assessment of alkylphenol ethoxylates and alkylphenols. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Nicol L. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Takenaka A. Fedtke N. Kolpin DW. Zaugg SD. et al.uk/resource/reports/ethoxylates_alkylphenols. pesticides. Chen J.44(8):1355-1361.116(1):39-44. Phthalates. McCoy GL. Food Chem Toxicol 2006. Estrogenic activity of octylphenol. Boockfor FR. Saito Y. Taya K. Roche JF. Marr MC. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol.15(6):683-692.S. Camann DE. Blake CA. 2003. Inoue K. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Katsuda S. and other organic wastewater contaminants in U. Biol Reprod 1997. Rudel RA. Indoor air pollution by alkylphenols in Tokyo. Cooper RL.pdf. Toxicol Appl Pharmacol 2000. Yoshimura S. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Izumi S. Reidy JA. Fail PA.141(7):2667-2673. Wang X. hormones. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Kawaguchi M. Maekawa A. Available at URL: http:// www. Reprod Toxicol 2001. Yoshimura Y. Ono H. 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. Williams B. et al. bisphenol A and methoxychlor in rats. Nakagomi M.71(1-2):112-122. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Paranko J. Maekawa A.18(1):43-51. Environ Health Perspect 2008. et al. Watanabe G.

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

2 (37.5) 13.S.8-63.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.29-12.1) 14.2) 12.2-46.4-19. Urinary Triclosan (2.50-10.0 (26.5-86.1) 9.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.7) 292 (151-432) 132 (78.6-111) 33.45 (5.40-17.6) 31.86-12.3 (26.7 (9.0) 9.60 (6.16 (6.1) 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 9.1) 9.5-14.22-10.6) 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 9.9-61.00-8.1) 11.89-11.6) 90th 212 (172-241) 03-04 03-04 03-04 9.4) 7.74 (5.4 (12.2 (10.0) 65.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14. interval) 12.9 (11.20-10.0-15.6-14.4) 73.0-213) 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 .6-14.2-58.8 (21.32-14. population from the National Health and Nutrition Examination Survey.3-67.4) 90th 249 (188-304) 03-04 03-04 03-04 8.90-10.30-14.7 (14.6 (10.45-13.8-85.20-11.8-112) 30.6-20.9) 75th 47.1) 9.3) 6.3 (11.3-35. Survey Geometric mean (95% conf.5) 20.4 (11.1) 9.0-73.9-236) 193 (90.11-11.8) 14. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 2.4.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.43-13.4.0 (8.8-127) 37.48-10.4 (38.6) 39.0 (36.7 (28.9) 8.5 (11.94 (7.50) 10.9 (50.Environmental Phenols Urinary Triclosan (2.9) 32.6 (9.2) 9.7 (39.92-12.0 (34.8) 116 (39.40-11.8) 9.2 (13.82 (8.18 (5.2-14.4) 25.3 (8.4-18.60 (8.2 (25.2 (27.6 (30.48 (8.S.10-9.20 (7.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.3-15.6-37.7 (11.0-15.10) 84.1) 7.6-65.93 (7.1 (8. interval) 13.3) 47.2) 13.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.7) 123 (36.8-60.4) 317 (231-433) 144 (96.1 (45.80 (5. population from the National Health and Nutrition Examination Survey.1-39.20-13.54 (8.4 (32.1 (15.9) 7.00 (4.3) 10.20 (7.3 (9.21 (6.9 (33.9 (8.6) 12.1) 13.1) 50.6 (12.38-18.6) 10.0) 49.0-19.4) 75th 43.0 (11.4) 51.45-10.2 (11.5) 11.7) 10.8) 7.72-13.5) 66.2-58.55 (4.70-16.6-15.3.4) 357 (225-456) 203 (87.3-31.

Wong LY. Bodey GP. Readman JW. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Aranami K. Photolytic degradation of triclosan in freshwater and seawater. Pinney SM. streams. Sandborgh-Englund G. Odham G.67(4):532-537. J Invest Dermatol 1976. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Aquat Toxicol 2006.83(1):84.7/2. Furia T. Toxicology of 2. Evidence of 2. Leonard PA. Pharmaceuticals. Wolff MS.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Kaneshima H. Pharmacokinetics of triclosan following oral ingestion in humans. Gomez MJ. Furlong ET. Bhargava HN. Clapson DJ. Levy SB. Environ Health Perspect 2008.4’-trichloro-2’hydroxydiphenyl ether). Ogawa H. hormones. Gunderson MP. IMS Ind Med Surg 1969. Nagao Y. 1999-2000: a national reconnaissance. Br J Clin Pharmacol 1987. The oral retention and antiplaque efficacy of triclosan in human volunteers. Fourth National Report on Human Exposure to Environmental Chemicals 39 . 4’-trichloro-2’-hydroxydiphenyl ether. Gilbert RJ.4. Hong HC.45 Suppl 2:S137-S147. et al. Thurman EM.Environmental Phenols References Aiello AE.115:116-121. 4. Kolpin DW. Moss T. Ye X.S. and other organic wastewater contaminants in U.66:1052-1056. Meyer MT. J Toxicol Environ Health A 2006. Chelimo C. Wigmore H. phthalates. Katsura E. Okui T. Teitelbaum SL.28(9):1748-1751.38(2):64-71. Barber LB. Pilot study of urinary biomarkers of phytoestrogens. Lyman FL. Anal Chim Acta 1004. Needham LL. Veldhoen N. Environ Sci Technol 2002.524:241-247. Windham G. Calafat AM. Ebersole R.17(5):637-644. Britton JA. Hirano M. Developmental evaluation of a potential non-steroidal estrogen: triclosan.38(4):361370. Ekstrand J.80(3):217-227. Am J Infect Control 1996. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Zaugg SD. Aguera A. Arch Environ Contam Toxicol 1988. Osachoff H. et al. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Howes D. Kanetoshi A. et al. population: 2003-2004. Matsumura N. Bennett ER. Biol Pharm Bull 2005. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). et al. Chemosphere 2007. Ferrer I.69(20):1861-1873. Fernandez-Alba AR. and phenols in girls. Williams FM. Reidy JA. Benson WH. Urinary concentrations of triclosan in the U. Foran CM. Mar Environ Res 2000. Williams PE.36(6):1202-1211..23(5):579-583. Triclosan: applications and safety. Watanabe N. Erratum in: Aquat Toxicol 2007.116(3):303-307. Mezcua M. Adolfsson-Erici M.24(3):209-218. Shiratsuchi H. Larson EL. Environ Health Perspect 2007. Skirrow RC.50(1-5):153-156.S. Hernando MD. Food Chem Toxicol 2000. Ishibashi H. Percutaneous penetration and dermal metabolism of triclosan (2.

47-3. and possibly of lindane (IPCS.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . Effects including hyperthermia.990 (<LOD-2. In the environment.350-1. 1976.350-2.62 (.650) 1.350 (.350 (.350 (. Acute.350-.350 (..90) 2.58-2.54-2.09) .10 (.g.01 (<LOD-1. and metabolic acidosis were observed in CAS No.40 (.S. bactericide.350-.350) < LOD .350 (.510-3.42) 696 680 521 696 603 951 Limit of detection (LOD.350) < LOD < LOD 75th . population from the National Health and Nutrition Examination Survey. PCP use in the U.75) 2.350 (.350) < LOD .350) 90th .350) .90 (1. with repeated or chronic exposure.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .650 (. After a single dose.350-2.350 (.350 (.850-2. herbicide.30) .350) < LOD .350-.350 (.98 (1.350) < LOD .350-.51) 1.25 and 0.350-2.83 (2.58-2.350-.350-.350-.350-.18 (<LOD-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.350 (.64) 1. 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) < LOD .350-.350-.350 (.53) size 1994 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .350 (.10 (<LOD-1.890-1. water and sediments because of the large amounts that were produced and used historically.10 (1. General population exposure to PCP may occur by inhalation of contaminated air.00) 1.94 (1.860-2.350-.990-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. which may vary for some chemicals by year and by individual sample.350-2. are eliminated in the urine.45-2.390 (. PCP is absorbed rapidly and well by all exposure routes.33) .30) 1.94 (1.590-1. plants. 1986). and dermal contact with PCP-treated products.960) 1.00 (.30 (1.00) 1.80) . 1979).350) < LOD .42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .5.65 (.350-. along with small amounts of tetrachlorohydroquinone and conjugates.350-. PCP is eliminated over a few days (Braun et al.76) 1.350) < LOD .350 (.350) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.67) 1. and animals.70) 2.37) . has been restricted.350-1.350) < LOD . high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.91 (1.980 (.350) < LOD . mollusicide. 40 Fourth National Report on Human Exposure to Environmental Chemicals .48 (.480-2.350 (..350 (. Kohli et al. 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.37 (. PCP has been detected in soils.530) 1.680-1.47-5.350-. so it is relatively non-persistent.350 (.70) .60) 1.60) 1.30) 1. Survey Geometric mean (95% conf.770 (.33-2.50) 1. ingestion of contaminated food or water.350-.08-3.76) .890 (. and it is used primarily as a preservative for wood to be used outdoors (e.350) < LOD .48-2.350-1.350 (. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown..350) < LOD .500-2. PCP is distributed to most tissues and is not extensively metabolized. PCP cannot be used on wood in residential or agricultural buildings.350 (. 1997).510-5.30 (.10) 1.78) 1.S. algaecide and insecticide.32 (.350-. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.23 (. To-Figueras et al. air. hypertension. After absorption.350-. < LOD means less than the limit of detection.660 (.350-.350-.350) < LOD .630 (..30 (.350) < LOD .350 (. The parent compound and conjugates.350 (.65 (.350-. PCP is degraded by sunlight and metabolized rapidly by microorganisms.390 (.350-..73 (1.04) 1.350-2. other polychlorinated benzenes.90) 1. Human exposure to PCP has become less common.350) < LOD . the elimination half-life may be a week or more (Uhl et al.350-1. Since 1984.350) < LOD . 2002.00) 2.350 (. utility poles and fence posts).350-.10) 1.

510-.00) 1.34 (. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.67 (1.40) 1.25-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.00-1.330-.25) 1.650 (.08 and 5.36) . Fourth National Report on Human Exposure to Environmental Chemicals 41 ..780) < LOD .260 (. 2004.250 (. OSHA has established an occupational standard.300 (.56) 1.40) 1.18 (1.900-1..40-2.. 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.16 (.52) 1.epa.580-.270-.25 (1.94 (1.340-.560) < LOD .82 (1.310) < LOD .13 (.21 (.html.06) 1.780-1.0 mg/L.290) < LOD .S.560-.S.26 (1.430-.40) 1.9 mg/L.35-2.950-1.30) 1. 2003). 1989).710-1.430) < LOD .73 (1.910-1.6 and 14. and the FDA has established a standard for bottled water.19) 2.490) < LOD .350) < LOD .300 (.S.25-2.420) < LOD .360-.10-2.92) 1.Fungicides adults and children severely exposed to PCP through ingestion.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .35) 1.67-3.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .800) < LOD 1.220-.240-.09-1.75) 1.55) 973 1190 1021 1337 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.310-.360 (.220-.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 .67 (1.30-2.84) 1.55) 1.40) 1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 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.25 (1.29-3..990 (.610 (.21-2. respectively) (Seifert et al. 2003). inhalation. population from the National Health and Nutrition Examination Survey.75 (<LOD-2.00-1.18) .950-1.630 (.500 (. 1991)..25-1.67-2.30 (.700-2.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 (4.51) 1.280) < LOD .09 (<LOD-2.67 (1. EPA has developed standards for PCP in drinking water and the environment. Among adults in the NHANES 1999-2000 subsample.06-3.570 (. 2000).57 (.90) 1.cdc.S.19) 2.290-. The U.380-.57 (1.19 (1.83 (1. environmental levels) and health effects is available from the U.10 (1. Death can result from seizures and cardiovascular collapse.510-.52 (1..67 (1.320 (..650) 90th 1. van Raaij et al.84 (1.800-1.94-3.78) 1. children in the 1980’s.EPA.. More information about external exposure (i.67 (1. 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. respectively) (Becker et al. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.11) 2.370 (.250 (.35-2.19) 2. carcinogenic. In a small sample of U.290-. 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.470 (.300 (.560) < LOD .850 (. or skin absorption.82) 1. In NHANES 2001-2002 subsamples.06 (.590) < LOD .52 (<LOD-1.650 (.400 (. Survey Geometric mean (95% conf.830) < LOD .320) < LOD .26 (1.84-4.79) 1.16-1.40) 1.500-1.94 (1. 1989).320) < LOD .320) < LOD < LOD 75th .730) < LOD .67-3. 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.52 (<LOD-1.500-. and adversely affected thyroid function (U.48-2. 1995). Pentachlorophenol is not mutagenic or teratogenic.gov/ toxpro2. In animals.920 (.95) 3. chronically administered high doses of PCP were hepatotoxic.950-1.gov/ pesticides/ and from ATSDR at: http://www. EPA at: http://www.760 (.590-1.S.atsdr.35) 1.440 (.78) 1.69 (1.270-.

Available at URL: h t t p : / / w w w. To T.58:182-186.S. urine. Rodamilans M. et al. van den Berg KJ. 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. 4/21/09 van Raaij JA. Can J Biochem 1976. Shealy DB. 2002.18:475-481. Seifert B.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Gregg M. Hill RH Jr. Seifert B. Blau GE. Arch Environ Contam Toxicol 1989. Notten WR. Needham LL. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. U.18(4):469-474. Bragt PC. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Environmental Protection Agency (U. hair. International Programme on Chemical Safety (IPCS). Jones D. Seiwert M. Becker K. Hill RH Jr. Pharmacokinetics of pentachlorophenol in man. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Arch Toxicol 1986.71:99108. Head SL. Braun WH.inchem. Krause C. Kaus S. Pesticide residues in urine of adults living in the United States: reference range concentrations. Fast DM. Schmid P. r e g u l a t i o n s . Sala M. Barrot C. Smith SJ. Safe A.10:552-65.org/documents/jmpr/jmpmono/2002pr08. house dust. Lindane. Santiago-Silva M. Environ Health Perspect 1997. PCP: Human Risk Characterization [online]. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. References Becker K. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Hill RH. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Environ Res 1995. Schulz C. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. 4/21/09 Kohli J. et al. Schulz C. available at URL: http://www. drinking water and indoor air. Bailey SL. Int J Hyg Environ Health 2003. Phillips DL. Engel R. Dev Toxicol Environ Sci 1979. et al. Arch Environ Contam Toxicol 1989. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Uhl S. To-Figueras J.54(3):203-208. Needham LL. Chenoweth MB. EPA). 11/30/2004. 206:15-24. J Expo Anal Environ Epidemiol 2000. Otero R. htm. Seiwert M. Cline RE. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects.4:289296. 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. Schlatter C. Baker S. Holler JS. Helm D. Toxicology 1991: 67(1):107-16. The metabolism of higher chlorinated benzene isomers.S.105(1):78-83.

450 (<LOD-.490 (<LOD-.20 (1. 2006).466 (. it was used in home sanitizers for surfaces. 2006).402-.50 (1. General population exposure can occur via dermal.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .600-1.621) * . such as fruits and vegetables.. population from the National Health and Nutrition Examination Survey.790) 2.550-1.370-.690-1. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.690) < LOD . Workers who manufacture.60-3.3.S.710-2.490 (<LOD-..14 (<LOD-3.349-.20 (.950) < LOD .540-2.50 (1.30) 1.645) * .780) < LOD .490 (<LOD-.40-5. and it has limited water solubility. OPP is considered to be moderately toxic after acute oral doses in animal studies.450 (<LOD-.386-.570 (.03) 1.770 (. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment. are antimicrobial agents used as bacteriostats.50) < LOD . but OPP and SOPP are still used on pears and citrus (U.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.480-1.970 (.390-. leaving the chemical residue OPP. 1989).552 (. Available evidence suggests that OPP does not accumulate in the body. Both have been used in agriculture to control fungal and bacterial growth on stored crops.389-.60 (1.00) .20 (1.30-7.389-.34) 1.50) 1.00) < LOD .840-1.90) 2.50) .Fungicides ortho-Phenylphenol CAS No.600) < LOD .EPA. OPP is volatile.09) 2.370-. sodium ortho-phenylphenate (SOPP).10-2.S.890 (.20) < LOD 2. EPA.570-2. 2006).88) 1.630) < LOD .10) 2.60 (1.20) < LOD 1. Cnubben et al.22) 2.880-2. 1998). formulate. SOPP is applied topically to the crop and then rinsed off.570-1.40-2.624) * .600) < LOD 75th .890) 1..90 (1. Survey Geometric mean (95% conf.410-.60-2.433-.61) 2.40 (.567 (.740 (.800-3.50-3.600) < LOD .50) < LOD . small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.710) 3. Timchalk et al. In the past.450 (<LOD-.02) 1.23) 695 680 520 695 603 953 Limit of detection (LOD.364-.90) 1. however.S. or apply these chemicals may be more highly exposed than the general population.890 (.496 (.10) 1.30 (1.570-.350-1.498 (.10 (1. in paints. OPP is still used as a disinfectant fungicide for industrial applications.490 (<LOD-. on ornamental plants and turfs. < LOD means less than the limit of detection.600) < LOD 1.30-2.696) * .S.670) 2.00 (1.00) .500-2.3 and 0.640) < LOD .610-1.20) 2. Most agricultural food applications have been revoked. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30) < LOD 90th 1.820 (.85) 2.17 (.770 (.00 (1.50-4.90 (1. inhalational.22 (.07 (. 2002.10) 1.590-2.80 (2.600-1.80) 1.30) < LOD 1.509 (. whereas SOPP is not volatile and is more water soluble.50-2.40-5.836) * .33 (.28 (.40-7. and as a wood preservative.76) 1.00 (1.10-1.50) < LOD . Both chemicals degrade within hours to weeks in the environment (U.00-2. or 2-phenylphenol) and its water-soluble salt.580-1.92 (.490 (<LOD-.420 (<LOD-.750-2.27 (.50 (1. Fourth National Report on Human Exposure to Environmental Chemicals 43 .600-1. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.520 (.930 (.60 (1.570 (. 90-43-7 General Information Ortho-phenylphenol (OPP.10) .508 (.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 .10 (1.28-3.860 (.742) * . OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.638) * .80) 1.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 . OPP is efficiently absorbed from the gastrointestinal tract and through the skin.470 (<LOD-. 2006). interval) .493 (. Estimated human intakes have been below recommended intake limits (U.EPA. 1998.10) .19 (.610 (. and sanitizers.370-. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.497 (.830 (. which may vary for some chemicals by year and by individual sample.850 (.00 (1.90) .20-3.10) .20-2.90) .860) * 99-00 01-02 99-00 01-02 99-00 01-02 . fungicides.30) < LOD .760-2.560-8.636) * .80-3.

93) .29) 1.74 (1.670) < LOD .666) * .382 (.81) 1.20) < LOD 3. 1999.epa. 1992.S. Survey Geometric mean (95% conf.29) 1. 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...910 (.301-.560-2.02 (.455-.4 mg dermally had urinary levels of OPP that were several hundred times higher than median levels found in NHANES 1999-2000 and 2001-2002 (Bartels et al.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.670 (.09-3. by possible genotoxic mechanisms (Hagiwara et al.12) < LOD 1.00 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.89 (1. Detectable levels were seen in over half the U.440 (.59) .43) 3.25-6.11 (.550) < LOD .96) 1.28 (<LOD-4. 2002.44 (1.S.780-14.. Zhao et al.97 (2. 1993.950) < LOD .380 (.61 (.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.S. 2005).EPA 2006).840 (..04-4.33-2.510-. Pathak and Roy.24-2.750 (.43-2.EPA 2006).670 (.480-.970) 1. or developmental toxicity was observed (Bomhard et al.420 (<LOD-..46) < LOD 1. or. CDC.980 (.05-2.420 (<LOD-.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 .570) < LOD 1.84 (1.93) .26) 1.31) < LOD .770-2.470 (<LOD-. OPP was not found to be mutagenic.59) 1.910-1.52 (. U.500) < LOD .09 (1.403-.800-1.640-1. 2000.11 (. Ito et al. Brusick. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.75 (1.38-3.75 (1.S.590) * .791) * .514 (.gov/pesticides/.28 (2. Bomhard et al.291-.43-2.360 (<LOD-. leading to production of two metabolites. Kwok et al.361-.18) 2. Volunteers exposed to 0.329-.900-1.568) * . 1999.550 (.EPA at: http:// www.27) < LOD .311-.17) 2..410 (<LOD-.980 (<LOD-1.17 (. 44 Fourth National Report on Human Exposure to Environmental Chemicals .S.750 (.560) < LOD 75th . 1998.11-1.12-2. Biomonitoring Information Urinary OPP levels reflect recent exposure.320 (<LOD-.444 (.33) .580-1.61 (2.64 (2.61 (1.17 (.96 (1.32) 1.550-.353-.11) < LOD 90th 1.580) < LOD . but no neurologic. 2005. 2002.780 (.93 (1.Fungicides anemia..08) 1.38) 2.01) 1. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP. 2002).58) 2.270-.47) . and it has classified OPP as not classifiable with respect to human carcinogenicity.53) 1. Nakagawa et al. 1984.656) * .08-2.21) 1. 1997. less likely. 1984.453 (. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.21-2.510 (<LOD-. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.473) * .860 (. 2005).460-.810) < LOD .06 (1.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 ...78 (2.21 (.940-2.13) 1.93) 1. 1986).385 (. U.38) 1.62) .96 (1.24-2.08-1. population from the National Health and Nutrition Examination Survey.248-.91 (1. reproductive.09-6.51-3.4) 3.88-4.343 (.508) * .496 (.620-1.484) * .900) < LOD .06-5.880-1.11) 4.. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) .96-4.610) < LOD 1.17) * 99-00 01-02 99-00 01-02 99-00 01-02 . Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.86 (1. Murata et al.650-1.07) 2.40-13.0) 1.810-1. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.600-1. In high dose animal studies.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .620-1.910 (<LOD-1.43 (1.690 (.00 (.69 (1.990) < LOD .860 (. IARC has classified SOPP as a possible human carcinogen.750-2.470) < LOD . Additional information is available from U.410 (<LOD-.06-4.32) 3. Smith et al.

Hakkert BC. et al. Kwok ES. Bartels MJ. Shirai T. Narang A.EPA). Arnold LL. 2005. Richter M.32(6):551-625. Ito N. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol.22(10):809-814. Environmental Protection Agency (U.286(2):309-319. Christenson WR. Toxicol Appl Pharmacol 1998. Gierthy J. Bormett GA.pdf. Smith RA.pdf. Bartels MJ.epa. Bartels MJ. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Brusick D. Leser KH. Elliott GR. Xenobiotica 1998. Sangha GK. Meuling WJ. Herbold BA. U. EPA-560/5-89-003.150(2):402-413. Toxicol Appl Pharmacol 1999. Food Chem Toxicol 1984. 2006. Kawanishi S. National Toxicology Program (NTP). Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. rat and man.35(2 Pt 1):198-208. Moore GA. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Hagiwara A. Stanley JS.gov/ntp/htdocs/LT_ rpts/tr301. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Freyberger A. Bartels MJ. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Hirose M. J Agric Food Chem 2002.(56):399-407. McNett DA. July 28. Shibata M.. 1989. Buchholz BA. Eastmond DA.Fungicides References Appel KE. 4/9/09.54(16):5731-5735. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Coelhan M. Murata M. Christenson WR. Atlanta (GA). EPA 739 R-06004. Environ Mol Mutagen 2005. Eadon G. Carcinogenesis 1999. Mutat Res 1993. et al. J Agric Food Chem 2006. Bromig KH. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. 4/13/09 Onstot JD. Hum Exp Toxicol 1998. Third National Report on Human Exposure to Environmental Chemicals. Turteltaub KW.28(6):579594.S. Roy D.niehs. Biochem Pharmacol 1992. U.S.74(2):61-71. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Vogel JS. Glas K. Office of Toxic Substances.S. Imaida K.gov/oppsrrd1/REDs/ phenylphenol_red. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Bomhard EM.50(11):3351-3358. St John MK.703(12):97-104.17(8):411-417. Fukushima S. Crit Rev Toxicol 2002. Available at URL: http://www. Timchalk C. Regul Toxicol Pharmacol 2002. Ito N. 90-43-7) in Swiss CD-1 mice (dermal studies). Drugs. Cnubben NH. Mendrala AL. Arch Toxicol 2000. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP).45(5):460-481. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Brzak KA. Sangha G. Identification of SARA compounds in adipose tissue. Roberts AL. Brendler-Schwaab SY.nih. Tayama S. March 1986.43(7):14311437. EPA). Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Selim S.S. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Pathak DN.20(5):851-857. Centers for Disease Control and Prevention (CDC). Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Moldeus P. Hagiwara A. Inoue S. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Timchalk C.159(1):18-24. Nakagawa Y. Zhao S. van de Sandt JJ. IARC Sci Publ 1984. Fukushima S. Environmental Protection Agency (U. Comparative metabolism of orthophenylphenol in mouse. Available at URL: http://ntp. Cano M. Moriya K. food additives and natural products as promoters in rat urinary bladder carcinogenesis. J Chromatogr B Biomed Sci Appl 1997. The carcinogenicity of the biocide ortho-phenylphenol.

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

renal injury.. Feng and Wratten. Davison et al. environmental levels) is available from U. 2006).. nasal epithelia. 2005. 1996).EPA 2000. General population exposure to acetochlor may occur through diet or drinking water.. Additional information about external exposure (i. Biomonitoring studies on levels of acetochlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of acetochlor than are found in the general population. Acetochlor has low acute toxicity.. mainly corn.. Kolpin et al. a major pathway for acetochlor metabolism involves mercapturate conjugation. in some species and at doses above maximum tolerated doses. but other pathways occur. In animals. Jefferies et al. 1989.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al. 1994. Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. and it is unlikely to be genotoxic at relevant doses (Ashby et al.Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure.gov/ pesticides/. Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8. People exposed to acetochlor will excrete acetochlor mercapturate in their urine. which are often more prevalent in the environment.e. and has been detected in watersheds of agricultural lands (Battaglin et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2006). 2000).S. animals have demonstrated tumors of the lung. including one that produces 2-methyl-6ethylaniline and its reactive metabolite. Urinary acetochlor mercapturate levels of 0. It is absorbed by plants and inhibits plant protein synthesis. NTP and IARC do not have ratings regarding human carcinogenicity.. EPA at: http://www.. 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. 2000.0 μg/L (Curwin et al. Fourth National Report on Human Exposure to Environmental Chemicals 47 . and hydroxymethyl ethyl aniline (U. Estimated human intakes of acetochlor have been below recommended limits (U. the latter which may account for some observed effects (Coleman et al.EPA. Acetochlor is not mutagenic. and thyroid (U. 2000. however. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2000.EPA. U. 2006).S. 2005). this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. 2005). 2007).EPA considers acetochlor likely to be carcinogenic in humans.EPA.S. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid. and neurologic movement abnormalities (U. However. Plants can degrade acetochlor to 2-ethyl-6-methylaniline.S. 2006). Acetochlor is moderately toxic to fish and honey bees. remains in soils for up to 3 months.epa.. Hladik et al. Acetochlor is microbiologically degraded..S. but it has produced testicular atrophy.S. 1998). CAS No. 2-hydroxyethyl-6-methylaniline..

Survey Geometric mean (95% conf.S. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 48 Fourth National Report on Human Exposure to Environmental Chemicals . Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor 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 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. 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.1. 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. < 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. see Data Analysis section) for Survey year 01-02 is 0.S.

Centers for Disease Control and Prevention (CDC). Kinney PL.248(2-3):123-133. Davison KL. EPA 738-R-00-009. 5/30/06 U. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Hum Exp Toxicol 1996. Bravo R. EPA).15(9):702-735. Barr JR. Environ Health Perspect 2000. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Volume 65. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Environmental Protection Agency (U. Chem Res Toxicol 1998.248(2-3):115-122. Roberts AL.Herbicides References Ashby J. Casida JE. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. and other herbicides in rivers. Linderman R. Battaglin WA.17(6):559-566. Sci Total Environ 2000. Environmental Protection Agency (U. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Atlanta (GA).24(10):1003-1012. Deddens JA. Third National Report on Human Exposure to Environmental Chemicals. et al. Olsson AO. 1998. Feil VJ. 2000. Striley CA. Feng PCC. Hines CJ. Federal Register: January 24. Acetochlor (Harness) Pesticide Petition Filing 1/00.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. acetochlor. March 2006. Hsiao JJ. Occurrence of sulfonylurea. pages 3682-3690. Thurman EM.pdf. et al.cce. U. Available at URL(non U. et al.cornell. Environ Health Perspect 2003.S. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Hein MJ. Lefevre PA. Green T. Andrews HF. Hladik ML. Larsen GL. Furlong ET. Linhart SM. Alavanja MC. J Agri Food Chem 1989.37(4):10881093. imidazolinone. Wilson AG. EPA). and metolachlor herbicides in rats. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Kolpin DW.39(17):6561-6574. Quistad GB. Comparative metabolism and elimination of acetanilide compounds by rat.108(12):1151-1157. Available at URL: http://www. Environ Sci Technol 2005. Curwin BD.S.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Heederik D.S. J Expo Sci Environ Epidemiol 2007. Peter CJ. Dialkylquinonimines validated as in vivo metabolites of alachlor. Rose RL. Reynolds SJ. Burkhardt MR. sulfonamide. Barr DB. reservoirs and ground water in the Midwestern United States. 2005. Jefferies PR.S. Sci Total Environ 2000.11(4):353359. Hodgson E.EPA): http://pmep. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.S. Barr DB. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Camann DE.15(6):500-508. Coleman S. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Ward EM. epa. 5/30/06.html. Whyatt RM. Tinwell H. Number 15. Xenobiotica 1994. J Expo Anal Environ Epidemiol 2005. Wratten SJ.111(5):749-756. Barr DB. Sanderson WT. Kier L.

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

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

revised February 15. Peter CJ. Occurrence of sulfonylurea.htm. Sci Total Environ 2000. EPA 738R-98-020. Clark JM. Davison KL. Kimmel EC. Thake DC. Kinney PL. Brown MA. Feil VJ.43(9):2504-2512.43(25):2087-94. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. 4/2/09 U. WHO/ FAO Data Sheets on Pesticides. 1998. Striley CA. Roberts AL. Casida JE. Hines CJ. 2/27/09 U. Xenobiotica 1994. Lau H. et al. Available at URL: http://water. Barr JR. 1999. Supplemental Technical Information (available on-line only). Martens MA. Biagini RE. Life Sci 1988. 86. Kolpin DW. Casida JE. Reregistration Eligibility Decision (RED) Alachlor. 1996. Centers for Disease Control and Prevention (CDC).39(17):6561-6574. Background document for development of WHO Guidelines for Drinking-water Quality. Jefferies PR. California. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Biagini R. U. Wilson AG. 2007. Hull RD. who. Deddens JA.gov/oppsrrd1/ REDs/0063. et al. December 1998. Gilliom RJ). MacKenzie B.S. Heydens WF.18(6):363-391.395(2-3):159-171. Shealy DB. Furlong ET. Sci Total Environ 2000. Hsiao JJ. Hines CJ. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Mutat Res. 1992-2001. Available at URL: http:// www.epa. Shoemaker DA. Am Ind Hyg Assoc J 1995. Sanderson WT. Bull Environ Contam Toxicol 1996. No. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Thelin GP.int/water_sanitation_health/dwq/chemicals/en/alachlor.inchem. 1997. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.Herbicides References Battaglin WA. Quistad GB. Alachlor in Drinking-water. sulfonamide. J Agri Food Chem 1989. Linhart SM. and other herbicides in rivers. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes.usgs. DNA adduct formation by alachlor metabolites. Hill AB. Geological Survey (USGS). World Health Organization (WHO).248(2-3):115-122. Environ Health Perspect 2003. ALACHLOR. Feng PCC. Hladik ML. Circular 1291. Identification of a major human urinary metabolite of alachlor by LC-MS/MS.47(6):503-517. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Available at URL: http://www. Burkhardt MR. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Available at URL: http://www.56(6):853-859. Wratten SJ. acetochlor.org/documents/pds/pds/pest86_e.44(18):1325. imidazolinone. 2/27/09 Jefferies PR.56(9):883-889. 2005.S. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Chem Res Toxicol 1998. 1999. Hill RH Jr. Driskell WJ. Quistad GB.111(5):749-756. Sacramento. Geneva.11(4):353359. 2003. Ann Occup Hyg 2003. Environ Sci Technol 2005. Tolos W. Casida JE. reservoirs and ground water in the Midwestern United States. Barr DB. Comparative metabolism and elimination of acetanilide compounds by rat. Brown KK. EPA).pdf. Erratum in: Life Sci 1989. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Kolpin DW. J Ag Food Chem 1995. Atlanta (GA).S. Third National Report on Human Exposure to Environmental Chemicals. Geological Survey (USGS). Larsen GL.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. and metolachlor herbicides in rats.S. Hum Exp Toxicol.24(10):1003-1012. Environmental Protection Agency (U. World Health Organization.248(2-3):123-133. International Programme on Chemical Safety (IPCS).pdf. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Henningsen G. March 2006. Andrews HF. 98-4245 (by Barbash JE. Dialkylquinonimines validated as in vivo metabolites of alachlor.php. Camann DE. Kier LD. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Thurman EM. Tessier DM.37(4):10881093. Whyatt RM.

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

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

J Toxicol Environ Health 1994. Perry et al. Stoker TE. Schmid J. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Cottica D. Shoemaker DA.html. Stoker TE.. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Barbieri F.atsdr. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. In small studies of Maryland residents in 19951996 (MacIntosh et al. Hayes TB. Tyrey L. 2001 [online]. In a small number of field workers. J Agric Food Chem 1982. Eldridge JC. Toxicol Sci 2000. Fleenor-Heyser DG. Cooper RL. Bersani M.76(1):190-200. Simpkins JW. Eldridge JC. 2005). 2000). Barr DB.. Gillis JH. Pfeifer KF. Biological monitoring of human exposure to atrazine. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Vonk A. Stoker TE. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Quandt SA. J Expo Anal Environ Epidemiol 2005. 1993). 2005.64(9):672-678. References Adgate JL. International Programme on Chemical Safety (IPCS). In a study of 60 farm worker children. Toxicol Sci 2000. Ferrell JM.gov/toxprofiles/tp153. 2003. Collins A. Extrom PC. Hein MJ.inchem.. Eberly LE. 2001). 3/11/09 Arcury TA. J Toxicol Environ Health 1994..cdc.htm. Mendoza M. Environ Health Perspect 2007.69(2):217-222. Tapia J. Lucas AD. The geometric mean of urinary atrazine mercapturate was 1.30(2):244-247. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Goldman JM. Stuart AA. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Seiber JN. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Goodrow MH. Barr DB. Ferioli A. Laws SC. et al. Toxicological profile for atrazine. Bradway DE. Geneva.47(6):503-517.53(2):297-307. Ferrell JM. Cooper RL. Pest Manag Sci 2005.109(6):583-590. Aldous CN. Sanderson WT. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Ann Occup Hyg 2003.115(8):1254-1260. Chen H.org/documents/pds/pds/pest82_e.61(4):331-355. Saiz SG. Lioy PJ. 1996. McElroy WK. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Third National Report on Human Exposure to Environmental Chemicals. Maroni M. et al. Proc Natl Acad Sci USA 2002. In the NHANES 2001-2002 subsample. World Health Organization. ATRAZINE. Stevens JT. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. 82. WHO/ FAO Data Sheets on Pesticides. Centers for Disease Control and Prevention (CDC). Available at URL: http:// www. Available at URL: http://www. Atlanta (GA).58(2):366-376. Gillis JH. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Reynolds SJ. Barr DB. Grzywacz JG. Clayton CA. Gammon DW. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Carr WC Jr. Wetzel LT. Moseman RF. Brown KK. Hermaphroditic. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. No. A risk assessment of atrazine use in California: human health and ecological aspects.. Agency for Toxic Substances and Disease Registry (ATSDR). 2005). levels of atrazine mercapturate were generally not detectable (CDC.43(2):155-167.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. Deddens JA. Wetzel LT. Noriega N. Blewett C. Environ Health Perspect 2001. Heederik D. Sanborn JR. et al. Striley CA. 3/11/09 Laws SC. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function.15(6):500-508. 2007). Freeman NC. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Breckenridge CB. et al. Steroids 1999. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Catenacci G. Curwin BD.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al.. et al. Biagini RE. diamino-S-chlorotriazine and hydroxyatrazine.. 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. Cooper RL. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Toxicol Sci 2003. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Jones AD. Lee M. Toxicol Lett 1993. Hines CJ.99(8):5476-5480.43(2):155-167. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. et al. atrazine was detected in only four children (Arcury et al.

Lansbergen GW. Available at URL: http://www. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat.58(1):50-59. Rayner JL. Laws SC. Singzoni B. Dagenhart D. 3/11/09 U. U. Tortorelli J. Cooper RL. Stoker TE. Delzell E. Breckenridge CB. Dryzga MD. March 2006. 1992-2001. Ann Epidemiol 2000. 0062. Crit Rev Toxicol 1997. Environmental Protection Agency (U. Pesticides in the Nation’s Streams and Ground Water. Environmental Protection Agency (U. May 2003a.S. Case No. 6/1/09 U. Toxicol Sci 2000.9(5):494-501.6(1):107-116. 2003b. Circular 1291. Chem Res Toxicol 1993. J Toxicol Environ Health A 1999. Kastl PE. Guidici DL. Environmental Fate and Effects Division. Fenton SE. Stevens JT.Herbicides development of a biomarker of exposure. Langvardt PW. Toxicol Appl Pharmacol 2004.gov/oppsrrd1/REDs/ atrazine_ired. The Quality of Our Nation’s Waters. A review of epidemiologic studies of triazine herbicides and cancer.S. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.pdf.S. Stoker TE. Cooper RL. A risk characterization for atrazine: oncogenicity profile. EPA Office of Pesticide Programs. 2007. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Washington (DC). Toxicol Appl Pharmacol 2002. MacIntosh DL. White paper on potential developmental effects of atrazine on amphibians. van den Berg M.27(6):599612. Ryan PB.php. EPA). Boerma J.S. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Interim Reregistration Eligibility Decision For Atrazine.195(1):23-34.10(7):479. Toxicol Sci 2002. Supplemental Technical Information (available on-line only). Christiani D. Geological Survey (USGS). Timchalk C. Available at URL: http://water. J Expo Anal Environ Epidemiol 1999. Hammerstrom KA. Wetzel L. Needham LL.usgs. Sanderson JT.S. A longitudinal investigation of selected pesticide metabolites in urine. Sathiakumar N. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats.67(2):198-206. Wood C.epa. Osborne DW. Available at URL: http://www. Pesticides and Toxic Substances. Laws SC.61(1):27-40.182(1):44-54. Toxicology 1990.epa.pdf. Urinary biomarkers of atrazine exposure among farm pesticide applicators. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Guidici DL. EPA). Perry M.56(2):69-109. revised February 15. Office of Prevention.

It was first registered with U.690 (. with a half-life of several days to several weeks.210 (<LOD-.10 (<LOD-1.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .410) < LOD .4-D were used in the U. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.22) < LOD . 2.690 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.952 and 0. the chlorophenoxy herbicide 2. agricultural. nausea. Once absorbed.S.670-1.16) < LOD . Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.10 (<LOD-1.4-D is rapidly absorbed via oral and inhalation routes.560-1.330 (. At low levels.32 (1.350) < LOD < LOD < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. MCPA. it acts as a plant growth hormone.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.760 (.27 (.30 (<LOD-2.20 (<LOD-1.07 (.4-D has low acute toxicity.43) 1. abdominal pain.40) 1.02-1.610 (. Fourth National Report on Human Exposure to Environmental Chemicals 57 . 2005). Similar to other chlorophenoxy herbicides.230 (<LOD-.420) < LOD .21) 1.680-1. and mecoprop). General population exposure to 2.05-2.490) < LOD < LOD < LOD .10) < LOD 1.27 (1.740 (. It is poorly bound in soils. which may vary for some chemicals by year and by individual sample. 2007). Recent estimates of chronic intakes of 2.03) 695 659 520 668 589 892 Limit of detection (LOD.66) < LOD 1.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.55 (1. Kohli et al. by direct contact with agricultural and residential areas after applications. Human health effects from 2.910) 1.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. dizziness.4-D can be applied either as an aqueous salt or as oil-soluble esters.320) 90th .00-2.4-D have been below recommended intake limits (U. hypotension.250 (<LOD-.730 (.27-2.08) < LOD .810-1.70) 1.210-. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. myotonia.S.250 (<LOD-.51 (1.890) < LOD .930 (. headache. As much as 62 million pounds of 2. 1989. in 2001 (U.230-.S. 1974.310) < LOD .370-. renal and hepatic injury.490 (.EPA in 1948..49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .S.960-1.610-.560-. and by consuming food or drinking water contaminated with 2.910) < LOD . 2004).690-1.EPA.420-. Sauerhoff et al. 1977). but at higher levels they are herbicidal.260 (<LOD-. 2. these herbicides can enhance plant growth. 4-D.60) 1.. 2.890 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. population from the National Health and Nutrition Examination Survey.4-D or exposed for prolonged periods.24 (. 2.400) < LOD . and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.S. and aquatic environments.4-dichlorophenoxyacetic acid (2. It is rarely detected in ground waters (USGS.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 . It is not well absorbed through the skin.20 (.13) < LOD .Herbicides 2.80) 1.660) 1.690 (..2.4-Dichlorophenoxyacetic Acid CAS No.440-1.550-1. Survey Geometric mean (95% conf. and delayed Urinary 2.4-D may occur during residential applications.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .540-.48) < LOD 1.4-D) controls broadleaf weeds in residential.EPA.930-1.310 (. 94-75-7 General Information Widely used throughout the United States. < LOD means less than the limit of detection.

820-1. liver.gov/pesticides/. and of adults and children (Baker et al. It is unclear whether these associations are related to the chlorophenoxy herbicides. 2005).41 (1.4-D levels were detectable in less than a quarter of the individuals studied. 1995).550-. IPCS.S.56) .. 1980. 1996.620-. and evidence of histological injury to the kidneys.4-D reflect recent exposure.32 (<LOD-2.640 (.670 (..S.13 (.3. other exposures.S. 2005).490 (.410 (<LOD-.890) < LOD 1. IOM. Acute high doses administered to laboratory animals produced ataxia.740 (..470) < LOD .4-D are eye irritants..epa. Post-application levels in farmers and home gardeners were dependent on Urinary 2. 1989). 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. 58 Fourth National Report on Human Exposure to Environmental Chemicals . 2003. U.610-.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. 1985. 2002.410) < LOD 1.480 (. 2005). IPCS. 2005.780) .780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S. or teratogenic effects in chronic rodent studies (Charles et al.890-1. 1996.410) < LOD < LOD < LOD . Knopp et al.570) < LOD .790) 1.790) < LOD . 2005. 2005. 2005. U.680) < LOD . 2002.380 (<LOD-.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 . 2006.930-1.4-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.920) < LOD 1. 2005). Average post-application urinary levels of 2.4-D does not have significant reproductive. in small samples of children (Hill et al.. 2.440 (. myotonia. Survey Geometric mean (95% conf. urinary 2.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .980) < LOD 1. 2.. CDC.73) .8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. 1996.700 (.EPA.380) < LOD .27-1.380 (<LOD-.390) < LOD < LOD < LOD . or to contaminants in the herbicide formulations (specifically 2.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .720 (.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.350 (<LOD-. population from the National Health and Nutrition Examination Survey. 1995. 1992). IPCS.590 (<LOD-1. Biomonitoring Information Urinary levels of 2. Kutz et al.4-D production plant workers and a few forestry workers spraying 2.. Kolmodin-Hedman and Erne.610-.340 (. Hill et al.05) . eyes. 2.08 (.S. U. U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.08 (.7. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. 2004).17 (.S.660 (. 1994).660) < LOD .16) 1.560-. thyroid.Herbicides neuropathy (Bradberry et al.330-. population (Hill et al.19) . 2000).580-.340-.410) 90th .4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.810-1.380-. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.35) < LOD .850) < LOD .270 (<LOD-. Pearce and McLean.670 (.EPA. In previous samples of the U.39) < LOD 1.780-1. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.810-1.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.590 (<LOD-1. developmental.EPA 2005).EPA at: http://www. adrenals and gonads (NTP. Additional information is available from U.13 (.. The acid and salt forms of 2.EPA. Epidemiological studies have reported associations of several types of cancer.14 (.24) 1..990-1. 2001. Frank et al.670 (<LOD-1.780 (.S.560-.270-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08 (.520-.

Arnold EK.4-dichlorophenoxyacetic acid and its forms. Ripley BD. Developmental toxicity studies in rats and rabbits on 2. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Baker SE. Barr DB.4-D than levels found in the general population. International Programme on Chemical Safety-INCHEM (IPCS). Hein MJ. Stephenson GR. Arch Environ Contam Toxicol 1989. Environ Res 1995. TOX-63: TOXICITY REPORT CURVES. Board on Health Promotion and Disease Prevention. J Expo Anal Environ Epidemiol 2000. National Toxicology Program (NTP). Barr DB. Centers for Disease Control and Prevention (CDC).5-T).4-D in urine does not mean that the level of the 2.4-. Available at URL: http:// www. 2005).4:427-435. 2005.gov/index. Carter-Pokras OD. 2. et al.inchem. Chapman P. Arch Toxicol Suppl 1980. 1992). Curwin BD. Biomonitoring of herbicides in Ontario farm applicators. Sirons G J. Tables. Mandel JS. Khanna RN.32(4):233-257. Sanderson WT.31(2):121-125. J Toxicol Environ Health 1992.4:318-321.4-Dichlorophenoxyacetic Acid). Philbert MA. Fast DM. Harris SA. Tandon JS. Alexander BH. Xenobiotica 1974. 2005). Solomon KR. the amount of pesticide applied. Absorption and excretion of 2.71(2):99-108. Forestry workers involved in aerial application of 2. Garabrant DH. and the use of protective clothing or equipment (Arbuckle et al. Reynolds SJ. Review of 2.4-D will result in an adverse health effect.edu/catalog.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. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Third National Report on Human Exposure to Environmental Chemicals. van Ravenzwaay B. Washington (DC): National Academies Press. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.nih. Kolmodin-Hedman B.4-D.15(6):500-508. Driskell WJ. Atlanta (GA).Herbicides the time since application. Veterans and Agent Orange: update 2002. Pesticides residues in food: 1996 evaluations Part II Toxicology. In farm families. 2005 Charles JM. Arch Environ Contam Toxicol 1985. Needham LL. Frank R. Bus JS. Heederik D.niehs. Ritter L. References Arbuckle TE. 2006. Biomonitoring for farm families in the farm family exposure study.31 Suppl 1:90-97. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Assessment of exposure to 2.18(4):469-474. Exposure of homeowners and bystanders to 2. Beeson MD. Erne K.4:97-100. Toxicol Sci 2001. Cook BT.4-dichlorophenoxyacetic acid in man.4-dichlorophenoxyacetic acid (2. Estimation of occupational exposure to phenoxy acids (2.37(2):277-291. Hill RH Jr.27(1):23-38. To T. Dhar MM. Honeycutt R. Murphy RS. 2003. Holler JS. Smith SJ.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Baker S. Biomonitoring studies of 2. Crit Rev Toxicol 2002. Occup Environ Med 1994. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.php?record_id=10603. Hanley TR Jr. et al. Gupta BN. 2005.4-D) epidemiology and toxicology... 914.4-D): exposure and urinary excretion. Updated March 7.htm. Bailey SL. Harris et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. Dichlorophenoxyacetic acid. general population. Acquavella JF. Available at URL: http://ntp. the number of acres to which it was applied (Curwin et al.nap. Scand J Work Environ Health 2005. 3/17/09 Knopp D. Selected pesticide residues and metabolites in urine from a survey of the U. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Mandel et al. Survival and Growth Curves from NTP Toxicity Studies.. Baker BA. Hill RH Jr. et al.4 dichlorophenoxyacetic acid (2. Kutz FW. 3/17/09 Institute of Medicine (IOM). Sircar KP.10(6 Pt 2):789-798. Kohli JD.51(3):152-159.. Campbell RA.31 Suppl 1:98-104. Needham LL. Beasley VR. Brody D.org/documents/jmpr/jmpmono/v96pr04.4-D were highest in the farmers who applied the 2. Available at URL: http:// www. J Expo Anal Environ Epidemiol 2005 Nov.S. Wilson RD. Cole DC. Gregg M. Head SL. Scand J Work Environ Health 2005. Shealy DB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4-dichlorophenoxyacetic acid (2.60(1):121-131. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Vet Hum Toxicol 1989. geometric mean urinary levels of 2. Finding a measurable amount of 2.4-D and 2.4-D).4. J Environ Sci Health B 1992. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. TOX-63 Peroxisone Project (2.

Blau GE. The fate of 2. Environmental Protection Agency (U.S.htm. Environmental Protection Agency (U.8:3-1U. Braun WH. 2004.S.php.S. March 2006.usgs.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.gov/oppsrrd1/ REDs/factsheets/24d_fs. EPA 738 F-05-002.epa. 3/17/09. The Quality of Our Nation’s Waters. 2.EPA). Supplemental Technical Information (available on-line only). Office of Prevention Pesticides and Toxic Substances. Pesticides in the Nation’s Streams and Ground Water. Gehring PJ. 2007.4-D RED Facts.pdf.EPA.S.4-D) following oral administration to man. May. gov/oppbead1/pestsales/01pestsales/market_estimates2001. 60 Fourth National Report on Human Exposure to Environmental Chemicals .EPA).Herbicides Sauerhoff MW. S. Toxicology 1977. Washington (DC): U. 3/17/09 U. Pesticide industry sales and usage . Geological Survey (USGS). Available at URL: http://www. 4/2/09 U. June 2005.S. 1992-2001. Available at URL: http://www.epa.4-dichlorophenoxyacetic acid (2. Available at URL: http://water. revised February 15. Circular 1291.2000 and 2001 market estimates.

1995. 2005). Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Hines et al. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. 2003). Feng and Wratten. formulators. and convulsions were observed at lethal doses in animal studies. 1998). Fourth National Report on Human Exposure to Environmental Chemicals 61 . This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment.S. 2003).S.. sorghum and other crops.200 μg/L (CDC. and it was not mutagenic in mammalian cells (U. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. including corn. The geometric mean metolachlor mercapturate was 4. U. 1999. and field workers may have significant exposures via this route. 1994. Salivation. though the 95th percentile for males was 0. 2000. Metolachlor has low potential for acute toxicity (U. 2005.. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample.S. Davison 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. Occasionally in the past. 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.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine.epa. Metolachlor is well absorbed dermally. WHO. USGS. in both ground and surface waters (Battaglin et al..Herbicides Metolachlor available from U.EPA. WHO. Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. Biomonitoring Information CAS No. 2007. mercapturate conjugates were the predominant metabolites. metolachlor levels in water have exceeded lifetime human health advisory levels (U. 1995). 2007. soybeans.EPA considers metolachlor to be a possible human carcinogen. People exposed to metolachlor will excrete metolachlor mercapturate in their urine. Estimated human intakes have been below recommended limits (U. 1995). Metolachlor did not show developmental or reproductive toxicity in chronic animal studies. 1995). Kolpin et al. and eliminated in urine and feces over two to three days (WHO.. lacrimation.S. so applicators.S. but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. (2003) showed that 2. It is absorbed by plants and inhibits plant protein synthesis.EPA. In animals. 1989.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. EPA at: http://www. Hladik et al.. General population exposure may occur through the consumption of contaminated food or drinking water. Gilliom. Jefferies et al. 2000. and on non-crop land for general weed control. 2003). NTP and IARC do not have ratings regarding human carcinogenicity. 2005). In animal studies. EPA.. 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. whereas 60% of applicators had detectable amounts.S. metolachlor was quickly absorbed after dermal or oral doses..gov/pesticides/. Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect.EPA.

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

Kolpin DW.php. Hsiao JJ. Pesticides in U. Third National Report on Human Exposure to Environmental Chemicals. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Striley CA.S. Thurman EM.S. Available at URL: http://www.47(6):503-517. 4/2/09 U. Ward EM. U. Kinney PL. Larsen GL. Linderman R. 98-4245 (by Barbash JE. 1998.pdf. Sci Total Environ 2000. 3/26/09 U. Gilliom RJ). R.html. Sci Total Environ 2000. Background document for development of WHO Guidelines for Drinking-water Quality. sulfonamide. Jefferies PR. and other herbicides in rivers. Furlong ET.39(17):6561-6574. Occurrence of sulfonylurea. EPA 738R-95-006. Hein MJ. Davison KL. Circular 1291. Environ Health Perspect 2003.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Comparative metabolism and elimination of acetanilide compounds by rat. March 2006. Reregistration Eligibility Decision (RED) Metolachlor. Peter CJ. Feil VJ. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. April 1995. Biagini RE.int/water_sanitation_health/dwq/chemicals/ metolachlor. Xenobiotica 1994. streams and groundwater. Wratten SJ. 2007. Hladik ML. et al. Curwin BD. Heederik D.pdf. Sanderson WT. Available at URL: http://www. Andrews HF.usgs. Kolpin DW. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Quistad GB.who. Coleman S.111(5):749-756. Barr DB. 6/1/09 Whyatt RM.11(4):353359. Thelin GP. 2005. Casida JE. Barr DB. Brown KK.248(2-3):115-122.24(10):1003-1012. Camann DE. Barr JR.epa. EPA). Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Burkhardt MR. Shoemaker DA.37(4):10881093.Herbicides References Battaglin WA. Environ Sci Technol 2005. usgs. Metolachlor in Drinkingwater.ESTfeature_gilliom. Hodgson E. Atlanta (GA). Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Gillion. Supplemental Technical Information (available on-line only). 1992-2001.41:3409-3414. Alavanja MC.108(12):1151-1157.pdf 3/30/09 Hines CJ. Available at URL: http://water. Rose RL. Environmental Protection Agency (U. Linhart SM.S.gov/nawqa/pnsp/pubs/files/051507. Environ Health Perspect 2000. California. World Health Organization (WHO).15(6):500-508. Available at URL: http://water. Ann Occup Hyg 2003. Geological Survey (USGS). Sacramento. Roberts AL. and metolachlor herbicides in rats. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.gov/oppsrrd1/ REDs/0001. Chem Res Toxicol 1998. acetochlor. 1999. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. J Expo Anal Environ Epidemiol 2005.S. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Centers for Disease Control and Prevention (CDC). imidazolinone. reservoirs and ground water in the Midwestern United States. Dialkylquinonimines validated as in vivo metabolites of alachlor. Available at URL: http://water. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.S. revised February 15. Geological Survey (USGS). 2003. Deddens JA. Feng PCC.usgs.248(2-3):123-133. Environ Sci Technol 2007. et al. Reynolds SJ.gov/nawqa/ pnsp/pubs/wrir984245/text. J Agri Food Chem 1989.

Herbicides 2. Given the commercial unavailability of 2. Nelson et al. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. 1974).5-T (Holson et al.4. 2. Survey Geometric mean (95% conf. Kohli et al. population from the National Health and Nutrition Examination Survey.4. 1992). 1986. 2. Human health effects from 2.. nausea.5T is rapidly absorbed via oral and inhalation routes.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.. ranging from several weeks to many months. headache.5-T degrades to 2.. 2.4. the general population is unlikely to be exposed to it. it is not well absorbed through the skin.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5-T is eliminated mostly unchanged in the urine.5-T use as a herbicide in 1985.4.4. < LOD means less than the limit of detection. myotonia. Although 2.4. Once absorbed into the body.S. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness..4. 1989.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.5-T in soil varies with conditions.5-trichlorophenol and other degradates. these herbicides can enhance plant growth. and concern about contamination with 2.3. dizziness.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.4. The half-life of 2. 93-76-5 General Information 2. 2. hypotension..5-Trichlorophenoxyacetic Acid CAS No. but higher levels are herbicidal.4. and delayed neuropathy (Bradberry et al.4.4. At low levels. 2007).2 and 0.5-T and 2.7. Chlorophenoxy herbicides act as plant growth hormones.4.g.. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD.5-T was once applied as either an aqueous salt or as an oil-soluble ester. which may vary for some chemicals by year and by individual sample. 2004).1.5-T.5-T has been rarely detected in ground waters (USGS. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. abdominal pain. Agent Orange).4.4-D were used as defoliants in the Vietnam War (e.4.5-Trichlorophenoxyacetic acid (2.4. 64 Fourth National Report on Human Exposure to Environmental Chemicals . renal and hepatic injury. Epidemiological studies have reported associations of several types of cancer. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. Mohammad and St. Omer.4. Ester forms of 2. with an elimination half-life of approximately 19 hours (Arnold et al. 1992.

or to contaminants in the herbicide formulations (specifically 2.gov/pesticides/. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Herbicides or contaminated herbicides.4.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.5-T also were below the limit of detection (Kutz et al..5-T does not mean that the level will result in an adverse health effect. Urinary 2.EPA at: http://www. 2005).5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. IOM. Fourth National Report on Human Exposure to Environmental Chemicals 65 . 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. Pearce and McLean. Biomonitoring Information Urinary levels of 2.5-T were generally below the limit of detection.4. 2004). Survey Geometric mean (95% conf. 1992). U.S.epa.4. 1980). 2003. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.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. IPCS. 2. Biomonitoring studies on 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. in which urinary levels of 2. 2002.S.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. Finding a measurable amount of 2.3.5-T reflect recent exposure.5-T than levels found in the general population.5-T itself is not mutagenic. Additional information is available from U.4.4.4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. similar to results of NHANES II (19761980). It is unclear whether these associations are related to the chlorophenoxy herbicides. population from the National Health and Nutrition Examination Survey.7. Mean urinary levels of 2.4. urinary levels of 2.4.S.EPA. 1996. other exposures.4. 2005.

Estimation of occupational exposure to phenoxy acids (2. J Toxicol Environ Health 1992. Available at URL: http://www.4.4-D/2. Developmental toxicity of 2.htm.23(2):65-73. St Omer VE.4.pdf. Beasley VR. Neurobehav Toxicol Teratol 1986.EPA.4-. Available at URL: http:// www. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Board on Health Promotion and Disease Prevention. Environmental Protection Agency (U. Available at URL: http:// www.4:318-21. LaBorde JB.19(2):298-306.S. Absorption and excretion of 2. Scand J Work Environ Health 2005. Crit Rev Toxicol 2002. S. Centers for Disease Control and Prevention (CDC). Nelson CJ.5-t mixture. Agricultural exposures and non-Hodgkin’s lymphoma. Vet Hum Toxicol 1989. Washington (DC): U.32(4):233-257. Arch Int Pharmacodyn Ther 1974. Mohammad FK. May. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Proudfoot AT. Gaylor DW.epa.nap.8(5):551-60. Review of 2.5-T). U. Pearce N.5-T in four-way outcross mice. 3/17/09 Kohli JD.S. Atlanta (GA). Gaines TB. Brody D.2000 and 2001 market estimates.4-dichlorophenoxyacetic acid (2. International Programme on Chemical Safety-INCHEM (IPCS). Sheehan DM. Carter-Pokras OD.4. I.5-trichlorophenoxyacetic acid (2.31(2):121-125. Holson JF. Tandon JS. McLean D. Erne K.5-trichlorophenoxy acetic acid in man.4.4-D and 2. Pesticides residues in food: 1996 evaluations Part II Toxicology. Behavioral and developmental effects in rats following in utero exposure to 2. Holson JF.5-trichlorophenoxyacetic acid (2. Fundam Appl Toxicol 1992.4-D) epidemiology and toxicology. 2005.4. Gupta BN. Nelson CJ. Khanna RN.4. Gaines TB. Bradberry SM.5-T).php?record_id=10603. Dichlorophenoxyacetic acid. Veterans and Agent Orange: update 2002.edu/catalog. Vale JA. gov/oppbead1/pestsales/01pestsales/market_estimates2001. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. II.4.org/documents/jmpr/jmpmono/v96pr04. general population. Cook BT. Sircar KP. discussion 5-7. Third National Report on Human Exposure to Environmental Chemicals. Toxicol Rev 2004.37(2):277-91. Arch Toxicol Suppl 1980. et al. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.Herbicides References Arnold EK. Poisoning due to chlorophenoxy herbicides. Office of Prevention Pesticides and Toxic Substances.4. Selected pesticide residues and metabolites in urine from a survey of the U.31 Suppl 1:1825. 210:250-255.EPA). et al. Kolmodin-Hedman B. LaBorde JB. Multireplicated dose-response studies with technical and analytical grades of 2. Murphy RS.5-T). Pesticide industry sales and usage . 2. 914.inchem. Garabrant DH. Fundam Appl Toxicol 1992. 2004. 3/17/09 Institute of Medicine (IOM). Kutz FW.19(2):286-297. Washington (DC): National Academies Press.S. Dhar MM. 2003. Developmental toxicity of 2. Wolff GL. Philbert MA. McCallum WF.

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

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

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

9 (14.110 (.100-.130) .062 (.190) .049-.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.30 (8.1 (18.2-15.103 (.077-.063-. 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.5) 19.5) 21.8-17.4-18.190) .088-.3 (14.6-24.80-10.9-23.8 (18.3 (19.5 and 7.4-17.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.0 (10.8-19.100) .5-15.9-22.4) 21.00-14.112) 95th .139 (.170) .160) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110-.1) 15.150 (.1) < LOD 9.160 (.5-17.3 (18. which may vary for some chemicals by year and by individual sample.098 (.3 (13.070) .90) 90th 15. which may vary for some chemicals by year and by individual sample.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 .4) 20.7 (<LOD-15.083-.100 (.8) < LOD 8.1) 13.160 (.2) 11.093) .056-.090-.6 (15.0-25.8-17.117) < LOD .103 (.090 (.0 (15.124) .0 (11.180) .1) 10.070 (<LOD-.102 (.080 (. Fourth National Report on Human Exposure to Environmental Chemicals 79 .058) < LOD .6-24.0-21.180) .5) 15.9-38.7-22.S.090-.084-.1-18.139 (.100-.140) .140 (.120 (.055 (.2) 14.S. 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 9.062-.073-.1-24.50) 15.064 (.40-9.062 (.120-.109 (.120 (.150 (.080-.100-.6-33.6) 19.9 (12.6) 9.138) .182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .149) .2) 15.158) .4) 95th 20.090-.110) .130) . Survey years 01-02 03-04 Geometric mean (95% conf.096-.110) .40-10.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .054-.112-.5-17.4) 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 8.1) 15.140-.7) 15.089 (.7 (14. population from the National Health and Nutrition Examination Survey.4) 539 456 484 487 980 885 Limits of detection (LOD.0 (10.080) .80 (<LOD-10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.060) .5 (16.053 (<LOD-.7-19. < LOD means less than the limit of detection.8.138 (.054-.1) 14. population from the National Health and Nutrition Examination Survey. 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 (<LOD-11.064) 90th .70 (7.147 (.130-.120 (.30 (8.10 (<LOD-16.8) 14. see Data Analysis section) for survey years 01-02 and 03-04 are 10.0) < LOD 9.4 (12.130-.120) .7 (15.00 (8.1 (13.0) 21.1-16.9 (12.6) 16.059 (.110 (.109-.50 (8.130 (.4) 14.109-.130) .8-24.6 (15.80-9.4 (12.242) .069) < LOD < LOD .1-19.8 (9.130-.3 (18.110 (.9 (13.108-.2) 12.0) 19.60-10.100) .116) .7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.086-.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.101) .070-.9 (13.8-25.8 (11.048 (<LOD-.1) 20.113 (.075) < LOD .090 (<LOD-. Survey years 01-02 03-04 Geometric mean (95% conf.6 (14.3-21.4) < LOD < LOD 16.8) 15.4) 19.077 (.054-.

International Programme on Chemical Safety (IPCS).27:405-421.47:1059-1087. 6/1/09 Ward EM. Fernandez MG. August 2008. 1989. Jr. Li AA. Narahashi T. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Sonnenschein C. J Toxicol Environ Health. 2007 [online]. 731-915. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Priestly BG. Environmental Health Criteria 91.atsdr. and epidemiology in the United States.htm. Cancer Epidemiol Biomarkers Prev 2000.usgs. and lymphocyte sister chromatid exchange. 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. Demographic and seasonal influences on human serum pesticide residue levels.org/documents/ehc/ ehc/ehc91. Roy ML. 4/21/09 Hoyer AP.html. Chung KL.gov/~dms/ pesrpts. Vol. Kanthasamy AG.352:1816-1820. Schulte P. Edwards JW. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.gov/ circ/2005/1291/. Corrigan FM. Serrano FO. Available at URL: http://www. Olea N. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. 4/21/09 Jorgenson JL. Mumtaz MM. Food and Drug Administration (FDA). Grajewski B. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Shore RF. Patterson DG Jr. Stehr-Green. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. In Hayes WJ. Carlson JN. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Organochlorine exposure and risk of breast cancer. VT. Available at URL: http://www.cdc. Facca A. Exp Neurol 1998. Available at URL: http://pubs. Teta MJ. Turner W. toxicology. Mink PJ. No:429-436. 4/21/09 Bates MN. 2 Classes of Pesticides.91(1):122-126.109(Supp1):113-139. Ellis H. David VL. Revised Feb. Handbook of Pesticide Toxicology. Int Arch Occup Environ Health 1994. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Eds. Psychopharmacology (Berl) 1987.fda. Academic Press. Inc. Smith AG. Chapin RE. Tully DB. Brock JW. Buckland SJ. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Environ Health Perspect 2001. Song S.gov/toxprofiles/ tp1. Garrett N. Six high-priority organochlorine pesticides.59:229-234. Kanthasamy A. Sanchez-Ramos J. Andersen A. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. References Agency for Toxic Substances and Disease Registry (ATSDR). Patterson DG Jr.54:1431-1443. Pesticides in the Nation’s Stream and Ground Water. J Occup Environ Med 2005. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Reprod Toxicol 2000. September 2002.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Daniel SE. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. are nonestrogenic in transfected HeLa cells. Frey JM.9:1357-1367. Wienburg CL.26:701-719. Part A 2000. United States Geological Survey (USGS). Toxicological profile for aldrin/dieldrin [online]. Aldrin and Dieldrin [online]. Mann D. Cox. Soto AM.cfsan. Grandjean P. et al. et al. 1992-2001. Lancet 1998. Kitzazwa M. Jr and Laws ER.inchem. 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. Jorgensen T. plasma dieldrin. Rosellini RA. Available at URL: http://www. Hartvig HB.html. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. bioaccumulation. PA. Toxicol Lett 1992. pp. Ginsburg KS. Environ Health Perspect 1995. 15. Finley B. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants.14:95-102. Chemosphere 2004.103(Suppl 7):113-122. Basit A.64-65 Spec. 1991. Anantharam V. either singly or in combination.150:263-271. New York. Neurotoxicol 2005.66(4):229-234. J Toxicol Environ Health 1989. Needham LL. Chlorinated Hydrocarbon Insecticides.

4) 18.3-43. and in soil.8-61.4 (30.1) * 11.7-14.2-21.3 (9.6) 36.2-49.5 (31.5) 21.6-53.2 (10.9 (15.3 (21.5-43.6) 11.6 (25.7 (34.3-32. see Data Analysis section) for Survey years 99-00.8-43.2 (21.6 (9. < LOD means less than the limit of detection.8 (40.9-38. 1994.4-45.1) * 11.2) < LOD 11.4 (35.4) < LOD < LOD < LOD 23.2 (28.2) 46.6) < LOD 11.3) 41.1 (44.5 (33.2-49.63 (8.7 (42.1 (27. 1994).0) 37.3) 10.0) 21.6-45.1-65.5-38.9 (11.3-49.7 (<LOD-13. foods high in fat such as meat.3 (25.0-61. and dairy products are the usual sources of exposure to these chemicals in the general population.2 (39.1-50.6) 48.1 (40.5.9 (15.6 (16.2) 22.8) 44.1 (15.0) 27. heptachlor use has been limited to treatment of fire ants near power transformers.0) 75th 20.8) 53.2) 37.74 (<LOD-10. respectively.4) 12. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.3-45.7) 42.9 (36.8) 27.2) * 12.6-12.0) 20.5-13. buildings.7 (43. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988. from the early 1950’s until the mid-1980’s.8-42.20 (<LOD-11.3 (11.0) 31.9) 37.5 (8.8) 18. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.9) 23.8 (42.7) 28.1 (11. Technical grade chlordane had contained 7% trans-nonachlor.2 (36.0 (16.8 (17.7 (17.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.1-51.1 (25.4) < LOD 11.7) 9.7 (10.5-44.5) 10. lawns.3 (20.1-19.7-39.1 (<LOD-12.6) 49.1) 22.4 (10. fish.1) 90th 34.6-18.6) 8.2-28.8-73.9) 23.5 (34.Organochlorine Pesticides Chlordane CAS No.1) < LOD < LOD < LOD < LOD < LOD 8.4-21.2 (9. Survey Geometric mean (95% conf.0-25.0) 41.4) 22.2-26.8) 52.7) 19.2) 33.7-25.3 (27.9 (21.6 (9.7) 31.5) < LOD < LOD 9. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.90 (8.9 (26.6) 20.5) < LOD < LOD < LOD < LOD 13.0-67. 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.S.3) 18.8 (18.8 (17.3-24.9 (29.4) 37.8-33.4) 29.8-23. which may vary for some chemicals by year and by individual sample.0 (20.7 (<LOD-32.5) 44.3) 37.6 (43.2-56.3-45. 01-02.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6) 23.4-40.9-21. 10.3 (26.2) 36.1-15.5) 37. population from the National Health and Nutrition Examination Survey.7 (19.36-11.5 (41.0 (26.2 (41.69-10.5-41.9) 39.6-24.7-56.0-12.7-12.9-42.5) 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 * * * * 11.6) 48. chlordane was used to kill termites and other insects on agricultural crops.89-10.9 (11.S.3 (<LOD-19.10-18.4-14.0 (37.2 (37. Until 1988.70 (<LOD-10.5) 9. 2007).1 (<LOD-12.9-21.5-40.3) 18.2) 34.1-25.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12. 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.1) 16.8-32. the technical grade product of each chemical contains 10%-20% of the other chemical.0 (<LOD-12.8.5-47.30-11. and 03-04 are 14.10-11. Chlordane is not currently produced or used in the U.7-70.10 (8.6-24.6) 39.9) 13.7 (34.0 (32.5.8-31.0-33.8) 52.1-25.5-65.5-42. Consequently.1 (20.8 (10.20-10.5 (<LOD-12.9) 17.0-18.1 (<LOD-12.8-33.4 (<LOD-12. Since 1992.4-51.3 (28.5) 38.6) 9.9) 47.9 (31.20-11.3) 10.9) 31.8-20.9) 36.37 (8.9) 11.4 (22.4 (30. 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.0-13. As a result of the manufacturing process.9 (18.5) 56.4) 39.82-11.7 (32.5-32.9 (17. in addition to trace amounts of numerous other related compounds (ATSDR.2) < LOD 11.9) 10.1 (16. 2007).1) 30.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.7) 19.9 (26.1) 30.. Fourth National Report on Human Exposure to Environmental Chemicals 81 .1 (17.8 (10.4 (31. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.S. and 7.9) 11.9-40. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6) 9. 57-74-9 Heptachlor CAS No.7) 35.

070 (<LOD-.310-.220 (.130-.300) .061-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.068) 75th .077) ..133) 90th .160) .207) . and the U.104) .S. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.080) .300) .S.230 (.430) .280) .128 (.230) . dermal.320 (.146) < LOD < LOD .165-.080) .120-.430) .063 (. Survey Geometric mean (95% conf.207 (.070-.360) .230-.115 (.240 (.136) .087-.110 (<LOD-.246-.300-.250-.070 (<LOD-.050 (<LOD-.200-. heptachlor.119 (..320 (. Acute.302) .057) * .350 (. OSHA has established occupational exposure criteria.148) .062) < LOD .260-.067 (.310) . Chlordane is metabolized primarily to oxychlordane and to a lesser extent.066-. Elimination of all these chemicals from the body occurs over months to years.170) .150 (.320 (.253-.058-. Le Marchand et al. Chlordane and heptachlor are absorbed after oral.082 (.063 (.245-.068) .220-.130-.140 (. 1991).100-.160) . 2007. 2006).063 (.210 (.280-.190-.280 (.310) .225 (.130 (. 82 Fourth National Report on Human Exposure to Environmental Chemicals .199-.073) < LOD < LOD < LOD < LOD .189-. Shindell and Ulrich. FDA established allowable residues of chlordane. The U.083) .063) * .190-.130-.090-.063-.080) .047 (<LOD-.148-.230 (.286 (.290) .300) .066 (.290) .070 (.170) .150-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.130 (.108-.112 (. 1986).140 (.070-.260 (.064) < LOD .077) .258 (.204 (.213) * .106-.258-.160) .200-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .350) .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.146) .230-.058 (.180) .057 (.271 (.210-.120-.050-.063) .053-.240) . The major metabolite of heptachlor is heptachlor epoxide.440) .260 (.130) . neonatal mortality.053-.120 (.286 (.140-.216-.269 (.170) .057-.070 (<LOD-. 1986).077) .071 (. 1977a.115-.077) .070-.079) .063 (.287) .315 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.310) .140 (.120-. 1977b.190-. which may vary for some chemicals by year and by individual sample.130-. Smith.066 (<LOD-.126 (.090) .070) .Organochlorine Pesticides (Dallaire et al. Takahashi et al.073 (.069 (<LOD-.348) .150 (.080 (.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .170) .075 (..290 (. characterized by seizures and paralysis.055-.510) .083 (.370 (.060 (<LOD-.270 (. and alterations in immune function of offspring. and heptachlor epoxide in foods and bottled water.250 (.130) .240-. 2007).250 (.227) < LOD .070 (<LOD-.200 (.370 (.048-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity. chronic doses of heptachlor have produced liver enlargement and injury.280 (.310 (.231) .320) .210 (.300) . 1981). 1991.070) < LOD < LOD < LOD < LOD < LOD .290-.160 (.223) .170) .150 (.270 (.330 (.280-.180-. 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.126) .230-.373) . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.100-. to heptachlor.100 (<LOD-.049 (<LOD-.560) .110-.189 (.260 (.208 (. 1996.410) .350 (.079) < LOD < LOD < LOD .340) .168-.242-.320 (. and breast milk is a major excretion route in lactating women.130-.220-.400) . population from the National Health and Nutrition Examination Survey.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .065-.104-.290-.058-.100 (.056 (. EPA has established environmental criteria for chlordane and heptachlor.270 (.090) .068-.340) .091) .400) .149 (. 2001.080 (.380) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.370 (.180) . Rogan.203-.170-.150) .140-.130 (..066-.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * . 2002.074-. which is also persistent in the body (ATSDR. In laboratory animal studies.450) .180-.140 (.450) . IARC.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 * * * * .S. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.200-.076) < LOD . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.320) .300 (. and inhalation exposure.092) .290-.140) .280-.240-.

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

1 (19.7 (16.2) 26. < LOD means less than the limit of detection.8) 13.6) 22.0) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.3) 18.6) 13.3-18.7 (10.20 (<LOD-9.0-17.5 (<LOD-32.7 (13.8.1) 20.6-21. 84 Fourth National Report on Human Exposure to Environmental Chemicals .8-24.4) 21.4 (<LOD-54. and 7.6-17.0-17.3) 18.6 (14.3) 18.5 (18.0 (11.8 (15.9 (15.5) < LOD 14.3) 16.0-19.1-38.9-29.3) 22.7-18.2-17. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24. respectively.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 (<LOD-19. which may vary for some chemicals by year and by individual sample.8 (13.6.6 (13.0-16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4 (11.0) 13.8 (<LOD-23.1) 13.2 (<LOD-25. population from the National Health and Nutrition Examination Survey.7-25.2-16.2) 20.3 (13.0 (15.4) 18.8-24.3) 27.5 (<LOD-21.50) < LOD < LOD < LOD 17.6 (8.5 (11.2) 13.9-29.6 (11.5 (10.8-23.1 (16.90 (<LOD-9.8 (18.2 (18.40) 15.2 (<LOD-16.6 (16.8) 14.2-27.2-27. Survey Geometric mean (95% conf.1-15.8) 19.8) 21.1-16.8) 14.S.8 (13.8) 19.4 (11.9) 15.8-46.0-54.9 (12. see Data Analysis section) for Survey years 99-00.4 (15.3 (<LOD-25.8 (18.6 (<LOD-27.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.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.3) 23.1-29. 10.8) 16.3) 10.9-25.5) 19.8) 20.5.6 (12.8) 15.8) 13.6) < LOD < LOD < LOD 27.8-24.10-13.1) 23.2) 15.6 (16. and 03-04 are 14.5 (11.2 (<LOD-62.6) 14.9-23.7-19.9) * * * 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 8.9-16. 01-02.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.

076-.S.170) .170) .170 (.101 (.270) .133 (.077-. Fourth National Report on Human Exposure to Environmental Chemicals 85 .090 (<LOD-.100-.190 (.200 (.240) .126 (.130-.120) .130 (.113-.087 (.190) .090-.101 (.310) .090-.090-.067-.200) .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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120-.120) .120 (<LOD-.111) .180 (<LOD-.161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .057 (<LOD-.180) .113) .170) .180 (.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 .100 (.110-.190) .097) < LOD .069 (.180) .180) .090-.190) .130) .380) .110-.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.140) .170 (<LOD-.096 (.053-.170 (.110 (. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.170 (.220) .108) .100 (.110) .055 (<LOD-.098 (.117) .094 (.130-.100-.090-.110 (.074-.090-.150 (<LOD-.071-. population from the National Health and Nutrition Examination Survey.111-.128 (.104) .107-.135 (.116) < LOD < LOD < LOD .310) .070-.110) .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.130-.200) .150 (.108-.130 (<LOD-.140-.150 (.063) .110 (<LOD-.106-.130) .140) .130-.077-.063) < LOD < LOD < LOD .180) .157) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .100 (.082-.135 (.149) .100 (.094 (.120 (<LOD-.100 (<LOD-.110 (<LOD-.108) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .090 (.120 (.

8-90.5 (44.S.8 (19.8 (42.7-17.2-17.9) 14.0 (60.1 (48.3 (56.1-16.0-38.9 (19.8 (28.8-79.2) 20.6) 25.5-87.3-21. 10.1-51.0-93.0) 40.6-54.3) 30.7) 78.2) 39.8-19.8 (<LOD-20.1 (10.4 (12.3) 18.5 (15.1) 32.6) 54.9 (28.6-66.5-95.0) 75th 31.3) 19.4) 19.2 (60.2-21.8-67.1-126) 67.4-35.8 (26.7 (11.0 (42.8 (26.3-74.4-22.4-52.1 (65.6) 56.1-20.9 (29.6 (<LOD-14. and 7.9-69.0 (13.6) 84.6 (50.3 (14.2 (36.1) 17. respectively.4-62.9 (15.1 (47.1 (41.8 (17.3 (14.4 (67.1 (17.3) 30.2) 30.8 (28.9-65.0-23.8 (15.2 (15.1) 31.7 (16.2-23.3 (58.5) 9.2) 34.1-28.0-123) 74.3) 36.0-93.0 (16.8-41.3) 32.6-88.9-58.6) 34.9) 51.6 (32.1) 30.4) 16.9-36.6 (56.4) 20.7-32.2) 19.8 (30.5) 26.1) 17.7-77.7) 35.5-111) 68.4 (30. which may vary for some chemicals by year and by individual sample.1) 17.5) 78.3) 15.7-22.5) 30.1) 14.9-65.5) 36.1) 16.7 (59.8-110) 59.0 (42.3 (49.8-21.9 (51.0) < LOD < LOD 8.6-20.8-77.86-13.7) 15.7) 56.4) 59.7-35.4 (16.7 (30.3) 16.8 (12.2 (27.3 (16.5) 48.8 (28.0) 49.0-59.2 (64.0-22.8-19.5.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.3) 32.0 (29.7 (28.7 (35.1-55.2) 59.7) 52.3-50.8 (11.5-69.6-19.5) 19.8-16.9-45.2-18.9) < LOD < LOD < LOD 20.3) 18.2 (25.4 (28.2-88.1-34.0) 33.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.0 (14.0-113) 68.0) 18. Survey Geometric mean (95% conf. 01-02.9-40.1) 17.0 (15.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.1-22.7) 17.0 (48.6 (52.3-86.4 (45.9 (36.2 (19.7) 78.2 (26.9 (66.9 (47.5) 20.0-37.6) 60.8 (71.1) 18.1) 17. population from the National Health and Nutrition Examination Survey.3 (17.6 (56.1) 18.6 (16. interval) 18. 86 Fourth National Report on Human Exposure to Environmental Chemicals .3-39.7) 73.6) 13.4) 55.1) 78.0) 19.8 (26.5 (15.9 (51.5-36.0) 13.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20. and 03-04 are 14.3-58.6 (57.9-20.2) < LOD 10.1-34.1 (22.2 (7.3-57.0 (62.5) 22.3 (45.8) 19.2-18.5) 90th 55.0-24.5) 77.9-89.6) 10.2 (14.8.7-20.8-90.0-68.8 (13.4) 48.5 (25.1) 17.6-22.1) 78.9) 51.4-36.1) 62.7-23.7-113) 68.5) 35.5 (45.7-18.0 (15.9 (<LOD-14.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.2-16.5-20.0 (16.10 (<LOD-11.7-160) 86.3) 25.1-18.3-30.3-32.8 (45.2) 17.7) 28.7 (59.4 (11.8) 47.70 (<LOD-12.2-37.6 (15.8) 80.0 (13.3) 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.7-38.1) 17.2 (14.4-67.7-29.7) 14.1-16.5 (13.0 (19.8) 51. < 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.5-19.7-21.9 (16.6 (12. see Data Analysis section) for Survey years 99-00.7 (74.7) 59.9-64.9-22.4) 107 (84.7 (13.6) 56.0-20.8 (16.5) 14.0-143) 112 (68.5.5-17.8-16.4-18.7 (18.8 (49.4-23.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.0-23.8 (13.7-34.2 (59.9-35.8-129) 74.6-82.9) 14.5) 14.9 (15.6) 82.

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.240-. which may vary for some chemicals by year and by individual sample.310 (.340) .220 (.288 (.120-.090 (<LOD-.161-.100-.260) .300-.113) .242) .069-.079-.081 (.210 (.690) .590 (.220) .960) .371) .286-.141) .285-.177-.108 (.210-.090 (.080) .590) .122) .130) .210 (.330-.250) .240) .060-.098) .230 (.370 (.084-.116-.470 (.111 (.120) .128 (.103 (.460) .497-.089 (.480) .237) .350-.096-.092 (.130 (.085-.110 (.240) . interval) .367) .340-.100 (.559) .085-.240 (.068-.090-.141) .395-.120) .370 (.080 (.055 (<LOD-.078 (.580 (.417 (.150) .320-.060) .078-.390 (.S.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .093-.100-.640 (.170 (.460) .397-.414 (.081-. Survey Geometric mean (95% conf.272-.190-.112 (.930) .520) . population from the National Health and Nutrition Examination Survey.520 (.190-.651) .113) < LOD .110) .390) .186 (.830) .232) .840) .288-.580 (.510 (.120) .210) .410-.210) .106 (.054-.830) .340-.490-.117) .470-.131) .120) .124) .301-.500) .300) .106 (.110 (.550 (.330-.343 (.116 (.600 (.114) .360-.250) .220 (.279-.202 (.061-.116) .270-.573 (.130) .091-.180-.250) .240) .390) .120 (.087 (.109 (.310-.590 (.103 (.100-.150) .108) 75th .090) .594) .470 (.580 (.080-.097) .220 (.327 (.104 (.093-.070 (.120 (.490) .096) .047-.310) .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 .400-.191 (.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .210) .360-.310-.110 (.100 (.090-.108) .390 (.440-.324 (.630) .127) < LOD < LOD .071 (<LOD-.060 (<LOD-.158-.440) .220 (.690) .134) .093-.355 (.085-.800) .110 (.094 (.220 (.565) .458 (.400-.090-.090-.220 (.099-.600) .111-.080-.460-.400 (.390-.380 (.210 (.630) .112 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.680 (.330 (.420 (.290-.310-.110 (.090-.120 (.119) < LOD < LOD < LOD .062 (.430-.310-.126) .234) .173-.409-.180-.125) .069) .098 (.630) .122) .092 (.095-.190-.395) .405) .160-.211) 90th .540) .470 (.760 (.140) .280) .400 (.080-.079-.186-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .130) .490 (.461 (.120-.210-.093) .129) .220 (.317 (.105 (.130 (.510-.098 (.106 (.390 (.110 (.125 (.205 (.410-1.104-.684) .183 (.260) .110-.490 (.180-.119) Selected percentiles ( 95% confidence interval) Sample 95th .109 (. Fourth National Report on Human Exposure to Environmental Chemicals 87 .099-.400) .520 (.350 (.220 (.680) .470-.420) .190-.130) .390 (.130) .096-.237) .041 (<LOD-.160 (.082) .098-.120-.190-.135 (.100-.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.20) .190-.145-.430-.130) .130) .171-.450) .090-.080-.161) .320-.430-.091) .

Drews K. Senie R. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States.nih. Bioassay of chlordane for possible carcinogenicity.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).cdc. Mortality of workers employed in the manufacture of chlordane: an update. 4/21/09 Baker DB. Siegel BZ. Covaci A. Aune M. Granath F.org/documents/iarc/ vol79/79-12.50(3):108-118. KalubaSkotarczak A. Available at URL: http://ntp. 1986. New York. Takei G. Berkowitz GS. Sci Total Environ 2004. LeMarchand L.html. August 2007. Poland. Stehr-Green P. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Environ Res 2000.html.atsdr. Saidein D. May 1994.pdf.372:20-31. Dewailly E. Willman E. Wohlleb JC.org/site/foundation/ research/projects2.org/ documents/cicads/cicads/cicad70.nih. Environ Health Perspect 2002. Atuma S. Baker DB. 9/25/07 International Programme in Chemical Safety (IPCS). 1994-1997 organochlorine compounds. Chlorinated Hydrocarbon Insecticides. et al.110:617-624. Arch Pediatr Adolesc Med 1996. Available at URL: http://ntp. Academic Press. Dendle WH. Available at URL: http://www. Chlordane and heptachlor [online].28:497501.41:145–148. 6/1/09 Rogan WJ. International Agency for Research on Cancer (IARC). Distribution of polychlorinated biphenyls.atsdr. 79. Dewailly E.150:981-990. Pollutants in breast milk.niehs. Brower S. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Barker J. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. et al. 2001. JAMA 1988. Vol.inchem. Laliberte C. Concise International Chemical Assessment Document 70 Heptachlor [online].inchem. Organochlorines in Swedish women: determinants of serum concentrations. Toxicological profile for heptachlor and heptachlor epoxide [online]. Hertz-Picciotto I. Toxicological profile for chlordane [online]. Glynn AW. In Hayes WJ. Muckle G. 1963-1967.cdc. et al.htm. Bioassay of heptachlor for possible carcinogenicity. Van Oostdam JC. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii.84:151-161. Odland JO.9:1-109. J Occup Med 1986. maternal serum and milk from Wielkopolska region.htm. Available at URL: http://www. 731-915.259(3):374-377. Takahashi W. Canada). International Agency for Research on Cancer (IARC) . 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Environ Health Perspect 2003. Chashchin V. Natl Cancer Inst Carcinog Tech Rep Ser 1977a.110(8):835-838. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Wong L. National Toxicology Program (NTP). Voorspoels S. Environ Health Perspect 2002. 4/21/09 James RA.gov/ntp/ htdocs/LT_rpts/tr008. Inc. Lawrence River (Quebec. Keller JA. Sci Tot Environ 2006.heptachlor. Handbook of Pesticide Toxicology. A Report to the Hawaii Heptachlor Research and Education Foundation. Shindell S and Ulrich S. Head SL. 2006. Bjerselius R. Available at URL: http://www. Eds. Jaraczewska K. Available at URL: http://www.330:55-70. Tartter P. 6/1/09 National Toxicology Program (NTP).Summaries & Evaluations. Smith AG. Hawaii Med J 1991. 4/21/09 Dallaire F. Bull Environ Contam Toxicol 1981:27:506-511. Lulek J. Jr and Laws ER. Royce W. 1979-1980. Hansen JC. Bleiweiss IJ. 1991 pp. Available at URL: http://www. Jr.gov/toxprofiles/tp31. Circumpolar maternal blood contaminant survey. 2 Classes of Pesticides.pdf. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort.8:1-123. et al. Charles MJ. Ayotte P. Gilman A. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Arch Environ Health. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Vol. Kolonel LN. Organochlorine exposures and breast cancer risk in New York City women. Darnerud PO.gov/ntp/ htdocs/LT_rpts/tr009.111:349355.html. gov/toxprofiles/tp12. Loo S. Organochloride pesticide residues in human milk in Hawaii.niehs. 1993. Wolff MS.

1’-dichloro-(2.6 (22.0) 20.8) 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 8.9 (21.2 (11.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. although DDT and DDE intakes have decreased over time (FDA.0-35.0 (21.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.0-53.9) < LOD < LOD 9.1 (23. Only a small proportion of DDT is metabolized and excreted (Smith. or dermal exposure. Survey Geometric mean (95% conf.9 (10.3-236) 24.S.0 (10. after World War II until 1972. particularly meat.8) 15. when virtually all use of it was banned. DDT is converted in the environment to other more stable chemical forms.2-95. In the general U. Fourth National Report on Human Exposure to Environmental Chemicals 89 . fish.7. 1991). o.p’-DDD (4% or less). 1991). Gunderson.9 (10.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.1 (33. Food imported from countries that still use DDT may contain the chemical or its residues.3) 21.50-11. The biodegradation half-life of DDT in soil varies from 2 to 15 years.0-155) 83. 2008.5 (23. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.8-39.1 (<LOD-39.4 (23.5-54. 17.9 (10. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR. DDT can be absorbed after ingestion.8-23. 2002. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3-590) 293 (104-541) 48.1-27.2-65.0-27. p.9) 29.3) 21. which may vary for some chemicals by year and by individual sample.7 (19.9-34.9-28.1’-(2. and 03-04 are 20. DDT is converted to DDE and several other metabolites. 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. These chemicals are highly persistent in soil. population.0 (18.7) < LOD 18.3 (<LOD-31.2) 155 (59.3 (27.6 (<LOD-25.8) 30. air.7 (15.3) 28.6-33. In the body. Smith.9) 14.00 (<LOD-10.5 (14. 01-02.10-13.S.10 (<LOD-12.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. as well as in plant and animal tissues.70 (8.5) < LOD < LOD 9. food. DDT was used at one time as a treatment for head and body lice.5 (15. continues to be the primary source of DDT exposure. resulting in fetal exposure.8.1) 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.p’-DDT (15%-21%).8-17.3 (<LOD-21.5-36.3) 22.9 (<LOD-20. respectively.6 (9.5) 25.2-bis(p-chlorophenyl) ethane (DDD). see Data Analysis section) for Survey years 99-00.5) 23.4. and dairy products.0) 19.8-26. which is a mixture containing p.0) 40. population from the National Health and Nutrition Examination Survey.6 (25. including 1.9) 17.8) 36.7) 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. It is still used in some countries.0-15.4) < LOD 17.0) 26. and trace amounts of several related compounds. and water. DDT and DDE can cross the placenta. < LOD means less than the limit of detection.S.1-71. 1988). depending on conditions. particularly for endemic vector and malaria control.0-37.7-16. and 7. sediments.p’-DDT (65%-80%).7) 12.4) < LOD < LOD < LOD 61.5 (23.6 (31.1) 31. It was produced and used in the U.90 (<LOD-12.2) 30. DDT usually refers to the technical product.3-16.2 (<LOD-40. inhalation.0 (18. Both Serum p.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2) < LOD < LOD 9.

62 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.075) 1.26) 1. and altered behavior after neonatal exposure (Eriksson and Talts.240 (.065-. Beard.061) < LOD < LOD < LOD .230) .146 (.112 (..142 (.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 . Mariussen and Fonnum. In laboratory animals.078 (.140-.064 (.132-. 2001). 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.p’-DDD and p.130-.203) .627) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .190-1.230) .570-4.106) < LOD < LOD .01) .051 (<LOD-.071 (. lung cancer.080-. Calle et al. A workplace standard for DDT has been established by Serum p.201 (..087 (.098-. 2006).120-.Organochlorine Pesticides chemicals are excreted in breast milk. 2006.114-. In high dose. premature delivery. fertility..180 (..054-.084 (. 2001).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. Snedeker. 1997).150-.130 (<LOD-.00 (.220) .. and leukemia have also been inconclusive (ADSDR. DDT may bind to estrogen receptors (Chen et al.150 (<LOD-.071-. Gray et al.400 (.530 (.106) .180) ..106-. Hayes et al. 2000.190 (..313 (.180 (. overt signs of acute human toxicity include vomiting. 2004. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.140) . 2001). tremor.170) .180-.530) .34) .330-4.143) < LOD < LOD .069) . 2006).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. dioxins and furans).167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * . which may vary for some chemicals by year and by individual sample.S. Reproductive effects in humans affecting birth weight. 2006..059-. 1995.190 (. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. Longnecker et al.189-.00) .074-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. 2006.097) 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 . and seizures.128 (. resulting in exposure to nursing infants (Rogan..343) < LOD . reproductive organ abnormalities.400) .g.250-1. 2006).130 (<LOD-.086 (.290) .105-.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 .108 (. Jusko et al. have not been consistently demonstrated (Beard. population from the National Health and Nutrition Examination Survey.220) .200 (. polychlorinated biphenyls.150 (<LOD-. Survey Geometric mean (95% conf. 1956). 2001).150) .250 (.095) < LOD . Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.170-. Jusko et al. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. other organochlorines.260) . Studies of DDT exposure and pancreatic cancer.048 (<LOD-.. 1998).160-.p’-DDE can produce anti-androgenic effects (Gray et al..146 (.180) .150-. 1996).. 2002. and duration of lactation. 2002. Gladen and Rogan. 2002.420) .130 (<LOD-. Animal studies reported reduced fertility. and o.170 (.068-.079) < LOD < LOD . 90 Fourth National Report on Human Exposure to Environmental Chemicals . accidental exposures.063 (<LOD-. 2002.240) .120 (<LOD-.078-.

6 (81. mean serum levels of DDT and DDE in the U.epa. interval) 260 (226-298) Selected percentiles ( 95% confidence interval) Sample 95th 1830 (1410-2300) 2320 (1830-2780) 1860 (1400-2380) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 226 (184-278) 251 (228-278) 203 (163-275) 75th 537 (476-631) 598 (521-699) 509 (376-655) 90th 1150 (976-1350) 1410 (1210-1500) 1170 (836-1570) 295 (267-327) 238 (195-292) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 118 (102-135) 124 (106-146) 105 (84. Smith. population declined by about fivefold to tenfold. Stehr-Green. NTP considers DDT as being reasonably anticipated to be a human carcinogen. 2004).7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. Heudorf et al. 2002. 01-02. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. Fourth National Report on Human Exposure to Environmental Chemicals 91 ..gov/ toxpro2. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. and 7.atsdr.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. 2003).gov/ pestcides/ and from ATSDR at: http://www. IARC classifies DDT (p. environmental levels) and health effects is available from the U. In a population-based sample of men and women from eastern Slovakia.. In general. EPA at: http://www..e. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.S. 2003. 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. 1989). see Data Analysis section) for Survey years 99-00.p’-DDT) as a possible human carcinogen. 2005).. and 03-04 are 18.S. population from the National Health and Nutrition Examination Survey. 2002.8. More information about external exposure (i. for males and females in the NHANES 19992000 subsample (Pavuk et al.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. Compared to females in the NHANES 1999-2000 subsample.cdc. Declining DDE levels over time have also been observed in the German population.Organochlorine Pesticides OSHA and a guidance established by ACGIH.. 8.3. respectively. Since the 1970’s. respectively. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. Survey Geometric mean (95% conf. compared to levels observed in this Report (Anderson et al.. Biomonitoring Information DDE persists in the body longer than DDT. 1998. 2004). Link et al.7-119) 113 (100-140) 93.. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. 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.html..6.S. 1991).

61 (1.635) 1.66) 1.22 (7.3 (9.965-1.59) 6.36-1.03-1.16 (2.55 (2.70-3.14 (1.81) 11.13) 4.6) 9.1) 40.11-1.18 (6.43 (5.9) 7. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.34-3.81 (7.11 (2.05 (3.6) 9.31 (1.32) 1.2) 26.21) 3.52 (1.43-4.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.9-17.50 (2.52 (3.40 (3.79) 4.47 (1.64-2.75) 2. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE than are found in the general population.590 (.59 (1.19) 4.90) 22.6 (8.38 (1.35) 1.2) 19.32-9. 2004).43-4.680-1. Survey Geometric mean (95% conf.7-48.07) 1. less than one percent had detectable serum levels of o.39-2.23 (7.69) 4.4) 13.66-17.6) 9.57) 2.6 (7.796 (.61-2.21) 90th 7.01-15.488-.22-1.18-1.0) 2.36 (3.51-49.14) 2.7) 13.37 (1.76 (2.18) 1. 309 versus 268 ng/g lipid.56-3.28) 1.60-13. 1971). 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.53 (2.69 (.50-17..557) 1.88 (2.96) .02 (2.85-4.69 (2.26) 3.36) 3.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .63 (1.600) .71) 32.01-1.8 (13.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.9-38.12 (. o.87-16.623 (. Finding a measurable amount of p.37-4.71 (5.4) 9.730) .53) 7.14-9.5) 5.90-8.45 (1.91-2. High mean levels of whole blood DDT (about 3.81-18.71 (6.27-1.87 (5.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.01-5.03-4.40-8.57-2.12 (6.7) 16.7) 9.8 (14.46 (1.13-2.43-8.06) 1.646) .91-3.14-1.6) 9. 1991).38 (1.46-2.75 (8.15-4.17 (3.4 (8.44) 1.994-2.00 (.820-1.34 (7.68 (2.2 (9.611-1.0 (9.06) 3.00) 7.92 (3.82 (1.4 (12.59) 3.10-1.7 (8.32-1.18-1.41-12.68) 2.30 (1.75) 1.57 (1.9 (26.07 (5.76) 1.49 (6.72) 1.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.860 ng/L) and DDE (about 14.31-2.68-4.37-16.2 (6.3-43.58) 75th 3.91) 3.85-10. or p.8 (13.77 (1.p’-DDT (Stehr-Green.26 (1.63 (1.4) 14.7-19.25-14.49 (1.45 (1.02) 1. population from the National Health and Nutrition Examination Survey.1) 7.56-6.10-5.37-10. In the NHANES 1999-2000.02-8.81 (1.19-14.72) 1.p’-DDT.56) 2.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.25) 8. 2004).726) .62-6. considerably higher than levels in this Report (Smith.10) 2.39-1.6 (17.84 (3.3) 13.30-1.49) 8.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.34) 6.6) 11.33-1.16-1.25) 1.26-2.51-8.51-15.59 (1.37-1.99) 1.52-6.80) 1.48 (6.63 (6.97-4.385-.1 (9.01) 1.1) 12.12-1.32 (1.76) 1.9) 5.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.20 (.97 (3.5) 10.36-11.66) 1.69) 8.13 (1.53-15.0) 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 .516 (.58) 1.64) 3.51) 3.39) 1.890-1.p’-DDT.69 (1.71) 12.54 (1.3) 10.2 (19.57 (1.5) 22.63-15.8-90.p’-DDT were below the limits of detection..25 (1.56-2.57-3.55-9.520 (.32 (1.3) 16.59 (4.32-1.870 (. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.80 (2.5) 7. In a subsample of NHANES II (19761980) participants.17-3.81-5.30 (1.05) 1.6) 13.57-13.39 (3.34) 2. serum levels of o.0 (12. 2005).6 (9.25-16.9 (15.48-4.27) 3.40-4.7-20.561 (.1 (8.18-4.75 (4.47) 3.77 (1.34-11. 1989).93 (7.66) 4.04-1..963-1.92 (3.65 (1.01) 1.26-10.49 (1.29 (1.75) 6.41 (1.01-11.00-1. interval) 1.31-12.92) 1.07) 1.88-35.14) 2.96) 1.46 (1. 2001-2002 and 2003-2004 subsamples.456 (.04 (6.80) 1.534-.10) .53) 1.5) 16.54-7.51) 1.24 (1.01-11.430-.419-.6) 8.01-1.09-1.4-19. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.66-4.91 (6.S.25 (.76-3.24-17.80) 3.6) 12.70) 1.500-.66) 3.30-1.36-2.66-2.2-32.24) 1.78 (4.00 (6.18-3.3 (8.54) 8.2 (9.65) 1.82) 1.84-3.Organochlorine Pesticides nearby agriculture (Botella et al.8 (9..83 (1.58) 1.22) . Serum p.51 (1.40-4.85 (1.57 (3.8) 15.

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

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.p'-Dichlorodiphenyltrichloroethane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.Organochlorine Pesticides Serum o. 94 Fourth National Report on Human Exposure to Environmental Chemicals .S. 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. 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.

Am J Epidemiol 2002. Becker K. Sci Tot Environ 2006. Parks L. Kulkarni PK.155(4):313-322.71(6):1200-1209. Hurd C. Calle EE. Gladen BC. Krause C.html.html. et al.54:1431-1443. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.gov/~dms/ pesrpts. Environ Health Perspect 1998. Cueto C. Zhou H. Chemosphere 2005. Savitz DA. August 2008. Maternal DDT exposures in relation to fetal and 5-year growth. Gray LE Jr. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Drexler H. Zhou H. Hayes WJ. Crespo J. Gabrio T. Toxicological profile for DDT. Jr. Wolf CJ. Gray KA. The effect of known repeated oral doses of chlorophenothane (DDT) in man. and other chemicals. Organochlorines in Swedish women: determinants of serum concentrations. Furr J. Schulz C. Chemosphere 2004. J Assoc Off Anal Chem 1988. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Herrman T. Hediger ML. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Environ Health Perspect 2003. et al. and polythelia among male offspring. et al. Barr DB.53(8):1161-1172. Patterson DG Jr. Swanson MK. Seiwert M. Klebanoff MA. Durham WF. Greenfield TA. Int J Hyg Environ Health 2002. Environ Res 2005.7(3):248-264.96:34-40. Talts U. and HCB residues in human blood in Ahmedabad. Willman EJ.cfsan. Zaidi SS. Environ Health Perspect 2004. September 2002. et al.17(6):692-700.cdc. 4/21/09 Anderson HA. Kaus S. and DDD [online].358:110-114. Piechotowski I. Angerer J. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Rogan WJ. Glynn AW. Buckland SJ. Frumkin H. Hum Reprod Updat 2001. JAMA 1956. Longnecker MP. Biochem Pharmacol 1997. Organochlorines and breast cancer risk.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Jr. Falk C. FDA total diet study. Henley SJ. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Needham LL. DDE and shortened duration of lactation in a northern Mexican town. Beard J. Bloom MS. Olea N. et al. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Atuma S. Olson J. selected elements. The Great Lakes Consortium. Maternal serum level of 1. Brock JW. Rivas A. Ostby J. Thun MJ. Baker RJ. hypospadias.106(5):279-289. Needham LL.21(1-2)37-48. Moysich KB. CA Cancer J Clin 2002. Vena JE. Levels of DDT. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Available at URL: http://www. Chen CW.58:1185-1201. Gunderson EL. Food and Drug Administration (FDA). Environ Res 2004. Katz SH. Brock JW. Zoellner I. Neurotoxicol 2000. Charles MJ.112(17):1761-1767. Biomonitoring of persistent organochlorine pesticides..fda. Effects of environmental antiandrogens on reproductive development in experimental animals. 4/21/09 Gladen BC. Int J Hyg Environ Health 2003.162:890-897. Lepom P.97(2):178192. Klebanoff MA.206:485-491. Notides AC. Epidemiology 2006. Hanrahan L. Lambright C. Burse VW.355:7889. Bjerselius R. Garrett N. Heudorf U. Jusko TA. Bull Environ Contam Toxicol 2004. dietary intakes of pesticides.85:504508.72:261265. Link B. hexachlorobenzene. Ellis H. DDT and human health. dichlorodiphenyldichloroethylene. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Klebanoff MA.52:301-309. HCH. Available at URL: http://www. Vorojeikina DP. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Paepke O. Longnecker MP. April 1982 to 1984. DDE. Lancet 2001. Bates MN. India. Kashyap R. et al. Cerrillo I. Koepsell TD.1-dichloro2.205:297-308. Olea-Serrano MF.111:349355. lindane (g-HCH). Saiyed HN. Eriksson P. Arnold SF. et al.gov/ toxprofiles/tp35. et al. Am J Public Health 1995. Bhatnagar VK. Darnerud PO. Davis MD. and dichloro(diphenyl)ethylene (DDE). Aune M. Needham LL. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Botella B. et al. Exposure of women to organochlorine pesticides in Southern Spain. Profiles of ortho-polychlorinated biphenyl congeners.atsdr. Granath F. Olson JR.

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

1992).50) < LOD 5. All uses of the pesticide in the U. 1992. Endrin has been detected in soils. 1979.20 (<LOD-5.. Over time. Endrin was used as an insecticide. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. In the body. 1987).S. endrin has been detected with declining frequency in U. anti-12hydroxyendrin. inhalation or dermal exposure routes. Endrin was not widely used as a termiticide. 1992). see Data Analysis section) for Survey years 01-02 and 03-04 are 5.60 (5.70) < 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 5.8. 72-20-8 General Information Endrin. endrin is converted rapidly to its major metabolite. Ketoendrin is a major photodegradation product (IPCS. An epidemic of acute endrin poisoning. endrin usually is not detected in serum of exposed individuals.. Hepatic effects of endrin exposure have included necrosis.09 and 7.Organochlorine Pesticides Endrin CAS No. total diet surveys (FDA.S. and inflammation (Smith.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.30 (<LOD-6.S. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al.S. endrin can persist for years. IPCS. 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 does not accumulate in body tissues (IPCS.30) < LOD 5. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. Because it is metabolized so rapidly. 2008).40 (<LOD-6. unlike aldrin and dieldrin. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. or from contact with contaminated soils and sediments in areas where endrin was applied. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. Kavlock et al. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1996.40) < 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 5.40) < 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. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al.10 (<LOD-5..20 (<LOD-5. manufactured. 1992). Depending on soil conditions. and occasionally at low levels in sediment and surface waters. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. 1981).10 (<LOD-5. 1991). is no longer manufactured in the U. a stereoisomer of dieldrin. have been cancelled by the U. or discarded. rodenticide and avicide. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. < LOD means less than the limit of detection. Survey Geometric mean (95% conf. unless the dose is high and the exposure is very recent. 1991). At high doses.50) < LOD < LOD < LOD 5. Fourth National Report on Human Exposure to Environmental Chemicals 97 .S.40-5. fatty infiltration. population from the National Health and Nutrition Examination Survey. EPA. Smith. Endrin is absorbed rapidly after ingestion. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals.

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

FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Chernoff N. Saleem M. Gray JA. Patterson DG Jr. Toxicology 1979. Toxicology 1981. 4/21/09 Bates MN. Schulte P. et al. Ginsburg KS. Grajewski B. Rogers E. Perinatal toxicity of endrin in rodents. Available at URL: http://www. New York. 2 Classes of Pesticides. Patterson DG Jr. Olea-Serrano MF. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.13:155-165. I. et al. Olea N.9:1357-136.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Fetotoxic effects of prenatal exposure in hamsters. Sokal D. Handbook of Pesticide Toxicology. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.atsdr. Academic Press. Hardjotanojo W. Smith AG. Needham LL.79(6):928-934. August 1996. Perinatal toxicity of endrin in rodents. Available at URL: http://www. Cancer Epidemiol Biomarkers Prev 2000. Convulsions caused by endrin poisoning in Pakistan. 731-915. Vol.64-65 Spec. Fourth National Report on Human Exposure to Environmental Chemicals 99 .cdc. Rivas A. Frey JM. Turner W. Liddle J. pp. Exposure of women to organochlorine pesticides in Southern Spain. Available at URL: http://www.html. Endrin [online]. et al. Cerrillo I.html. 1991. Whitehouse DA. Eds. Environmental Health Criteria 130. Andersen A. Chernoff H. Roy ML. August 2008. Burse VW. Hanisch RC.21:141-150. Chemosphere 2004. Narahashi T. Inc. Gray J. Food and Drug Administration (FDA).gov/~dms/ pesrpts. Rab MA. Hanisch RC.inchem.96:34-40. 4/21/09 Kavlock RJ. Environ Res 2004. Rowley DL. Ward EM. Toxicol Lett 1992. Chlorinated Hydrocarbon Insecticides. Crespo J. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.htm. Buckland SJ. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Jr. In Hayes WJ.gov/toxprofiles/tp89. Gray LE. Jr and Laws ER.54:1431-1443. II. 4/21/09 International Programme on Chemical Safety (IPCS). Pediatrics 1987. Fetotoxic effects of prenatal exposure in rats and mice. Toxicological profile for endrin [online]. Kavlock RJ.org/documents/ehc/ehc/ ehc130. Garrett N. Gray LE. Botella B. 1992. No:429-436.fda. et al.cfsan. Ellis H.

3 (16.0-16. and has been detected in soil.1 (14.2-31. The FDA dietary surveys have shown that over time.4. and 7.6 (21.2 (24. particularly by consuming fish.0-28. 2.7-15. and foods with a high fat content.S. 2008. HCB is well absorbed after oral administration.9) < LOD < LOD 20.0-19. 1976). 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. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR. 100 Fourth National Report on Human Exposure to Environmental Chemicals .5-18.7-29.1 (14.4) < LOD < LOD 33.4 (11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 24.4. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.4.5) < LOD < LOD 18.5 (14..9) 19. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.9) < LOD < LOD 28.6) < LOD < LOD 24. Gunderson.8-15.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.6) < LOD < LOD 25..3-22.0.9-24. and accumulates in fatty tissues where it persists for years.7-26.9 (25.2) < LOD < LOD 13. and elimination occurs by renal and fecal routes.1 (13.9-30.6 (24.9-15.6-trichlorophenol (2. HCB is slowly metabolized.5-14.5-trichlorophenol (2. air.4) < LOD < LOD 23. HCB has been detected in fewer foods since the 1980s (FDA.0) < LOD < LOD 15.6) < LOD < LOD 14.5-15.9 (25.6-44.1) < LOD < LOD 15.9) < LOD < LOD 15. Urinary metabolites include pentachlorophenol (PCP). distributes widely throughout the body.0 (14.0) < LOD < LOD 15.3 (12.4) < LOD < LOD 18. or game taken from areas with HCB contamination.7-30.4) < LOD < LOD 14. and sediment (Barber et al.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.0 (18.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.6-TCP) (To-Figueras et al.1-20.8. 31. and 03-04 are 118. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.7 (19. Although it is not manufactured as an end-product in the U.5 (13.Organochlorine Pesticides Hexachlorobenzene CAS No.7-16.5-15.5-TCP) and 2. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.1 (17. respectively.6-19. EPA cancelled its use in 1984.7) 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. wildfowl. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) * * 15.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.7 (15.4-15.7) < LOD < LOD 24.S.3 (14.3-20.6-33.9) < LOD < LOD 20.3-26.7-22.2 (14.2 (14.9) < LOD < LOD 19.4 (18.9 (14.5-14.9-17.2) < LOD < LOD 29. Therefore. 1988).6-32. primarily as a fungicide and seed treatment until the U.2 (17.4) < LOD < LOD 19.0-25.8 (22.7 (15. water.S.0 (25.1-16.9-32.7-21.3 (22.2 (13.6) < LOD < LOD 26.7 (27.3 (20. breast milk is an additional route of elimination in nursing women.4) < LOD < LOD 22. 2005).2-15.4. The general population may be exposed to HCB through diet..8 (26.8) < LOD < LOD 27. 1997). Survey Geometric mean (95% conf.0) < LOD < LOD 24.0 (18.9 (23.4-16.6) < LOD < LOD 26. < LOD means less than the limit of detection.5-33.7) * * 14.9) < LOD < LOD 16.. 01-02.7-16.2-15.3) * * 15.5 (13.6 (23. see Data Analysis section) for Survey years 99-00.3 (22.4 (22.4.8 (15.3) < LOD < LOD 20.1) * * 15. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.6-26. 2002).9-20.3) < LOD < LOD 29.4 (18.

Infants were exposed transplacentally and through breast milk.gov/toxpro2.163-..082-.155) < LOD < LOD .114-.088-.145-.102) < LOD < LOD .091-.163 (.095 (.120 (.099) < LOD < LOD . which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.086) < LOD < LOD .095 (.163) < LOD < LOD . population from the National Health and Nutrition Examination Survey.atsdr. Survey Geometric mean (95% conf.077-.147-. The U.157-. 1960).152) < LOD < LOD . Schmid. reproductive and developmental toxicities. and many died before 2 years of age (Peters et al.095) * * .212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .065 (.175) < LOD < LOD .109) * * .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 * * .090-. very high.S.Organochlorine Pesticides chemical. and liver and thyroid cancers (ATSDR. 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. immunologic abnormalities.085-.129) < LOD < LOD .176-.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.094 (.135-.140 (.095) < LOD < LOD 75th < LOD < LOD 90th * * .104 (.069) * * .090 (.122) < LOD < LOD .098 (.089-.258) < LOD < LOD .115 (.169-.092-. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown.081-.064 (.107) < LOD < LOD .182 (.097) < LOD < LOD .062-.078 (.121 (. arthritis.123 (..186 (.081 (.089-.111) < LOD < LOD .178-. 2002). ACGIH has developed workplace exposure limits for HCB.145-.e. More information about external exposure (i.225 (.173) < LOD < LOD .114-.094) < LOD < LOD .epa. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Biomonitoring Information Serum concentrations reflect the body burden of HCB.083) < LOD < LOD .111-.167 (.S. EPA has established a drinking water standard.191 (.159-. and the FDA has established a bottled water standard for HCB.156 (. acute doses produce central nervous system depression and seizures.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 * * .190 (. thyromegaly.100) < LOD < LOD . 1982. as well as hypertrichosis. HCB interferes with normal heme synthesis.203) < LOD < LOD .196) < LOD < LOD .203) < LOD < LOD .132) < LOD < LOD .086-.069) < LOD < LOD . and weakness.160 (.073-.085) * * .176) < LOD < LOD .092 (.gov/pesticides/ and from ATSDR at: http://www.099) < LOD < LOD .079 (. which may vary for some chemicals by year and by individual sample.141) < LOD < LOD .107-.097 (.113-. Chronic feeding studies in animals have demonstrated kidney injury.127-. This condition. EPA at: http://www. anorexia.179 (.099) < LOD < LOD .102 (. environmental levels) and health effects is available from the U.167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .148-.123 (.087 (.171 (.097) .157 (.html. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.118-.060-.125 (. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.092 (. With chronic exposure.143-. In humans. Fourth National Report on Human Exposure to Environmental Chemicals 101 .123 (. 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.088-.086-.090 (.147 (.130) < LOD < LOD .072-.118-.cdc.S.126) .174-.118) < LOD < LOD .090 (.088-. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.095-.092 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .

van Wijk D. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Lackmann.9% of participants had quantifiable levels (Stehr-Green.58:1185-1201. et al. Canada). and the geometric mean concentration of HCB in whole blood was 0. 2005). FDA total diet study. et al.. References Agency for Toxic Substances and Disease Registry (ATSDR). Zoellner I.. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.39(12):744-749. HCB detection in serum also was proportional to age. Biomonitoring of persistent organochlorine pesticides. but overall. Safe A. 4/21/09 Glynn AW. Kaus S. Peters HA. Kemper FH.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Arch Dermatol 1999. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Muckle G. Laliberte C. Toxicological profile for hexachlorobenzene update [online]. Schulz C.71(6):1200-1209. J Exp Sci Environ Epidemiol 2007. 2006). Schwartz JM. In the 1976-1980 NHANES subsample.205:297-308. Bertram HP. HCB levels were directly related to age. 1999). Lawrence River (Quebec. more HCB levels were quantified. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Jones KC.44 mg/L..html. Can J Biochem 1976. Link et al. Cripps DJ.. Arch Neurol 1982. Available at URL: http://www. 2002.html. Piechotowski I. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. et al. Biol Neonate 2002. Holland NT. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Becker K. Bryan GT. Environ Health Perspect 2003. however.atsdr. Lackman. Bertram et al. Ayotte P. Over the past two decades. 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. April 1982 to 1984.. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates.. 2002. Link B. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Hexachlorobenzene in the global environment: emissions. Bjerselius R.. 2002) and among children (Link et al. Kohli J. 2002. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Ozalla D. only 4. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Gunderson EL.17:388–399. 2003). Lepom P. Bradman et al.135(4):400404. Chemosphere 2005.111:349355. In Spain. Granath F. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Muller C. As a result of the lower limit of detection in NHANES 2003-2004.fda. Dallaire F.54(3):203-208. 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. 2005).cfsan. Fenster L. Reference values updated. et al. Food and Drug Administration (FDA). Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. The metabolism of higher chlorinated benzene isomers. Sci Tot Environ 2005. Glynn et al. September 2002. Eskenazi B. Bradman A. IARC Sci Publ 1986. Gocmen A... Sala M. Paepke O. Seiwert M. Lackmann GM.349:144. 2002). Otero R. 2005. Organochlorines in Swedish women: determinants of serum concentrations. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Gabrio T. Aune M. Environ Health Perspect 2002. trends and processes.110(8):835-838. distribution. Available at URL: http://www. Dewailly E. Herrero C. Jones D. 2002.77:173182. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. respectively. 1989). Krause C. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. FDA Pesticide Program Residue Monitoring 1993-2006 [online].gov/ toxprofiles/tp90. Sweetman AJ.81(2):82-85. and other chemicals. levels. August 2008. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al.cdc. Atuma S.. 4/21/09 Barber JL. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. dietary intakes of pesticides. In a representative sample of the 1998 German adult population.gov/~dms/ pesrpts. Lecha M. Herrman T. Barr DB.. Santiago-Silva M. 1986. Darnerud PO. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Int J Hyg Environ Health 2002. Dogramaci I. selected elements. J Assoc Off Anal Chem 1988.

Fourth National Report on Human Exposure to Environmental Chemicals 103 . Cutaneous porphyria in Turkey. Rodamilans M. Barrot C. N Engl J Med 1960.Organochlorine Pesticides Schmid R. Otero R. Santiago-Silva M. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. et al. J Toxicol Environ Health 1989.27:405-421. Stehr-Green. Demographic and seasonal influences on human serum pesticide residue levels.105(1):78-83. To-Figueras J. PA. Sala M.263:397-398. Environ Health Perspect 1997.

80 (<LOD-14.6-18. and have been used either as fungicides or to synthesize other chemicals.66-12.5) 11. EPA cancelled agricultural uses of lindane (ATSDR.36.4) 10.4-111) 84.6) 35.6-14.5 (37.1-32.68 (<LOD-10. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.50) 8.3 (42.5 (14.87 (9.2 (9.3 (26.1) 31.80 (6. commonly known as lindane. soil.9) 45.S.7 (62.9 (32.8) 27. particularly alpha and gamma have been detected widely in air.8) 39.1-16.6 (33.8 (23.0-111) 70.5) 90th 42.4) < LOD < LOD < LOD 46.1 (9.9 (62.6 (22.7 (30.2-98.1) 71. See the section “What’s New” at the beginning of this Report for details. 104 Fourth National Report on Human Exposure to Environmental Chemicals .3) 37.6 (10.4 (50.1-15.8) 52. gamma.8-68.6) 50. population from the National Health and Nutrition Examination Survey.6-135) 69.8-54. 58-89-9 General Information Hexachlorocyclohexane (HCH).3 (13.3-38.9 (9. 608-73-1 beta-Hexachlorocyclohexane CAS No.Organochlorine Pesticides Hexachlorocyclohexane CAS No.2 (18.6) 18.1-49.6 (16.9-24.9) 17.60-13.5) 16.0-23.9) 81.4-50.7) 73. and 03-04 are 9.8-19. 6.4) 44. However.2) 9.9 (26.2-67.7-20.5) 67.9-51. The other isomers can be formed during the synthesis of lindane. the U.4) < LOD 9.0) 41.3) 14.6 (40.61-12.8-199) 134 (85.1) 13.4 (11.46-11.9-81. 01-02.7 (<LOD-16. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.4) 21. < LOD means less than the limit of detection.5 (8.S.6-20.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.0 (35.6) 653 758 589 1240 1533 1370 20 years and older 10.S.8) < LOD 10.9) 15.0-34.2 (48.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.5 (43.1) 12.0-70.4) 901 1067 952 992 1224 1007 Females 11. environmental levels declined.2) 36.5528. and 7. beta. The gamma isomer.4 (16.7-96.9 (11.6-89.0 (8.6-37.7) 18. which may vary for some chemicals by year and by individual sample.9 (50.2 (34.2) 62.0) 17.90) 7.8-87.8.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.1-27.6-47.7) 27.56-12.30-11.5 (11.6 (17.0 (19.76. It is no longer produced or sold in the U.3) 25.0-21. so they can accumulate in fatty tissues of animals. 2005).09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.0) 7.7) 10.7) 10.1 (16.7) 32.8 (64.4 (52.20-16.9 (30.4) 27.6-62. interval) 9. 2005).3-56.3-85.8 (32.90-8.6) 36.3 (62.5 (16.1) 12.70-19.4) 51.3 (42.0) 8. each result has been multiplied by 1.5) 22.8 (21.70 (6. HCH isomers. Lindane has a half-life of about two weeks in soils and water.7-166) 70.5) 40. water.7-96.5) 14.0 (37.2) 13. **In survey period 2001-2002.2-17.7 (53.0 (33.4 (12.4-73.2-87.0) 35. 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.8) 12.7-26.70 (8. exists in several isomeric forms. respectively.1 (9.0-70.04-10.0) 71. containing about 64% alpha and 10%-15% gamma isomers.0-20.2-52. including alpha.3) 34.1 (18.4 (8.9-21.4) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD 21.1-32.7) 97.4-45. In 2006.7) 56. HCH isomers are lipophilic.1 (30.9-178) 48.2 (29.7) < LOD < LOD < LOD < LOD < LOD < LOD 37. and delta. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.90-8.2-46.1 (27.7-69.89 (<LOD-9. formerly referred to as benzene hexachloride.8) 7.5 (24.2) 142 (99.8) 95th 68.8-16. and sediment as a result of historic production and use.7 (25.5) 29.6-42.2 (50.2 (31.9-56.6) 47.4) 11.7 (35.7-69. As pesticide applications of HCH were increasingly restricted or eliminated.70-12. Technical grade HCH is a mixture of all four isomers.7) 23.1 (21.5-29.9 (40.8 (17.2-55. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.2-22.7 (13.1-37.0 (14.1-36.8 (10. 319-85-7 gamma-Hexachlorocyclohexane CAS No.9-14.7 (29.3) 51.5-123) 49. see Data Analysis section) for survey years 99-00.0 (<LOD-12.1 (12.8) * * * * * * 15.1 (11.6) 16.2-42.8 (33. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-20.43 (<LOD-9.8 (9.

100 (.070 (.140 (.077) < LOD .560) .070 (. probably by blocking inhibitory neurotransmitters in the central nervous system.070-. ingestion.S.294-.5528.330-.050-.180-.840) . and nephropathy developed (IPCS.210) . The beta isomer accumulates in fatty tissues and is metabolized more slowly. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.390-.200 (.S.250-.100-.120 (. Gunderson 1988).170-.083 (. tremors.330 (.290 (.01 (.580-1.068-.260-.244-.510) .072 (. 1996.100) .250) .305) .360) .170-.200-. 1983).174) .410) .110-.220-.120 (.100-.260) .051 (<LOD-.130 (.410) .319) .470) .680) .580 (.120) . hepatic enzyme induction.331 (.501) .050 (<LOD-.119) . each result has been multiplied by 1.310) .080-.216 (.120-. the serum half-life was about 20 hours among children (Ginsburg et al.091) .410-.410 (.210 (. See the section “What’s New” at the beginning of this Report for details.130) .047-.160) .620-1. 2008.480 (.100 (..460 (.450 (.050 (<LOD-.073-.124-.690) . The U.910 (.150) .140) .080 (.220) .100) .404) .360 (.080-.191-.089) . resulting in a half-life of about seven years.372 (.050-. and seizures.380 (.110) .057-.620) . 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. 1977).096) .382-.214) .230-.120-.587) 653 758 589 1240 1533 1370 20 years and older .150 (.160-.069) .190) .057 (<LOD-.056-.290) .560 (.. Workers who directly handled HCH have complained of headache. HCH isomers are absorbed after inhalation.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 . U.083) .090 (.060) . Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.450) .400) .700) . After dermal application of lindane 1% lotion.S.300-.220-. population from the National Health and Nutrition Examination Survey.400) .050-.160 (.290 (. and FDA has established a bottled water standard and food residue tolerances for lindane. Saxena et al.080) * * * * * * .056-.240-.254) 95th .058 (<LOD-.086) < LOD < LOD < LOD < LOD < LOD < LOD .661) 901 1067 952 992 1224 1007 Females .250 (. Distribution is mainly to fatty tissues.Organochlorine Pesticides exposure to HCH is through the diet. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.173-. 1986).05) .710) .190-1.048 (<LOD-.098 (. respectively. OSHA and ACGIH have established workplace standards and guidelines.210-.600) .570 (.350) . 1981).. **In survey period 2001-2002.130-.210 (.521 (.070) .280-.110) . Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.460) .080-.150) .144 (.120 (.146-.190) .067 (.103) 90th .190-.280-. which may vary for some chemicals by year and by individual sample..32) .310) .064 (.040-.150-.120) .360-.220 (.350 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.480 (.281 (.070-.290) . 1971. Fourth National Report on Human Exposure to Environmental Chemicals 105 .470 (.051-. Rogan.270 (.100-.287 (.103-.260) .814) .081-.080 (.290 (. EPA has established a drinking water standard.057-.340-.118-.090 (.234 (.080) .110) .250-.221-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.050 (.250 (. ataxia. 2002).420-.340) .070-.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .059-.390 (.139 (. for lindane.125) < LOD < LOD < LOD .175 (.480) .064) . interval) .320 (.450-. and memory loss (Nigam et al.120-.050-.310 (.222 (.090 (.067) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .140) .103 (.092 (.050) . enlarged livers. When animals were chronically fed lindane at high doses.131-.167 (.442 (.370-. paresthesias.308-.077) < LOD . or dermal exposure. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.089-.050 (.37) 1.062 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.065 (.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 ..065 (.062 (.250 (.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.191-.140) .078 (.090-.412 (.240 (.297-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.118 (.200-.

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

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

J Assoc Off Anal Chem 1988. Exposure of women to organochlorine pesticides in Southern Spain. August 2008. Falk C. Bai KM. org/documents/jmpr/jmpmono/2002pr08. Nigam SK. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Saxena MC. Bhargava AK. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Glynn AW. FDA total diet study. Int J Hyg Environ Health 2002.57(4):315-320. Gabrio T. Absorption of lindane (g benzene hexachloride) in infants and children. Piechotowski I.111:349355. Olea N.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). et al. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Heinrich R. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Lepom P. Schulz C.72:261265. children and newborn infants. Chemosphere 2005. Bjerselius R. Environ Health Perspect 1998. Patterson DG Jr. Zaidi SS. et al. Organochlorines in Swedish women: determinants of serum concentrations. Burse VW.106(5):279-289. Cancer Causes and Control 1998.150:981-990. Gunderson EL.atsdr. Aune M. Potischman N. VI. Atuma S. Sturgeon SR.96:34-4Food and Drug Administration (FDA). Krause C. Needham LL. Cerrillo I. Brinton LA. and other chemicals. Astolfi E. Bull Environ Contam Toxicol 2004. et al.58:1185-1201. Kulkarni PK. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. J Pediatr 1977. Radomski JL. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Majumder SK. dietary intakes of pesticides. Wood PH. et al. selected elements. et al. Bottimore DP. Maass R. Occupational exposure to hexachlorocyclohexane.9(4):417-424. Granath F. Arch Toxicol 1981. Hanrahan L. Lindane. and HCB residues in human blood in Ahmedabad. Olson J. Reisch JS. Link B. Angerer J. Rothman N. Environ Health Perspect 2003. Garrett N. Int Arch Occup Environ Health 1986. Olea-Serrano MF.120:1-82. HCH.fda. Kutty D. Saiyed HN. Needham LL.71(6):1200-1209. Kaus S. April 1982 to 1984. Placental transfer of pesticides in humans. Bates MN. Toxicological profile for hexachlorocyclohexanes update [online]. Demographic and seasonal influences on human serum pesticide residue levels. gov/toxprofiles/tp43. Arch Pediatr Adolesc Med 1996. Biomonitoring of persistent organochlorine pesticides. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Needham LL. Metabolism of gammahexachlorocyclohexane in man. Krishna Murti CR.48:127-134. Zoellner I. Kashyap R.54:1431-1443. Visweswariah K. Buckland SJ.cdc. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.gov/~dms/pesrpts. Pollutants in breast milk. Int Arch Occup Environ Health 1983. Becker K. 4/21/09 Kutz FW. Siddiqui MKJ.html. Rogan WJ. Brock JW. August 2005.27:405-421. India. PA. Ellis H. Seiwert M. J Toxicol Environ Health 1989.cfsan. Rivas A. 4/21/09 Anderson HA.htm.html. available at URL: http://www. et al. 4/21/09 Ginsburg CM. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 2002.91:998-1000. Rev Environ Contam Toxicol 1991. Herrman T. Karnik AB. Available at URL: http://www. Deichmann WB. Stehr-Green. Environ Res 2004. Botella B. Rey AA. Crespo J. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. International Programme on Chemical Safety (IPCS).205:297-308. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. The Great Lakes Consortium. Bhatnagar VK. Paepke O. et al.inchem. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.20(2):186-193. Lowry W. Darnerud PO. Raju GS. Available at URL: http://www. Levels of DDT. Toxicol Appl Pharmacol 1971. Chemosphere 2004.52(1):59-67.

mirex was detected in human adipose samples.10-37.0-374) 11.6 (<LOD-31. (Kutz et al.5-82.5 (9. and foods. Mirex has been detected in air.3-225) 15.0 (14. 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. especially those from persons living in the southeastern U.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. where it was applied directly to soil and by aerial spraying.2-230) 13. and 03-04 are 14.S.0 (<LOD-108) < LOD < LOD 50. 10. 01-02.5-291) 11. Fourth National Report on Human Exposure to Environmental Chemicals 109 .6-305) 15.6 (<LOD-108) 9.2 (7.4 (8. 1995). soil. after which it is widely distributed in the body and stored in fat. Some states and the U.7) < LOD 66.70-40. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. respectively. 2385-85-5 General Information Mirex has not been produced or used in the U.8.7) 8.6 (<LOD-23. disposal.5-425) 40. aquatic organisms.2) 51.8 (<LOD-73..8 (12. Mirex binds strongly to soil.6) < LOD < LOD < LOD < LOD 71. Mirex is absorbed through the skin and from the gastrointestinal tract.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Mirex is not metabolized in the body.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.0 (12.5 (<LOD-42.3) 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. it is a highly persistent chemical in the environment. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. where it has a half-life of 12 years.S.4) < LOD 63.10 (<LOD-15.1 (13.6. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. resulting in exposure to newborns and nursing infants.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1991). since 1977.6) 9.90-29. Survey Geometric mean (95% conf.1 (8.S.70-24. population from the National Health and Nutrition Examination Survey. animals. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.70 (<LOD-15.Organochlorine Pesticides Mirex CAS No.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 19.7 (<LOD-47.3 (15. 1985. and 7. which may vary for some chemicals by year and by individual sample. Occupational exposure is limited to workers at sites where mirex contamination is present. < LOD means less than the limit of detection.5 (<LOD-115) 153 (30. In studies conducted in the 1970’s and 1980’s.5. or pesticide application.S.4) < LOD 15.40 (<LOD-13.3 (15. see Data Analysis section) for Survey years 99-00.8) < LOD 15.7 (12.. Mirex can cross the placenta and be excreted in breast milk. water.4-230) 18.1 (<LOD-65. sediments. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. Formerly.S.1) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 16. Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental Serum Mirex (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.

053-.064 (<LOD-.090 (<LOD-.430 (.410 (. 1991). 7. and 2003-2004 subsamples.106) < LOD .090 (<LOD-. Smith.470 (. 1995.108 (.8.. which may vary for some chemicals by year and by individual sample. EPA has established environmental standards for mirex.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .080-1.635) < LOD .112 (. population from the National Health and Nutrition Examination Survey.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .110 (<LOD-.atsdr.470) .100 (<LOD-.140 (<LOD-. IARC classifies mirex as possibly carcinogenic to humans. The U.450) 1.170) 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 .052-.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.gov/toxpro2. 2004).610) < LOD < LOD < LOD < LOD . and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.08 (.470) .79) .220 (<LOD-. and 4.090-1..062-. 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.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.html. More information about external exposure (i. In samples obtained between 1994 and 1997. 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.170) < LOD .370 (. 2005).450 (. serum mirex levels were generally below the limits of detection (Stehr-Green.S.106 (.220) .080-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . environmental levels) and health effects is available from the ATSDR at: http://www. 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.055-. Survey Geometric mean (95% conf.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 . Biomonitoring Information In the NHANES 1999-2000.37) .077 (<LOD-.059 (<LOD-.7 ng/g of lipid.02) .690) .73) .090 (<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..e.090-1.054 (<LOD-. reproductive toxicity included decreased fertility and testicular damage.510) < LOD < LOD .079 (<LOD-. In addition.92) . developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.102) < LOD < LOD < LOD < LOD . 2001-2002.089-.79) . The geometric mean mirex levels of the Inuit mothers were 8.256 (.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 .268) < LOD . 1989).093 (.170-3.Organochlorine Pesticides exposures are unknown.cdc.090-1. as well as in a subsample of NHANES II (1976-1980) participants.070-1. Laboratory animals fed high doses developed liver enlargement and liver tumors. 110 Fourth National Report on Human Exposure to Environmental Chemicals . and NTP classifies mirex as reasonably anticipated to be a human carcinogen.100 (<LOD-.41) .310 (.

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

50-16.6-trichlorophenol (2.0 (4.30-3. EPA. may occur by inhalation or dermal routes.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.20) < LOD 1.00 (2. including hexachlorobenzene and hexachlorocyclohexanes.50-63.30-40.5-Trichlorophenol CAS No.30-27.6-Trichlorophenol CAS No. soils. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.80 (2.40) < LOD 6.0 (4.00 (3.7.920-3. usually at herbicide production or waste incineration facilities.20) < LOD 90th 5.S.72) < LOD 1. 2.0 (3.940-3.30-44.30-27.30) < LOD 4.9 (<LOD-121) 9.50) < LOD 1.4. and sediments. Historically. Exposure to trichlorophenols also may result from metabolism of lindane.0) 2.50 (1.40 (2.0) 5.4.0) < LOD 11.50 (.7) 24. Occupational exposures. public drinking water systems did not detect 2.40) < LOD 1.20 (4.50 (2.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Trichlorophenols are no longer manufactured commercially.27) 696 661 521 696 603 939 Limit of detection (LOD.900-2. Such workers would probably Urinary 2.4. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. 112 Fourth National Report on Human Exposure to Environmental Chemicals .30-11.0 (8. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.0) < LOD 5. Survey Geometric mean (95% conf.40 (1.90-33.5-trichlorophenol (2.40) < LOD 4. Formation of 2. Both chemicals have been detected in air. however.4.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.63) 18.9.30) < LOD < LOD < LOD < LOD < LOD 1. population from the National Health and Nutrition Examination Survey.80-41.40-18.4.3.60-8.5-TCP) and 2.40-11. recent sampling of U.40 (1.71 (<LOD-8.0) 2.0) < LOD 5.60 (2.20-71.80) < LOD 1.60 (. which may vary for some chemicals by year and by individual sample.19 (<LOD-6.40 (2.S.60) < LOD 8.980-3.20) < LOD 5.0 (3.60-18.4.71 (<LOD-8.5TCP and 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.50-25.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 2. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.6-TCP)..40 (. 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) < LOD 11.30 (.950 (<LOD-1. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.9 and 0.0) 14.4. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.4.4.Organochlorine Pesticides 2.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4.0) < LOD 5. 1999). 1999). other organochlorines.00-3.40 (2.42 (<LOD-8.980-3. surface water.40 (2. are metabolites of several organochlorine chemicals. 1976).8) 21. and polychlorinated benzenes (Kohil et al.57 (<LOD-15.30-27.31 (<LOD-9.40 (.20-36.4.27) 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 1.00-3. 2. hexachlorobenzene.6-TCP were used as intermediates in the production of certain pesticides.4.60 (4.0) 2.0) 2.0) < LOD 21.10-3.0 (5.5-trichlorophenol.S. 95-95-4 2.0) 2.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.42 (<LOD-12.6-TCP in any of the samples (U. 2006).03) 9.0 (4.80 (1.0) 2.00-8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

6) 4.4. Neither 2.62-20.1) 2.4) < LOD 3.32) < LOD 4.15) < LOD 2.2) < LOD 5.2 (2.37-11. population from the National Health and Nutrition Examination Survey.17) 9. the 95th percentile urinary 2.24) < LOD 5.5-TCP or 2.44 (.4 (6. The 95th percentiles for 2.73 (<LOD-8.53-3.19-4. which includes trichlorophenols. 2003).4.29 (1.81 (<LOD-9. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.6) 4.43) < LOD 12.atsdr.60-3.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.80 (1..53-3. At lower doses..00) < LOD 4.00-19.57 (<LOD-7.24-11.9) 12. the 95th percentile urinary 2.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).6-TCP.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.980 (<LOD-1.2) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20-6.49 (1. Among 6-11 year old children in NHANES 1999-2000.67 (1.57 (<LOD-7.4. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.93-11.cdc.78 (3.4) 5.5) < LOD 12.4.69-18.8 (5..83-12.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . Fourth National Report on Human Exposure to Environmental Chemicals 113 .57 (3. leukemias.4.47-8. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.67 (1.6-TCP had increased rates of hepatic tumors.24 (3.11) 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 2.74) 11.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.html.4. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.02-3. 2004).43 (2.75 (<LOD-6..02) < LOD 7.55 (4. NTP classifies 2.4.50) < LOD 2.05-8.. 2003.gov/toxpro2.6-TCP levels at the 95th percentile were up to eight times higher than 3.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.64 (4.6-TCP as reasonably anticipated to be a human carcinogen.33) < LOD < LOD < LOD < LOD < LOD 2.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2. urinary 2. 7.5-TCP nor 2.05-17. Radon et al..44 (1.31) < LOD 2.27-17. 1989). animals showed hepatocellular abnormalities.95 (3.88-16.82 (<LOD-32.3 mg/L reported in German adults aged 18-69 years (Becker et al.920-2.820-2.4.37) 16. environmental levels) and health effects is available from ATSDR at: http://www. and lymphomas. and other chlorinated compounds.24) < LOD 1. Survey Geometric mean (95% conf.68 (<LOD-8.6) 4.68-4.Organochlorine Pesticides be exposed to mixtures of chlorophenols. furans.28-25. 1995) were similar. 1995) and up to 19 times higher than the 95th percentile value of 1.69 (2.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.90 (4.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4.78-19. 1989). 2003).5) 11.4. in addition to dioxins.19-12.e.4.4) < LOD 3..16 (. as being possibly carcinogenic to humans.13-13.1 (<LOD-58. Urinary 2..5-TCP.8) 4.86 (3.36 (1.5-TCP and limited for 2.0 mg/L.3 (5.7 (4. Human health effects from 2.24) < LOD 6.4.. IARC classifies combined exposures to polychlorophenols.9 (5.75 (3.4. In the same 2-6 year old children.79-4. Laboratory animals chronically fed high doses of 2.78) < LOD 1.46 (1. More information about external exposure (i.0) 7.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.16) < LOD 90th 5. However. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.S.00-29. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.8) < LOD 9.

2 (14.40 (2. In harbor workers exposed to chlorophenol-contaminated river silt.0 (6.9) 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 2.85) * 3.0 (20.6-TCP (0.40-7.0 (7.1) 16.7) 33. Urinary 2.0) 14.4 (10.7) 21.8 (9.20-23.3) 20.72-10.09-7.40-4.20 (3.4.0 (15.0-38. interval) 2.02) 2.6) 26. similar to the limit of detection for this Report (Anderson et al.0 (4.24 (2.0 (15.79 (5.4.7 mg/L.67-12.80 (2.45 (2.60) 6.20-6.0-50.45) < LOD 11.0 (14.8-24.0) 12.3) 23.0 (14.30-33.5-TCP or 2.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.5-TCP level of 0.0) 7.7 (9..33-4.10-3.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.3-26.4.95 (4.3) 37.0-37.0 (14.3 (11.4.52-3.32) * 3.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.0) 6.50-5.0 and 1.54) 6.59-6.89 (3.00-4.6 (11. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.53) 4.73-9.09) 15.0 (11.00 (4.87-14.70) 1.7-16.06) * 2.95) 3.36 mg/g creatinine.0) 19.26 (2.70-3.28) 24.1 (10.70) 5.6-TCP level.55-3.0 (16.6TCP causes an adverse health effect.32-4.0) 7.80-25.40-2.36 (1.8-13.4 (17.4-17.4.30) 4.0) 17.80-6.60-3.70) 5.0) 15.4.6-TCP exposure and health effects.60-21.. Survey Geometric mean (95% conf.0 (9.92 (2.98-7.4 (9. 2003).57 (<LOD-2.0-43. for males in NHANES 19992002 (Agramunt et al.9 (11.90 (4.10-2.84) 2.07 (<LOD-3.S.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.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.6-19.4.91-4. Finding a measurable amount of 2.56 (3. population from the National Health and Nutrition Examination Survey.0) 19.23-2.1 (8.20-3.0-38.3. Biomonitoring studies on levels of 2.60 (3. was about six times lower than the median urinary levels for males in this Report (Radon et al.58 (1.28) * 2.89-6.65 (5.6TCP values.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.0) 11.70-6.66 (8.85 (2.90 (3. Biomonitoring data will also help scientists plan and conduct research about 2.0 (20.10) 2.0) 10.80 (3.60 (2.0) 13.01-6.00 (1.46-3.18-3.7-3.80-20.23) 2.10 (5.69 (3. which may vary for some chemicals by year and by individual sample.0 (13.4.2) 25.40-32.4.70 (2.0) 17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08 (2.2) 12.70-6.63) 90th 15.0) 11.8) 18.5-TCP or 2.59) 4.60-37.51-12. < LOD means less than the limit of detection.65) 15.0 (6.8) 32.45-9.5-TCP or 2.5-46.4 (8.0-44.5-TCP or 2.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.53) 2.78 (2.5-TCP and 2. 1991).20) 4.40 (2.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.4.25-11.0-68.04) 2.4.4.6-22.4.6) 21.0) 9.74-3.0) 13.4.40) 4.5-TCP and to the median 2.6-TCP in urine does not mean that the level of 2.0) 13.0 (12.0-54. the median urinary 2.35-3.76) 3. 2004).10-3.0 (6.50 (2.20 (3.98-11.95-6. Urinary 2.4. 1998).70) 3.9) 694 677 519 696 602 931 Limit of detection (LOD.40-2.31) * 2. Mean values of 2. respectively.30-11.60 (3.0 (8.30-2.80) 1.0-18.9 (13.6 mg/g creatinine) and 2.68 (<LOD-2.40) 3.44) 75th 4. 0.10) 6.67) 4.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.70 (2.5-TCP and 2.6 (12.3-17. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.6-TCP than are found in the general population.00-21.4.00 (2.7 (13.74 (2.0) 13.40-14.5 mg/g creatinine) were similar to the limit of detection for 2.30-2.80 (2.60) < LOD 5.0) 10.0) 9.6-17..58-3.4.0) 14.2-0.45 (5.40) 2.80-7.31 (3.40) 2.78 (2.75 (8.0 (8.99) 6.52 (2.4.9) 13.23) 3.1-25.5-TCP (0. 114 Fourth National Report on Human Exposure to Environmental Chemicals .49 (6.47 (3.32) 3..0-41.12) 2.8-15.14 (2.48-26.90) 2.36-5.90-8.4.4.3 (11.

43 (<LOD-2.14-13.02 (1.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.2 (13.6) 8. Fourth National Report on Human Exposure to Environmental Chemicals 115 .5 (8.33-2.76-8.04-2.38) 22.54 (2.9 (9.9-29.81) 2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.48-2.5 (10.1-21.29-4.4) 9.49) 4.0) 8.10-9.05 (6.83 (3.23 (1.2) 19.73-22.18-4.2 (12.6 (9.42) 2.4 (11.15 (1.00 (3.77-4.40 (2.52 (5.56 (7.06) 4.91 (3.46-14.22-2.53) * 2.26-13.81-9.19-5.20-2.53) 4.87) * 2.63) * 4.8) 21.89) 10.55-2.41 (3.73) 5.8) 11.82 (8.40 (7.29-4.1) 14.25-15.32 (2.6) 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 2.62-15.59 (2.83-5.22 (1.87 (3.5) 11.5) 11.53-11.88) 4.9-34.78 (2.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.68) 2.8 (8.04-16.72-16.4 (12.9) 19.00) 4.22 (3.98) 10.22 (<LOD-2.63 (2.82-2.15 (6.63-15.9) 8.3-37.33 (1.6 (6.56-5.63 (<LOD-2.25 (3.60-2.51 (2.32-19.5) 9.96) < LOD 4.1) 11.13 (1.10 (6.60 (4.88-7.18-2.65) 18.24 (1.67-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (5.02) 3.76) 4.78) 90th 12.6 (10.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.0 (6.22-9.63) 4.3) 8.79-17.7) 25.70-9.82 (3.27-9.06) 11.82) 2.56) < LOD 11.17) 13.52 (3.58 (4.88) 4.3 (9.94-13.91 (7.65) 2.83-6.6 (22.87) 2.28-4.87-6.35 (3.72) 32.6) 12.43-7.Organochlorine Pesticides Urinary 2.01 (3.44 (3.1 (8.10) 4.43 (2.26 (6.51) 18. Survey Geometric mean (95% conf.52) 2.51-21.9-64.3-23.41-6.91-2.4) 4.21-11.2 (8.9-32.88) 1.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.78) 2.53 (3.17-4.98 (1.5-28.13-6.5) 12.87-7. population from the National Health and Nutrition Examination Survey.63-13.6 (9.76) 1.8) 12.90) 2.09-3.83-6.95-2.77) 2.25 (3.16-10.8) 19.38 (4.S.92) 4.6 (12.9) 7.11) 10.1-32.25-2.23) 4.42 (2.5) 8.00 (2.88) 5.75) 75th 4.7 (14.50-8.90 (1.0 (11.6-31.2 (7.4) 8.76) 2.38 (2.49-3.52) 2.30-2.14-2. interval) 2.6) 13.99-2.08-2.7) 6.9 (9.05 (3.88) * 2.65-2.50 (2.5 (7.1 (13.7-36.33 (7.88 (2.65-21.47-5.9) 8.0) 10.29 (6.71 (3.68) 2.33) * 2.00) 4.89-2.25-17.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.66-4.17) 2.4.0 (9.06-2.38-5.8 (7.

Environmental Protection Agency (U. Baur X. Poschadel B. Kohli J. Pesticide residues in urine of adults living in the United States: reference range concentrations. Safe A.71:99108. Falk C. et al. Needham LL. July 1999. Szadkowski D. Smith SJ.S. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Pekari K.gov/toxprofiles/tp107.cdc. Becker K.epa. Gregg M. Domingo JL. Available at URL: http://www. Urinary excretion of chlorinated phenols in saw-mill workers. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population.106(5):279-289. Hanrahan L. et al. Wegner R. Environ Res 1995. Anderson HA. Toxicol Lett 2003. Jones D.pdf. Bailey SL. Am J Ind Med 2004. Can J Biochem 1976. Shealy DB. Fast DM. Domingo A.atsdr. Int J Hyg Environ Health 2003.54(3):203-208. Corbella J. Burse VW. U. The Great Lakes Consortium. Lindroos L. Available at URL: http://www.EPA). Jarvisalo J. Holler JS.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 206:15-24. Hill RH Jr. Aitio A. 4/21/09 Agramunt MC. Olson J.63:57-62. To T. Needham LL. Toxicological profile for chlorophenols [online]. Seifert B. 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]. Head SL. html. et al. Hill RH Jr. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Heinrich-Ramm R. Seiwert M. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Environ Health Perspect 1998.18(4):469-474. S. Radon K. December 2006 Draft. Schulz C. Baker S. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Luotamo M. Int Arch Occup Environ Health 1991.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Arch Environ Contam Toxicol 1989. Kaus S.146:83-91.45:440-445. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. The metabolism of higher chlorinated benzene isomers.

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

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

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

840-1.27-15.600 (<LOD-1.80) 11.40 (.74 (8.16 (2.30 (2.61) 4.95) 5.00) 3.52) 6.26-6.70) < LOD < LOD 1.34-7.830 (<LOD-3.3-15.740-2.43-12.91) 4.81) 1.S.71-9.5) 20.08 (<LOD-2.70) < LOD < LOD 75th 3.00) 3.9-18.80) .0) 11.80-22.58 (3.10 (2.599-1.0 (4.81) 11.8) 11.670-1.02) 4.2) 16.80) 2.30-4.99 (5. respectively.58 (5.981 (.97) 90th 7.32) 1.0) 6.4 (9.1-17.33 (5.42) .2 (14.82-12.10 (2.8-32.20 (2.8 (12.4) 20.50) 2.4 (7.80) .83 (5.955 (.7 (12.0) 10.530 (<LOD-2.23-5.55-8.0 (9.620-1.60-11.00 (1.60 (1.63) 1.4 (9.46) 10.50 (4.20-30.04) < LOD 1.623-1.16) 4.954 (.1) 95th 13.0) 9. < LOD means less than the limit of detection.21 (.8 (8.0) 10. interval) 1.8) 7.90-4.07-10.01) * * 1.758-1.40-19.86 (1.0) 7.73) * * .2 (14.53) 4.9) 8.44-38.700-1.2 (9.80 (4.717-1.00 (4.93-24.93 (4.76 (2.68-7.52-11.579-1.89) 9.40-16.2) 16.1) 10. population from the National Health and Nutrition Examination Survey.17-3.9) 14.780) < LOD 3.20 (.10) < LOD < LOD 4.00-19.55-6. see Data Analysis section) for Survey years 99-00.58 (2.890 (<LOD-2.0) 20.79 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0) 11.60-25.20-7. 0.38-5.60 (5. and 0.2 (11.970-2.0) 5.10 (.750-1.5) 15.4) 17.0) 6.48-7.0) 15.80) 3.00 (5.22 (.1 (9.7 (14.51) 2.2-20.4 (7.290 (<LOD-.56 (1.0) 12.15-12.0) 6.98-5.0-28.5 (11.90-5.50-5.85 (3.0) 10.30 (2.1-23.290 (<LOD-1.47) * * 1.33-18.44-3.2.2 (7.35-11.0 (7.70) .90 (1.00-12.5-17.70-23.1) 13.757-2.2) 14.30 (4.30-6.00-27.0 (7.2) 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 1.60) .70 (2.5 (8.0) 11.00-12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 120 Fourth National Report on Human Exposure to Environmental Chemicals .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 1.0) 11.70-11.860-2.3) 16.80) 2.52) * * 1.28) 1.71 (2.26-8.4) 18.94) * * .2 (7.0 (9.42-3.86-15.10 (.5-16.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.98-12.34-3.0) 10.13-2.74 (8.56 (4.29) * * 1.0 (12.90) 3.67) 3.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.54 (3.3) 17.45 (2.08-2.70-14.70-19.0) 10.8 (14.10-7.15) 14.94) 3.0) 5.08-15.0 (8.57-7. 01-02.6) 18.0 (6.40-5.0 (6.13 (2.82) 10.90) 2.1 (10.37 (3.9 (8.80-24.50 (.12) 4.39 (8.36-4.8 (9.05-7.0-27.3) 14.60-18.60) < LOD < LOD 4. which may vary for some chemicals by year and by individual sample.79-7.0 (5.35-16.00-7.40-14.80 (2.61 (3.81) 11.8) 7.20 (.0 (7.11 (.03 (.27-3.66) * * 1.810-1.2.2 (7.1.14) * * .20 (.56 (6.0) 5.20-4. and 03-04 are 0.26 (5.2) 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 1.97) 8.40-11.21) 9.47) 5.50-36.40-1.20 (.56-13.6) 7.2 (9.0 (8.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.39 (3.0 (7.44 (2.0 (8.80) 4.80-4.96-3.32 (.02-5.490-2.72) 5.35-12.7) 11.80) 2.13 (2.10) < LOD .70 (4.19) 9.12-19.8) 19.50 (2.00-27.

60-9.71) 10.5) 12.69 (4.61-13.7 (9.40-5.83) 8.03) 2.56) .9 (5.40-28.9) 16.570-1.47) * * .89-3.98 (3.430-1.66 (5.88-10.66 (1.90-8.5-16.8) 6.2) 8.98) .10 (3.93) 9.890 (<LOD-1.52) 4.4) 13.440 (<LOD-2.7) 5.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.900 (.6 (9.34 (6.82-14.06-2.80 (7.47) 2.79-9.62-5.28 (4.98-22.34 (6.15-10.924 (.27) < LOD 2.42) 12.6) 9.69-10.1 (7.6) 11.4) 4.23 (4.28 (5.89) * * 1.87 (1.60) * * .8) 8.45-11.73 (1.13) 4.34) < LOD < LOD .14 (3.3) 12.02-14.84) 7.82-6.650-1.82-14.1 (9.95 (3.47 (3.11-6.3) 5.870-2.28-9.94-22.40-3.66 (2.39 (2.56-13.29) * * .28) 10.510-1.54) .2 (10.03-6.0) 7.40-12.51-5.6 (10.53-11.53 (6.92-2.66-34.85 (6.7 (8.960 (.26) * * .03 (7.42 (3.710 (<LOD-1.46) 2.61-29.25) 6.00-13.9) 12.45-5.7) 12.88 (5.6) 13.07 (.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 1.61 (1.54-2.780 (<LOD-1.75 (7.03 (2.35) < LOD < LOD 3.54-11.34) * * .55-20.818 (.608-1.05 (1.68) < LOD < LOD 3.94-23. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40 (3.09 (.47 (3.30) 2.2) 13.2) 5.5) 7.56) 4.64-5.2) 5.960 (<LOD-2.69) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (4.87 (3.855 (.21-23.50) 7.25) < LOD .80) 9.19 (4.5) 7.75-7.1 (8.57 (6.890 (<LOD-1.8 (10.5) 8.66-15.92-5.00-19.93-5.94-10.31-14.09-11.0 (8.00) 8.98-5.750 (<LOD-1.98) 9.56) 7.4) 4.81 (1.9 (9.61 (1.38) .920 (.94 (2.88) 2.533-1.82-26.40) < LOD < LOD 75th 2.560-1.7 (10.83 (7.28 (2.37-5.996 (.2) 95th 12.54-15.00 (4.4 (9.37 (4.40) 4.8) 16.72) 11.57 (4.90-5.566-1.0) 6.05 (.94-9.10-13.31 (3.1 (10.7) 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.37 (5.35 (1.41) Selected percentiles ( 95% confidence interval) Total * * 50th .01-2.77 (6.4 (4.5-13.09) 2.6) 8.43 (.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 1.790 (.3) 15.74) 4. interval) .75 (3.94 (4.1) 4.549-1.30 (1.29 (2.41-12.860 (.1) 4.58) * * 1.03) 2.02 (2.820 (.57) 4.620-1.71-2.7) 18.87-5.2) 9.68-4.67) 1.80 (2.5 (4.88-15.93-9.43 (3.62) .830-1.37) 9.02 (7.9-28.69) 4.84 (5.79-3.S.883 (.38 (1.98) .1 (11.9) 11.1-15.04 (1.44 (2.74) 90th 7.54-4.04-6.53) 9.5-20.1 (6.7) 471 576 308 664 821 699 814 1122 921 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .05) .633-1.932 (.18 (.60) 2.81-5.75) 2.43) 2. Fourth National Report on Human Exposure to Environmental Chemicals 121 .75) 14.41) .574-1.20-8.57-10.85) 2.8) 12.5-32.5) 11. population from the National Health and Nutrition Examination Survey.2) 7.02-2.00-17.40-14.46-5.76-4.8) 7.95) 2.37-3.76) < LOD .2 (6.45-5.23) 4.47 (1.500-1.36) * * 1.67) 4.540-1.2 (8.80 (6.773-1.24-3.9 (9.3) 16.78 (2.32-12.67-19.

9) 95th 14.0) 12.70 (1.37) 2.650-1.0) 7.04 (3.77-3.00-4.35) 4.0) 19.0 (10.80-12.58.90 (1.4) 7.7) 10.81-6.6 (10.5.00) < LOD .9-17.10-15.95 (2.22 (6.17 (7.790 (<LOD-1.61 (3.0) 14.70) 2. 122 Fourth National Report on Human Exposure to Environmental Chemicals .1) 11.10) 6.90 (2.4 (10.00) 7.6) 11.0) 12.29-4.8) 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 1.90 (2.88) 3.9) 10.0 (14.37 (3.1-23.3 (9.80) .62-17.7-19.80-4.670 (<LOD-1.25 (2. 01-02.31) 1.18) * * * * * * * * 1.22) 8.70-5.10-4.00-18.89) 2.31-12.22 (6.00-9. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .8) 8.5 (8.9) 16.06 (2.89 (2.70-9.0 (7.00) 8.670 (<LOD-1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 9.6) 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 * * * 1.24-5.9-14.7) 22.3 (12.27 (3.66) 4.70-8.80 (2.8-17.51) < LOD 1.8) 9.40) < LOD < LOD 75th 2.80-6.20 (<LOD-2.7) 14.9) 9.6-41.92) 9.4) 11.53 (3.41-5. population from the National Health and Nutrition Examination Survey. and 0. which may vary for some chemicals by year and by individual sample.740 (<LOD-1.60 (5.34-5.9-15.10-10.01 (2.96) 3.0) 23.90 (5.0 (15.4 (10.1 (10.16-1.0 (8.86-10.40 (2.39-13.30) 3.20-8.27) 9.70 (8.8-21.00-18.88) 10.46-28.0-24.60 (2.27) .00) 3.60 (6.3 (9.80 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.67) 3.0) 12. and 03-04 are 0.58 (1.3) 8.63-14.90) 8.5-26.80-21.92-17.33-11.66-13.90 (2.670 (<LOD-1.80-14.84-4.80-3.0) 13.11-6.4-17.3 (7.50) .90-15.00-4.90 (6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (8.95-9.9 (7.60) < LOD < LOD 2.12 (4.29) < LOD < LOD < LOD < LOD 3.6) 14.0 (9.20-4.98-9.8 (12.20) 3.95 (5.34-3.15-6.0) 13.30) < LOD < LOD 4.30) 3.0) 14.50) 3.00-16.22-12.3) 22.7 (10.S.3) 20.3 (6.0) 6.0-19.99 (3.9 (12.10 (<LOD-1. 0. see Data Analysis section) for Survey years 99-00.41) 3.90-31.96) 90th 7.18 (3.97-4.2 (9.5) 21.30) < LOD < LOD .20) .74) * * * * * 1.31-7.90-9.580-2.680 (<LOD-1.0-24.1 (10.24 (2.46-4.75 (2.73) 7.34 (6.61-32.20) 3.910 (<LOD-2.0) 9.30) 8.27 (7.82) 8.50-5.77-14.6) 18.7) 15.15-2.0-33.00) 3.970 (<LOD-2.67-10.2) 14.10 (.40 (2.0 (13.0) 18.2 (7.28 (7.90 (6.7 (11.80) 5.42 (1.3 (11.50) 5.5 (9.6 (10.59-3.0-29. < LOD means less than the limit of detection.0) 11.90 (6.8 (12.80-8.52 (6.7) 16.8-20.4 (14.70-9.45 (3.72) 2.7-21.00 (.6-19.6) 14.0 (5. respectively.3) 10.67) 4.0 (10.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.20-18.39 (5.80) .27) 4.90-15.0 (9.0) 11.90) 4.5) 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 * * * * * * .8-20.3) 14.5.35-3.78) 5.35 (6.50-4.49-4.14 (6.670 (<LOD-1.34-10.90 (6.47-6.80 (2.64) 10.75 (3.

70-2.36 (2.63 (2.05-3.75-3.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.94-14.1 (13.91-9.30-5.68-10.09-11.0 (10.68) .14 (2.2 (9.43 (2.2) 12.06) .2) 12.92) 3.890-2.63 (6.9) 19.97-4.88-7.4) 15.6) 12.620 (<LOD-.58 (4.28-12.950) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.41 (7.61 (2.53-8.38-13.6 (11.89) 5.6) 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 * * * * * * . Fourth National Report on Human Exposure to Environmental Chemicals 123 .80) 3.78-10.7) 14.07) 2.3-34.2-30.20-3.7 (11.42) 8.23-3.3-17.810 (<LOD-1.4-16.94 (5.64-11.2) 8.920 (<LOD-1.38 (2.81 (7.27) * * * * * * * * 1.73 (5.4) 16.0) 14.1 (19.72) 4.6 (12.33-10.2) 16.11-3.530-1.97) < LOD .27) 1.910 (<LOD-1.82-11.03 (2.9-25.5 (15.89-3.45) 6.93 (6.67 (1.51-10.4) 6.6) 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 * * * .940) < LOD < LOD 1.4 (11.38 (1.5) 8.83 (7.68-4.00 (2.2) 15.38) 1.6) 14.68-19.12) < LOD < LOD 4.86) 9.6) 13.5 (8.4-15.4) 7.34-18.99) 2.27-13.34) < LOD < LOD < LOD < LOD 3.95) 90th 8.7-23.39-17.5) 13.89-13.7) 14.51-7.3) 12.690 (.09-11.04) 9.88 (1.0 (11.86-3.780-1.590 (<LOD-.29) 3.82-8.850 (<LOD-1.92 (5.760 (<LOD-1.77 (2.95 (2.54 (7.55) .2) 12.0 (8.6) 6.37-5.16-14.6) 95th 16.45) 3.33) 3.69-11.95) 3.54-5.7) 15.25-9.01-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.38 (.71) < LOD < LOD 2.7 (8.18) 2.42-19.9) 16.0-19.6) 7.93 (<LOD-2.4-18.77) 3.3-17.12 (7.42) 7.4) 7.3 (7. population from the National Health and Nutrition Examination Survey.89-10.32) 2.7) 9.48 (2.973 (.2) 19.2-15.00 (3.79-6.8) 16.71 (1.54) 9.3-15.47-9.1) 10.93-10.07 (5.6 (13.4) 9.25 (4.93 (2.2 (9.15) < LOD < LOD 75th 2.9 (9.55) 16.3) 9.27) < LOD .1) 20.85-17.29 (5.3-21.29 (2.6 (11.8) 14.89 (3.02-4.06 (<LOD-1.00 (7.5 (10.37) 3.99 (4.78 (6.32-8.2) 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.S.86 (3.74-4.00 (<LOD-1.8) 11.70-35.6 (10.03 (6.07-3.00) 2.3) 8.78) 4.1 (8.30) 8.19) 3.50 (6.00) 8.67 (7.9 (9.52-3.8 (8.55 (2.30) 2.6) 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 1.59-3.0-21.4-16.7 (10.8 (10.50-17.15 (1.21-21.28 (1.07) 2.00 (<LOD-1.1) 13.11 (5.5-17.44-6.83 (6.77 (2.7 (10.96-10.9-17.78 (4.29-2.89-3.91) 3.30) 7.7) 12.7-19.96-11.5) 22.4) 7. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .87 (3.9 (9.75-3.03) 3.6 (13.79-9.2) 10.3) 6.5 (9.72-4.27) 5.0 (13.89 (2.85-8.21) * * * * * 1.16 (3.28) 6.74-19.5) 10.5 (11.00 (5.6-19.

820 (.201-.76 (1.14-1.47) 2.830 (.740-.303-.880 (.86 (1.449 (.64 (1.54) .77 (1.657) * * .960) 1.780 (.455 (.380) .10-1.720-1.37-2.25-1.01-1.00-2.14 (1.16-3.70-7.74-5.89) 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 * .600 (<LOD-.00 (1.400) .336-.83) .58 (1.597) * .10) 1.618) * .20) 1. which may vary for some chemicals by year and by individual sample.65 (2. < LOD means less than the limit of detection. 0.910 (.50 (1.560-.75 (2.30) 1.80 (1.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.20-1.78) 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 * .91) 2.47 (1.29) 1.20-2.15) 2.960) .820 (.880) < LOD .29-2.19-1.83 (2.74) 3.20) 3. 124 Fourth National Report on Human Exposure to Environmental Chemicals .13) .70 (1.710) .740-1.740 (.17) 1.45 (2.759) * .59-2.20) 2.50-2.27 (2.860) < LOD < LOD .580-1.22-3.73 (2.08 (2.930-1.710 (.240 (<LOD-.570 (<LOD-.760 (.98) .459 (.970) .61 (1.930 (.10-1.650-.749 (.26) .592) * 50th . see Data Analysis section) for Survey years 99-00.750) 1.740 (.930) 1.38) 1.467 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.48 (1.20) 3.88) 1.80) 3.680-1.50 (1.80) 2.90) 2.05-2.960) .90) 2.980) 1.22-8.04) .260 (<LOD-.20 (1.46 (1.15) 2.83) 1.90-4.2.350-.90 (1.22-3. and 0.680-1.10) 1.22 (1.30-3.42-2.690-1.960-1.720-1.40 (1.453 (.70 (1.570-1.380-.17) 1.970) 1.39) 2.22-2.73-5.359-.75-2.45 (1.21) 3.31) 95th 2.600-.20 (1.89-6.32) 3.950) 90th 1.584) .89) 1.880) < LOD 75th .98 (2.97 (2.60) 3.23-3.17-4.94 (3.910) 1.16) 2.425 (.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.55 (3.41-5.670) .46-3.30-1.30) 2.30) 4.80) 5.34) 2.57 (1.382-.930) < LOD .63 (1.550 (.54 (2.30 (.390-.98-3.398-.570 (.570) * .18 (.700) .549 (.11-3.78) 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 * .31-3.510 (.57 (2.33-2.80 (2.03) 1.68-5.20 (2.41 (2.35) 1.570 (.390-.457 (.840 (.380-.08 (2.31) 2.30 (.440-.60 (2.34) 2.45-4.690 (.86) 3.700) .00) 2.04) 1.800 (.710 (.96-5.18 (1.89) .79) .730) .690-.36-4.280-.580-.540 (.78) .95) 2.990-1.00) 1.750-1.09.59-6.60-4.01) .45 (1.05-3.50-2.54-2.592-.40 (1.01-3.S.160 (<LOD-.50 (1.30 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20 (1.20-3.73 (1.49) 2.1.30) 4.09 (.10) 1.20) 1.20-2.460-.31-3.50 (1.720 (.590-.83 (2.940) < LOD .13) 2.810) .80) 3.340-.780) .70-2.570 (<LOD-.600-1.46) 1.585) * * .50) 1.70 (1.343 (.620-1.388-.32-1.550 (.587) * * . interval) Selected percentiles ( 95% confidence interval) Total * .76-6.16) 1.505 (.26 (2.80) 3. population from the National Health and Nutrition Examination Survey.500 (<LOD-.90) 3.00-4.850) < LOD .79) .95-5.353-.48 (2. 01-02. and 03-04 are 0.690) .94) .49) .77-2.592) * .450 (<LOD-.790 (.83) 2.780 (.94 (2.960 (.11-3.30 (1.350-.96-3.46 (2.210 (<LOD-.910-1.32 (1.80) 2.30-3.510 (<LOD-.490 (<LOD-.87-3.60) 2.95 (2.27 (3.69-4. respectively.20) 2.949) .50 (1.10) 3.

77 (3.444-.57 (3.490 (.560-.60 (2.45 (2.580-.640 (.57-2.23) 2.742) * * .88 (1.72 (1.480) .660-.560-.28 (1.710 (.58 (1.72) 1.67) .33) .94) .560 (.17-2.550-.77-3.07) 1.448 (.710 (.84 (2.470 (<LOD-.80) 2.18-2.14 (2.71) .22-3.07) 5.29-4.00 (3.540-.250 (<LOD-.69 (3.380) .79) 1.270 (<LOD-.07 (.64 (2.00-3.460) .19 (1.310 (<LOD-.73-3.38-3.22 (2.850) 1.348-.57-4.99) 1.64 (2.591 (.310-.00-1.55-3.380-.42 (.552 (. Fourth National Report on Human Exposure to Environmental Chemicals 125 .690) < LOD < LOD .08-2.460 (.02-6.04) 95th 2.447 (.58-6.11) 1.58) 3.16) 1.67 (1.990-1.32) 2.830) 90th 1.485) * * .20) 1.580) .380-1.180 (<LOD-.730) .17) 2.253-.270-.67-3.22-2.89 (1.08-2.71) 2.840) 1.60 (1.460-1.75 (2.99) 2.02-3.43) 2.305 (.08) 2.509 (.310 (<LOD-.92-8.76) 1.590 (.08-3.44-2.940-1.44) 2.98) 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 * .77-4.800-1.08-3.65) 2.70 (3.320-.234 (.230 (<LOD-.38 (2.20-2.92) 3.597) * . interval) Selected percentiles ( 95% confidence interval) Total * .11 (.790) .84-6.62 (2.700 (.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.61-3.760) < LOD 75th .22) 4.318-.07-2. population from the National Health and Nutrition Examination Survey.41 (.08-3.700 (.05-4.08-3.61-3.52) 3.97) 1.32-1.688) * .920) .550-1.645) .47-4.280 (<LOD-.70 (2.06) 4.07-3.95) 1.92 (1.510 (.42-6.510 (.20-7.32) 5.88) .440-1.23 (.57 (1.270-.700 (.830 (.43) 1.52 (1.820) 1.60) .400) .471-.870) .580 (.136-.640 (.67) 1.80) 471 575 296 664 821 689 814 1122 918 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .630) * .62 (1.750 (.07) 1.69 (1.710 (.350) .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.590-1.17) 2.510-.72 (2.60) 1.840) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.61 (3.23) 3.82) 2.81) 2.520 (.47 (1.07) 1.800) < LOD .22-3.330-.900) 1.930-1.72-4.820) .08 (2.590) * 50th .23) 1.520-.403) .43 (1.24) 4.870 (.980-1.30-2.43) 2.320-.S.750 (.23) 2.06-2.720 (.500-.91 (1.72) 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 * .16-2.330 (<LOD-.05) < LOD .97 (1.71 (1.63 (1.13 (1.285-.61) 2.89-3.53) .42-8.22) 1.11-2.535 (.368) * .790 (.75-3.75) 6.04-1.75 (1.67 (1.453 (.50 (1.09) .39) 2.78) 3.45 (1.05 (1.50) 1.372 (.32) 1.03-1.31-1.49-4.950-2.335-.73 (2.04-5.470) .550-.16-1.670 (.10) 2.740) .400-1.550) .03-2.390-1.38 (1.90) 2.390) .47 (1.33 (1.739) * .760) .393 (.300 (<LOD-.82 (2.640 (.97) 2.05-2.740) < LOD 1.97 (1.22) .66) .42) .55 (1.32 (.36) 3.300-.08) 1.02-3.39 (1.25-3.910) < LOD .30) 3.880) 1.840) 1.05) 1.530 (.79 (1.720-1.08 (.34 (1.98) 1.87 (2.680 (.480-1.412-.250 (<LOD-.515) * * .66 (2.08-2.377-.49 (1.370-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.

9) 18.04 (<LOD-2.3) 31.830-4.0 (20.2-39.18) 14.8 (22.19) 2.8 (12.0-110) 34.0-52.74-2.1-40.13 (1.9 (10.1 (11.06) * 2.50-7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4-22.0 (38.61-2.8) 39.0-49.0 (8.1) 38.60) < LOD 1.59 (1.71) 5.80) 1.23-2.81-2.0-260) 34.05) 1.3 (12.98) * 2.10 (1.0-41.69) 2.6-54.50-5. and 03-04 are 0.0-39.7-22.80) < LOD 1.90 (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.64-8.41) 1.2-27.70) 1.79 (2.20) 1.0 (38. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7) 20.3) 28.0) 5.92-5.4 (15.0) 20.82 (1.0) 32.86 (1.0 (38.46-2.95 (5.0-43.10 (1.7 (28.57-2.8) 62.2-80.43-7.5-27.0-31.0 (8.0-53.90-8.11) 2.8) 41.4 (19.0) 3.8) 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 (38.87-7.80) 90th 38.0 (13. 126 Fourth National Report on Human Exposure to Environmental Chemicals .9 (19.16) * 1.0 (38.05) * 2.80-2.7) 47.1) 38.5-40.05-3.8 (12.0) 16.45) 2.11 (4.27-6.830-3.93-3.79-2.88) 3.10 (7.30-14.4 (10.04) 3.13) 12.16) 2.0-58.0 (26.530-4.5 (24.0) 18.0) 3.31-6.75-14.4) 38.42) 1.07-5.9 (19.32 (2.0) 17.0) 42.79 (1.0 (38.7-41.6 (15.2-47.90) 11.610 (<LOD-1.90 (1.49-2.0 (7.6-45.0-39.0) 28.0 (17.00 (.76 (2.83 (3.0) 28.33 (5.0 (11.17-2.46-6.25-3.1) 95th 48.1-46. population from the National Health and Nutrition Examination Survey.0-29.41 (1.00-24.1 (22.44) Selected percentiles ( 95% confidence interval) Total * 2.96) 5.50-20.0-53.600-2. see Data Analysis section) for Survey years 99-00.45) 2.29) 2.3 (14.2-62.0) 45. and 0.1 (10.85 (1.30) 4.0) 3.70 (1.70 (1.0) 15.40-16.76 (2.0-41.78 (1.26) 75th 11.20-4.57-2.9) 48.67 (1.83-2.10 (1. which may vary for some chemicals by year and by individual sample.0) 17.70) 5.5-20.50 (2.1 (26.99 (2.04-8.64-3.18) 20.3) 33.40) 50th 2.0-41.S. 01-02.88) 1.48-2.21 (4.1-25.41-4.85) * 2.41) 1.0) 31.5) 30.70-17.30) 11.59 (1.13 (1.09 (4.0-62.9-51.44) 3.23) 9.0 (25.1-19.9) 38.2) 31.6-27.0) 13.70) 1.18.58-2.6-22.21 (3.470 (<LOD-1.30 (.0) 33.0) 4.50-17.23-2.81-3.83 (1.10-13.2-26. respectively.2) 16.54 (1.44-7.83-2.50-2.3 (12.44) 2.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8-21.29-9.0 (32.690-3.3 (10.0) 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 2.0-69.0 (20.0 (6.3) 26.2-27.80-18.20 (2.3) 38.97) 6.10) .660-2.35-6.0 (21. 0.7 (12.53) 1.94 (1.6 (9.0 (8.40) < LOD 1.0-230) 35.66-5.5-74.19-2.0) 6.0 (37.29-4.2 (19.63-6.2-33.12 (3.40-4.0-92.4.92) * 2.0 (19.4) 19.02 (2.2 (12.52 (4.14) 5.8-24.1) 140 (46.71 (4.40) < LOD 2.41) 5.0) 8.1) 18.0 (33.3 (24.58) 16.72 (1.10-4.18) 6.78) 9.9) 17.53) 40.9-21.4-76.53) * 2.36-2.70-6.21 (1.77) 38.0-47.98 (1.10 (1.48-2.54 (3.0) 4.0 (24.26 (.0) 4.0) 15.7 (12.3 (23.6 (26.0-62.10) 39.77 (1.00 (.60 (2.0) 20.6 (11.0) 3.1 (25.0) 19.5) 69.1-47.61 (1.46 (.71-2.0) 16.48) 5.0) 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 2.65 (4.0-58.9 (27.0) 30.8) 32.80) . interval) 1.0-50.5-45.0 (38.70 (7.12) 1.1 (25.91 (4.06 (1.70 (.5. < LOD means less than the limit of detection.0 (40.86-3.8 (26.9 (23.0-110) 42.1-20.6) 52.53 (1.

16 (1.61-22.9-18.67 (1.930 (<LOD-1.4 (11.69-5.18) 3.46-5.6-49.03-2.48) 1.88 (1.7) 34.38) 5.0) 13.7 (18.32-3.9 (7.35) .80-8.50 (2.1) 17.9 (39.2) 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 1.6 (24.7-20.2 (22.3-42.2) 33.6) 11.9-52.43-2.3-19.11-2.6-51.39 (1.4-39.4 (25.9 (19.1-22.33-5.2-47.43-12.22 (2.27-3.53) 1.28) 1.4) 14.27) 50th 2.79 (2.46-22.70 (1.899-2.1) 25.8-37.97 (1.8) 31.16 (1.27 (6.60) 4.2 (8.94) 19.3 (9.23) 37.50-5.S.1 (34.66) 8.7) 61.6) 7.58-17.59-2.6 (7.94-20.5 (8.5 (17.8) 15.14-8.4 (5.68) 47.47-17.46) 1.7) 26.66 (1.71) 8.72) 2.35 (2.14 (.2) 13.00 (4.18-1.37-2.20-5.58-2.60 (. interval) 1.7-19.5 (15.29-5.7) 95th 51.1) 15.9) 3.3-22.54-15.7-37.9 (10.08) 1.6) 19.0) 25.7 (10.1) 52.25-3.4-67.22-2.34) * 1.23) < LOD 2.57) 4.0) 30.870-3.8 (7.8) 11.09 (5.75 (1.67-3.5 (6.47 (3.82 (2.51) < LOD 1.83 (.4-21.40-7.17-3.38-1.95-16.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.31) 2.43) * 2.71 (1.95-16.2-38.26-4.0) 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 1.69-18.96) 2.02 (.3 (8.33) 1.32 (3.0 (6.1-63.40 (5.0 (25.0) 3.9-36.3-27.26-2.67 (1.75-6.67-16.1) 13.19-6.3) 13.96-16.1 (33.5 (41.0 (14.9-37.6 (11.33) 2.5) 27.7-38.0 (17.0) 10.7) 30.86) * 2.93) 5.19) 5.0) 48.54-2.23-1.4 (12.38-5.82) 1.21 (4. population from the National Health and Nutrition Examination Survey.06) 75th 9.68 (1.8) 3.22 (.36-13.36) 10. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.91 (6.6 (27.7 (11.08 (1.7) 15.38 (3.56) 1.33) < LOD 1.35) 1.0 (19.1) 36.07) 9.71-2.16 (1.47 (1.1 (12.63-5.20) Selected percentiles ( 95% confidence interval) Total * 1.4 (21.6) 3.4) 12.22-3.95 (2.44) 9.07-2.6-38.11) < LOD 1.12) 3.30) 28.16-2.9 (13.52 (1.1-60.83) .36 (4.7-47.6) 112 (40.1) 25.40 (2.0 (23. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (39.7 (18.0-71.59-2.2) 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 2.860 (<LOD-1.00) 6.66 (1.0-70.1 (50.79-17.7-43.670-1.5 (15.75) * 1.6) 3.3 (10.3 (20.3) 28.64 (1.2 (16.5-97.7) 66.5-43.84-13.2-34.4-71.02) * 1.7 (24.2 (9.4 (9.61 (1.1) 27.48 (4.5-36.15 (.55 (2.1) 27.90 (.01 (.70-4.4) 3.19-14.890-4.680-4.02) 1.750 (<LOD-1.1 (39.88 (1.9) 24.07-2.46-6.5) 70.06-1.2) 4.88 (4.52-4.62) 4.0-40.03) 1.59-15.51) .2) 13.61-2.1) 13.0 (32.00-16.6) 23.24 (1.28 (1. Fourth National Report on Human Exposure to Environmental Chemicals 127 .8) 23.9-41.18) * 2.57 (6.2 (21.2 (15.45 (1.4-34.5-190) 30.4) 12.12 (1.40-4.7-109) 22.56 (2.8-45.9-95.75 (1.88 (4.45-1.95) 90th 32.4 (19.2) 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.27) 10.62 (2.41 (2.06) 1.8-26.888-1.4 (25.19) 5.8-34.9 (26.9) 12.2) 36.2-28.9) 3.870-3.0 (23.7) 23.76-2.17) 2.0-118) 29.91-2.80 (1.870-3.9) 24.06) 1.8) 32.9) 54.99-4.3 (10.1 (25.00) 1.86) * 3.2) 41.8-43.0) 47.19 (1.37 (1.5 (34.5 (13.6-32.94) 1.2-70.

630 (.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.280) < LOD < LOD < LOD < LOD .410-1.15) .850) < LOD .860) .300-.830) < LOD .780) < LOD 1.310-.150) .570) .990 (.260 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.460-.560 (.640-1. population from the National Health and Nutrition Examination Survey.120-.870 (. 0.140-.990) .680) .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 .860-1.42) .840) .190 (.130-.310 (.140-.03) .20) .270 (.720) .450 (.110-.162) * * * * * .230) .090 (<LOD-.640) .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.680 (.430-.540 (<LOD-.080 (<LOD-. 128 Fourth National Report on Human Exposure to Environmental Chemicals .050-.640) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .10) . which may vary for some chemicals by year and by individual sample.740) < LOD .600 (.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 * * * * * * .36) .370-.40) .160) .10 (.130) .240 (<LOD-.S.10) .090 (<LOD-.084-. see Data Analysis section) for Survey years 99-00.650 (.130) .870 (.200) < LOD < LOD .140) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.630 (.450 (.12 (.770) < LOD 95th .290) < LOD < LOD < LOD < LOD 90th .170-.220 (<LOD-.350) .100 (.230-.850 (.10) .430 (.870 (.180) .171) * * .310) < LOD < LOD < LOD < LOD .190 (.300-1. < LOD means less than the limit of detection.090 (<LOD-.610-1.660 (.820 (.610 (.760) < LOD .140-.320-.870 (.1.870 (. respectively.117 (.650) .730-.130-.120 (<LOD-.650-1.540) 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 (.830 (.550) .210 (.30) .850 (.13) .410-.099-.160-.540) .700-1.700-1.220 (.900 (.390 (.360-.470 (.090 (<LOD-.650) .940 (.730) .510-1.190 (.610 (.380-.530-.990) .640 (.410) < LOD < LOD < LOD < LOD .290) < LOD < LOD < LOD < LOD . and 0.870) < LOD .470-1.840) .160) .330-.58) .30) .620 (.690-1.150 (<LOD-.290 (<LOD-.400-.680-1.310) < LOD < LOD < LOD < LOD .32) .210 (.60) 1.090 (<LOD-.560 (.680-1.450 (.830) .350) < LOD < LOD < LOD < LOD .720 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .1.05.540) .490 (.830 (. and 03-04 are 0.320 (.360-.720-1.390) < LOD < LOD .130-.650-1.130 (.440-1.120-. 01-02.090 (<LOD-.420-.00) .42) .460 (.30) .080 (<LOD-.930 (.700-1.820 (.380-.700-1.310 (.370-.410-.610-.380-.

330-.360 (.560 (.990) .300-.660-1.100 (<LOD-.540 (.060-.86) .450) .190 (.140-.320 (<LOD-.410 (.120) .180-.200 (.270) < LOD < LOD < LOD < LOD .410) .43) .460 (.370 (<LOD-.400) .720 (.410-.170) < LOD < LOD .380-.140) .610-1.161) * * .380-.084-.67) .140-.66) 1.580 (.540) .890 (.220 (.730) .700 (.36 (1.03 (.700 (.990) .410-.520-.410) < LOD < LOD .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 .670-1.057-.230) < LOD < LOD < LOD < LOD .970) .550 (.01 (.00) < LOD .580 (.510-.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .470 (<LOD-.050 (<LOD-.550 (.360) < LOD < LOD < LOD < LOD .730) .260) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.880 (.03 (.300-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.140-.110) .190-.730) .140-.86) .730 (.220) < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .850 (.38) 1.450 (.140-.650-1.080 (.190 (.090 (<LOD-.14) 1.12) < LOD .170 (.111) * * * * * .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 * * * * * * * * * .760) .490-1.60) .340-.330-.360-.570 (.070 (<LOD-.440 (.03 (.940) .740) < LOD 1.710-1.230 (<LOD-.880-1.380-1.380-.380 (.070 (<LOD-.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.860 (.700-1.02-1.580) < LOD .810 (.960) .310) < LOD < LOD < LOD < LOD .800-1.740 (.700) .250-.860 (.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.78) .330 (.940) .280) < LOD < LOD < LOD < LOD .570-.780 (.600) .S.09) .600-1.300 (.440-1.240-.110) .270 (.080 (<LOD-.330 (.860-2. Fourth National Report on Human Exposure to Environmental Chemicals 129 .170 (.580-1.330-.360-.640-1.780) < LOD 1.570-1.540) 471 576 310 664 821 715 814 1118 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .500) .720 (.100-.540 (.090 (.24 (.20) 1.080) .110) .580) .110) .210 (.650) < LOD .670 (.500-1.070 (<LOD-.400 (<LOD-.500 (<LOD-.260-. population from the National Health and Nutrition Examination Survey.02) .62) 1.58) 1.29 (.670 (.290) < LOD < LOD < LOD < LOD 90th .390-.390-.19 (.03) .750) < LOD 95th .110-.870) .230-.150-.200 (.410 (.120) .24) .116 (.070 (<LOD-.

15) 14.730 (.40-20.11) .0-39.67 (2.0-44.00) 1.840-3. and 03-04 are 0.00-17.05 (3.800) 90th 13.S.96 (1.10-9.0) 5.65) 1.0-38.770) 2.720) 2.40 (1.48) 13.20-4.12-1.350-.35-10.70) 2.0 (5.70-3.0) 2.0) 2. population from the National Health and Nutrition Examination Survey.40) 2.94 (1.610) < LOD < LOD < LOD < LOD < LOD 2.691 (.99) 19. respectively.0 (13.99 (1.37) .35) 5.0) 7.62-8.83-3.14) 2.840 (<LOD-1.90) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.870) < LOD < LOD .32-9.0 (3.60) 1.00) .97) 20.83-3.580 (.0-40.380-.42) 2.50) 2.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.11) 13.0 (5.49) 17.83) 2.90-28.51-8.0-38.67) .50) .88-3.0 (17. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.110 (<LOD-.30) 95th 19.74 (3.640 (.10 (3.10 (.86) 4.1.59-5.66) 4.63) 32.90-9.24-7. and 0.28) 1.08.90) .97) 20.68) 2.48 (2.840 (.0 (7.16) 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 .890 (.0 (17.0) 3.35) 11.47 (3.32 (1.0) 2.90) .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 * * * * * * * * * .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 * * * * * * .26 (2.0 (5.00 (.0-38. 0.43-4.6) 5.94-3.0 (4.0 (5.03 (.55-4.07 (3.46 (1.0) 2.20 (1.36-3. see Data Analysis section) for Survey years 99-00.53-7.21) 3.0) 4.85-3.690 (.14-5.40 (1.0-40.600 (.67 (1.0 (16.0) 4.800-4. 01-02.0) 4.20 (1.82-4.0 (17.52 (1.61 (1.0 (4.0 (6.94-8.42) .20-17.10-3.00) .36-3.70-30.07-3.620-1.0 (5.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.39 (2.1.40-4.10 (3.40) 1.13 (3.830 (.51 (2.425-1.31) .20) < LOD < LOD < LOD < LOD < LOD 1.99) 11.30-6.53 (2.70-17.400-1.30-7. < LOD means less than the limit of detection.00 (1.60) .55-8.52 (1.30 (.10-3.07 (3.0) 5.07) 1.590 (.750-2.30 (2.770 (<LOD-1.90 (2.28) .21-3.080-1.960 (.80 (4.0) 2.90-37.330 (<LOD-1.640 (.05-3.510-.0 (17.87) 5.00-17.880) 5.360-1.76 (1.900 (.90-20.40-7.45 (2. which may vary for some chemicals by year and by individual sample.23-6.910) 2.740 (.850) 16. 130 Fourth National Report on Human Exposure to Environmental Chemicals .63 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.39) .38-3.49 (1.0) 2.0 (17.30-3.960 (<LOD-1.14) .750-1.53) 20.52) 5.28-9.11 (1.0) 5.800) 17.190-1.610 (.30) .480-.30 (1.350-.90 (1.370-.12) * * * * * * * * .170-1.07 (1.33 (4.260-.0) 5.01) 5.15) 19.20-4.31-10.40-8.0) 2.70-7.0) 4.30 (1.210-1.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.05 (2.250 (<LOD-.70-50.07-3.49 (1.29-10.30 (1.18) 1.87) 12.74) 5.

11) .270 (<LOD-.8) 2.40 (.83 (4.S.96-8.73 (4.150 (<LOD-.450 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.66-47.40-2.730-3.62 (1.60 (1.340-.90-6.5 (9.590) 2.64) 30.47-10.55) 21.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.31) .74 (2.91) 2.6) 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 * * * * * * * * * .32) 9.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.820) .53) 27.04-16.12-4.700) 6. population from the National Health and Nutrition Examination Survey.00-19.540 (.10 (2.1) 471 575 306 664 820 697 814 1122 924 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .08) .830 (.18) * * * * * * * * .33-5.250 (<LOD-.85-3.07 (2.14-6.650) 90th 10.17 (1.81-17.39) 20.48 (4.390-.49-2.06 (.370 (.960 (.52 (.340-.31-18.23-7.4) 2.85 (1.710 (<LOD-1.3) 3.470 (.28-6.800-2.7) 6.80) 3.8) 7.53) .56) 2.61) 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 .8) 1.25 (1.09-3.40-12.04 (1.62-17.13 (2.29 (4.22-27.41) 18.51-44.580-1.15) 9.40) 1.310-.430 (<LOD-.86) .620-3.17) 5.41 (4.9) 6.1 (7.190-1.748 (.38 (2.0 (9.44-11.7 (6.45 (1.780-4.890 (.05) .650 (.370) < LOD < LOD < LOD < LOD < LOD 1.25-38.260-.5) 2.55) 21.84) 9.96) 2.320-1.770) .33-3.89 (2.88-3.31-7.560 (.33-4. Fourth National Report on Human Exposure to Environmental Chemicals 131 .77 (.970-3.35 (.12 (4.92 (2.360 (.43) .98 (4.850-3.55 (3.02) .56 (1.97) .03) 2.47-10.660) < LOD < LOD .69-7.690-5.370-1.27 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8 (20.82-11.540-1.57) 1.4-34.24) 3.630-1.21-3.1) 2.240-.57-40.50) .00) .580) 1.67-6.7) 5.580) 16.75) 5.30 (4.69) 2.79 (.5) 7.02-4.07-21.330-1.5 (11.8) 2.14 (1.56) .340 (.18) 1.700) < LOD < LOD < LOD < LOD < LOD 1.01 (1.57 (.33 (1.31) .270-.59 (1.790) 11.83-11.7) 4.71 (2.86 (3.22) 2.2 (8.91-4.10-3.02 (.44) .8) 7.11-5.3) 2.0) 4.830-3.1 (5.1) 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.7 (12.670 (.9) 5.474-1.67) 1.47) .9 (11.820 (.430) 1.47) 5.96-25.50) 11.500 (.02 (1.51-4.4 (4.5 (8.33 (3.88 (.8) 4.64-4.18) 95th 21.8-33.840-3.10) 2.25-9.740-1.03) 16.5) 2.88) 17.340-.600 (<LOD-1.48-42.0 (4.7) 3.36 (.67 (2.930) .67) 2.37) 4.50 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.29-4.57) 8.940-4.80 (.32-6.260-.88 (2.5-40.48-7.790 (.65 (2.580 (.71 (.2-38.860-2.50 (4.

7(5):715-731. J Toxicol Environ Health 1981. 132 Fourth National Report on Human Exposure to Environmental Chemicals .53(1):714. Demers P. Am J Ind Med 2006.113(12):1802-1807.16(5):417-426. Occup Environ Med 2003. Bradman A. Leffingwell JT. Metabolites of organophosphorous insecticides in urine specimens from inhabitants of a residential area.110(8):829-833. Anger WK. Fenske RA. Checkoway H. Environmental and biological monitoring of exposure to organophosphorus pesticides: application to occupationally and non-occupationally exposed adult populations. Barr DB. Eaton DL. Franklin CA. Lu C. Reprod Toxicol 1998a. Regul Toxicol Pharmacol 2003. and incidental exposure to organophosphate pesticides using urine alkyl phosphate and phenolic metabolite measurements. Arch Environ Health 1998. Environ Health Perspect 2003. Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets. Gillham RA. Aprea C. Fenske RA. Griffith W. Chevrier J. 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Barr DB. low-level exposure to the organophosphate diazinon. Thompson ML.332(1-3):71-80. Pesticides in the Diets of Infants and Children. Bull Environ Contam Toxicol 1994. McCauley L. Ames RG. Savage EP. Stokes L.24(1):18-29. Rothlein J. Occup Environ Med 1995. Keifer M. Pilkington A. Chronic central nervous system effects of acute organophosphate pesticide intoxication.52(2):190-195. Salvini S. National Research Council (NRC).338(8761):223-227. Wickremasinghe AR.345(8958):11351139.30(2):98-103.S. Aprea C. 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. Vitayavirasak B. vibration sense and tremor among South African farm workers. et al.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. EPA). Pedersen L.php?record_id=2126&page=1. Stark A. Irish RM. Gladstone EA. Schenker M. Dinoff TM. McConnell R. Environ Health Perspect 2005. O’Malley M. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Environmental Protection Agency (U. Saieva C. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Effects of chronic.113(4):504-508. Mounce LM.68(3):209-227 Maizlish N.84(5):731-736. Tumino R. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Am J Public Health 1994. Malathion deposition. Jamal GA.20(2):115-22. Myers JE. 1993 [online]. Lambert WE.43(1):38-45. Kidd M. Rohlman D. Lasarev M. Int J Occup Environ Health 2006. Weerasekera G. Stephens R. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. 4/7/09 Young JG. low-level organophosphate exposure on delayed recall. Visuthismajarn P.58(11):702710. van der Hoek W. Rodnitzky RL. Scand J Work Environ Health 1998. Russo J. Neurotoxicology 2005. Takamiya K. Marshall E. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Lu C. Arch Environ Health 1988. Muniz J. Nell V. Neurotoxicol Teratol 1998. Bradman A. Sci Total Environ 2004.pdf. Steenland K. Office of Prevention Pesticides and Toxic Substances. Samuels S. Spurgeon A. Petchuay C. Seiber J. and spatial learning in monkeys and rats. London L. Rosenstock L. Weisskopf C. The Pesticide Health Effects Study Group. Lancet 1995. Am J Ind Med 1987. Caltabiano LM. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Berry H. et al. J Occup Environ Med 2002. Smit LA. Lancet. Johnson C. Levy LS. Heaton RK. discrimination. Frasca G. Keefe TJ. May. Scherer J. 1991. Ruberu DK. Beach J.38(4):546-563. Prendergast MA.52(10):648-653. Bravo R.S. Narang A. 2004. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Neurotoxicity among pesticide applicators exposed to organophosphates. Hansen S. gov/oppbead1/pestsales/01pestsales/market_estimates2001. J Toxicol Environ Health A 2005. Hore P. Lasarev M. Terry AV Jr. Chrislip D. Buccafusco JJ. Environ Health Perspect 2006. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. et al. 1/12/09 Peiris-John RJ. Pesticide industry sales and usage . Arch Environ Health 1975.114(5):691-696. Robson MG. Jenkins B. National Academy of Sciences. A behavioral evaluation of pest control workers with short-term. S. et al. Burcar PJ.2000 and 2001 market estimates. Calvert IA. U. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Occup Environ Med 2001. Masala G. Eskenazi B. Lewis JA. Rothlein J.epa. metabolite clearance. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. and cholinesterase status of date dusters and harvesters in California. Available at URL: http://www. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. EPA.12(2):134-141. Washington (DC). Arch Environ Contam Toxicol 2000.edu/ openbook. Washington (DC): U. Muniz J. Effects of long-term organophosphate exposures on neurological symptoms. Chronic neurological sequelae to organophosphate pesticide poisoning. Claypoole K.nap.44(4):352-357. Available at URL: http://books. Daniell WE.26(2):199-209. et al. Santana J. Gillham R. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Phillips J. Buchanan D.12(2):153-172.

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

60) 5. and sprayed to kill mosquitoes.1) 5.95 (4.83) 1.50-4.50 (2.02) 1.37) 5. although some tolerances for specific food crops have been reduced in the past to avoid exceeding recommended intake limits for total dietary intake in special groups (U.70 (1.97) 2.91) 16.60 (5. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.5) 7.72) 2.8-15.4 (9.30-2.78 (7.96) 3.95) 7.9 (10.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.13 (1.9 (9. Approximately 21-24 million pounds per year were used domestically from 1987-1998.03) 1.09 (3.0) 8.68-2.20-14.16) 2.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.44 (3.8) 9.S.20) 10.5.3 (11..0) 12. 2005).0) 14. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration. interval) 1.60-3.7) 9. 1999.47-9.03) 99-00 01-02 99-00 01-02 99-00 01-02 2. 2921-88-2 Chlorpyrifos-methyl CAS No.9 (7.20-3. Fourth National Report on Human Exposure to Environmental Chemicals 135 .44-5.02 (7.97) 7. staying bound to soil particles.24-3. It has low leachability.000 pounds are used per year.10-17. Survey Geometric mean (95% conf.74 (1.92 (1.30-1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.50 (2.77-6.0) 12. 2002).90 (1.24-1.2 (10.29-1.44-2.31-2.60-3. Approximately 80.64) 3.70-16.9) 697 660 521 701 602 947 Limit of detection (LOD.20 (4.99-4.43-2.70-11.17 (1.68 (7.81-2.71 (6. air.1-16. After 2001.4.51 (1.0) 10.80 (7.46-2. chlorpyrifos was no longer registered for indoor residential uses in the United States.97) 4.20) 4.19-3.5-24. Chlorpyrifos is Urinary 3.4 and 0.35) 1.94 (4. 5598-13-0 General Information The chemical 3.20-16.71 (1. dermal. and dust.26) 7. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.63 (1. and on plants for days to several weeks. population from the National Health and Nutrition Examination Survey.32-1.50-14.4-15.98-15.84) 1. For instance.34) 1.80) 4.7-23. pre.0 (7.3 (10.70) 1.51) 1.20-2.37 (1. applied to structures to kill termites.30) 4. 2007).0 (7.61 (1.72-4.30-11. in 142 urban homes and preschools in North Carolina.15 (1.40) 2.90-4.62-2. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.0) 11.61) 75th 3.10 (3.0) 15.89-2.10 (5.90 (6.47) 1.05) 1.0 (7.31-2.97-7.63 (8.20-4.30-5.50 (2.40 (5.00-24.91 (1.EPA.20-11.60-2.50-8.47 (4.0-28.10) 6.60 (4.and post-construction structural applications for termite control were to be phased out by 2005 (U.0) 12.9-18.66-4.70-17.10 (4.67 (2.76 (1.40-13.28-3.80 (1.30 (2.0 (7.50 (1.25) 1.90) 3.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.47-13.40 (5.36 (4.S.00) 1.0) 7.00) 2.05-5.51-2.39-2. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.40) 9.57 (2.00-8.60 (2.53 (1.30) 4.6) 7.60-4.30 (2.90-8.3) 8. and inhalation routes.0 (7.79-2. The general population may be exposed to chlorpyrifos via oral.28) 2.50 (1.70 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.40-2.55-5.80-10.0) 18.04-10. USGS.30-12.0 (10.74-9.27 (7.20 (2.67 (2.4 (10.66-15.50-2.90-7.4 (8.40-10.02 (1.76 (1.35) 2.39) 4.21) 3.67 (1.86) 4.10 (1.80) 1.45 (1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.3 (8. It also has been applied directly on animals to kill mites.13-3.40-26.30-9.50-5.EPA.59) 2. 2002).9) 11.71 (2.50-4.01) 1.90 (1.80) 12.90-2.37 (4.40 (6.20) 2.97) 2.19 (1.52-2.20) 2.04-10.5.77) 1.70-5.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30 (4.47-11.22) 2.63 (2.87-6. and is infrequently detected in ground water (IPCS.0 (9.77-15.0) 12.7) 8.00) 3.8) 10.0) 10.30) 5.90 (3.70-15.90) 7.50-2.22 (1. but can be detected in streams receiving runoff from application sites.59-2. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.38 (3.90 (2.3) 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 1.5 (8.29) 90th 7.10) 2. Estimated intakes from diet and water have not exceeded recommended intake limits. Exposure can also result from contact with contaminated surfaces.0) 12.25) 3.0) 6.0) 8.09 (2.89 (2.7) 13.88 (1.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.0) 9.S.80-8.0 (13.77 (1.80) 2.0) 10.43-2.32) 2.61-7.52-12.

55 (1. vomiting.43 (4.80) 3. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.45 (1.12) 1.39) 6.0) 6.70-4.97 (2.0) 16.0) 10.16 (4.57) 9.05) 3.12-1.28) 2.98 (6.65-15.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.43-10.93) 2.24-5. Thus.55) 1.1-38.40) 1. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.71 (1.12-3.49-2.22 (4.91 (4.. 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.05-4.3 (7.09-1.84-6.05-3.73 (1.29 (3.62) 1.48 (1. 2005.72) 2. Ricceri et al.53 (2.22 (6. and producing acute symptoms such as nausea. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.07) 5.23) 14.90-9.97-3.S.64-7. Howard et al.0) 12.81 (3.54 (2.94-14.66 (1.91) 1.58) 1. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.27-1.97) 3.93) 5. 2002).33 (1.5 (6.44 (5. population from the National Health and Nutrition Examination Survey.44 (6. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.26-14.11) 7.27-7. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.62) 90th 5.14) 1.86 (1. TCPy is more persistent in the environment than chlorpyrifos itself (U.01) 1.32) 1.5.08) 6.25-12.6) 9.54) 5.3) 8.88) 6.58 (4.47-2.89) 4..5) 5.42-2.91-13.69 (1. 2006b).24-4.88 (1.00 (7.42 (5.21-1.66-11. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.00-8.24) 75th 2.95 (3.11 (2.4) 4.3) 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 1.91-4.20 (2.74) 1.06 (1. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.75 (1.44-6.34-1.60 (1. Roy et al.85 (2.80-4. 1984).80-6.EPA.95 (1.44 (1.05-8..09-2.56-2.3) 9. Slotkin et al.79-13.94-12.85) 1.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.99-8.91) 1.91 (3. 2006.78 (1.47 (1.63 (4.49-2.11 (2.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.24-1. 2005.15 (4. Betancourt et al.39 (4.47 (5.57-2. resulting in excess acetylcholine at nerve terminals.56 (1. Based on animal data and human cholinesterase monitoring during occupational exposure.09 (1.24) 5.88-9.85-4.45-1.1-21.33-7.940-1.71) 3.85) 4.39-1.. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.30-4.8) 9.01) 3.57) 2.96) 3.91) 2.30-1.03) 1. paralysis.02) 7.56) 2. 2000).92) 3.88-8.49 (1.9 (12.58 (1.66) 1.97 (3.55 (4.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1. and other metabolites.93 (1.44 (5.S.20-1. 2006a.93 (2.24-24.57-2.88 (1.63 (5.31-4.39 (2.3) 8.38) 3.85 (3.80-11.97) 3.28) 2.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.59-2.46 (2.22-6. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).65-11.60-3.52 (5.86 (3.33) 2. weakness.58) 5.64 (1. and seizures.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .68) 1.47 (1.33 (5.09-3.7) 7.07) 1.24 (1.53-5.19-1.46 (1.31-1.82-4.35-1.88-8.42 (6.11-9.. neurotransmission.83-11.23-1.75) 6.56) 5.82 (2.2) 6.35) 1.25-11.68) 6.99) 1.22) 1.05-1.19) 3.62-7.83-2.83) 1.72) 1.64-2.59) 3.06-4.00-13.92-2.93 (4.91) 10.87-3.63-2. Survey Geometric mean (95% conf.2 (7. Metabolic hydrolysis leads to the formation of TCPy.35) 2.49-2.01) 3.14-8.. Once absorbed.. In pesticide applicators.98 (7. 2006.50 (4.21-6.72-2.82 (3.17-4.36) 1. TCPy can also occur in the environment from the breakdown of the parent compounds.56 (4.33 (.19-2. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.88-10. 2005.92 (1.48 (2.82) 8. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.58 (1.00) 1.1 (7. Urinary 3.1 (10.76 (2.81) 2.31) 1.06 (5.44 (1.19) 6.41 (1.16) 6..77) 1..76 (3.25-1.37 (1. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.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.86 (1.17-4.58-5.6) 10.51 (1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.02 (5. cholinergic effects. interval) 1.

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

Needham LL. Slotkin TA. Gurunathan S. J Expo Anal Environ Epidemiol 2000. 1999. Atlanta (GA). Chuang JC. Environ Health Perspect 2005. et al. Exposures of preschool children to chlorpyrifos and its degradation product 3. Steenland K. Environ Health Perspect 2004. Chrislip DW. Pesticide residues in urine of adults living in the United States: reference range concentrations. February 5. Morgan MK. MacIntosh DL.nih. Venerosi A.S. Freshour NL.155(1):71-80. et al. International Programme on Chemical Safety-INCHEM (IPCS). Int J Hyg Environ Health 2001.9(5):494-501. Angerer J. J Expo Anal Environ Epidemiol 1999. Interim registration eligibility decision for chlorpyrifos. Jett DA. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Curwin BD. Alexander BH.114(2):260-263. Lorenzini P.6-trichloro-2-pyridinol. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Rick DL. Available at URL: http://www. Shealy DB. 4/7/09 Perera FP. Meeker JD. Environ Health Perspect 2006a. Chapman P. Environ Health Perspect 2006. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. EPA). Head SL. 1992. Kromhout H. Cometa MF. 2921-882. Lu C. Hines CJ. Pellizzari E. Lein PJ.6-trichloro 2-pyridinol in their everyday environments. et al. Howard AS.73:8-15. Robson M. Mandel JS. Jones PA.111(2):201-205. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Toxicol Appl Pharmacol 1984. Weltzien E. Gregg M. Camann D. Hardt J.inchem.S. Environ Health Perspect 2000. Kinney P. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Sharma V. Acquavella JF. Neurologic function among termiticide applicators exposed to chlorpyrifos. Bravo R. mothers and fathers living in farm and non-farm households in Iowa. Baker BA. Yang D.31 Suppl 1:98-104. Bennett DH. Ozkaynak H. Edwards RD. Reid TM. A longitudinal investigation of selected pesticide metabolites in urine. Brain Res Dev Brain Res 2005. et al. et al. et al.15(4):297-309. Howell RJ. Ryde IT. 2005. Harley K. Seidler FJ. et al. Ann Occup Hyg 2007. J Expo Anal Environ Epidemiol 2005. Available at URL: http://ntp. Bucelli R. Levin ED. Fortuna S. J Expo Anal Environ Epidemiol 2005. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Herrick RF. National Toxicology Program (NTP). Adgate JL. Levin ED. Honeycutt R. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Chlorpyrifos: pharmacokinetics in human volunteers. chlorpyrifos. Sanderson WT. et al. Scand J Work Environ Health 2005.org/documents/jmpr/jmpmono/ v99pr03. Freeman N. Environmental Health Criteria 198.htm. Robertson GL.71:99108.112(10):1116-1124. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Seidler FJ.114(5):746-751. Dick RB. Rauh V. Hammerstrom KA. Urinary pesticide concentrations among children. Baker S. Striley C. Hore P. Toxicol Sci 2006. Hein MJ. Croghan CW. Ryan L. Jewell NP. Ryan PB. Capone F. Nolan RJ.15(3):271-281.114(10):1542-1546. Tsai WY. Slotkin TA. Saunders JH. Executive summary of safety and toxicity information. Eskenazi B. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Barr D. et al. Irish R. Bravo R. Hill RH Jr. gov/ntpweb/index. Ricceri L. Bailey SL. et al. Environ Health Perspect 2006b. 4/7/09 Koch HM.93(1):105-113.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Sheldon LS. Freeman N. Toepel K. Environ Res 1995. Environmental Protection Agency (U. U. Zhang J. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Barr DB. Slotkin TA.207(2):112-124.niehs. Environ Health Perspect 2003. Heederik D. Tate CA. Wartenberg D. Biomonitoring for farm families in the farm family exposure study. Seidler FJ. Fenske RA.10(4):327-340. Toxicol Appl Pharmacol 2005. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3.108(4):293-300. Bruun D. Barr DB. Chlorpyrifos. Bradman A. Roy TS.5. 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.204(2-3):175-180.51(1):53-65.5.113(2):211-219. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Lioy PJ. Third National Report on Human Exposure to Environmental Chemicals. Barr DB.

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

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

Survey Geometric mean (95% conf. < 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 . population from the National Health and Nutrition Examination Survey.270) < LOD 659 701 920 Limit of detection (LOD.27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-.670 (<LOD-1. see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf.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 .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. Fourth National Report on Human Exposure to Environmental Chemicals 141 .200 (<LOD-.S. population from the National Health and Nutrition Examination Survey.380 (<LOD-. 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.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.

12(6):619-645.S. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos.gov/oppsrrd1/ REDs/0018tred. 2005. Freshwater KJ. Atlanta (GA). Olsson AO. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . Reprod Toxicol 1998. Third National Report on Human Exposure to Environmental Chemicals. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Environmental Protection Agency (U. Centers for Disease Control and Prevention (CDC). September 2000. Sadowski MA. Available at URL: http://www. Nguyen JV.epa.S. EPA 738-R-00-010. U. EPA). Eigenberg DA. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies.pdf. Barr DB.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. Anal Bioanal Chem 2003.376(6):808-815.

Diazinon is not well-absorbed through the skin.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. but these uses have been phased out. Inhalational and dermal routes of exposure can be significant for pesticide applicators. Most granular formulations. Survey Geometric mean (95% conf. Once absorbed. Estimated intakes from diet and water do not exceed recommended intake limits (U. which may vary for some chemicals by year and by individual sample. and forage crops. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. 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. diazinon produced wild bird kills before use restrictions were in place. aerial. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. seed and foliar applications are planned to be phased out (U. fruits. 1998. 1998). since 2004.49 (<LOD-2. * 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 143 . Before these restrictions.7. in the past.EPA.EPA. diazinon cannot be sold for residential use. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. an organophosphorus insecticide that is used to control insects on nuts. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. 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.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. 2004). 2004). diazinon was widely used in residential and garden application. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. see Data Analysis section) for Survey years 99-00 and 01-02 are 7.2 and 0. and particularly when it was ingested in granular form. 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. It is also used for cattle ear tag applications to control flies and ticks and. USGS. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). but is rapidly absorbed orally (IPCS. It is toxic to birds. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine.45 (<LOD-3. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. 2007). Prior to 2000. in some pest strips. population from the National Health and Nutrition Examination Survey. and other metabolites.S. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon.S. vegetable. < LOD means less than the limit of detection.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No.S.

vomiting.. At high doses. environmental levels) and health effects is available from ATSDR at: http://www. Survey Geometric mean (95% conf. in the 2001-2002 subsample (CDC. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. cholinergic effects.S. 1998).. diazinon does not accumulate in tissues (IPCS. population from the National Health and Nutrition Examination Survey. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. weakness. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants. 1992). and indoor applications have been documented.S.72 (<LOD-4. Additional information about external exposure (i.EPA considers diazinon unlikely to be carcinogenic in humans. paralysis. Seifert and Pewnim. animal carcinogen. Diazinon has moderate acute toxicity in animal studies. 1986 Rajendra et al. The U. agricultural. 2003)...epa. or reproductive toxicant (IPCS.. In the U. Thus.html and from U.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. 1998).S. In animals.49 μg/L. respectively (Baker et al.e. 1986.cdc. 2000.. 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. respectively. 144 Fourth National Report on Human Exposure to Environmental Chemicals . and producing acute symptoms such as nausea. Diazinon is not considered to be a mutagen. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. and seizures.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al.76 (<LOD-3.45 and 1. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. Olsson et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In two nonrandom samples of United States adults and children. subsamples of NHANES 1999-2000 and 20012002. Intoxications in humans from intentional overdose. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound.48) < LOD < LOD 644 678 484 699 554 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.atsdr.gov/toxpro2. In addition to being a human metabolite of diazinon. 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. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al.gov/pesticides/. 2002). EPA at: http://www. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. resulting in excess acetylcholine at nerve terminals. teratogen. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown.

Bull Environ Contam Toxicol 1986. Bouchard M. Sadowski MA. Geological Survey (USGS). Atlanta (GA). Banister E. Toepel K.pdf. Swan SH.inchem. Redmon JB.50(5):505-515. 2006). Toxicol Lett 2002. 4/7/09 Lu C. revised February 15. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Biochem Pharmacol 1992. Seifert J. Kruse RL. Barr DB. Pesticides in the Nation’s Streams and Ground Water. Banister EW. Available at URL: http://www. Drobnis EZ.44(11):2243-2250. et al. In 23 children. Diazinon. Diazinon. 2005. Environ Health Perspect 2006. 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. Carrier G. Olsson AO. Barr DB.S. May 2004.10(6 Pt 2):789-798. Oloffs PC. Liu F. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Fenske RA. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.. Semen quality in relation to biomarkers of pesticide exposure.134(1-3):105-113. Driskell WJ. Centers for Disease Control and Prevention (CDC). In 54 Canadian greenhouse workers.S. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Cocker J. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon..usgs. Dumas P. References Anthony J. Barr DB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http://www. Mason HJ.376(6):808-815.Organophosphorus Insecticides: Specific Metabolites 2005).htm. Environmental Health Criteria 198. Study for Future Families Research Group.111(12):1478-1484.9(2):117-131.gov/circ/2005/1291/. Drug Chem Toxicol 1986. International Programme on Chemical Safety-INCHEM (IPCS). 2006). Interim reregistration eligibility decision (IRED. 1992-2001. Third National Report on Human Exposure to Environmental Chemicals.S. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Jones K. U. Available at URL: http://pubs. EPA). J Expo Anal Environ Epidemiol 2000. Oloffs PC. Swan et al.37(4):501-507.org/documents/ehc/ehc/ehc198. Nguyen JV. Noisel N. March 2006. The Quality of Our Nation’s Waters. 1998.gov/ oppsrrd1/REDs/diazinon_ired. Effect of sublethal levels of diazinon: histopathology of liver. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Ann Occup Hyg 2006. 2007 [online]. Baker SE. Environ Health Perspect 2003. Beeson MD. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Pewnim T. Environmental Protection Agency (U. Brunet RC. Anal Bioanal Chem 2003.epa. Rajendra W. Garfitt SJ.114(2):260-263. Barr DB. 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. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Bravo R. 1/14/09 U. In a small number of men visiting fertility clinics in Missouri and Minnesota. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. EPA 738-R-04-006. Needham LL. Irish R.

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

2000). representative subsample from NHANES 19992000 (Adgate.. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC.e. 2006). Pluth et al. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample.. but cholinesterase activity was not affected.S. Survey Geometric mean (95% conf.S. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid.74 (<LOD-5. Lu et al. 1999. 1993. 2003). 2001. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al.S. 1999).gov/pesticides/.EPA. 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. 1996.epa. Additional information about external exposure (i.. environmental levels) and health effects is available from ATSDR at: http://www.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.S. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. 1990). 2005). 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.cdc.EPA. 2002. Human studies of single oral doses between 0.. 2004).html and from U. 2006).Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions...5 and 5. 1987. Fourth National Report on Human Exposure to Environmental Chemicals 147 . population from the National Health and Nutrition Examination Survey.atsdr. and it is not considered an animal teratogen or a reproductive toxicant. 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. Flessel et al... Thomas et al. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. 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. EPA at: http://www. 2006). A study of 13 children from an agricultural region of Washington State reported median levels that were below the detection limit in the NHANES 1999-2000 subsample (Kissel et al. but isomalathion..S. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. Urinary Malathion dicarboxylic acid (creatinine corrected) Metabolite of Malathion Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.gov/toxpro2. Of 382 pregnant women living in an agricultural community. Malathion itself has not been considered genotoxic (U.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. 2005). Giri et al.. 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. Toxicity from unprotected bystander exposure during applications is rare (U. 2005. CDC. IARC considers malathion not classifiable as a human carcinogen. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Third National Report on Human Exposure to Environmental Chemicals. A longitudinal investigation of selected pesticide metabolites in urine. Flessel P. Centers for Disease Control and Prevention (CDC). Needham LL. MacIntosh DL. Neutra R.77:1009-1010. The Quality of Our Nation’s Waters. Trzeciak A. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Reregistration eligibility decision (RED) Malathion. U. Harley K. EPA 738-R06-030.S. Petitti D. Available at URL: http://pubs. Irish R. Pesticides in the Nation’s Streams and Ground Water. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues.S. htm. Kedan G. Dumoulin MJ.pdf. et al. Gosselin NH. Environ Mol Mutagen 1993. metabolite clearance. J Expo Anal Environ Epidemiol 1999. Toxicol Sci 2003 May. Arch Environ Contam Toxicol 2000. Malathion deposition.112(10):1116-1124.gov/oppsrrd1/REDs/ malathion_red. Nicklas JA. Blasiak J. Krieger RI. Clayton CA. Lu C.S. Cancer Res 1996. Barr DB. Bouchard M. International Programme on Chemical Safety-INCHEM (IPCS). 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . 1992-2001. Available at URL: http://www.gov/circ/2005/1291/. Jaloszynski P. Barr DB. 2007 [online]. J Expo Anal Environ Epidemiol 2005. 2005. Environmental Protection Agency (U.109(6):583-590. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. 6/1/09 U. Environ Health Perspect 2006. Harris JA. O’Neill JP. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Reproductive outcome in women exposed to malathion. Bradman A.org/documents/jmpr/jmpmono/v2003pr06.73(1):182-94. Bravo R. Eskenazi B. Szyfter K. March 2006. Environ Health Perspect 2004. Hertz-Picciotto I. July 2006. Ryan PB. Erratum in: Toxicol Sci 2003 Aug.epa. Fenske RA. Am J Epidemiol 1990. Mutat Res 2002.514(1-2):223231. Albertini RJ.132(4):794-795. 4/7/09 Kissel JC. Jewell NP. Griffith W. et al. Rappaport E. Carrier G. Freeman NC.445(2):275-283. Giri S. Environ Health Perspect 2001. Atlanta (GA). Grether JK. Available at URL: http://www. Barr DB. Lu C. Samuel O. Quintana PJ. Lioy PJ. Malathion (addendum). Geological Survey (USGS). Dinoff TM. Hooper K.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Sharma GD. Weltzien E. Swan SH.74(2):following table of contents. Brunet RC.38(4):546-553. Hammerstrom KA. Curl CL.9(5):494-501. Am J Public Health 1987.15(2):164-171. Goldhaber M. Pluth JM. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Barr DB. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Genetic toxicity of malathion: a review. Giri A.usgs.22(1):7-17. Prasad SB. et al.56(10):2393-2399.114(2):260-263. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Thomas D. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Eberly LE. Toepel K. EPA). revised February 15.inchem. and cholinesterase status of date dusters and harvesters in California. Mutat Res 1999. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure.

Ethyl parathion.80 (2.60 (4.09-1.70-6. In animal studies.37-4. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. 2003).11) 2.49 (1.70 (2. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.27) 2.70-6.40-3.11-4. and has a short half-life in soils and on plants. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80 (2.10 (3.16) < LOD 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.71 (2.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .70-3. Once absorbed..50 (1. more slowly absorbed through the skin.10) 22. first registered in 1948.33 (1.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .28 (1.30-3.910) < LOD < LOD < LOD 1.44) 2.0) 3.01-4.28-4.10) 4. and aquatic invertebrates.20 (<LOD-2.26 (1.40) 4.40 (1. Methyl parathion has low water solubility.12) < LOD < LOD 1.47) 2. Increased risk of exposure via dermal. Methyl parathion is not registered for residential use in the United States.70 (2.40-4. Both are toxic to birds.70) 2.66 (2.67 (1. methyl parathion was rapidly absorbed after ingestion.18-3.92-2.30 (1. In the 1990s. It had been applied to cotton.74) 5. fish.32 (1.700 (<LOD-.50 (1.0) 3. with limited applications in agriculture.01) 695 660 518 679 603 941 Limit of detection (LOD.70) 2.80) 2. but by 2003.0) 4. Given its limited use.20-5.10-11.790 (<LOD-.0 (3. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides. pulmonary.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 1.40-4.61) < LOD 1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.10-1.EPA.50) 3.28 (1.72 (3.60) 1.990-1.37) 2.70-6.57-4. 1977). 2000). < LOD means less than the limit of detection.33) 2.10 (<LOD-6.850) < LOD .41-4. binds tightly to soils resulting in low leachability.21 (2.62 (1.85 (2.70 (2.00) 3.32-1.S.91-3.32-1. was once a restricted-use insecticide with limited applications on certain agricultural crops.298-00-0 Ethyl Parathion CAS No. and eliminated rapidly from the body after absorption (Kramer et al.90-9. all registered uses were voluntarily cancelled (U.19 (.92) 5.00 (2. population from the National Health and Nutrition Examination Survey. 2007). Methyl parathion use is highly restricted. 2006). Survey Geometric mean (95% conf.37-2. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.48) 90th 2.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Morgan et al.10 (3.15-3.22-3.50 (1.90 (1.910) < LOD < LOD .60-36.40) 1.50) 3.02-6.69 (2.50 (1.770 (.70 (<LOD-3.S. Fourth National Report on Human Exposure to Environmental Chemicals 149 .30-16.30 (2.70 (3.20) 5.21-1.90-11. on cereal grains. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate..8 and 0.13-1. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.EPA.50-9.940 (<LOD-2.70-3. Many previous registered agricultural uses of methyl parathion have been cancelled (U.1. 2002.80 (1.01) 4.730 (<LOD-.00 (2.36-1. ethyl parathion.67) < LOD 1.S.0) 3.910) < LOD .50) 2..20 (2.89 (2.60-19.69) 4.46 (3.05) 4. and oral routes can occur in pesticide and agricultural workers (Muttray et al.0) 3. which may vary for some chemicals by year and by individual sample.50-14.57) 1.60-5.70) 2.45 (1.34 (3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. Estimated intakes from diet and drinking water have been below recommended limits.300-.50) 1.71 (3.0) 2. and to a lesser extent.45) 5.37-4.50 (2. peak domestic use was as high as 5-6 million pounds per year. Methyl Parathion.0) 3.60-24.58) 3.50 (2.860 (<LOD-1.40) 2.30-5. and of the chemical nitrobenzene.32-3.79) 4.61) < LOD 1.

17) . U. 2006.23) 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 .800-1.60-2. paralysis.78 (2.3) 2. Slotkin et al.04) 1.. 1991).950) < LOD .06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .870) < LOD . 2003. gov/pesticides/.97-10.720-1.91 (1. 1978.00) 2.41-2.e.690-1.39 (1. 1995). Parathion and methyl parathion have high acute toxicity in animal testing.500) < LOD < LOD .Organophosphorus Insecticides: Specific Metabolites Metabolites”).720 (<LOD-.08 (1.08-3.78) 2.73 (1..78-2.310-.97 (<LOD-4.07 (1.82) < LOD . or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.57) 6.S.84) 3.33-6. teratogenic.89 (2. paranitrophenol. does not inhibit acetylcholinesterase enzymes.98-7.72-2.78-2.680 (<LOD-1.23) 1. Lores et al. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.55) 2. 2004).87 (1.09) 2.S.43) 4.86 (2.88 (1.S.850-1.930 (. but lists ethyl parathion as a possible human carcinogen. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.540) < LOD .79 (1.atsdr. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.EPA considers methyl parathion unlikely to be carcinogenic to humans.20) .840 (.970 (.59 (1. 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.29 (2.61) 4.940 (<LOD-1.29) 1..96 (1. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.01-3.30) 3.7) 3.35-3.21) 1.15-10.440 (<LOD-.cdc.37-1.11) 1. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.30-1.94-4. environmental levels) and health effects is available from ATSDR at: http://www.4 (3.88) 1. and other metabolites. 2005. Methyl Parathion.2) 2.. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.76-14.14-3.71) 1.29) 2.01 (...83 (1.25 (2.1) 2. Additional information about external exposure (i.33-3.980 (.730-1. Jaga and Dharmani. At high animal doses of methyl parathion. Zurich et al. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.70) 3. 150 Fourth National Report on Human Exposure to Environmental Chemicals .11-4.17-4. and producing acute symptoms such as nausea.90 (1.48-4.80 (1.15) 3.20) 3.01 (2.05) 4.21-21.57-2.430 (. In addition to being a metabolite of methyl and ethyl parathion. WHO.830-1.91) 1. 2004). population from the National Health and Nutrition Examination Survey.9) 1.57-7.970 (.2) 2.html and from U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .80 (1.55 (<LOD-3.71 (1.77-7. Thus. 2006. vomiting. 1990.00 (1.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .07) 2.13) 4.31-3. The metabolite.640) < LOD < LOD 1..530) < LOD < LOD < LOD .93 (2.20 (3. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. Orsorio et al.400 (<LOD-.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Methyl parathion is not considered genotoxic.95) 1.epa. Karanth and Pope et al.82 (2.16-4.790-1.26) 17.60) 2.56-2.94-47.67-2.10 (1. EPA at: http://www. and seizures.04 (2.44-3.880 (. In large doses.96 (1.38-3.26 (1.35-3. accidental exposure.13-12.39) 1. 1995.60 (1.44-3.97 (2.370 (<LOD-.930 (. ethyl parathion. weakness.10) 90th 2.79) 1.33-3. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. gov/toxpro2.08) < LOD ..00 (1. cholinergic effects. and unintentional acute or chronic high-level occupational exposure (Hill et al.67 (3.25) 1. resulting in excess acetylcholine at nerve terminals.92 (2.790-. methyl parathion. Survey Geometric mean (95% conf.89 (2.31) < LOD .

Lewalter J.9:311-320. population (Olsson et al.33(5):270-276. Kramer RE. Head SL. 2005). Neurotoxicol Teratol 2003. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. McClure PC.5 mg (500 µg)/g creatinine for workers at the end of shift. Harley K. Methyl parathion: an organophosphate insecticide not quite forgotten. general population (CDC. Barr DB. 2005)..org/documents/jmpr/jmpmono/v95pr14. Hill RH Jr. Environ Health Perspect 2002. Baker SE. Curl CL. Costa LG. Rev Environ Health 2006. Chicago area methyl parathion response. Arch Environ Contam Toxicol 1977. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure..15(2):164-171.110 Suppl 6:1085-1091. 1999). Pesticide workers may have much higher levels following pesticide applications. et al. Kissel JC. DiPietro E. Bradway DE. Griffith W.56(7):449553. Shealy DB. 2002.htm. Moseman RF. oral or dermal administration. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Morgan DP. Dharmani C. Available at URL: http:// www. Bradman A. Baker S. 2002. ACGIH recommends a BEI of 0. Giordano G. 1995. Role of individual susceptibility in risk assessment of pesticides. Weltzien E. Pesticide residues in urine of adults living in the United States: reference range concentrations. J Expo Anal Environ Epidemiol 2005. Moomey CM. 2002). Barr DB. Fourth National Report on Human Exposure to Environmental Chemicals 151 . 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.S. a range of values several hundred times higher than levels found in the U. Third National Report on Human Exposure to Environmental Chemicals. References Barr DB. Levels of para-nitrophenol in the NHANES 1999-2000 and 2001-2002 subsamples were similar or slightly lower than those in a nonrandom subsample of NHANES III (19881994) participants (CDC.. Turner WE. Pathak S. Parathion-Methyl (addendum). Pharmacokinetics of methyl parathion: a comparison following single intravenous.14(4):213-216. Rubin et al. 2005. Guizzetti M.21(1):5767. Slach EF. 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. Jewell NP. 2004). Head SL. 4/7/09 Jaga K. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Karanth S. McCann et al. Hill RH Jr. Arch Environ Health 1978.215(3):182-190. In a study of workers who handle parathion. Bailey SL.. Eskenazi B.25(5):599-606. International Programme on Chemical Safety-INCHEM (IPCS). Pope C. et al. 2005. Clark JM.inchem. et al. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation.S. Occup Environ Med 1999.112(10):1116-1124. Barr DB. Cline RE.110 Suppl 6:1075-1078. Centers for Disease Control and Prevention (CDC). Ashley DL. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Baker RC. Kedan G. Runkle KD.71:99108. McCann KG. J Biomed Sci 2002. Alley CC. 1995). and many residents were symptomatic (Barr et al.. et al. Environ Health Perspect 2004. Leng G.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.6(2-3):159-173. Hryhorczuk DO. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Lin LI. Hill et al. Barr JR. Gregg M. Toxicology 2005. 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. Environ Health Perspect 2002. Wellman SE. et al. 2005. Rockhold RW. Lores EM. Hetzler HL. Needham LL. Environ Res 1995. Laboratory investigation of a poisoning epidemic in Sierra Leone. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. CDC.. Lu C. J Anal Toxicol 1990. and levels were similar or slightly lower that those in a small convenience sample of the U. Atlanta (GA).

Ohio. Hill RH Jr. Letzel S. The Quality of Our Nation’s Waters. 6/1/09 World Health Organization (WHO). Available at URL: http://pubs. WHO/SDE/WSH/03. Ames RG. Slotkin TA.pdf. Nguyen JV.S. revised February 15.S. Available at URL: http://www. 1/12/07 U. 0153.S. Schilter B. May 2003. Methyl parathion in drinking water.376(6):808-815. March 2006. Environmental Protection Agency (U.110 Suppl 6:1047-1051. Dunlop B.gov/oppsrrd1/REDs/factsheets/0155fct. Rubin C. Yacovac R. R.Organophosphorus Insecticides: Specific Metabolites Muttray A. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Investigation of a fatality among parathion applicators in California. Pesticides in the Nation’s Streams and Ground Water. Costa LG.D. September 2000. EPA-738-FOO-009. Toxicol Appl Pharmacol 2004. Toxicol Lett 2006. Monnet-Tschudi F. et al. 1/14/09 U. Facts.gov/circ/2005/1291/. Seidler FJ. 5/19/09 Zurich MG. Jung D. Mengle DC. 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. Environ Health Perspect 2002. Available at URL: http://www.pdf.usgs. Olsson AO.04/106. 1995-1996.who. Geological Survey (USGS). gov/oppsrrd1/REDs/methylparathion_ired. Rosenberg J. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Esteban E. Barr DB. Environmental Protection Agency (U.114(10):1542-1546. Case No. Environ Health Perspect 2006.20(4):533-546. Available at URL: http://www. Ryde IT. Levin ED.E. External and internal exposure of wine growers spraying methyl parathion. pdf.162(2-3):219-224. Sadowski MA. Backer G.S. U. 152 Fourth National Report on Human Exposure to Environmental Chemicals . 1992-2001. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County.S. Osorio AM. Tate CA. Honegger P. 2004. Ethyl parathion. Am J Ind Med 1991. Hill G.201(2):97-104.epa. EPA). Kieszak S. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Anal Bioanal Chem 2003.int/water_sanitation_health/dwq/chemicals/ methylparathion. 2007 [online]. EPA).epa.

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

94) .410 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.840 (. which may vary for some chemicals by year and by individual sample.210-.840) 669 687 929 Limit of detection (LOD.680 (<LOD-.850 (. 154 Fourth National Report on Human Exposure to Environmental Chemicals .580-1. < LOD means less than the limit of detection.740-1.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .07) . population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey.950) < LOD < LOD 1.31) .210-1.64) .780 (.15) < LOD .210 (<LOD-. 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 .250 (<LOD-.700-1.27) .500 (.670 (<LOD-1.300-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0.610 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .820) < LOD < LOD .00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.760 (<LOD-.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 .780 (<LOD-1.780 (<LOD-1.55) .700-. 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.430 (<LOD-.740 (.S.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .200-.2.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.21) < LOD .Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.17 (.470 (.780 (.

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

and greenhouses.S. but pyrethroids are highly toxic to fish and some aquatic invertebrates. There are about 30 different pyrethroid pesticides in use. Adverse effects from large doses are related to the action of pyrethroids on the nervous system.. After absorption from inhalation or ingestion. Woollen et al. They are ranked as having moderate acute oral toxicity. Permethrin is also used in skin lotions and shampoos as medical treatments for lice and scabies. Estimated intakes from diet and drinking water are below recommended limits. Pyrethroid pesticides are generally formulated as complex mixtures of different chemical isomers.. 1997. so usage is restricted near water (U. 1992). Compared with other classes of insecticides such as organochlorines. by either ester hydrolysis or hydroxylation. Unmetabolized pyrethroids have been measured in breast milk. such as piperonyl butoxide. Certain pyrethroid insecticides (such as permethrin. agricultural fields. warehouses. or carbamate pesticides. Outside the U. WHO.2-dimethylcyclopropane carboxylic acid (55701-03-6) cis-3-(2. 2003. Dermal exposure with the potential for inadvertent ingestion may occur when lotions or shampoos are applied to treat lice or scabies. Soderlund et al. The table shows the urinary pyrethroid metabolites measured in this Report. which are natural chemicals found in chrysanthemum flowers. and are rarely detected in ground waters (USGS. bind to soils.. followed by conjugation.S.S. In agriculture... where these chemicals prolong sodium channel opening when a nerve cell is depolarized (Shafer et al.2-dimethylcyclopropane carboxylic acid (55701-05-8 ) trans-3-(2. About two million pounds of permethrin and one million pounds of cypermethrin have been applied annually (U. They are also applied on livestock to control insects. solvent oils. Generally. and then eliminated over several days in urine and bile (Kuhn et al. cypermethrin. 2005). Pyrethroid pesticides have low volatility. and sumithrin) are also registered for use in mosquito-control programs in the United States. pyrethroids are rapidly metabolized. they are not persistent in the environment due to their rapid degradation within days to several months. EPA. and deltamethrin have been used frequently on cotton. Pyrethroid insecticides are the most common active ingredient in commercially available insect sprays and are also used as structural termiticides. Leng et al. Possible other additional actions on neuroreceptors Pyrethroid Insecticides Metabolites in this Report Pyrethroid (CAS number) Cyfluthrin (68359-37-5) Cypermethrin (52315-07-8) Cyfluthrin (68359-37-5) and Permethrin (52645-53-1) Deltamethrin (52918-63-5) Cyhalothrin (68359-37-5) Cypermethrin (52315-07-8) Deltamethrin (52918-63-5) Fenpropathrin (39515-41-8) Permethrin (52645-53-1) Tralomethrin (66841-25-6) Urinary metabolite (CAS number) 4-Fluoro-3-phenoxybenzoic acid (77279-89-1) cis-3-(2. 1992). deltamethrin has been used for indoor protection against mosquitoes that carry malaria. but may be poorly transferred across the placenta (ATSDR. in some situations replacing the use of DDT. 2006a. Pyrethroids are not well absorbed through the skin (ATSDR.2-Dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid 3-Phenoxybenzoic acid (3739-38-6) 156 Fourth National Report on Human Exposure to Environmental Chemicals .2-Dichlorovinyl)-2.Pyrethroid Pesticides Pyrethroid Pesticides General Information Pyrethroid pesticides are synthetic analogues of pyrethrins. Woollen et al. pyrethroid pesticides have less acute toxicity in animals and people. 2002)..2-Dichlorovinyl)-2. organophosphorus. 2002. This class of pesticides has low toxicity in birds and mammals. 2005. Pyrethroid pesticides are used to control a wide range of insects in public and commercial buildings. resmethrin. Pesticide applicators can be exposed to pyrethroid pesticides via dermal and inhalation routes from powders and liquid formulations. The general population may be exposed to pyrethroid insecticides primarily from the ingestion of food or from residential use. cyfluthrin. and synergists. 2002).. animal facilities. 2007). 1999. Human health effects from pyrethroid pesticides at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2006b).EPA. 2003. Soderlund et al..

References Agency for Toxic Substances and Disease Registry (ATSDR). Regul Toxicol Pharmacol 2002. Moniz et al. Bull Environ Contam Toxicol 1999. epa. In developing rodents. September 2003. Int J Hyg Environ Health 2002.8(1):18-21. Hu et al. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Berger-Preiss E. 2005). Yang J. 1999. Shaw IC. Richardson JR.. Pyrethroid pesticide-induced alterations in dopamine transporter function. Elwan MA. Generally. Wang SL.211(3):188-197. Neurosci Lett 2001. Idel H. bioallethrin and deltamethrin. et al. Song L.. Elwan et al. Ray et al. Varoli FM. Ose K. Kim et al. Zhao RC. J Environ Monit 2006.html. Leng G. 1991. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. dopaminergic.. Florio JC. EPA at: http://www. Bernardi MM.107(3):173-177. Garey J. Lee SJ..S.gov/toxprofiles/ tp155. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Sugiri D. Hu JY. Garey J. Kuhn KH. 2005). Estrogenicity of pyrethroid insecticide metabolites. Indoor pyrethroid exposure in homes with woollen textile floor coverings. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. 2005). hypersensitivity. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats.1/15/09 Aziz MH.. Spinosa HS. Miller GW. Guillot TS.gov/pesticides/ and from ATSDR at: http://www. Moniz AC. Additional information about pesticides is available from U. Salzgeber SA. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Seth PK. Shin JH. Cruz-Casallas PE. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Ranft U. tremor. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Go et al. Pauluhn J.27(12):1273-1283.. Garey and Wolff.cdc. neurochemical changes in cholinergic.atsdr. McCarthy AR. Bernardi MM. Yamada T. Environ Health Perspect 1999. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. and striatal dopamine levels in male and female rats.gov/toxpro2. salivation.8(1):197-202. Thomson BM. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. McCarthy et al. 2003. Chen JH. Abell AD.251(3):855-859. 2006. 2001. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Kim HS. and permethrin) in the Hershberger and uterotrophic assays.. Lemonica IP.. Sunami O. Available from URL: http://www. Toxicol Appl Pharmacol 1991. motor activity. 2004. Pogo BG. 1998. 2003. 2001. Biochem Biophys Res Commun 1998. 2006). Shukla Y.. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Leng G. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Lazarini CA. Lazarini et al. 2003. Kamita Y. cdc. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. and seizures (ATSDR. Neurotoxic effects of two different pyrethroids. Agrawal AK. 2002.27(4):609-614.50(2):245-255. Fredriksson A.108(1):78-85. et al. Soderlund et al. Lewalter J. 2002). Leng A. In California.atsdr. Fourth National Report on Human Exposure to Environmental Chemicals 157 .. Idel H. Wieseler B. 2000. choreoathetosis. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Wolff MS. et al.. Kim TS.. on immature and adult mice: changes in behavioral and muscarinic receptor variables. 2002). WHO. Kunimatsu T.35(2 Pt 1):227-237. Leng G. 2003.300(3):161-165. Xenobiotica 1997.23(6):665-673. Eriksson P. Okuno Y.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. 2005). Shafer. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Levsen K. Wolff MS. Eriksson and Fredriksson. Kunimatsu et al. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. J Reprod Dev 2004. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. 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.. Kim IY. Neurotoxicol Teratol 2005. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Adhami VM.html.205(6):459-472. Kang IH. Effects of prenatal exposure to deltamethrin on forced swimming behavior.62:101-108. Toxicological profile for pyrethrins and pyrethroids. Neurotoxicol Teratol 2001. fenvalerate. Go V. Caudle WM. Toxicol Appl Pharmacol 2006. et al. Kuhn K.

June 2006a. Sheets LP. Pesticides in the Nation’s Streams and Ground Water. Available at URL: http://www.S.pdf. Soderlund DM. Clark JM. June 2006b.10. Pesticide and Evaluation Scheme. et al.113(2):123-136. Crofton KM. Rev Environ Contam Toxicol 2006. Available at URL: http://www. 19962002. U. April 2002. Piccirillo VJ. synergies.171:3-59.38:95-101. Environmental Protection Agency (U. O’Malley M. Environmental Protection Agency (U. EPA). 5/26/09 U.usgs.htm. Pyrethroid illnesses in California.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. 5/26/09 U. Toxicology 2002. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). Xenobiotica 1992.22(8):983-991.gov/ circ/2005/1291/.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes.S. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. World Health Organization (WHO).Pyrethroid Pesticides Ray DE. and therapy. Reregistration Eligibility Decision for Cypermethrin. 1992–2001. 2007. Revised February 25.epa.S.186:57-72. 2005. EPA). EPA). Mullin LS. Marsh JR. 5/26/09 Woollen BH. Spencer J. Laird WJ.htm. Forshaw PJ.S. J Toxicol Clin Toxicol 2000. Environ Health Perspect 2005.S. Lesser JE. Available at URL: http://whqlibdoc.who.gov/oppsrrd1/REDs/cypermethrin_red. March 2006.epa.epa. Available at URL: http://pubs. Meyer DA. pdf. Geological Survey (USGS). sumithrin synthetic pyrethroids for mosquito control.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. resmethrin. 5/26/09 U.S. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . Pyrethroid insecticides: poisoning syndromes. Shafer TJ. Environmental Protection Agency (U. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Permethrin. Sargent D. Safety of pyrethroids for public health use.S. Available at URL: http://www.

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

Survey Geometric mean (95% conf.2 and 0.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2. * 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 < 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. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 160 Fourth National Report on Human Exposure to Environmental Chemicals . < 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.S.

S. population from the National Health and Nutrition Examination Survey. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. 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.

209(3):293-299. Sugiri D. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Barr DB. 162 Fourth National Report on Human Exposure to Environmental Chemicals . 2005. Rev Environ Contam Toxicol 2006. O’Malley M. J Expo Anal Environ Epidemiol 2003. Hoppe HW. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Schulz C. Third National Report on Human Exposure to Environmental Chemicals. Heudorf U. Centers for Disease Control and Prevention (CDC). Int J Hyg Environ Health 2006.206(2):85-92. Pyrethroid illnesses in California. Krieger RI. Berger-Preiss E.209(3):221-233. Environ Health Perspect 2001. Ranft U. Olsson AO. Int Arch Occup Environ Health 2004.46(3):281-288. Arch Environ Contam Toxicol 2004. Angerer J. Seiwert M. Williams RL. et al. Int J Hyg Environ Health 2003. Angerer J.186:57-72. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Hadnagy W. Leng G.77(1):67-72. Angerer J. Human exposure to indoor residential cyfluthrin residues during a structured activity program. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Kolossa-Gehring M. Heudorf U. Idel H. Bernard CE.13(2):112-119. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Drexler H.Pyrethroid Pesticides References Baker SE. 19962002. Angerer J. Ball M. Spencer J. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Heudorf U. Butte W.109(3):213-217. Atlanta (GA). Int J Hyg Environ Health 2006. Becker K.

and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.850 (.470 (.460-.610) .160 (. and trans-cyfluthrin.53) .200 (.580-1.110-.202 (.420-.140 (.180) .120-.07 (. Generally.340-.500 (.490-.430-.530 (.2dichlorovinyl)-2.690) .300 (.180 (.410) .510 (.2-dichlorovinyl)-2.120-.600 (.250 (.240) .630) .220-.200) .160 (. but it can also reflect exposure to cis-3-(2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.13 (.300-.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.490-1.15) . In the body.12 (.340) .780) .270 (.710-1.2-Dichlorovinyl)-2.S.240) .740-2. Fourth National Report on Human Exposure to Environmental Chemicals 163 . Survey Geometric mean (95% conf.740) 1.380) .470-1.520) .380-. 1985.44 (.600) .140 (<LOD-. Kuhn et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. cis-cypermethrin.200-.08) .880 (.570 (.740-1.580) 1..68) .2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.11) . Kuhn et al.820 (.380-.210) .600-1.1. 52315-07-8 CAS No.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George. but can also reflect exposure to trans-3(2. 1999).260 (. the presence of trans-3-(2.680-3.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .120-.270 (.670-2.35) . trans-cypermethrin.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . The chemical trans-3(2.510 (.200-.630-. trans-permethrin. which may vary for some chemicals by year and by individual sample.770-1.630) .250-. Biomonitoring Information Urinary levels of cis.24) 1.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.54) .43) .730 (.670-1.68 (.280 (. ciscypermethrin and cis-cyfluthrin.410) .870) 1.and trans-isomers.68) .890 (.1 and 0.710) . The presence of cis-3-(2.28) 671 680 518 701 591 957 Limit of detection (LOD. cis-3-(2.220-.550) .280-.50) . more of the trans-metabolite than Urinary cis-3-(2.210-.68359-37-5 Cypermethrin Permethrin CAS No.262) * * * < LOD < LOD .460 (. population from the National Health and Nutrition Examination Survey.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.230) .110 (<LOD-.890 (.150 (.490-.47 (.210) 90th .790-1.730 (.110-.510 (.2-dichlorovinyl)-2. 1999).680 (..670 (.270-.155-.640 (. 1985.10) 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 .77 (.500 (.910-5. Cyfluthrin. and ciscyfluthrin.2-dichlorovinyl)-2.770) .570-. < LOD means less than the limit of detection.200) < LOD < LOD < LOD .790-1.920) 1.610) .350) .2-dichlorovinyl)- CAS No.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.490-1. cis-permethrin.700) .340) .310) .110-.300 (.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.380 (. Similarly.790 (.650-1.220) .2dichlorovinyl)-2. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.or trans-3-(2.460-1.32) .200-.220-.270 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.300-.950-2.440 (.330) .670-1.80) .160 (<LOD-.380-.740 (.630 (.790) .370 (.400-.2-dichlorovinyl)2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. transcypermethrin and trans-cyfluthrin.21) .730 (.200) .960 (.220-.35) 1.330 (.900 (.370-.120-.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.170 (.

270) .33 (..160 (<LOD-.260 (.290 (.260-.24) .120 (.12-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.410) .Pyrethroid Pesticides 2. Schettgen et al.2-dimethylcyclopropane carboxylic acid did not increase.530 (.550-1.200 (.S.220) .400 (.320) .570) .640) 1.680-1.750-1.750 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.170) < LOD < LOD < LOD .380-.290) .138 (.440-.2dichlorovinyl)-2.320-.290-.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.and trans-3-(2.840 (.550) .540) . 2003).350 (.. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.550) .2-dichlorovinyl)-2..430-.. Studies in Germany of 396 children and adolescents (Becker et al. 2006.880) . 2004.420 (..250) .240 (<LOD-.170 (.150-.59) .890) .300 (.130-.340) .260 (. In a study of urban residents in Germany (Berger-Preiss et al.250-.680-1.300) .440-.182) * * * < LOD < LOD .210-. Lu et al. 2002). 2003).400-1.11) 1. population from the National Health and Nutrition Examination Survey.270) .360-1.840 (.280-..830) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC. urinary trans-3-(2. 2006) and 1177 urban adults and children (Heudorf et al.540 (.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al. the median and 95th percentile of urinary levels of cis-3-(2.2-dichlorovinyl)-2.190 (.59) .780) 1. 2001.230-. Cyfluthrin.510-1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.200-.S. 2005).080-.230-.220 (.300 (.440 (.700) . 2005).37) .200) .11 (. 2001) showed urinary levels of cis.590) .390-.2-dichlorovinyl)-2. median urinary levels of trans-3-(2.59 (1.710 (. 2005).370-.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .450-.230 (.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.49) .29 (..550-1.380 (.500 (.21) .250) .810 (.640-1.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.33) .440 (.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 .900 (.250-.230-. 2005). 2005) In a small group of indoor pest-control operators.600 (.280 (.2-dichlorovinyl)-2.2-Dichlorovinyl)-2.250-. In the same residents.560) . In these volunteers. 164 Fourth National Report on Human Exposure to Environmental Chemicals .180-.390-.450 (.370-.12 (.300-. post- Urinary cis-3-(2.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.300) ..640-.540 (.31) .350) ..11) .640-1.250 (<LOD-.220 (. 2006).370-.340) .80) ..580) .890 (.2dichlorovinyl)-2.260 (.580-1.640 (.67 (.530 (.690-1.200-.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .700-2. 2004).450-1.150-.190) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.710-3.470-1.190) . urinary levels of cis-3-(2.800 (.250) 90th . Survey Geometric mean (95% conf.680 (.550 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.780 (.11) .180 (.270 (.and trans-3(2. 2002)..67) .920 (. 2006.380) .260) .700) .2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.170 (.03) 1.340-. 2006).150-.390 (.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.270-.430 (. In a study of volunteers. representative NHANES 2001-2002 subsample (CDC.290) .590 (.430-1.104-. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.560) 1. Other studies have provided evidence that urinary levels of cis.140-.

which may vary for some chemicals by year and by individual sample.800-1.42) 1.56 (1.910-1.66) 691 680 518 690 595 954 Limit of detection (LOD.08-4.69) 1. < LOD means less than the limit of detection. however.69 (1.460-.940 (.17 (. Biomonitoring studies on urinary levels of cisor trans-3-(2.22 (1.55-3.23 (.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .11-1.10) 2.7) 2.19 (3. Finding a measurable amount of cis.660) 1.4 and 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.03-1.840-1.2-dichlorovinyl)-2.620) < LOD 2.760) .670) .610) 1.14-2.13) .28 (1.42 (2.40 (1.560 (.16) 1.84 (1.63) 1.410-.39 (1.750) .54) 4.410 (<LOD-.56 (1.14-6.25-3.39-5.64-4.94 (1.55-5.500-. 2005). The maximum post-application urinary levels.27 (1.60) 1.20 (.01) 4.97-11. population from the National Health and Nutrition Examination Survey.49-3.670) .20 (.Pyrethroid Pesticides application median urinary levels of summed cis. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.410-.90) 1. 2005).and trans-3-(2.77 (1.89 (2.95) 2.68) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.63) 1.5) 2.550 (.520) .87 (1.41-14.26 (.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.850-1.68-3.or trans-3-(2.12-6.09 (.530) .58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .19 (2.710 (. Urinary trans-3-(2.490 (<LOD-.500 (.60) .830-1.55-4.780 (.59 (1.490-1.56) 2.700-1.54 (1.910-1.20 (.56) 2.820) .76-4. Fourth National Report on Human Exposure to Environmental Chemicals 165 .14) 1. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.62 (1.400-.480-.48) 4.68) 1.470 (.60-4.560 (.580 (.85) 4.2-dichlorovinyl)-2. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.81) 2.68-2.76-3.41 (1.920-1.470 (<LOD-.440 (<LOD-. Survey Geometric mean (95% conf.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.970 (.680-1.25 (1.08) 1.77) 2.07-3.37 (1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .49-5.17 (.520-.460-.400 (<LOD-.19) 1.560 (.91 (1.08-6. trans-Cypermethrin.28 (2.95) 3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.07 (1.50 (1.860) .810-1.68) 2.03-1.11-2.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.420 (<LOD-.S.410 (<LOD-.700) .43) 2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2dichlorovinyl)-2.01 (1.23) 2.17-1.70) 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 .66) .77) 1.2-Dichlorovinyl)-2.35) 1.500) .49-3.570) 90th 1.730) .4.

86 (2.87) 1.570 (<LOD-.12-1.60 (1.530 (.880-1.780) .15-3.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.22-2.60) 2.470-.44) 2.16 (1.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.39 (1.540) .740) .19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .08 (.31) 1.00) 1.15-3.20 (1.42 (.36 (1.880 (.31 (.780 (<LOD-.67 (2.35 (1.56-2.89) 2.440-.820-2.56 (1.87-3.580 (.12 (.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 .91) 1.700 (.15 (1.530 (<LOD-.33-1.470 (.07) 2.74) .07-2.27-2.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.45-2.27-2. trans-Cypermethrin.61) 1.570 (.11) .48 (1.15-3.87-8.33-2.08 (.31 (2.800-1.570-.970 (.480-.15) 2.2-Dichlorovinyl)-2.30-3.900 (<LOD-1.930-1.760 (.55 (2.750) .55 (2.610-.700 (.07) 2.55 (2.20-2.S.56-5.98 (1.39) 1.65 (2.57) 3.68) 3.780) 90th 1.00) 5.28) 2.00) 1.47 (1.81 (2.800-1.22-1.850) .47-2.33 (1.48-2.74) 2.91 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.64 (1. Survey Geometric mean (95% conf.720-1.850) 1.07-3.47-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.36) 2.880 (<LOD-1.640) .45 (1.660) . and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.37 (1.75 (1.02-1.13) 1.91-11.70 (.730) .57 (1.15) 3.580) .19 (1. population from the National Health and Nutrition Examination Survey.34-4.00-5.13) .520 (<LOD-.26 (1.720 (<LOD-.87) 1.60) 2.560 (.720-1.34-3.670) .11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .770) < LOD 2.850-3.19) .80) 1.00 (1.41) 1.3) 2. 166 Fourth National Report on Human Exposure to Environmental Chemicals .07-1.30-6.65) 1.Pyrethroid Pesticides Urinary trans-3-(2.22) 1.35) 1.410-.700-.87 (1.40-2.500-.29) 1.42) 1.

Centers for Disease Control and Prevention (CDC). Hardt J. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Sugiri D. Lu C. Kuhn K. Heudorf U. Leng G.209(3):221-233. Int J Hyg Environ Health 2006. Angerer J. Barr DB. Angerer J. Idel H. Berger-Preiss E. Drexler H.109(3):213-217. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Environ Health Perspect 2006.206(2):85-92. J AOAC 1985.77(1):67-72. Schettgen T. Bartell S. Int Arch Occup Environ Health 2004. Angerer J. Levsen K. Butte W.134(1-3):141-145. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Hadnagy W. Ranft U. Bull Environ Contam Toxicol 1999. Angerer J.68(6):1160-1163. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Seiwert M. George DA. Int J Hyg Environ Health 2002.205(6):459-472.Pyrethroid Pesticides References Becker K. Heudorf U. et al. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002.209(3):293-299. Angerer J. Idel H. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Schulz C.76(7):492-498. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Fourth National Report on Human Exposure to Environmental Chemicals 167 . 2005. Angerer J. Third National Report on Human Exposure to Environmental Chemicals. Leng G. Atlanta (GA). Permethrin and its two metabolite residues in seven agricultural crops. Sugiri D. Berger-Preiss E. Heudorf U. Pearson M.114(9):14191423. Kolossa-Gehring M. Ball M. Environ Health Perspect 2001. Leng G.62:101-108. Bravo R. Biological monitoring of workers after the application of insecticidal pyrethroids. Ranft U. Drexler H. Int Arch Occup Environ Health 2003. Wieseler B. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Idel H. Heudorf U. Hoppe HW. Int J Hyg Environ Health 2006. Int J Hyg Environ Health 2003.

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 at the 95th percentile ranged slightly higher (0.2-dibromovinyl)-2. 2005).2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.3-0. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2004).. Outside the U. (2004) reported a geometric mean concentration of cis-3(2.2-dibromovinyl)-2.5 μg/L) than the detection limit (0. 1990). Thus. Following residential spraying with deltamethrin for malaria protection in Mexico.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. Studies in Germany of 396 children and adolescents (Becker et al. 2005)..2-dibromovinyl)-2..39 µg/L. 168 Fourth National Report on Human Exposure to Environmental Chemicals .. in some situations replacing the use of DDT. Deltamethrin can degrade to cis-3(2. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population. 2006) and 1177 urban adults and children (Heudorf et al.. mean peak urinary levels of cis-3-(2.2-dibromovinyl)-2.Pyrethroid Pesticides Deltamethrin CAS No.1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dibromovinyl)2. deltamethrin has been used against mosquitoes that carry malaria. 2001.2-dibromovinyl)-2. 2005). urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. in detection of cis-3-(2. In the NHANES 2001-2002 subsample. Urinary levels for adults and children in these studies were similar (Heudorf et al.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.2-dibromovinyl)-2. Biomonitoring Information Urinary levels of cis-3-(2.2-dibromovinyl)-2..S.2dimethylcyclopropane carboxylic acid formed in the environment. 2001) showed that urinary levels of cis-3-(2. Baker et al. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2-dibromovinyl)-2. 52918-63-5 General Information Cis-3-(2.2-dimethylcyclopropane carboxylic acid of 0. Finding a measurable amount of cis-3-(2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.

Pyrethroid Pesticides Urinary cis-3-(2.1 and 0. < 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.1. Fourth National Report on Human Exposure to Environmental Chemicals 169 . 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.S. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.2-Dibromovinyl)-2.

Pyrethroid Pesticides Urinary cis-3-(2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.S. 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. 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. population from the National Health and Nutrition Examination Survey.2-Dibromovinyl)-2.

Third National Report on Human Exposure to Environmental Chemicals.113(6):782-786. Lopez-Guzman OD. International Programme On Chemical Safety (IPCS). Centers for Disease Control and Prevention (CDC).209(3):221-233. Heudorf U.inchem. and genotoxicity in exposed children. Deltamethrin. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Batres LE. Int J Hyg Environ Health 2006. Environ Health Perspect 2005. Seiwert M. Angerer J. 5/26/09 Ortiz-Perez MD. Angerer J. 2005. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Hoppe HW.htm. et al. Grimaldo M. Carranza C. et al. Kolossa-Gehring M. Int J Hyg Environ Health 2006. toxicokinetics. Heudorf U. Int Arch Occup Environ Health 2004. Angerer J. [online] 1990. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Ball M. Environmental Health Criteria 97.109(3):213-217. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.77(1):67-72. Available at URL: http://www. Torres-Dosal A.org/documents/ehc/ehc/ ehc97.Pyrethroid Pesticides References Becker K. Butte W. Drexler H. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Environ Health Perspect 2001. Heudorf U. Atlanta (GA). Schulz C.209(3):293-299. Angerer J.

Saieva et al. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. 2005. 2002.. 2003). A study of 396 German children (Becker et al. 2004). Thus... 2005). median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. 2003. 2006. In one study of 145 urban residents in 80 private homes in Germany. 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. In a small group of indoor pest-control operators.. CDC.Pyrethroid Pesticides Cyhalothrin CAS No.. CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. CDC. Becker et al. representative NHANES 2001-2002 subsample (CDC. 2005). 39515-41-8 CAS No. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides.S.52315-07-8 CAS No. 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 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Hardt and Angerer. the postapplication median urinary levels of 3-phenoxybenzoic acid were 24-fold higher than those for adults in the NHANES 2001-2002 subsample (CDC. 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 . 52645-53-1 Tralomethrin CAS No. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. 2005). (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. 68359-37-5 Cypermethrin Deltamethrin CAS No. Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al.. 2003. In the New York City study. Baker et al.. 52918-63-5 use and house dust levels (Lu et al. 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. 2005). 2005). 2005. Fenpropathrin Permethrin CAS No. 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). 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). 2006). The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. Following residential spraying with deltamethrin for malaria protection in Mexico.

328 (.240 (.86 (1.200-.39) 2.69) 3.62) 5.417 (.314) .1 and 0.620-1.250-.51-3.190-.680 (.820) .260 (.550-.630) .160-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.300 (.38 (2.740 (.710 (.13) .590-.290 (.01 (1.49 (1.246-.390) .34-6.590 (.297 (.960 (.190-.850) .226-.750-1.780) 4.276-.200-.210-. population from the National Health and Nutrition Examination Survey.850) .230-. Deltamethrin.75 (1.64) 697 680 524 701 603 957 Limit of detection (LOD.288-.710 (.600 (.72 (1.48-2.810) 1.610) .320) .65-2.54) 1.800 (.265-.81 (1.830) 90th 1.700-1. interval) .364) .320) .650 (.510-.38 (2.273 (.570-.49-2. Fourth National Report on Human Exposure to Environmental Chemicals 173 .1) 3.428-.1) 3.940) 1.384) .470-.93 (1.260 (.35 (2.90) 1.76 (1.69 (1.570-1.355) .277-.640 (.33 (1.238-.430-.42-2.730 (.320) .353 (.50 (2.53-3.1.21 (2.311 (.434) .233-.300 (.73) 1.298 (.227-.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .387) .267 (.760 (.S.92-3.05) 1.1) 3.340) .36) 1.41-2.16-1.586) .320 (.330) .601) .26) 2.180-.230-.25-7.43) 3.510-.560-1.670 (.260 (.230 (.250 (.25-4.27-2.16) 1.41 (1.78) 6.02-6.160-.336 (.990) .750) .240 (.490) .560-.28) 1.427) .440) .230-.30 (1.362) .266-.33 (2.406) .210-.520 (.270 (.190-.04) .41) 3.32 (1.34) 8.507 (.78) 1.230 (.300 (.325 (.44) 5.490-.430-.247-.27-2.41-3.78) 1.190-.321 (.12) .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 .370) .320) .49 (1. Survey Geometric mean (95% conf.450 (.35) 2.18 (2.330) .740 (.840-1.530-.83-11.56-5.360) .45-5.25 (2.315 (.65 (1.33) .18 (1.35) 2.295) .314 (.454 (.12) 4.26-2.373) .13 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.34 (2.560-.89-71.374) 99-00 01-02 99-00 01-02 99-00 01-02 .750) .280 (.79) 3.29-1.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.62-8.830-2.292-.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .27-11.820) .52-4.60) .530-.340) 1.25-1.352-.35 (1.340) 75th .05) .71 (1.288 (.200-.53) 1.45 (2.595) .03 (3.46) 2.8) 3.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.300) .63 (3.250 (.49-2.25 (2.62-6.270) .46) .30 (.32 (2.220-.55 (1.369) .32-21.870 (.12 (.23 (2.420) .78 (1.26) 2.04-5.253-.700 (.271-.800) 1.51-6.292 (.63-3.260-.48-2.35) 1.250 (.30) 3.14-6.52-5.350-.

534) .590) .330) .11 (.84 (1.278) .400-.27) 1.450 (.280) .730-1.357) .480-.67 (1.570) .36-6.94 (1.37) 1.510 (.440-.720) 90th 1.350) .316 (.590-1.420-.67 (1.64-5.740) .35 (1.73-4.86 (1.610 (.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.04 (3.323 (.200-.19 (2.530-.760) .350 (.150-.362 (.43) 1.640 (.49-2.860-1.09-2.311 (.80) 4.190-.63) 1.280 (.290) .10 (2.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .226-.16-4.41) 1.49) 3.378 (.91-4.240-.13-1.05-3.96 (1.490-.270 (.490 (.240-.275 (.240 (.44) 2.238-.299-.270-.72 (1.00) 5.330) 75th .590) .225-.550 (.240 (.630) .365) 99-00 01-02 99-00 01-02 99-00 01-02 .00) 1.07-5.460-.15-2.81 (1.240-.22 (1.590) .380 (.240 (.410-.09 (.52) 2.387) .48 (1.06-3.300-.234 (.40 (1.290-.700-1.11 (.190-.83 (1.35) .720 (.19) 2.274 (.37 (1.250 (.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .400-.230) .91 (2.25) 2.370-.49) 1.35-3.43 (1.250) .73) 1.330) .51-7.580) .580 (.440-.320) .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 .264 (.730) .840-1.309 (.860-1.440-.190 (.43 (2. Survey Geometric mean (95% conf.21 (1.240-.410) .560 (.272) .210 (.261-.74) 3.230-.280 (.25-5.730) .60-4.200-.35) 1.55 (1.330 (.329) .540 (.310) .41-4.490 (.62) 1.510 (.930) .335-.860 (.640 (.67) 1.32 (2.670) .446) .224-.437) .330) 1.930) 1.17 (.91) 9.54 (1. population from the National Health and Nutrition Examination Survey.21-4.55) 3.380-.670) 3.329) .03 (.372) .60) 1.274-.02 (2.230-.160-.53 (1.43-64.00) 1.280-.261 (.300-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.321-.550 (.271-.750-1.328) .44 (1.272 (.13-1.227 (.960-1.240 (. Deltamethrin.95) 1.460-.229-.270) .0) 3.90) 3.290) .173-. interval) .49 (1.210-.253) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.370 (.36 (1.309) .75-8.216-.61-2.423 (.401) .83) 1.677) .25-2.52 (1.220 (.810) 1.200-.91) .63-3.62) .17-1.200-.220-.280 (.210 (.312 (.250 (.40) 2.480 (.88-5.510 (.246 (.178-.270) .400) .S.530-.550 (.280) .500) .13 (.202-.390-.270 (.09) 3.04 (.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .09-2.07) 2.39) 1.650) .02-1.03-1.19-6.

Int J Hyg Environ Health 2003. Sugiri D. Olsson AO. 2005. Bartell S. Ranft U. Hardt J.114(9):14191423. Sugiri D.205(6):459-472. Leng G. urban cohort. Lu C. Levsen K. Environ Health Perspect 2003. et al. Fourth National Report on Human Exposure to Environmental Chemicals 175 . GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.76(7):492-498.Pyrethroid Pesticides References Baker SE. Lapinski R. Bravo R. Angerer J. et al. Berger-Preiss E. Liu Z. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Angerer J. Leng G. Grimaldo M. Centers for Disease Control and Prevention (CDC).206(2):85-92. Ranft U. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Batres LE. Carranza C. Lopez-Guzman OD. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides.113(6):782-786. Exposure to indoor pesticides during pregnancy in a multiethnic.46(3):281-288.111(1):79-84. Arch Environ Contam Toxicol 2004. Berkowitz GS. and genotoxicity in exposed children.209(3):221-233. toxicokinetics. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Third National Report on Human Exposure to Environmental Chemicals. et al. Seiwert M. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Ball M. Biological monitoring of workers after the application of insecticidal pyrethroids. Ortiz-Perez MD. Barr DB. Kolossa-Gehring M. Hoppe HW. Int J Hyg Environ Health 2006. Torres-Dosal A. Obel J. Pearson M. Godbold J. Int J Hyg Environ Health 2002. Idel H. Atlanta (GA). Environ Health Perspect 2006. Environ Health Perspect 2005. Becker K. Int Arch Occup Environ Health 2003. Berger-Preiss E. Idel H. Barr DB. Hadnagy W. Deych E.

087-.570) . Stibine is a metal hydride form of antimony used in the semiconductor industry.180 (.270) .260) .120 (.100-. solder.140 (.390) .128 (. from air and drinking water.180-.142 (.220) 95th .160 (.130-.130) .130 (.220-.158 (. +3.156-.170-.180 (. ammunition.210-. 176 Fourth National Report on Human Exposure to Environmental Chemicals . People are exposed to antimony primarily through food and.210) . interval) . to a lesser extent.154) .280) .120) .460) . and 03-04 are 0.160) .350 (.410) .178) . and glass.230-.200 (.110-.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 .330 (.197) . water.320-.120) .360 (.120-.350) .210 (.240 (.115) .200-.250 (.200 (.120) .210) .320 (.210) . It is also used in paints. respectively. see Data Analysis section) for Survey years 99-00.300-.280 (.110 (.099 (. fireworks.340) .440) .350-.140) .350 (.200-.170) .070-.080) .122 (. 0.130 (.130-.140) .400 (.190 (.200) .220-.230 (.160-.460 (.140) .190-.220-.250 (.150-.190 (.240) .400) .150 (.290-.120 (.140-.320) Total .134 (.340 (.120-.220 (. which may vary for some chemicals by year and by individual sample.140) . It is used in metal alloys.170-.350) .119) .250-. coal-fired plants.169 (.200 (.207) .220 (.190 (.240-.130) < LOD .350 (.160) .120-.310 (.Metals Antimony CAS No.390 (.120 (.350 (.04.110-.270-.470) .154-.310) .200) .190-.230) .130 (.164-.500) .120-.160) .460 (.093 (.280) .260) .175 (.370-.120 (. < LOD means less than the limit of detection.140 (. and +5.210 (.080-.280-. enamels.176 (.110-.150 (.310 (.330) .400) .090 (.360) .120-.136) * .440) .160-.230 (.330) .280-.170-.120 (. storage batteries.230) .390) . 01-02. sheet and pipe metal.160) .200) .160 (.290 (.120-.04.300 (.160 (.117-.150) .190-.114) .250-.350-.170 (.112-.136-.330 (.250-.200 (.190) .200) .140 (.230-.300 (.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 .280) .260) .310) .220-.144) .160) .260 (.240 (.126-.150-.137) .360-. Dermal contact with soil.150) .330-. 7440-36-0 General Information Antimony is found in ores or other minerals.260 (.230 (.240 (.320-.180 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Antimony enters the environment from natural sources and from its use in industry.150-.160-.320 (.150) .200 (.310 (.090-.390-.07.330) .100 (.350) .157) .105 (.350) .080 (<LOD-.530) .141-.150) 90th .510) .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 .070 (<LOD-.280-.108-.130-.320) . distribution.145) Selected percentiles ( 95% confidence interval) 50th .300-. metal bearings.170-.180-.430 (.190-.130-.120-.109-.250 (. ceramics.130-.180 (.230-.710) .400 (.270 (.133) * .180) .184) .130 (.200-.090) 75th .310-.119-.170 (.070 (<LOD-.200-.190-.390-.280 (.220-. and as a fire-retardant in textiles and plastics. The absorption.250) .100) .137) .410-.300) .560) .320-.190 (.180-.130 (.140) .460 (.230-.440 (. castings.S. and refuse incinerators that process or release antimony.143 (.095 (.420) .600) .330) .280-.180 (.130 (.100-. population from the National Health and Nutrition Examination Survey. or other substances containing antimony is another means of exposure.220-.210) .370) .110) .430 (. and 0.190) . Antimony can exist in one of four valences in its various chemical and physical forms: -3.130) .132 (.400-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.130-. and excretion of antimony vary depending on its oxidation state.095-.080) .430 (.131-.098-.140) .180 (.220) .134-.230-. Workplace exposures can occur at smelters.130-.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.125 (.190) .120-.130 (.161) .300-.290-.360) .110-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.154) .270) .160) .220) .130) .145 (.120-.090 (<LOD-.350 (.090-.108 (.190) .135) * .240-.250-.079-.180) .160-.100 (.180-. and pewter.117-.190 (.115-.150 (.123 (. 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) .230) .390-.310 (.500) .270 (.128 (.280-.400 (.130 (.490 (.310-.390) .400) .146 (.300) .340 (.350-.210) .190) .120) .280) .220) .330-.210-.330 (.180-.148-.320-.088-.260 (.240 (.200 (.260-.470) .270 (.410) .360 (.240 (.150-.390) .170-.140 (.150-.270 (.300) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.260-.126 (.470 (.132 (.103) . 0.

250 (.164 (.098-.127) .124-.727) .741) .114 (.321) .149-.150-.178-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.085) .269 (.131-.317) .159-.187) .385 (.181) .266 (.182 (.079 (<LOD-.133) .146-.265-.206-.338) .241-.173 (.200-. and eyes.277 (.417) .357-.255) .298 (.092) .333 (.081 (<LOD-.167 (.148-.106-. and route of exposure (Elinder and Friberg.195-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.320) ..138-.281-.338 (.113-. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.129) * .138) * .230) 95th .295 (.107-.205-.080 (<LOD-. resulting in hemolysis with abdominal and back pain (Dernehl et al.500) .109 (.120 (.114 (.471 (.176 (.111 (.095-.253-.112-.172-.308) .288 (.176-.229-.121) .125-.444) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.138 (.250) .119-.115 (.198) .115) .135) .152) .167-.144-.113) .120 (.115 (.320-.127) .272) .228 (.175 (. abdominal pain.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 . 1958) and occupational exposures (Briegner et al.167 (.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 .129 (. liver.183) .315) .235-.082 (<LOD-.265 (.146) .242-.425) .239-.071-.209 (.135 (.126 (.255-.391) .238) .263 (.233) .148) * .208-.236 (.121 (. 1954).391) . Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.124) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.127) .224 (.421) .135) .118 (.161) .130) .222 (.Metals than for trivalent compounds (Elinder and Friberg.132) .471) .147-.247) ..061-.102-.121 (.485) .145) .257) . 1973).226 (.214) . 1995).196 (.140) .373) .132 (.068-.119 (.181) .092-.161) .238) .200-.333-1.162-.116 (.207) .104-.126-.211) .111-.228-.200-.126) .130) .120 (.271-.199-.112 (.417) .076-.313-. skin.120 (.173) .089) .069-.352 (.146-.263-.203) .310 (.127 (.195 (.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 .181) .268) .259 (.146-.233-.447 (.082) .147) .116-.170 (.186) .333) . and kidney have been demonstrated in high dose animal studies depending on the dose.143) .153-.317) .225 (.122 (.276 (.193) .086) 75th .176 (. myocardium.278 (.154-.227-.068 (.109-.318-.139 (.119-.333 (.204-. and ulcers (Werrin.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.200) .250-.075 (.115 (.102-.253 (.156 (.300) .099-.230-. Inorganic antimony salts irritate the mucous membranes.333-.320-.138-.280-.122 (.380 (.250-.256 (.245) . diarrhea.267-.077) .320 (.300 (.193 (.115-. 1944).163 (.308-. and gastrointestinal symptoms such as vomiting.250-.104-.352) .107-.364 (.108 (.250-.107-.261) . The toxicity of stibine after acute inhalational exposure is similar to that of arsine.333 (.371 (.414) .113-.357) .208 (.343 (.238 (.087) .318-.081) .189 (.192-.192) .278) .280 (.115-.310) .178 (.152) .248) .127) .317) .364 (.209) .429 (.143) 90th .098-.438) .244-.153 (.203) .480) .134) . Ming-Hsin et al.130) .109 (.123) .233 (.444) .129) .095-.333-.430) .213 (.098) .143) Selected percentiles ( 95% confidence interval) 50th .118 (.151) .159-.097-.173-.135 (.136) .124 (.108-.148-.075 (.076-.125 (.074 (.250 (.220) .320 (.194-.225) .167 (.143) .117-.171) .267) . 1953)..248-.30) .103-.084) .099-.163 (.185-.300) .173 (. Histopathologic inflammatory and degenerative changes in the lung. Fourth National Report on Human Exposure to Environmental Chemicals 177 .150-.192 (.108-. 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.069-.310) .106-.286 (.294) Total . 1988.100 (.123 (.112 (. 1986). 1962).160 (.130 (.405) .267 (.082) .179-.. species.124-.131 (.129 (.400 (. interval) .140) < LOD .086 (.078 (..149) .164-.209) .185 (.209-.143 (.156-.228 (.333-.117-.741 (.080 (. Acute antimony poisoning may cause a metallic taste.185 (.195-.241-.217 (.159-.096-.338 (.117-. population from the National Health and Nutrition Examination Survey.188-.114 (.429) .137 (.188) .S.105-.131) .103-.139 (.135) . 1986).191 (.128-.164) .108-.

. Antimony in blood and urine of infants. Rev Infect Dis 1988. Stasney J. J Occup Environ Med 2004. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Shao-Chi C. 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.67:119-123. Antimony.76:432436. Schaller KH. Semisch CW.. Weltle D.16: 33-39. Mahieu P. Kuo-Juie Y.. Element reference values in tissues from inhabitants of the European community.. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Sabbioni E. Stone FD. Industrial antimony poisoning. J Trace Elem Med Biol 2002. Information about external exposure (i.106:33-39. Cordasco EM. Yu H-S.59:469-474. Apostoli P.atsdr. Minoia C. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Ming-Hsin H. Gebel TW. Review of elements in blood.46:931-936. Kiberd B.10(3):560-586. 26-42. Environ Health Perspect 1998. Cullen A. pp. Pulmonary edema of environmental origin. 2002. Iavicoli I. Yang C-Y.S. Ludersdorf et al. Leinemann M. O’Regan M. Suchenwirth R. Liao Y-H et al. Pietra R. Trace element reference values in tissues from inhabitants of the European community I. and 2003-2004.. Buchet JP. and hydrogen sulfide. 1998) or compiled reference ranges (Hamilton et al. Industrial Medicine and Surgery (Dec. Cheng-Wei L. New York: Elsevier.. Atlanta (GA).48:93-97.html. Vouk VB. Earlier measurements in general populations (Minoia et al. Industrial Medicine 1944.Metals to antimony have been established by OSHA and ACGIH. Bailly R. Third National Report on Human Exposure to Environmental Chemicals. indium. Pozzoli L. Schacke G. gallium. References Berman JD. In: Friberg L. Biological monitoring of exposures to aluminum. arsenic. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. 1991. EPA. Arsine. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Antimony trioxide is rated by IARC as a possible human carcinogen. Paschal et al.158:165-190. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Petrucci F. Dunkelberg. which may be due to methodologic. Mayer P. Biological assessment of exposure to antimony and lead in the glass-producing industry. et al. et al. even when exposure levels were below workplace air standards (Bailly et al. and a drinking water standard has been established by the U. Roland H.. Sci Total Environ 1994. HH. 1994) have reported values slightly higher than those in this Report. 1995.64(2):182-185.521-523. Iavicoli et al. VI. clinical efficacy.. Kentner et al. Carelli G. Chen J-R. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Konings J. Friberg L. Br J Ind Med 1991. and antimony in optoelectronic industry workers. Centers for Disease Control and Prevention (CDC). 1987). Mayne P.e. External and internal antimony exposure in starter battery production.51:238-240. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. J Clin Pathol 1998. 20012002. Nau CA. Stocks J. 2004. Luedersdorf R. Biomonitoring of a worker population exposed to low antimony trioxide levels. Liao Y-H. Pilgrim L. Ju-Sun P.. Lenert G. 2nd ed. Arch Dis Child 1997. Stead FM. Ho C-K. 1997). Lauwerys R. et al. Piatnek DA. Alimonti A. Dezateux C. stibine. 1998. 1998). Handbook on the toxicology of metals.13:361-362. Delves HT. Caroli S.. environmental levels) and health effects is available from ATSDR at: http://www. Int Arch Occup Environ Health 1995. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Wu M-T. Costeloe K.. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Chia-Yu H. Urinary antimony in infancy. Fuchs A.76(2):103-115. Briegner H. Nordberg GF. and future strategies. Dernehl CU. Sabbioni E. eds.. Wade A. Hamilton EI. population. Gallorini M. Chin Med J 1958. gov/toxpro2.)1954. Van der Venne MT. Int Arch Occup Environ Health 1987. 1986. Delves HT. or exposure differences. Chest 1973. Matthews T. Dezateux et al. Chemotherapy for leishmaniasis: Biochemical mechanisms.cdc. Bolten C. Skulsukai G. 2005. 1990. Elinder CG. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. respectively. Kentner M.

Sci Total Environ 1990. Ting BG. Antimony poisoning in industry. Paschal DC. and serum of Italian subjects. blood. et al. Chemical food poisoning. Trace metals in urine of United States residents: reference range concentrations. Environ Res 1998.76(1):53-59.95:89-105. Werrin M. 27:38-45. Industrial Hygiene and Occupational Medicine 1953. Renes LE. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Sampson EJ.Metals in urine.99-108. Pirkle JL. Morrow JC. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Jackson RJ.

and arsenates (oxidation states of -3.10-10.2) 15. Arsenic is measurable in most soils.40) 7.3) 10.4-65. the smelting of copper.7 (11. and play sets.1 (38.84) 8. Arsenic and its compounds have had many uses in the past and present as medicines. to a lesser extent.84) 8.4 (24.3-19.9-46.19-9.7-95.4) 60.74. and. copper arsenates. Water sources contain mostly inorganic arsenate. solders. to a lesser extent.3-15. sodium arsenite.8) 34.90-7. as alloy in metal bearings.0 (11.8-77.7) 90th 37.6-141) 53.5) 66.8) 7.2 (12.9) 21. mostly for use in wood preservation (ATSDR. 2001).10-7.20 (8. see Data Analysis section) for Survey year 03-04 is 0.000 metric tons annually. and as homicidal poisons.30) 17.2-17.90-8.7) 65.57) Selected percentiles ( 95% confidence interval) 50th 7.10 (6. and indium arsenides are used in the semiconductor industry.5-52.4 (31. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.2 (41. Gallium.90 (7.90 (7. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. population from the National Health and Nutrition Examination Survey.90) 75th 16. and other metals. trimethylarsine oxide.5 (23.Metals Arsenic CAS No. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.S.5 (34. and arsenosugars.34-10. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80 (5.0-60.5-178) 46. black.9-34.3-111) 78.25-9. gaseous hydride manufactured in small quantities for use in the semiconductor industry. lead. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.29 (8. referred to as inorganic arsenic compounds. cancers.4) 13.2 (13. particularly arsenic trioxide. psoriasis. In the last century.1) 290 725 1542 03-04 03-04 9. arsenic compounds.00 (6. cacodylic acid.27) 9. and produce.0-19.6 (15. The United States no longer produces arsenic from mining but imports about 22.5-41.2 (51.6) 11. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.8 (48.50 (8.10) 10. and as a cosmetic to lighten complexion. Although it is still widely used in the United States.41 (7. though in some locations arsenite may be prevalent (WHO.8) 30.5) 95th 65.34-9. retaining walls.0 (43.9) 68.50-14. and gray forms).5 (40.02-8. such as arsenopyrite (FeAsS) and realgar (As4S4).0 (22. were used as treatments for syphilis.9-62.66-8.00-9. alloys. arsenic as elemental metalloids may be used in some ammunition.90) 16.7-83.9 (8.9 (17. 2005).8) 29.90-8.1-18.5 (14. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.8-61. arsenocholine.1) 15. and in lead-acid storage battery grids.77) 6. Survey years 03-04 Geometric mean (95% conf.2) 46.12 (6. semiconductors.90-14.4 (48.30 (6. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. mental disorders. pesticides. from coal burning.8) 17. +3 and +5).0 (14.70) 8.1) 7.8) 7.5-19.7) 24.5) 43. meats.90-11.80-9.6 (9.6) 618 722 1074 Limit of detection (LOD.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 7.1 (32.2-20.70 (6.4 (7.2-93.97) 8. Before the 20th century. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. arsenites.4 (26. lead hydrogen arsenate.5 (36. 180 Fourth National Report on Human Exposure to Environmental Chemicals .6-43.0 (15. and foods.8) 33.2-61. Since the 1940s. Arsine (AsH3) is a reactive. Various arsenic compounds were used in paint pigments and for tanning animal hides.6 (32. it is found in over 200 crystalline or mineral forms.55 (7. Arsenic trioxide is approved to treat acute promyelocytic leukemia. or rarely as elemental metalloids (yellow.80) 6.13-8. Also. In nature.30 (7.1-40. Arsenic trioxide (As2O3. General population exposure to inorganic arsenic can occur through consumption of drinking water and.70-9.1) 1281 1276 03-04 03-04 03-04 9.5) 41. interval) 8.6 (13.12-10. aluminum.08 (5.6-35. grain.4) 40. ocean and fresh waters.90 (5.

Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established. In aquatic organisms.5-17.7 (25.4 (12.45) 5. WHO.1) 8.3-62.8 (27.7) 95th 50.3-41. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.0-69.4 (26.93-9.93-8.18 (5.7) 28. 2001).2-15.. After absorption.2-46.0) 42.58-10.66-8...30-9. 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.9-56. 2001). selenium. 2003. U.4-64.20-9.0) 12. Steinmaus et al. Extremely high groundwater arsenic levels. organic arsenic can be converted back to methylated and inorganic arsenic.59) Selected percentiles ( 95% confidence interval) 50th 7. 2007. and some other seafood can contain organic forms of arsenic including arsenobetaine.0 (31.0-26.0) 33.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . Tseng.0) 1281 1276 03-04 03-04 03-04 8. WHO. arsenocholine. 2007. inorganic arsenic is widely distributed within the body. 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.2) 15. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.8-75.8-32.6) 45.6 (10.86-17. mine tailings).4 (24. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.8-62.81-9.23-7. shellfish.S. Fish.8 (11.5-120) 40.50 (6. Inorganic forms of arsenic demonstrate high acute toxicity..7 (9.3 (24..11 (5.3-53. 2001).47-6.3) 9.8 (21.2 (12. trimethylarsine oxide (TMAO).3) 6.04 (5.66-8.44) 6.4 (40.4) 32. 2007. 2006.0-18.47 (7.96) 12.5) 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 8.06 (4. Direct exposure to DMA and MMA may result from use of the two pesticides. but is poorly absorbed dermally (WHO. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.31 (6. dose level. and folate status (Chen et al. 2001)..04) 7.5) 290 725 1542 03-04 03-04 8.88 (5.00 (6.51) 75th 14.01) 11.7-188) 27.24 (7. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. and contact with CCA-preserved wood structures.5) 17.75) 13.7-34.6 (35. NRC.0-38.28-7.9) 13. dust. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. age.07-9. 2001). 2001. 2001).1-36.5 (9. Gamble et al.4 (11.9) 53.25 (6. Children may have additional exposures from ingestion of contaminated soils (e.8 (20. EPA’s maximum contaminant level (Hughes.3-64.7-18.1) 24. Though modest bioconcentration occurs in some aquatic life. population from the National Health and Nutrition Examination Survey. EPA. In aquatic sediments.33 (6.38-10.S.99-9.3 (27.0) 14. are used in enclosed ultraclean operations within the semiconductor industry. Survey years 03-04 Geometric mean (95% conf. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. 2001). 2006. Arsenate is reduced in the body to arsenite (oxidation state +3).1) 58.41) 6.6-17.10-16. 1988).1 (14.75 (5. though some reduction may occur in the gut prior to absorption.25-9.32 (5. interval) 8.40) 8.61 (7.7-17. The semiconductor dopants.1) 6.01) 7.66 (7.12-10.44-11. 2001.7 (11. Chowdhury et al.0) 26. and arsenosugars.1 (11.6 (17. have caused clinical arsenic poisoning.g.8 (12.76 (6.88) 7.2) 40.10-8.33-10. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. as observed in Bangladesh where millions of people have been exposed.0 (17.8) 27.47 (6.4) 54.7-35.S. gallium arsenide and indium arsenide.64 (7.4 (42. kelp.8) 22. cacodylic acid and monosodium methyl arsenate. so exposure to the general population is extremely limited. arsenic does not show biomagnification in the food chain (WHO.1) 7.2) 90th 30.9 (45. Smoking tobacco is also a source of inorganic arsenic.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.35) 7. 2001).13) 8.

and DNA repair inhibition (Cohen et al.20 (<LOD-1. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. but additional or confirmatory research is needed (Kapaj et al.10 (<LOD-1.. WHO. 2001. 2006. renal failure.. vomiting.S. increased oxidative stress.20 (<LOD-1. Chronic arsenic exposure in humans is considered to be a cause of skin.20 (<LOD-1. cell transformations. 2001). hepatotoxicity.30) 1. The organic forms of arsenic occurring in seafood have little known toxicity. The U.. Arsenic has many actions demonstrated in cellular studies. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and production of glutathione may be affected as well.60) 1. including inhibition of numerous enzymes.S. leading to a decrease in adenosine triphosphate energy production.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1..10 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 1. U. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. interference in signal transduction pathways. Such actions may lead to decreased energy production. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. and diarrhea. and by uncoupling oxidative phosphorylation (NRC. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. Bredfeldt et al. Acutely.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al.50) 1. 2004). 2001).50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. NRC. and endothelial injury (Kumagai and Sumi. food residue. lung. Bangladesh.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.. and bladder cancer (IARC. Cellular glucose uptake. WHO. NRC. and hyperpigmentation of the skin (NRC. noncirrhotic portal hypertension. WHO. respectively. which may vary for some chemicals by year and by individual sample. cytotoxicity. Studies of arsenic at levels typical of U.. and environmental standards for arsenic and arsenic Urinary Arsenic (V) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and it also will inhibit succinate dehydrogenase. gluconeogenesis. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. 2001. 2006) or when exposure occurs in smokers (Chen et al. 2006.10 (<LOD-1.EPA. arsenic trioxide) includes hemorrhagic gastritis with nausea. Survey years 03-04 Geometric mean (95% conf. Raml et al.20 (<LOD-1.S. drinking water have not been associated with increased cancer rates (Schoen et al. Although arsenate is reduced in the body to arsenite. hyperkeratosis. some of these effects may take years to develop.10 (<LOD-1. 1998. and altered gene expression.. 2001).S. hypertension.g. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. 2001). which can lead to dehydration and shock.. 2004). fatty acid oxidation.60) 1. Chronic elevated arsenic intakes have been associated with diabetes. WHO. 2007). Taiwan. 2001).0. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. and childhood neurodevelopmental effects in observational human studies..EPA has established drinking water. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al.10 (<LOD-1.. apoptosis.g. Cohen et al. With chronic exposure. 2007. hematocytopenias. Chile).. peripheral vascular disease. see Data Analysis section) for Survey year 03-04 is 1. can cause peripheral sensorimotor neuropathies. 2004. 182 Fourth National Report on Human Exposure to Environmental Chemicals . 2006. Cardiac arrhythmias. 2001). Chronic human intake of arsenic at less than acutely toxic doses. including drinking water sources with elevated arsenic levels (e. population from the National Health and Nutrition Examination Survey. substitution in phosphate metabolism.50) 621 725 1078 Limit of detection (LOD. 2007. 2000. < LOD means less than the limit of detection..80) 1.

2004.00) 1.41) 3. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. 2006).. Though CCA-treated wood contains several thousand times more arsenic than untreated wood.. had decreased since the prior 1990– 1992 survey. Shalat et al. gov/toxpro2.33 (<LOD-3.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2000). and were about two-fold lower than those for the U...S. Caldwell et al.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 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 < LOD 90th < LOD Sample size 3. In a Nevada town where groundwater levels were naturally elevated.80 (<LOD-4.. 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. Compared with this Report. 2000.19) 3. 2001)...S. 2008). 1998. 2001). population in NHANES 2003–2004 (Schulz et al.69 (<LOD-3.html. Pellizzari and Clayton..cdc..atsdr.75 (<LOD-2. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.18 (<LOD-3. arsenic has been fetotoxic and teratogenic.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2.04 (<LOD-3. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. 2006. and the FDA has established a bottled drinking water standard. 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. 1999. 2008). Pellizzari and Clayton. 2006).50) 1. Caldwell et al. * 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... 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.18) 3. 2007. Consequently. 1986). WHO. In animal studies.. Meza et al. DMA produced bladder cancer in some chronic rat studies (Cohen et al.Metals compounds. Survey years 03-04 Geometric mean (95% conf. 1999. environmental levels) and health effects is available from ATSDR at: http://www...e. median urinary total arsenic levels in 4052 adults varied with seafood intake. 2008. 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. Additional information about external exposure (i. Fourth National Report on Human Exposure to Environmental Chemicals 183 . Calderon et al.. 1992.. 2006.S. 2001). Shalat et al. 1999).S. but generally only at maternally toxic doses (WHO... 2004.61 (<LOD-3.. Offergelt et al. Pellizzari and Clayton 2006). 2007.. 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. 2006). Vahter et al.. although urinary arsenic levels were not associated with CCA contact (Shalat et al. 2006). though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. Josyula et al. In the German Environmental Survey III of 1998. Several studies have shown that urinary arsenic levels are not correlated with low levels of arsenic measured in house dust or in washings taken from hands (Hysong et al. Valenzuela et al. 2006. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. Levels of total urinary arsenic in the U.. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. 2003.75 (<LOD-2. population (Rubin et al.33 (<LOD-3..95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

90-29.66 (1. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.20 (2.800-1. Tseng et al.83) Selected percentiles ( 95% confidence interval) 50th 1. China. population from the National Health and Nutrition Examination Survey.8-50.17-1.3) 95th 35..3 (21. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.9 (7.80) 1. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. Valenzuela et al.S.00-4.00-12.70 (5.74 (1. and two methylated metabolic products. interval) 1.3) 1284 1284 03-04 03-04 03-04 1. geometric mean levels were about 70-fold higher than for the U..800 (.30 (2.9-23. In the residents of a Chilean town who consumed water with high levels of arsenic.45 (1. Chowdhury et al.6-44.10) 4. Aposhian et al. 2007) with higher levels of arsenic in the drinking water.50) .5 (14. and 0. Survey years 03-04 Geometric mean (95% conf.500-1. when seafood organic arsenic is subtracted). 2008).0) 4. population in the NHANES 2003–2004 subsample. 2001.2 (6. and other factors such as nutrition.Metals other areas of the world (Ahsan et al. Blom et al.80 (4. arsenite.6 (11.40) 5.S.20 (4.. In most human studies.37 (1. These associations are stronger at higher urinary levels. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20-190) 31. MMA.40-7. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. For residents of Inner Mongolia.70 (3. 1.4 (16.S..6 (13. methylation capacity.7-22. Sun et al.S.30) 2.2-35.8-40.30 (1. 184 Fourth National Report on Human Exposure to Environmental Chemicals . population (Ahsan et al.70-21.0) 29.60) 1.70-21.1-25. 4. Pellizzari and Clayton.80 (. 2006).800 (. 2005. Total arsenic measured in the urine includes all species of inorganic and organic arsenic..00 (1. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level. population (Sun et al.2-38..50-6.68) . arsenocholine. 1985. 2008.5) 32. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8) 35.900-1.20) 18. 2001). and duration of exposure are also considered important. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.29 (1. The higher percentiles of total urinary arsenic levels in the U.0 (27.5 (26.700-1. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.28) 1..60-3.8.62) 2. Caceres et al.1-51. In the late 1980s.80 (3.3) 35.800) 1. After recent seafood ingestion.0-23.0 (26.871-1. arsenocholine.4) 31.40-6.70) 6.700-1. Individually measurable species resulting from inorganic arsenic exposure are arsenate. 2000.48-2.00 (. 2008). 2005.7) 15.05) < LOD .00-1.4.20-3..90-7...7) 13.20-25.800-4.4) 23..50) .1) 45. 2000..50) 90th 16. dermal keratosis. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.e. respectively. with DMA.10) 8. Caldwell et al.31-1. and TMAO were detected in only 7.55 (1..3% of a representative sample of the U.7 (13.6) 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 * * 1.00) 3.g.93) 1. Arsenate. 2007). Some noncancer effects of arsenic (e.S.4-35. population showed a higher contribution of arsenobetaine (Caldwell et al... vasospasm. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. Also. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.3 (9. 2000.5) 621 725 1078 Limit of detection (LOD. and TMAO. in NHEXAS 1995–1996. 1996.. Measurable organic arsenic species in this Report are three biologically generated environmental forms.11-1.1) 18. which may vary for some chemicals by year and by individual sample.600 (. 2003).6 (25.80-5.6. arsenobetaine. WHO. 2005. 2008). 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.19 (. 1990. Caldwell et al. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.5) 292 728 1548 03-04 03-04 1.30) 10..43-1.20 (1.40) 75th 5.7 (21.10 (4.8 (17.00-6.6..20) 7.5) 29.. When seafood intake is avoided.9) 13. 2008).1-94.8 (12.3-39.9 (6.400-.900 (.20) 3. 2008. Caldwell et al. DMA and MMA.. arsenite. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. see Data Analysis section) for Survey year 03-04 is 0. < LOD means less than the limit of detection.20 (.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 292 728 1548 03-04 03-04 1. In recent years.58 (3.79 (1.05 (. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.5) 26.51-2.80-153) 17.638) 1.93 (1.2 (12.5-20.72) 12. 2003.S. interval) 1.9 (25.43) 75th 5. Fourth National Report on Human Exposure to Environmental Chemicals 185 .67) 1.1 (26.531 (.5 (18..55) 1.82) 4.50-7.54 (1.68 (1.39-3.91 (4.47 (1.67) 4.S.6) 19.47 (2.8) 29.901-2.959-1.4-21. which is below the ACGIH BEI (Caldwell et al.400-.9 μg/L.786-1.76-27.5) 17. 2008).05) 1.19-2.4) 32.0-36. not to imply a safety level for general population exposure.. 1992.15-4. WHO.88) 2.18-1.80) .25 (.88 (5. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.877 (. 1986.00 (1.25-7.32-7.7) 17.45) 1. Sun et al.3-24. 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.15-1.28) 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..612-1.. 2008).833-1.Metals as with DMA.43) 14. Survey years 03-04 Geometric mean (95% conf.14 (1.2 (13.16 (. population from the National Health and Nutrition Examination Survey. 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.6 (9.9) 32.37-2.4) 13.. Information about the biological exposure indices is provided here for comparison.64-29.4-28.53 (.50-15.938-1.13-39. 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.36) 2.1-18.4 (24.30-1.15-1. The 95th percentile of the U.81 (4. 1998.6 (6.73-6. 2001).1) 26.1-36.40) 1.0 (9.3) 1284 1284 03-04 03-04 03-04 1.44 (1.83) 2. 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.3 (10.7) 30.21) 5.65 (1.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.6-46.51) 5.5 (18..4-82.3 (10.2 (4.. 2001).4 (11.12) < LOD . population for the sum of inorganic related species was 18.7) 9.9) 14.70) 5.00 (3. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.909-1.6-32. 2006.78 (3.6-29.61-6.2 (12.62-6.11 (.. Caldwell et al.29-14. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.40 (1.29 (4.4) 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 * * 1.9 (13.3) 95th 29. Offergelt et al.9-18. 2007).82) Selected percentiles ( 95% confidence interval) 50th 1.30) 1.10 (.83) 8.91) 90th 16.78-5. Vahter et al.

see Data Analysis section) for Survey year 03-04 is 0. 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. which may vary for some chemicals by year and by individual sample. Urinary Arsenocholine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey years 03-04 Geometric mean (95% conf.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. 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.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey years 03-04 Geometric mean (95% conf. 186 Fourth National Report on Human Exposure to Environmental Chemicals .Metals Urinary Arsenocholine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.6.

2.S.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. which may vary for some chemicals by year and by individual sample.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.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. < 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 1.20 (<LOD-1. Survey years 03-04 Geometric mean (95% conf. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) 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. Fourth National Report on Human Exposure to Environmental Chemicals 187 .44) 2. Survey years 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) < LOD 621 725 1078 Limit of detection (LOD.08 (<LOD-4.00 (<LOD-3.00 (<LOD-2. population from the National Health and Nutrition Examination Survey.40 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 1.00) 1.95 (<LOD-2.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.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.

00-7.0 (10.00 (6.95-3. population from the National Health and Nutrition Examination Survey.71 (3.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0 (10.7) 12.39-3. Survey years 03-04 Geometric mean (95% conf.0-25.45 (8.16 (2.61-11.9) 12.92) 3.00 (3.73) 6.00-10.78) 4.00 (5.0) 16.20-4.00-7.00 (6.0) 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 4.34-4.46 (4.0 (13.60-6.80) 2.5) 95th 13.0 (12.82-9.00-12.44) 5.05) 3.19) Selected percentiles ( 95% confidence interval) 50th 3.97-3.05) 5.00 (3.62) 4.91) 75th 5.00) 9.31) 4.80) 7.3 (8.90) 2.0-12.0) 17.45) 3.69 (3.55 (2.34 (3.90 (3.24) 3.00-4.0) 11.17-6.95-6.27-5.1-18.1-15.57 (3.80-6.00) 6.0) 9.60-4.00) 12.37 (2.5) 12.0 (13. population from the National Health and Nutrition Examination Survey.59 (6.11) 4.8) 7.70) 5.20) 11.00 (3.00 (6.15) 4.52) 3.50 (4.69-3.70-4.0-17.50-15.1 (8.49-4.0) 13.00-8.9) 13.3 (8.60-3.82-5.22) 4.00 (4.65-6.00-4.32 (8.77 (3.0) 95th 16.95-4.03-6.49) 10.57-5.70-3.00-15.80-3.00-15.00 (5.7 (10.74 (2.00) 7.86-21.0) 17.00 (5.0 (9.2) 10.03 (3.9 (11.00 (5.0) 621 725 1078 Limit of detection (LOD. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.84-18.00) 5.69 (3.00) 6.00-4.0 (12.09 (7.9) 11.94-3.0) 13.12-4.0) 12.37 (3.00) 6.86-7.00-4.7) 1284 1284 03-04 03-04 03-04 4.90) 5.6) 1284 1284 03-04 03-04 03-04 4.00-15.61-16.88 (4.0) 9.00-4.00-3.80 (4.00-5.00) 4.72 (4.6 (9.00) 6.0-17.00) 3.84-8.00) 90th 11.7) 13.00-11.71-4. Survey years 03-04 Geometric mean (95% conf.9) 5.00 (5.32-10.0 (8.8) 7.12 (3.20-12.31-4.82) 3.79 (3.25 (4.38 (3.1-22.67) 8.70 (3.34-4.27 (3.16-11.30 (7.95 (4.11 (3.78 (4.0 (10.00 (3.89 (3.45) 8.00 (3.8) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 3.7-16.0-18.00-13.6) 292 728 1548 03-04 03-04 3.S.48 (3.0) 14.33) 3.00) 3.7.14) 3.0) 16.44 (2.00-4.81 (5.00) 4.00 (7.0 (9.60-7.10) 6.08 (2.50-5.13-4.34) 3.32 (4.16 (4.14) Selected percentiles ( 95% confidence interval) 50th 3.10) 3.0 (8.00-12.6-18.0-16.0-16.33-4.71) 3.0) 11.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .71 (4.05) 10.92-12.00-7.00-11.S.06) 5.00-3.80-5.18 (6.00-11.17-4.27-2.00-7.85 (3.65-8.3 (7.0 (9.30) 3.86 (2.42) 3.48 (2.00-22.17 (2.73 (3.27 (2.0 (10.00-9. interval) 3.0) 9.0 (14.67) 9.5 (11. interval) 3.0 (11.28) 2.94) 3.34 (3.70-12.00) 75th 6.9 (7.69-6.00 (3.0) 10.29-4. see Data Analysis section) for Survey year 03-04 is 1.0-19.00 (7.98) 4.74) 90th 9.4 (7.0) 292 728 1548 03-04 03-04 4.24-4.

93) .70-2.52 (2.22 (1.62) 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. which may vary for some chemicals by year and by individual sample.10-3.50) 1.50) 621 725 1077 Limit of detection (LOD.73-2.816 (<LOD-.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.22) 3.10-1.30 (1.54) 90th 2.88 (1.07) 2.79) 2.00 (<LOD-1.30) 1.20-3.80 (1.84-3.70-3.31 (1.60) 2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.53 (1.33 (1.00-2.S.00 (<LOD-1.10 (1.86) 2.50 (1.31-3.75) 621 725 1077 < 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.70-2.30 (2.70) 2.80-2.20 (1. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf.81) 1.00-2.50 (1.40) 2.90) 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 1.10-1.00 (1.34) 2.60) 2.00-1.18-1.15-1.20 (1.57) 95th 2.10) 2.37 (1.90 (1.985) 1.45) 3.20 (1.88 (1.20 (1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60 (1.16 (2.40-3.20 (1.40) 1.61-3.90) 1.10 (<LOD-1.88-2.30) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.36 (1.10) 95th 2.40-2.60) 1.30-2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.20-1.900-1.85) 1.90) 2.07-3.00) 1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.63 (<LOD-1.71-2.28 (1.61) 2.40-3.10 (. see Data Analysis section) for Survey year 03-04 is 0. Survey years 03-04 Geometric mean (95% conf.86 (2.00-1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.80 (1.40 (1.50 (<LOD-1.43-3.53-2. < LOD means less than the limit of detection.07 (1.30 (1.30) 1.00-4.80 (2.17) 2.05-1.20 (1.30) 90th 1.86 (2.80) 1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .58) 2.00) 1.50-2.60-2.00 (2.18-1.86) 3.853-1.28 (1.30-1.20) 2.00) 2.10 (.70-2.50 (2.80 (1.30-1.82-2.40 (2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.00) 1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.30 (1.46-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33 (1.S.70-2.60 (2.96-2.82-2.9.46 (1.80-2.40) 1.10 (1.77) 1.40-2.11-1.23) 1.35-3.90 (2.80 (1.00) 2.80) 1.36) 1.00 (2.14-1.85) 2.

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

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71) 2.54 (2.18-1.50 (6.15 (6. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).90) 2.12 (2.56) 4.25 (1.80) 1.41-3.30 (5.20-8.63) 1.20-8.71) 95th 6.36-1.90 (4.46) 1.17-1.48) 1.20 (1.20) 2.50) 2.49) 2.70-6.35) 5.50-6. fireworks.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 1.01 (4.51) 1.73 (6.30-5.43) 2.70-3.76) 1.64-3.20-1.93-2.62 (1.53) 2.20-6.30-2.75) 2.61-8.21-8.S.48-4.30-1.90-2.65) 1. barium sulfate and barium carbonate). and ceramics.69 (1.80) 7.72) 4.66) Selected percentiles ( 95% confidence interval) 50th 1. interval) 1. are high in barium (Genter.63 (1.60-6.00) 4.60-10.4) 9.60-3. 01-02.27 (1.95 (4.97 (1.54-1.82) 1.19-1.37 (4.27 (1.60-6.73-5.81-2.32) 8.41) 1.8) 5.30) 3.22-1.60) 3.61 (1.49-1.22-1.40) 7. 7440-39-3 Medically.48-4.40 (1.15-1.80-2.80 (1.28) 90th 5.43 (1.18) 3.61 (5.51) 2.53-5.44-2.12-1.31 (2.70 (5.10 (3.50 (3.1) 9.61 (3.20-5.4) 7.45) 7.30) 5.60-2.70) 5.75-3.52 (1.00) 1. respectively.16 (1.62) 1.02 (7.49) 11.48 (6.37-8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40 (5.88) 4.56 (1.80 (1.25-11.86 (4.56) 1.15 (1.55-3.51) 7.31-2.57 (5.05% of the earth’s crust.01-7.05-2.81-3.70) 3. Barium compounds are used by the oil and gas industries to make drilling muds.32-7.40 (1.50) 1.98) 1.65) 3. rubber.09 (1.20 (3.40 (5.73 (5.63 (2.12) 7.80-5. Fourth National Report on Human Exposure to Environmental Chemicals 193 .39-1.50-1.46) 1. glass.93-8.49 (1. and 0.11-1.14-6.74) 3.87-3.73) 3.00-3.71-9. Some barium salts are freely soluble in water.32-1.60) 1.26-1.30-3.80-7. such as barium chloride.00-76.74-3.76-3.08 (6.90-13. whereas others are practically insoluble (e.29-1.44 (1.34 (2. and food.72) 75th 3.68 (1.54 (6.87) 7.43 (1.70) 7.85) 1.30) 4.34) 2. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.39) 1.39 (1.49-9.78-2. bricks.30-2.20-1.30 (5.50 (1.30-1.07 (2.03 (1.62) 1.76-7.12.35 (1.63) Total 1.43 (5.35 (3.70-2.87 (5.2) 6.11 (3.73) 1.50 (1.38) 8.91) 2.36 (4.15-11.46-1.50 (2.36 (1.47-1.09 (2.64 (1.10-5.35-1.20-8.76-2.87-14.38) 2.90) 1.08-8.82) 2.21 (1.30) 5.52 (4.15-1.36-1.70-5.9) 5.10 (4.12) 6.45 (1.54) 1.30) 5.28-1.62 (1.54) 1.59) 3.60) 1.49) 8. In nature.33 (1.59-11.51 (1.84) 5.25-1.10) 3.20-1. Small amounts of barium can be released into the air during mining and other industrial processes.99 (4.24-1.04-2.12. The general population can be exposed to low amounts of barium in air.12 (2. and 03-04 are 0.26) 2.14 (6.64) 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 2.00 (2.37-1.50 (4.35 (2.Metals Barium CAS No.16) 5.80 (2.90) 4.78) 1.50 (5.65) 1.40 (5.27) 2. population from the National Health and Nutrition Examination Survey.65 (5.26) 5.53) 1.77 (3.88) 7.57-7.34 (1.77) 1.37) 5. it combines with other chemicals such as sulfur or carbon and oxygen.54-8.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.49) 4.94-6.95-6.40 (4.65-5.50-6.20-1.50 (1.65-1. water.24-1.42 (1.50 (1.55-7.10) 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. see Data Analysis section) for Survey years 99-00.8 (6.50 (1.00) 6.87 (6.80-3.21 (1.43) 6.15 (2.11 (2.41-1.30 (2.30) 8.4) 6.70) 1.40 (1.87-9. soluble forms of barium.00) 1.30) 2.54) 2. Barium salts have also been available as rodenticides.60 (2. Workers employed by industries that make or use barium compounds can be exposed to barium dust.50) 2.47) 4.48) 1.92) 2. 2001).90 (1.61 (2.11 (3.35-1.10-4.35-4.66 (4.86-4.71) 1.00-8.72) 1.g.04-6.57) 3. Certain foods.65-8.70 (1.00 (1.50 (4.36) 5.39 (1.06-1.81-2.30 (1.40) 7.31.54-1.67) 6.91 (2.85) 1.88 (5.90) 2.47-1.14-1.44-5.50 (4.38 (1.24 (4..91) 6.80 (1.60 (1.86) 6.61 (1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.77-3.39) 4.74-2.34 (1.76 (3.30 (3.29) 5. 0.10) 5.06-2.88) 1.70) 4.82-6.93 (4.70-8.29-5.63 (8.70-2.18 (6.96-2.70) 1.63) 1.21-2.90 (6.80) 6.86-5.37) 1. depilatories. such as brazil nuts.99-5.40) 3.20 (4.90-9.56 (1.40-13.71 (2.56 (2.87-7.60) 4.85 (2.78-3. tiles.80 (2.19) 2.10 (2.50) 4.26-7.63 (5. Barium compounds are also used commercially in paint.80 (5.56 (6.86 (4. In single dose animal studies.38 (1.22) 6. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.8) 9.78) 1.50-1.15) 5.

28 (1.10-1.45-8.10) 3.84) 2.36-1.84-5.29-7.69 (5.39-10.04 (2.00) 4.00) 6.2) 5.68 (3.905 (.96) 7. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.01) 1.48-3.96 (4.38) 1.57) 2.921 (.43-6.62 (4.77) 1.83) 2.30) 2.32 (1. Chronic high doses in animals resulted in kidney damage (McCauley et al.24-11.39 (2.22-4.91) 2.80) 4.20) 4.51) 6.19-2.13-2.41) 4.24-1. Toxicity from soluble barium salts is rare.59-7.41 (1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.23-1.81-7.37-1.34-1.47) 1.76-3.38) 4.91 (3. 1984.47) 1.97 (5.02-5.03) 3. 2001).2) 6.52) 7.56 (1.57-7.76 (4. paralysis.75-3.36 (1. NTP.29) 1.26-1.86 (2.38 (1.81-6.11) .14-2.64) 7..33 (1. and cardiac dysrhythmias.963 (.00 (5. 1990). a benign condition that may occur among barite ore miners.68) 3.11-2.51) 4.20 (1.39 (3. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.10-2.56) Selected percentiles ( 95% confidence interval) 50th 1.42) 1.50) 1.47) 4.18 (1. and route of exposure.31 (4.00) 4.19-1.15-4.92 (4.20-1.54) 2.77) 5.3 (6.74 (5.26-1.62 (2.96) 4.55 (1.22-1.72) 4..33) 1.48 (1.23-2.29-1.27) 7.24) 3. 1986).06) 2.64 (1.51 (1.34-3.60) 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 2.00-1.44-2.68-3.55 (5.09) 6.36 (3.06) . vomiting.04) 1.39 (2.5) 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 1.73) 2.40 (1.31 (1.76 (3.32) 2.50) 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 1.33-1.73-4.77-5.36 (3.70) 10.51) 4.59) 2.34 (1. such as those used in medical radiographic procedures.50 (4.41 (2.71 (5.57 (6.91 (3.32) 2.55-5.38 (4.Metals was eliminated primarily in feces and to a lesser extent.75-22.37) 2. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.18 (1.76) 2.82) 1.55-6.97) 1. weakness. Symptoms following acute high dose include perioral paresthesias.00-7.29 (3.880-1.50) 1.47 (2.31-1.56) 4.52-4.89) 90th 4. Insoluble barium salts.32 (1.19-1.81-6.65 (2. The health effects of exposure to barium compounds depend on the dose.55) .40-1.53-21.703-1.20-2.39-1.891 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.51 (3.38 (1.33 (5.97 (4.99) 1.33) 6.56 (1.49 (1.48) 2.88 (6.68 (3.44 (1.58-6.63-4.83) 3.40 (1.10 (6.4 (5.58) 1.75) 2.46) 1.63) 1.96) 4.42) 1.58) 4.45 (1.22-2.55 (1.80) 3.38-7.96) 4.03) 2. chemical form.48-1.34-5.29-4. Following intravenous injection in animals.31-1.03-1.28) 5.16) 11.64 (1.36 (5.75) 1.21 (1.74) 1.76) 2.24-6.64) 7.39 (2.53) .05-1.30 (1.47-8.44-2.S.915 (.24-1.67-6.96-6.29-3.01 (5.27-3.20-8.58 (4.00) 1.24 (5.60 (2.52-10. 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.16 (1.51-3.97-4.90-2.46) 3.79) 1.45) 95th 6.45-1.25) 4.60 (5.02) 4.82) 1.99 (4.38-1.45-6.3) 6.51 (1.37 (1.40 (1.96 (4. population from the National Health and Nutrition Examination Survey.31-1.02 (3.45-1.28-11.49 (1.54 (1.39-1.70) 4.41) 5. in urine.56-3.24-3.62 (1.75) 1.28-6.33-4.77) 1. interval) 1.23-5.76 (2.26-1.38-5.53 (2.73-2.36 (1. Perry et al.57-10.0) 6.39) 4.2 (3.31) 5.52) 1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. are not absorbed when administered.61) 2.74) 1.25-11.881 (.832-1.59) 1.64 (1.35-3.99 (2.91-2.710-1.86) 5.37-2.41 (1.00 (2.49-1.26) 4.72) 6.59) 1.98 (2.68 (2.03-1.27 (2.68-3.4) 5.08-1.13-3.66 (1.55 (4.19-1.35-1.46-22.60 (2.75) 2. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.77) 1.08-2.60 (1. Barium is not rated for human carcinogenicity.54 (2.62) 2.48 (1.50) 2.11) .58 (2.35-1.59 (1.84 (3.45) 1.22-1.54) 1.00 (3.04) 5.36-2.8) 4.88 (2.34) 1.26-4.77) Total 1.28-7.43) 1.777-1.26-1.46 (2.42 (4.76) 1.52) 2.79-5.69-9.16-1.28-1.10) 6. water solubility.64 (1.24-6. 1985.49-1. diarrhea. 1989).85-5.46) 2.27) 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 .68) 1.48-5.87) 1.29 (1.89 (2.0) 7.70) 1.58) 75th 2.36-1.38) 1.92) 2.47 (5.00 (3. Wones et al.0) 5.29-4.57-5.84-2.72 (2.32 (2.01 (4.27-1.47) 10.60 (1.38 (4.03) 1.61 (4.52 (3. 1994.80-6.02) .25 (1.86-7.24 (3.97-3.45 (3.65 (5.37 (1.59 (1.12) 2.39-5.49-1.30 (1.48 (1. hypertension.78 (2.754-1..33 (1.

J Toxicol Environ Health. Sci Total Environ 1990.html?charset=iso-88591&url=http%3A//ntp. 2nd Ed. et al. Trace metals in urine of United States residents: reference range concentrations. Minoia C.niehs. National Toxicology Program (NTP).cdc.nih. [online]. and serum of Italian subjects. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies).S. 84-94.. Sabbioni E. Environ Health Perspect 1990. McCauley PT. Schaller KH. Investigations into the effect of drinking water barium on rats. et al. Cohressen B.gov:8080/cs. p. 2005. Fourth National Report on Human Exposure to Environmental Chemicals 195 . A study of 46 elements in urine. and 2003-2004 (CDC.64(1):13-23.gov/toxpro2. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. strontium. EPA. 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. 1984. Comparison of representative ranges based on U. Minoia et al. Morrow JC. Nordberg GF.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. and a drinking water standard has been established by U. et al. In Friberg L. patient population and literature reference intervals for urinary trace elements. barium. Sampson EJ. References Brenniman GR... Environ Res 1998.95:89-105.e. eds. Trace element reference values in tissues from inhabitants of the European community I.85:355-359. 5th ed. Patty’s toxicology.S. 4/8/09 Paschal DC. Zschiesche W.. Gallorini M. Ash KO. Lack of effect of drinking water barium on cardiovascular risk factor. Frohman. eds. Calabrese EJ. Inc. Pietra R. pp. Clin Chim Acta 2000.. p. Magnesium. Apostoli P. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. Princeton (NJ): Princeton Scientific Publications. Paschal et al. Powell C. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. Vol 2: Specific Metals. 2005. 1985. Information about external exposure (i. Epidemiological study of barium in Illinois drinking water supplies. Third National Report on Human Exposure to Environmental Chemicals. 221-252 Komaromy-Hiller G. 1986. Exposure to soluble barium compounds: an interventional study in arc welders. 2001. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report.niehs. Jackson RJ. Wones RG.28(3):373-388. blood. ed. Douglas BH. Advances in modern toxicology. Biomonitoring Information Levels of urinary barium reflect recent exposure. New York: John Wiley & Sons. Atlanta (GA). Handbook on the Toxicology of Metals. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Centers for Disease Control and Prevention (CDC). Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect.197210. 1992). p. Perry HM. Costa R. Pozzoli L.. Stadler BL. Princeton NJ: Princeton Scientific Publications.atsdr.296(1-2):71-90. Barium. Int Arch Occup Environ Health 1992. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. NTP. ed. 1994. Jr. Pirkle JL. 231-249. and radium In: Bingham A. In: Calabrese EJ. Weltle D. Available at URL: http://ntp.. Vouk VB. Kopp SJ. 1990. Reeves AL. the welders had no obvious adverse clinical effects (Zschiesche et al. Perry EF. In: Inorganics in drinking water and cardiovascular disease. Genter MB. calcium. 1989.gov/ntp/htdocs/LT_rpts/tr432. 1998)... Howerton K. PS. Laurie RD. 2001-2002. Levy.nih. New York: Elsevier.html. LA. Ting BG.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. 2000) to levels in NHANES 1999-2000 and 2001-2002.76(1):53-59. environmental levels) and health effects is available from ATSDR at: http://www. et al.

and volcanic dust.130 (<LOD-. or drinking water containing the metal. and can be found in mineral rocks. 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 .130 (<LOD-. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. computer. beryllium is used in instruments. Exposure to beryllium occurs mostly in the workplace. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. 7440-41-7 General Information Pure beryllium is a hard gray metal.S. * 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.13. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. which may vary for some chemicals by year and by individual sample. and 0. Low-level beryllium exposure in the general population can occur through breathing air. 196 Fourth National Report on Human Exposure to Environmental Chemicals . In studies of laboratory animals. < LOD means less than the limit of detection. 0. 01-02. near some hazardous waste sites. Two types of minerals.Metals Beryllium CAS No.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. soil. respectively. see Data Analysis section) for Survey years 99-00.150) < 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 . electrical. and from breathing tobacco smoke.140 (<LOD-. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. eating food. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. aircraft. Beryllium compounds are commercially mined.13.170) < 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 . x-ray machines. and dental bridges. and machine-parts industries. and 03-04 are 0. and refined beryllium is used in mirrors and special metal alloys for the automobile. nuclear.13. In medicine. are mined for commercial recovery of beryllium. bertrandite and beryl. coal. the lightest of all metals. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames.

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

Atlanta (GA) 2005. Weston A.gov/toxpro2. Genetic and exposure risks for chronic beryllium disease. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Ting BG. and the 95th percentile for males in NHANES 2001-2002. Pozzoli L. Trace element reference values in tissues from inhabitants of the European community I. Andrew M.atsdr.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. 1998). 0. 1990. population are lower than levels in workers. et al.cdc. 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.e. McCanlies EC.S. Element reference values in tissues from inhabitants of the European community. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Pietra R.76(1):53-59. Environmental Health Criteria.html. Kriess K. Paschal et al. population were generally undetectable in NHANES 1999-2000.13 μg/L.1 μg/L). less than 0. In other studies. VI. Hamilton et al. and the fact that most NHANES participant levels were undetectable. Clin Chest Med 2002. Ash KO. Sci Total Environ 1990. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect.. Sampson EJ. 3/27/08 Komaromy-Hiller G. Am J Epidemiol 2003.23:827-839.. Minoia et al. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. and serum of Italian subjects. References Apostoli P. which approximate this Report’s limit of detection. Paschal DC. HLA-DPB1 and chronic beryllium disease: a HuGE review. 2000.Metals (i. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. and 2003-2004. Environ Res 1998. Third National Report on Human Exposure to Environmental Chemicals. it is likely that urinary beryllium levels in the U.inchem.S..12 to 0. Hamilton EI. 1990. Morrow JC. They reported urinary beryllium levels ranging from 0.296(1-2):71-90.e. Levels of beryllium in urine for the U. Minoia C. Sabbioni E.157:388-398. blood.158:165-190. Clin Chim Acta 2000. Pirkle JL. Given these results. Comparison of representative ranges based on U. A study of 46 elements in urine. Available at URL: http://www. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Beryllium [online]. patient population and literature reference intervals for urinary trace elements. International Programme on Chemical Safety (IPCS). Gallorini M. Sabbioni E.htm.74:162-166. Van der Venne MT.95:89-105. Apostoli P. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. 20012002. Schaller KH. Review of elements in blood. Centers for Disease Control and Prevention (CDC). et al. Int Arch Occup Environ Health 2001. Jackson RJ. Maier L. Sci Total Environ 1994. Costa R.org/documents/ehc/ehc/ ehc106. Trace metals in urine of United States residents: reference range concentrations...S. environmental levels) and health effects is available from ATSDR at: http://www. 106. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Howerton K. 2001).

00-1. EPA.10) 1.283 (.20) 1.500-.500 (.513) .20) .60) Total * .10) 1.300) .200 (<LOD-.403) .400) .300) .30 (1.300 (.900-1.30) 1.200-.40 (1.S.600) 1.400-.600-. or copper smelters (U.3.00) .70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.500-.441) * .344) .600 (.400-.50 (1. as zinc sulfide) and to a lesser extent.10) 1.10 (1.800-1.10) 1.700-1.70) 1.235 (.50 (1.468 (.700) .00-1.300) .60 (1. interval) . Since 2001.400) .00 (.30-1.90) 1. which may vary for some chemicals by year and by individual sample.313 (. Other uses include pigment production.50-1.600 (.400) < LOD < LOD < LOD .600 (.300 (<LOD-.200-.470) * .60-1.700) .20-1.300) .900-1.usgs. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.60 (1.Metals Cadmium CAS No.10 (1.398) < LOD < LOD < LOD < LOD < LOD < LOD .700) .600-.14.400) .800-1.400) < LOD .500) .300-.00 (.600-1.500 (.400 (.309-.20) 1.700) .00-1.376-.500) . The predominant commercial use of cadmium is in battery manufacturing.50) 1.20) 1.600) .60) 1.600 (.600) 90th 1.300-.50-1.359-.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 .40 (1.20-1.420 (.30-1.400-.300) 75th .400 (.20) 1.300 (<LOD-.400 (.10) 1.10) 1.200) .500-.400 (.296-.300) .500 (.700) .S.900-1.300 (.30-1.200 (.600) .500-.400 (.20) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (.400) .600) .378 (.00-1.800 (.216-.300-.30) 1.300 (.300-.300) .300 (.386-.300) .500 (.500-.300 (.500 (.337) .00-1.361-.300 (.300 (.378-.300) .289-.400) .900-1.500-.426-.40 (1.200 (.600 (.400-.400 (.400) < LOD .80) 1.50-1.600) .449) Selected percentiles ( 95% confidence interval) 50th .80) 1.70) 1.700-1.900 (.400 (.500-. lead.400 (.10) 1.500-. Fourth National Report on Human Exposure to Environmental Chemicals 199 .600) .300-.40 (1.382 (.500 (.400) .600 (.300-. Cadmium also may be emitted into the air from zinc.300 (<LOD-.400) .460) . and incineration of municipal waste materials. respectively.30-1.30-1.326 (.900 (. and 0.600 (.700) .50) 1.200-.500 (.400-. cadmium use has declined in response to environmental concerns (http:// minerals.60 (1.700 (.200) .300-.00 (.900-1.40 (1.800 (.60 (1. 0.400 (. < LOD means less than the limit of detection.00 (.20-1.00-1.gov/minerals/pubs/commodity/cadmium).20) 1.300) 1.275-.00 (.60) 1.300) .500) .500) .600 (.500 (.400) .500-.400 (.427) * .00 (1.300-.20-1.403 (.300-.00-1.300-.00 (.200 (<LOD-.300 (.304-.400 (.425 (.800) .400) < LOD . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.900-1.00-1. malleable.30) 1.500) .421 (.200 (.00 (1.362-.40) 1.500-.50) 1.10 (1. and nonferrous alloys.30) .70) 1.20-1.500-.00 (.800) 1.20-1.452) .300) .20) 1.400) .366) * * .255) .700) .400 (.500-.412 (.3. and 03-04 are 0.300) .368-.500-.500) . 01-02.600 (.304 (.400) .395 (.500-.00 (. U.40-1.500-.600 (.50-1.300-.200-. during refining of lead and copper from sulfide ore.10 (1.900-1.700) 1.20) 1.300-.60) 1. coatings and plating.900-1.700-1.600 (.600) .10 (1.200-.400 (.400-.333 (.367-.400-.S.80 (1.400 (.400) .600) .400 (.10) 1.00 (.20) 95th 1.300 (.300 (.10 (1.300-.600 (.40) 1.600) .331) . Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.800) .304 (.900-1.600 (.300 (.300-.300 (.266-.400) .300-.60 (1.400) .900-1.300-.300-.20 (.300-.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .300) .500-.600-.500-.600 (.50 (1.400-.300-.424) * .40-1.00-1.40 (1. see Data Analysis section) for Survey years 99-00. population from the National Health and Nutrition Examination Survey.393 (.40 (1. plastic stabilizers.400-.700) .10 (1.300 (.20) .70) 1.70) 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 .300 (<LOD-.10 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.500-.50 (1.00) .300 (.400 (.300-.300-.400) .20 (1. 7440-43-9 General Information Cadmium is a soft.20-1.500) .500 (.400-.300) .400 (.600) .300-.400-.

Cadmium in soil is absorbed by plants.273 (.092) .195-.192-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 0.238-.82) 1.206) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.22 (.226) .065-.178-.34) 1.170 (. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.283 (.790 (.253-.858 (..13) .550 (.03) .28-1.519) . 2003.433-.219 (.510) .148-.790 (.870) .115-.919) .241) .15) .202 (.190-. and 0.25) 1.238) .160) .299) .150) . an inducible metal binding protein.247) .306 (.41 (.219 (.189-. including many food crops such as cereal grains.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.450 (.360) .43) 1.918-1.200 (.170-.481) .239 (.492 (.310) .766 (.077 (.530 (.263) .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.135-. rice.817 (.220 (.202-.482) .350 (.151-.173) .S. Cadmium absorption may be increased with iron deficiency (Berglund et al.067-.280 (.329 (.38) .623) .855-1.171-.189) .400-.733) .193 (.980-1.880) ..394-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.366) .763-.960 (.705-.13-1.430-.112-.310 (.090) .190-.875 (.279 (.381-.06.72) 1.078 (.717-.388-.38) 1. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.270 (.800-.462 (. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.860) 1.458 (.452 (.220) .839 (.366-.231) .194-.977) .32 (1.281 (.13 (. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.980 (.20 (1.989-1.800 (.320) .390-.455 (.390-.153-.255) . 200 Fourth National Report on Human Exposure to Environmental Chemicals .290-.730-.201 (.240) .261-.38) 1.963-1.313) .06-1.282 (.160 (. and 03-04 are 0.067-.170-.475 (.04 (. population from the National Health and Nutrition Examination Survey.436-.211 (.507) .200-.25 (1.216 (.184-.110-.519) .128 (.596) .249-.980-1. 2003).308) .51 (1.192-. wheat.741-1.700-.510-.191-.260 (. For nonsmokers who are not exposed to cadmium in the workplace.092 (.20 (1.15 (.810-1. see Data Analysis section) for Survey years 99-00.960) 1.01 (.210) .300 (.387) .500) 90th .100-.980) .450 (.229) .260-. respectively.47) 1.493-.12 (.700-.400-.210 (.820-1.714-1.191 (.17 (.196-.193-.203) .101) . potatoes.219 (.200 (.640) .316 (.38) .01) .198) .20-1.06) .713) .322 (. interval) .57) 1.230) .06.302 (.061-.892 (.220-.220-.633-1.081) .36) 1.848 (.134) .540) .351-.22 (1.221 (.** Survey Geometric mean (95% conf.177-.295) .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 .204 (.061 (<LOD-.300) .249) .30-1.Metals 2000).277 (.24) 1.700-.189-.10 (1.107-. 01-02. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.04 (.886-1. 2003).210 (.466 (.232 (.206 (. ingestion through food is the largest source of exposure.17 (..109 (.426 (.221) .456-.17 (.222) .551 (.753-.087-.48 (1.160) .210 (.633 (.181 (.843-1. and various seeds.261-. however.20 (1.199 (.813 (.136) .580) .06-1.157-.12-1.412) .227 (.09-1.390 (.890 (.890-1. whose body burdens of cadmium can be approximately twice that of nonsmokers.362) .26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .836-1.077 (.490) .74) 1. 1999.214-. Kikuchi et al.167-..15) 1.610) .589 (.120 (.209 (.141 (. Diamond et al.440-.160-.820 (.551) .326) .210 (.211-.423-.06.090) .17) . zinc.530) .940-1..255) . To a lesser extent.366-.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .289-.28) 1.820) 1. copper) and protein.272-.080 (.150-. calcium.440 (.237-.210) .235) .233) .445 (.126) .233) .169-.190-.232) .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 .393-. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.07-1.354) .607) .440 (.02-1.140 (.886) .447 (.179-.748-1.20) 1.243-. 2001).223 (.470-.262) .372) .430) .498-.251) . The kidney is a critical target and shows the earliest sign of cadmium toxicity.818 (.180 (. drinking water is a source for cadmium intake.230 (. 2004a.148) .875) .135 (.234 (.479) .806) .972 (.285-. Inhalation of cigarette smoke is a predominant source of exposure in smokers. With chronic exposure.980) . Renal tubular and glomerular damage.246) .733-.229) .255) .01-1.680 (.500) .339) .109-.686-.892-1.270 (.060-..203 (.545 (.208-.284) .19) 1.52 (1. Cadmium is absorbed via inhalation and ingestion.157) .229-.191-.330-.175 (.28 (1.165-.183-. 1994).539) .210 (.990) .207-.476-.480) .257) .130 (.265 (.187 (.260-.200-.83) 1.490) 1.559 (.230) 75th .175 (.520-.817 (.327 (. 2003).445 (.240-.114-.257-.265) . Horiguchi et al.336) .121 (.

077-.075-.653) .518) .274) 1.719 (.687 (.767 (. At lower environmental exposures.792 (.927-1..08) 780 682 614 546 667 717 760 1132 1070 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 * Not calculated: proportion of results below limit of detection was too high to provide a valid result.813-.156) .150-.329 (.364) .487 (. 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.484 (..884) .157-..093 (.757 (.700) .304) .184-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.158-.071 (.551) .263-.754) .856 (. 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.. 1996. can result from high dose chronic exposure.350) .288 (.280 (.166 (.423-.144-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.218) .500-.228-.391-.441-.168-.917) .338 (. population from the National Health and Nutrition Examination Survey.795) 1.219 (.240) .225) . 1999).126 (.140-.423 (.238-.00 (.147-.813-1.516-.181-.199 (.740 (.236-.789 (.224 (.107) .086 (.767) .223) .828) .075 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 201 .184-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.112) .210 (.222-.10) 1.722-.839) .700 (.136-. 1999).255-.674-1.537-.229) .201-.202 (.204-.729 (.381-.154-.085 (. 2002.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .101) .174-.216-.143-.253 (.300-.208 (.207) .865 (.304-.873 (.171-.802 (.440) ..104) .476) .545) .449) .507-.183 (.247-. 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..712 (.806-1.929) .388-.267 (.531 (.318 (. Jarup et al.906) .414-.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 .281) .412 (.421 (.630-.02 (.687-.07) .17) .377-.234) .00 (.691-.645-.12) 1.137 (.148 (.219 (.38) .479 (.247-. 2002.21) 1121 1334 1277 1136 1355 1266 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 .919 (.536 (.783) .282 (.263 (.194-.209) .481 (.05) 1.084 (.856) .501 (. 2004b).273 (.163) .074-.098) .418-.473 (. 2004).232) .444-.175-.159 (.559-.168 (. most often a result of occupational exposure (Roels et al.113-.663 (.316) .209) Selected percentiles ( 95% confidence interval) Sample 95th .727-.826-1.440) .433-.336-.091 (.206-.162 (.292) .909-1.196 (.725-1.253) .288-.325 (.178) .185 (.560-.199-.130-.252 (..067-.191 (.123-.784) .09 (.690-.818) .267 (.226) 75th .234-.175 (.541) .321) .239-.414 (.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .06 (.266) .159 (.446) .122 (.631) .S.123-.208-.16) 1.084-.288) .261 (.268 (.189-.250) .187-.415) .238) .205 (.826-1.200 (. During the 1950’s and 1960’s.085-.779 (.146-.136-.716-.100 (.757) .382) .667) .940 (. Noonan et al.135) .340) .708-1.296 (.143-.297) .431) .693 (.538) . However. 2003.106) .210) .352) .225) .308) .091) .491-.182) .178-.096) .261-.154 (.311) . 2002.241) .432 (.293-.833-1.678-.418) . 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.07 (.650-.614) .850) .163 (.210 (.998) .185) .215 (. 2000.438-.183) .931 (.696-.147 (.181 (.104) .668-.156 (.** Survey Geometric mean (95% conf.979 (.818) . Staessen et al.303) .131-.690 (.240) .191) .156-.242) ..Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.197-.783 (.247-.187) .212 (.111-. Horiguchi et al.175 (.533) .490 (.398-.137-.289) .343-.830) .181) .917 (.094) .874-1.16) .232) .173 (. 1999).198) .078-.227-.182) . Olsson et al..830-1.270 (.387 (. 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.097) .591 (.562-.470) .283 (.063-.850) .168-.245 (.051-.716) .177) .266-.718 (.261) .157-.181 (.190 (.256-.426-.617 (.147-.827) .438) 90th .192) .470) .472) .235) .622 (.182) .191-.387-.434 (.140-.331 (.666-.170 (.281) .316 (.940-1.184) .308 (.08) .078 (.278) .941 (.173-.170-..690-. interval) .161-.876-1.404 (.688-.211 (.083-.190 (.647-.176 (.207-.950) .686 (.221 (.13) .143) .382-.234 (.962) .678 (.335 (.221-.090 (.404) .233 (.985 (.769 (.289) .607) .176 (.220 (.091 (.

Salpietro et al. Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 mg/gram of creatinine (Akesson et al. Women had higher blood and urine cadmium levels compared to men of similar ages.. 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).. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. Creatinine-corrected urine cadmium values in U. Staessen et al. potentially fatal pneumonitis (Fernandez et al.. Noonan et al. as may occur from welding cadmium-alloyed metals. 2000. Jin et al. 2002. 1999). 2000).. 2003. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. Moriguchi et al. maternal blood or maternal urine and birth weight (Nishijo et al.html. Friedman et al. Zhang et al... Ezaki et al. 2003). 2004.. 1988). Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al.. For NHANES 19992000.. 2006). Olsson et al. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.1 mg/L (Alfven et al.. Information about external exposure (i.. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. 2002. 2002. Occupational standards are provided here for comparison only. 2005. intermediate in former smokers and lower in never-smokers (Becker et al.. CDC. Becker et al. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. Olsson et al. Jarup et al..cdc.. 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. 2002. 2002). 1996). 2006). Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. Olsson et al.... 2000.. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. 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. environmental levels) and health effects is available from ATSDR at: http://www. 2004b. Cadmium can produce lung. 2006... Becker et al. 2000.. 2005). 2002)... 2002. Horiguchi et al. Both IARC and NTP consider cadmium a human carcinogen. has resulted in severe. Wennberg et al... In postmenopausal women. 2006. 1999).. Becker et al. with peak values observed in the fifth to sixth decades (CDC. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. 2004). Komaromy-Hiller et al. and drinking water and environmental standards have been established by U. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles... decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al.. Jarup et al. 2003. Further research is needed to address the public health consequences of such exposure in the United States. 2005. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. not to imply a safety level for general population exposure. respectively. In the typical environmental exposure. Wennberg et al. Suwazono et al. 2002).46 mg/gram of creatinine) (Ezaki et al. 2005. 2003. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH.. 2004.. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. In adults aged 60 years and older. 2004b). 2004. 2003.. 2002). Staessen et al. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Wilhelm et al. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . respectively. Staessen et al.e.atsdr. 2002).. However.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. 2005. data (CDC. 2004.. Acute and heavy exposure to airborne dusts and fumes. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. 2002) and length at birth (Nishijo et al... approached these values associated with subclinical changes in renal function and bone mineral density. 2002.. Horiguchi et al..gov/ toxpro2.S. 2003...26 and 3.S. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC.. 1996. Mannino et al. study subjects living near a former zinc smelter were similar to those from an unexposed community and to those in this Report (Noonan et al. Animal studies have demonstrated reproductive and teratogenic effects. EPA.S. Ezaki et al.. 2003.

Seifert B. Nerbrand C. Ukai H. Jarup L.354:1508– 1513. 206:15-24. Occup Environ Med 2000. Kaus S. Occup Med 1996. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Furuki K.46:372-374. Seiwert M. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Kundiev YT.76:186-196. Oguma E. Mucha A. 196:114-123. Toxicological profile for cadmium update. Sanz P.110:699-702. Taylor AJ. Diamond GL. References Akesson A. Elinder CG. Lukyanova EM. Jones RL.95:20–31. Lepom P. Kaus S. Palomar M. Consonni D. Horiguchi H. Kikuchi Y. Costa R. Atlanta (GA). Schulz C. Fayers PM. et al. Agency for Toxic Substances and Disease Registry (ATSDR). Fatal chemical pneumonitis due to cadmium fumes.59:497]. possibly better than b2microglobulin. Centers for Disease Control and Prevention (CDC).gov/toxprofiles/tp5. Vahter M. Komaromy-Hiller G. Sasaki S. Ash KO. Choudhury H. Environ Health Perspect 2005. Toxicol Lett 2004. Fernandez MA. et al. et al. Machida M.13(11):1627-1631. Lundh T. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Uemura T. Anthropometric. Moriguchi J. Mascagni P. 102:10581066. Moriguchi J. Clin Chim Acta 2000. Friedman LS. J Toxicol Environ Health 2003. Environ Health Perspect 1994. Bregante G. Fukui Y. Hellstrom L. patient population and literature reference intervals for urinary trace elements.148(1-2):11-20. Toxicol Appl Pharmacol 2004a.S. Chislovska NV. Miyamoto K. Nermell B. Venables KM. Krause C. Nomiyama T. et al. Persson B. Mannino DM. Ezaki T. 1999 [online]. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Alfven T. iron deficiency. Thayer WC. Thorax 2004. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. et al. Machida M. Hotz P. Environ Res 2006. et al.cdc. Akesson A. Environ Res 2004.96:353-359. Comprehensive study of the effects of age. Gadea E. Chiappino G. Jin T. Holguin F. Berglund M. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Available at URL: http://www. Bo M. Toffoletto F. Schulz C. Zhu G. Lidfeldt J. Ikeda Y. Environ Res 2004b. et al. Ezaki T. Okamoto S.205:297-308. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Nordberg G. Bernard A. Darbyshire J. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Ikeda Y. Environ Health Perspect 2002. Carlsson MD. Becker K. Horiguchi H.66(Pt A):2141-2164.102:83-89.S. Kumagai N. Wang H. Buchet JP. Fukui Y. Lison D. et al. Dekio F. Int J Hyg Environ Health 2002. Oguma E. Int Arch Occup Environ Health 2003. Bellerup P. J Occup Health 2003. Grubb A. Takebayashi T. Stock AL. Cadmium fume inhalation and emphysema. Third National Report on Human Exposure to Environmental Chemicals.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. 4/8/09 Alfven T.html. Int J Hyg Environ Health 2003. Vahter M. et al.296(1-2):71-90. Savage-Brown A. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake.atsdr. Tsukahara T.1(8587):663-667. et al. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Tsukahara T. Howerton K.000 women in the Japanese general population: a nationwide large-scale survey. ShkiryakNizhnyk AZ. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Olfactory function in workers exposed to moderate airborne cadmium levels. Lauwerys R. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Ye T. Lancet 1999. Davison AG. Greves HM. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. et al.57:668-672. Miyamoto K. Serra J. population.59:194-8. Pickering CA. Comparison of representative ranges based on U. Furuki K. Jarup L.24:717-724. Becker K. Sasaki S. environmental. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Neurotoxicology 2003. diabetes mellitus.45:43-52. Seiwert M. Lancet 1988. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. 2005. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers.

Bergdahl IA. Lundh T.epa. et al. Kobayashi E.110:151-155.gov/ttn/atw/ hlthef/cadmium. Honda R. et al. Zhu HD. Staessen J. Relationship between newborn size and mother’s blood cadmium levels. Bruiglia S. Biological monitoring of cadmium. Roels H. Noonan CW. Nakagawa H. Sager PR. et al.84 (Section A):4455.S. Lauwerys R. Mutat Res 2003. Toyama. Ginucchio G. Arch Environ Health. lead. Biological monitoring of toxic metals. eds. Int J Hyg Environ Health 2006. dietary intake. Environmental exposure to cadmium. 2001. Nakagawa H. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. Vangronsveld J. Japan. Environ Res 2000. New York: Plenum Press. Jansson J-H. Cadmium in blood and urine – impact of sex. and former smoking – association of renal effects. Nordberg M. Kathman SJ. Hazard Summary. Lybarger JA. lead. Schultz C. et al. Environ Res 2006.3:26-41. 4/8/09 Waalkes MP. and mercury in the population of northern Sweden.Metals Nishijo M. Environ Health Perspect 2002. Skerfving S. Emelianov D. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. Occup Environ Med 2002. United States Environmental Protection Agency (U. Buchet JP.209:301305. cadmium. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Kido T. et al. Minciullo PL. Suwazono Y. Cadmium carcinogenesis. Bensryd I. Schwenk M. Tanebe K. Campagna D. Lison D.39:2507-2515. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Stegmayr B. Stelitano A. created 1992. Gangemi S. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. Lundh T. Ottosson H. Zhang YL. EPA). Time trends in burdens of cadmium. Kuznetsova T. 2000. J Cardiovasc Risk 1996. Cadmium compounds. Okubo Y. Mueller PW. Honda R. Merlino MV. lead. iron status. age. Wennberg M. Sarasua SM.353:1140-1144.110:1185-1190. Nishijo M. Staessen JA. Olsson IM.59(1):22-25. J Environ Sci Health B 2004. Wilhelm M. Fan YG.21(3-4):251-262. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Wang JX. 2004. Environ Health Perspect 2002. Nogawa K. Effects of exposure to low levels of environmental cadmium on renal biomarkers.59:394-397.533(12):107-120. Revised 2000 [online]. Available at URL: www.html. and risk of fractures: prospective population study. Revised and new reference values for arsenic. Lancet 1999. Liu QF. Salpietro CD. Lijnen P. forearm bone density. Nordberg GF. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Tanebe K. Friberg L. Nordberg GF. pp. J Perinat Med 2002. Zhao YC. Nakagawa H. Tawara K. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Ren Fail 1999. Saito S. Roels HA. In: Clarkson TW.100:330-338. Gallmans G. 151-168. Oskarsson A.30(5):395-399. Thijs L. Hoet P. Usefulness of biomarkers of exposure to inorganic mercury. Roels HA. et al.

0) 12.04) 7.83) 6.63-4.55 (4.4) 95th 11.89-5.49) 4.56) 5.20 (4.87-7.59-5.26-11.1-13.2-13.9) 12.95 (3.5) 12.87) 5.60-12.0) 11.99-11.2-13.40-5.77-8.12-5.30 (6.90 (6.90-12.5-16.8) 12.80-10.16-6.9) 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 4.3 (8.68) 9.13 (5.9 (11.08 (7.95-4.20 (6.8) 11.80) 7.38) 5.20) 5.81) 4.08) 7.70 (6.0) 11.77 (4.60) 5.14.25) 4.53 (6.44 (8.87 (4.70) 5.50 (7.40) 5.01) 7.5-14.03 (4.2.83-4. infrared lamps.42) 6.2) 11.47-8. For absorbed cesium salts.49 (4.4) 10. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.70 (8. cesium hydroxide is corrosive and irritating at high concentrations.50 (4.62 (5.96 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00.4-13.60-5.67 (4.99-6.26 (3.00) 4.29 (4.94 (4.30-5.3-15.81) 4.08-5.60-6.32 (3.52-9.40-5.6) 11.8) 12.6 (11.3) 9.0) 12.20) 8.5) 10.40) 5.50) 9.35 (4.40-5.17) 4.4) 10.13-8.26) 4. and as polymerization catalysts.59) 7.34 (4.3) 10.77 (9.20-5.54-11.56-11.10-5.97) 4.91-8.36) 3.25 (3. Radioactive 137Cs has been used medically to treat cancer.90 (4.22 (4.81-14.56 (4. However.1 (9.74) Selected percentiles ( 95% confidence interval) 50th 4. photographic emulsions. and high-power gas-ion devices.00-8.05) 5.86-12.8) 12.94-4.10 (6. scintillation counters.3) 12.12) 5.7) 11.20-8.81) 9.97-7.84 (4.55 (7.80 (4.8 (10.98 (7.0-15.50 (4.32-5.53-11.70 (8.02 (4.61) 7.7 (9.4 (9.98 (7.71 (8.33 (6.2 (9.80 (8.40-11.16-6.39) 7.60-7.64 (4.37) 7. and 03-04 are 0.35 (4.34) 9.71-9.2) 12.3) 10.50-7.7 (11.63 (4.79 (4.64) 5.64-5.13 (8.90) 7.76-6.24) 4.59 (5.87 (4.09) 5.84-5.33 (5.89) 4.60-6.62 (5.03 (4.82-4.7 (10.9 (11.90-10.20) 4.1-12.61-6.7 (9.20-4.54) 4.68 (7.30-10.62) 4.30) 7.49) 75th 7.9 (10.14. respectively.86 (7.08-5.6 (11. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.08 (6.3-13.80-11.86-11.13 (7.00-8. 0.90) 4.7 (10.73-5.10-7. semiconductors.36 (6.3) 10.5 (8.6 (9.30 (6.04 (4.4) 9.57-5.9 (11.6) 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 4.1-12. although cesium was generally of low toxicity when given to animals.1) 11. 2004).Metals Cesium CAS No.3 (8.71) 4.40 (4. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.80 (8.3) 10.90-10.29) 4.0) 9.95) 5.1) 9.64) 5. and cardiac arrhythmia (ATSDR.80-6.5-13.55-11.88 (8.7) 10.81 (4.4 (10.74 (4.10 (6.27) 4.64-10.43-8.40-7.26) 7.5-14.17-6.00 (7. interval) 4.70 (9.99) 7.93 (4.31-8.43 (5.32) 4.21) 90th 9.7 (8.5) 9. nausea.50) 5.01-8.25-5.09-5.5 (10.39-4.3-13.8) 11.94) 4.20) 7. Most human exposure to cesium occurs through the diet.27 (7.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.01-6.4 (9.40) 7.12 (4.59-5.69-6.63) 6.8) 9. the body half-life is estimated to be 70-109 days based on 137Cs exposures.10-8.37) 5.30) 5.2-13.73-11. soil.97 (7.80-10.00-10.17 (6.42-7.50 (4.70-8.6 (9. Little is known about the health effects of this metal. Inorganic cesium compounds are used in photomultiplier and vacuum tubes. and 0.00) 6.4) 11.2-14.33-5.4) 12.7) 10.0) 10.99-11.20-7. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.94 (4.0 (9. and clay.23-4.80 (4.00-9.03-4.56 (4.59-5.05-5.77 (9.2 (9.80 (4.10-9.70 (5.50 (6.1) 9.46) 7.80-13.45-5.70) 5.70) 7.00) 7.90-12.1) 10.80-10.10 (8.99) 9.70-5.22-4.90-10.60-7.84) 8.8 (11.71-5.9) 11.40-11.90) 9.0) 12.35-5.4) 12.47-4.6 (9.0 (10.10 (8.23) 9. population from the National Health and Nutrition Examination Survey.05-5.2-12.07-11.9 (10.82) 5.40-5.45-8.8 (10. Fourth National Report on Human Exposure to Environmental Chemicals 205 .0-13. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.15-8.42) 7.6 (9.90) 5.90-8.60) 7.14 (4.66 (7.84) 5.60) 7.27-5.74-5. diarrhea.80 (8.89) 5.72-7.6) 10.05) 5.07) 4.7-14.72) 4.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.8) 9. 01-02.21 (4.1 (10.S.7 (10.92-13.12-11.70 (4.9 (11.60 (7.49 (5.7) 11.52) 7.60 (8.1 (11.70 (6. Whether cesium compounds are carcinogenic is unknown.00-4.7 (9.71-8.9) 8.1) 11.91 (7.36 (3.9) Total 4.84-9.87 (4.64) 4.71 (4.90) 5.8-13.

68) 4.94) 7.89-4.43) 8. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.14-6.22 (3.65-3.59-8.76-9.88-4.39) 8.17-4.05 (4.92) 3. population.27 (6.10 (3.97) 8.83-7.40-5.52-5.08-3.24-4.08) 4.13) 7.21 (2.71) 6.99) 4.55 (3.0 (7.47) 7.16) 5.47 (7.63 (6.42 (4.29) 4.84-7.77 (6.16-5.28 (5.3) 11.99-9.20) 5.40) 7.63 (4. and were also roughly similar to those in this Report.78) 4.08 (5.64) 4.10 (5.43 (8.57) 3.96-4.81 (4.93-7.05) 6.47 (4.50) 4.04-11.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.66 (6.3 (9.08-7.97-5.07-4.81 (4.13-9. population from the National Health and Nutrition Examination Survey.24-10.4) 10.29-3. Two small studies of European populations reported urinary cesium levels similar to U.15-11.83) 8.3 (8.91 (5.27-4.84-7.07) 8.46-8.67) 5.27 (8.91) 4.50 (6.90-8.87) 5.17 (6.95) 4.03) 6.30 (7.43-6.10 (3.41-7.8 (9.50) 4.06) 4.20-4.68) 3.73-4.43 (4.75-11.93-9.13 (3.29-3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.41) 4.56 (4.03) 5.5) 9.44-9.0) 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 .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 (3.22-11.30) 10.41 (4.84-9.26-6.79) 4.99-4.82-4.41 (8.19-6.70 (7.14-7.08) 4.79 (5.98) 5.77) 4. (2000) found urinary cesium levels that were slightly lower than those reported for the U.18-7.05-4.22) 6.99 (3.18-6.86 (4.51 (3.85) 5.31-6.35) 3.27-6.65-4.47) 6.30 (3.02-4.9) 10.9 (9.41 (5.54 (4.S.11 (5.50-5.20-4.03-5.5 (9.63-6.17) 4.60 (3.56) 3.06 (3.21-4.51) 4.39) 5.27) 4.71 (7.00-10.60) 3.6 (9..70) 6.88-10.53 (4.55-5.90-8.63) 6.38 (3.91-7.37-3.24 (3.54 (5.00-5.96) 4. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.51 (7.68) 6.53) 6.12) 3.95-6.6 (9.54 (4.08) 3.98) 5.8) 6.56) 4.20-4.66 (5.33 (5.2 (8.47) 6.56) 4.43-11.51 (3.35-7.60-20..84-9.96 (4.75 (7.79) 9.36-6.38-12.14 (6. Minoia et al.64 (4.74 (4.14) 4.11 (5.62-8.78) 4.18 (7.26 (4.60-10.95 (3.73 (3.42-6.30-4.5) 7.78 (3.0) Total 4.91-9.66-6.03-6.09) 8.51 (4.82) 7.91) 5.53) 3.94 (5.15 (7.46) 6.33-3.42-4.68-11.29) 4.77-5.2 (8.47) 4.96) 4.04-5.09 (4.55) 4.30 (4.39 (5.00-8.8) 10.43 (4.97-4.56-10.85) 4.S.26 (3. Using clinically submitted specimens.80) 6.36-3.78 (3.91-6.68 (4.61-3.05-3.74 (5.33 (5.58 (6.29) 5.8) 5.01-8.87) 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 5.65 (6.62) 5.49) 3.27 (6.77 (7.14-4.58-5.09) 4.6) 6.50 (5.S.37) 4.21-5.42 (5.16-8.59) 4.83-6.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.95-12.38-7.95) 10.41-4.12 (3.74) 3.21-3.98 (6.44) 3.44 (4.04) 5.76-6.50) 8.79) 6.3) 9.58) 3.5) 9. 2005.1) 11.72 (4.00 (8.7) 10. 2004).10) 7.30-4.66 (5.48) 7.06 (5..64) 5.02 (5.07 (5.67 (5.63-6.08 (6.96-4.31 (4.04) 6.33-8.2) 11.53 (6.91) 5.05-3.7) 10. population results shown in this Report (Alimonti et al.87 (5.28 (4.58 (4.72) 4.51 (4.74-11.17) 9.77 (4.54 (3.48) 90th 7.48-6.43 (3.34 (5.44-5.46 (8.79-5.41) 9.46 (7.91 (5.64-6.19-3.95 (5.70) 7.0) 7.67 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.35 (4.36-10.50 (7.60 (5. 1990).95) 8.58) 8.10-4.61 (7.25) 4.23 (7.20-8.74) 75th 5.12-6.98 (7. interval) 4.13-9.90 (7.00) 6.30) 10. Komaromy-Hiller et al.50) 4.63 (7.35-11.14) 4.15) 95th 8.06) 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.85-4.16-8.00-4.45-6.31-4.64) 9.92 (5.99-9.15-4.46-4.18) 8.75 (6.40) 6.38) 10.00-9.38 (3.00-5.7-12.07) 8.3-15.25) Selected percentiles ( 95% confidence interval) 50th 4.45 (4.31 (4.05) 3.42-4.3 (10. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.84-11.28) 7.28) 8.72-5.87-4.44 (8.9 (10.64 (8.90-3.35 (3.

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

950) .07.04) 1.428-.04 (.431) . Cobalt compounds are used as catalysts in producing oil and gas.15-1.280-.570-.07-1.583) .350-. 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. varnishes. industry is imported or obtained by recycling scrap metal that contains cobalt.470 (.810-.380-.23-2.16 (.12) 1.33 (1.73) 1.850-1. and soil. Usual human exposure is from food sources.410) .880-1.29 (1.81) 1.400-.520) .333-.710 (. large appliances.670 (.700) .820 (.390 (.520-.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.640) . and in synthesizing polyester and other materials.99) 1. and inks. Cobalt occurs naturally in airborne dust.540-.460) .32 (1.03) 1. steel-belted radial tires.350-.496) .650-.22-1.07-1. blue-colored pigments.440-.390 (.640) .340) .660) .285 (.910-1.316-.360-.610-.16 (1.490-.515 (.434 (.750 (.370 (.543) .600 (.480-.16-1.398 (.930) .390-.760) .480 (.01-2.690-.359 (.S.22) 1.740-.790-.890) 95th 1. interval) .461 (.369 (.290-.377-.460 (.499 (. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.05 (.08.320 (.418 (.370-.610 (.620-.416) .16) 1.570) . and 0.370-.950 (.370) .17 (1.465) .940-1.370-.790 (.770) .590-.04-1.650 (.291-.424) .950-1.373-.435 (.520-.430 (.430 (.56) 1.23) .28 (1.460 (.48) 1.380 (.380 (.394) .460) .550-.45 (1.930-1.64) 1.32 (1. and fertilizers.670-.820 (.940 (.650 (. The cobalt used in U.452 (.660-.373) .67) 1.364-.810) .08-1.980) .07 (.570 (.270-.540-.410 (.600-.39) 1.09 (.339 (.890-1.374 (.52 (1.487) .330 (.310 (.09) .890-1. and magnetic recording media.01 (.670 (.640) .630-.06 (.313) .520-.47) 1.810) .590-.790) .523) .270-.510) 1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.393-.28 (1.42) 1.430) .26) 1.850) .870-1.760 (.59 (1.399) .47) 1.379 (. and 03-04 are 0.410 (.355-.316 (.540-. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.460) .340-.450-.750 (.417) .530) .340) .47 (1.S.16 (1.14-1. shiny. hard metal (alloys of cobalt and tungsten carbide). 0.350-.460-.331-.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 . 01-02.850-1.520 (.33-1.710) .17-1.680 (.301 (. Cobalt is used as a drying agent in paints.300-.710) 1.890) .580 (.26-2.350 (.610) .690-.259-.470) .05 (.500) .348-.65) 1.305-.410 (. Cobalt compounds are also used in manufacturing battery electrodes.22 (1.950 (.07.294 (.386) .20 (1.620-.17 (1.319) .880 (.02-1.340-.900-1.860 (.327-.16) 1.580 (.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 .581) .06 (.430-.519 (.410-.360-.26) Total .430) .380-.950-1.900-1.430 (. population from the National Health and Nutrition Examination Survey.630 (.28-2.700) .900) . see Data Analysis section) for Survey years 99-00.404) .570-.25-1.550) 90th .820 (.371 (.03) .334) .800-.333-.450) .390 (.450) .390) .900) .343 (.564) .680 (.68 (1.16-1. diamond-polishing wheels.480 (.454 (.03 (.960-1.32-2.450) .469-.21) 1.06-1.920) 1.00) .388-.360-.04-1.08) .410-.19) .48) 1.580 (.420) .463-.900) .570) .352 (.690 (.630 (.53) 1. It is emitted into the environment from burning coal and oil and car and truck exhaust.12) 1.550 (.60 (1.420 (.379 (. hard metal or in combination with other elements.24 (1. It is also a component of porcelain enamel applied to steel bathroom fixtures.01-1.15 (1.05) 1.980-1.730) 1.75 (1.420) .590) .520 (.500 (.350) 75th .50) 1.590 (.28 (1.680) .920-1.930 (.26-1.520) .338-.03) 1.670-.530 (.410) .850) 1.32) 1.14) .398) .740-.13) 1.348-.Metals Cobalt CAS No.840) .610) .04-1.410 (.502) .520 (.620) . seawater.03 (.50 (1.740 (.427-.830-1.490-.670 (.01 (.540) 1.380 (.414) .600) .308-.47 (1.410-.24 (.03-1.450-.375 (.890-1.310-.800-.620-.660) .37-1.450) . 208 Fourth National Report on Human Exposure to Environmental Chemicals .680) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.81) 1.92) 1.940-1.870 (.336-.36) 1.520-.530-.431) .340 (.17 (. automobile airbags.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 .372) .419) Selected percentiles ( 95% confidence interval) 50th .520 (.410 (.540-.270-.32) 1. respectively.800) .750 (.870 (.750-.09 (.367 (.300 (.46 (1. and kitchenware.405-.330) .44) 1.330-.560 (.

826-1.313-.500-. with pulmonary clearance half-lives of from one to two years (Hedge et al.550-.963-1.16) .847) .303-.644 (.487-.563-.616-.595) .707) .471-.435-.455 (.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 .361-.28) 1.378 (.272-.353 (.786-.833-1. 1994).25 (..457-.243-.368) .667-1.363) .290 (.29) 1. 1972).306) 75th .54) 1. 1979).898 (.976 (.248-.632-.358 (.442-.593) .634-.895-1.781-1.50 (1.638-1.03 (.278 (.561) .691 (.257 (.15 (.337 (.372) .328 (.421) .15) 1.317 (.29 (1.298 (.06 (.452-.335 (. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. cobalt is excreted predominantly in the urine.582-.02 (.600-.326-.990) .407 (. 2003).417 (.844 (.234 (.215-.275-.409) .983) .324-.463-.57) 1.417) .393-.381) .378-.11-1.09) 1.402 (.360) .268 (.513 (.444 (.279) .16 (.342-.313-.708) . Once absorbed and distributed in the body.49) 1.378-.662) .316 (.753-.895-1.301-.60) 1.505) .938) .343 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.376 (.12 (.23 (1.328 (.785) .821 (.257-.319-.495 (.615) .781) 95th 1.457) . Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.872 (.24) .469-.300) .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 .301) .256-. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.362-. Cobalt is absorbed by oral and pulmonary routes.50) 1.04-1.289) .760-1.479) .27) 1.50) 1.581) . interval) .829) .393 (.286) .296-.353-.331-.861 (.428-.792-1.259-.314 (.554 (.16 (1.728 (.282 (.407) .362) .911-1. or using diamond-polishing wheels that contain cobalt metal. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.10 (.277-.36) 1.297-. population from the National Health and Nutrition Examination Survey.522) .396) .487-.468) . A portion of cobalt retained for long periods is concentrated in the liver.700 (.857-1.250) .369 (.929) .606 (.667-1. 1994.757-1.313 (.738 (.278-.425-.736-.327 (.384) .523 (.523 (.29) .273 (.309) .737 (.382-.361 (.290 (.534-.365-.694) .429) 1. in the feces.513-.433) .290 (.10-1.400 (.598 (.251-.963) .975 (.329-.337) .313-.700 (.380-.963-1.324) .S.608 (.35) .352) .753) 1.534 (.03-1.344-.296) .44 (.352 (.11-1.33) .750-.457 (.35) 1.346 (.537 (.542 (.756 (.552 (.669) .738 (.388 (.842) .387) .964 (.352 (.471-.500 (. and to a lesser extent.548 (.673-.547 (.439) .703-.626-.310) .562) .00 (.33) 1.594) .640) .19) .396) ..274-.392 (.481) 90th .10) .723 (. Smith et al.479-.591 (.609) .04 (.515 (.388 (.475 (.960 (.476-.630-.361 (.Metals fabricated from cobalt alloys (Lhotka et al.850-1.900-1.704-.275-.529 (. using hard metal cutting tools.237-.829-1.533 (.29 (1.471 (.378-.362 (.990-1.333-.304-.259 (.304) .386 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin)..508-.488) .16 (.247 (.333-.635 (.00 (.259) ..279 (.248-.792 (.804) 1.281) .513) .297) .952 (.333-. refining or processing alloys.937 (..339-.29 (1.327-.365) .500-.963) .60) 1.850 (.434-. 1972).368 (.917) .302-.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 .449-.349) .611) .30 (1.419) .824 (.689 (.12-1.426 (.368) .774 (.574-.955) .355) .313-.27) 1.408 (.879-1. respectively.830 (.744) 1.293 (. an essential human nutrient.848 (.313-.683-.438) .329 (.348) . but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.36) 1.750) .467-.25 (.00-1.660-.10) Total .727 (.949) .733-1.435 (.462) ..333 (.599) .394) .425) .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 .391) Selected percentiles ( 95% confidence interval) 50th .821-3.323) .861-1.280-. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.73) 1.461) .777-.282-.503-.239-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.630-.838 (.938-1.955) .55) .562) .00 (. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.343-.391 (.306 (.449) .291 (.585) .983-1.543) .404-.554 (.83) 1.560-.361-.00) .647) .905) . Exposure in the workplace may come from electroplating.679-.728) .328) .611) .740-1.00) .932-1.294-.271 (.851 (.14 (.00 (.334) .17) .

White and Sabbioni. 2001.43(4):299-303. 2006. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. Dunstan et al.gov/ exposurereport/. usually in combination with tungsten carbide (Cugell et al. environmental levels) and health effects is available from ATSDR at: http://www. 1998). 2001. 1990). Alexandersson R. Morgan WKC. 2003. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al. not to imply that the BEI is a safe level for general population exposure. Swennen et al..S. Atlanta (GA). “Hard metal” disease. 1988). 1955). a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Hailey JR. 4/3/08 Christensen JM. Lison et al. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L. Urinary measurements mainly reflect recent exposure.. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. 1998). Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al.. Poulsen OM. Centers for Disease Control and Prevention (CDC). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Perkins DG. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al. Linnainmaa and Kiilunen. Information about external exposure (i.cdc. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda.. 1994.. 1994. For workers exposed to cobalt in the air. 1989). with mean levels that were about 15-20 times higher than in the general U. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al..atsdr. 2005...Metals Toxic effects of cobalt have been encountered in workplace settings. Available at URL: http://www.....e. Sills RC. 1972). Blood and urinary concentrations as estimators of cobalt exposure. Thomassen et al.gov/toxpro2. Haseman JK. Grumbein SL. 1992). Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. References Alexander CS. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. Sci Total Environ 1994. population results in this Report (Kristiansen et al.S.. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. MacDonald et al. 2005 [online]... 210 2006. Iavicoli et al. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. 1997). 1997. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals ... Cugell DW. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. Cobalt was once added as a foaming agent to beer. 1999).50(13):95-104. 1994). Rubin A. 1993). Am J Med 1972. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. Lauwerys and Hoet.. Toxicol Sci 1999. Krause et al. 2005. 2001. 1988). Cobalt-beer cardiomyopathy. Roycroft JR. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. Bucher JR. 1985. population (CDC. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al.. Third National Report on Human Exposure to Environmental Chemicals. Arch Environ Health 1988. Daniel et al. 2003).49:56-67. A clinical and pathological study of twenty-eight cases. although substantial occupational exposures have produced elevated urinary levels for many weeks. et al. A 1982-1992 surveillance programme on Danish pottery painters. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al.. Information about the BEI is provided here for comparison... 2001).html. Shirakawa et al..53:395417.cdc. has been associated with exposure to dusts that contain cobalt. 1993). Lisi. 2003.. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis.. 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. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al.

Schaller KH. Daniel J. Hammon E. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up.157:117121. et al. Moulin JJ.58(10):631-634. Hedge AG. Goto S. Falcone G. Dunstan E. Lauwerys RB. Bozec C.48:172-173. J Bone Joint Surg Br 2006. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Pradhan C.533:135-152. et al. Kriss JP. Outcome of occupational asthma due to cobalt hypersensitivity.87(5):628-631.242:1412-1415. Mosconi G. Lasfargues G. Int Arch Occup Environ Health 1997. Ghat IS. Linnainmaa M. Fujimura N. Occup Environ Med 1994. Laippala P. J Occup Med 1992. a study of 13 elements in blood and urine of a United Kingdom population.” Contact Dermatitis 2001. Hoet P. Long-term clearance of inhaled 60Co. Clin Orthop Relat Res 2003. Leghissa P. Zweymuller K. Peltier A.Metals effects of cobalt. Contact Dermatitis 2003.(1-3):133-139.51(7):447450. MacDonald SJ.28(5):1121-1128.148:241-248. Dickel H. Schramel P. Dunning SP. Rorabeck CH. Occupationallyinduced “isolated cobalt sensitization. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Heki S. 2001. Molders J. Angerer J. Cresti R.34:620-626. Smith T. Science 1988. Absorption and retention of cobalt in man by whole-body counting. Co-sensitivity between cobalt and other transition metals.20(1):25-31. et al. Buchet JP.22:359367.21(2):189-195. et al. Szekeres T. Cannon SR. Ichikawa Y. Boca Raton (FL): Lewis Publishers. Cleland D. salt. Schank M. Radulescu M. Epidemiological survey of workers exposed to cobalt oxides. J Rheumatol 2001. De Boeck M. Chest 1989. A report of two cases from mineral assay laboratories and a review of the literature. Zobelein P. Diepgen TL. Trace element reference values in tissues from inhabitants of the European Union. Kuska Y. Lhotka C.216:253-270.69(3):193-200. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Am J Ind Med 2003. Sanghrajka AP. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements.50(9):835-842. 1985. McCalden RW. Romazini S.204:147-160. et al. Iversen BS. 3rd ed. Tilley S. Kiilunen M. Int Arch Occup Environ Health. Thomassen H. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Am J Epidemiol 1998. Robinson C. Salvatori S. Sabbioni E. Sabbioni E.95:29-37. Goto S. Sci Total Environ 1994. Occup Environ Med 2001. Alessandrelli M. Swennen B.36:732-734.150.150:177-183. Swennen B. and cobalt metals. Cobalt and antimony: genotoxicity and carcinogenicity. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Blunn G. Vitali MT. Jarvis JQ. Lauwerys R.406:282-296. White MA. Kraus T. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Respiratory health of cobalt production workers. Br J Ind Med 1993. The release of metals from metal-onmetal surface arthroplasty of the hip. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Kristiansen J. Meier R. Chess DG. Thabe H. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Hoher T. Health Phys 1972. Linna A.44:124-132. Lung cancer risk in hard-metal workers.88(4):443448. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Oksa P. Gross RT. Palmroos P. Edmonds CJ. Ziaee H. oxides. Shirakawa T. J Orthop Res 2003. J Bone Joint Surg Br 2005. Lison D. J Trace Elem Med Biol 2006. Arch Intern Med 1990. et al. Barnaby CF. Bourne RB. Iavicoli I.45:246-247. Lauwerys R. Roto P. Goldberg MA. Zhuber K. and hard metal dust. cobalt salts. Stanescu D. Weyher I. Kato M. Biological monitoring of workers exposed to cobalt metal. Lison D. Uitti J. Buchet JP. Sabbioni E. Steffan I. Lison D. Wild P. Weber A. Bacis M. Christensen JM. Salama A. McMinn DJ.55(4):269-276. Unwin P.150(1-3):167-171. Zedda S. Kirsch-Volders M. DeSantis V. Bunn HF. X. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Mutat Res 2003. Sci Total Environ 1998. Pisati G. Sci Total Environ 1997. Meyer zum Buschenfelde K-H. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Health Phys 1979. HoffmannB. Thakker DM. Lisi P. Kusaka Y. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Sci Total Environ 1994. Carnes WH. Cobalt cardiomyopathy.

31) 1.87) 1.00 (5.40) 2.20) 4. ammunition.90 (3.10 (1.60 (1.70) 4.20-3.40 (3.75) 1.20-3.00-1.50) 75th 2.50-2.40-1.43 (1.942 (.50-2.90 (1.30-2.50-1.80) 2.30) 1.87 (1.00 (4.60) 3.60-2.90) 1.69 (1.20 (2.10 (4.20 (1. antique-molded or cast ornaments.90 (3.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.80-4.70 (1.10) 1.3.80-4.10-2.900 (. brass. 0.10) 2.S.00) 6.20-1.50 (4.90) 1.40-5.19 (1.30-4.80-3.93-2. blue-gray metal that occurs naturally in soils and rocks.81) 1.34-1.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.60-3.20) 3. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.90-2.62 (1.00 (4.60 (3.70-6. the main source of lead exposure for the general U.50-4.20-2.30-1.30 (2.20-3.00) 1.23 (1.80 (1.30 (4.37 (1.86) 1.30-1.90) 2.50-2.40-1.52 (1.20 (3.00) 4.40-2.60) 5.40) 2. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.50) 2.20) 5.00 (1.32-1.3.90) 2.80 (4. 212 Fourth National Report on Human Exposure to Environmental Chemicals .20) 3.90) 2.40-3.00) 5.90-2.60) 2.60-6.55-1.00) 3.20 (3.20) 3.80 (1.10-2.90-4.90 (1.40-3.50 (1. respectively.10-2.50 (1.37 (1. interval) 1.10-2.60) 2.40-1.14-1. solders.60) 1.90) 2.70) 1.60 (2.50 (3.36-1.70-5. leaded glass.00) 2.10-2.70 (3.10 (2.40 (2.60-1.30-2.80-3.50) 1.30 (1.32-1.39) 1.30-1.30 (2.40) 1.899-.60-4.39-1. Lead is most often mined from ores or recycled from scrap metal or batteries.60) 4.91) 1.71-1.10-1.60 (2.90) 2.80 (2.60 (1.43) 1.95) 1.40) 3.00-6.50 (4.66 (1.10-1.09) 1.20 (3.50-4.70) 1.90) 1.10 (2.30-6.60 (3.90-4.10-3.10) 2.10) 1.70) 1.80-3. Lead has a variety of uses in manufacturing: storage batteries.60 (3.60 (1.00 (1.90-3.900 (.70 (2.g.50-3.20 (4.25 (1.60) 4.70) 4.20 (1.00) 1.40-6.78 (1.70-1.60) 3.69 (1.30 (4.80 (5.20) 3.45 (1.50-3.55 (1.60) 2.45-1.65 (1.90) 3.70) 4.70 (5.20 (1.20 (3.80) 2. lead was added to gasoline and residential paints and used in soldering the seams of food cans.80 (2.30 (2. Before the 1980’s.10-4.50 (1.60-1.00) 1.50) 1.30 (2.01 (1.46 (1.30 (2.48) 1.30) 2.30-5.14-1.80 (5.30-1.60 (2.50) 5.10 (3.40 (2.70 (2.10 (1.90 (4.56 (1.72) Selected percentiles ( 95% confidence interval) 50th 1.50 (2. Since lead has been eliminated from gasoline.20-2. 01-02.40 (4.80) 3.12-1.20) 4.20-3.69) 1.40-4.70) 1.80 (2.60-2.80) 1.00) 3.60) 2.60) 3.10-3.80-4.60-1.80 (1.90) 3.62-1.60) 5.70) 1.10) 1.75-1.50-2.70) 2.60-4. malleable.80) 1.00-1.80-3. and 0.10-6.30 (1.50) 4.52-1.50-1.30) 95th 5.60 (4.40-1.50-5.60 (2.00) 2. ceramic glazes.40) 5.51 (1.90 (2.50-5.40) 2.66) 1.10) 3.70) 3.60) 3.04-1.90) 5.40) Total 1.40 (1. such as lead phosphate and tetraethyl lead.986) .50-1.00) 2.60) 1.20) 2.70 (2.00-5.00 (2.90-2.40-6.43 (1.80 (1.50) 1.60 (1.90 (3.60) 4.30 (1.20-6.50-1.20 (3.70-1.25 (1.80 (1.37-1.20 (1.60) 4.900-1. and for radiation shielding.60 (1.50) 1. Elemental lead can be combined with other elements to form inorganic and organic compounds.36-1.70-2.60 (1.36) 1.10-2.17) .14-1.40 (1.40 (1.50-1.90-4.00) 1.20 (2.75 (1.50 (2.90-2.50 (2.69) 1.60 (2.70-4.50) 4.90-4.40 (5.70 (1.70 (1.00-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40 (1.50) 5.75-2. population from the National Health and Nutrition Examination Survey.60) 1.10 (2.25) 1.878-1.53) 1.49-1.83 (1.90 (3.00-2.50) 2. see Data Analysis section) for Survey years 99-00.40) 1.30 (4.946 (.68-1.00-4.10 (1.62) 1. 7439-92-1 General Information Elemental lead is a soft.50 (1.10-8.50 (2.60 (3.10-3.80 (1.80 (4.60 (2.80) 1. Lead was used in plumbing for centuries and may still be present.20-1.40-2. dense.20) 1.50) Sample size 7970 8945 8373 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.70-3.30) 5.60-1.30-2.80) 2.20) .55-1.60) 1.50-6.00 (6.S.02) 1.70) 3.80) 1.77 (1.60) 2.50 (2.10-6. and 03-04 are 0.80-5.80) 2.70) 4.80) 1.40-1.10-3.50) 3.40-2.Metals Lead CAS No. metal alloys (e. population was aerosolized lead emitted from combustion engines that used leaded gasoline.50) 7.10) 3.70-2.30 (2.80 (3.70-2.70-1.89) 1.00 (3.40-3.00) 2.00-4.30 (1.30-1.30) 2.80-2. plastics.00) 4.20) 90th 3.90 (2.10) 5.50 (3. bronze).40) 4. In the past.800-1.90-6.43) 1.10) 4.30 (2.10-4.60) 1.28.70) 3.10) 3.30-1.40) 2.90 (3.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.43-1.30) 2.20-4.20 (3.30-2.70 (1.30 (3.96-2.40) 1.60 (1.40-1.52-1.00) 1.22 (1.20 (1.10-1.70 (3.00) .20 (3.51) 1.

940 (.50 (2.688 (.20) .20-1. respectively.04 (.80 (2.800 (.700 (.18-1.10-3.570-.40 (2.70) 1.600-.915-1.857) .10 (1.674) 1. Approximately half of the absorbed lead may be incorporated into bone.540 (.29 (2.00) 2.600-.80 (1.14-1.17 (1.70 (2.00 (2.80-2.506-.800-1.03-2.600 (.40) 1. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient.04) 2.701) .625-.20-2.70 (2.630 (.50) 3.90) 2. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. see Data Analysis section) for Survey years 99-00.20-1.00-2.06) .671-.66 (2.941) . and 03-04 are 0.800 (.80) 2.09) 1.651) .70) 3.40) 1.579-.700) 1.20) 1.800) .731 (.620 (.600 (.828) Selected percentiles ( 95% confidence interval) 50th .690) 75th 1.86-2.613) .640-.595-.800-1.10-3.78-2.30) .30-2.20 (2.900) .591 (.795 (.80) 3.80) 1.11) 2.10-5.818) . absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.90 (1.40) 1.30-1.40-2.60-3.82 (1.535-.13) .86) 1.33-2.40) 2.800-.500-.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.07-1.20-2.20 (2.650) 1.19 (1.30-1.30) 1.752 (.80) 2.33 (2.00 (1.00 (1.820-1.04-2. bullet fragments retained in human tissue.579-.738) .700) .710-.10-1.553-.20) 1.616) .700-1.10-1.80) 2.00) .11 (1.S.10-3.70-2.604 (.900-1.10-1.708-.22) 1.745-.60 (1.833 (.659 (.636 (.30-1.75) 3.691-.960-1.00 (.75) 4.00) 1.700-.600-.20) .920 (.80-2.70) 3.40-1.900) .40-1.52 (1.g.753 (.70) 1.540-.20 (1.02 (.97) 4.40-3.785) .628) 1.986) .80) 2.60 (1.70) 2.20 (1. interval) .30-3.800) . population from the National Health and Nutrition Examination Survey.40-1. or water contaminated by mining or smelting operations. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.20) .70 (2.931) .20 (1.90-2.10 (.52-1.Metals occupational (e.900) .970-1.564 (. stained glass framing.10-1.10 (. Fourth National Report on Human Exposure to Environmental Chemicals 213 . or after soluble lead compounds are ingested.920 (.00-1.10 (1. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.572-.600-.40) 2.773) .749) .700 (.790 (.50 (2. imported children’s trinkets and toys.480-.30 (2.620) 1.13-3.40) 2.910-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 1.637-.04) . 0.62) Total .02) 1.560-. 2000).80) 1. battery and radiator manufacturing) and recreational sources.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 .680-.80) 2.50-3.815 (.30 (3.90-2.52-1.590 (.70 (2.70-3.21 (2.00) .900-1.700-.600-.848 (.50-1.766 (.700 (.900) .80) 3.10 (.40 (2.60-3.730 (.90) 2.50-2.700-.40) 1.800 (.14 (1.10) .700 (.10) .800 (.31 (1.89) 2.40) 3.78-2.580-. and contact with soil.30) 1. and 0.91) 2.00-1.07 (.900-1.800-.14 (1.60-2.700-.90-2.50 (1.10-1.40-1.90 (1.90 (2.40 (1.23) .30) 2.50) 1.710-1.00) .862) .30) 1.960 (.935) 1.800) .800) .90) 2.00 (1.680-.90-3.700 (.900 (..661-.660) .62-4. CDC.32 (1.12) 90th 2.33.49 (1.641-.20) 1.00) .900-1.40) 2.30-5.729-.41) 2.990) 1.810-1.86 (1.40 (1.900) .10) 2.44-2.20 (3.90 (2.29) 2.40 (1.03 (1.30) 2.78-2.66 (2. 2007.90 (1.800) . dust.20 (2.90 (2.680) .695 (.700 (.90) 1.60 (2.757-.82 (2.718) . older plumbing systems with leaded pipes or lead soldered connections.60 (1.90-3.00 (1. lead-contaminated dust in indoor firing ranges.40 (2.40) 1.80 (1.20-1.60-1..1.558 (.900 (.30) 1.677 (.73 (1.40 (2.00) 2. lead-based painted surfaces undergoing renovation or demolition.589-.30-1.40 (1.86) 95th 2.923 (.00-1.10 (1.50) 2. pewter utensils and drinking vessels.50-2.990) 2.900 (. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.642 (.50 (1.20 (1.808 (.10 (1.70 (1.23-4.1.10) 2.610 (.20) .556-. However.640 (.59-2.50 (2. 1991). lead-containing folk remedies and cosmetics.960-1. In the blood.60-2.80-3.30) 1.40-5.31-3.10) 1.59) 1.850 (.50) 1.24-1.60 (1.840 (.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. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.50) 1.90-2.600) .955-1.526-.20 (1.50-2.40 (1.64) 2.90-4.60) 2.833-1.72) 1.27 (1.20 (1.600) .625 (.00-2.573 (.70) 1.00-2.30 (1.700-.822-1. 01-02.50) 2.35 (.900) .30) 2.04 (.80) 1.27) 1.605) .

72-2.963-1.67-4.796-1.64) 95th 2.635 (.851) .655-.603-.702-.725) .508) .644) .988-1.61) 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 .62-2.460-.914-1.702) .763) .870 (.654) .18) 2.86 (1.41 (1.971 (.85-2.63) 4.71-2.55 (1. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.721 (.11) .594-.33 (1.755 (. 1993).774 (..08-2.739) . and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.639 (. Lead can cross the placenta and enter the developing fetal brain.765) .383-.541-. 2003.66 (1. through the inhibition of certain enzymes.50-2.914 (.00 (1.08) .72-2.618 (.11) 1. In 1991.07) .33) 2.03) .605-.01 (.07-1.622 (.898) .06 (.900 (.920-1.02) 1.718) . Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.50) 1.612-.707 (.00 (1. zinc.05-1.917-1.673) .87) 1.33) 1.400) .753) .48 (1.696 (. The toxic effects of lead result from its interference with the physiologic actions of calcium.43 (1.603 (.659-.25-1. 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. interval) .679-.00 (1.75-2.03 (.49 (1.731-.70 (1.Metals 90% of the body lead burden in most adults.92) 2.77) 2.862-.28) . 1991.720 (.670) 1.461) . Approximately 70% of lead excretion occurs via the urine.03 (.43) 1.31 (2.492-.15-3.71 (1.09-1.62) 2.05 (1.469 (.655) .20-3.97) 1.09-1.15-2.31) 1.722 (.43 (2.50-1.82) 1.65 (1. population from the National Health and Nutrition Examination Survey.14) 1.73) 2.88) 2.586-.66 (1.63) 1.701) .11 (. scant amounts are lost through sweat.657) 1.992-1.990 (. 1995.44) 1.78 (2.78-4. 2007).00) .641 (. CDC.18 (1.644 (.50-2.718) 1.977) 1.29 (1.96 (1.18) 1.887 (. BLLs and associated toxic effects differ in children and adults.404 (.588-.18) 1.918 (.06) .793-1.571-.68 (1.667-.992-1.535) .03) 90th 1.404 (.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 .380-.34-1.639 (.529-. Large amounts of lead in the body can cause anemia.571-.625 (.53-1.15-2.69 (1.510-.938-1.28-1.742) Selected percentiles ( 95% confidence interval) 50th .64 (1. Schwartz.01) .88-2.85 (1.790) . O’Flaherty.S.708 (.97 (1. hair.702) .853-1.375 (.31 (1. abdominal pain.79 (1.608-.03) 1.39-1.75 (2.66) 2.72) .615 (.04) 2.47 (1.17-1.649 (.26) Total .03) 1.05-1.56-2.20) .83) 1.979 (.933) .781-1.688) .841-1.559-.10 (1. 2004.838) .588-.31 (1.47) 1.561-.681-. 1993.36-2.593 (.94 (1.51) 1.43) 2.97) 1.988 (.62-1.914 (.09) 1.61) 3.11 (1.20) .03) .940 (.926 (.683-.14 (1.10) 1.85) 1.722 (..933-1.31) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.812-1.981-1.603-.38 (2.946-1.03-2.882-1.623 (.56-3.61) 1.94-2.03) 2.551-. with lesser amounts eliminated via the feces.65-2.88) 2.61) 1.667-.58) 1.00 (.38 (2.98-2.592-.594-.50 (1. encephalopathy.64-2.604-.682) .633 (.408-.957-1.08) .73-2.02-1.56 (1.61) 1. The skeleton acts as a storage depot.698) .615 (.03) 2.668-.606-. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.725) . For instance.828-1.720 (.05 (.758) .79) 1.701 (.89-2. 1996).44 (1.64) 2.59-3.18) .98) 2.587-.609 (. based on prospective population studies.698) .677-.652 (.38 (2. with a half-life of years to decades.04-3.608 (.997-1.56) 3.11 (1.12-1.686) .607-. and iron.730) 1.45 (1.893) .693 (.583-.645-.33-1.62-3.51 (1.26) 2.648 (.19-5.53) 1.52) 1.742) .41-1.712 (.40-1.671 (. and through binding to ion channels and regulatory proteins.83 (2.667) .703) .22) 1.15) 1.55 (1.89-5.22-1.85-2.15) 1.432 (.496 (.621 (.37-1.700-.677 (.710) .639) .677) .43-1.662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.579-. and paralysis.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 .734) . 1995). seizures.98 (1.37-1.569 (.50-2.35) 2.428) .645-.17 (.975-1.41) .22) 1.918-1.800-.07 (.46 (1.79) 2.709 (.19) 1.25-1.655) 75th 1.632 (.11-1.23 (1.06) 1.658 (..601-.74 (1.97-18.47 (2. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.681-. kidney injury.0) 3.46 (2.639 (.11 (.09-1.638 (.03 (1.342-.404-.44 (1.617-.22) .962 (.10 (.88 (1.810 (.876-1. Staessen et al. and nails (Leggett.22-2. Nash et al.88) 1.436) .746) .03 (.52 (1.676) .623 (.06 (1.679) 1.938 (.24 (1.28) 2.27 (1.828) .

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.. Bellinger 2005. High dose occupational lead exposure. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. 1991. 2006). 2009).. premature delivery. 2003.atsdr. reduce sperm count. Jones et al.. 2000). and low family income (CDC. with overt encephalopathy. both the geometric mean (1. Borja-Aburto et al. Data submitted through state public health programs from 2006 showed that 1.000 adults. 2005b). Telisman et al. More recently. 2002... Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. which is an 84% decline. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. 1996. lead in women may be associated with hypertension during pregnancy.4% of children had BLLs of 10µg/dL or higher (CDC. Staessen et al. Information about external exposure (i. and decrease fertility (Alexander et al. 1995.. However.. 1996. IARC considers inorganic lead compounds probable human carcinogens. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR.. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC..gov/toxpro2.21% of approximately 3. and organic lead compounds not classifiable with respect to human carcinogenicity. 2005a). Muntner et al. environmental levels) and health effects is available from ATSDR at: http://www.. Both drinking water and ambient air standards for lead have been established by the U. when the geometric mean BLL was 2. Schwartz et al.3 million children tested had BLLs of 10 mg/dL or higher (http://www. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. In NHANES 1999-2002 in children 1-5 years old. Fourth National Report on Human Exposure to Environmental Chemicals 215 . the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.2 µg/dL in males and 3.7 µg/dL and 4. 2001).9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 2003). Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. seizures. Payton et al. 2000). NTP considers lead and its compounds reasonably anticipated to be human carcinogens. adults in the 19992000 NHANES sample (Apostoli et al. The U. Surveillance data reported by U. usually with BLLs greater than 40 mg/dL. 1999).S.. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3.S. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. Overall. 1987.cdc. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. the geometric mean BLL was 3. urban residence. EPA.75 µg/dL in U. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH..e. At low environmental exposures. 1999). In occupationally exposed adults. 2002a). residing in housing built before the 1950’s. Schwartz. respectively..Metals µg/dL or higher as the level of concern in children.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. Korrick et al. 1998).html.. adults in the 1999-2000 NHANES sample. 2003. 2006).000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample. Lanphear et al. approximately 11..S. almost double the geometric mean of 1. For example. and peripheral neuropathy generally occurring at much higher levels (e. 2002). including minority race or ethnicity. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. though there is greater individual variation in urine lead than in blood and greater potential for contamination.xls).6%) were lower than those from NHANES 1991-1994.. 1996. CDC. 2007).07 µg/dL (Becker et al. Pirkle et al. Urine levels may reflect recently absorbed lead. BLLs reflect both recent intake and equilibration with stored lead in other tissues.cdc. and spontaneous abortion (Baghurst et al.. 1994). may alter sperm morphology.S.S.4% in NHANES 1999-2004. particularly in the skeleton. the prevalence rate has declined annually since 1994 (CDC.g. 2003. 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.6% in NHANES 1988-1991 to 1. adult residents..5 per 100. 1984. 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.. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al.. 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.. higher than 100-200 µg/dL).0 µg/dL in females (Soldin et al...S.

doi:10. Neurotoxicol 1987. 2002 [online]. gov/mmwr/preview/mmwrhtml/mm5420a5. JAMA 1996.275:1177-1181.8(3):395-401. Weiss ST. Blood lead reference values: the results of an Italian polycentric study. et al. 1999-2002. Adult blood lead epidemiology and surveillance—United States.htm. Hernberg S. 4/14/09 Alexander BH. Available at URL: http://www. Kaus S. Rojas LM. Muller CH. Leggett RW.gov/mmwr/preview/mmwrhtml/ mm5532a2.cdc. Ewers TG. N Engl J Med 2003. Chiodo LM. Ganzi A. Acquisition and retention of lead by young children. IARC Monogr Eval Carcinog Risks Hum 2006. Korrick SA.gov/nceh/lead/publications/ books/plpyc/contents. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Rotnitzky A. Intellectual impairment in children with blood lead concentrations below 10 µg/dL.cdc. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. 2005. Wager C. Cory-Slechta DA. Manton WI. Atlanta (GA). Lanphear BP. Sci Total Environ 2002. Hu H. Scand J Work Environ Health 1984. Batuman V. Luukkonen R.73:409-420. Seiwert M. Am J Epidemiol 1999. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Ga. Borja-Aburto VH. Bellinger D. 2005b. Lanphear BP. Mantere P. Jones RL. Atlanta (GA). Am J Public Health 1999. Neurodevelopmental effects of postnatal lead exposure at very low levels. Brody DJ.275(15):1171-1176. Available at URL: http://www.gov/toxprofiles/tp13. Stanek KL. Weiss ST.htm. Pirkle JL.html. Occup Environ Med 1996.cdc.89:330-335. Payton M. Inorganic and Organic Lead Compounds. Available at URL: http://www. Muntner P.htm. Managing Elevated Blood Lead Levels Among Young Children. Pediatrics 2004. Environ Res 2000. Toxicological profile for lead. Speizer FE.205:297-308. Aug 2007 [online]. Canfield RL. et al. Sparrow D. Jacobson SW. Becker K. Dietrich K. Sparrow D.101(7):598-616. Rios C. MMWR Morb Mortal Wkly Rep 2006. 1991 [online]. Vupputyuri S.113(4):1016-1022. Blood lead levels measured prospectively and risk of spontaneous abortion.123:e376-e385. Reese YR. 4/14/09 Centers for Disease Control and Prevention (CDC).87:1-471. Environ Health Perspect 1993. Baj A. Coresh J. Atlanta. Ronchi L. Available from URL: http://www. Jusko TA. Preventing Lead Poisoning in Young Children.26:359-371. Centers for Disease Control and Prevention (CDC). Hu H. Teratogen update: lead and pregnancy. Lead.cdc.cdc. Wigg NR. 4/14/09 Centers for Disease Control and Prevention (CDC).115:521-529. Public Health Rep 2000. Roberts RR. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Birth Defects Research (Part A). et al. Cox C. Caldwell KL. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Robertson EF. Blanco J. JAMA 1996. Hertz-Picciotto I. Neri A. Neurotoxicol Teratol 2004. Blood lead levels—United States. van Netten C. Baghurst PA. Krause C. Farias P. et al. Aro A.82:60-80.htm.54(20):513-516.150(6):590-597. Auinger P. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. 1988-2004.10:43-50. Third National Report on Human Exposure to Environmental Chemicals. CDC. Rotnitzky A. Int J Hyg Environ Health 2002. 4/14/09 Centers for Disease Control and Prevention (CDC). German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 4/14/09 Centers for Disease Control and Prevention (CDC). Henderson CR. Hu H. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Bavazzano P. Angle CR. Hänninen H. Cox C. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Apostoli P. The relationship of bone and blood lead to hypertension.1542/peds:2007-3608. A prospective follow-up study on psychological effects in workers exposed to low levels of lead.53:411-416. Semen quality of men employed at a lead smelter. Homa DM. Lead and hypertension in a sample of middle-aged women. Kaufman JD. Hunter DJ. Schulz C.atsdr. References Agency for Toxic Substances and Disease Registry (ATSDR). MMWR Morb Mortal Wkly Rep 2005a. Checkoway H. Pediatrics 2009.348:15171526. Korrick S. et al.287:1-11. Kuehnemann TJ. Jacobson JL.55(32):876-879. Vimpani FB. 2003-2004. McMichael AJ. Age-specific kinetic model of lead metal in humans.gov/nceh/lead/ CaseManagement/caseManage_main. Available at URL: http://www. Kim R. Meyer PA. Lepom P.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. Bellinger D.

Amery A. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. 50:31-37. Nash D. Lee BK. Soldin SJ. Use of endogenous. Am J Epidemiol 1994.108(1):45-53. Int J Hyg Environ Health 2006.153(5):453464. blood pressure. Blood lead. Low-level lead exposure and blood pressure. Staessen JA. Gavella M. et al. J Hum Hypertens 1995. Pizent A. lead. Kaufmann RB.289(12):1523-1531. Wilhelm M.Metals results from NHANES III. Pirkle JL. Gunter EW. Low-level lead exposure and renal function in the Normative Aging Study. Lustberg M.104(1):60-66. Sparrow D. Arch Environ Health 1995. Stewar WF. Environ Health Perspect 1998.63:1044-1050. Blood lead concentrations in children: new ranges. Schulz D. JAMA 2003.9:303-327. Lee SS.327:109-113. cadmium. Association of blood lead. cadmium. Magder L. Osterloh JD. and tibia lead with neurobehavioral test scores in South Korean lead workers. Lauwerys RR. Hanak B. Payton M. blood pressure and cardiovascular disease in men. Schwenk M. Revised and new reference values for arsenic. Cvitkovic P. stable lead isotopes to determine release of lead from the skeleton. Weiss ST. Schwartz J. population to lead: 1991-1994.106:745-750. zinc. Fourth National Report on Human Exposure to Environmental Chemicals 217 .118:16-29. Lead. O’Flaherty EJ. Telisman S.209:301305. Brody DJ. Flegal AR. and copper in men. Environ Health Perspect 1996. Hickman T. Kinetics of lead disposition in humans. Environ Health Perspect 2000. and hypertension in perimenopausal and postmenopausal women. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Soldin OP. Toxicol Appl Pharmacol 1993. Sherwin R. et al. Rocic B. dimercaptosuccinic acidchelatable lead. Kidney Int 2003. Physiologically based models for bone-seeking elements. Smith DR. IV. Kaufmann R. Hwang KY. Jurasovic J. Am J Epidemiol 2001.140:821-829. Schwartz BS.S. Rubin R. Clin Chim Acta 2003. Roels H. Exposure of the U. Hu H. Paschal DC. Lee GS.

sphygmomanometers and barometers.781 (.. predominantly from fish and other seafood. may contain inorganic mercury.484) .10) . The ingestion of methyl mercury. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. which can bioaccumulate in aquatic and terrestrial food chains.689-.574) .60-6. Hursh et al.472-.800 (. inorganic.860-1. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.12) .80 (1.800-1. Accidental spills of elemental mercury.800 (.30-6. Woods et al.00 (.30 (1. thimerosal. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).700 (. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.. have often required public health intervention (Zeitz et al. Apart from methyl mercury.90) 95th 4.02) . Poorly absorbed from the gastrointestinal tract.400 (.490 (.60) 2085 2293 3478 Limit of detection (LOD.60) 1.60-2.60) 1.700-. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.g.30-2..800-1.672) .60-5.50-1.00 (2.700) .50) 5.00) 1.80) 1.40-1.80 (1.900) 75th 1.30) 4132 4241 03-04 03-04 03-04 .70 (1.300 (.60-3.40-1. The kinetics of the different forms of mercury vary considerably.g. see Data Analysis section) for Survey year 03-04 is 0.40-2.50) 2.60-6.00 (. elemental mercury is absorbed mainly by inhaling volatilized vapor.714-. such as chlorine (e.419 (.30) 1.30) 5. an organic form of mercury.600) 1. and is distributed to most tissues.900) 1.00) 4. with the highest concentrations occurring in the kidneys (Barregard et al.g. 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. 1999 . synthetic organomercury compounds were once used in pharmaceutical applications. mercuric chloride).30 (2.30-4.814 (. Atmospheric elemental mercury can be deposited on land and water.326 (. 2002).80 (3.90 (4.00) 1.500-.700-.703-.500 (. 1993).363-.700-. Other major uses include electrical equipment (e.80 (1.753-1.800 (.40 (3.00 (.797 (.00 (2. constitutes the main source of dietary mercury exposure in the general population.40 (4.Metals Mercury CAS No.70 (1.418-.500-.30-5.300) .700) .70 (4.70 (3.563 (. or oxygen.927) . merbromin).900) .900 (.2.50-3.979 (.400-.400-..500 (. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).20-3.500) .372) .00-5.. and mercury compounds are still used as preservatives (e.700-.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 . Survey years 03-04 Geometric mean (95% conf. 1998. which create an episodic potential for volatization and inhalation of mercury vapor.40 (3.90 (1. 1994.30) 1.655-.80) 4. and dental amalgam. and mining and smelting. Also. solid-waste incineration.20-4.300-. and organic forms.60 (1. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.800-1.40 (4.40-3.40) 3.50-2.877 (. phenylmercuric acetate) or topical antiseptics (e.00-1.919) .776 (. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore. population from the National Health and Nutrition Examination Survey. thermostats and switches).00 (2. Elemental mercury is a shiny..60 (1. to form inorganic mercury compounds or salts.80) 3. 2007).g. Kingman et al.700-.20) 2..S.10-3.903) Selected percentiles ( 95% confidence interval) 50th . After elemental mercury is absorbed.30) 3.800-1.900) 1.S. IARC.70) 911 856 2081 4525 03-04 03-04 .30) 3. sulfur. 1980. interval) .70-2.00) . Some cosmetic skin creams from countries other than the U. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.40) 1. thermometers.90) 3.00 (1..90) 90th 3.00) 3.800 (. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.285-. In addition..60 (2.50) 1.40-2.900) 1.600 (.20 (2. electrical lamps.50) 4.90-3.800-1.886) .20-4. 218 Fourth National Report on Human Exposure to Environmental Chemicals .00 (.

10 (1.800) 75th . interval) Selected percentiles (95% confidence interval) 50th .60) 2.400-.30 (1.50) 95th 2.30-2.200-. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.10-3.377 (.00 (2.06-1. a measure of accumulated dose (Cernichiari et al..00) 7.40) 2.50) 1.700 (.00 (2.343 (..00-2.500-.00 (2. Myers et al.824) 1. Methyl mercury is incorporated into growing hair. 1994).700 (.40-2.820 (.14 and 0.90) 3. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.10-1.30-11. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.50) 3. 1999).. 2003). 2005).200-..300) .269-.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 .600) . 1992). Vimy et al.500-.944 (.50-12.80 (1.Metals the tissues to mercurous and mercuric inorganic forms.60 (1.300) .940) Race/ethnicity (females.300) .500 (. thereafter.. 2004.800-1.407) .10 (.297-.06 (.00) 2.60 (2.10) .70-6. Jonsson et al..600 (. 1998).01) .500-.10 (1.30-5.667 (.700-1.475) .200-.70-3.60) 3. Excretion occurs by renal and fecal routes. Smith et al.10 (5..90) 2. 1975.30-6.800) .30) 1..70 (1. 1994.30 (1.10) .200-.697-.60) 1.29) . 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .871-1.726-1.800) 1.60 (1. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.800) . and the newborn’s levels decline gradually over several weeks (Bjornberg et al.. Sandborgh-Englund et al.00-2.23) .40 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.300 (. 1984.900 (.500-.256-.. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.800 (.90) 90th 1.20 (. and a useful marker of exposure in epidemiologic studies (Grandjean et al..60 (3..50 (2. 1969.70 (1.800-1. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.265-.80-3.900-1.318 (.20-3.700 (.800 (.. Smith and Farris.377) .374) .300 (.900-1.20 (2. 1990).369) 1..919) .00 (1.27) ..700-..317 (. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.35 (1.20-3.30 (1.20-3. population.299-.30) 1. McDowell et al.00-1.329 (. with most elimination occurring through in the feces (Sherlock et al.50) 2. the transfer Total Blood Mercury−1999-2002 Geometric mean and selected percentiles of blood concentrations (in µg/L) for males and females aged 1 to 5 years and females aged 16 to 49 years in the U.700-.70-5.90 (4.800) 1.800-1.200-.300 (. for both acute and chronic exposures.70) 1.70-5. 1992.307 (.900 (.40 (1.00) 6. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith. 1994) and then undergoes slow dealkylation to inorganic mercury.825-1.10 (1.3) 4.40) 1.00) .40-1.10) 1.60 (1.00-2.00-3.500-1.00 (3.50) 1. Fourth National Report on Human Exposure to Environmental Chemicals 219 .02 (. 1992 and 1999.70-3.0) 4.7) 4. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.. 1996).00) 4. 1998).80 (3.70) 4.60 (3.90 (3.S.700 (.833 (.300 (.395) . 1999-2002..40) 5. 1993).00) 1.500-.50-3. 1973).80) 1.40-2. Suzuki et al.10 (3.70 (1.00-6.90) 2.200 (.20-2. Vahter et al.200-.30-6.500 (.90) 5.73) 1..50 (1.80) 579 527 370 436 588 806 Limit of detection (LOD. National Health and Nutrition Examination Survey..700) 2.300) .30-6.20-11. 1971).738-.200 (. 1996.300) .20) 1.900 (.90 (1.541-.90 (4. After exposure to elemental mercury.20) .30 (. 1993). Methyl mercury enters the brain and other tissues (Vahter et al.20) .800 (. Miettinen et al.664-1.70) 4.14.268-.30-3.600) . 2003). Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.00) 1.30) 3.10 (. 1995.50-2. Blood concentrations decline initially with a rapid halflife of approximately 1-3 days followed by a slower half-life of approximately 1-3 weeks (Barregard et al.700-1.90 (1. Geometric mean Survey years (95% conf.. 1991.300) ..30-4.30-4.60) 1.

.. overt signs and symptoms of chronic inhalation may include tremor. Smith et al.700) .500-. 220 Fourth National Report on Human Exposure to Environmental Chemicals .800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .700 (.700-. dysarthria.700 (. hearing impairment.600) .800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .500-. fatigue.600-. gingivitis.600) . Vupputuri et al. Stern 2005.. maculopapular rash. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. hypertension.700-. Rissanen et al. The constellation of findings may include anorexia. dysarthria.600-. 2000). Salonen et al. DeRouen et al.Metals may be more efficient for inorganic mercury (Grandjean et al..600 (. Drexler and Schaller. 1995.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Bellinger et al. In recent epidemiologic studies. which may vary for some chemicals by year and by individual sample. Sakamoto et al. 2004).600-. short-term memory loss. Sakamoto et al. the existence of a causal relation is unresolved (Chan and Egeland. 2005). ataxia.500-.S.700) 2007 2240 3406 Limit of detection (LOD.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 . High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.500-. 1993)... 1996). Overt poisoning from methyl mercury primarily affects the central nervous system.500-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Survey Geometric mean (95% conf.600 (. and cerebral palsy (NRC.500-. Smith et al. see Data Analysis section) for Survey year 03-04 is 0. 1983). 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.700 (. insomnia. typically after a latent period of weeks to months.800) .500-. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. Inorganic mercury exposure usually occurs by ingestion.. 2004.. and progressive constriction of the visual fields. depression. 2000..600) ..500) . 2006. Rice. Once absorbed. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.. 1987).. 1998.500 (. < LOD means less than the limit of detection. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. particularly irritability. 1970. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. 1995. 2002. and sleep disturbance (Bidstrup et al. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.500 (..500-.600) . At levels below those that cause acute lung injury. and pinkish discoloration of the hands and feet (Tunnessen et al.500 (<LOD-. Factor-Litvak et al. high-dose exposure to elemental mercury vapor may cause severe pneumonitis.600 (.800) . 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. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.600) .600) . pain in the extremities.600 (. altered physical growth.600 (.500-. causing parasthesias. 2004. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al.. cerebellar ataxia..700 (. Oskarsson et al.600 (..600-.600) . and neurocognitive and behavioral disturbances. limb deformities.600) . Acute. sensory impairments. 2005.700 (.600 (.. 1951. 2000. 2003). Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.600 (.42.. 2006.600) .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.700 (. 1963). anorexia.500 (<LOD-. 2004). irritability. population from the National Health and Nutrition Examination Survey.

EPA at: http://www.S.19 (2.76-4.555) .54 (2. Over the NHANES 1999-2006 survey periods. interval) .416 (.78-2. In Germany the geometric mean for blood mercury was 0. see Data Analysis section) for Survey year 03-04 is 0. and the age-related changes differed across the groups (Caldwell et al. Kingman et al.S..78 µg/L for adults and 0.12 (.67-2. Among the three racial/ethnic groups.360-.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 . 2002).480 (.epa. aged 18 to 69 years.16 (1.88) 287 722 1529 03-04 03-04 . et al.atsdr..55 µg/L.280-.410-.. Information about external exposure (i.430 (. 1997.. total blood mercury increased with age..46) 3. 1998).580) .90) 2.360 (. range 40 years to 78 years) had an average total blood mercury concentration of 2.840-1.09 (2.463) . 2001.870-1.530) .24) 1.76-3.530-.160-. From 1996 through 1998.770-1.60) 619 713 1066 Limit of detection (LOD.480) 75th 1.03-4.97) 2.413-. and increased slightly in non-Hispanic white children (Caldwell. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.405-. 1998). population from the National Health and Nutrition Examination Survey. Grandjean et al.430 (.549) .440 (. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC. the total blood mercury concentration is due mostly to the dietary intake of organic forms.42) 95th 3.77-2.313-. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al..96 (1.370) .492) Selected percentiles ( 95% confidence interval) 50th .520) .01 (.14) 90th 2.442-.28) 1.433 (.gov/toxprofiles.840-1.61) 1. military veterans (mean age 52.66) 3.05) 3. who participated in a 1998 representative population survey (Becker et al.29) 1.S.58 µg/L for 4645 adults.400 (.89) 3. total blood mercury geometric mean levels in females aged 16-49 years did not change.408) .30) 3.05) 1.gov/mercury and from ATSDR at: http:// www. Benes et al.63-2.24 (2.00 (.67-3. 2001.39-3. A cohort of 1127 U.33 (2.S. average age 9.200 (.S.cdc. 2003).840) 1. the median concentration of blood mercury was 0.960 (.9 years). 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. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al. Biomonitoring Information In the general population.31) 2. 2000).07 (.304) .430) .19 (1.46 µg/L for children.530) .700 (.08 (1.441 (.16 (.60 (1.52) 2.18) 2.330 (.99-6..20 (1.890 (. 2004.509) .8 years.Metals standard for inorganic mercury has been established by U.570) .85-2.93 (1.23) .495 (. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females. slightly higher total blood mercury levels were found in U.360-. particularly methyl mercury.. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.340-.14..65) 1.14-2..26 (1.250) .23) 2.08 (1. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.. EPA.88 (1.350-. 2003).358 (. 2006).68 (2. In NHANES 19992002. 2009). Mahaffey et al. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children. However.e.870-1.330-..940 (.509) .60-2.330-. Sanzo et al.290-.460) .254 (. 1995. Fourth National Report on Human Exposure to Environmental Chemicals 221 . These distinctions can help interpret mercury blood levels in people. 758 children. average age 33 years.. adult women in several ethnic subgroups (Hightower et al.930-1. Survey years 03-04 Geometric mean (95% conf.13-2.00) 1.460 (. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.213-. environmental levels) and health effects is available from the U.406-.420 (.420 (. 2009).700-1.88-3.534) . During the same survey periods.610-1.382-.476 (. Schober et al.34-3.96 (1.396-.330-.447 (. Total blood mercury levels increase with greater fish consumption (Dewailly et al..31) 1266 1272 03-04 03-04 03-04 .76-3.

333-.Metals 2000). 2002).87 (1.508 (.347) . In the study of U.376-. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.619-.532 (.06 (..225-. 2005).S.217 (.447-.. Department of Health and Human Services noted that several studies have observed a modest.566) . population from the National Health and Nutrition Examination Survey.307-.498) 75th . 2006).522-.358) .67 (1.13-2.. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.385-.S.28 (.909 (.785-1. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.537) .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 .44) 1.88-2.535) 1.309-.09) 1.30) 1.32-2.545 (. Urine mercury and the number of dental amalgams were correlated.06 (.25 (.875-1. mean urinary mercury was 3. and on average.S.784) 1. An expert-panel report recently prepared for the U.63) 1.362 (.455-. 1998).18-1.35 (1.01) 2.1 µg/L for each surface with a dental amalgam (Kingman et al.40 (1. 2002) adult population surveys were similar to those in a U.306 (.61) 1.255 (. and Italian (Apostoli et al. 2009).54 (2.275) .86) 95th 2. the urine mercury increased by approximately 0.00) 90th 1.368) .455) .400) .246-.969-1.455-.667-1..443 (.476 (.616) ..39) 1.620-... Urinary mercury levels in recent German (Becker et al.62 (1.391) .31 (1.652) .404-.40-1.486) Selected percentiles ( 95% confidence interval) 50th .07) 1. a biomarker of perturbation in renal tubular function.88 (1.800-1. 1992). among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.485 (.00) 286 722 1529 03-04 03-04 .11) 2. 2006.21) 1.03) 2.696 (. et al. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.56) 1266 1271 03-04 03-04 03-04 .208-.280-. women of childbearing age have generally been much lower than these levels (CDC.S.464 (.391-.384 (.78-4. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.964-1.1 µg/L. military veterans with dental amalgams.365 (. not to imply a safety level for general population exposure.265-. reversible increase in urinary N-acetyl-glucosaminidase.400-.768 (.12-3.11-2.599) . 1988.447 (.990) .289) .23-2.687) .S.79 (1. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.00 (.32 (1.11) 1.587 (. DeRouen et al.51-2.365 (. Langworth et al. 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.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals . Czech (Benes et al.417) .196-.67 (1.87) 2.525 (. 2003).630) .16) 1. 2009). Information about the biological exposure indices is provided here for comparison.463 (. et al. interval) .301-. 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..41-2.13 (1.65 (1.30) 2.276 (.04-3.480) .79) 1. Survey years 03-04 Geometric mean (95% conf.46-2.77 (2.76 (1.64-2.588) .970 (.343 (.392-. Levels in U.297 (. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell..88-2..714-1.472-.

670) 75th 1.16-5.95 (2.53-3.05 (3.32-3.560 (.48 (2.00 (2.699) 1.799) .592 (. 1999-2002.760 (.00) 2.84 (2.46-4.657 (.62 (3.17) 95th 5.526-.809) .610-.832-1.24-1.615 (.909-1.910) .742-1.99 (2.23-1.79) 3.77) 2.47) 1.99) 1.710 (.656-.05 (2.774) .62 (4.13-4.21 (2.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .45-3.32 (1.92) 3.07-2.42) 2.500-.475-.631-.57-4.42-3.83-3. National Health and Nutrition Examination Survey.68 (3.709) 75th 1.45) 2.09-1.14) 3.09-1.76) 2.45-2.35 (1.450-.76-5.540 (.16) 5.97) 2.719 (.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .27-1.39-3.522 (.622-.46) 3.65) 1.870) .51 (3.Metals Urinary Mercury−Females Aged 16-49 Years Old. 16-49 years) 99-00 01-02 .30 (2.30 (1.87-4.06 (.540-.41-6.91-7.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.27 (2.709) .98 (5.624-.723 (.81-6.79) 1.824) .616-.59-5.92) 4.632 (.580-.51) .62 (1.520-.724 (. interval) Selected percentiles (95% confidence interval) Survey years 50th .516 (.07-5.650 (.21 (1.806) .54) 595 531 381 442 594 826 Limit of detection (LOD.508-.68-3.664) .605-. Geometric mean (95% conf.21-3.25) 2.553-.665) .63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.42) 90th 2.03 (.14-1.84 (2.55-3.15-1.579-.41 (1.55) 90th 3.30-2.85) 4.23-1.31-1.30 (2.637) .S.43-1.03) 1.22-3.97) 2.91 (2.772 (.420-.35) .18) 3.14-2.37) 1.69 (1.76 (1.68) 3.721 (.831) .56) 3.810) .650) 1.686) .89 (2.41 (2.502-.56 (1. population.831) .582-. interval) Selected percentiles (95% confidence interval) 50th .639 (.636-. 1999-2002.27 (1.45 (1. 16-49 years) 99-00 01-02 .650 (.606 (.45) 95th 3.61) 1.97) 2.10-4.50-4.32) 2.578-.850-1.710) 1.15 (2.50 (1.46 (1.45) 2.22 (.65-4.706 (.99 (3.10-2.600 (. National Health and Nutrition Examination Survey.569-. 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.03-2.580 (.560-.685 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.99-2.56) 4.892) .72) 1.85-3.04-1.846) .426-.24) 6.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .38) 4.740 (.710 (.44) 3.41 (1.97 (1.387-.930) .81 (3.61-6.00 (3.47) 1.655 (.596 (.14 and 0.13 (2.3) 5.28 (1.744) 1.691) .04-10. population.92) 2.77) 1.14. Geometric mean Survey years (95% conf.966) .620 (.790) . Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.37 (1.658 (.70 (2.94) 1.565 (.410-.S.557-.18 (3.520-.69-3.52) 3.31 (1.833) .07) 1.03 (.501-.50 (2. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.

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Aguinagalde FX. Environ Health Perspect 2007. Lorscheider FL. Sinks TH. Friberg L.124:221-229. et al. Schober SE. Environ Health Perspect 2003. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Public health consequences of mercury spills: hazardous substances emergency events surveillance system.Metals Sanzo JM. Toxicol Appl Pharmacol 1994. Stern AH.31:687-700. Mottet NK. Orr MF.115(10):1527-1531. Smith JC. Yoshinaga J. Sherlock J. Turner MD. Langolf GD. The hair-organ relationship in mercury concentration in contemporary Japanese.97(2):195-200. 1993-1998. Blood mercury levels in US children and women of childbearing age. Matsuo N. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish.110:129-132. Toxicol Appl Pharmacol 1994. Am J Physiol 1990.98(1):133-142.4(5):981-988. Acrodynia: exposure to mercury from fluorescent light bulbs. Dorronsoro M. Smith JC. Hongo T. et al. Amurrio A. Goldberg J.37:245-252. Effects of exposure to mercury in the manufacture of chlorine. et al. Guo S.48(4):221229. Shen DD.289(13):1667-1674. Pediatrics 1987. McMahon KJ.40:413-419. Arch Environ Health 1993. Takahashi Y. Environ Res 2005. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Mooney TF. Hall LL.128(2):25125-25126. Burbacher T. Environ Res 2005. Methyl mercury pharmacokinetics in man: a reevaluation. Vorwald AJ. JAMA 2003. Farris FF. Kaye WE. Amiano P. The kinetics of intravenously administered methyl mercury in man. Osterloh J. Jones RL. Smith AE. Longnecker MP. Zeitz P.2:117-131. Imai H. Public Health Nutr 2001. Lind B. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury.79:786789. 1999-2000. Effects of occupational exposure to elemental mercury on short term memory.258(4 Pt 2):R939-945. Leroux BG. Martin MD. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Environ Health Perspect 2002. Tunnessen WW. Allen PV. Whittle K.111(12):1465-1470. Vupputuri S. The contribution of dental amalgam to urinary mercury excretion in children. Bernardo MF. Vimy MJ. McDowell M. Sandler DP. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Stern AH. Leitao JG. Suzuki T. Patil LS. Bolger PM. Azpiri MA. Woods JS. Baser M. Am Ind Hyg Assoc J 1970. Most B. Smith RG. DeRouen TA. Hum Toxicol 1984. Topping G. Newton G. Daniels JL. Smith PJ. Br J Ind Med 1983. Fisher HL. Vahter M. Hislop D. Nakazawa M. Toxicol Appl Pharmacol 1996. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000.

3) 41. hydrogenation catalysts.7-41.6) 53.3 (84.2) 53.9-56.9-109) 97. and 1.0-65.1-48.3 (71.7) 46.5-52.5.7-39.6-55.1) 126 (106-147) 109 (94.3 (55.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45. Fourth National Report on Human Exposure to Environmental Chemicals 227 .6-72.6 (55.3 (53.9-55. 1996).1 (91.7-68.7) 57.5 (43. which exert homeostatic regulation over molybdenum balance.2-91.2-59.2 (49.4 (79.0) 97.6-46.2 (49.9 (33.1) 35.1-88.7 (50.0) 39.2) 52.. semiconductor and battery industries have begun to use molybdenum.0 (46.8) 39.4) 76.5 (48.7) 78.0 (42.0-77. 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.0-110) 90. chemical reagents in hospital laboratories. and in pigments for ceramics.7) 77.3 (79.7 (73.0-85.5-91.4-75. interval) 45.0-56.8) 40.3 (38.7 (37.8-106) 88.2) 41.9-85.9) 34.3 (64.5 (41.1) 59.7) 51.9 (52.9 (73.4 (48.1 (71.0) 45. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0-38.8-49.0-71.7 (44.3-115) 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.6-58.7 (51. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.3 (73.4) 42.3 (55.0-100) 63.3 (37.3 (46.0 (48.8 (85.2-53. More recently.0-101) 82.7-84.0-62.2 (83.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52.2-59.0) 54.8-94. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.2) 79.3) 85. 2001.6 (73.0) 55.5 (37. 01-02.2 (61.7) 86.3) 83.1-63.8-108) 87.6 (40.5-41.3-47.7-50. 0. molybdenum is a cofactor for three enzyme classes— sulfite oxidase. aldehyde dehydrogenase.9-55.Metals Molybdenum or ore deposits.3) 65.9 (37.5-66.7) 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 78.5) 85.7 (58. Excretion occurs predominantly via the kidneys.2-79.3-44.5-46.2 (56.8) 46.4-52.6-82. and 03-04 are 0.5) 80.4 (72.4 (34.6-42.9 (78.7-96.7-122) 93.1) 82.4) 49.0) 62.4-61.6) 71.4) 41.2-42.1-44.2) 48.1-52.0) 60.6 (43.4-82. In humans.8-46.2 (55.5 (67.5 (81.5-65. lubricants.S.5 (49. 7439-98-7 General Information Elemental molybdenum is a silver-white.9) 67.6 (55.1-52.3-91. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.9 (32. Compounds of molybdenum are also used as corrosion inhibitors.6-62.2-37.1 (38.5 (41.1-59.6-96.5-124) 108 (92.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.3) 54. 2001). WHO.3-75.1-55.2-70.6 (52.6 (40.2 (69.6) 93.6) 51.9 (40.6) 71.8 (42.1-51.2) 40.9 (34.4 (80.7) 75th 84.0 (81.5 (74. see Data Analysis section) for survey years 99-00.1) 60.4) 45.2 (63.8.1) 46.7-60.8-90.7-105) 69.0) 84.2 (40.7 (45.0 (43.5-68.3-108) 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 47.7-51.3) 37. At a daily oral molybdenum dose of 24 µg.0-53.9-82.6) Selected percentiles ( 95% confidence interval) 50th 50.9) 62.7-47.7) 45.4) 56.0 (76.4) 52.7-91.2) 37.5) 60. inks.5) 47.3 (47.7-73. respectively.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. urinary excretion over six days CAS No. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.8 (82.5) 44.0 (42. and xanthine oxidase (Kisker et al.2 (38. 1997).8.2) 178 (147-259) 169 (138-197) 138 (127-152) 146 (112-171) 145 (129-159) 118 (105-125) 126 (114-134) 114 (103-124) 105 (98.1) 57.0 (41.8) 44.8) 48.3) 47. and paints.7) 78.7 (71.5-52.1 (34.9-83.8 (67.8) 75.5) 80.9 (44.7-92.4 (48.7 (36. population from the National Health and Nutrition Examination survey.

A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP. In industry.2 (33.8) 38.7 (30.3-68.1) 40.1-81.3) 61. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1-43.1-34.9 (49.5 (50.3) 41.4) 60.1 (38.8-67. of the ingested dose (Turnlund et al.1 (42.1-100) 86.7) 112 (95.8) 62. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.5) 90th 108 (97.2-80.1-43.0) 53.5 (37..4 (78.7) 41..1-40.5 (35.6 (36.5 (41.1 (44.1-39.2) 42.0) 72.2-103) 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 42.4-106) 85.2-41.7-38. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.1-41.2) 37.4-39.5) 71.7-100) 77.5-97.4-185) 106 (94.8) 79.6) 39.2 (73.3) 37.5 (65.0-46.3-52.3 (71.1-109) 89.4 (37.5 (34.6) 39.1 (33. urinary excretion over six days rose to 50% and 67%.8-66.7 (66.0) 38.7-62.6-88.3) 57.9-61.1 (54.3-56.6) Selected percentiles ( 95% confidence interval) 50th 41. 1999).8-47.1-67.8) 37.8-42.1 (30.3-141) 109 (81.0 (74. respectively.1) 37.6-63.8) 71.4 (56.6 (38.9) 92.8) 39. Biomonitoring Information Molybdenum is an essential element for health.7-40. 1997).9 (64.3 (51.8-118) 81.7) 57.9) 31.5 (83.2 (40.5-92.5-69.5) 63.9-87.9-71.4-42.1-38.9-117) 57.5 (40.2 (69.4 (53. but available epidemiologic data are scant.5 (80.6-63.5-48.4) 89.7) 115 (93.9) 79.3 (37.9 (39.7) 62.3-115) 98.4) 48.7-43.3) 64.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al. 1961.9 mg/kg/day and established a tolerable upper intake level of 0.1) 101 (83.5-60.6-78.5) 73.4 (55.S.2 (52.9-45.9 (39.4) 47. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.8-47.7-120) 87. EPA.2-49.7-52.5 (65.0) 39.9-41.4) 40.4) 77.2) 42. 1993). Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.6 (36.5-50.8 (37.4-41.9-42.2 (37.5-70.0) 44.5 (54.4-107) 85.2 (43.2-65.0-133) 119 (88.4 (67.0-120) 85.3 (55.8 (57.3 (36.5 (35.9-40.8) 61. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1 (40.0 (35.4-118) 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 (57.3) 40.2-40. and clinical or epidemiologic evidence of adverse effects is limited.1-112) 78.2 (50.5 (37.7) 75th 63.3) 43.4 (44.9) 41.4-120) 101 (84.1-79.9-96.4) 116 (101-126) 104 (88.5 (39.2) 38.0 (80.3-46. and urinary levels reflect intake from all sources.3 (83.7-93.2 (40. population from the National Health and Nutrition Examination survey.2) 58.7-44.2-96.1) 43.3) 44.9 (64.3-102) 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 40.1 (49.5 (78.2-121) 107 (92.4-76.9-68.0) 36.8 (75.0) 33.2 (36.3 (36.6-45.2) 55.5-119) 90.2-46.9 (40.5 (41.2-47.5-35.2-96.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.9-118) 91.0) 39.5 (40.6) 36.3) 56.2) 37.2 (40.9) 40.8-52.8-46.8-84.5 (39.7 (75. 1995).1 (82.6-76. interval) 43.5-46.0-41. 2001).0 (58.1 (38.8) 38.6 (71.8 (36.1) 56.9 (73.0) 62.5 (38. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.5-62.6 (59.Metals was 18% of the ingested dose.1 (37.3-59.3-43.3-45.3) 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 85.2) 43.4) 122 (107-133) 109 (99.8) 45.5 (59.4) 44.3 (71.0-56.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.8-65.7-137) 129 (109-155) 112 (97.5) 60.3 (58.1-39.5-44.7) 45.5 (36.9-45.6-61.9 (36.0) 88.1) 65.5-45.6-61.6-41.5-99.0-38. U.6) 43. Molybdenum is generally considered to be of low human toxicity.4 (59.7) 53.2) 39.9) 44. at daily oral doses of 95 µg and 428 µg.7 (77.9 (35.1-45.03 mg/kg/day in humans (IOM.2) 39.8 (90.1-127) 90.5) 72.4 (40.3 (53.0-103) 103 (90.6 (42.3-44..3 (37.1) 37.4-66.8 (56. Based on studies finding adverse reproductive effects in rats and mice.1 (39.5 (79.7) 42.S.4) 58.6 (57.4) 61.6) 48.9 (79.0-46.

(DC): National Academy Press.. Sciarra G. 56:322-327. vanadium. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Schindelin H. iodine. edu/openbook. Yarovaya GA. Occup Environ Med 1999. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Sabbioni E.niehs. Institute of Medicine (IOM). Van Meerbeeck JP.nap.htm. Molybdenum-cofactorcontaining enzymes: structure and mechanism.62(4):790-796. 2005). J Trace Elem Med Biol 2001.nih.66:233-267. vitamin K. Turnlund JR. manganese. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. 2001). et al. Rapid Comm Mass Spectrom 2002. Kisker C. White MA. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. chromium. Am J Clin Nutr 1995. Christensen JM. Zhurnal Obshchey Biologii 1961.S. Analyst 1998. Third National Report on Human Exposure to Environmental Chemicals. Gatti A. Minoia C. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. 1998.epa. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. nickel. Aprea C. Available at URL: http://www. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Atlanta (GA). 4/14/09 Iversen BS. 16:1313-1319. Rees DC. 144-154. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. excretion.216:253-270. pp. 2001.15(2-3):149-154. In: Trace elements in human nutrition and health..Metals in urine for the U. X. U. Available at URL: http://ntp. Keyes WR. Fourth National Report on Human Exposure to Environmental Chemicals 229 . A study of 13 elements in blood and urine of a United Kingdom population. 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.123(1):81-85. Kristiansen J. Menne C.22(3):179-191. and zinc: a report of the Panel on Micronutrients. Trace element reference values in tissues from inhabitants of the European Union. 2002. Washington. Schleyerbach U. Molybdenum in infancy: methodical investigation of urinary excretion. National Toxicology Program (NTP). arsenic. Dietary reference intakes for vitamin A. Shmavonyan DM. Droste JHJ. silicon.gov/iris/ subst/0425. World Health Organization (WHO). Peiffer GL. iron.S. Available at URL: http://books. Molybdenum absorption. Sabbioni E. 1998).. Weyler JJ. Environmental Protection Agency (U. Sci Total Environ 1998. Molybdenum. Food and Nutrition Board. 4/14/09 Sievers E. molybdenum. Schaub J. Ann Rev Biochem 1997. Ronchi A.S. 1996. Geneva: WHO. 4/14/09 White MA. TR-462. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect.php?record_id=10026&page=420. 2005. Vermeire PA. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. copper. EPA). References Centers for Disease Control and Prevention (CDC). Turci R. Minoia et al. van Sprundel MP. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Koval’skiy GA. Occupational risk factors of lung cancer: a hospital based case-control study. 420-441. pp. White and Sabbioni. Molybdenum 1993 [online]. boron.gov/index.

04. cisplatin. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. 0. 230 Fourth National Report on Human Exposure to Environmental Chemicals ..07.04. strength at high temperatures.Metals Platinum CAS No. respectively. carboplatin) in the treatment of cancer. 01-02. as oxidation catalysts in chemical manufacturing. 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. and high catalytic activity. and 03-04 are 0. dental alloys. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. thick-film circuits printed on ceramic substrates.S. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.g. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. which may vary for some chemicals by year and by individual sample. Important properties of platinum are resistance to corrosion. 7440-06-4 General Information Platinum is a silver-gray. < LOD means less than the limit of detection. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Platinum compounds are used in electrodes. and as drugs (e. 1998). 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. see Data Analysis section) for Survey years 99-00.. and 0. population from the National Health and Nutrition Examination Survey. and iron. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. jewelry. however. copper.

route of exposure (e.g. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 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. and duration of exposure. 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. The pharmaceutical cisplatin is an animal carcinogen and reasonably anticipated to be a human carcinogen as determined by NTP. 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.. or organometallic).e... Platinum metal is biologically inert..S. Fourth National Report on Human Exposure to Environmental Chemicals 231 ..Metals doses or at biomonitored levels from low environmental exposures are unknown... 1969).g.g. Workplace air standards for external exposure are established for soluble salts of platinum by OSHA and ACGIH. Platinum metal and insoluble salts can produce eye irritation. When ingested or inhaled. whereas soluble platinum compounds (e. inorganic salt. inhalational. Animals exposed to cholorplatinate salts used in industry have demonstrated severe hypersensitivity with asthma-like symptoms and anaphylactic shock (Parrot et al. 1975a. The carcinogenicity of other platinum compounds remains uncertain. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. halogenated salts) encountered in occupational settings can cause platinum salt hypersensitivity with symptoms that include bronchitis and asthma after inhalational exposure and contact dermatitis after skin exposure. metallic. 1969. cutaneous. Information about external exposure (i. Saindelle et al. 1975b). Toxicity is determined by the type of compound (e. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. oral). Most absorbed platinum accumulates in the kidneys and is excreted in urine (Moore et al. intravenous medicinal use. 2000). population from the National Health and Nutrition Examination Survey. or recommended for the metal form by NIOSH (Czerczak and Gromiec.

et al.. 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. Environmental Health Criteria 125. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. In: Bingham E. International Programme on Chemical Safety (IPCS).70(3):205-208. Gieler U. Gromiec JP. Schierl et al. Fruhmann G. Kelly J. Huber R. Urinary platinum levels associated with dental gold alloys. Cohrssen B.207(1):69-73. 1998). Arch Environ Health 2001. Allergy and histamine release due to some platinum salts. Hysell D. 2003. New York: John Wiley & Sons. Wilhelm et al. 206:15-24. 2003). and platinum. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Moore W Jr. palladium. 2000. Schierl R. Neuendorf J. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al.61(7):636-9. Parrot JL. Crocker W. Hebert R. Schierl.19:685-691. Saindelle A.01 µg/L (Becker et al. which elevate urinary platinum by five to twelve-fold (Begerow et al. Herr et al.55(2):138-140.. van de Weyer C. Turfeld M. Jankofsky M. Angerer J.org/documents/ehc/ehc/ ehc125. Powell CH. Boos KS. Fries HG. Duneman L:Long-term urinary platinum. ruthenium. Pethran et al. Hall L. Nowak D. References Becker K. Int J Hyg Environ Health 2004.. Schierl R.. and gold excretion of patients after insertion of noble-metal dental alloys. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Influences on human internal exposure to environmental platinum. 1999.. 1991 [online].04 µg/L) in this Report.org/documents/ehc/ehc/ehc125. Ewers U.inchem. Uptake of antineoplastic agents in pharmacy and hospital personnel.htm. Herr et al. Biomonitoring of traffic police officers exposed to airborne platinum. eds. J Expo Anal Environ Epidemiol 2003. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations.76(1):5-10. Schulz C. Petrucci F.4(1):27-36. Arch Environ Health:1969. Alimonti A. Campbell K. Environ Res 1975a.. et al. Occup Environ Med 1998.S. Begerow J. 289-380. pp.005 µg/L (Iavicoli et al. Schierl R. Pethran A. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Herr CE. Seifert B. 3/31/08 Moore W Jr. Int Arch Occup Environ Health 1997. Analyst 1998. rhodium. Carelli G.htm. Kaus S. Urinary excretion of platinum from platinum-industry workers. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum.35:313-321. Raab W. Kavanagh P. Part 1: monitoring of urinary concentrations. 5th ed. Nickel. Occup Environ Med 2004. Hauff K. Seiwert M.123(3):451-454. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Patty’s Toxicology. Wilhelm M. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Ruff F: Histamine release by sodium cholorplatinate. 1998). Modest (ten-fold or less) elevations in urinary platinum concentrations were associated with handling of cisplatin and carboplatin by pharmacy and other hospital personnel (Ensslin et al. Levels of platinum in urine for the U. et al. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Stilianakis NI. Biomonitoring Information Urinary platinum levels reflect recent exposure. Kulka U. Kuster W. and in blood and urine in the United Kingdom. Grimm CH. Ruff F: Platinum and platinosis. Hysell D. Blanks R.56(3):283-286. Several studies have shown that background concentrations in general populations were usually less than 0. Available at URL: http://www. Farago ME. Thornton I.9:152-158.. population were below the limit of detection (0. Schierl R. 2004) or less than 0. 2003. 2004. 2001). Czerczak S. Platinum. Environ Health Perspect 1975b. 2003.. Biomarkers 1999.10:63-71. Pethran A. Platinum concentrations in urban road dust and soil.. Rommelt H.Metals the International Programme on Chemical Safety at http:// www. palladium.inchem. 1997. Saindelle A. Bocca B. Kazantzis G. Senofonte O.13(1):24-30.. Br J Pharmacol 1969. Int Arch Occup Environ Health 2003. Ensslin AS. 2004). et al. International Journal of Hygiene and Environmental Health 2003. Iavicoli I. Schulz C. osmium.

390-.380 (.170) .280) .400 (.154-.430) .147-.470) .330-.240-.170 (.330-.180-.270-.220) .280 (. respectively. it has not been specifically mined or refined in the United States since 1984.400) .191 (.410 (.290 (.350-.167-.250-.220 (. 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.188) .200-.640) .180-.360-.137-.173) .450 (.230-.178) .220 (.290) 90th . In addition.162-.410) .197 (.150-.220) .420) .200-.390) .218) .430 (.360 (.220 (.159 (.340 (.350 (.02.190-.390) .370-.290) .239) .350) .02.240) .145-.330-.210-.146 (.350-.181-.180-.190 (.160-.270 (.520) . see Data Analysis section) for Survey years 99-00.185-.410-.250-.490 (.290-.160 (.170-.280 (.520) .260-.460-.380-.134-.360-.250-.590) . It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.167 (.410 (.160-.480) .290 (.420) .240-.230) .440 (.190 (.300-.430 (.400 (.380-.420) .200) .200) .500) .490) Total .310 (.163) .200 (.370 (.200) .147-.400-.410 (. interval) .500) .420) .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 .02.170) .150-.390 (. and 03-04 are 0.144 (.470) .300) .196) .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 .300 (.190 (.340) .440) .160 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.320) .187-.156) .180 (.176 (.390-.390) .230-.410-.420-.250 (.196) .350-.360 (.180 (.390) .215) .190 (.430-.330-.480) .500 (.230 (.330-.510) .250-. population from the National Health and Nutrition Examination Survey.370 (.290-. 01-02.210 (.133-.330-.330) .320) .410 (.450 (.170) . In the United States.430) .450) .470 (.330) .460 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.185 (.250-.420-.270-.360-.340-.320 (.149 (.160 (.410-.159 (.206) .260-.150-.220) .360-.450 (.167-. the latter being the current major industrial consumer of thallium in this country.290 (.400 (.280-.180) 75th .230-.250-.490) .370 (.220) .400 (.280-.202 (.520 (.280) .390 (.370-.410-.440 (.440) .550 (.240-.202) .450 (.460) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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 .260-.170 (.145-.180) .290) .153-.230) .370-.350) .173-.290) .201 (. representing distribution into other tissues.450 (.220 (.430-.400-.310-.360) .310 (.490) .320) .350-. Human health effects from thallium at low environmental CAS No.165 (.400 (.260 (.270 (. Fourth National Report on Human Exposure to Environmental Chemicals 233 .420) .200 (.240) .150-.380 (.220-.200 (.300) .430 (.148-.420) .260 (.420-.217 (.290 (.230) .480) .310) .250 (.140-. 2005).470 (.171 (.520) .420-.260-.690) .210 (.400-.370 (.350 (. 0.170 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.190 (.350-.330) .197-.280) .420) .410-.192) Selected percentiles ( 95% confidence interval) 50th .230) .158) .290) .177) .180-.159 (.360 (.184 (.470) .560) .450 (..160-.330) .390-. Thallium disappears from the blood with a half-life of several days.200 (.160 (.170-.400-.270 (.370 (.147-.350-.500) . From these and other sources.170-.450 (.217) .200 (.330-.370 (.430 (. thallium was obtained as a by-product of smelting other metals.380) .420 (.430-. In the past.340-.440-.400) .630) .490) .400) .180 (.S.243) .370) .200-.157-.260) .220) .170-.156) .190 (.220 (.210) .300 (.156-.172 (.440 (.270-.182-.270) .340) .270) .410 (.590) .270 (.145 (.440) .183) .160-.250-.410-.170-.480) .480) . and 0.310 (. thallium readily crosses the placenta and also distributes into breast milk.200 (.340-.370-.280 (.150-.150-.400) .250-.225) .170-.175) .220) .300) .240) .390-.173) .300 (.320-.400-.410 (.218) .510 (.360-.170-.290 (. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.200) .160-.172 (.Metals Thallium depilatory cosmetics.450 (.370 (.201 (.260 (.202 (.270 (.200) . however.155 (.450 (.360 (.370) .440 (.200) .160 (.172) .183) .290 (.260-.179-.340-.300) .250) .200-.400) 95th .135-.

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

Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L.Metals (CDC. 1990. Environ Res 1998. Trace metals in urine of United States residents: reference range concentrations. Jackson RJ. Sci Total Environ 1990. 1985). Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect.35(1):4-9.5 μg/L. Buhlmeyer G. 1992 [online]. 2005. Celier D. Paschal DC. 2005) and are shown with results from NHANES 2003-2004 in this Report. Martin J-C. 7/15/09 Blanchardon E.S. Sabbioni E. 1981.76(1):53-59. et al.1 mg/m3 (Marcus. A study of 13 elements in blood and urine of a United Kingdom population. Manke G. Brockhaus et al. J Soc Occup Med 1985. Brockhaus A. Investigation of a working population exposed to thallium. Trace element reference values in tissues from inhabitants of the European community I. Int Arch Occup Environ Health 1981. Challeton-de Vathaire C.. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. White and Sabbioni.. Trace element reference values in tissues from inhabitants of the European Union.cdc.47(3):223-231. A study of 46 elements in urine. 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. Minoia C. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U.95:89-105. Ting BG. Centers for Disease Control and Prevention. 1998). et al. population) are thought to correspond to workplace exposures at the threshold limit value of 0.atsdr. Soddemann H. Ewers U. Pirkle JL. Schmidt M. Pozzoli L. 1998. with concentrations ranging up to 76.216:253-270. White MA. Sampson EJ. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Gallorini M. X.265 people living near a thallium-emitting cement plant in Germany. Radiat Prot Dosim. 1980. Schaller et al. Int Arch Occup Environ Health 1980. Raithel HJ. et al.48(4):375-389. Apostoli P. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Schaller KH. Dolger R. and serum of Italian subjects. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Kramer U. References Agency for Toxic Substances and Disease Registry (ATSDR).. Minoia et al.html. Sci Total Environ 1998. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://www.gov/toxprofiles/tp54.113(1):47-53. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Valentin H. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Pietra R. Atlanta (GA). Morrow JC.. Sabbioni E. Paschal et al. Marcus RL. Toxicological profile for thallium. Investigations of thallium-exposed workers in cement factories. Cassot G. 2005. Boisson P. Wiegand H. 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. (1981) studied 1. blood.

380-.204) .060-.090 (. Evidence is lacking for the carcinogenicity of tungsten.500 (.082) .080 (.620 (.550) .073) . and as catalysts in the petroleum industry.090-.090) .056-.04.140 (.130) .250) .290-.530 (.130-.300 (.400-.190-.270 (.080 (. which is used in the steel industry.200) .120 (.620) .070) .065-.160) .170) .092 (.550) .360-.470) .210-.510-.100) Selected percentiles ( 95% confidence interval) 50th .123-.810) .180) .320) .084-.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 .110 (.770 (.130) .370-.00) .790) .170 (. filaments for incandescent lamps.070) .105) . Tungsten compounds are used as lubricating agents.650) .122) .470 (.170) . and for producing ferrotungsten. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.330 (.110-.060-.070) .230-.370 (.330) .107 (.097-.093) .120) .04.560) .360) .130) .090-.250) . population from the National Health and Nutrition Examination Survey.350) .090-.096 (.110) .080) .090) .090-.110 (.071-.080-.101 (.420-.113 (.130-.070 (.140 (.060 (.090-.180 (.560) .151) . Tungsten is used mainly for producing hard metals.126) .250-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.620) .190 (.210 (.400 (.073-.260 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).120) .170) .064-.210 (.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 .120) .130) .060 (.330-.100) .460 (.430-.S.250-.220) .310-.100 (.430) .400) .360-.160 (.130) .470) .380-.110 (.092) .150 (.230-.340-.280-.320 (.100-.250) .260-.04.350) .100) .091) .240-.370-.113 (.230) .073 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.078-.069-.300-.310-.380-.380) .180) .140 (.210 (.120) .560) .113 (.290) .160 (.082-.220) .240 (.360 (. and 0.100 (.460 (.270 (.092 (.080 (.190-.133) .062 (.590) .070 (.480) Total .310-.090) .056-.270-. interval) .060 (.460 (.135) .200-.230) .270-.640 (.260-.220 (.086 (.180) .180-.230-.420-.073-.081 (.070) . Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.140-.090) .390 (.070-.120) .330-.070-.460) .Metals Tungsten CAS No.120-.160) .077-.520) .53) .310 (.400 (.300) 95th .120) .110-.490) . 01-02.101-.190) .084 (.140-.074-.190 (.080) .830) .060 (.330) .113 (. and 03-04 are 0.190-.180) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.111-.120-.150) .440) .470 (.370 (.510-1.800) .280 (.080-.170-.320-.110 (.500) .087) .180-. 236 Fourth National Report on Human Exposure to Environmental Chemicals . Little information is available on the toxicity of tungsten. which are used in rock drills and metal-cutting tools. mainly as scheelite (CaWO4). 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.050-.050-.520) .300 (.370 (.800) .068) .070-.310-.100 (.050-.500 (.340) .200 (.060 (.270 (. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.180-.290 (.290-.137 (.065 (.060-.220) .180-.130-.270-.060-.350) .690) .100) .380-.210 (.080) .390) . see Data Analysis section) for Survey years 99-00.140 (.250) .100-.340-.260-.400 (.670) .100) .300) .250) .270-.430-.350-1.410-.210) .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 .120-.350 (.160-.490 (.160-.180 (.095-.360 (.160-. bronzes in pigments.071 (.530 (.082 (.158 (.132) .300 (.320-.360 (.430 (.410 (.116) .150 (.093 (.090-.058-.310-.250) .460) .080 (.070-.140) 90th .130 (.069) .160 (.090-.450 (.190-.380 (.080-. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.076 (.260 (.110) .550 (.160 (.430 (.105 (.340-.060 (.570 (.520) .370) .290-.470-.110 (.090 (.380 (.160-.230 (.280 (.060-.310) .082 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.510 (.260) .076 (.080 (.110-.170) .062 (.230-.087-.070 (.290) .100 (.093-.070-.084) .160 (.580) .150-.100-.450-.560 (.220-.320 (.530 (.100) .210 (.096-.060-.088 (.560) . 0.630) .090-.090 (.130-.570 (.430 (.104) .050-.400 (.130 (.066-.095-.109) .150 (. respectively.080) 75th .120-.550) .170 (.120-.120-.950) .088) .

069-.131-.426) .436-1.301) . Patients with medically-inserted tungsten found at increased levels in drinking water.094) .067 (.167-.154) .301) .199 (.279 (.253 (.072-.154) .077-.130 (.340 (.071-.089 (.439 (.074 (.122 (.133) .120) .116 (.500) .253-.245-.139) .138) .S.294 (.122-.120) .353 (. 2001).081-.125 (.333) .072-.431) .091) .090-.462) .237-.880) .279 (.158) .315-.105 (.073 (.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 .099-.087 (.237) .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 (.364 (.217-.082) .078 (.180-.385 (.317-.453) .302-.063-.091) .300 (.347 (.188-.216-.484 (. (1987) found possibly due to methodologic.426) .138 (.250 (.174) .086) .436) .169) . 2005).054-. measure urinary tungsten.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 .091) .255-.125) .079 (.080-.167) .117 (.124-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.064-.331-.124 (. population (CDC. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.308) . population.053-.084 (.091 (.100 (.S.098-.126-.667 (.231-.061-.308) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.412 (.119-.300-.103-.094-.270 (.431) .071) .555 (.060 (.151 (.074-.167) .306) .105 (.224) .198) .059-.216 (.360 (.497 (.121-.237) .096) .218 (.179-.283) . 2001-2002.158) .197) .071) .215) .075-.078) .605) .086-. similar to those in this Report (Schramel et al.074) .233-.065-.098-.079) .301) .068-.187) .061-.148 (.071) .067 (.157) . population from the National Health and Nutrition Examination Survey.077-.062 (.098) .088) .130-.063-.150 (.214) .258-.153) .121 (.085) .329-.250 (.333 (.069 (.439) Total .119 (.333 (.216-.439 (.174 (.302-.139 (.386) .063-.136-.085 (.063 (.375) .333-.075) .358) .095-.143 (.459) . population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.216-.164 (. 2003.082 (.075 (.084) .452-.117) .201 (.554) . 1998).216 (.181 (.084 (. Using neutron activation analysis to 2000.072 (.169 (. 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.083 (.431) .083) .059-.258 (.055-. 1997).379 (.255 (.056-.106 (.341 (.170-.333-.222) .111 (.215 (.255 (.482 (.28) .075 (.090-.089) .634 (.339 (.100) .138 (.083 (.091) .150-.060-.081 (.354-.279 (.161) .133) .143-.(Kraus et al.098-. and 2003-2004 (Paschal et al.144 (.199 (.205-.240-. Nicolaou et al.087) .073 (.079) .079) .359 (.083) .333 (.116-.197-.317) .484) .071 (.206-.060-.049-.084) .293 (.261-.209-.095) Selected percentiles ( 95% confidence interval) 50th .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.136 (.158 (.081 (.231 (.088) .267) .214-.267-.167-.208-. or exposure that a control group of non-metal workers had mean levels differences.082) .078) .285) .353 (.582) .061-..155-.344-.150-.079) .354) .074-.359 (.198-.063-.797) .176-.077) .823) .059-.465) .136-.146 (.065-.109-.074) 75th .201) .091 (.727) .197) .116) .133) 90th .148) .066 (.168 (.145 (.329 (.287) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.381) .253) 95th .083-.071 (.065 (.146 (.326) .538) .739) .080-.144-.122-.080 (.217-.203-.064-.086) .146) .056-.158) .054-.080 (.068 (.333 (.222-.107-.136-.465) .176-.109 (.136-.300) .057-.286-.067-.152-.075) .200-.100) .300-.284) .069 (..108) .065) .667) .070 (.153-.086) .333) .299 (.085-.063 (.211 (..272-.339 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.S.414) .078-.065-.092) .073 (.073 (.058-.139-.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 .079 (.392) .078 (.081) .278-.165) . interval) .317 (.410-.098 (. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.186 (.190) .179-.077) .093) .383 (.075-.065 (.104-.108-.250-.059 (.070 (.066 (.265 (.275 (.200-.093-.071 (.197 (.094) .057-.

Angerer J. and hair (Bachthaler et al. Jackson RJ. Link J. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. Nevada Exposure Asssessment. Cancer Clusters. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. The determination of metals (antimony. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Mosconi G. National Center for Environmental Health. Paschal DC. tellurium. Feuerbach S. Int Arch Occup Environ Health 1997. Seghizzi P. Pietra R. et al. Schramel P.62:380-384. Environ Res 1998.69(3):219-223. bismuth. References Bachthaler M. Sabioni E. Zobelein P. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis.(2):73-77. Angerer J. Occup Environ Med 2001. 238 Fourth National Report on Human Exposure to Environmental Chemicals .gov/nceh/clusters/Fallon/study. Wendler I. Weber A. platinum. Third National Report on Human Exposure to Environmental Chemicals. Nicolaou G.. 2004). urine. Manke C. Lenhart M.58(10):631-634.cdc.76(1):53-59. Schramel P. lead. Ting BG. [online] 2003. Pirkle JL. Trace metals in urine of United States residents: reference range concentrations. 4/15/09 Centers for Disease Control and Prevention. Kraus T.htm. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Centers for Disease Control and Prevention. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Metals blood. Schaller KH. Churchill County (Fallon). Paetzel C. mercury. Cassina G. Sampson EJ. J Trace Elem Electrolytes Health Dis 1987. Atlanta (GA). palladium. thallium. 2005. Available at URL: http://www. Catheter Cardiovasc Interv 2004. 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. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. cadmium. Morrow JC.

033 (.020) .007) .016-.158) .013-.012 (.009-.012) .011-.007-.028 (.056) .043 (.034-.018 (.034) .007-. 235U (about 0.042) .009) .030) . Uranium has many commercial uses.009-.045) .021 (.007 (. In workplaces that involve uranium mining.008 (.011 (.031-.007-.009 (.009) .020) .030 (.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 .017) .007-.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.026) .008-.048) . population from the National Health and Nutrition Examination Survey.009 (.017-.016 (.013) .009) .011-.008) .028 (.127) .009 (.020-.056) .010) .029 (. see Data Analysis section) for Survey years 99-00.021) .016) .011) .014 (.006 (.015) .007) .017) .008 (. nuclear fuel.017-.037 (.039-.040 (.022 (.037) .067) .016) .007-.023-.013) 90th .008) .036-.004.032 (.006-.006 (.008 (.010-.009) Selected percentiles ( 95% confidence interval) 50th .008 (.022-.038) .015 (.021-.027) .019-.009) * . human exposure occurs primarily by inhaling dust and other small particles.022-.S.008 (.023) .049) .013 (.036) .046) .007-.069) .007-.024-.053) .009 (.009-. milling.055 (. respectively.010) .030-.010) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.007 (.006-.007-.013 (.006-.017 (.033) .012) .008 (.031 (.023-.007-.012-.008 (. and as an aid in electron microscopy and photography.014 (. and 0.006-.050) .009-. 0.016) .010 (.008) .030 (. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.054) .048 (.010-.022-.044 (.009) .010-.013-.016) .010) .012 (.013-.011) .062) .031 (.027 (.033-.009-.016) .008 (.008-.010-.013 (.017-.018) .017) .010 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.027 (.012) .027) .017-.007 (.009 (.024 (.016-.023) .023 (.010) * .012-.009) . Variable concentrations of uranium occur naturally in drinking water sources.027 (.018 (.005-.007-. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).007 (.043) . interval) .046 (.034-.007) . including nuclear weapons.053 (.030 (.011 (.047 (.026) 95th .017 (.037) Total .009-.026 (.008 (.009 (.019-.011-.063) .026) .041 (.021 (.012 (.031 (. 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. 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.027 (.007-.023) .005-.028-.027-.012-.020-.012 (.006-.028-.012-.027) .027-.033 (.015 (.010-.008 (.009) .011) .045) .023-.046 (.010) .008-.007 (.006-.013 (.009-.007) .027-.007 (.006-.029-.039) .024-.011-.007-.022) .007-.036) . and 03-04 are 0.007-.040 (.008 (.040-.026-.021) .009 (.009 (.016) .008 (.060 (.012-.005-.011) .007-.009-.008) .012 (.008 (.008-.035) .015) .018) .007-.008-.073) .015-.064 (.015 (.025-.007-.006-.012 (. and 234U.017-.011-.009) .011) .005-.009) .008 (.010) * .013 (.008-.029-.007 (.013 (.006-.036-.008) .010-.037) .036 (.009 (.041 (.007) 75th .279) .018) .026 (.050) .065) .028 (.009) .018) .046 (.008-.042 (.026 (.015 (.031 (.020-.038 (.014 (.054-.006-.040-.040) .017) . Thus.011-.005.007 (.Metals Uranium CAS No.017) . 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.010) .008 (.007 (.014 (.019-.004.052 (.72%).072) .005-.026-.040) .006 (.021) .037) .010 (.014 (.010 (.049) .046 (.035) .008-.065) .019 (.039) .011) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks. Fourth National Report on Human Exposure to Environmental Chemicals 239 .009 (.009) . Since the 1990’s.023 (.014 (.020-.067) .007-. in some ceramics.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 .013 (.021-.008 (.009) .020 (.046-.066) .023 (.036 (.054) .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 .017-.009) . or processing.007 (.020-.009) .031 (. 01-02.114 (.012) .006-.019-.009-.018-.007 (.023-.011) .016-.027) .006-.012-.021 (.008 (.010) .009-.088) .007) .010) .035-.006 (.011-.024-.010 (.006-.051) .037-.

010-.006-.019-.067) .006-.009-.013) .044) .009-.018-.006) .035 (.020-.032) .027 (.019 (.010) .006 (.027-.007 (.005-.018) .025-.020-.025-.005-.051) .050 (.011-.008) .008 (.033 (.010-.026 (.014) 90th . In cases of retained DU shrapnel.013 (.007 (.008 (.021-.017) .030) .035 (.042-.007 (.005-.056) .027-.007 (.027) .010 (.015) .006-.006) .006 (.S.063) .017-.007) .008) . 1992).007 (.020 (.008-.006-.006-.020 (.010) * .007-.010) .080) .016-.006 (.013 (.006-. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.008) .027-.028) .016) .007 (.058) .100 (.016-.006-.008 (.004-.050) .007-.006-.017-.013 (.011-.006 (.024) .031-.007 (.039) .077) . which can occur occasionally from high occupational exposure.034 (.027 (.033 (. Radiation risks from exposure to natural uranium are very low.006-.042) .037 (.013 (.006-.015) .012) . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.009-.011-.008-.019-.021 (.009 (.034) .007 (.020 (.016) .009 (.007 (.008 (.019-.008 (.006-.006-.016) .006-.025 (.007-.024) .009) .008 (.015) .016-.011-.011-.019) .007 (.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.021) .028) .007-. with much slower elimination from bone.034 (.004-.006-.270) .007 (.015-.021 (.016) .007 (.010-.040 (. Inhaled uranium-containing particles are retained in the lungs.018-.009) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.047) .018-.014-.009) .026 (.028 (.025-.014 (.010) .074) .006-.015 (.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 .007 (.014) .025-.010) . low level exposure.009) .007 (.012 (.015-.008 (.011-.027-.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 .017) .028 (.031 (.006-.029) .045 (.010-.006-.006 (.028) .024) .030-.006) .008 (.015 (.016) .006-.010-.007 (.034-.016 (.017-. liver..013 (.025 (.033 (.012 (.013 (.007-.029 (.013) .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 .010-.039) .005-.019-. 240 Fourth National Report on Human Exposure to Environmental Chemicals . kidneys.050) .010-.011) .048) . population from the National Health and Nutrition Examination Survey.030 (.032) .007 (.029) .012) .020-.024 (.021 (.042) .009) .011) * .006-.008) .028-.012 (.051) .026 (.011 (.016) .024) .019-.1%-6% of an ingested dose may be absorbed.024 (.008) .011-.012 (. 2003).022 (.059 (.010 (.015-.017 (.019) .008-. interval) .041) .017) ..009 (.015) .029 (.015-.022-.007-.024-.007 (. After inhalation.012) .006-.016-.009) . Health effects from uranium exposure result from chemical toxicity to the kidney.029 (.009) .008-. which represents distribution and excretion.012-.020-.029) .022-.008) .018-.007) .014-. 0. After long term or repeated exposure.021 (.024-.048) .030 (.019 (.008) .034-.043 (.013 (.006 (.008) .051 (..005 (.008) 75th .034 (.009-.007-.030) .009) .013 (.034 (.033 (.014) .009) Selected percentiles ( 95% confidence interval) 50th .005-.028) .013 (.019 (.015 (.013 (.034 (.008) .009 (.033) .008) .009) .011) .007 (.027 (. where limited absorption occurs (less than 5%).012 (. After exposure to soluble uranium salts.010 (.016) .024) .010-.006-.007) .010-.058) .005-.007-.011 (.022 (.016) .027) .026-.023-.010 (.010 (.022-.009) * .039) .030-. Depending upon the specific compound and solubility.051) .026) .054) .007 (.009-.053) .008-.011-.007-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.018-.014 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.025) 95th .010) .010-.040) 883 682 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites * Not calculated: proportion of results below limit of detection was too high to provide a valid result.015 (.009) .017-.005 (.005-.006-.013-.053) .014) . Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.146) .017 (.014-.007 (.015-.007 (. Uranium is eliminated in feces and urine.061) .009) .008 (.006) .Metals impact.012 (.010-.018 (.008) .012-.022) .013) .030 (.022 (.005 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.009-.024 (.020) .029) .005 (.008-.006) . the shrapnel acts as a source of chronic.011-.010) .009 (.024-.039) Total .011) .006-.006-.008 (. 2005).012 (.

.168(8):600-605. 2006). 28 soldiers who may have been exposed to DU by inhalation. 41 (1). Radiation protection dosimetry. Sci Total Environ 1991. 2006)..066 μg/g creatinine (Gwiazda et al. 2006. Muggenburg BA.. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. Mil Med 2003. Uranium content of blood.S. Vol. or wound contamination. EPA.gov/ toxpro2. Carmichael AJ. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. 2006). 1978). the median urinary uranium concentration was 2. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. Drinking water and other environmental standards have been established by U. Centers for Disease Control and Prevention (CDC). The U. Stradling GN. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. 2001-2002..110 to 45 μg/L (Ejnik et al. IARC and NTP have no ratings for uranium human carcinogenicity.162 μg/L) (Orloff et al. and 2003-2004 (Dang et al..65 μg/L).1992. 2003. In 17 U. Dietz LA. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. In the same study. Six workers in a depleted uranium program showed concentrations of 0. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population.Metals injury associated with elevated urinary uranium levels (Kurttio et al.107:143-157. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Third National Report on Human Exposure to Environmental Chemicals..55 μg/L (median 0..S. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.1996.. Ejnik JW.011 μg/L (McDiarmid et al.. (May et al.e. Volf V.61 μg/g creatinine. in that the levels were below their respective detection limits (Byrne et al. McDiarmid et al. Benedik L.. respectively.78:143-146. with emphasis on quality control. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. population. (Kurttio et al. 1991. 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. Boyd P. et al. Durakovic A. Galletti. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. 2000). Thomas RG.html. but in whom no shrapnel was embedded. Atlanta (GA). 2004).S. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.. NRC. soldiers evaluated before. 2006). 2000). Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts..cdc. In a study of 105 persons exposed to natural uranium in well water. pp. eds.. Karpas et al. Zimmerman I. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Hamilton et al. and no consistent effects on multiple endpoints of kidney function were found. 1-49. Byrne AR. Fourth National Report on Human Exposure to Environmental Chemicals 241 . Dang HS. environmental levels) and health effects is available from ATSDR at: http://www. References Bhattacharyya MH. although slightly increased during and after deployment. during.. Breitenstein BD. Health Phys 2000. McDiarmid M. Hamilton MM. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U.. 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. 2005.S. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. 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. Metivier H. 2002). A cohort of 46 U. 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. Squibb K. the median urinary concentration was 0. Tolmachev et al.S. Pillai KC. 2004).. Komaromy-Hiller et al. Kent (England): Nuclear Technology Publishing.S.078 μg/L (ranging up to 5.. 2002. the geometric mean urinary uranium concentration was 0. urinary levels of uranium were as high as 9. In: Gerber GB. 1994.atsdr..62:562-566. had a mean urinary uranium concentration of 0. Information about external exposure (i. Horan P. 2004). 1992. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. Pullat VR. 2004). ingestion. Health Phys 1992.

Ting BG. Orloff KG. Pirkle JL.91(2):144-153. Lorber A.S.79(1):11-21. Saha H. Shelly T. Element reference values in tissues from inhabitants of the European community. Jackson RJ. Health Phys 2004. et al. VI. McDiarmid M. Biologic monitoring for urinary uranium in Gulf War I veterans. Uranium daily intake and urinary excretion: a preliminary study in Italy. Squibb K. Engelhardt SM.67(8-10):697-714. Kurttio P. Komulainen H. July 1978. Oeh U. Biokinetic modeling of uranium in man after injection and ingestion.158:165-190. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. et al. Int Arch Occup Environ Health 2006.Metals Galletti M. Kuwabara J. Sci Total Environ 1994.S. Heller J. Inductively coupled plasma mass spectrometry as a simple. Makelainen I.47(6):972-982. Noguchi H. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. concentration and daily excretion of uranium in urine of Japanese.22–Bioassay at uranium mills. Harmionen A. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Health Phys 1996. Charp P. patient population and literature reference intervals for urinary trace elements. Metcalf S. Costa R. Sampson EJ. Oliver M. Auvinen A. Van der Venne MT. May LM.S. Halicz L. Clin Chim Acta 2000. Paretzke HG. NRC). Englehardt SA. rapid. McDiarmid MA. Renal effects of uranium in drinking water. Salonen L. Cordero S. Paschal DC. Uranium and thorium in urine of United States residents: reference range concentrations. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo.110(4):337-342.S. Radiat Environ Biophys 2005. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Jarrett JM. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Roth P. Washington (DC): NRC.85:228-235. D’Annibale L. Salonen L. Health Phys 2006. Oberbroekling KJ. Sabbioni E. Wilson PD. Environ Health Perspect 2002. Smith D. Cremisini C. Marino R.94:319-326. Katorza E. Gucer P. Health Phys 2002. Bennett LG. Am J Kidney Dis 2006. Kalinsky V. U. Nuclear Regulatory Commission (NRC) Guide 8. et al. Kidney toxicity of ingested uranium from drinking water. Howerton K. Roiz J. Squibb K. Ejnik J. Mistry K. Environ Res 1999. Saha H. Ough EA. Kane R. Environ Res 2004. J Toxicol Environ Health A 2004. Pinto V. Lewis BM.71(6):879-85. Li WB.87:51-56. Karpas Z. Hollriegl V. U. McDiarmid MA.44:29-40. Karpas Z.296(1-2):71-90. Gwiazda RH.86:12-18. Human exposure to uranium in groundwater. et al. et al. Nuclear Regulatory Commission (U. Kurttio P. Komaromy-Hiller G. et al. Tolmachev S. Hancock RG. Pekkanen J. Review of elements in blood. 242 Fourth National Report on Human Exposure to Environmental Chemicals .81:45-51. Scott K. Auvinen A. Andrews WS. Comparison of representative ranges based on U. Hamilton EI. Health Phys 2004. Ash KO. Marko R. Health Phys 2003. Wahl W.82(4): 527-532.

32 (3.80) 3.11) 4.0) 13.0 (9. Perchlorate is stable under most environmental and physiological conditions.70 (3.10) 12.30-6.30-7. 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.90-3.0) 13.12) 3.66) 3.75 (3.0) 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 3.50) 3.0) 13.10-4..39-4.20 (7.0) 14.51 (3.40 (3.76 (3.50-3.0 (8.79 (2.81-16.0 (8. interval) 3.10-11.0) 12.40) 3. matches.70 (3.S.0 (11.40-7.0) 708 617 681 652 1228 1092 Limit of detection (LOD.0) 11.0 (12.67-5.16) 3. Other manufactured uses include fireworks.30) 6.0) 11.50-11.80 (3.0) 9. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.00-5. milk.29-3.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.90-12.0) 8.30 (5.0-15.05 (2.09) 3.80-12. 1998).0) 14.90 (2.. and reducing agents. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.40) 6.40 (4.0-17.40 (4. 2005).20-11.45-4.0 (9.70-3.18-3.0) 10.54 (3.07-4.60-6.60 (4.68) 4.0) 15. population from the National Health and Nutrition Examination Survey.20 (2.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4. laboratory analysis.88) 3.90 (5.0 (11.0 (11.22 (2.00) 3.0) 13.0 (9.30 (2.0-19.75-3.21 (2.0) 13.26 (2.40) 2.11) 3.60 (4.S.80 (7.0 (8.80) 75th 6.80-15.60) 8.0 (12. and certain plants with high water content (e.01 (2.S. or ammonium salt.0 (11.90-10.70-12.50 (8.70-9.93-4.0) 9.0 (8.50-4.0) 15.76) 4.40 (3.20 (2.90 (4.40) 3.20 (4.40 (5. and limited applications in pharmaceutics.0 (9.00) 5.0-18.05 and 0.90-6.10-7.40-11.40-6.20 (8.56) 3.30 (2.0) 95th 14.40) 4.0-15.0 (13.90-3. fabric dyeing.0 (8. but has strong oxidant properties in the presence of concentrated acids.0 (9.90 (5.0-17.90 (3.20 (5.40 (8.10-12.70-7.10 (6.40 (5.38) 5.70-6.0) 9.90) 5.84) 14.80-4.0 (12.19 (3.0 (11. Drinking water.10 (5. 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. 2007).30-19.00) 4.00) 3.50) 6. certain catalytic metals.0-20.60-7.0-18.19-4.96 (3. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.89-3.93 (4.50-7.80 (3.90-11. 2005).90) 6. lettuce) can be the main sources of intake for humans (FDA.65) 3.00-6.31) 2.0) 9.70-3.0-17.80-4.0) 10.20) 7.20-4.81) Selected percentiles ( 95% confidence interval) 50th 3.40-13.30-17.20 (6.10) 3. potassium. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .74-3.0 (10.50 (3.20 (4.46) 3.70 (3.80 (6.10-11.0 (11.0 (11.35 (3.0 (11.08-3. Survey years 01-02 03-04 Geometric mean (95% conf.60) 3.0) 11.40-5.60 (7.44-4.0) 10. and electroplating.0) 8.0 (11.90-9.93-3.20) 4.0) 16.20-3.90-11.50-4.0 (11.0-18. leather tanning.10 (2.50 (5.40) 3.49-3.0) 13.90-9.0) 14.0-23.50) 5. In addition.80) 7.80) 12. 2002).87-3. 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. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.0 (9.0-17.50) 11.80-6.05.80-8. 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.10) 3.10 (7.03) 3.90 (5. It is normally found and produced as the anion of a sodium.20-12.30 (5.70) 3. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.00) 7.20) 3.EPA.0) 9. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.10) 5.70-5.g.40-4.51 (3.70-11.60) 5.0 (12.30) 6.0) 13.0-14.10) 5.62 (3.40) 90th 10.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.0) 13.02 (3. Perchlorate was added to the U.0) 19.40 (5.0) 9.50) 5.0-17.22-5.20-4.00-6.10 (6.0 (9.0-29. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.47-4.5 hours and has a small estimated volume of distribution (Crump and Gibbs.40-4.Perchlorate Perchlorate (Urbansky.0-17.

50-3. gender.51 (3.20 (6.60-6. Survey years 01-02 03-04 Geometric mean (95% conf.0) 10.46 (3.0 (9.73) 3.44) 3. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.72 (3.45-2. menopausal status.61-10.87 (7.0-17.18-3.20 (3.00-3..46-4.4 (11.07 (2.10-3.87-3.2) 8. However.00) 9.Perchlorate inhibition (RUI). chronicity of exposure.0 (10.71 (5. Steinmaus et al.30-5.90-2.60-11.1 (8.90-9.80 (7. 2001.45) 3.4 (10.93-7.70 (2.05 (4.09) 3. 2006.84) 2.25) 5. 2005).0 (9.20 (7.24-2.76-3.96) 2.70) 10.0) 11. in a representative sample of U.42 (3.3) 8.20 (4.74) 7.60) 3.2) 8. 2007).10 (4.87) 2. 2005.10-7.0) 13..3 (10.98) 3.50 (6.60-15.39-4.80-3.87) 7.77 (3.20-9.29) 2.76 (3.37-13.0) 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 .30 (3.91) 4.02) 3. 2005.30) 5.0) 4.20-3.22-6.8 (11.90 (2.56 (3.20 (2.24 (4.EPA.58) 2.10 (6.93-5.66) 3.67) 5.0 (11.70 (4. women with urinary levels of iodine less than 100 micrograms per day.60-8. and the presence of other substances known to affect thyroid function (e.10 (2.22 (2.64-3.29-6.EPA.60 (3.70-5.12 (6..08 (3.83 (5.90) 5.90 (2.22-4.70-4.5) 8. levels.00-11.4 (11.40) 3. 2002).39) 2.20-3.1-16..60-5.21 (2.0 (9.0) 12. Lawrence et al.20) 8.51-4.4-16. 2000).10) 6. U. Follicular cell thyroid tumors would Urinary Perchlorate (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.30) 3.08) 3.03 (2. During gestation and infancy.56-3.S.35 (2. Li et al.33 (7. Lamm and Doemland.1-13.80-3. 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.4 (8.0-14. dietary iodine intake..25) 5.6) 20.0) 12.1-22. population from the National Health and Nutrition Examination Survey.0 (8. Greer et al.87 (5.1) 8.6-17.50) 5. nitrate.34-3.20) 3.14 (2.82 (5.37 (4..30) 90th 9.41-9.30 (5.00 (4.40-10.25 (3.0-19. 2002.30 (6.40 (7.30-5.75) 3.54 (2.60-11.0 (11.32) 5.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3..59) 3.4) 8.60-5.90-11.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.43) 6.1 (11.44-6.70) 2.89-3.7 (11. In the U.16-3.3) 12..00-2. interval) 3.0 (11. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.00 (6.60-8.19-6.40) 17.90-3.19-10.61-5.61 (5.20-4.50) 2.25) 5.S. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.93) 3. up to 68% RUI has been demonstrated.80 (4. 2002.35 (4.90 (7. 1999.26) 4.40 (3.04-3. Also.20-10.81-3.10 (4.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3. 2005). age. thiocyanate.10 (1.60) 8.54 (3. perchlorate is negative in most genotoxic assays (U.50) 2. although iodine intake was higher than U. 2005).52-9.22-4.95 (2.0) 7.S. 2003.99 (5.12-2. medications).60) 10.10) 3.90 (4.1-14.S.33-12.64) 5.70-15.30-10.90-20.86) 4.50-9. NAS.00 (2.93-8.70 (2.0) 13..33-6. altered thyroid function was not found in Chilean pregnant women or their newborns with mean urinary perchlorate levels about 40-fold higher than average U.47) 2. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.80 (7.S.39 (3.3) 11. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.97-5..0-14.0) 9.6) 12.3-14.04-3.40 (4.70-3.26 (3.0 (8.S. 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.0) 12.15-12.40) 5.50) 6.80) Selected percentiles ( 95% confidence interval) 50th 3. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.0) 6.90-15.89 (2. levels and sufficient in most participants (Tellez et al.36 (8.00) 4.50 (3.52 (8.09 (7.50) 9.30) 75th 5.4) 13.0-44. Many factors may be important in consideration of perchlorate action on the thyroid: dose.10) 13.46-13.S.0) 14.53 (2.g.02-4.0) 12.00) 3.35) 3.93-5.50) 95th 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 3.40 (3.50-5.5 (13.60-3.99-3.0) 9. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.10) 4.

17(4):400-407.40(21):6608-6614. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Deyhle GM.htm. J Expo Sci Environ Epidemiol 2007. Braverman LE. Chacon PM. Health Implications of Perchlorate Ingestion.fda. National Academy of Sciences (NAS).atsdr. Perchlorate in the United States. Magnani B. Valentin-Blasini L. 2005. Blount BC. et al. May 2007. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 .110(9):927-937. most of the population is considered to be below the U.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Environ Health Perspect 2006. (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. and nitrate on thyroid function in workers exposed to perchlorate long-term. Environ Health Perspect 2007. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Erratum in: Environ Health Perspect 2005. Tellez RT. Osterloh JD.41(5):409-411. Blount BC. Abarca CR. Food and Drug Administration (FDA). Additional information about exposure and health effects is available from the U. Crump KS. Primary congenital hypothyroidism. Richman K. Daaboul JJ. newborn thyroid function.90(2):700-706. Dyke JV. Thyroid 2000. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. He X. J Clin Endocrinol Metab 2005.115(9):1333-1338.S. Environ Health Perspect 2002. and environmental perchlorate exposure among residents of a Southern California community. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Miller MD. epa. Barnard JC. 6/2/09 Greer MA. et al. EPA reference dose (Blount et al.S.. thiocyanate. Lamm SH. The effect of short-term low-dose perchlorate on various aspects of thyroid function.11(3):295. 2001-2002. The effect of perchlorate. Sesser DE. Greer SE. Pino S. 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.113(11):A732. Braverman LE. Doemland M. Page Last Updated: 05/28/2009. J Occup Environ Med 2000. Landingham CB. et al. Valentin-Blasini L. Low dose perchlorate (3 mg daily) and thyroid function. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lawrence J. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Osterloh JD. 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. Washington (DC): National Academy Press. Benchmark calculations for perchlorate from three human cohorts. Crump KS. Mauldin JP. Dasgupta PK. Jackson WA.html. Howd R. Perchlorate Exposure of the US Population. Gibbs JP. Li FX. Lamm SH. 2007). J Occup Environ Med 2003. Environ Sci Technol 2006. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. 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. Braverman LE. Lamm SH. Environ Health Perspect 2005. Erratum in: J Occup Environ Med 2004. Pleus RC. Goodman G. Pirkle JL. Blount et al..45(10):1116-1127. Caldwell KL.. CFSAN/Office of Plant & Dairy Foods.113(8):10011008. Neonatal thyroxine level and perchlorate in drinking water.cdc. Lawrence JE. Thyroid 2001. Buffler PA. Li Z. Rutherford GW. Lamm S. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey.42(2):200-205.10(8):659-663. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Pirkle JL. Analysis of relative source contributions to the food chain. Pino S.EPA at: http://www.46(5):509. 2005). Skeels MR. References Blount BC.114(12):1865-1871. Lau EC. Kelsh MA. Also. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. National Research Council of the National Academies. Cross M. et al.html and from ATSDR at: http://www. Available at URL: http://www.gov/toxpro2. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans.S. 2005). Kirk AB. Byrd D. Steinmaus C. population.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653.gov/safewater/ccl/perchlorate/perchlorate.

Revised 2/11/05. Environmental Protection Agency (U. U. Integrated Risk Information System (IRIS).S. EPA/600/F-98/002 Washington (DC).15(9):963-975.Perchlorate pregnancy and the neonatal period. Perchlorate. Perchlorate as an environmental contaminant.gov/iris/quickview.S. Environ Sci Pollut Res Int 2002. 246 Fourth National Report on Human Exposure to Environmental Chemicals .9(3):187-192. cfm?substance_nmbr=1007. EPA).epa.S. Doc. Thyroid 2005.S. No.1/15/06 U. Available from URL: http://cfpub. Drinking Water Contaminant Candidate List. 1988. Environmental Protection Agency (U. EPA). Urbansky TF.

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

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

2007). elderly and children.. 2003).700) . and there was no clear evidence of excess all-cause or diseasespecific mortality. 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.. perfluorohexanesulfonate (PFHxS). see Data Analysis section) for Survey year 03-04 is 0.. Survey Geometric mean (95% conf.500) 90th .. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. U..10 (.S. 1999.. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.700 (. 2007b).20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .400-. In comparing three separate reports on adults.400-1.500 (.900 (.400-1. 2005). Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. 2003a). Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. 2003a. Olsen et al. Cook et al. and humans.80) 485 538 962 Limit of detection (LOD.40) . 2004a. 2003a.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 2003).800) 1.. reproductive. < LOD means less than the limit of detection.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al.300 (<LOD-.80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th . thyroidal).400-. 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. Harada et al..80) 640 1454 03-04 03-04 * * < LOD < LOD .00) . population. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.3.500-1. EPA. At high but non-toxic maternal doses of PFOS.500) . monkeys. 2007.50) . 2007a. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. 2005).800) 1. 2004b).300-1.. 2003.500-1. 2007a. Animal studies of PFOS have demonstrated weight loss.900 (.. 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. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.400-1. development in offspring was stunted and hypothyroxinemia was observed.800 (. or increased cancer rates (Alexander et al. U.. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003).. 2004. 2004.00) .800 (. PFOS.500-3. At doses causing maternal toxicity. In such studies. Fei et al. 2003. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years.S.10) .500-1. Olsen et al..400-1.. Fourth National Report on Human Exposure to Environmental Chemicals 249 .400-1. the potential to estimate risks to humans from animal doses is uncertain. PFOS. 2003. 2007b.500) . However.300 (<LOD-. 2001.500 (. EPA. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.600 (.400) .. 2003a)... PFOA. which may vary for some chemicals by year and by individual sample.800 (.. PFOA. Kennedy et al. 2003a. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.800 (.600-2.600 (. 2004). 2004)...10) * 03-04 03-04 * * < LOD < LOD < LOD . Thibodeaux et al.S.00) . hepatotoxicity.400 (<LOD-. population from the National Health and Nutrition Examination Survey. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.400 (<LOD-.500-1. Olsen et al..600 (. 1992.10) . and changes in thyroid hormone concentrations (Grasty et al.300 (<LOD-. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. Lau et al.20) .400 (<LOD-.500-. developmental and teratogenic effects were demonstrated in offspring.500) . A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. possibly related to lung immaturity (Lau et al.108 times higher than background serum levels in humans (Butenoff et al.500) .00 (.900 (.500 (<LOD-1.

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

Fourth National Report on Human Exposure to Environmental Chemicals 251 .400 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300-. see Data Analysis section) for Survey year 03-04 is 0.300 (<LOD-. population from the National Health and Nutrition Examination Survey.500-.600) < LOD .500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .500) 485 538 962 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (<LOD-. 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.S.600 (.400 (<LOD-.0.3. see Data Analysis section) for Survey year 03-04 is 1.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. < LOD means less than the limit of detection.300 (<LOD-.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum 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. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400) .S. which may vary for some chemicals by year and by individual sample.900) < LOD .500 (<LOD-. population from the National Health and Nutrition Examination Survey.

10) 4.10 (1.900-1.5) 8.00 (.3.70-6.00 (.90 (1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.80-4.50) 6.30 (1.20 (1.10 (.90-2.70) 1.05-2.30) 3.30 (1.900 (.40 (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 1.0) 1053 1041 03-04 03-04 03-04 1.809) 1. 252 Fourth National Report on Human Exposure to Environmental Chemicals .50 (4.80-8.80-8.10 (.50-6.60) 9.20-1.10) 1053 1041 03-04 03-04 03-04 .90 (1.10 (.826-1.40) 1.90) 90th 5.80) 4.50 (6.80 (1.90 (4.00-1.S.30 (6.60-7.10) 4.60 (1.03) 1.90 (1.09 (.40 (1.10) 75th 1.50) 2.70) 2. interval) .90) 3.80) 5.27) 1.40-3.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.90) 1.20) .50 (1.10 (4.20 (1.861 (.42 (1.62-2.30) 3.00) 1.912-1.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.689 (.900-1.91) 2.00 (1.70-2.30) 03-04 03-04 .30) 3.50 (4.10) 1.20-1. population from the National Health and Nutrition Examination Survey.00-1.20-1.70-2.60-2.90) 1.40) 4. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.40) 640 1454 03-04 03-04 2.72) 1.60-4.00-7. see Data Analysis section) for Survey year 03-04 is 0.86 (1.20 (6.30 (1.60 (1.54) .10) 1.800-1.30) .1) 485 538 962 Limit of detection (LOD.90 (1.20) 03-04 03-04 2.80-7.51) 1.60) 3.80 (1.80-7.50) 2.816-1.80-6.20-2.20-3.80) 90th 2.900) 1.80-3.30 (3. Survey Geometric mean (95% conf.17-1.20-1.10) 75th 3.852 (.721-1.70) 2.50-10.73-2. interval) 1.00 (5.20 (1.40 (1.20) 2.90-10.00) 1.60-2.60) 2.60-3.30-12.40) 1.80-4.700-1.16) .20) 1.900 (.586-.12) .30-9.70) 3.60 (6.90) 8.90) 1.80) 1.40) 2.08) 2.40 (1.10) 6.S.70 (1.44 (2.80-3.67-2.30 (2.70 (2.17 (1.70-5.70-7.00-6.60) 1.10) 8.60-2.14 (.10-9.70) 1.20) 485 538 962 Limit of detection (LOD.60-4.697-1.40) 640 1454 03-04 03-04 1.600-.984 (.900-1.10-9.70) 13.90 (2.90-19.20) 1. Survey Geometric mean (95% conf.40-1.80 (4.00 (1.80-2.50 (1.3 (9.5) 5.00 (2. population from the National Health and Nutrition Examination Survey.80-4.30 (1.50-6.60-8.87-2.00 (1.56-1.10-5.30-2.835-1.6) 7.04) .40) .20 (1.834-1.90 (4.00) 3.40 (2.77-2.70-10.900-1.900-1.93 (1.963 (.80-12.50-3.00) 2.800 (.50 (2.20 (6.10) 6.700 (. see Data Analysis section) for Survey year 03-04 is 0.01 (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 1.92 (1.50 (1.10) 5.30-6.30 (2.30 (7.00 (1.80) 3.50 (1.72 (1.26) 2.60 (1.1.900-1.40-1.0) 8.10 (4.00-8.966 (.50 (6.60-3.

7 (19. Survey Geometric mean (95% conf.35) 3.70-10.90-4.5) 57.2-22.9) 22.6-50.60 (3.0) 21.40 (6.47-4.53) 3.40) 75th 5.0-16.60 (4.3-61.0) 23.40-14.30 (3.0) 03-04 03-04 19.4) 75th 30.95 (3. interval) 20.37 (2.9 (22.3) 42.30-3.0 (27.9 (19.30 (5.80 (7.1.30-8.5) 9.30-11.00) 3.6) 9.9) 27.60-13.6) 7.3) 485 538 962 Limit of detection (LOD.0) 43.65-4.89 (3.3) 41.60) 8.90 (5.20) 4.10-3.4 (19.3 (28.5-62.40 (4.8-81.4-42.70-9.6) 42.2 (27.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.2) 30.20) 7.6) 35.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.90 (7.9-23.90 (7.80) 8.6) 21.2-57.90-4.40) 90th 7.70 (5.9-38.40-6.4) 20. see Data Analysis section) for Survey year 03-04 is 0.20 (4.1-33.70-5.1 (24.7 (7.7 (35.4-25.90-12.9) 9.30 (3.2 (21.40-6.79) 4.8) 27.1) 57.60-14.85-4.2) 30.7-23.6-45.80 (5.30) 7.8-22.5) 32.40) 5.3 (44.9-19.3) 28.6-24.84-3.91) 3.30) 6.5) 8.6) 62.6 (42.3-22.1-35.4) 640 1454 03-04 03-04 23.9 (17.8-30.80 (6.6) 18. interval) 3.60 (5.70-7.7-53.18 (3.1-25.60-6.6) 1053 1041 03-04 03-04 03-04 3. Survey Geometric mean (95% conf.8-78.90 (7.1 (23.3 (35.7-69.4 (17.47 (4.10) 5.7 (35.70 (3.1) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 4.5) 7.40-17.7-49.3 (35.80-4.20) 5.7 (13.20-9.60) 03-04 03-04 3.27) 4.8) 32.7 (43.0) 90th 41.0-20.60 (7.70-7.5-23.5) 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 21.67-4.50) 4.5 (28.10 (3.S.7 (43.6 (44.20-5.50-6.99-3.82) 4.00 (5.96 (3.5-33.80-9. Fourth National Report on Human Exposure to Environmental Chemicals 253 .4 (28.7-33.4.8-35.0 (20.1) 15.4-17.2) 640 1454 03-04 03-04 4.6 (35.70) 3.0-66. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.8 (34.40) 3.4 (23.60 (6.90) 6. see Data Analysis section) for Survey year 03-04 is 0.50 (3.11 (2.5) 18.5 (28.1-24.4) 21.50) 7.2 (18.0) 485 538 962 Limit of detection (LOD.1 (19.S.10 (3.21-3.70) 4.20-4.40-10.07-4.0) 21.50-4.80-12.30-6.50 (4.7) 39.10 (6. population from the National Health and Nutrition Examination Survey.6 (19.70 (5.60 (6.5-21.20) 5.50-13.20) 10.5) 1053 1041 03-04 03-04 03-04 14.2) 45.1-52.00 (3.2 (16.20) 7.1-36.8-22.3 (17.20 (4.4) 56.5) 19.7-30.60-9.2 (19.30-5.80 (6.0-70.8) 46.9 (13.8-22.9) 22.70) 6.8 (37. population from the National Health and Nutrition Examination Survey.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.0) 36.8 (45.00 (5.4 (19.2 (28.

300 (. population from the National Health and Nutrition Examination Survey.300 (.300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (.300-.500) < LOD 485 538 962 Limit of detection (LOD. Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (.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 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .300 (. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.300 (.300 (. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.200-.300-. which may vary for some chemicals by year and by individual sample.400 (<LOD-.300 (.2.200-.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300) .500) . see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey.300 (.300 (.200-.300) . < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300) .200-.200-.300 (.4. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300 (.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300) . 254 Fourth National Report on Human Exposure to Environmental Chemicals .200-.200-.300-.200-.500) .200 (<LOD-.300) .500) 485 538 962 Limit of detection (LOD.300-.S.S.200-.500) .300) .200-.

50 (1.700) 1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .60) 640 1454 03-04 03-04 * * < LOD < LOD .500 (<LOD-.10-1.600 (<LOD-1. which may vary for some chemicals by year and by individual sample.10-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .70) 1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.10) * 03-04 03-04 * * < LOD < LOD .30) 1.700 (<LOD-.30 (1.00) < LOD .S.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .00 (.10) 1.800) .600 (<LOD-1.6.600 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.900 (.300 (<LOD-1.900 (<LOD-1.900) 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 . < LOD means less than the limit of detection.900-1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .10 (1.300-2.00 (.10 (.700) 90th 1.700 (<LOD-.00 (.700 (<LOD-.700 (<LOD-.30 (1.20) 1.10) .80) 1.900-1.20 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.10) .40) 1.30 (1.900-1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .10-1.50 (1.80) 1.800 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (.700) .900) 485 538 962 Limit of detection (LOD.10-1.900-1.600) .900) .3.S. < LOD means less than the limit of detection.900-1.400 (<LOD-.900-1.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.400 (<LOD-1.60) 485 538 962 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample.00 (.10) 1.00-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .30) 1.20-1. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 0. Survey Geometric mean (95% conf.10 (.700) 1.700 (<LOD-. population from the National Health and Nutrition Examination Survey.300 (<LOD-.40) < LOD < LOD .90) .10-1.800) .700 (<LOD-.700 (<LOD-2.30) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900-1.600 (<LOD-1. population from the National Health and Nutrition Examination Survey.

Environ Health Perspect 2007.115(11):1596-1602. Cook JC. Kannan K. Seneviratne HR. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Rev Environ Contam Toxicol 2003. Liu RC. Morikawa A. Chemosphere 2006b. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Halden RU. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Environ Health Perspect 2007. Laane RW. et al.41:2237-2242. et al.115(11):1670-1676. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Mandel JS. Hurtt ME.39(3):363-380.63:490496. et al. Inoue K. Kuklenyik Z. Yoshinaga T. Hurtt ME. Grasty RC.Perfluorochemicals References Alexander BH. Environmental and toxicity effects of perfluoroalkylated substances. Reidy JA. Day RD. Kannan K. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Rogers JM. Reidy JA. Environ Health Perspect. Calafat AM. Butenhoff JL.1968--2003. Sasaki S. Crit Rev Toxicol 2004. brominated.39(1):80-84.7(4):371-377. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Aguilar-Villalobos M. Hekster FM. Environ Sci Technol 2004.113(2):209-217. Toxicol Appl Pharmacol 1995. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Edwards EA. Kennedy GL Jr. Tully JS. Mandel JH. Perkins RG. Bignert A. Inoue K. Kawashima Y. Murray SM. Mohotti KM. Toxicol Sci 2001. Apelberg BJ.34(4):351-384. Butenhoff JL.115(11):1677-1682. Keller JM. Environ Sci Technol 2007a. Yamashita N. Wong LY. Saito N.99(2):253-261. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion.39(23):9101-9108. Reidy JA. Yamashita N. et al. Loganathan BG. et al. Toxicol Appl Pharmacol 1990. Environ Sci Technol 2006a. Chem Biol Interact 2000. Environ Sci Technol 2005. Katakura M. Peterson RE. Chlorinated. and ex vivo studies. Holmstrom KE. Fillmann G. Fei C. and perfluorinated contaminants in livers of polar bears from Alaska.124(2):119-132. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. de Voogt P. Caudill SP. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Environ Sci Technol 2005. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years.179:99-121. Ingall GB. Hurtt ME. Calafat AM. The toxicology of perfluorooctanoate. Caudill SP. Mabury SA. Yoshinaga T. Yun SH. Wijeratna S. McLaughlin JK. Fluorotelomer alcohol biodegradation yields poly. Moore RW. Mandel JH.60(10):722729. Bandai N. Ye Y. Kuklenyik Z. Needham LL. Biegel LB.39(23):9057-9063. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000.Koizumi A. Kuklenyik Z. O’Connor JC. Burris JM. Kannan K. Occup Environ Med 2003. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Needham LL. Toxicol Appl Pharmacol 1992. Tarone RE. Saito N. Kuklenyik Z. Koizumi A.38(17):4489-4495. 2007b. Seacat AM. Herbstman JB. Calafat AM. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Witter FR. Corsolini S. Harada K. Biegel LB. Perfluorinated chemicals in selected residents of the American continent.68(6):465-471. Polyfluoroalkyl chemicals in the U.46(2):141-147.S. Taniyasu S. Birth Defects Res B Dev Reprod Toxicol 2003. Environ Sci Technol 2005. Rodricks J. Reidy JA. Kudo N.and perfluorinated acids. in vivo. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro.134(1):18-25. Lau CS. Jarnberg U.38(10):2857-2864. Olsen GW. Cook JC.104(2):322-333. et al. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea.40:21282134. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Olsen GW. Taniyasu S. Harada K. The influence of time. Regul Toxicol Pharmacol 2004. et al. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. J Environ Monit 2005. Suzuki E.60(1):44-55. Tully JS. Frame SR. Environ Res 2005. Needham LL. Olsen GW. Calafat AM. Gaylor DW. Evans TJ. Guruge KS. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Sci Technol 2004. Moore JA. Dinglasan MJ. Watanabe T. Falandysz J. Grey BE. Needham LL.S. Olsen J. Arendt MD. Calafat AM. Characterization of risk for general population exposure to perfluorooctanoate. Bookstaff RC. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Kamiyama S. J Occup Health 2004. Frame SR. Cook JC. Kumar KS. O’Connor JC.

Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. EPA). Hansen KJ. Toxicol Sci 2002. Lundberg JK. Environ Health Perspect 2003a. et al. Mandel JH.68(1):249-264. Washington. Available from URL: http://www.54(11):1599-1611. Thibodeaux JR. Mandel JH. Hanson RG. Olsen GW. Toxicol Appl Pharmacol 2004. J Occup Environ Med 1999. and perfluorooctanoate in retired fluorochemical production workers. Burlew MM. Olsen GW. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat.115(9):1298-1305. Olsen GW. Kannan K. perfluorooctanoate andother fluorochemicals in human blood. Burris JM. et al. Church TR. J Children’s Health 2004b. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Environmental Protection Agency (U. Bronson R. Seacat AM. Mair DC. Butenhoff JL. Korzeniowski SH.perfluorohexanesulfonate. Olsen GW.51(8-12):658-668. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle.111(16):1900) Olsen GW. Peterson RE.1177(2):183-190. U. The developmental toxicity of perfluoroalkyl acids and their derivatives. Lau C. Mar Pollut Bull 2005. Reagen WK. 2007a. Hansen KJ. Mandel JH.113(5):539-545. Froehlich JW. Buck RC. Church TR. Lau C. 2003a. Chemosphere 2007b.26(1):47-51. Prevedouros K. Biol Pharm Bull 2003. et al. Olsen GW. Ehresman DJ. Helzlsouer KJ. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Hansen KJ. Olsen GW. Yamashita N.111(16):1892-1901.74(2):382-392. Butenhoff JL.68:105–111. Hansen KJ. Barbee BD. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Burris JM. Toxicol Sci 2003. fish. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. 1/15/06 Vanden Heuvel JP. Thibodeaux JR. Thomford PJ. Horii Y. (Erratum in: Environ Health Perspect.gov/opptintr/pfoa/pfoara. Ehresman DJ. Kannan K. Grey BE. Taniyasu S. Butenhoff JL. Rogers JM. Coordinate induction of acyl-CoA binding protein. Hanson RG. Olsen GW. Zobel LR. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. fast foods. Butenhoff JL. Historical comparison of perfluorooctanesulfonate.41(9):799-806. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Ellefson ME. Lundberg JK. Cousins IT. I: maternal and prenatal evaluations. (Erratum in: Toxicol Sci 2004. fish. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Olsen GW.epa. Grey BE.37(12):2634-2639. Rogers JM.S. Church TR. Butenhoff JL. Larson EB. Yamashita N. van Belle G. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. et al. Biochim Biophys Acta 1993.82(1):359. J Occup Environ Med 2003b. Chemosphere 2004a. Environ Sci Technol 2006.Perfluorochemicals Kudo N. birds. et al. Seacat AM. Mandel JH. Horii Y. Sterchele PF. Cao XL et al. and humans from Japan. Taniyasu S. htm. Petrick G.198(2):231-241. Case MT. Gamo T. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts.2(1):53-76. Half-life of serum elimination of perfluoroo ctanesulfonate. II: postnatal evaluation. Hanari N. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Burris JM.45(3):260-270. Burris JM. Hansen KJ. Nesbit DJ.) Tittlemier SA. Pepper K. J Ag Food Chem 2007.S. and food items prepared in their packaging. fate and transport of perfluorocarboxylates. Butenhoff JL.55:3203-3210. A global survey of perfluorinated acids in oceans. Rogers JM. 2003. Sources. Moisey J. et al.40(1):32-44. Toxicol Sci 2003. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Miller JP.. Kawashima Y. Environ Sci Technol 2003. Environ Health Perspect 2005. Environ Health Perspect. Richards JH. Stanton ME. Seymour C. Huang HY.74(2):369-381. Burris JM.

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

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

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7 (70.2-31.8) 63.9 (11.1-116) 122 (93. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives. vinyl tile.8) 33.8.6-150) 94.0) 34.4 (59.9 (12.5) 16.S.1) 32.5-33.7-82.8-98.5) 55. and diet is the major source for general population exposure.1 (13.7-119) 99.0-85. can produce developmental and reproductive toxicity in rodents.9 (39.8 (21.2-20. and 0.0 (55.9-49.2-17.6-17. 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.3-27.8-64.1-61.4) 98.9) 18.S.7-14.6) 15. including MBzP.8-13.1-43.0) 32.2) 14.4) 108 (96.4) 49.3 (13.1) 29.4-25.4) 35.4 (27.3-125) Total 15.1 (13. NTPCERHR.1-39.9 (70.2) 13. 2000). because it is not bound to products in which it is incorporated.1-16.6) 29.1 (14.8-14.7 (13.6-72.9 (13.2) 32. some personal care products. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine..2-183) 101 (78.6) 25.3 (22.7-13.4 (10.3 (29.4-16.7-58.5-35.3 (12.8) 14.6) 13.3) 15.0) 16.9-190) 86.4 (29.2) 15.3) 54.7-17.6) 14.8-17.1) 31.8) 24.8 (38.1) 12.4 (10.9-30.3 (54.0-130) 101 (86.8 (14.3-75.8-35.5) 65.0 (26. and 2003-2004 were generally similar those reported in U. car care products.4 (68. respectively.4 (32.1 (14.5-94.5 (66.4 (48.1 (58. and 03-04 are 0.7-16.6) 37.3-18.2-40.9-28.5-145) 138 (106-241) 143 (127-179) 120 (99.4-15. interval) 15.0 (11.5 (26.8 (86.3-82.0 (30.7 (12.6 (53.7 (15.2-16.7-15.3) 23.1) Selected percentiles ( 95% confidence interval) 50th 17. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7 (82.7-35.0 (27.6) 24.1-18.3 (12.1) 13.4-92.6) 63.1-214) 166 (116-191) 145 (110-213) 88.4 (53.3-91.0 (14.9 (12.0-55. 0.4 (31.3-34.0) 24.0 (43.8 (28.3-12.8 (80.9-27.6) 13.6) 50.7-16. it can be released into the ambient air during use or disposal of the products.9) 13.6) 35.2-116) 122 (102-143) 101 (84.3-74.8 (71.3-130) 122 (88.9) 14.0 (34.8-17.9-14.6 (13.0) 33.8-18.2-33.9 (22.3-43.2) 22.8 (50.8-133) 89.6-18.5 (47.2 (19.8-76.4) 38.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.5) 82.7-170) 169 (134-198) 152 (99.2) 78.6 (32.5-97.9) 11. sealants.5-41.6-79.5 (55.5-14.6 (41.1-15.2 (25.4-120) 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. residents (Blount et al.8 (30.6-92.6-132) 103 (84.5) 27.6-43.5-18.5-25.3-18.6) 35..7) 23.7-172) 103 (74.0-26.5) 15.7) 38.8-16.7 (80. particularly male animals (McKee et al.2 (19.5 (61.6 (66.2) 17.9) 14.5 (57.9-62.5) 23.0) 20.3) 94.6-29.8-121) 79.9) 49.0 (23.0 (30.4) 75th 35.1-120) 52.5-62.2 (11.1-35.0 (12.5-84.9) 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 39.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 262 Fourth National Report on Human Exposure to Environmental Chemicals .2-39.0) 70.0 (33.7 (51.7) 40.1) 14.3-21.2) 14.6 (13.5 (76.9-47.7 (11. and to a lesser extent.3-161) 99.9 (16.6 (13.3) 13.5 (13.9) 43.7-25.3 (30.2-19.3) 63.4) 65.6-92.1 (55.6-39.1-15.3 (29.4) 129 (98.4) 35.4 (53.8 (10.3.2 (47.Phthalates Benzylbutyl Phthalate CAS No. BzBP can be released into the environment during its production and.7-16.4 (13.8-41.2) 33.0 (15. population from the National Health and Nutrition Examination Survey.9 (21.4) 80.0 (15.1 (10.0-106) 58. High dose BzBP and its monoester metabolites.1-90.4) 71.4 (32.2-16.6) 95th 103 (94.8) 28.4-127) 80.5 (27.5-36.2 (43. 2004.6 (21.8 (12. 01-02.2 (14.2 (10.1-16.2) 69.0 (20.9 (28.1 (20.7 (53.8 (53.4 (63.8-14.9-16.1 (19. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.6) 16. 2000).0) 23.3 (44.1) 67.9) 15.4-62.1.1) 68.6 (12. IARC considers BzBP not classifiable with respect to human carcinogenicity. see Data Analysis section) for Survey years 99-00.6) 67.1 (32.3) 37.4-24.5) 30.3 (12.4) 33.2-38.2) 66.8-16.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16.3-88.2-155) 91. Food crops take up BzBP.8-48.6-116) 122 (102-142) 101 (85.4) 12.4) 14.9) 12.5-36. 2001-2002.9-87.0) 90th 67.6 (13.6-38.4) 51.1) 76.3 (33.8 (71.6) 14.3) 13.5) 15.5-40.4) 81.2) 12.2-115) 113 (91.5 (67.1-38.8-72.

8-13.0 (49.5-99.3) 16.9 (10.9-16.5-58.1 (21.6) 53.8 (13.9-13.1-120) 77..8-13.5 (10.9) 24.8) 68.5 (49.4 (34.5-26.0 (12.5-26.7-123) 77.8 (10. 2007). 2002.9 (9.4 (46.9) 64.1-79.9) 12.4) 21.2-13.1 (19. adolescents compared with adults.8-15.0) 49.8-14. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6 (30.6-116) 74.4-93.7 (11.6-40.0 (12.1-14.9) 100 (80. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.3) 37.3) 29.4-116) 73. 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.7 (55.6 (24. 2005).4-14.6) 12.1-27.5-23.8) 16.1-12.8-14.4) 14.4 (25.5-38.5 (42.4) 17.5-76.2-12.3) 13.4-60.6 (22.0) 12.7) 38.1 (14.2 (56.4) 13.6 (11.7-31.8-80.4) 12.3 (39.3-73.6 (19..3) 13.7 (12.8-42.8-27. and in a small sample of German residents (Koch et al.5) 78.2) 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 12.9) 12.8 (57.5) 14.2-49.9-23.5) 17.9-62.7-397) 70.8-13.9 (22.Phthalates York City (Adibi et al.7-90.3 (38.8) 54.6-26.1 (21.2 (69.1 (53.5 (10.9-14.2) 12.3) 36.8-60.5) 16.2-15.6 (34.3 (12.0 (10.4) 90th 50.3-34.2-51.5-13.2-21.2-117) 95.0 (33.2-17.8) 24. 2004.0-90.0-48.6 (30.8-173) 195 (121-305) 229 (99.4 (12.9 (29.7 (38. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.3) 67.7 (59.6) 73.73-12.1) 27.6) 30.7) 19.9 (55.4-14.0-15.3-38.0 (62.1) 24.1 (21.9 (24. in men attending a Boston infertility clinic (Duty et al. 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.5-16.8-64.4 (21.0) Selected percentiles ( 95% confidence interval) 50th 13.3) 12. In NHANES 1999-2000.8-39.3) 18..9 (10.1 (11.4 (11.4) 13.5-58.7) 11.4-17.4 (11.8) 34.2) 32.0-109) 65.6 (15.3) 21.5 (12.4) 50.3) 13.6-13.4) 25. 2004)..7) 56. 2003).0 (67.7 (23.4-23.8 (30.1 (23.4-142) 134 (116-176) 136 (85.2-57.4-42.8) 53.9 (39.9-115) 57.7-14.8 (64.1 (43.2 (41.4) 15. 2007).4 (10.0 (41.9 (15.9 (43.5-57.8-85.1 (13. 2005.7-14.3 (60.5-42. 2006).8) 53. Weuve et al.4-18.9 (54. A small study of African-American women in Washington.5 (56.0 (38.8) 13.0) 24.3 (13.5) 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 .9-40. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.9) Total 14.1 (9.3-11. Hoppin et al.6-81.9 (51.3) 14.3-16.6 (11.8 (46.7-19.4-27.1 (21.2 (27.3-64.6) 13.4) 44.S.1 (18.4 (74.8) 108 (75.1) 39. 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.4-102) 70.0) 13.5) 41. In an annual sample of German university students..6-47..4 (11.4-19.2) 26.0-51.7 (13.2-13.4 (26.1 (25.6) 58.1 (13.7-15.9-13.5) 13.1) 17.4 (63.0 (41.69-11.8-34.2) 11.1-35.95-14..9) 11.1-12.7-15. interval) 14.5) 46.5-29.9 (12.8) 11. 2003).8-48.7-56. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.7 (11.1 (15.4-99.7-20.4-90.1-29.7 (21.7 (13.4) 60.6 (57.7) 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 40.1) 80.7-69.5-31.8-16.8 (49.7 (19.6-86.7-19.0 (11.8) 56..7 (18.9) 12.7-29.0) 24.7) 25.6) 38.8-15.2) 11.6 (36. in young Swedish men (Jonsson et al.6-15.9 (15.5-79.4 (69.0 (13.1 (41.5-61.8) 33.4-15.3 (23.8) 46.0) 15.1) 142 (99.9 (12..8) 71.4) 51.6) 12.6) 75th 25. 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) 28.3) 90.1 (34.8) 26.2) 11.3) 89.4) 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 12.7 (14.3 (15.4 (33.6-12.0-53.6-20.2) 67.9) 42.7-12.9-28.6 (11.3) 73.0-27.7 (54.1-58.1-125) 86.2-15.9-83.3) 55.8 (11.6) 25.1) 23.6 (51.5 (9.9-69.0) 60.5 (35.7 (11.4 (13.9-104) 62.5) 10.8-69. 2002).7) 46.6 (14.1) 12.8) 33.5 (48.1) 35.7-20. and females compared to males (Silva et al.3) 14.5) 23.2) 15.4) 104 (89.4-79.8 (50.5) 95th 77.5) 20.1 (46.8) 80.9) 52.0-26.8) 15.0) 11.9) 11. Hauser et al.9 (24..3 (24.5-213) 49. population from the National Health and Nutrition Examination Survey.2-26.6-99.8 (12.4 (60.3 (35.7-61.2-78.2 (40.5 (11.1) 24.8 (69.

Environ Health Perspect 2000. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Brock JW.93:177-185. Blount BC. Third National Report on Human Exposure to Environmental Chemicals. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Rossbach B. Reprod Toxicol 2004. Baird DD. Ryan L. Koch HM. Eckard R. Barr DB. Davis BJ. David RM. Epidemiol 2005. et al. Silva MJ. Available at URL: http://cerhr.108(10):979-982.22(3):688-695. Wiesmuller GA. Hauser R. et al. Brock JW. Drexler H. Meeker JD. et al. Rylander L. McKee RH. Sanchez GN. Gans G. Singh NP. Hilborn ED.25(2):293-302. Hodge CC. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP).S. Duty S.68:309-314.112(3):331-338. Calafat AM.210(3-4):319-333. Hagmar L. Chen Z.Phthalates References Adibi JJ. Camann DE. Silva MJ. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Barr D. Angerer J. et al. Reidy JA. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Environ Health Perspect 2003. Weuve J. Brock JW. Caudill SP. et al. Caudill SP. Environ Health Perspect 2004. Richthoff J. 4/20/09 Silva MJ. J Androl 2004. Prenatal exposures to phthalates among women in New York City and Krakow. Jacek R. Poland. Bull Environ Contam Toxicol 2002. Malek NA. Urinary levels of seven phthalate metabolites in the U. 2000 [online]. Koch HM. Int J Hyg Environ Health 2007. Giwercman A. Ryan L. Jedrychowski W.114(9):1424-1431. Pirkle JL. Needham LL. Levels of seven urinary phthalate metabolites in a human reference population.niehs. Wittassek M. Reproducibility of urinary phthalate metabolites in first morning urine samples. Environ Res 2003. Schettler T. Sampson EJ. 2005.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Environ Health Perspect 2002.110(5):515-518.16(4):487-493. Butala JH. Centers for Disease Control and Prevention (CDC). NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Hoppin JA. Hum Reprod 2007. Atlanta (GA). NTP-CERHR. Jonsson BAG. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Caudill SP. Hu H. Phthalate monoesters levels in the urine of young children. et al.111(14):1719-1722. et al. Duty SM.18(1):122. Green RA. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Perera FP.html. Silva MJ. Silva MJ. Helm D. Calafat AM. Research Triangle Park (NC). Needham LL. Dobler L. Environ Health Perspect 2006. 112(5):A270]. Urinary phthalate metabolites and biomarkers of reproductive function in young men.nih.

90 (4.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.. 2005.40-12.60 (5.90-7.44-2. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.5 (20.6 (9.80 (5.40 (2.60 (2.4 (14.71 (2. Survey Geometric mean (95% conf.30) 6.1-17.3-24. NTP-CERHR.7) 18.10-2.1-12...5) 23.6 (14.30-11.67 (5.0-14.56-4.1) 25.3 (11.17) 4.60-6.00 (5.10) 3.10) 11.11-3.50) 7.10 (4..50 (6.5) 19.72-3.10) 9.97) 4.40 (3.. 2004.6 (14.48 (2. they have been referred to as monobutyl phthalate (MBP).0 (13..5) 18.2-22. mostly as MnBP (Anderson et al..6 (11.49-2.97-7.40-3.0) 9. Biomonitoring Information Median concentrations reported in the NHANES 19992000.4) 22.30 (4.7) 15.5-16.80 (2. 2004. When total DBP metabolites have been measured.97) 2.50-6.50-2. and insecticides.40 (7.3 (18.68 (2. 2003).81 (3. Fourth National Report on Human Exposure to Environmental Chemicals 265 .50-4.6 (29.9 (16.70) 3.28-5. 2005).20-2.3-19.7 (16. 2005).2-33.96) 3.Phthalates Di-n-butyl Phthalate CAS No.5 (17.6 (13.07 (3.30) 10.40-9.7) 7.70-4. Studies of children found age-related differences in urine MBP levels.20-6.00-4.24-8.70 (2.5) 12.20-9.1) 22.8) 40.17 (2.80 (2.30-3.50) 90th 12.85-6.3 (19. interval) 2.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.40-17.1-25.S.3) 33.90 (6.4) 12.59) 3.0) 13.7 (9.30-13.6-14. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.2 (8.22 (3.80 (5.56 (5.00-6.3) 18.0) 20.4) 5.00) 4.40 (6.6) 12.6) 10.8) 677 652 703 699 1216 1088 Limit of detection (LOD. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.37) 6.00) 4.7 (18.50) 5.3) 3.3 (16.5-24.30-6.40) 5.0 (19.3 (13.70-4.4-27.00) 10.5 (10. 2003).S.90 (4.6 (13.26 (2.5-29.30 (1. Following oral administration of DBP to humans. DBP can produce reproductive toxicity in male rodents (McKee et al.2 (11. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.70) 5.63) 3.20-12.9) 10. In addition.5) 18. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.00) 6.6) 17.6-34. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.50) 18.5 (27.6) 17.60 (8.22) 3.43) 6. pharmaceutical coatings.00 (7.7 (17.2 (12.70-8.02) 4.30) 5.19-3.3 (16.56 (3.50) 2.2) 5.66) 2.50-10.80) 75th 5.00-11.3 (13. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.7-31.33 (2.10 (4.6 (10. 2001).73 (2.00) 7. about 65% to 80% of a dose is eliminated in urine within 24 hours.6 (10.84) 4.9) 15.3-48.30) 2.80 (3.0 (13.7-31.40 (2.40-4.5) 14.90-4.20 (3.1) 16.0) 12.10) 2. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.6) 26.1 (13.7 (7.1-20.5 (11.60) 3.0) 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.. 2007).0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.10 (3.90 (3.0) 24.46 (3.6) 16.70 (5.9-14.00-9.40-3.1 (8.30-2.6) 16.9-23.0 (11. CDC.7) 4. in a small sample of pregnant women in New York City (Adibi et al.82-3. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.80-5.20) 4.91) 4.60 (4.8 (9.9 (16.40-4. population from the National Health and Nutrition Examination Survey. Koch et al.56) 3.6-20.90-4.00-6.30-6.50) 8.0-18.4-12. 2000).20 (7.3-43.90) 12.46) 2.3.50 (3.7 (17. 2000.40-5.3-20. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.80-5.30 (3. 2005).90-2.5) 25.0-38. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.3-18.20-12.30) 10.5-16.7-20.3-30. and in a small sample of Japanese adults (Itoh et al.6-18.30-7.55) 2.7) 14.46 (2.20) 7. 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.0-25.46-5.20 (6.10-9.0 and 0.10) 8.4 (20.73-5.7-18. residents (Blount et al.8) 21. 84-74-2 Di-isobutyl Phthalate CAS No.2-14.6-26. Hauser et al..5) 22. and also in some printing inks. in men attending a Boston infertility clinic (Duty et al.10-9. OSHA has established a workplace air standard for external exposure to DBP.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.55 (3.

00 (3.15) 3. 2004).4) 23.27-12.3) 13.5 (11.6) 11.47-5.38-10.1) 11.7) 10.20 (2.82 (4.0) 11.62-12.39) 5. population from the National Health and Nutrition Examination Survey.43) 3.1) 10.7 (9.64-7.30) 2.76 (3.56-15.00-3.56-4.29-8.89) 6.5-19.69) 4.29-3.66) 2.26-2.37) 3.11 (5.83 (2.52-3.96 (3.78-8. than adults in NHANES subsamples during the same time period. In an analysis of NHANES 1999-2000.25) 5.7) 19.53-3.4 (12..42) 2.1-12.08) 75th 4.34 (3. interval) 2.57 (3.3 (17.7-28.28-13.7 (11.86) 6.2) 24.84 (4.91-6.7 (13.03-11.02-10.8-18.5) 13.01-2.33-9.05) 2. 2005).7) 11.45) 3. to about two to fourfold higher (Fromme et al.3 (13..56) 2.98 (2.56) 5.66) 4.18-4.03 (5.3) 13.09-2.2-13. Over this time.72) 5. An analysis of NHANES 2001-2002 showed similar age.8 (8.18) 4.78) 8.15-4.54 (4.33 (2.89-5.17 (2. ranging from more than one-tenth the NHANES median (Itoh et al.28 (4.3) 18..0 (8.1) 15.65-11.19 (2.02 (7.9) 12.79 (4.76-3.75 (4..58-4.65 (4.13-6.2) 8.07-5.21 (5.18 (4.73 (5.10-5.65-4.35) 3.18) 3.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .81 (6.81 (3.18-10.99) 7.08-2.4) 15.53-5.47 (3. 2006).1-24. 2007).95) 10.03-7.8 (9.6 (10. 2004).43) 3.94-12.4-16..9-16.31) 2.68) 3.41 (2.61-3.8-18.97-2.1) 13.59 (4.68) 5.89 (3.80) 7.57-4.6 (15.53-4.72-7.7 (21.30 (6.82) 4.0) 3.6 (12.04) 3.7) 3.51) 15.74-3.20-4.6) 13. Between 1998 and 2003. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2007).84 (8.26 (2.1 (10.5) 15.6-19.69-7.11-2.2) 9.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.24) 3.9 (11.52-20.78) 9. Survey Geometric mean (95% conf.8) 10.99-4.92 (7.2 (10.00-7.95-3.31 (7.74 (4.69) 6. the students’ median values for MiBP levels remained relatively unchanged.0-18.66 (8.46 (2.0) 7. while MnBP declined (Wittassek et al. respectively.11) 5.04) 7.0 (12.80 (3.64-7. Weuve et al.20-3.0) 15.5 (9.67-5.1) 4.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.86-4.20-2.6 (8.1-25.36-7.75 (6.57 (3. samples from German university students had consistently higher median urine levels of MnBP and MiBP.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.44 (3.80-3.39-3.76-15.1-15.81) 4.3) 16.14 (4.32 (3.66) 10.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.6-19.64-10. 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.S.4) 7.17-12.17) 90th 8. 2005). 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..55-6.54 (2.2-15.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.8-13.43) 3.46) 3.9 (15.8-36.31 (2. 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.04-5.8 (10.33 (3.51) 2.07 (2.9-26.85 (2.94) 6.79-8.52) 3.31) 2.93-6.47-12.46-11.68 (2.33) 3.54) 2. 2002.94 (5.6 (9.0 (10.18 (1..and gender.76-3.79-6.32) 7.2 (11.1) 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 2.22 (2.38 (6.00-3.1 (11.58-3.81) 9.6 (8.36-2.51) 5.69 (2.3) 28.62 (6.9 (9. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples. 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.95) 2.13 (2.88 (2.9-40.20 (2.32 (7.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.20 (7.52 (2.21) 10. up to four and 13 fold. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.

9) 21.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.0-32.7) 52.0) 120 (98.3) 24.0 (23.5) 95.7) 42.3-76.1-75.1 (51.1.6-69.6 (19.1 (19.9 (17.0) 31.5-117) 95.3-136) 137 (107-162) 119 (90.5) 47.3) 40.1-51.3 (56.2-159) 92.2 (21.9 (79.0) 27.4-42.4-159) 107 (84.3) 36.6) 20.6) 46.1-80.3 (60.5 (59.5 (30.6 (32.4 (38.2 (75.7 (51.7-106) 69.2 (78.2) 62.1-92.2-114) 73.2) 42.9) 18.2-32.2-21.1) 20.7-53.9 (17.1) 23.1) 23.0 (31.1) 30.5 (59.0) 20.7 (38.9) 36.6 (90.4 (71.8) 75th 51.9) 46.7-24. 01-02.1 (34.9-114) 116 (97.1) 36.1) 47.2 (20.7-42.2-24.1 (36.9-87.4-18. *In the 1999-2000 survey period.7-111) 64.0) 30.1-27.2) 38.6) 71.3 (23.0-19.5) 65.0 (18.1-20.5-43.9) 75.3-60.4 (23.9 (79.3) 18.5) 34.7) 74.2-63.0) 21.6 (48.6) 38.2-93.6-40.6-33.1) 31.6 (16. interval) 24.4-25.2 (79.4 (84.8) 62.7) 92.8-132) 95.7-116) 95.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.5) 19.7-42.4-26.1 (28.5 (29.0 (30.3) 19.7) 124 (98.7-127) 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 22.0) 84.4 (36.1-29.3) 21. respectively.5-47.6-36.0-51.6 (26.S.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.9-33.6-29.9 (20.1 (62.7 (64.3) 26.7 (18.6-37.0 (36.4 (35.4-20.2) 20.1) 19.9) 29.8-111) 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 23.2 (59.6-24.6 (65.3-24. Fourth National Report on Human Exposure to Environmental Chemicals 267 .8-29.0 (45.2-56.2 (21.0) 38.0 (20.0-24.7-121) 97.8) 58.2 (17.0-21.8-25.3 (42.8-22.3-96.3 (36.9.2-87.1 (19.4) 64.6 (55. see Data Analysis section) for survey years 99-00.2-22.7-117) 118 (108-143) 93.7-34.4 (25.2) 68.0-26.2-49.6 (22.9-22.4) 20.0 (17.2 (58.4.5-27.2 (25.5-42.7 (28.8) 43.5) 40.6) 21.6-48. population from the National Health and Nutrition Examination Survey.2 (19.2) 26.1-22.4 (19.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.2-33.8-42.1) 46.7 (43.8-123) 101 (90. 1.7-92. Survey Geometric mean (95% conf.9-28.5) 21.5) 78.7) 28.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.0 (25.7 (70. and 03-04 are 0.6-143) 127 (99.7 (24.3-145) 85.8) 23.0-24.9-22.0-19.9) 26.6) 80.0 (72.0-58. and 0.4) 59.1) 23.1 (26.5-47.4 (35.4-31.1 (16.5) 85.3-40.1 (31.9-53.9-42.2-23.4 (72.4 (21.3 (51.6-29.9) 71.9-79.1 (19.7-26.7-34.5) 31.6) 39.5 (74.3) 23.2 (74.6-44.5-44.3 (17.4-44.8 (19.5-121) 106 (94.9-101) 77.2) 90th 98.1) 17.0 (78.3 (37.1 (21.2) 32.5-60.6 (61.1 (17.6 (44.3 (23.3-21.0-73.3 (30.5) 36.1-82.1 (58.8 (57.0) 117 (104-131) 112 (84.1-24.6) 35.7 (18.4) 22.4) 52.5) 37.5-53.5) 24.7-20.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.7 (16.8) 19.5 (28.5) 26. referred to as monobutyl phthalate (MBP). concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.5) 36.1 (41.3-67.3-85.7 (19.3-79.7 (33.5) 17.6-49.6) 17.1) 25.4 (35.8-119) 90.3 (30.7 (22.4 (35.1 (18.9-92.5) 20.6-20.1 (19.2 (18.8) 48.6-113) 108 (90.1 (54.4-60.0 (15.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.7-91.6-31.

5 (18.9 (35.5-16.3-71.0-90.0) 70.6 (31.7-21.9-34.8) 75th 38.5-30.5-70.7 (57.4 (19.3 (42.2-61.3 (21.9) 49.6) 64.8-235) 137 (108-198) 88.3 (76.5-142) 81.0-47.8) 20.0-19.1-21.0) 53.9-36.4-131) 81.1-128) 97.6) 39.3-106) 74.7 (12.2) 59.4) 53.9 (20.5-21.1 (61.3-18.6) 14.8-43.6-16.0 (61.7 (27.7 (19.5 (81.9 (39.0 (50.3 (46.3-21.2 (16.7) 19.8 (18.3 (55.1) 44.6) 25.8) 63.3) 52.0) 55.2-22.9-56.3) 59.9-38.0) 19.8 (33.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9) 14.0-38.1) 22.2-108) 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.3) 35.3 (17.3 (48.5-23.5) 21.9-68.2-85.4) 62.5) 91.1 (21.3 (69.8) 19.3-20.2) 159 (102-263) 147 (93.9 (35.3 (28.6) 24.9 (21.3) 19.9) 20.4-76.1 (56.7 (16.8) 13.6-155) 91.4) 19.6-28.8) 40.0 (27.0) 41.3-49.1-32.0 (16.7) 42.0) 26.0-60.0 (15.1-23.5-76.8) 17.6-22.9) 28.4 (31.3 (60.6-23.5) 60.3) 33.3 (71.3 (24.9-68.6-24.7-37.4-24.2-48.5) 84.7 (28.0 (34.9-70.2) 65.0 (19.8-24.6-26.3) 17.9 (30.5) 134 (93.9 (73.4 (16.5-15.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.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.7 (73.6-32.2) 31.1) 17.1) 35.4 (68.7 (60.1-99.8) 34.9-49.4-135) 71.6-43.3 (17.4-34.1 (34.4-72.2 (38.4 (50.6) 65.3-114) 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 17.9) 19.2 (83.8) 28.6) 18.2-22.2-106) 64.3-32.1) 20.5 (30.6-44.6) 83.7-26.4 (17.1 (32.4 (50.3 (16.6-53.3 (52.0) 108 (71.5) 82.6) 24.8) 34.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.0) 28.9-105) 85.2) 74.2-73.4 (47.8 (17.2 (19.0 (18.3-23.4) 15.9 (56.7-20.8 (65.7 (43.7-42.2-27.6 (25.6) 38.3-26.0 (43.3) 18.3) 19.7-80.0 (70.0 (20.3) 67.1) 20.4 (20.0-113) 104 (83.4 (13.2 (35.3 (19.8) 20.1) 42.8 (18.7-28.1) 21.3-40.9) 24.4-164) 96.9 (19.7-39.5-18.6-119) 63.8 (50. interval) 22.9 (16.3-38.7 (81.3-81.3) 20.4 (31.4 (16.6 (74.5 (18. population from the National Health and Nutrition Examination Survey.9 (58.5 (14.8) 35.5 (64.6) 34.2-86.6 (19.2) 16.4-47.4-65.8-23.7-19.6 (61. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value. Survey Geometric mean (95% conf.3-78.5) 90th 68.7-19.7 (14.3-17.4 (17.8) 30.4) 20.9) 52.6 (25.0 (26.1 (29.7-78.6-92.7) 36.4 (33.9 (64.0 (52.4) 16.0-75.2-16.5-64.7-51.0 (71.0) 81.9) 39.0-41.1 (15.4 (31.9-26.4-103) 117 (83.3) 33.2-21.6-24.2-18.0-92.8) 17.3 (52.6-128) 96.1) 61.1-62.8 (25.6 (57.3 (17.5-41.0) 25.8 (13.4 (23.5-22.9-100) 86.9 (30.6 (72.8-32.4) 21.4) 51.4 (53.3-39.7 (60.0) 94.2-179) 84.6-50.6-44.S.2-28.9-84.8-24.0) 75.9) 62.9-14.6 (17.4 (18.7 (54.4) 15.5 (15.8) 23.5-142) 89.8 (18.1 (46.4 (45.2 (19.6) 31.6-74.0) 29.9 (37.1) 37.2-22.6) 37.3-21.0 (69.4-61.9) 30.0) 35.1-83.4 (37.7 (20.5-37.6 (41.4 (56.0 (18.5) 39.8 (16.6 (27.8) 22.6 (29.1-18.6-19.9 (30.1-99.6-27.8 (22.1) 53.9) 91.6-23.2) 21.6) 23.1) 50.6-42.0-17.7) 20.8) 17.7-23.5) 17.0) 59. 268 Fourth National Report on Human Exposure to Environmental Chemicals .6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.3) 21.

Brock JW. Barr D. Ryan L. et al. Helm D. Butala JH. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].68:309-314. Wittassek M. Fromme H. Silva MJ. Masunaga S. Int J Hyg Environ Health 2007. Reprod Toxicol 2004. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Jedrychowski W. Caudill SP. Green RA. Jacek R.nih. 112(5):A270]. Itoh H. Anderson WA. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Hagmar L. et al. et al. Int J Hyg Environ Health 2007. Calafat AM. Koch HM. Needham LL. Pirkle JL. Ryan L. Hauser R. Rylander L. Schettler T.gov/chemicals/ phthalates/dbp/dbp-eval. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. J Androl 2004. Scotter MJ. Castle L. Malek NA. Drexler H. Yoshida K. Springall C. Meeker JD. Duty S. Environ Health Perspect 2003. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Reidy JA. Sampson EJ. Prenatal exposures to phthalates among women in New York City and Krakow. Angerer J. Food Addit Contam 2001. 2005. Caudill SP.114(9):1424-1431. Centers for Disease Control and Prevention (CDC). Brock JW. Singh NP. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Hodge CC. Urinary levels of seven phthalate metabolites in the U. Angerer J. Bolte G. Camann DE. Massey RC. Koch HM. Poland. Dobler L.111(14):1719-1722. Calafat AM. et al.18(1):122. Drexler H.108(10)979-982. Silva MJ. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.Phthalates References Adibi JJ. Blount BC. Levels of seven urinary phthalate metabolites in a human reference population. Duty SM. Gans G. Environ Health Perspect 2006. Bull Environ Contam Toxicol 2002. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Third National Report on Human Exposure to Environmental Chemicals. 2000 [online].22(3):688-695. Eckard R. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. et al. Sanchez GN. Richthoff J. Epidemiol 2005. Silva MJ. NTP-CERHR. Environ Health Perspect 2000. Koch HM.html. Perera FP. Caudill SP. David RM. Boehmer S. et al. Needham LL.112(3):331-338. Environ Res 2003. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Jonsson BAG. Phthalate monoesters levels in the urine of young children. Int J Hyg Environ Health 2005.208:237-245. Wiesmuller GA. Hum Reprod 2007. McKee RH. Silva MJ. Hilborn ED.S. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Available at URL: http://cerhr. Rossbach B. et al.25(2):293-302. Hu H. Atlanta (GA). et al. 4/20/09 Silva MJ. Environ Health Perspect 2004.210(3-4):319-33. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Barr DB.93:177-185. Weuve J.18(12):10681074. Chen Z. Research Triangle Park (NC).210:21-33. Giwercman A.16(4):487-493.niehs. Fourth National Report on Human Exposure to Environmental Chemicals 269 .

500 (.500 (.500 (.300) < LOD .400 (<LOD-.500-. and 03-04 are 0.500) < LOD < LOD .400-.S. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.70) .200-.700) . Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.400-.00 (<LOD-1.500 (.500) < LOD < LOD .500 (.10 (<LOD-1.300-.Phthalates Dicyclohexyl Phthalate CAS No.00 (<LOD-1. polyvinyl acetate.300-.400-.500) 1.90) .600) < LOD .400) 1.400 (.300-.200-.200-.400 (.10 (.400 (.300-. only levels at or above the 90th percentile could be characterized.400-.300 (<LOD-. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.300-. population from the National Health and Nutrition Examination Survey.00 (<LOD-1.20) .500) .600) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70) .300) < LOD .400 (.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 .400 (<LOD-.80) .500) < LOD 1. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.700) .400 (<LOD-.10 (<LOD-1.70 (1.400-.500 (.500) 1.400) < LOD 1. 270 Fourth National Report on Human Exposure to Environmental Chemicals . 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.600) .500 (.600) . and polyvinyl chloride.500 (.700) . 0. and polymers.600 (.00) . which may vary for some chemicals by year and by individual sample.300 (.70 (1.500) 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 .300-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. < LOD means less than the limit of detection.900-1.500) .500) . In this Report.400 (<LOD-.400 (. 01-02.300 (. and 0.300 (.300 (.300-.50) .300 (.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . respectively.400 (.3. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.600) .400-. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Survey Geometric mean (95% conf.10 (<LOD-2.600) .10) .400 (. including nitrocellulose.00-2.500) < 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 1.200 (<LOD-.300 (.2.200-.400) 1.500) 1.300 (. resins.300-.00-3. see Data Analysis section) for Survey years 99-00.200-.300-.500 (.50) .300-.9. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.400-.200-.400) < LOD < LOD .500) .

910 (.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 .250 (.710) .54-6.34) .420-.770-1.500 (.510 (.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 1.00 (<LOD-3. population from the National Health and Nutrition Examination Survey.610 (.770) < LOD 2.530-1.590 (.630 (<LOD-.690) < LOD 2.420-.310) < LOD .530-.470 (.16 (<LOD-3.36-1.82) .44) .05) .220 (<LOD-.880 (.830) 1.54 (<LOD-2.390 (.500-.53) .350-.290-.740) < LOD < LOD .690-1. Fourth National Report on Human Exposure to Environmental Chemicals 271 .770 (.770-1.420-.770-1.14 (<LOD-3.54) .370 (<LOD-.590 (<LOD-.620) < LOD .660) .330 (.S.670-1.490) .33 (<LOD-3.310-.530) 1.530) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.240-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .43 (1.690) < LOD < LOD .10) .660) < LOD < LOD .330 (.270) < LOD .670 (<LOD-.400-.12-1.170-.740) .410 (.910 (.800-1.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .06) .00) .360-.510-.560) 1.450 (.470) 3.380 (.530 (.630 (<LOD-.33) .910 (.17) .53) .480 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.11) .260-.400-.500) 3. Survey Geometric mean (95% conf.450 (.67 (1.690 (.910 (.940 (.790-1.82 (1.06) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.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.74) .950 (.380-.18) .16) .22 (<LOD-1.

Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. shampoos. 272 Fourth National Report on Human Exposure to Environmental Chemicals . 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 91.9 (61. 2007).9-92.4. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. colognes.3-103) 193 (141-256) 184 (148-227) 221 (165-294) 180 (140-221) 181 (152-212) 188 (158-219) 197 (129-249) 183 (142-217) 196 (170-241) 564 (419-818) 479 (387-651) 557 (432-695) 482 (390-590) 498 (441-567) 533 (471-629) 378 (290-730) 451 (315-636) 521 (295-571) 1510 (1050-2150) 1260 (983-1480) 1250 (973-1560) 1340 (1010-1660) 1350 (1060-1660) 1590 (1220-2070) 756 (379-1070) 808 (572-1090) 827 (542-1440) 3260 (1550-4420) 2070 (1470-3050) 2310 (1360-3310) 3480 (2230-4640) 2720 (2160-3670) 2980 (2250-3800) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 179 (149-215) 182 (157-211) 197 (173-224) 178 (154-206) 174 (153-198) 189 (160-225) 154 (119-197) 171 (139-199) 171 (148-201) 174 (138-210) 167 (139-194) 182 (138-219) 523 (372-650) 502 (419-603) 536 (449-654) 425 (350-508) 427 (387-498) 478 (392-564) 1440 (1020-2280) 1450 (1060-2110) 1520 (1210-2070) 988 (880-1230) 1050 (879-1310) 1260 (969-1640) 3500 (2130-4560) 3100 (2110-4390) 2910 (2210-3480) 2230 (1370-3880) 1860 (1490-2500) 2590 (1800-3420) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 181 (157-209) 226 (195-262) 267 (239-298) 322 (275-377) 352 (324-384) 357 (310-412) 152 (133-175) 158 (141-178) 167 (145-193) 174 (146-210) 220 (190-264) 249 (212-307) 306 (