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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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3-Dichlorobenzene (m-Dichlorobenzene) 1.1.2-Dichlorobenzene (o-Dichlorobenzene) 1.2-Trichloroethane Trichloroethene (Trichloroethylene) m.4.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.2'.5'-Tetrachlorobiphenyl (PCB 49) 2.2’.4'.2'.4.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.2'.4.2-Dichloroethene trans-1.6-Pentabromodiphenyl ether (BDE 100) 2.4'-Pentabromodiphenyl ether (BDE 85) 2.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.5'-Tetrachlorobiphenyl (PCB 44) 2.cdc.3.1-Dichloroethane 1.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.2'4.5-Pentabromodiphenyl ether (BDE 99) 2.4.1.2'.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals . The process for selection is described at http://www.1.5.4-Dichlorobenzene (p-Dichlorobenzene.6.gov/exposurereport/chemical_selection.3’.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.3.4’.4.html.4'-Tetrabromodiphenyl ether (BDE 47) 2.2'.4'-Tetrabromodiphenyl ether (BDE 66) 2.5.What’s New in this Report What’s New in this Report In this Fourth Report.2'.1-Trichloroethane (Methyl chloroform) 1.2-Dichloropropane 2.5.3.4.3'.4.5'-Hexabromodiphenyl ether (BDE 153) 2.5'. Table 1.2.2'.4’.2'3.4'.4. Paradichlorobenzene) 1.1.3-Tetramethylbutyl] phenol) Triclosan (2.2-Dichloroethene Dichloromethane (Methylene chloride) 1.1-Dichloroethene (Vinylidene chloride) cis-1.2-Dichloroethane (Ethylene dichloride) 1.4'.4'.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.4-Tribromodiphenyl ether (BDE 17) 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.4.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.4'-Tribromodiphenyl ether (BDE 28) 2.4.6'-Hexabromodiphenyl ether (BDE 154) 2.5.2'.6-Heptabromodiphenyl ether (BDE 183) 2.3. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.2'. 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 (2.4'.4.4.5’.

Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. 2003-2004) have been re-computed by use of this improved procedure. Explanations for each change are provided in Appendix B. Only slight differences should be noted when one compares the recomputations to previous releases of the Report.5-dichlorophenol for the 1999-2002 survey periods.4-dichlorophenol and 2. urinary 2.1).g. and these data will be included in the next release of the Report.g. Percentiles for all three NHANES survey periods (1999-2000. Details of this procedure are provided in Appendix A. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. Fourth National Report on Human Exposure to Environmental Chemicals 3 . Data for other pesticides are included only for 1999-2000 and 2001-2002.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.. 2001-2002. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report.. the presence of an interference) that produced results of inadequate quality. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. five results that all have the value 90.

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

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

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

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

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

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

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

2 (62.0-58.7 (65. People may be exposed to acrylamide from foods. FDA. smoking. EPA reference dose of 0. Fourth National Report on Human Exposure to Environmental Chemicals 11 .2 (58.2-59.5 (74. as an absorbent in disposable diapers. 2005.7-64.1 (52. and from dermal contact with products that contain residual acrylamide. 2005).6-108) 61.0.6 (81.4-60. mineral processing.0 (67. and in the synthesis or compounding of dye materials.3-71.7-64.9-61. glycidamide. in some sealing grouts.4 (53.5 (79. soil conditioners.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 61.1) 101 (95. are heated at temperatures used for frying and baking.0) 85. EPA.7) 73.9-52. In 1997. Since acrylamide has limited volatility and high water solubility.6-65.6) 90. it was discovered that acrylamide is formed when starch-rich foods.1-57.2-67. In humans.0-66.5 (44.8-57.4) 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. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. 2006. 2005). acrylamide has produced upper airway irritation following inhalation of high levels. Acrylamide is not thought to accumulate in the body at environmental doses. ocular and dermal irritation from direct contact with acrylamide containing materials.6-66.1) 62.8 (52.9) 63.0-108) 152 (139-175) 126 (111-142) 108 (86.9 (69.S. 2005).2 (75.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.6-75.1) 46.7) 58.S.3) 63.2 μg/kg/day (U. and is either metabolized to the reactive epoxide. 2002)..4 (54. Polyacrylamides are useful water-compatible polymers used in water treatment. pulp and paper production.2-118) 98. Foods such as french fries and potato chips can contain acrylamide at levels up to 100 times greater than levels found in cooked fish or poultry (DiNovi and Howard.0) 57. but are generally above the U.8-55.9-105) 86.4) 57..6 (56.4-89.5-85.4 (51.5) 66. gels. and an average daily intake is estimated as 0.9) 58.1-61. acrylamide is synthesized and used in the production of polyacrylamide polymer. Survey Geometric mean (95% conf. such as potatoes and some grains..2) 57.4 (54.0 μg/kg for adults (FAO/ WHO. 2006). the main source of exposure is from the diet.8 (57.4-60.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. These estimated intakes are hundreds of times lower than occupational exposures.4-83. 2004).1) 55.3-2.7) 96.2) 57. 217 million pounds of acrylamide were produced commercially in the U. or to glutathione conjugates (Calleman et al.6-104) 82. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.0 (57.7 (58. 2004.8 (81.7) 75th 79. and in some cosmetics.4-76.9 (54.0 (53. see Data Analysis section) for Survey year 03-04 is 3. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.1 (47.1 (83.S.8 (91.2-114) 163 (147-191) 96.4) 100 (89. drinking water.2-93.6 (51.4) 57. and well below doses known to cause nerve damage or carcinogenicity in animals.6-61.7 (63. 2005).2-77. population from the National Health and Nutrition Examination Survey. EPA. 1990. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.5-80.9) 57. Elimination occurs mainly in the urine as mercapturic acid conjugates.0-49.1 (73.1 (88. Recently.9 (60. Fennell et al.0 (69.S. 2005). Commercially. Tareke et al.2-91.3) 70. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.S.7 (55. widely distributed in tissues.7-60.2-70.4 (59.1-64.6) 50. and cosmetics (NTP-CERHR. In the general population. Natural substances in the food are converted to acrylamide.3 (55.5) 58. Estimated intakes in children are about twice that of adults (DiNovi and Howard. interval) 61. but can covalently bind to form adducts with proteins.7) 54.6) 71. 1994).6) 73. Animal studies indicate that acrylamide is well absorbed. in permanent press fabrics.3) 86.5 (52.3 (53.1) 53.Acrylamide Acrylamide CAS No.1-64. and binding agents. (NTP-CERHR. FAO/WHO.9) 75.

2006). thyroid. EPA.7-86.0 (80.. 1997.5 (59. 2005).2 (63.3-78.8-48.1 (57.9) 65. 2001).. 2005.5 (42. 2006.7-62.1 (70.S. 2005..3) 59. uterine.3) 85.9-64.6-62. 2005. 1997.. scrotal.7-64. Schettgen et al. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.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. Puppel et al.4-98. 12 Fourth National Report on Human Exposure to Environmental Chemicals .. Additional information is available from U. 2002.9 (57. 2009).. Puppel et al.5-94.4 (90.S.2) 55. 2008).1-70.1) 60. 2006). 2005) and sperm DNA adducts (Xie et al. Vesper 2005) and smoking (Bergmark.5 (83.6 (90. presynaptic nerve terminal binding (LoPachin.9 (58. male germinal cell injury.6-64.5) 71.int/ ipcs/food/jecfa/summaries/summary_report_64_final.3-101) 95. most non-smokers had levels less than about 100 pmol/gram hemoglobin.0 (75.4-59. dominant lethality). 2006) have been demonstrated after acrylamide dosing.3) 59.1 (66.4 (56.8-61.4 (81.5-66. 2005.S.7) 90. EPA.1 (82.0) 94.9-77.0. NTP-CERHR. 2002. 2005.1-62.5-92.9-62.6-90.. Survey Geometric mean (95% conf. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.0 (52.Acrylamide occupational exposures.pdf.4) 46..5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.5) 75th 85.. 2005).7) 74..4 (61.9) 75.5-64.1-60. Maniere et al.4) 83.2) 65.. U. and neuronal DNA reactivity (Doerge et al.8 (44. 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.7) 61. 2003. Hagmar et al. Acrylamide is clastogenic and can produce dominant lethal mutations. Mucci et al.7 (57. fetal death.2-90. U.. 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.8) 60.4) 53. although different analytic methods can affect results. reproductive effects (reduced litter size.2-91. Glycidamide has been shown to react with DNA (Doerge et al. 2005).3) 59. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. 2005. In addition. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.0 (70.9) 59. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. and cancer (mammary. EPA at: http://www..2-68.4-65..0-62.9) 87.9-76.4 (51.0-103) 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 64.1) 56. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. population from the National Health and Nutrition Examination Survey. Schettgen et al. 2005. 2004).2 (56. AHA levels have been shown to increase with dietary intake (Hagmar et al. altered gene expression in testicular tissues (Yang et al. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.8 (51. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. and other sites) (FAO/WHO. Klaunig et al.5) 87.0) 118 (103-126) 121 (112-134) 113 (94. Rice.7) 60. 2008). After exposure ceases. probably through its epoxide metabolite.8-49.7 (84.9-138) 143 (130-159) 96. IARC classifies acrylamide as probably carcinogenic to humans. 2004.2 (72..4 (57.epa. 2005. interval) 59. 2005. Axonal degeneration. 2005) have been demonstrated in animals. adrenal.0-93.8) 45.. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. 2005)..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 59.2) 87. 2005..1-56..6 (66. respectively) are markers of integrated acrylamide exposure over the preceding few months.9-78.7 (87. see Data Analysis section) for Survey year 03-04 is 4. glycidamide (NTP-CERHR.4-103) 79.S. 2005..5 (56.who.7 (61.1) 62. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).3 (56.1 (56.9 (81. Vesper et al.

[Epub ahead of print] Dybing E. Mechanisms of acrylamide induced rodent carcinogenesis. Mucci LA. et al. Farmer PB. The Updated Exposure Assessment for Acrylamide. Bruze M. Mutat Res 2005. Hagmar L.fda.. Haugen M. In another study. Summer SCJ. Adv Exp Med Biol 2005. 2/3/09 Klaunig JE. 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. Mutat Res 2005. Paulsen JE. Kautiainen A. July. Axmon A. Human exposure and internal dose assessments of acrylamide in food. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. J Agric Food Chem 2008. 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. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin.580(1-2):157-165. Chem Res Toxicol 1997 Jan. et al. Magnusson AL. Toxicol Sci 2005. DiNovi M and Howard D. Alexander J. McDaniel LP. Available at URL: http://www. 2/3/09 Perez HL.cfsan.43:365–410.niehs. Uncertainties. gov/~dms/acrydata. 1994). 2/3/09 Hagmar L. Chicago.580(1-2):131-141. Toxicol Appl Pharmacol 1993. Acrylamide neurotoxicity: neurological..pdf. Available at URL: http://www. Doerge DR.. Churchwell MI. 054472. Tornqvist M.120(1):45-54. Tornqvist M. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Rome.3:406-412. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Calleman CJ. Costa LG.nih.580(1-2):119-129. Hagmar et al. Joint FAO/WHO Expert Committee on Food Additives. et al. Wirfalt E. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Available at URL: http://cerhr. Illinois. 8-17 February 2005. February. Metabolism and hemoglobin adduct formation of acrylamide in humans.. 1993. Bergmark E. Becher G. Calleman CJ. Granath F. Cheong HK. smokers and nonsmokers. Food Chem. smoking habits and gender. 2001. References Bergmark E. Beland FA. Kamendulis LM.gov/chemicals/ acrylamide/Acrylamide_Monograph. Bergmark E. Chem Res Toxicol 1990. Malmberg B. 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. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. CFSAN/Office of Plant and Dairy Foods. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. He F. LoPachin RM. Maniere I. Toxicol 2005. 2009 Jan 8. He F.56. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.10(1):78-84. Adv Exp Med Biol 2005. Survey data on acrylamide in food: individual food products.pdf. morphological and molecular endpoints in animal models. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Bridson WE. Italy. 2001). 6013-6019. Churchwell MI. Burgess J. Nordander C. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Calleman CJ. Costa LG. Laurentie M. Bjellaas T.126(2):361-371. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. da Costa GG.who. Tian G. 2005. 2004. April 13-15. Zhang S.561:49-62.Acrylamide In occupational settings. Guffroy M. Toxicol Sci. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Yang JS. NIH Publication No. Fennell TR. National Toxicology Program. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Wu Y.Toxicol Appl Pharmacol 1994. et al. Doerge DR.27(4):219-226. Mutat Res 2005. Andersen M. Scand J Work Environ Health 2001. Spicer R. Wilson KM. Rosen I. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Paulsson B. Perez et al.85:447-459. Snyder RW. Fennell TR.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Twaddle NC.html#u1004. Aprea P. Acrylamide intake through diet and human cancer risk. and Research Strategies. 2006.561:21-37.. Osterman-Golkar S. 1999). DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. 64th Meeting: Summary and Conclusions (FAO/WHO). Food and Drug Administration (FDA). et al. Duale N. Godard T. Bergmark E.

Ospina M. Acrylamide. Fueller F.580(1-2):3-20. a carcinogen formed in heated foodstuffs. Angerer J. Rydberg P. Drexler H.561:89-96. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Drexler H. Tjønneland A. J Agric Food Chem 2008. Int J Hyg Environ Health 2004. Adv Exp Med Biol 2005. EPA).epa. Benetou V. Slimani N. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Han CH.gov/chemfact/s_acryla.S.163(2):101-8. Kutting B.gov/iris/subst/0286. 2/3/09 Vesper HW. U. Schettgen T. Myers GL. Hemoglobin adducts of ethylene oxide. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine.134(1-3):65-70. Gray JG. Lee SH. Letzel S. 1994.epa. Agudo A. Vesper HW. Available at URL: http://www. The carcinogenicity of acrylamide. Eriksson S. Chemical Summary for Acrylamide.S. Fu D. Schettgen T.50(17):4998-5006. Angerer J. Han DU. Toxicological effects of acrylamide on rat testicular gene expression profile. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Environmental Protection Agency (U. Hallmans G. 2/3/09.56(15):6046-53. et al. Toxicol Lett 2002. Analysis of acrylamide. EPA).207(6):531-9. Available at URL: http://www. et al.580(1-2):71-80. Choi JH. September. Yang HJ.274(1):59-68. Rice JM. U. Liu Y. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Drexler H. Angerer J. Office of Pollution Prevention and Toxics.206(1):9-14.S. Sun H. Smith A.htm. Rapid Commun Mass Spectrom 2006. Chae C. Puppel N. Washington (DC). Vesper HW. Schettgen T. Karlsson P.txt. Int J Hyg Environ Health 2003. Tornqvist M. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. propylene oxide. Environmental Protection Agency (U.S. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Rossbach B. Toxicol Lett 2006. Mutat Res 2005. Meyers T. Broding HC. Licea-Perez H. Integrated Risk Information System (IRIS).19(4):527-34. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Xie Q. Anal Biochem 1999. Mutat Res 2005 Feb 7. Ding X. Marko D. Ospina M. Tjaden Z. Meyers T. J Agric Food Chem 2002.20(6):959-64. Reprod Toxicol 2005. Liu K. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Weiss T. Tareke E. Ingham L. Lee MH. revised 1/3/06.Acrylamide glycidamide by gas chromatography-mass spectrometry. Jin Y.

470-.30) 2. 1998). Fourth National Report on Human Exposure to Environmental Chemicals 15 .190-.17) .312) .96) 2.302) .50 (1.20 (.81-2.077) .060) .310) .350-.061) < LOD .066-.23 (.19) 1.22) 2.150) .210 (.89) 1.308 (.23 (1.300) .260) 1.060 (<LOD-.78) 2.S.49) 1.216 (. respectively. maternal exposure during pregnancy can result in lower birth weight. and various other disorders (U.160 (.260-1.094) .020-.88 (1.086 (.160-.142-.62 (2.30) 2.00) .050) .076-.180 (.175 (.050-. Children exposed to ETS are at increased risk for sudden infant death syndrome.040 (.09-3.050) .99) 2.54) 1.148-.075 (.21-1.240 (. see Data Analysis section) for Survey years 99-00.071) .180) .83-2.840) 3.213) . 83% of measurements had an LOD of 0.34 (1.770-1.93) .12 (1.047-.92) 1174 1415 1252 1773 1902 1783 3052 3502 3285 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 20 years and older Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 ..110) .030-.14-1.620 (.126) . 2004).09-2.05.44 (2.625) .42 (1.115-.26-1.160 (.015 ng/mL.02) 1.77 (1.32) 1.20 (1.60-2. acute respiratory infections.160) .040 (.410) .Cotinine Cotinine CAS No.39 (1.070) 75th .060-.910-1.030 (.180) . Survey Geometric mean (95% conf.220) .50-4.40) . stroke.066) .120 (.68 (1.030-.110-.05 ng/mL.050 (<LOD-.180) .850 (.47-3.110 (.21-1.77 (2.44) 2. Cigarettes contain about 1.23 (2. cardiovascular disease.068) .080) < LOD .124 (.084) .580) .48-2.70-2.87-3.050-.145) .193) . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.047-.76 (1.100-.163) . and exacerbated asthma (U.320) .54 (1.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .120 (. acute respiratory illness.050 (<LOD-.050 (.533-.95) 1.052 (<LOD-.710 (.088-. which may vary for some chemicals by year and by individual sample.154-.040-.50) 3.060-.164 (. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.190-.110 (. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.050 (<LOD-.062 (.110-.050 (<LOD-.137 (.200) 1.17 (.30) * .92 (1.62) 2.040-.111-.370-.071 (.70) 2.990) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140 (.090-.180 (.070-.080-.66-3.058 (.087) < LOD < LOD .23-2.310-1.621-1.480-.17 (1.350 (.33-2.740-1.28) . and 17% had an LOD of 0.106-.726) .087 (.730 (. 2004).280 (.630 (.201) . 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.570-1.054 (.16) .030-. population from the National Health and Nutrition Examination Survey.45) 1.09-3.997-3.55 (1.144 (.090-.500 (.43 (1.087-.160 (.163 (.790) .580-1.600-1.49) 2241 1878 1707 1333 1602 1704 1950 2847 2500 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02** 03-04 Limit of detection (LOD.960-1.070) .S.860 (.800 (.950-1.01) 3.84-3.120 (.190-.20) 1.060 (.12 (2.120 (.570 (.94) 1.18-3.620-1.44 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.32-2.080 (.137-.660) .505 (.12) 1.198) * .220-.310) 90th 1.110 (. and 0.630 (. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.15 (2.920 (.39) 3. < LOD means less than the limit of detection. ** In the 2001-2002 survey period.130) .077) .108) * .153-.120) .360) .44) 2.05) 1.85 (1.950 (.110-.131 (.14) .670) .5% nicotine by weight (Kozlowski et al.040 (.540 (.070) .220) .820) .68) .310-1.480-1.140-. DHHS.053 (<LOD-. emphysema.140 (.120-.080 (.130 (.00) 1.104-.21 (.99) 2.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * . 2006).167 (.015.080-.14) .052 (<LOD-.740-1.35 (2.02) 1.68) 2.65 (1.234) .15) 2.96-4.11) .19) .53-4.28-1.55-2.180) .089) Age group 3-11 years 99-00 01-02** 03-04 .230) .75) 1.770) .073) < LOD .110) .164 (.63-2.139) * .510 (.38-2.400-.900-1.580 (.428-.20) .12-4.450-.54 (1.188) .506 (.060 (<LOD-.990 (.49) 1. ear problems.19-2.120 (.110 (. DHHS. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.520 (.630 (.63 (2.057-.059-. 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.540-.430-1.50-1.53 (1.20-2.930 (.48-3.063) .080-.350-.160) . and 03-04 are 0.32-2.230 (.04 (1.187) .57) 2.42-4.090-.180) .150) .043-.066 (.66) 1.96 (1.080-.66 (1.S.690 (.059-.080) < LOD < LOD .120-.060-.88 (.770) .77 (1.79) 3.110 (.01 (1.070 (<LOD-.060 (.140-.068) .197) .02 (.

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

S. Tobacco Smoke and Involuntary Smoking. Benowitz NL.S. Office on Smoking and Health [online] 2006. International Agency for Research on Cancer. Bernert JT. Herrera B. Aiba M. Available at URL: http://monographs.pdf. 4/13/09 U. Giovino G. Brody DJ. et al.iarc. 11th ed. U. Tobacco related exposures. Third National Report on Human Exposure to Environmental Chemicals. Tob Control 1998. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Jacob P III. available at URL: http://mtn. Houseman TH. 1999-2002. Jacob P III.niehs. IARC Monogr Eval Carcinog Risks Hum. Racial/ethnic differences in serum cotinine levels among adult U. Turner DM.275:1233-1240. Jacob P.S Department of Health and Human Services (U.S. JAMA 1996. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary.cdc. Cotinine as a biomarker of environmental tobacco smoke exposure.S Department of Health and Human Services (U. Kira S.57(1):79115. Absorption and metabolism of nicotine from cigarettes. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. BMJ 1975. Soliman S.15:302-307.63:139-43. Vol 38. Schwartz SS. Nicotine metabolism and intake in black and white smokers. George CF. Exposure of the U. Pickett MA. Mowery PD.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Summary of Data Reported and Evaluation [online] 1986.cancer. Int Arch Occup Environ Health 1991. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. and the United States. Pirkle JL. Jarvis MJ. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Bernert JT. 2004. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency.S. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Trends in the exposure of nonsmokers in the U. DHHS). Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. National Toxicology Program (NTP). DHHS).114(6):853-858. Centers for Disease Control. 1988-1991. Strauss WJ.fr/ENG/Monographs/ allmonos90. Pechacek TF. JAMA 1998. Herrera B. Sosnoff CS. Vogler GP. Clin Pharmacol Ther 1994. the United Kingdom.S.gov/library/ secondhandsmoke/. 1988-1991.php. iarc. Benowitz NL. J Pharmacol Exp Ther 1999. Dollery CT. Caraballo R. U. Department of Heath and Human Services.4:313-316. Respiratory nicotine absorption in non-smoking females during passive smoking. Curtin LR.fr/ENG/Monographs/allmonos90. Benowitz NL. June. Available at URL: http:// cancercontrol. Vol 83. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. References Armitage AK. Centers for Disease Control and Prevention.gov/eid/rmca/critdocs/ criteriadoc/33.surgeongeneral.S.18:188-204. 4/13/09 International Agency for Research on Cancer. Mehta NY. Available at URL: http://ntp.gov/tcrb/monographs/10/.niosh. Metabolism and disposition kinetics of nicotine. 4/13/09 National Cancer Institute (NCI). et al. Tobacco Smoke. Caudill SP.S. [online]. 4/13/09 Perez-Stable EJ. Environ Health Perspect 2006. 1991. Modin G.280:135-140. Benowitz NL. Available at URL: http://www.56:483-493. U. Coordinating Center for Health Promotion. Brody DJ. Pirkle JL.291(3):1196-1203. Schober SE. Ethnic differences in N-glucuronidation of nicotine and cotinine. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Atlanta (GA): 2005. Smoking and Tobacco Control Monograph 10 [online]. Available at URL: http://monographs. Kozlowski LT. Warner K. Lewis PJ. JAMA 1998. 4/13/09 Iwase A.php.gov/ntp/roc/eleventh/profiles/ s176toba. In Report on Carcinogens. Hukkanen J. Fong I. Pharmacol Rev 2005. Benowitz NL.pdf. 4/13/09 Centers for Disease Control and Prevention (CDC). Am J Public Health 2004. Coordinating Center for Health Promotion.nih. Maurer KR. Richter PA.7:369-375. Jacob III P. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Pechacek TF. National Institute for Occupational Safety and Hygiene (NIOSH). Summary of Data Reported and Evaluation [online] 2004.94(2):314-320. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Epidemiol Rev 1996. Flegal KM. National Center for Chronic Disease Prevention and Health Promotion. IARC Monogr Eval Carcinog Risks Hum. Sweeney CT. Giovino GA. Perez-Stable EJ. Department of Heath and Human Services. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 .280:152-156. Tob Control 2006. Pollack HA. Centers for Disease Control and Prevention. population to secondhand smoke: 1988-2002. Etzel RA. 1999. cigarette smokers: the Third National Health and Nutrition Examination Survey.

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

110 (. (Kolpin et al. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.100-. Neurological effects in humans.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 .270) 688 678 518 700 598 956 Limit of detection (LOD. After absorption.140) < LOD . 2002).100-. About 3-8% of dermally applied DEET is absorbed. 134-62-3 General Information N.S.S. which may vary for some chemicals by year and by individual sample.210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .190) < LOD .130 (. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. have been reported as result of self-poisoning by ingestion or excessive dermal application..N-Diethyl-meta-toluamide (DEET) N. Sudakin and Trevathan. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.160) < LOD .100 (<LOD-. 2002).100-.180 (.180) < LOD .449 and 0. Additional information is available from U.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . 1998). General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.S. Survey Geometric mean (95% conf. Its use is recommended for prevention of several vector-borne diseases.250) < LOD .110 (.110-.180 (. < LOD means less than the limit of detection.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1998).120-.180 (.220 (.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.110 (.130) < LOD .170 (.120-.EPA.210 (.S. EPA.520) < LOD . and they range in concentration from 4% to 100%.140 (. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. 2005).N-Diethyl-meta-toluamide (DEET) CAS No. 2003).130-.100-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. DEET can be applied to clothing and the skin to repel biting insects.140) < LOD . DEET has low acute toxicity. (U. Fourth National Report on Human Exposure to Environmental Chemicals 19 .130 (.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 .110 (<LOD-.. 1995. DEET is not a developmental or reproductive toxicant in animals (U.EPA.170 (.100-.epa.130-.130-.N.110-.140-. One survey detected DEET in 74% of sampled streams in the U. including seizures and encephalopathy. There are over 225 insect repellents brands containing DEET.100-.240) < LOD .1.130) < LOD .560) < LOD ..140) < LOD . 2003). Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.110 (. Urinary N. population from the National Health and Nutrition Examination Survey.EPA at: http://www.130 (.130-.gov/pesticides/.S. DEET is not genotoxic.110 (<LOD-. DEET is not registered for use on agricultural commodities.150) < LOD . DEET is also used in combination with dermal sun screens (U. and it has not been rated by IARC or NTP with respect to human carcinogenicity. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.

140-.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 .190 (. 1992). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.490) < LOD .480 (. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.270-.230-. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.270 (.. Urinary N.93) < LOD .350) < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.270) < LOD . Survey Geometric mean (95% conf.300 (.190 (.130 (<LOD-.240-.630) < LOD .390-.S.410-.290-. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.230) < LOD .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.410 (.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.350-.330 (. In this survey period.170-. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.350) < LOD . 20 Fourth National Report on Human Exposure to Environmental Chemicals . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.250 (.N.S. Urinary DEET levels as high as 5.200 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . 2007). population from the National Health and Nutrition Examination Survey.370-. 2005). 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.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .320 (.190-.150-.320) < LOD ..640 (.280-1.500 (.150) < LOD .440) < LOD .250-.280 (.250) < 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 .270 (<LOD-.190 (<LOD-.240) < LOD .300) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . representative subsamples from NHANES 2001-2002.370) < LOD .230-.330 (.410 (.

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

Park S. hormones. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Howdeshell KL. Klinefelter GR. Research Triangle Park. Kim YH. NC. Environ Sci Technol 2002. Sottas CM. bisphenol A glucuronide. C. 2/4/09 Ouchi K.68(1):121-146. U. niehs. Timms BG. Available at URL: http://cerhr. Reidy JA.14(2):149-157. Regul Toxicol Pharmacol 2002. Keimowitz AR. Pyo MY. Human Health. Exposure of the U. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). vom Saal FS. Lynch BS. Gray GM. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Needham LL. Ema M. et al. Life Sci 2001. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. May 22. Joskow R. Ye X. Barber LB. K.niehs. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection.102(19):7014-7019.gov/chemicals/bisphenol/BPAFinalEPVF112607. September. National Institutes of Health. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP).pdf. Inhibition of testicular steroidogenesis by the xenoestrogen bisphenol A is associated with reduced pituitary luteinizing hormone secretion and decreased steroidogenic enzyme gene expression in rat Leydig cells. and Hardy MP.. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. Gender differences in the levels of bisphenol A metabolites in urine.pdf . Endocrinology 2008. Marr MC.. Calafat AM. Richter CA. Calafat AM. Myers CB.780(2):365-370. Pharmaceuticals.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Hughes C. Kawamura N. Brussels. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. and other organic wastewater contaminants in U. Hara K. Leranth. streams.gov/chemicals/bisphenol/bisphenol. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Koh WS. Biochem Biophys Res Commun 2003. niehs. Imai H. 2002. Available at URL: http://ntp. Kroes R. Bradley S. Available at URL: http://ec. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Needham LL. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Doull J.nih. Ispra. European Commission.116(1):39-44. Joint Research Centre Institute of Health and Consumer Protection. Caudill SP. Ekong J. Occup Environ Med 2002.145:592-603. Italy.S. Cunha G. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Yoshinaga J. 2007. Koulova AI. Zacharewski TR. 2008. Calafat AM.pdf. Available at URL: http://ecb. Environ Health Perspect 2005. Watanabe S. National Toxicology Program. T. Barr DB.eu/ health/ph_risk/committees/sct/documents/out156_en.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. N. Kuklenyik Z. Rubin C. Twomey K. 2/4/09 Fujimaki K. Harazono A. Rhomberg et al. 2/4/09 European Commission.pdf. Hanaoka T. and Hajszan. Tsugane S. Han SS. McConnell EE. Ikka T. Nippon Eiseigaku Zasshi 2004. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Cha SW. Hum Ecol Risk Assess 2004. Thurman EM. August 2001. Brine DR. Reidy JA. Haighton LA.S.pdf . 2003. Munro IC.36(6):1202-1211. Needham LL. National Institute of Environmental Health Sciences. Thomas BF. Meyer MT.Environmental Phenols References Akingbemi BT. Wong LY. Environ Health Perspect 2008.35(2 Pt 1):238-254. An evaluation of the possible carcinogenicity of bisphenol A to humans. Watanabe C. J Am Dent Assoc 2006.10:875-921.Scientific Committee on Toxicity.S. Ecotoxicity and the Environment (CSTEE). Matthews JB. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. In vitro and in vivo interactions of bisphenol A and its metabolite. with estrogen receptors alpha and beta. DirectorateGeneral Health and Consumer Protection. MacLusky. Available at URL: http://cerhr.312(2):441-448. Furlong ET.jrc. Hlywka JJ.nih. Belgium.59(9):625-628. Furukawa M. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Szigeti-Buck.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report.149:988-994. Rat two-generation reproductive toxicity study of bisphenol A. Serizawa S. Barr JR. Tyl RW. Chem Res Toxicol 2001. Proc Natl Acad Sci USA 2005. Toxicol Sci 2002. Kim CS. 1999-2000: a national reconnaissance. Bisphenol A. Chung MK. Shin HC.. Zaugg SD.137(3):353-362. Arakawa C. Han SY. 5: 505-523.69(22):2611-2625.J. Fujii S. November 26.nih. Barton L. Department of Health and Human Services. Reprod Toxicol 2001. Kiguchi M.113(4):391-395. Cohen JT. et al. Yang M. et al. Kolpin DW.59(4):403-408.europa. 4. Kim JC. Endocrinology 2004.

Witorsch RJ. Biological monitoring of bisphenol a in a Korean population. Environ Health Perspect 2005. Environ Res 2007. Sheldon LS. Hughes C. Yang M. and nonylphenol at home and daycare. Nagel SC. Lee SM.44(4):546-51. Large effects from small exposures. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Kawamoto T. Colnot T. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Jang JY. Wilson NK. Vom Saal FS. Filser JG. bisphenol-A. et al. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment.147(6 Suppl):S56-69. Morgan MK. Food Chem Toxicol 2002.40(7):905-12. Chang SS.15:12811287. Welshons WV. Csanady GA.113(8):926-33. vom Saal FS. Endocrinology 2006. III. Lordo RA.Environmental Phenols Volkel W. Chem Res Toxicol 2002. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Fourth National Report on Human Exposure to Environmental Chemicals 33 .103(1):9-20. Arch Environ Contam Toxicol 2003. Dekant W. An observational study of the potential exposures of preschool children to pentachlorophenol. Chuang JC. Kim SY.

500-1..40 (1.00 (. and some of their degradation products are toxic to aquatic life. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. Indoor and to a lesser extent.80 (1.10) 2. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.80 (1.40) 2. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown. fish) and drinking water. through sewage.. 2000.600-1.00 (.00 (1.10-2.. 2006.20-2.600-1.900 (.40) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.507) * < LOD .60-3.300 (<LOD-.90) 2.50 (1.70 (1.10 (.80 (1. to shorter chain alkylphenol ethoxylates..200-.500) .477) ..20) 2.. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.30 (1. < LOD means less than the limit of detection.00) 1229 1288 03-04 03-04 03-04 * . In rats. testicular atrophy.600-1.20-2. did not bioaccumulate.30 (1. which may vary for some chemicals by year and by individual sample.40) * 03-04 03-04 03-04 . Saito et al. Several alkylphenols. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.299-..900 (.60) 613 652 1092 Limit of detection (LOD. Katsuda et al.300 (<LOD-. and through manufacturing waste streams (Warhurst. and some personal care products.60-3.000 tons of alkylphenol ethoxylates were produced annually worldwide. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).357 (. impaired steroidogenesis. the various alkylphenols have also been used as emulsifiers and modifiers in paints.5% of 139 U.20-2. textiles.800-1.389 (. Bian et al.500) .500-1..50) 1.900 (.10 (1.400 (.30) 1. Less frequently. leading to inhalation as another potential exposure route (Rudel et al.10 (.600) .10) 1.900 (. an alkylphenol.20 (1. Disposition in humans has not been studied sufficiently.80) 2. 2003. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.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 . which are anionic surfactants used in detergents.50) .70 (1.30) 90th 1. orally administered 4-tert-octylphenol was well absorbed. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. including 4-tert-octylphenol. over 500.20-2. 1997. The alkylphenol ethoxylates enter the environment through human use of products containing them.500) 75th .20-2. see Data Analysis section) for Survey year 03-04 is 0.30 (1.600-1.400 (. population from the National Health and Nutrition Examination Survey.300 (<LOD-.Environmental Phenols 4-tert-Octylphenol CAS No.60) 1.300 (<LOD-. 34 Fourth National Report on Human Exposure to Environmental Chemicals .30 (. In 1999-2000.70 (1.50) . Ying et al.300-. During the 1980s and 1990s. and to alkylphenoxycarboxylates.30 (1. is used to manufacture alkylphenol ethoxylates.50) 1. The alkylphenols can bioaccumulate in some fish.274-. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.20) 1.900 (.60) .500 (. and was quickly eliminated from the blood (Certa et al.60-3.g. altered neonatal sexual development.497) * . Survey Geometric mean (95% conf.400) 1..200-.40) 2.50-2. and the polyethoxy chain may consist of up to 50 ethoxy units. 2004).. and emulsifiers.30-2. streams in 30 states (Kolpin et al.60-3. Blake and Boockfor.3.40) 1. pesticides. 1995.20) 314 715 1488 03-04 03-04 * * .60-3.90) 2. 1996).700-1.600) 1. and impaired spermatogenesis (e. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.60-3. altered estrus cycles and reproductive outcomes. In the 1990s. 2002).g.50) 1.S.30) 2.70 (1. 4-octylphenol monoethoxylate was detected in 43.2. have demonstrated estrogenic effects particularly when injected at high doses in animals. 2000. 140-66-9 General Information 4-tert-Octyphenol.300 (<LOD-.600-1. industrial cleaners.500) .400 (.50-3. 2002).268-.600) .3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.369 (.600) .1. Laws et al.300-.600-1. and from contact with some personal care products and detergents. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.S.20-2. Urinary 4-tert-Octylphenol (4-[1.

78) 3. 2000.640-1. Calafat et al. representative subsample of NHANES 2003-2004.43) 1.31-2.. Sweeney et al.276 (.41) .770 (.730-1.270 (.33) 3.03 (1.S.68) 2.40 (1. nonylphenol.270 (.03-6.18-4.337-.81 (1.14) 314 713 1487 03-04 03-04 * * .33 (2.630-1.62 (1.560) .540-1.280-.410 (.860 (.43) 1. 1999).00) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (. Nagao et al..60 (1.450) 1.850 (.620-1. Urinary 4-tert-Octylphenol (4-[1.29) 2.207-.470-1.20 (1. 4-tert-Octylphenol is not considered directly genotoxic.740 (. Tyl et al. Yoshida et al.67-2.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf.17 (.25-2. Kawaguchi et al.11) 1.03 (1. 2004.25) 2.349) * < LOD .269 (.550-1.Environmental Phenols Myllymaki et al. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.76 (2. Fourth National Report on Human Exposure to Environmental Chemicals 35 .54) * 03-04 03-04 03-04 .890-2.570) . 2001.500-1.270-. 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. In a small number of adult Japanese volunteers.78) 1228 1286 03-04 03-04 03-04 * . 2004).78 (1.3.62 (1.10-2.15) 1..22) .470-1.00) 2.420) .00) 2.460 (.620) .59 (1.25) 90th 1.320 (<LOD-.40-4.300 (<LOD-.06 (2..85 (1.43-3. population from the National Health and Nutrition Examination Survey. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.68-2.S. 2001)..08) 1.384) * . Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.170-.450) . 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.02-4. IARC and NTP have not rated octylphenol.64 (.11-2.199-.05-2.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00 (. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.470) 75th .160-.50 (2. at lower or environmentally relevant doses (Blake et al. or their corresponding ethoxylates with respect to human carcinogenicity.36-3.910 (. It is unclear if estrogenic or other effects occur in animals through oral dosing..59) 1.610) .73) 2.1.260 (<LOD-. 2005.400) .435 (.31 (1.370 (<LOD-.740 (.11) 2.380 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.53-3. 2003.62) .96-4.65-3.00) 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 .530) .71) 2.

2003. Taya K. 1995. bisphenol A and methoxychlor in rats. et al. Toppari J. Yoshida M. Seto H. Bodman GJ. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. et al. and testosterone. Seely JC. Available at URL: http:// www. Cooper RL. Okada F. Spengler JD. McCoy GL.207(1):59-68. Maekawa A. Taya K. polybrominated diphenyl ethers. Saito Y. Endocrinology 2000. 2/4/09 Ying GG. Nagao T. testis size. Horie M. Haavisto TE. Makino T. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Onuki A. Rudel RA. Qian J. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Maekawa A. Indoor Air 2004. Tyl RW. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Fedtke N. et al. Toxicol Lett 2001. nonylphenol. Yoshimura Y. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. pesticides. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Wiegand HJ. and other organic wastewater contaminants in U. Inoue K. Raychoudhury SS. Brooks AN. and sertoli cell number. Exposure of the U.14(5):325-332. Ye X. Korn LR. Kookana R. Environ Int 2002. Inoue K.18(1):43-51. Toxicol Appl Pharmacol 2005. Thurman EM.36(6):1202-1211. Myers CB. Brine DR. Toxicol Appl Pharmacol 2000. Nakagomi M. Karjalainen M.co. Reprod Toxicol 2001. Saito I. Arch Toxicol 1996. Biol Reprod 1997. Izumi S. Katsuda S. Katsuda S. Takenaka A. Watanabe G.28(3):215-226.uk/resource/reports/ethoxylates_alkylphenols. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Environ Sci Technol 2002. Meyer MT. hormones. Warhurst AM. Boockfor FR. Reidy JA. Xu L. Zaugg SD.116(1):39-44. Sweeney T. Sakui N. Paranko J. Kolpin DW. Kawaguchi M. Millette CF. Usumi K. Takai N.44(8):1355-1361. Environ Health Perspect 2008. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. 1999-2000: a national reconnaissance. streams. Bolt HM. Nicol L. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Boockfor FR.S. Myllymaki SA. Blake CA. Ferrell JM. and other endocrine-disrupting compounds in indoor air and dust. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Yoshimura S. Wang X. Camann DE. Environ Sci Technol 2003. Furlong ET. Calafat AM. Ono H. Marr MC.folliclestimulating hormone. Yoshida M.57(2):255-266. prolactin.foe. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Estrogenic activity of octylphenol. Laws SC. Carey SA. Toxicol Sci 2000.S. Food Chem Toxicol 2006. Barber LB. Regul Toxicol Pharmacol 1999. Brody JG. Two-generation reproduction study with para-tert-octylphenol in rats. Blake CA. Reprod Toxicol 2004. Chen J.165(3):217-226. Phthalates. alkylphenols. Muller AM. Anal Chim Acta 486:41-50. et al. Wong LY. Ito R. Certa H.141(7):2667-2673.799(1):119-125. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Nair-Menon JU. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Indoor air pollution by alkylphenols in Tokyo.37(20):4543-53.pdf. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Watanabe G. Pharmaceuticals. Needham LL.30(2 Pt 1):81-95.121(1):21-33. Kawaguchi M. Fail PA.15(6):683-692. 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.71(1-2):112-122.Environmental Phenols References Bian Q. Song L. Williams B. Roche JF. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol.54(1):154-167.

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

6) 90th 212 (172-241) 03-04 03-04 03-04 9.1) 14.8 (21.70-16.2 (11.45-13.5) 20.40-17.9-236) 193 (90.38-18.6-14.0) 65.10-9.2) 9.0 (34.S.6) 10.20-11.50-10.32-14.7 (28.2-58.4 (38.8-85.0-19.1) 7.89-11.45 (5.0-15.4 (11.2 (10.4) 25.4 (32.5) 11.8) 14.6 (30.8-63.20-10.6-15.92-12.0) 49.7 (14.6-20.9-61.3 (26.93 (7.10) 84.20 (7.4 (12.3-35.9) 32.21 (6.50) 10.8-112) 30.40-11.6) 39.6) 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 9.86-12.3 (9. interval) 13.Environmental Phenols Urinary Triclosan (2.6 (10.7 (9.2-58.3) 6.8) 116 (39.4) 90th 249 (188-304) 03-04 03-04 03-04 8.9 (33.1) 50.6 (12.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.2 (13.7) 292 (151-432) 132 (78.1 (45.1) 9.1 (8.5-86.2) 12.7 (11.90-10.2 (27.5) 66. Urinary Triclosan (2.3) 47.9) 7.6-65.3 (8.8-60.4) 73.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.29-12.0 (8.9 (11.1) 11.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.6) 12. see Data Analysis section) for Survey year 03-04 is 2.3-15.80 (5.74 (5.4) 357 (225-456) 203 (87.4.00 (4. population from the National Health and Nutrition Examination Survey.82 (8.4) 75th 43.8) 7.16 (6.72-13.4) 7.3.0 (11.48 (8.20-13.0-73.1) 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 9.4) 51.0-213) 213 (160-272) 453 (263-1150) 260 (127-513) 358 (276-480) 612 651 1091 38 Fourth National Report on Human Exposure to Environmental Chemicals .5-14.7 (39.4-19.7) 10.4-18.0 (36.S. interval) 12.1) 9.4.60 (8.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.45-10.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.9) 8.43-13.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf.0-15.1) 9.94 (7.0) 9.3 (11.9) 75th 47.6-37.11-11.5 (11.3) 10.22-10.55 (4. population from the National Health and Nutrition Examination Survey.18 (5.2-46.6 (9.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.54 (8.4) 317 (231-433) 144 (96.60 (6.9 (50.7) 123 (36.3-31.6) 31.8) 9.20 (7.2-14.6-14.1 (15.3-67.0 (26.9 (8.2 (37.48-10.1) 9.00-8.30-14.6-111) 33.1) 13.5) 13.8-127) 37.2) 13.2 (25.1-39.

Okui T.80(3):217-227. Reidy JA. Nagao Y. Gunderson MP. population: 2003-2004. Am J Infect Control 1996. Matsumura N. 1999-2000: a national reconnaissance.23(5):579-583. Leonard PA. et al. Pharmaceuticals.66:1052-1056. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Osachoff H. Aranami K. Foran CM. Ebersole R. Odham G.69(20):1861-1873. Food Chem Toxicol 2000. Percutaneous penetration and dermal metabolism of triclosan (2. Erratum in: Aquat Toxicol 2007. Bhargava HN.S. Environ Sci Technol 2002. Ferrer I. Benson WH. Furlong ET. Howes D.67(4):532-537. Larson EL. Pinney SM. et al. Pilot study of urinary biomarkers of phytoestrogens. Urinary concentrations of triclosan in the U. Williams PE. 4. Hirano M. and phenols in girls. et al. Chelimo C. Ogawa H. Gomez MJ. Furia T. Br J Clin Pharmacol 1987. Toxicology of 2. The oral retention and antiplaque efficacy of triclosan in human volunteers.Environmental Phenols References Aiello AE. Barber LB.115:116-121. Wolff MS. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. and other organic wastewater contaminants in U. Environ Health Perspect 2007. Biol Pharm Bull 2005. Wigmore H. Levy SB. Chemosphere 2007.4’-trichloro-2’hydroxydiphenyl ether). Photolytic degradation of triclosan in freshwater and seawater. J Invest Dermatol 1976. Calafat AM. Wong LY. Veldhoen N. Sandborgh-Englund G.38(2):64-71.7/2. Arch Environ Contam Toxicol 1988. Mezcua M. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice.24(3):209-218. Fernandez-Alba AR. Adolfsson-Erici M. Aguera A. Williams FM. phthalates. Readman JW. Evidence of 2. Lyman FL. Pharmacokinetics of triclosan following oral ingestion in humans.28(9):1748-1751. Ye X. Environ Health Perspect 2008. Needham LL. Triclosan: applications and safety. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Hernando MD. Zaugg SD. Britton JA. Ishibashi H. Moss T. Gilbert RJ. et al. IMS Ind Med Surg 1969. Watanabe N.83(1):84. Developmental evaluation of a potential non-steroidal estrogen: triclosan. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Katsura E. Hong HC.116(3):303-307. Kanetoshi A. Fourth National Report on Human Exposure to Environmental Chemicals 39 .S.45 Suppl 2:S137-S147. Kaneshima H.36(6):1202-1211.. streams.50(1-5):153-156. hormones. Shiratsuchi H.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples.524:241-247. Thurman EM. J Toxicol Environ Health A 2006. Bodey GP. Bennett ER.4. Anal Chim Acta 1004. Kolpin DW. Meyer MT. Clapson DJ. Aquat Toxicol 2006. Mar Environ Res 2000. Skirrow RC. Teitelbaum SL.17(5):637-644. Windham G. Ekstrand J. 4’-trichloro-2’-hydroxydiphenyl ether.38(4):361370.

78) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation. bactericide.660 (.40 (. ingestion of contaminated food or water.630 (.350) < LOD .75) 2. To-Figueras et al. PCP use in the U.350) < LOD .350 (. with repeated or chronic exposure. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1..350-. PCP is absorbed rapidly and well by all exposure routes.62 (. General population exposure to PCP may occur by inhalation of contaminated air.60) 1. and metabolic acidosis were observed in CAS No. utility poles and fence posts).65 (.33-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.850-2.960) 1.350 (. along with small amounts of tetrachlorohydroquinone and conjugates. 1976.770 (. The parent compound and conjugates.510-3.350) < LOD . Kohli et al.10) 1.530) 1.350 (. PCP is eliminated over a few days (Braun et al.S.350-2.350-.00 (.73 (1.98 (1.350-.350) < LOD . After absorption.04) 1.350-. PCP cannot be used on wood in residential or agricultural buildings.350) < LOD . After a single dose. PCP is degraded by sunlight and metabolized rapidly by microorganisms. mollusicide.350) < LOD .47-3.08-3.990 (<LOD-2. 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.390 (.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .30) 1.25 and 0. PCP is distributed to most tissues and is not extensively metabolized.350-.350 (.67) 1. Acute.350-.70) .76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350) < LOD ..860-2. hypertension.S. Survey Geometric mean (95% conf.480-2.350-.350-.30) .30 (. 40 Fourth National Report on Human Exposure to Environmental Chemicals .350-.990-2.10 (.37) .350 (.50) 1.10 (1. plants.350 (.30 (.00) 1.350-. and animals. Effects including hyperthermia.350 (. the elimination half-life may be a week or more (Uhl et al.70) 2.350-1.650 (.10) 1.350-.350 (.350-. 1979).350 (.23 (.590-1.350) < LOD .350) < LOD . which may vary for some chemicals by year and by individual sample.91 (1. has been restricted.510-5. PCP has been detected in soils.58-2.48 (.48-2. Since 1984.90) 1.350-.47-5.09) .30 (1.350-2.30) 1.60) 1.350-.65 (.350) < LOD .350) .390 (. herbicide.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 . water and sediments because of the large amounts that were produced and used historically.54-2.80) . are eliminated in the urine.18 (<LOD-1.10 (<LOD-1. and it is used primarily as a preservative for wood to be used outdoors (e. 2002..350 (.350) < LOD .350-.42) 696 680 521 696 603 951 Limit of detection (LOD.76) 1. and possibly of lindane (IPCS. 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. and dermal contact with PCP-treated products.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .500-2.890 (.g. < LOD means less than the limit of detection.83 (2.350) < LOD .350 (.350-. In the environment.58-2.90) 2.350 (.00) 2.350 (.350-1. other polychlorinated benzenes. Human exposure to PCP has become less common.350) < LOD < LOD 75th .64) 1.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.350 (.350 (.01 (<LOD-1.350 (.350-2.350 (.350 (.350 (.350) 90th .32 (.350) < LOD .90 (1.5.350-. so it is relatively non-persistent.350 (.94 (1.350-1.350-.350-1. algaecide and insecticide.45-2.350-2.350-2. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1986).94 (1. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.51) 1.890-1. air.350) < LOD ..350-.76) ..33) .350-.980 (. population from the National Health and Nutrition Examination Survey.00) 1.680-1.650) 1.37 (.350-.350) < LOD . 1997).350-.350) < LOD .

710-1.09-1.510-.94 (1.800) < LOD 1.52 (<LOD-1.500-.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .850 (.300 (...30-2.360-.35) 1.340-.90) 1.34 (.420) < LOD .73 (1.06-3.350) < LOD .gov/ pesticides/ and from ATSDR at: http://www.290) < LOD .500 (.52 (<LOD-1. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.990 (. respectively) (Seifert et al. Survey Geometric mean (95% conf. respectively) (Becker et al.910-1.35) 1.82) 1.06) 1.36) .75) 1.67 (1. 2003).35-2.920 (.380-. chronically administered high doses of PCP were hepatotoxic.21 (. More information about external exposure (i.84) 1.21-2.94 (1.25-2. Death can result from seizures and cardiovascular collapse.30) 1.490) < LOD . In animals..650) 90th 1.19) 2.26 (1.57 (1.52) 1.19) 2.25-1.270-.270-.EPA.79) 1.67 (1.16-1. and the FDA has established a standard for bottled water.310) < LOD .51) 1.92) 1.67 (1.html.25-2.35-2.S. 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.40) 1.40) 1.30 (.gov/ toxpro2.590) < LOD .430) < LOD . the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.310-.430-.82 (1.40-2.250 (. inhalation. Pentachlorophenol is not mutagenic or teratogenic.830) < LOD .84-4.950-1. 2003).25) 1.40) 1.83 (1..360 (.260 (.250 (..55) 1. EPA has developed standards for PCP in drinking water and the environment.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. Among adults in the NHANES 1999-2000 subsample.700-2..16 (.290-. carcinogenic.290-.220-.25 (1.25 (1. 2004.19) 2. environmental levels) and health effects is available from the U.40) 1.320) < LOD .78) 1.650 (.580-..e.S.650 (.400 (.760 (.800-1. 1991).590-1.630 (.40) 1.S.950-1.78) 1.94-3.500-1. 2000)..Fungicides adults and children severely exposed to PCP through ingestion.320 (.9 mg/L.95) 3.09 (<LOD-2.52 (1.730) < LOD .epa.280) < LOD .610 (.320) < LOD < LOD 75th .560-.560) < LOD .950-1.240-.atsdr.69 (1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .18) .330-.570 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.320) < LOD .10-2. 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.56) 1.780-1.48-2. 1995).900-1. and adversely affected thyroid function (U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.00-1.26 (1.11) 2.470 (.00-1.00) 1.06 (.0 mg/L.560) < LOD .67-3.08 and 5.67-2.30) 1.510-.220-.780) < LOD .08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.84 (1. EPA at: http://www. In a small sample of U. The U.370 (. population from the National Health and Nutrition Examination Survey.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . 1989). In NHANES 2001-2002 subsamples.300 (.13 (.6 and 14.57 (. or skin absorption. children in the 1980’s. 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. van Raaij et al.19 (1.440 (.S.67 (1. Urinary Pentachlorophenol (creatinine corrected) Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. OSHA has established an occupational standard.300 (. Fourth National Report on Human Exposure to Environmental Chemicals 41 .29-3.75 (<LOD-2.cdc. 1989).18 (1.67-3.10 (1. 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.

Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Seiwert M. 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. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Schulz C. 42 Fourth National Report on Human Exposure to Environmental Chemicals . International Programme on Chemical Safety (IPCS). To-Figueras J. J Expo Anal Environ Epidemiol 2000.10:552-65. 2002. 4/21/09 Kohli J.org/documents/jmpr/jmpmono/2002pr08. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Hill RH Jr. References Becker K. Holler JS. Environmental Protection Agency (U. Kaus S. hair. Arch Environ Contam Toxicol 1989. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. house dust. 4/21/09 van Raaij JA. van den Berg KJ. Fast DM. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Chenoweth MB. 206:15-24. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Rodamilans M. Needham LL. Smith SJ. Barrot C. Notten WR. PCP: Human Risk Characterization [online].S. Becker K.105(1):78-83.18(4):469-474. Bailey SL. Safe A. Schlatter C. Sala M. Arch Environ Contam Toxicol 1989. Bragt PC. Dev Toxicol Environ Sci 1979. Jones D. Shealy DB. et al. et al. Seifert B. Needham LL. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Uhl S. Hill RH. urine.18:475-481. Cline RE. Blau GE. Krause C. EPA).71:99108. Schulz C. Braun WH. Seiwert M. Pharmacokinetics of pentachlorophenol in man.4:289296. Head SL. Schmid P. Int J Hyg Environ Health 2003. drinking water and indoor air. 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.58:182-186. 11/30/2004. et al. available at URL: http://www. Seifert B. Otero R. Lindane. Available at URL: h t t p : / / w w w.54(3):203-208.inchem. Can J Biochem 1976. Arch Toxicol 1986. Engel R. To T. Pesticide residues in urine of adults living in the United States: reference range concentrations. htm. U. Environ Res 1995. Toxicology 1991: 67(1):107-16.S. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Phillips DL. Gregg M. Hill RH Jr. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Baker S. r e g u l a t i o n s . The metabolism of higher chlorinated benzene isomers. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Helm D. Environ Health Perspect 1997. Santiago-Silva M.

386-.497 (..90) 2.10 (1.80 (2.621) * .480-1.50) < LOD .3 and 0.638) * .20-3. 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. Both chemicals degrade within hours to weeks in the environment (U.50) < LOD .20) < LOD 2.600) < LOD 75th .600-1.00) < LOD .490 (<LOD-.890 (. Fourth National Report on Human Exposure to Environmental Chemicals 43 .690) < LOD .850 (.550-1.490 (<LOD-.790) 2. it was used in home sanitizers for surfaces.349-. SOPP is applied topically to the crop and then rinsed off. 2006).28 (.30-2.420 (<LOD-. however.402-.00) .800-3.570 (.836) * .466 (. and it has limited water solubility. 2006). Survey Geometric mean (95% conf.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .742) * .09) 2.EPA.00) .85) 2. which may vary for some chemicals by year and by individual sample.470 (<LOD-.S.710) 3.600) < LOD .80-3.570-1. Both have been used in agriculture to control fungal and bacterial growth on stored crops.830 (.570 (.92 (.508 (. or 2-phenylphenol) and its water-soluble salt.370-.600-1.645) * .600) < LOD 1. whereas SOPP is not volatile and is more water soluble. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.10) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.90) .390-.840-1.630) < LOD .23) 695 680 520 695 603 953 Limit of detection (LOD.410-.930 (.389-.770 (.07 (. 2002.40-7.740 (.820 (.590-2.696) * . Most agricultural food applications have been revoked.40-2..76) 1.61) 2.14 (<LOD-3. fungicides.50-4.22) 2.567 (.88) 1. leaving the chemical residue OPP.610 (.30) < LOD .350-1. 2006). 1998). In the past. 1998.570-2.500-2. EPA. interval) .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 .860) * 99-00 01-02 99-00 01-02 99-00 01-02 .770 (.950) < LOD . such as fruits and vegetables. or apply these chemicals may be more highly exposed than the general population.20) 2.28-3.80) 1.433-.624) * . or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment. OPP is still used as a disinfectant fungicide for industrial applications.27 (.890 (.50) < LOD .750-2.10-1. Estimated human intakes have been below recommended intake limits (U.10) .30) < LOD 1.Fungicides ortho-Phenylphenol CAS No.10) .90) .60 (1. OPP is efficiently absorbed from the gastrointestinal tract and through the skin. population from the National Health and Nutrition Examination Survey. General population exposure can occur via dermal.40-5.710-2.880-2.50-2. OPP is considered to be moderately toxic after acute oral doses in animal studies.498 (.02) 1.560-8. 90-43-7 General Information Ortho-phenylphenol (OPP.50-3.60 (1.670) 2. are antimicrobial agents used as bacteriostats. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.17 (.40-5.600-1.S.760-2.90) 1. Workers who manufacture.640) < LOD . sodium ortho-phenylphenate (SOPP).60-2.552 (.20 (.30-7.20 (1. Cnubben et al. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.890) 1.370-.50) . but OPP and SOPP are still used on pears and citrus (U.490 (<LOD-.30) < LOD 90th 1. OPP is volatile.30) 1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.00-2.610-1.10) 2.690-1.970 (.40 (. inhalational.496 (.20) < LOD 1.600) < LOD .780) < LOD .10) 1. formulate.450 (<LOD-.570-. and sanitizers.50 (1.490 (<LOD-.490 (<LOD-.10) .509 (.450 (<LOD-.S.33 (. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.03) 1.60-3.00 (1.19 (. Available evidence suggests that OPP does not accumulate in the body.520 (.60 (1. Timchalk et al.3.580-1.50) 1.S.34) 1.30 (1.20 (1. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.90 (1. < LOD means less than the limit of detection.370-.. in paints.20-2. and as a wood preservative.80) 1.860 (.493 (.90 (1.364-.10-2.22 (.636) * .50 (1. 1989). on ornamental plants and turfs.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .10 (1.00 (1. 2006).00 (1.EPA.50 (1.540-2.389-.00 (1.450 (<LOD-.

353-.990) < LOD .11) < LOD 90th 1. 1997.248-.650-1.550 (.11 (. Murata et al.510-. but no neurologic.750 (.970) 1.470 (<LOD-.Fungicides anemia.420 (<LOD-.64 (2. leading to production of two metabolites. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.470) < LOD .06-4.840 (.666) * .07) 2.33) .656) * . OPP was not found to be mutagenic.62) .61 (1. CDC.514 (.11-1.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.38-3.21 (.980 (<LOD-1. 1998. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.910-1.84 (1.28 (2. Brusick.43-2.24-2. Pathak and Roy.46) < LOD 1.93 (1. Detectable levels were seen in over half the U. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.31) < LOD .496 (.93) .33-2.52 (.410 (<LOD-.361-.29) 1.08-1.11) 4..91 (1.670) < LOD .791) * .75 (1.640-1. U.S.40-13.568) * .440 (.311-.410 (<LOD-.. Smith et al. 44 Fourth National Report on Human Exposure to Environmental Chemicals .. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.0) 1.33) 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 .380 (.29) 1. In high dose animal studies.26) 1. 2000.43-2.25-6.51-3.53) 1.460-. 2002. less likely. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.508) * ... Ito et al. 1999.560-2.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .690 (.32) 3.17 (.04-4.96 (1.670 (.28 (<LOD-4.06-5.S.750-2. Bomhard 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.21-2. and it has classified OPP as not classifiable with respect to human carcinogenicity. 1993. Volunteers exposed to 0.21) 1. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. by possible genotoxic mechanisms (Hagiwara et al.00 (.44 (1. 2002.270-.620-1.18) 2.750 (.900-1.09-6.320 (<LOD-..02 (. Additional information is available from U.09 (1.gov/pesticides/.43) 3.980 (.59) .385 (. interval) .510 (<LOD-.4 mg dermally had urinary levels of OPP that were several hundred times higher than median levels found in NHANES 1999-2000 and 2001-2002 (Bartels et al.96 (1.32) 1..382 (. Zhao et al.910 (.329-.. Biomonitoring Information Urinary OPP levels reflect recent exposure.EPA 2006).550) < LOD .590) * . or developmental toxicity was observed (Bomhard et al.97 (2.EPA at: http:// www.301-.12-2.403-.780-14.444 (.17) 2.670 (.910 (<LOD-1..12) < LOD 1.09-3.01) 1.940-2.580) < LOD .770-2.EPA 2006).96-4.43 (1. 1984.860 (.58) 2.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .780 (.360 (<LOD-.484) * .47) .343 (. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.06 (1.00 (1. Nakagawa et al. Kwok et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.75 (1.800-1. 1999. 2005).610) < LOD 1. 1986). or.61 (2.480-.S.570) < LOD 1.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .89 (1. 2002).950) < LOD .08-2. population from the National Health and Nutrition Examination Survey.550-.11 (.S.17 (.453 (.810-1.560) < LOD 75th .61 (.620-1. Survey Geometric mean (95% conf. IARC has classified SOPP as a possible human carcinogen. 1992.96) 1.580-1. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect..78 (2.69 (1. reproductive.epa.455-.81) 1.20) < LOD 3.880-1. 2005.88-4.38) 1.S.08) 1. 2005).27) < LOD .59) 1.600-1.93) .473) * . 1984.4) 3.05-2.500) < LOD .900) < LOD .291-.86 (1.810) < LOD . U.38) 2. 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.24-2.420 (<LOD-.13) 1.93) 1.74 (1.860 (.

Arnold LL. Hagiwara A. et al. Glas K. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Leser KH. Meuling WJ.286(2):309-319. Environ Mol Mutagen 2005. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). Freyberger A.nih. Roberts AL. Environmental Protection Agency (U. Hagiwara A. Bartels MJ. J Chromatogr B Biomed Sci Appl 1997. Imaida K. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Toxicol Appl Pharmacol 1999. Coelhan M.20(5):851-857.(56):399-407. Brzak KA. J Agric Food Chem 2002. Bartels MJ. Pathak DN. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Carcinogenesis 1999. Available at URL: http://www. Sangha GK. EPA-560/5-89-003. The carcinogenicity of the biocide ortho-phenylphenol.43(7):14311437. Shibata M.S. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Fukushima S. Xenobiotica 1998.32(6):551-625. McNett DA. Hirose M. Christenson WR. Kwok ES. 2005.niehs.150(2):402-413. St John MK.28(6):579594. Bormett GA. Cnubben NH. Cano M.35(2 Pt 1):198-208.pdf. Toxicol Appl Pharmacol 1998.EPA). et al. Timchalk C. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries.17(8):411-417. Mutat Res 1993. IARC Sci Publ 1984.gov/ntp/htdocs/LT_ rpts/tr301. July 28. Environmental Protection Agency (U. Brusick D. Turteltaub KW. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. March 1986.159(1):18-24. Inoue S. Elliott GR. Third National Report on Human Exposure to Environmental Chemicals. Fukushima S. Selim S. J Agric Food Chem 2006. Arch Toxicol 2000. Comparative metabolism of orthophenylphenol in mouse. Vogel JS. Roy D. Eastmond DA. Narang A. Office of Toxic Substances. Regul Toxicol Pharmacol 2002. Bartels MJ. Kawanishi S. Atlanta (GA).pdf. Gierthy J.50(11):3351-3358. Bromig KH. Christenson WR. Moore GA. Moriya K. Tayama S. Timchalk C. Centers for Disease Control and Prevention (CDC). EPA 739 R-06004. Ito N. Hakkert BC. Biochem Pharmacol 1992. Richter M. 2006. Moldeus P. Ito N. Fourth National Report on Human Exposure to Environmental Chemicals 45 .gov/oppsrrd1/REDs/ phenylphenol_red. Bomhard EM. van de Sandt JJ.74(2):61-71. Identification of SARA compounds in adipose tissue.S. Zhao S. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Smith RA.Fungicides References Appel KE. Eadon G. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Hum Exp Toxicol 1998.54(16):5731-5735. Crit Rev Toxicol 2002. Stanley JS. Available at URL: http://ntp. EPA). Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Drugs. U. National Toxicology Program (NTP). Brendler-Schwaab SY. 90-43-7) in Swiss CD-1 mice (dermal studies). Mendrala AL. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol.epa.703(12):97-104. Murata M. Bartels MJ. Shirai T. rat and man. Nakagawa Y. Sangha G. U.45(5):460-481. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice.S. 1989.S. Herbold BA. Buchholz BA.22(10):809-814. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. 4/13/09 Onstot JD. 4/9/09.. Food Chem Toxicol 1984. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol.

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

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

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

pdf.cce. Larsen GL. pages 3682-3690. Camann DE. Sanderson WT. Barr DB. Occurrence of sulfonylurea. et al. and metolachlor herbicides in rats. Davison KL. Olsson AO. Atlanta (GA). U. acetochlor. Wilson AG. Lefevre PA. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor.108(12):1151-1157.cornell. Third National Report on Human Exposure to Environmental Chemicals.248(2-3):115-122. Linhart SM. EPA). Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Striley CA. Kinney PL. Volume 65. Environ Health Perspect 2000. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Feil VJ. epa. Tinwell H.html. Heederik D. Kier L. Chem Res Toxicol 1998. Rose RL. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Ward EM. Bravo R. Dialkylquinonimines validated as in vivo metabolites of alachlor. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Barr DB.S. Environ Health Perspect 2003. Alavanja MC. Available at URL(non U. 1998. Environmental Protection Agency (U. Curwin BD. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Sci Total Environ 2000. Hein MJ. Barr DB. Hines CJ. Thurman EM.11(4):353359. reservoirs and ground water in the Midwestern United States. Environmental Protection Agency (U. Quistad GB. Acetochlor (Harness) Pesticide Petition Filing 1/00. Feng PCC. Environ Sci Technol 2005. March 2006. Hsiao JJ.37(4):10881093.15(6):500-508. 2000. Hladik ML. Burkhardt MR. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Barr JR.248(2-3):123-133. et al.EPA): http://pmep.S. Sci Total Environ 2000. Federal Register: January 24. 5/30/06. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. J Expo Sci Environ Epidemiol 2007. Comparative metabolism and elimination of acetanilide compounds by rat.39(17):6561-6574.Herbicides References Ashby J. Xenobiotica 1994.S.24(10):1003-1012. Hum Exp Toxicol 1996. Linderman R.17(6):559-566. Andrews HF. imidazolinone. Coleman S. J Agri Food Chem 1989. sulfonamide.S. Casida JE. Furlong ET. Wratten SJ. 5/30/06 U. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Battaglin WA. Whyatt RM. Available at URL: http://www. Peter CJ. Reynolds SJ. et al. 2005. Hodgson E.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Green T.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. and other herbicides in rivers. EPA). J Expo Anal Environ Epidemiol 2005. Deddens JA.S. EPA 738-R-00-009.111(5):749-756. Centers for Disease Control and Prevention (CDC).15(9):702-735. Number 15. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Jefferies PR. Kolpin DW. Roberts AL.

In a study of applicators and workers exposed to alachlor. EPA at: http://www. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. 1999. 1998.. but another metabolic pathway can produce 2.S. U. 1997. 1996). 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.. IPCS. stomach. 2000.1 mg/L at various collection times (Sanderson et al. ranged from 0. Additional information about is available from U.EPA. 1998). 1995). hemosiderosis. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. Estimated human intakes have been below recommended limits (U. 2003). 1996. Because it can be absorbed through skin. NTP and IARC do not have ratings regarding human carcinogenicity. WHO.S.EPA. Kolpin et al.. U. 15972-60-8 General Information Alachlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural cropland. 2003). Since the late 1980s alachlor use has been declining. Jefferies et al.EPA considers alachlor to be a probable human carcinogen at high doses. 1996. Alachlor itself is not considered mutagenic.S. 1998.epa. WHO.S. 1998. 1989.. Hines et al. In chronic animal testing.EPA. In 1993-1995.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. and uveal degeneration. 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 absorbed by plants and inhibits plant protein synthesis.EPA. Alachlor has low potential for acute toxicity. 50 Fourth National Report on Human Exposure to Environmental Chemicals . corn cropland was treated with alachlor. 1994.. mean values of urinary concentrations of alachlor metabolites. and on non-crop land for general weed control. soybeans. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. as measured through conversion to deethylamine. Hladik et al. Tessier and Clark. Hill et al. the latter may account for some observed effects (Davison et al.6-diethylaniline and its reactive metabolite.S. 1999 and 2007. and field workers. the dermal exposure route is potentially significant for applicators. 1995. 1998). (2003) showed that 2. WHO. 2005. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. alachlor has demonstrated hepatotoxicity. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. WHO. whereas 60% of applicators had detectable amounts. about 20-25% of the U..gov/pesticides/. but has not shown developmental or reproductive toxicity in mammalian systems (U.1 to 1..EPA. but shows little bioaccumulation.. USGS.S. peanuts and other crops. In animal studies. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. U.. formulators. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. In animals. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment.. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. 2003). 2005). Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. U. Feng and Wratten. mercapturate conjugates were predominant metabolites. 1998). 2003).Herbicides Alachlor CAS No. 2000.S. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. Alachlor has a soil half-life of a few weeks.S. 1988. but not likely at low doses. including corn.

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 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Fourth National Report on Human Exposure to Environmental Chemicals 51 . see Data Analysis section) for Survey year 99-00 is 1. population from the National Health and Nutrition Examination Survey. 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. < LOD means less than the limit of detection.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.Herbicides Urinary Alachlor mercapturate Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Urinary Alachlor mercapturate (creatinine corrected) Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf.18.S.

Tolos W. imidazolinone. Mutat Res. Comparative metabolism and elimination of acetanilide compounds by rat. Background document for development of WHO Guidelines for Drinking-water Quality. 86.248(2-3):123-133. EPA 738R-98-020. Xenobiotica 1994.htm. Supplemental Technical Information (available on-line only). Burkhardt MR.18(6):363-391. Shealy DB. DNA adduct formation by alachlor metabolites. Jefferies PR.S. Sci Total Environ 2000. Quistad GB. Feng PCC. Heydens WF. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. World Health Organization. Brown KK. MacKenzie B. 1997. Am Ind Hyg Assoc J 1995. WHO/ FAO Data Sheets on Pesticides. Erratum in: Life Sci 1989. No. Alachlor in Drinking-water. Casida JE.56(9):883-889.S. Life Sci 1988. Roberts AL. 98-4245 (by Barbash JE. Quistad GB. Feil VJ. Biagini RE. 2005.pdf. Available at URL: http://www. Available at URL: http:// www. California. reservoirs and ground water in the Midwestern United States. Striley CA.11(4):353359. Third National Report on Human Exposure to Environmental Chemicals. 1992-2001. Andrews HF. Hill RH Jr. 4/2/09 U. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Camann DE. Ann Occup Hyg 2003. Atlanta (GA). Kolpin DW. 2003. J Agri Food Chem 1989. EPA).56(6):853-859.pdf. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Sci Technol 2005. 2/27/09 Jefferies PR.24(10):1003-1012. Chem Res Toxicol 1998.php.43(9):2504-2512. Casida JE. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Henningsen G. Thake DC. 1999. et al.43(25):2087-94. Shoemaker DA.44(18):1325. Hsiao JJ. Gilliom RJ). Thurman EM. Davison KL. Available at URL: http://water. Hill AB. Kolpin DW. Larsen GL. acetochlor. 2/27/09 U. et al. Kinney PL. Barr DB. World Health Organization (WHO). Geological Survey (USGS). sulfonamide. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. and other herbicides in rivers. International Programme on Chemical Safety (IPCS).37(4):10881093. Kimmel EC. Clark JM. Kier LD. December 1998. Circular 1291.Herbicides References Battaglin WA. who.int/water_sanitation_health/dwq/chemicals/en/alachlor. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Martens MA.39(17):6561-6574. Centers for Disease Control and Prevention (CDC). Reregistration Eligibility Decision (RED) Alachlor. Lau H.248(2-3):115-122.111(5):749-756.org/documents/pds/pds/pest86_e. Sci Total Environ 2000. Driskell WJ. U. Occurrence of sulfonylurea. Biagini R. 1999.S. Geneva. Casida JE. Thelin GP. Bull Environ Contam Toxicol 1996. Hines CJ. Sacramento. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. and metolachlor herbicides in rats.S. ALACHLOR. Peter CJ. 2007. 1996.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Geological Survey (USGS). Hum Exp Toxicol.gov/oppsrrd1/ REDs/0063. Whyatt RM.epa. Hull RD. revised February 15. Barr JR. Environmental Protection Agency (U. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Hladik ML. Brown MA. Environ Health Perspect 2003.395(2-3):159-171. J Ag Food Chem 1995.usgs. Linhart SM. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Available at URL: http://www.47(6):503-517. Tessier DM. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Wratten SJ.inchem. Hines CJ. Furlong ET. Deddens JA. March 2006. Dialkylquinonimines validated as in vivo metabolites of alachlor. 1998. Sanderson WT. Wilson AG.

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

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

International Programme on Chemical Safety (IPCS). Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Noriega N. et al.inchem. Sanborn JR. Grzywacz JG. Deddens JA. Toxicol Lett 1993.15(6):500-508. Proc Natl Acad Sci USA 2002. Mendoza M. Toxicological profile for atrazine. Environ Health Perspect 2007.47(6):503-517. 2001 [online]. Agency for Toxic Substances and Disease Registry (ATSDR). Collins A. Tapia J. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Ferioli A.64(9):672-678. J Toxicol Environ Health 1994. Curwin BD. Schmid J. Simpkins JW. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. 2007). Eberly LE. Cooper RL.. Brown KK. Barr DB. Hayes TB. Atlanta (GA). Fleenor-Heyser DG. Clayton CA.. Barr DB. Geneva. 1993). Stoker TE.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. In a small number of field workers.76(1):190-200. Hermaphroditic. Gammon DW.htm. Saiz SG. Cottica D. Stoker TE. Chen H. Cooper RL. diamino-S-chlorotriazine and hydroxyatrazine. ATRAZINE. Steroids 1999. Vonk A. Cooper RL. Bradway DE.. Quandt SA. Eldridge JC.99(8):5476-5480. Hein MJ. 2005. McElroy WK. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence.109(6):583-590. Biological monitoring of human exposure to atrazine.58(2):366-376. J Toxicol Environ Health 1994.cdc.. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). 82. 2005). Jones AD. Gillis JH. Ann Occup Hyg 2003. Centers for Disease Control and Prevention (CDC). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Stuart AA. Extrom PC. 3/11/09 Arcury TA. In a study of 60 farm worker children. Reynolds SJ. Available at URL: http://www. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Carr WC Jr. Gillis JH. Wetzel LT. et al.. Blewett C. Stoker TE. Catenacci G. 2003. Lee M. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. 1996. et al. 3/11/09 Laws SC. In the NHANES 2001-2002 subsample. Eldridge JC. Hines CJ. Ferrell JM. World Health Organization. Heederik D.30(2):244-247. Pfeifer KF. Lioy PJ.org/documents/pds/pds/pest82_e. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. The geometric mean of urinary atrazine mercapturate was 1. Aldous CN. Goodrow MH.gov/toxprofiles/tp153. 2005). Perry et al. Laws SC. Ferrell JM.atsdr. 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. Stevens JT. Freeman NC. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . 2000).Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. J Agric Food Chem 1982.43(2):155-167.115(8):1254-1260. Pest Manag Sci 2005. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L.69(2):217-222. Sanderson WT. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Third National Report on Human Exposure to Environmental Chemicals. Wetzel LT. A risk assessment of atrazine use in California: human health and ecological aspects. Goldman JM. Environ Health Perspect 2001. Biagini RE.61(4):331-355. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Maroni M. et al. Seiber JN. et al.. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. No.. In small studies of Maryland residents in 19951996 (MacIntosh et al.43(2):155-167. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Lucas AD. Barr DB. Toxicol Sci 2000.53(2):297-307.html. 2001). Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. atrazine was detected in only four children (Arcury et al. Toxicol Sci 2003. J Expo Anal Environ Epidemiol 2005. et al. References Adgate JL. Striley CA. Barbieri F. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Tyrey L. Moseman RF. Available at URL: http:// www. Breckenridge CB. WHO/ FAO Data Sheets on Pesticides. Shoemaker DA. Bersani M. levels of atrazine mercapturate were generally not detectable (CDC. Toxicol Sci 2000.

Perry M. Toxicology 1990. A risk characterization for atrazine: oncogenicity profile. May 2003a. Cooper RL. Interim Reregistration Eligibility Decision For Atrazine.epa. Singzoni B. 3/11/09 U.php. Sanderson JT. Christiani D.56(2):69-109. 6/1/09 U. Pesticides in the Nation’s Streams and Ground Water. Boerma J. Ryan PB. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Rayner JL. Supplemental Technical Information (available on-line only). Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats.S.epa. Guidici DL. Available at URL: http://water. Timchalk C. Laws SC. Environmental Fate and Effects Division.67(2):198-206. Chem Res Toxicol 1993. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. revised February 15. Geological Survey (USGS). Toxicol Appl Pharmacol 2002. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Available at URL: http://www. Available at URL: http://www. A review of epidemiologic studies of triazine herbicides and cancer.182(1):44-54.195(1):23-34.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. EPA). Ann Epidemiol 2000. Pesticides and Toxic Substances.9(5):494-501. March 2006. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Circular 1291. J Toxicol Environ Health A 1999.Herbicides development of a biomarker of exposure. Tortorelli J. van den Berg M. Wood C. EPA Office of Pesticide Programs. 2007.pdf. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Needham LL. Environmental Protection Agency (U. Toxicol Appl Pharmacol 2004. Office of Prevention. White paper on potential developmental effects of atrazine on amphibians. Fenton SE. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat.6(1):107-116.58(1):50-59. Kastl PE. Case No. MacIntosh DL.10(7):479. J Expo Anal Environ Epidemiol 1999.usgs. Breckenridge CB. Dagenhart D. 0062. Osborne DW.gov/oppsrrd1/REDs/ atrazine_ired. 1992-2001. Crit Rev Toxicol 1997.S. Stoker TE. Guidici DL. U. Cooper RL. Toxicol Sci 2002. 2003b. Stoker TE.27(6):599612. EPA). A longitudinal investigation of selected pesticide metabolites in urine.S. Toxicol Sci 2000. Sathiakumar N.61(1):27-40. Hammerstrom KA. Delzell E. Stevens JT. Washington (DC).S. Lansbergen GW. Dryzga MD. Langvardt PW. Wetzel L. Environmental Protection Agency (U. The Quality of Our Nation’s Waters.S.pdf. Laws SC.

930 (.350) < LOD < LOD < LOD .22) < LOD .690-1. 4-D.24 (.320) 90th .66) < LOD 1. 94-75-7 General Information Widely used throughout the United States.70) 1..32 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.330 (. agricultural.690 (.40) 1.370-.930-1.660) 1.230 (<LOD-. renal and hepatic injury. As much as 62 million pounds of 2.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80) 1. Similar to other chlorophenoxy herbicides.210-. myotonia. it acts as a plant growth hormone.27 (.4-D have been below recommended intake limits (U. It was first registered with U.410) < LOD . 2005).05-2.310) < LOD .49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . and delayed Urinary 2. and mecoprop).960-1.260 (<LOD-.740 (.680-1. 2.4-Dichlorophenoxyacetic Acid CAS No. It is not well absorbed through the skin.S. Human health effects from 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.2.250 (<LOD-. abdominal pain.4-D is rapidly absorbed via oral and inhalation routes.51 (1.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Once absorbed.27 (1. dizziness. in 2001 (U.00-2.560-. Survey Geometric mean (95% conf. 2004). < LOD means less than the limit of detection.4-dichlorophenoxyacetic acid (2.S. 1974.490 (.610 (. nausea. 2007). General population exposure to 2.4-D or exposed for prolonged periods.02-1.EPA.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .21) 1.230-.4-D has low acute toxicity.420) < LOD .440-1.550-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. but at higher levels they are herbicidal.310 (.560-1. Sauerhoff et al.30 (<LOD-2.250 (<LOD-. population from the National Health and Nutrition Examination Survey.690 (. At low levels. 2. hypotension.03) 695 659 520 668 589 892 Limit of detection (LOD. It is rarely detected in ground waters (USGS. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.. with a half-life of several days to several weeks.20 (.760 (.Herbicides 2. headache.890 (.540-.4-D can be applied either as an aqueous salt or as oil-soluble esters. 1989. 1977).EPA in 1948.S.08) < LOD .4-D) controls broadleaf weeds in residential. Recent estimates of chronic intakes of 2.. MCPA. Fourth National Report on Human Exposure to Environmental Chemicals 57 . and by consuming food or drinking water contaminated with 2. these herbicides can enhance plant growth.10 (<LOD-1.27-2.730 (.60) 1. Kohli et al.690 (. 2.48) < LOD 1. 2.43) 1.810-1.S. the chlorophenoxy herbicide 2. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.37) size 1977 2413 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD .4-D were used in the U.S.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.10 (<LOD-1.490) < LOD < LOD < LOD .910) < LOD .13) < LOD .910) 1.4-D may occur during residential applications.10) < LOD 1.EPA. It is poorly bound in soils.952 and 0. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.55 (1.20 (<LOD-1.670-1.420-. and aquatic environments.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.610-.16) < LOD . by direct contact with agricultural and residential areas after applications.210 (<LOD-. which may vary for some chemicals by year and by individual sample.07 (.890) < LOD .400) < LOD .

gov/pesticides/.7.810-1. or teratogenic effects in chronic rodent studies (Charles et al. 2005. population (Hill et al. adrenals and gonads (NTP.EPA. 1992).580-.17 (..08 (.270 (<LOD-.890) < LOD 1.850) < LOD .27-1. Average post-application urinary levels of 2. and evidence of histological injury to the kidneys.490 (.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . other exposures.640 (.380 (<LOD-.410) < LOD < LOD < LOD .570) < LOD . 2005).4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Knopp et al.EPA.410 (<LOD-.670 (.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.620-.16) 1. Survey Geometric mean (95% conf. Biomonitoring Information Urinary levels of 2. 1996.. urinary 2.. 2005.05) .8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. IPCS.41 (1. Frank et al.810-1. Kolmodin-Hedman and Erne. 1985.270-.550-. 2005.590 (<LOD-1. Hill et al.S. U. 2.14 (. CDC.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2006.S. IPCS. IPCS.08 (.. 1996. U.340-. 1980. 2002. 2.330-.19) .13 (.700 (. thyroid. 2005.3. 2003.. developmental. or to contaminants in the herbicide formulations (specifically 2.920) < LOD 1.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.340 (. Epidemiological studies have reported associations of several types of cancer. 2004).410) < LOD 1.790) < LOD . population from the National Health and Nutrition Examination Survey.480 (.740 (.560-.780) .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..39) < LOD 1.440 (.980) < LOD 1.390) < LOD < LOD < LOD ..29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .4-D are eye irritants.EPA at: http://www.35) < LOD .670 (.660 (.EPA 2005).520-.410) 90th .670 (<LOD-1.. U.S.24) 1. 2002.470) < LOD . The acid and salt forms of 2. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. Post-application levels in farmers and home gardeners were dependent on Urinary 2.56) . Kutz et al. IOM. 58 Fourth National Report on Human Exposure to Environmental Chemicals . and of adults and children (Baker et al.32 (<LOD-2. in small samples of children (Hill et al.680) < LOD .S. 2005).73) . It is unclear whether these associations are related to the chlorophenoxy herbicides.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 . 1994). myotonia.4-D does not have significant reproductive..4-D reflect recent exposure.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.930-1.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.660) < LOD .EPA.Herbicides neuropathy (Bradberry et al. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. Pearce and McLean. 2001. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.780-1. 1995. 1996.590 (<LOD-1.790) 1.S. eyes.780 (.380 (<LOD-.4-D levels were detectable in less than a quarter of the individuals studied. 2005). Additional information is available from U. 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. 1995).13 (. 1989). 2000).380-.890-1.08 (.720 (.990-1. U.epa. 2. 2005). In previous samples of the U. liver. Acute high doses administered to laboratory animals produced ataxia.610-.380) < LOD ..820-1.S.4-D production plant workers and a few forestry workers spraying 2.610-.350 (<LOD-.560-.

Environ Res 1995. Biomonitoring studies of 2.php?record_id=10603. Third National Report on Human Exposure to Environmental Chemicals. Carter-Pokras OD.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. Holler JS. In farm families. Tables. et al. Chapman P. Curwin BD.18(4):469-474. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .4-D than levels found in the general population. van Ravenzwaay B. 2005 Charles JM. Sircar KP.4:427-435. Arch Environ Contam Toxicol 1985. Scand J Work Environ Health 2005. Pesticide residues in urine of adults living in the United States: reference range concentrations. TOX-63 Peroxisone Project (2. Khanna RN. References Arbuckle TE. Forestry workers involved in aerial application of 2...inchem. Acquavella JF.4-dichlorophenoxyacetic acid (2. Review of 2.4-D): exposure and urinary excretion. Selected pesticide residues and metabolites in urine from a survey of the U.4-D) epidemiology and toxicology. Needham LL. 914. general population. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Arnold EK. Baker BA. National Toxicology Program (NTP). Baker SE. Assessment of exposure to 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4-dichlorophenoxyacetic acid in man. Smith SJ.31 Suppl 1:90-97. Vet Hum Toxicol 1989.4-D).nih.Herbicides the time since application. Campbell RA. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. the number of acres to which it was applied (Curwin et al. Driskell WJ. Barr DB. Cole DC. Hanley TR Jr.niehs.4-D will result in an adverse health effect. Ritter L. Developmental toxicity studies in rats and rabbits on 2.4-D and 2. the amount of pesticide applied. Dichlorophenoxyacetic acid. Head SL. Updated March 7. Available at URL: http://ntp.4-D. International Programme on Chemical Safety-INCHEM (IPCS).4-.31(2):121-125. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Shealy DB. Hill RH Jr. Estimation of occupational exposure to phenoxy acids (2.4:318-321.71(2):99-108. Pesticides residues in food: 1996 evaluations Part II Toxicology.. Available at URL: http:// www. Xenobiotica 1974.S. 1992).5-T). Centers for Disease Control and Prevention (CDC). et al. Harris et al. Garabrant DH.31 Suppl 1:98-104. Tandon JS. Survival and Growth Curves from NTP Toxicity Studies.4:97-100. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.4-D were highest in the farmers who applied the 2. Barr DB.27(1):23-38. Absorption and excretion of 2.4-D in urine does not mean that the level of the 2. Washington (DC): National Academies Press. Veterans and Agent Orange: update 2002. 2006. 3/17/09 Institute of Medicine (IOM). Kutz FW. Ripley BD.4 dichlorophenoxyacetic acid (2. Hill RH Jr.15(6):500-508.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Erne K.4-dichlorophenoxyacetic acid and its forms. Harris SA. 2005. Finding a measurable amount of 2. Beasley VR.4-dichlorophenoxyacetic acid (2. Baker S. J Toxicol Environ Health 1992. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Needham LL.nap. Cook BT. 2005. Alexander BH.edu/catalog. Beeson MD. Gupta BN. Toxicol Sci 2001. Wilson RD. Kolmodin-Hedman B. Kohli JD. Sirons G J. Heederik D. Fast DM. Bus JS. Board on Health Promotion and Disease Prevention.51(3):152-159. Gregg M.4-Dichlorophenoxyacetic Acid). Honeycutt R. Murphy RS. Scand J Work Environ Health 2005. Biomonitoring for farm families in the farm family exposure study. Exposure of homeowners and bystanders to 2. geometric mean urinary levels of 2. TOX-63: TOXICITY REPORT CURVES. Occup Environ Med 1994.10(6 Pt 2):789-798. 2005). Mandel et al. Philbert MA. Brody D. Biomonitoring of herbicides in Ontario farm applicators. Crit Rev Toxicol 2002. J Environ Sci Health B 1992. Atlanta (GA). 2. Dhar MM. Reynolds SJ. et al. Arch Toxicol Suppl 1980.60(1):121-131. 3/17/09 Knopp D.htm.org/documents/jmpr/jmpmono/v96pr04. To T. and the use of protective clothing or equipment (Arbuckle et al. Sanderson WT.4. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Frank R. Bailey SL.gov/index. J Expo Anal Environ Epidemiol 2000. Arch Environ Contam Toxicol 1989. Stephenson GR.32(4):233-257. Mandel JS. 2003.. 2005). J Expo Anal Environ Epidemiol 2005 Nov.37(2):277-291. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Available at URL: http:// www. Solomon KR. Hein MJ.

Pesticides in the Nation’s Streams and Ground Water.epa. 4/2/09 U.usgs. Available at URL: http://www. Available at URL: http://water. June 2005. March 2006. The Quality of Our Nation’s Waters. gov/oppbead1/pestsales/01pestsales/market_estimates2001.EPA). May. Environmental Protection Agency (U.4-dichlorophenoxyacetic acid (2. Available at URL: http://www. Toxicology 1977. 3/17/09. Braun WH. Pesticide industry sales and usage .4-D) following oral administration to man.S. Circular 1291. 60 Fourth National Report on Human Exposure to Environmental Chemicals .epa. 2004.gov/oppsrrd1/ REDs/factsheets/24d_fs.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. 2. Blau GE. EPA 738 F-05-002.S.4-D RED Facts. Washington (DC): U. The fate of 2.EPA).Herbicides Sauerhoff MW.php.pdf. 3/17/09 U. Gehring PJ. Environmental Protection Agency (U.S.8:3-1U. Geological Survey (USGS). 1992-2001. 2007. Office of Prevention Pesticides and Toxic Substances. Supplemental Technical Information (available on-line only).S.htm. revised February 15. S.2000 and 2001 market estimates.S.EPA.

mercapturate conjugates were the predominant metabolites.. sorghum and other crops.S. It is absorbed by plants and inhibits plant protein synthesis. and eliminated in urine and feces over two to three days (WHO. 2000.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al. 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. EPA at: http://www. Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. 2003). Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect. In animals. so applicators. Estimated human intakes have been below recommended limits (U. 1995).S. formulators. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample.Herbicides Metolachlor available from U. and convulsions were observed at lethal doses in animal studies. Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. The geometric mean metolachlor mercapturate was 4.S.. Biomonitoring Information CAS No. 2007. U. 2005). in both ground and surface waters (Battaglin et al.. metolachlor levels in water have exceeded lifetime human health advisory levels (U.S. Metolachlor has low potential for acute toxicity (U.. soybeans. Hladik et al. Kolpin et al.EPA. General population exposure may occur through the consumption of contaminated food or drinking water. including corn. Jefferies et al. 2003). Gilliom. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. and on non-crop land for general weed control. but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. WHO. Fourth National Report on Human Exposure to Environmental Chemicals 61 . and field workers may have significant exposures via this route. 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.. 2003). This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment. 1989. 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. USGS. though the 95th percentile for males was 0.EPA considers metolachlor to be a possible human carcinogen. metolachlor was quickly absorbed after dermal or oral doses. 2000. 2005. 1994. People exposed to metolachlor will excrete metolachlor mercapturate in their urine. In animal studies. 2005). Feng and Wratten.EPA. Davison et al. Hines et al.. WHO.S. Metolachlor did not show developmental or reproductive toxicity in chronic animal studies.200 μg/L (CDC. Metolachlor is well absorbed dermally. Salivation. EPA. lacrimation. NTP and IARC do not have ratings regarding human carcinogenicity. 1999. 1998). Occasionally in the past.gov/pesticides/.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine.epa. 1995). 1995. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. (2003) showed that 2. whereas 60% of applicators had detectable amounts. Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. and it was not mutagenic in mammalian cells (U. 2007. 1995)..EPA.

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

248(2-3):115-122. Available at URL: http://www. Thelin GP. Kolpin DW.gov/nawqa/pnsp/pubs/files/051507. Centers for Disease Control and Prevention (CDC). 6/1/09 Whyatt RM. World Health Organization (WHO).pdf 3/30/09 Hines CJ.who.gov/oppsrrd1/ REDs/0001. and metolachlor herbicides in rats. Sci Total Environ 2000.S. 98-4245 (by Barbash JE. R. Sacramento.24(10):1003-1012.php. Curwin BD.41:3409-3414. Occurrence of sulfonylurea. Reregistration Eligibility Decision (RED) Metolachlor. Comparative metabolism and elimination of acetanilide compounds by rat. Available at URL: http://water. Hodgson E.html. Linderman R. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Barr DB.epa. Casida JE. Peter CJ. Hein MJ.gov/nawqa/ pnsp/pubs/wrir984245/text. Ann Occup Hyg 2003. reservoirs and ground water in the Midwestern United States. Rose RL. Davison KL. 1999. Atlanta (GA). EPA 738R-95-006.108(12):1151-1157. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. usgs. et al. Sanderson WT. Geological Survey (USGS). Biagini RE. Hladik ML. 1998. Striley CA. Environ Sci Technol 2007. Ward EM. sulfonamide. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Wratten SJ. Available at URL: http://water. Gillion. Coleman S.S.S. Metolachlor in Drinkingwater. Supplemental Technical Information (available on-line only). Environ Health Perspect 2000. Shoemaker DA. Linhart SM. streams and groundwater. revised February 15. Andrews HF. Environ Sci Technol 2005. EPA). Burkhardt MR. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Brown KK.248(2-3):123-133. Geological Survey (USGS). 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 .11(4):353359. imidazolinone.ESTfeature_gilliom. Hsiao JJ. Third National Report on Human Exposure to Environmental Chemicals.pdf.S. Roberts AL.111(5):749-756. Reynolds SJ.Herbicides References Battaglin WA. Environ Health Perspect 2003.47(6):503-517. et al. 4/2/09 U. Xenobiotica 1994. Quistad GB. Furlong ET. 1992-2001. Environmental Protection Agency (U. Circular 1291. March 2006. April 1995. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. J Expo Anal Environ Epidemiol 2005. U.usgs. Feng PCC. and other herbicides in rivers. Feil VJ. Camann DE.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.S.int/water_sanitation_health/dwq/chemicals/ metolachlor. 2003. Alavanja MC. Gilliom RJ). J Agri Food Chem 1989. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Barr JR.usgs. Heederik D. Background document for development of WHO Guidelines for Drinking-water Quality. Sci Total Environ 2000. Available at URL: http://www. 2007. Jefferies PR. Pesticides in U. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Larsen GL. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. acetochlor.15(6):500-508. Available at URL: http://water. Kinney PL. 3/26/09 U.pdf. 2005. Deddens JA.39(17):6561-6574. California. Kolpin DW. Dialkylquinonimines validated as in vivo metabolites of alachlor. Chem Res Toxicol 1998. Barr DB. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.37(4):10881093. Thurman EM.

.4.5-T use as a herbicide in 1985.4. with an elimination half-life of approximately 19 hours (Arnold et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Human health effects from 2. renal and hepatic injury. abdominal pain.. the general population is unlikely to be exposed to it.4. Epidemiological studies have reported associations of several types of cancer.4. nausea.2 and 0. but higher levels are herbicidal.5-T is eliminated mostly unchanged in the urine. ranging from several weeks to many months. 2.4.4-D were used as defoliants in the Vietnam War (e.5-T was once applied as either an aqueous salt or as an oil-soluble ester. and delayed neuropathy (Bradberry et al. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.4.5-Trichlorophenoxyacetic acid (2. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 2. dizziness. and concern about contamination with 2.3. it is not well absorbed through the skin. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.S. these herbicides can enhance plant growth..5-T and 2.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2. Nelson et al.5T is rapidly absorbed via oral and inhalation routes.4. Although 2. Chlorophenoxy herbicides act as plant growth hormones. population from the National Health and Nutrition Examination Survey.g.5-Trichlorophenoxyacetic Acid CAS No.4. Survey Geometric mean (95% conf. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. 2004). headache.. 1992).5-trichlorophenol and other degradates. 93-76-5 General Information 2. hypotension.4.4. Ester forms of 2. which may vary for some chemicals by year and by individual sample.4. Kohli et al.4.Herbicides 2. At low levels. 1986.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.1. Given the commercial unavailability of 2.4. 1974). 64 Fourth National Report on Human Exposure to Environmental Chemicals . Omer.4. 2. The half-life of 2.5-T in soil varies with conditions. myotonia. 2007).5-T. Once absorbed into the body. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.. 1992.5-T (Holson et al.7.4. 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. < LOD means less than the limit of detection.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. 1989..5-T degrades to 2.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. Agent Orange).5-T has been rarely detected in ground waters (USGS.4. Mohammad and St.

4.3. Biomonitoring Information Urinary levels of 2.4.gov/pesticides/.EPA. IOM. IPCS.7. 2.5-T in urine also provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2. Urinary 2.4. other exposures.S.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. Additional information is available from U. urinary levels of 2. 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. or to contaminants in the herbicide formulations (specifically 2.5-T does not mean that the level will result in an adverse health effect.4.EPA at: http://www.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.Herbicides or contaminated herbicides. Biomonitoring studies on 2. 1980). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4.4.4.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. similar to results of NHANES II (19761980). population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 65 .epa. 2003.S. 2005)..5-T reflect recent exposure. U. 1996.5-T than levels found in the general population. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 2004).4. 1992).S. Survey Geometric mean (95% conf.5-T also were below the limit of detection (Kutz et al. It is unclear whether these associations are related to the chlorophenoxy herbicides.4. Mean urinary levels of 2.5-T itself is not mutagenic. Pearce and McLean.5-T were generally below the limit of detection. Finding a measurable amount of 2. in which urinary levels of 2. 2005. 2002. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Cook BT. Kutz FW.4-dichlorophenoxyacetic acid (2.php?record_id=10603.37(2):277-91.5-T in four-way outcross mice. May.8(5):551-60. S.5-t mixture. Office of Prevention Pesticides and Toxic Substances. Crit Rev Toxicol 2002. Review of 2. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Board on Health Promotion and Disease Prevention. Holson JF. Centers for Disease Control and Prevention (CDC).org/documents/jmpr/jmpmono/v96pr04.4. Nelson CJ.htm. Khanna RN.4. St Omer VE. 210:250-255. Wolff GL. et al. Available at URL: http:// www. Arch Int Pharmacodyn Ther 1974. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Washington (DC): National Academies Press.pdf.19(2):298-306.4. 2005.4-D and 2. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http:// www.EPA). Fundam Appl Toxicol 1992. Murphy RS. Beasley VR. Pesticide industry sales and usage . LaBorde JB. Poisoning due to chlorophenoxy herbicides. Vale JA. Gaines TB. Sircar KP.31 Suppl 1:1825. Atlanta (GA).4:318-21. Nelson CJ.2000 and 2001 market estimates.5-trichlorophenoxyacetic acid (2.4.EPA. Kolmodin-Hedman B. Arch Toxicol Suppl 1980. Estimation of occupational exposure to phenoxy acids (2. Neurobehav Toxicol Teratol 1986. Gaylor DW. Vet Hum Toxicol 1989. Sheehan DM. Dhar MM. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Scand J Work Environ Health 2005. Carter-Pokras OD. Developmental toxicity of 2. McCallum WF.nap.Herbicides References Arnold EK. Proudfoot AT. Dichlorophenoxyacetic acid.4. LaBorde JB. Pearce N. Behavioral and developmental effects in rats following in utero exposure to 2. Brody D.5-trichlorophenoxy acetic acid in man. I. Agricultural exposures and non-Hodgkin’s lymphoma. Garabrant DH.4-D) epidemiology and toxicology. 2. 2003.5-T). Environmental Protection Agency (U. Pesticides residues in food: 1996 evaluations Part II Toxicology. 2004. Toxicol Rev 2004.S. general population. Veterans and Agent Orange: update 2002.5-T). Fundam Appl Toxicol 1992. Holson JF. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Erne K.4-. Philbert MA.32(4):233-257.S. Available at URL: http://www. discussion 5-7. J Toxicol Environ Health 1992.4.23(2):65-73. Selected pesticide residues and metabolites in urine from a survey of the U.4. II. Bradberry SM.4-D/2.31(2):121-125.epa.5-T). Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.inchem. Mohammad FK. Absorption and excretion of 2. 3/17/09 Kohli JD. McLean D.19(2):286-297. Developmental toxicity of 2. et al.4. Multireplicated dose-response studies with technical and analytical grades of 2. International Programme on Chemical Safety-INCHEM (IPCS).edu/catalog. 914. Washington (DC): U.S. Gupta BN.5-trichlorophenoxyacetic acid (2. U. 3/17/09 Institute of Medicine (IOM). Tandon JS. Gaines TB.

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

Carbamate Insecticides

Carbofuran

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 827 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1340

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

* * * * * *

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

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

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

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

696 680 521 696 603 953

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

68

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 826 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1339

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

* * * * * *

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

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

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

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

696 680 521 695 603 953

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

Fourth National Report on Human Exposure to Environmental Chemicals

69

Carbamate Insecticides

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

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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

population from the National Health and Nutrition Examination Survey.. which may vary for some chemicals by year and by individual sample. and seizures. similar to results in a subsample of NHANES II (19761980) (Stehr-Green. dieldrin at higher doses caused irritability. Kanthasamy 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. the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al. In samples obtained between 1973 and 1991 from Norwegian women. the median serum dieldrin level was generally similar to the 90th percentile for females in this Report (Ward et al. nausea. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity. OSHA has established workplace exposure standards for aldrin and dieldrin. 2000).e..atsdr. Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al. 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. Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al.. The U. When fed to experimental animals.6% of the subsample had dieldrin levels above the limit of detection (Stehr-Green 1989). 1998) and behavioral changes (Carlson and Rosellini.. In a study of pesticide applicators with occupational exposure to aldrin. environmental levels) and health effects is available from ATSDR at: http://www.. vomiting. 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. and the FDA monitors foods for pesticide residues.gov/toxpro2. 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. 1987). 2004). but no estrogenic effect was noted in a study that used cultured cells (Tully et al. 1995). 2000).S. tremors. 1991). 2004). Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. in which only 10..Organochlorine Pesticides twitching.cdc. both aldrin and dieldrin caused liver enlargement and liver tumors. 2000. seizures (Smith. Survey Geometric mean (95% conf. Information about external exposure (i. 2005)... 2005. Epidemiologic and animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al. 78 Fourth National Report on Human Exposure to Environmental Chemicals . serum aldrin levels were below the limit of detection.. 1989).S. and occasionally.html. 1998). EPA has established environmental standards for aldrin and dieldrin. Li et al. When dieldrin was fed to pregnant rodents.. Serum dieldrin levels at the 95th percentile in NHANES 2001-2002 and 2003-2004 subsamples were approximately ten times lower than the corresponding percentile measured in NHANES II (1976-1980)..

Survey years 01-02 03-04 Geometric mean (95% conf.60-10.054-.100-.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 8.9-38.5) 21. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD .7-19.080-.048 (<LOD-.4 (12.50 (8.100) .9 (13.8.147) 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 .6 (14.3 (18.180) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 10.2) 14.090-.50) 15. Fourth National Report on Human Exposure to Environmental Chemicals 79 .00-14.30 (8.055 (. which may vary for some chemicals by year and by individual sample.8 (9.1) 15.112-.9 (12.089 (.098 (.090-.130-.1-16.124) .090 (.103 (.9 (12.139 (.8-24.5) 19.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.108-.4) 19.4) 95th 20.40-9.110 (.110) .070) .150 (. 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.180) .8 (18.5 (16.4) 539 456 484 487 980 885 Limits of detection (LOD.0) 21.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.112) 95th .3 (18. Survey years 01-02 03-04 Geometric mean (95% conf.8-25.6) 19. see Data Analysis section) for survey years 01-02 and 03-04 are 10.4-18.130-.062-.9-23.8) 14.S.6) 9.00 (8.9 (14.116) .100) .190) .130-.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .170) .80-9.063-.190) .100-.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .1-24.1) 14.5 (<LOD-11.4) 20.138) .0 (15.0-21.6-24.2) 12.2) 11.147 (.1-18.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.083-.6 (15.9-22.060) .102 (.10 (<LOD-16.113 (.S.130) .6 (15.077 (.7 (<LOD-15.053 (<LOD-.1-19.8) 15.056-. which may vary for some chemicals by year and by individual sample.075) < LOD .090 (<LOD-.242) .093) .6-33.109-.9 (13.101) . 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 9.109 (.160 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30 (8.8 (11.054-.062 (.0-25.130) .100-.6-24.5-15.3-21.103 (.7-22.120) .080) .4) 21.130) .3 (13.0) 19.090-.110 (.2-15.080 (.1) 20.086-.90) 90th 15.110) .064 (.3 (14.130 (.1 (13.40-10.084-.5-17.049-.070 (<LOD-.120-.096-.80-10.077-.80 (<LOD-10.158) .6) 16.1) 13.100 (.4) 14.138 (.3 (19. < LOD means less than the limit of detection.5 and 7.139 (.088-.8) < LOD 8.8-17.0) < LOD 9.0 (10.140-.160) .140 (.058) < LOD .109-.149) .160 (.150 (. population from the National Health and Nutrition Examination Survey.110 (.5-17.120 (.8-17.8-19.1 (18.4) < LOD < LOD 16.064) 90th .7 (14.110-.140) .073-.0 (10.120 (.117) < LOD .069) < LOD < LOD .062 (.4-17.070-.5) 15.7) 15.1) < LOD 9.70 (7.054-.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.0 (11.4 (12.120 (.059 (.7 (15.2) 15.1) 15.

Priestly BG. bioaccumulation. Serrano FO. 2 Classes of Pesticides. PA. Part A 2000. Grajewski B. Environ Health Perspect 2001. Psychopharmacology (Berl) 1987. 1989. et al.109(Supp1):113-139. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Li AA. United States Geological Survey (USGS). Garrett N. Schulte P. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Ellis H. VT. No:429-436.html. Available at URL: http://www. Pesticides in the Nation’s Stream and Ground Water. Carlson JN. Andersen A. Turner W.gov/toxprofiles/ tp1. Shore RF. Roy ML. Rosellini RA. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Six high-priority organochlorine pesticides. McIntosh LJ. pp. Mumtaz MM. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. J Occup Environ Med 2005. Eds.352:1816-1820. Available at URL: http://www. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. either singly or in combination. 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. 4/21/09 Hoyer AP. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. and epidemiology in the United States.47:1059-1087. Tully DB. Mink PJ. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Basit A.cdc. Effect of occupational exposure to aldrin on urinary D-glucaric acid. 6/1/09 Ward EM. 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. Organochlorine insecticides in substantia nigra in Parkinson’s disease. 1991. 731-915.html. Reprod Toxicol 2000. Jr. 1992-2001. Mann D.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Facca A. Available at URL: http://pubs. International Programme on Chemical Safety (IPCS). and lymphocyte sister chromatid exchange.usgs. Edwards JW. Anantharam V.103(Suppl 7):113-122. August 2008. et al. Aldrin and Dieldrin [online]. J Toxicol Environ Health 1989. Available at URL: http://www. Organochlorine exposure and risk of breast cancer. Soto AM. David VL.org/documents/ehc/ ehc/ehc91. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Finley B. Narahashi T. Int Arch Occup Environ Health 1994. Demographic and seasonal influences on human serum pesticide residue levels. 80 Fourth National Report on Human Exposure to Environmental Chemicals .66(4):229-234.gov/ circ/2005/1291/.54:1431-1443. Daniel SE. are nonestrogenic in transfected HeLa cells. Jr and Laws ER. Environ Health Perspect 1995. Inc. Food and Drug Administration (FDA). Grandjean P. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. plasma dieldrin. Toxicological profile for aldrin/dieldrin [online]. J Toxicol Environ Health. Revised Feb. Chemosphere 2004. Sonnenschein C. 4/21/09 Bates MN. Smith AG.fda. Teta MJ. New York.64-65 Spec. Hartvig HB. Academic Press. Wienburg CL. Kanthasamy AG. Needham LL.cfsan.gov/~dms/ pesrpts. Cox. Patterson DG Jr. Neurotoxicol 2005. Exp Neurol 1998.inchem. Kitzazwa M.9:1357-1367. toxicology. Patterson DG Jr.htm.150:263-271. Environmental Health Criteria 91. Lancet 1998. 2007 [online]. Stehr-Green. References Agency for Toxic Substances and Disease Registry (ATSDR). 4/21/09 Jorgenson JL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kanthasamy A. Fernandez MG. Vol. Brock JW.14:95-102. Sanchez-Ramos J. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. 15. Chung KL. Buckland SJ. Song S.59:229-234.26:701-719. Corrigan FM. Cancer Epidemiol Biomarkers Prev 2000. Jorgensen T. Olea N. Toxicol Lett 1992. Frey JM. Handbook of Pesticide Toxicology. In Hayes WJ. Ginsburg KS.91(1):122-126.atsdr.27:405-421. September 2002. Chlorinated Hydrocarbon Insecticides. Chapin RE.

< LOD means less than the limit of detection.5) 38.5) < LOD < LOD 9.5-38.7) 9.8 (40..6) < LOD 11.2-26.4 (30.1 (40.1 (17. fish.1) 16.5) 21.8-32. 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.8-42.4) 39.5-40.6-18.1-50.4) < LOD < LOD < LOD 23.3 (21.6) 9. Chlordane is not currently produced or used in the U.7) 42.6-24.9) 11. from the early 1950’s until the mid-1980’s.20 (<LOD-11.9 (15.8-33.4 (30.9 (29.4) 29.10-11.8) 52.9) 36.8) 27.4 (35.0) 20.6) 8.8-61.1) * 11.2) 36.1-25.4) < LOD 11.3) 18. and in soil.3 (25.9 (31.9) 23.7-56.2 (28.8 (10.1) 90th 34.5) 44.3-49.7 (34.5-13.10-18.7) 31.1-65.4-45.9) 37.6 (43.6-53.7 (42. foods high in fat such as meat. Technical grade chlordane had contained 7% trans-nonachlor.9 (17.5) 9.0 (26.6) 48.5-65.8 (17.4-40.2) * 12.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2-56. Fourth National Report on Human Exposure to Environmental Chemicals 81 .9-21.2) 22.5.1-15.90 (8.0-12.3-32.S.70 (<LOD-10.6-45.S.7-70.5 (<LOD-12.7 (32.6 (9. 10.1-25.4 (22.2) 37.0) 27.10 (8.1 (11. 1994.3) 37.7 (<LOD-32. and 7. 1994).3 (20.7-25. and 03-04 are 14.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.8 (10.74 (<LOD-10.6) 11. lawns.6 (25.0 (<LOD-12.1 (27. respectively.2 (36.2 (39.8 (17.2 (41.6) 23.63 (8.9 (26.9) 39.7 (34.9-42.5.0-18. 01-02.3) 10.8) 18.9) 31.9-21.3 (27.7) 19.9 (36.0-13.5-43.7 (10. which may vary for some chemicals by year and by individual sample.6-12.7-39. 2007).3 (<LOD-19.0) 21.89-10.9 (26.9 (15.0 (16.6 (16. 57-74-9 Heptachlor CAS No.9) 13.5 (33. which results in exposure to the fetus and nursing infant Serum Oxychlordane (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.0-25.30-11.20-10.0) 41.1 (<LOD-12.8.2-21.9 (18.0-67.6) 9.0) 75th 20.9 (11.0 (20. buildings.8-31.5 (31. Consequently.9) 11.5) 37. population from the National Health and Nutrition Examination Survey.2 (21.4) 12.2) 34.4 (<LOD-12.4 (31.5 (8.69-10.5 (34.7) 28.4-21.8-20.9-40.6) 39.1 (15.3 (11. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk. Until 1988.2 (10.3) 18.2 (9.2) 33.6) 49.5-41.1) * 11.1-19.9 (11.0 (37.3 (26.1 (44.5) 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 * * * * 11.8-43.6) 48. see Data Analysis section) for Survey years 99-00.0-61.1-51.6) 36.20-11.3-45.7) 35.7) 19.1 (<LOD-12.1 (25.3) 10. Survey Geometric mean (95% conf.S.5-44.8-23.7 (19.Organochlorine Pesticides Chlordane CAS No.8) 44.7 (<LOD-13.2) 46.8 (42.5) < LOD < LOD < LOD < LOD 13.37 (8.2-28. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.9) 10.9) 23.3-45. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.2) < LOD 11.4) 22.8 (18. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.4) 18.3 (9.4-14.2) < LOD 11.9) 47.1 (16.9 (21. 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.1 (<LOD-12.6) 20.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.4) 37.2 (37.9-38.9) 17.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11. chlordane was used to kill termites and other insects on agricultural crops.3-43.1) < LOD < LOD < LOD < LOD < LOD 8.6 (9.2-49.5-32.1 (20.3) 41. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.7-12.8) 52.7 (17. 2007).36-11.8-33.1) 30.4-51.3 (28. and dairy products are the usual sources of exposure to these chemicals in the general population.1) 30.7-14. in addition to trace amounts of numerous other related compounds (ATSDR.5 (41. heptachlor use has been limited to treatment of fire ants near power transformers.6-24.5-42. As a result of the manufacturing process. Since 1992.4 (10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3-24.0) 37.0-33.8) 53.82-11.8-73.2-49.5-47. the technical grade product of each chemical contains 10%-20% of the other chemical.0) 31.1) 22.0 (32.7 (43.5) 56.5) 10.

1991.170) .070-.140 (.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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.210 (.073 (.230 (.049 (<LOD-.270 (.057-. OSHA has established occupational exposure criteria.260 (.130 (.310) .130-.106-.208 (.280 (.140 (.130-.340) . and breast milk is a major excretion route in lactating women.050 (<LOD-.290-.320 (. and alterations in immune function of offspring.260 (.180) .210-.320 (.082 (.271 (.115 (.300) .119 (.230 (.280-.230-.100 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.070) < LOD < LOD < LOD < LOD < LOD .130) .075 (.270 (.070 (.063 (.200-.199-.063 (.190-.223) .120-.203-.071 (.300 (.560) .140 (. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.066 (.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .370 (.180-.300) .240 (.269 (.170) .180) .240-.100-. heptachlor. 1996.148-.320) .250 (.150-.130 (.207 (.302) .083 (.058-.242-.060 (<LOD-. neonatal mortality. Le Marchand et al.216-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.270 (.112 (. In laboratory animal studies.370 (.087-.165-.079) .104) .230) .. 2006).160) .063 (.170) .290) . 1977a.064) < LOD .246-.070) .070-. Survey Geometric mean (95% conf. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.092) .130 (.083) .320 (. 2007.340) .315 (.070 (<LOD-. chronic doses of heptachlor have produced liver enlargement and injury.055-.067 (.310) .136) .204 (.077) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al. 82 Fourth National Report on Human Exposure to Environmental Chemicals . to heptachlor.110 (<LOD-.S.290 (.200 (.063-.048-.073) < LOD < LOD < LOD < LOD .280 (.290) .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .410) .220-.140) .150 (.280) . and inhalation exposure.130-.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .290-.350 (.100-.148) .080 (. dermal.150 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.230-. 1991). FDA established allowable residues of chlordane.258 (. 1981).140-.108-. which may vary for some chemicals by year and by individual sample.068-.320 (.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 * * * * .350) .231) ..260-.057 (.400) .227) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .190-.133) 90th .430) . EPA has established environmental criteria for chlordane and heptachlor.189-.080) .286 (.230-. 1986).062) < LOD .074-. 2001. Chlordane and heptachlor are absorbed after oral.180-.160) .063) .300) . and the U.310 (.069 (<LOD-.050-.100 (<LOD-.150) .160) .240) .320) . characterized by seizures and paralysis.126) .061-. Acute.510) . Takahashi et al.207) .400) .066 (<LOD-.380) .245-.330 (.066-.Organochlorine Pesticides (Dallaire et al. and heptachlor epoxide in foods and bottled water.450) . 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. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.210 (.077) .110-.076) < LOD .150 (. population from the National Health and Nutrition Examination Survey.220 (.047 (<LOD-.053-. Rogan.160 (.120-. which is also persistent in the body (ATSDR. Smith.440) .115-. The U..280-.068) . Shindell and Ulrich.056 (.080 (.057) * . IARC. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.373) .168-.080) .146) < LOD < LOD .170) .225 (.066-.058-.070-.070 (<LOD-.080) . The major metabolite of heptachlor is heptachlor epoxide.190-.065-. 2007).091) .370 (. Elimination of all these chemicals from the body occurs over months to years.090) .200-.149 (.170-.063) * .S.120 (.140-.090) .310-. 1986).146) .104-.189 (.140 (.430) .053-.250 (.130) .450) .240-. 1977b.348) .200-.250-.079) < LOD < LOD < LOD .360) . 2002.213) * .170) .070 (<LOD-.063 (.058 (.310) .220-.300) .077) .287) .128 (.120-.090-.S.260 (.253-.077) .286 (.068) 75th .300-.130-.070 (<LOD-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.280-.350 (.290-.126 (. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.130-.258-.

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

8) 14.6 (8. Survey Geometric mean (95% conf.8) 13.4) 18. 01-02.7 (10.8) 15.5) 19. and 03-04 are 14.9-23.8) 19.8-23.90 (<LOD-9.8-24.6-17.8 (13.1) 23.8 (18.0 (11.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6 (13.6 (12.3 (<LOD-25. 84 Fourth National Report on Human Exposure to Environmental Chemicals .1 (16.4 (11.9-29.0 (15.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.0-17.3 (13.2-16.6 (<LOD-27.5.5) < LOD 14. < LOD means less than the limit of detection.6 (16.1-29.7-18.3) 10.4 (<LOD-54.2) 26.5 (11.1 (19.40) 15.4 (<LOD-19.6.5 (<LOD-32.2-17.0) 13.5 (10.3) 18.2 (<LOD-16.5 (11.5 (<LOD-21.1-16.3) 22. which may vary for some chemicals by year and by individual sample.7 (16.6) 13.3) 16.9-29.8) 20. 10.2-27.7-25.5 (18.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.6 (16.0-17.8) 14.4 (15.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8.9-25.4 (11.2) 15.6) 22.9 (15. and 7.8 (<LOD-23. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8-46.3) 23.4) 21.2 (18.9-16.0-19.6 (11.8) 16.1) 20.2 (<LOD-25.8-24.1-38.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.8) 13. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00.50) < LOD < LOD < LOD 17.6-21.3) 18.6) < LOD < LOD < LOD 27.3) 27.20 (<LOD-9.9 (12.8 (15.6 (14.7-19.0-54.8) 19.8) 21.8 (13.S.3) 18.3-18.2) 20.0) 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 13.10-13.1-15.7 (13.6) 14.0-16.2) 13.8 (18. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.9) 15. respectively.2-27.8-24.2 (<LOD-62.1) 13.

190) .180) .110) . which may vary for some chemicals by year and by individual sample.077-.082-.110-.053-.170) .063) .270) .130) .130 (<LOD-.094 (.150 (.180) .106-.116) < LOD < LOD < LOD .108) .111-.170) .074-.380) .076-.200) .150 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .200) .094 (.135 (.100 (.150 (<LOD-.149) .069 (.120-.063) < LOD < LOD < LOD .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.180) .090-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.100 (.200 (.110) .130-.100 (.055 (<LOD-.130 (.170 (.110 (.101 (.100-.110 (.180 (.090-.090-.113) .161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .130-.113-.310) .157) .090 (.111) .173) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .090-.097) < LOD . population from the National Health and Nutrition Examination Survey.070-.140) .240) .133 (.130-.190 (.108-.087 (.130-.120 (<LOD-.057 (<LOD-.140) .190) .180 (<LOD-.170 (.090-.071-.120) .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. Fourth National Report on Human Exposure to Environmental Chemicals 85 .100 (<LOD-.100-.130) .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 .107-.S.117) .170 (.098 (.135 (.101 (.120) .104) .110-.126 (.120 (.170 (<LOD-.110 (<LOD-.100 (.128 (.090 (<LOD-.067-.096 (.090-.110 (<LOD-.120 (<LOD-.140-.170) .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 .310) .077-.190) .220) .

0 (29.7) 52.4) 48.6 (52.3 (45.9) < LOD < LOD < LOD 20.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.8 (17.10 (<LOD-11.1-22.0-23.7-21.3) 30.S.7-22.1-16.9 (36.4 (16.3-86.8) 51.9-58.8 (28.5-19.2) 34.0 (13.1 (10.0) 19.6 (50.0-113) 68.4) 55.1 (17.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.5 (44.9 (28.9-65.6-82.9 (51.6 (32.1) 14.7) 73.2 (19.0-20.6) 56.9) 14.4) 107 (84.3 (17.0-22.1) 17.3) 15. respectively.1 (22.9 (47.3 (16. interval) 18.1) 18.3-32.5 (45.4-36.2 (14.5) 90th 55.2 (60.7) 17.6) 10.3) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 Limit of detection (LOD.3-30.0) 13.8-79.6) 56.9) 14.3-74.6 (56.1) 17.1) 17.4) 16.5-17.4-18.2-21. 86 Fourth National Report on Human Exposure to Environmental Chemicals .8 (30.0-93.2-16.5-111) 68.2) < LOD 10.7-38.7-17.3) 32.7 (13.2 (64.5) 9.3 (58.2) 39.0-93.8 (71.6-20.1) 17.0 (48.4 (67.2) 20.1-20.9-40.8 (26.7) 35.4 (30.7-18.1-34.7 (30.2-18.0) 33.8) 19.9-35.5) 14.0 (13.8-77.7-34.5) 30.8 (26.5-69.5) 77.8 (<LOD-20.9 (66.4-23.1-126) 67.5) 22.7 (35.8-67.0-143) 112 (68.6) 60.3 (14.6 (15.8 (12. Survey Geometric mean (95% conf.9 (15.7) 59.7-20.9-64.7-113) 68.0) 40.7) 78.5) 20.1-55.1) 31.1 (41.4 (11.1) 16.8 (19.6) 82.9-45.5-87.8 (28.8-19.8 (42.0-37.9) 51.4) 59.7-29.5 (13.0-68.5) 78. 10.2-17.0 (60.6-66.2) 30.3 (56.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.6-19.1) 17.1) 32.8) 47.9-20.4 (45.1 (47.1-18.9 (51.6 (57. and 03-04 are 14.1-51.8-21.7 (18.5.0 (15.7-23.8 (49.0) 49.2-88.8 (26.5 (15.7 (11.2-23.0 (14.5) 48.3) 25.9 (15.2) 59.5) 36.1) 17.8 (28.8-90.7-77.1-34.7) 56.6 (16.4 (28.3-39.7 (74. 01-02.9-65.9) 51.2 (26.1) 30.9-89. population from the National Health and Nutrition Examination Survey.3-57.3) 18.3 (14.3) 19.3-21.6-88.2) 17.7) 78.7) 14.0) 75th 31.2 (7.5-36.0) 18.3-50.6) 13.0-123) 74.7) 15.2 (59.0 (15.8-16.0 (16.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.0 (16.86-13.2) 19.4-22.4-67.0 (42.2-18.4 (12.8 (13.8-129) 74.7 (28.6 (56.8-110) 59.9-69.2 (25.8 (16.8.9 (29.1 (48. < LOD means less than the limit of detection.6 (12.7-32.0 (42.5-95.0 (62.4-62.8-90.2 (15.5) 35.0 (19.3) 30.6-22.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.0-24.5) 26.6) 34.9-22.7 (59.1) 78.7-160) 86.0) < LOD < LOD 8.7-35.8-16.8 (15.9-36.8 (13.1-28.2 (27.5) 19.3 (49.5) 14.6) 84.4) 19.1 (65.7 (59.5-20.4-52.3) 18.9 (19.70 (<LOD-12.2-37.5 (15.1) 18.1-16.8-19.3) 32. and 7.3) 16.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.1) 17.4-35.5 (25.6-54. see Data Analysis section) for Survey years 99-00.7 (16.1) 78. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-59.0-23.8) 80.8 (11.5.3-58.9 (<LOD-14.7) 28.0-38.2 (36.2 (14.8-41.6) 54.6) 25.6 (<LOD-14.3) 36.8 (45. which may vary for some chemicals by year and by individual sample.1) 62.4) 20.9 (16.

085-.122) .106 (.110 (.100 (.120 (.110 (.096-.160 (.082) .093) .111-.120 (.093-.220 (.106 (.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.580 (.390 (.134) .130) .290-.186 (. Survey Geometric mean (95% conf.202 (.098 (.093-.180-.210-.340-.090-.301-.090-.400 (.100-.087 (.068-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.343 (.310-.127) < LOD < LOD .690) .078-.145-.461 (.237) .125) .520) .330-.070 (.573 (.680 (.100-.550 (.390 (.410-1.390-.600) .417 (.130) .085-.510 (.190-.054-.310-.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .330 (.041 (<LOD-.113) < LOD .180-.288-.460-.150) .470 (.090-.330-.310-.104-.480) .270-.110-.173-.497-.109 (.590 (.651) .580 (.630) .171-.210 (.350 (.220 (.371) .090 (<LOD-.340-.594) .420 (.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.116) .161) .047-.559) .317 (.220 (.630) .190-.085-.096) .130 (.109 (.370 (.220 (.460) .458 (.105 (.062 (.240 (.400 (.081-.120-.400-.191 (.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 .540) .170 (.104 (.490) .210-.420) .093-.800) .069-.395-.240) .117) .580 (.099-.260) .080) .240) .080 (.108) .110 (.069) .108 (.367) .320-.400-.380 (.140) .630) .090-.460) .640 (.590 (.097) .084-.094 (.110) .158-.141) .130 (.190-.111 (.150) .110 (. population from the National Health and Nutrition Examination Survey.099-.400) .324 (.091) .119) < LOD < LOD < LOD .830) .078 (.600 (.098) .120) .100 (.210 (.220 (.320-.090 (.590) .120-.124) .061-.220) .108) 75th .116-.430-.680) .126) .409-.081 (.760 (.096-.190-.190-.110 (.113) .390 (.370 (.260) .240) .450) .106 (.079-.520 (.180-.071 (<LOD-.490-.130) .098-.205 (.470-.120) .390) .130) .120) .160-.125 (.327 (. which may vary for some chemicals by year and by individual sample.080-.103 (.286-.272-.430-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .092 (.930) .122) .250) .250) .220 (.440-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .210) .129) .220 (.300-.960) .250) .090) .092 (.395) .830) .490 (.242) .177-.310) .430-.310-.520 (.080-.20) .080-.288 (.079-.211) 90th .161-.055 (<LOD-.131) .390 (.116 (.510-.279-.114) .103 (.690) .100-.360-.100-.565) .355 (.410-.130) .060) .414 (.098 (.120) .119) Selected percentiles ( 95% confidence interval) Sample 95th .230 (.090-.340) .080-.237) .234) . Fourth National Report on Human Exposure to Environmental Chemicals 87 .095-.141) .060-.060 (<LOD-.240-.440) .210 (.089 (.112 (.405) .310 (.684) .300) .110 (.470 (.285-.280) .397-.130) .190-.112 (. interval) .183 (.210) .120-.390) .490 (.360-.135 (.350-.232) .220 (.186-.840) .470 (.210) .120 (.S.470-.500) .128 (.130) .090-.091-.

J Occup Med 1986. 6/1/09 National Toxicology Program (NTP). Covaci A.cdc. 6/1/09 Rogan WJ. Bioassay of chlordane for possible carcinogenicity.heptachlor. Available at URL: http://ntp. 1963-1967.pdf.28:497501.org/site/foundation/ research/projects2. Eds. New York.htm. Jaraczewska K. Arch Pediatr Adolesc Med 1996. Takei G. Tartter P.html. et al. 4/21/09 James RA. 2001. LeMarchand L. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Canada). 2006. Gilman A. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Stehr-Green P. Sci Total Environ 2004. Arch Environ Health. Chlorinated Hydrocarbon Insecticides. National Toxicology Program (NTP).8:1-123.110:617-624. KalubaSkotarczak A. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Concise International Chemical Assessment Document 70 Heptachlor [online]. Ayotte P. Drews K. Head SL. Toxicological profile for heptachlor and heptachlor epoxide [online]. Jr and Laws ER. August 2007. Organochloride pesticide residues in human milk in Hawaii. Environ Res 2000. 1991 pp. May 1994. Available at URL: http://www. Smith AG. Chashchin V. 4/21/09 Dallaire F.org/documents/iarc/ vol79/79-12.372:20-31. Berkowitz GS. 4/21/09 Baker DB. Bjerselius R. 9/25/07 International Programme in Chemical Safety (IPCS). Vol. Kolonel LN. Bioassay of heptachlor for possible carcinogenicity.atsdr. Van Oostdam JC.pdf. Granath F. Hansen JC.84:151-161.inchem. Laliberte C. Wolff MS. Brower S. Darnerud PO. Bull Environ Contam Toxicol 1981:27:506-511. Vol. Handbook of Pesticide Toxicology.111:349355. Organochlorines in Swedish women: determinants of serum concentrations. Academic Press. Available at URL: http://www. Atuma S. Available at URL: http://www. 1979-1980.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Aune M.330:55-70. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Dewailly E.html.gov/ntp/ htdocs/LT_rpts/tr008. Muckle G.gov/toxprofiles/tp31.150:981-990. Chlordane and heptachlor [online].nih. et al. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Lulek J. et al. Voorspoels S. Siegel BZ. Pollutants in breast milk. 1994-1997 organochlorine compounds.nih. 1993.259(3):374-377. Environ Health Perspect 2002. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor.9:1-109. Available at URL: http://ntp. Dewailly E. Circumpolar maternal blood contaminant survey. Senie R. Wong L. Takahashi W. Wohlleb JC. 1986. International Agency for Research on Cancer (IARC) . Lawrence River (Quebec.atsdr. Mortality of workers employed in the manufacture of chlordane: an update. Loo S. Available at URL: http://www.50(3):108-118. Environ Health Perspect 2002. Bleiweiss IJ. JAMA 1988.Summaries & Evaluations. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum.cdc. Hertz-Picciotto I.niehs.gov/ntp/ htdocs/LT_rpts/tr009. Environ Health Perspect 2003. Organochlorine exposures and breast cancer risk in New York City women.html. Available at URL: http://www. Inc.org/ documents/cicads/cicads/cicad70. gov/toxprofiles/tp12. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Hawaii Med J 1991. Glynn AW. Sci Tot Environ 2006. Royce W. Barker J. Dendle WH. Natl Cancer Inst Carcinog Tech Rep Ser 1977a.htm. Jr.41:145–148. 731-915. Baker DB. A Report to the Hawaii Heptachlor Research and Education Foundation. 2 Classes of Pesticides. International Agency for Research on Cancer (IARC). Poland. Charles MJ. Willman E.inchem. Toxicological profile for chlordane [online]. 79. maternal serum and milk from Wielkopolska region. Saidein D. Keller JA.110(8):835-838. Shindell S and Ulrich S.niehs. Odland JO. In Hayes WJ. et al. Distribution of polychlorinated biphenyls.

5-54.00 (<LOD-10. including 1.5 (15.3 (27. 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.5 (23.8-23. Food imported from countries that still use DDT may contain the chemical or its residues. continues to be the primary source of DDT exposure.0) 19.7) 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 10.4) < LOD < LOD < LOD 61.4. Survey Geometric mean (95% conf.2 (<LOD-40.5) 23.1-71.50-11.9) 17.9 (21. Only a small proportion of DDT is metabolized and excreted (Smith. DDT is converted to DDE and several other metabolites. and water.1) 31.7 (19.3-590) 293 (104-541) 48.2) < LOD < LOD 9.6-33.1 (<LOD-39. DDT was used at one time as a treatment for head and body lice. fish. Both Serum p. DDT and DDE can cross the placenta.0-15. It is still used in some countries. and trace amounts of several related compounds.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 8.3) 28.9) < LOD < LOD 9. air.2-bis(p-chlorophenyl) ethane (DDD).0 (18.9 (10. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. In the general U. DDT can be absorbed after ingestion.3 (<LOD-31. and 03-04 are 20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-155) 83. 2008. In the body.2-95.9 (10. DDT is converted in the environment to other more stable chemical forms. 1991).2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. as well as in plant and animal tissues.2 (11.6 (9. p. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.9-28.2) 155 (59. Fourth National Report on Human Exposure to Environmental Chemicals 89 .0 (10.10 (<LOD-12. and 7. which is a mixture containing p.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.1) 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. 2002.8) 15.8) 30.2) 30.p’-DDD (4% or less).8) 36. These chemicals are highly persistent in soil.7-16.6 (25.70 (8.7) < LOD 18.10-13. o. 1991).5) 25. It was produced and used in the U.0-37. particularly for endemic vector and malaria control. see Data Analysis section) for Survey years 99-00. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.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.8-39.S. < LOD means less than the limit of detection. inhalation.0-35. and dairy products.7. The biodegradation half-life of DDT in soil varies from 2 to 15 years.8.1’-(2.2-65.7) 12.3-236) 24.6 (31.0) 20.5 (23. sediments.6 (<LOD-25.8-17.9-34. when virtually all use of it was banned. 1988).4) < LOD 17.8-26.3-16.9 (10.S. although DDT and DDE intakes have decreased over time (FDA.3 (<LOD-21. Smith. depending on conditions.6 (22.0) 40.S.1’-dichloro-(2.9 (<LOD-20.90 (<LOD-12.0 (18.3) 21.3) 21.1-27.p’-DDT (15%-21%).Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5 (14.3) 22.p’-DDT (65%-80%). 17.9) 14.5) < LOD < LOD 9. or dermal exposure. food.9) 29. resulting in fetal exposure. after World War II until 1972.0 (21. Gunderson.1 (33.0) 26.4 (23. particularly meat. respectively. population.0-27. DDT usually refers to the technical product.0-53.1 (23.7 (15.5-36. 01-02.

128 (. which may vary for some chemicals by year and by individual sample.079) < LOD < LOD .071 (.080-.105-.130-. population from the National Health and Nutrition Examination Survey.051 (<LOD-.160-.220) . DDT may bind to estrogen receptors (Chen et al. 2001). 2006. Calle et al.069) . tremor.200 (.26) 1.00) .106-. 1995. 90 Fourth National Report on Human Exposure to Environmental Chemicals .. 2000.143) < LOD < LOD . fertility.130 (<LOD-.120 (<LOD-.087 (. resulting in exposure to nursing infants (Rogan.054-.190-1.132-.627) .230) .201 (.130 (<LOD-.530 (.01) . 1997).140) ...048 (<LOD-. Mariussen and Fonnum. Gladen and Rogan. Animal studies reported reduced fertility.240 (.170 (.074-.189-. Gray et al. 2006). Reproductive effects in humans affecting birth weight.240) . Jusko et al.063 (<LOD-.250 (. premature delivery.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. and seizures.330-4. 2001).230) . Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.290) . 2006).220) . interval) Selected percentiles ( 95% confidence interval) Sample 95th . Snedeker. other organochlorines. 2002.203) .095) < LOD .S. Survey Geometric mean (95% conf. 2002. lung cancer.120-.112 (.084 (.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .. 2006.071-.059-..420) .260) .180) . and altered behavior after neonatal exposure (Eriksson and Talts. Studies of DDT exposure and pancreatic cancer. 1956).343) < LOD .400) .150) .150 (<LOD-. reproductive organ abnormalities.. and duration of lactation.570-4. Beard..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..098-.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 . In high dose. 2002. polychlorinated biphenyls.34) . 2002.Organochlorine Pesticides chemicals are excreted in breast milk. and o.180) . Hayes et al.530) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.180-.g.p’-DDE can produce anti-androgenic effects (Gray et al.146 (.065-.170) .140-. 2006. 1998).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 . Longnecker et al..180 (.170-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. 2006).p’-DDD and p..150-.. 1996).075) 1.086 (.190 (.061) < LOD < LOD < LOD .00 (.250-1. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.064 (.146 (. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.150-.078 (.106) < LOD < LOD .180 (.400 (. have not been consistently demonstrated (Beard. accidental exposures. 2004. In laboratory animals.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 .130 (<LOD-.108 (. overt signs of acute human toxicity include vomiting. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.313 (.190 (.078-. and leukemia have also been inconclusive (ADSDR.106) . dioxins and furans).068-. Jusko et al. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.150 (<LOD-.114-..62 (. 2001). 2001).142 (. 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. A workplace standard for DDT has been established by Serum p.

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.. Compared to females in the NHANES 1999-2000 subsample. 1989). see Data Analysis section) for Survey years 99-00.. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. and 03-04 are 18..S. 2002. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. Link et al. IARC classifies DDT (p.S. and 7.0-114) 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. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. compared to levels observed in this Report (Anderson et al. In general.p’-DDT) as a possible human carcinogen.cdc. mean serum levels of DDT and DDE in the U.6. EPA at: http://www. Fourth National Report on Human Exposure to Environmental Chemicals 91 . Heudorf et al..7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. Biomonitoring Information DDE persists in the body longer than DDT. Smith.e.gov/ pestcides/ and from ATSDR at: http://www. A study of New Zealand adults sampled in 1996-1997 reported median DDE levels that were about threefold higher than the median for adults in the NHANES 1999-2000 subsample (Bates et al.3. 2004). Stehr-Green. 1998.. 01-02.atsdr.S. In a population-based sample of men and women from eastern Slovakia.. 2002. Since the 1970’s. Survey Geometric mean (95% conf. More information about external exposure (i..6 (81. 2003). 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. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. 1991).gov/ toxpro2. population declined by about fivefold to tenfold. 2004). 2005).Organochlorine Pesticides OSHA and a guidance established by ACGIH.epa. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person.7-119) 113 (100-140) 93. population from the National Health and Nutrition Examination Survey. Declining DDE levels over time have also been observed in the German population.8.. respectively. respectively. NTP considers DDT as being reasonably anticipated to be a human carcinogen.html. 8. 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. for males and females in the NHANES 19992000 subsample (Pavuk et al. environmental levels) and health effects is available from the U.

82 (1.81-18.2 (9.75 (8.16 (2.34) 2.46-2.63 (1.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.90-8.430-.93 (7.00) 7.2-32.66-2..63 (6.2 (19.7) 13.36) 3. Survey Geometric mean (95% conf.68 (2.0) 2.25) 1.39-2.41 (1.10) 2.890-1. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE than are found in the general population.99) 1.26 (1.2 (6.56-2.00 (.24 (1.51-8.48 (6.77 (1.48-4.22-1.25 (1.97-4.534-.04-1.46 (1.8 (13.71 (6.30 (1. High mean levels of whole blood DDT (about 3.21) 90th 7.9-38.01) 1.76) 1. 2005).6 (17.53-15.71 (5.3) 13.51-49.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .6) 9.58) 1.36-2.69 (.37-16.5) 7.34) 6.91-3. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.488-.p’-DDT.870 (.66-4.34-11.56) 2.57 (3.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.59) 3.80) 3.00 (6.79) 4.80 (2.38 (1.62-6.88-35.456 (.24) 1. 1971).32-9.03-4.14-9.91 (6.9 (15.5) 16.4 (12.22 (7. 1991).80) 1.96) .32) 1.44) 1.0 (12.51) 3.57-13.40-8.S.66) 4.56-6.635) 1. Finding a measurable amount of p.3 (8.61 (1.31-12.994-2.33-1.90) 22.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. In a subsample of NHANES II (19761980) participants.15-4.7-20.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.p’-DDT were below the limits of detection.04 (6.81 (1.49 (1.25) 8.4) 13.65 (1.18-4.63-15.11-1.385-.0 (9.66-17..68-4.82) 1.7) 16.43-8.2 (9.1) 40.69 (1.92) 1. less than one percent had detectable serum levels of o.965-1.47 (1.860 ng/L) and DDE (about 14.516 (..58) 75th 3.01-15.2) 19.1 (8.1) 7.1 (9.75 (4.Organochlorine Pesticides nearby agriculture (Botella et al. Serum p.51 (1.92 (3.51-15.59) 6.13) 4.66) 1.14-1.25-14.50 (2.85-4. serum levels of o.600) .58) 1.01) 1.36-1.963-1.01-5. In the NHANES 1999-2000.51) 1.8-90. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.53) 7.9 (26.796 (.3) 16.611-1.10) .41-12.12-1.5) 22.14 (1.71) 12.61-2.64-2.21) 3.4) 14.07) 1.30-1.72) 1.43 (5.66) 3. population from the National Health and Nutrition Examination Survey. 2001-2002 and 2003-2004 subsamples.63 (1.7-19.419-.39-1.77 (1.12 (.34-3. considerably higher than levels in this Report (Smith.623 (.26-10.6) 9.22) .79) Selected percentiles ( 95% confidence interval) Sample 95th 11.17 (3.4 (8.97 (3. 2004).55-9.75) 2.27-1.34 (7.18-1.8 (14.32-1.29 (1.76) 1.561 (.59 (1.3) 10.6 (9.5) 5.0) 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 .7 (8. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.25 (.3 (9.37-4.13-2.53) 1.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.19) 4.59 (1.8 (13.12 (6.75) 1.87-16.8 (9.9) 5.30 (1.02) 1.02 (2.05 (3.18-1.26-2.70-3.32 (1.81 (7.52 (3.36 (3. o.76 (2.726) .557) 1.88 (2.07 (5.p’-DDT.47) 3.6) 13.75) 6.72) 1.56-3.68) 2.66) 1.4-19.p’-DDT (Stehr-Green.65) 1.01-11.14) 2.81) 11.10-5.71) 32.81-5.57 (1.49 (1.31 (1.32-1.50-17.57-3.57-2.28) 1.45 (1. interval) 1.83 (1.13 (1.30-1.680-1.78 (4.6 (7.6) 11.64) 3.05) 1.35) 1.7-48.18) 1.39 (3.37-10.54 (1.09-1.49) 8.70) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.54-7.87 (5.2) 26.52-6.01-1.06) 1.27) 3.26) 3.8) 15.92 (3.590 (.730) .06) 3.37-1.57) 2.40-4.36-11.32 (1.6) 8.69 (2.80) 1.24-17.19-14.43-4. 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. 2004).4) 9.84-3.9-17.20 (.00-1.54) 8.820-1. or p.96) 1.7) 9.76-3.45 (1.85-10.18-3.57 (1.03-1.55 (2..6) 9.91) 3.69) 4.85 (1.500-.14) 2.646) .6) 9.91-2.07) 1.6 (8.31-2.53 (2.520 (.40-4.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.23 (7.52 (1.49 (6.40 (3.43-4.6) 12.16-1.25-16.46 (1.69) 8.59 (4.18 (6.5) 10.38 (1.37 (1.11 (2.17-3.01-1. 1989).60-13.9) 7. 309 versus 268 ng/g lipid.01-11.02-8.10-1.84 (3.3-43.39) 1.1) 12.

which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00.4.Organochlorine Pesticides Serum o. 17. respectively. Fourth National Report on Human Exposure to Environmental Chemicals 93 . < LOD means less than the limit of detection.7. and 03-04 are 20. 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.8. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.S. 01-02. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and 7.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.

S. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf. * 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. 94 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.Organochlorine Pesticides Serum o. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.

et al. Bull Environ Contam Toxicol 2004. Gray LE Jr. Chemosphere 2005. Environ Health Perspect 1998. Ostby J. Atuma S. Environ Res 2005.53(8):1161-1172. Ellis H. Parks L. et al. Saiyed HN. Longnecker MP. Falk C. Jusko TA. DDE and shortened duration of lactation in a northern Mexican town. Krause C. Hurd C. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. The Great Lakes Consortium. Link B.7(3):248-264. August 2008.112(17):1761-1767. Klebanoff MA.52:301-309. Food and Drug Administration (FDA). PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.21(1-2)37-48. Beard J. Klebanoff MA. Organochlorines in Swedish women: determinants of serum concentrations. et al. FDA total diet study. Olson JR. Int J Hyg Environ Health 2002. Barr DB.71(6):1200-1209. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Wolf CJ. DDE. Cueto C.. Hanrahan L. Hediger ML. Olea N. Available at URL: http://www. Hum Reprod Updat 2001. Angerer J. Schulz C. et al. et al. Piechotowski I.html.358:110-114. Zhou H. and dichloro(diphenyl)ethylene (DDE). Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Int J Hyg Environ Health 2003. et al. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. September 2002. Toxicological profile for DDT. Gunderson EL. Granath F. Frumkin H. Environ Health Perspect 2003.355:7889.atsdr. Rivas A.97(2):178192. Cerrillo I. Chen CW. Longnecker MP. Charles MJ. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Moysich KB. Heudorf U.html. Botella B. Bloom MS. Vena JE. Biomonitoring of persistent organochlorine pesticides.1-dichloro2. dietary intakes of pesticides. Needham LL. Biochem Pharmacol 1997. JAMA 1956. Buckland SJ. Needham LL. Olson J. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells.gov/~dms/ pesrpts. Gabrio T. Brock JW. Am J Epidemiol 2002. Hayes WJ. HCH.96:34-40. Darnerud PO. Savitz DA. and polythelia among male offspring. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Chemosphere 2004. dichlorodiphenyldichloroethylene. Patterson DG Jr. Kulkarni PK. Zoellner I. Calle EE. lindane (g-HCH). 4/21/09 Anderson HA. India. Maternal DDT exposures in relation to fetal and 5-year growth.106(5):279-289. Environ Health Perspect 2004. and DDD [online]. Baker RJ.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Lambright C. Organochlorines and breast cancer risk.54:1431-1443. Available at URL: http://www. Jr. Kashyap R. Vorojeikina DP. Maternal serum level of 1. Koepsell TD. Levels of DDT. selected elements. Becker K. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Henley SJ. DDT and human health. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Arnold SF. Davis MD. Rogan WJ. Olea-Serrano MF. Thun MJ. hypospadias. Klebanoff MA.58:1185-1201. The effect of known repeated oral doses of chlorophenothane (DDT) in man.17(6):692-700. Zaidi SS. Seiwert M. Drexler H. and other chemicals.111:349355. Herrman T. Garrett N. Greenfield TA.gov/ toxprofiles/tp35. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Kaus S. Paepke O. and HCB residues in human blood in Ahmedabad. Needham LL.162:890-897. Brock JW. April 1982 to 1984.155(4):313-322. CA Cancer J Clin 2002.cdc. Exposure of women to organochlorine pesticides in Southern Spain. Zhou H.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism.85:504508. Profiles of ortho-polychlorinated biphenyl congeners. Durham WF. Willman EJ. Am J Public Health 1995. Katz SH. Environ Res 2004. Sci Tot Environ 2006. Aune M.205:297-308. Bjerselius R. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Glynn AW. Bates MN. hexachlorobenzene.cfsan. Talts U. Effects of environmental antiandrogens on reproductive development in experimental animals. Lancet 2001.72:261265. Eriksson P. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Furr J. J Assoc Off Anal Chem 1988. Jr. 4/21/09 Gladen BC. Swanson MK. Lepom P. Gladen BC. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study.206:485-491. Notides AC. et al. et al. Neurotoxicol 2000. Gray KA. et al. Epidemiology 2006. Burse VW.fda. Bhatnagar VK. Crespo J.

Stehr-Green. Chovancova J. Nims R. DDE. et al. and DDD in male rat liver and cultured rat hepatocytes.36:253-589. New York. Snedeker SM.20(2):186-193. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Jones CR. Jr and Laws ER. Fonnum F. Toxicol Appl Pharmacol 1971. Cerhan JR. DDE. Comparative pharmacodynamics of CYP2B induction by DDT. et al. Demographic and seasonal influences on human serum pesticide residue levels.53:455-477. Arch Pediatr Adolesc Med 1996. children and newborn infants. Eds. Pavuk M. Inc. J Toxicol Environ Health Part A 1998. Smith AG. and dieldrin. Pesticides and breast cancer risk: a review of DDT. Vol. Handbook of Pesticide Toxicology. 1991 pp. Fox S. Chemosphere 2004.Organochlorine Pesticides Mariussen E. Rogan WJ. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Astolfi E. Lynch CF. Radomski JL. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Thomas PE.54:1509-520. In Hayes WJ. 96 Fourth National Report on Human Exposure to Environmental Chemicals . 731-915. Academic Press. Petrik J. Environ Health Perspect 2001.150:981-990. Lubet R.109:35-47. PA. Chlorinated Hydrocarbon Insecticides. Crit Rev Toxicol 2006. Reddy AB. Pollutants in breast milk. 2 Classes of Pesticides. Deichmann WB.27:405-421. Jr. Rey AA. J Toxicol Environ Health 1989. Schecter A.

40 (<LOD-6. endrin usually is not detected in serum of exposed individuals. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. endrin is converted rapidly to its major metabolite. manufactured. IPCS.20 (<LOD-5.8. unless the dose is high and the exposure is very recent. have been cancelled by the U. Endrin does not accumulate in body tissues (IPCS. Kavlock et al. 72-20-8 General Information Endrin. Endrin was not widely used as a termiticide. EPA. 1991). largely the result of historical agricultural application or run off from contaminated soils (ATSDR.50) < LOD 5. inhalation or dermal exposure routes. Endrin was used as an insecticide. 1979. a stereoisomer of dieldrin.S. is no longer manufactured in the U.60 (5. At high doses. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. 1981). Hepatic effects of endrin exposure have included necrosis. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1992).30 (<LOD-6.S. Depending on soil conditions.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 5.70) < 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. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. In the body. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. total diet surveys (FDA.10 (<LOD-5..20 (<LOD-5.S. Fourth National Report on Human Exposure to Environmental Chemicals 97 .. endrin has been detected with declining frequency in U.10 (<LOD-5.40-5.09 and 7. Because it is metabolized so rapidly.. 1987).30) < LOD 5. 1991). and inflammation (Smith.. rodenticide and avicide. fatty infiltration. 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. Ketoendrin is a major photodegradation product (IPCS.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample. 1992). All uses of the pesticide in the U. 2008). Endrin is absorbed rapidly after ingestion. and occasionally at low levels in sediment and surface waters. Smith. unlike aldrin and dieldrin. Endrin has been detected in soils.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. 1992). 1996. anti-12hydroxyendrin. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.Organochlorine Pesticides Endrin CAS No. endrin can persist for years.50) < LOD < LOD < LOD 5.S.S. Over time. An epidemic of acute endrin poisoning. 1992. or from contact with contaminated soils and sediments in areas where endrin was applied. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. or discarded.

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

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

9-24.4.5 (13. 1976). Urinary metabolites include pentachlorophenol (PCP).6) < LOD < LOD 26. Therefore.2-31. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.4) < LOD < LOD 19.8 (22.S.4-15. 100 Fourth National Report on Human Exposure to Environmental Chemicals .. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.9) < LOD < LOD 19.9) < LOD < LOD 20.9) < LOD < LOD 28. wildfowl. 01-02.3) < LOD < LOD 29.1-20.2 (24.1 (17.3 (22. respectively.S.0) * * 15. and accumulates in fatty tissues where it persists for years.5-33.3 (16.9-30.3 (20.0.0 (18. 2005).4) < LOD < LOD 23.2 (14. see Data Analysis section) for Survey years 99-00. < LOD means less than the limit of detection.4. particularly by consuming fish.0 (14.6) < LOD < LOD 25.6-26. 2.1) * * 15.4 (18.4 (22.8 (15.6 (21.2 (17.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.3-26.0-25.5-trichlorophenol (2. primarily as a fungicide and seed treatment until the U.5 (14.7 (15.5-18. HCB is well absorbed after oral administration. or game taken from areas with HCB contamination.0-16.5-15.5 (13.1) < LOD < LOD 15.S.7) < LOD < LOD 24.7-26.6 (24.7 (19. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.3 (14. HCB has been detected in fewer foods since the 1980s (FDA.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.2 (14.6-32. air. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U. and elimination occurs by renal and fecal routes. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and has been detected in soil.2 (13.5-14.4) < LOD < LOD 18.8) < LOD < LOD 27.2-15.0-28.9) < LOD < LOD 15.0-19. breast milk is an additional route of elimination in nursing women. Although it is not manufactured as an end-product in the U..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 * * 16.4 (11.6) < LOD < LOD 14.5) < LOD < LOD 18..4. distributes widely throughout the body.2) < LOD < LOD 29.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6) < LOD < LOD 26.9) 19.3 (12.7-16.9) < LOD < LOD 16. and sediment (Barber et al. The FDA dietary surveys have shown that over time.4) < LOD < LOD 14.9-20. 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.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.4) < LOD < LOD 33.0 (25.2) < LOD < LOD 13.3) 24.7-21.S.6-TCP) (To-Figueras et al. water.7-29.6 (23.5-15. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.1 (14.8. Survey Geometric mean (95% conf.8-15.8 (26.6-44. 1997).9 (14.5-TCP) and 2. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.1 (13..9-32.Organochlorine Pesticides Hexachlorobenzene CAS No.4.6-33.9-17.7-22.7) * * 14. 2008.7 (27.6-trichlorophenol (2.3 (22.3-20.3) * * 15.0) < LOD < LOD 15.7-15.2-15. 1988).1-16.3) < LOD < LOD 20.4 (18.7 (15. which may vary for some chemicals by year and by individual sample. and 7.6) < LOD < LOD 24.9 (25. The general population may be exposed to HCB through diet. EPA cancelled its use in 1984.0) < LOD < LOD 15.0 (18.7-30.9 (25.0) < LOD < LOD 24.7-16.9-15.9 (23.3-22. 31. and foods with a high fat content.4-16.5-14.4.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.1 (14. Gunderson.9) < LOD < LOD 20. 2002).6-19. HCB is slowly metabolized. and 03-04 are 118.4) < LOD < LOD 22. population from the National Health and Nutrition Examination Survey.

epa.065 (.174-.S.140 (.html. The U. Fourth National Report on Human Exposure to Environmental Chemicals 101 . Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown. as well as hypertrichosis. population from the National Health and Nutrition Examination Survey.Organochlorine Pesticides chemical.082-.089-.086-.135-.099) < LOD < LOD .114-. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.064 (.092 (. 1960).115 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .088-.175) < LOD < LOD .085-. Biomonitoring Information Serum concentrations reflect the body burden of HCB.gov/toxpro2.113-.cdc.122) < LOD < LOD .167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .086-.121 (.147-.062-.167 (.125 (..e.069) < LOD < LOD .104 (.155) < LOD < LOD .095) * * .178-. In humans.095) < LOD < LOD 75th < LOD < LOD 90th * * .176) < LOD < LOD . arthritis.086) < LOD < LOD .157 (. and the FDA has established a bottled water standard for HCB. Chronic feeding studies in animals have demonstrated kidney injury.107-. 2002).118-.095 (.092 (.100) < LOD < LOD .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.077-.258) < LOD < LOD .079 (. reproductive and developmental toxicities.118-.060-.130) < LOD < LOD .159-.107) < LOD < LOD . With chronic exposure. 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.094) < LOD < LOD .143-.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .090 (.176-.095-.109) * * .191 (.123 (.097 (.114-. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.087 (.098 (.069) * * . 1982. Survey Geometric mean (95% conf.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 * * .129) < LOD < LOD . a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda. immunologic abnormalities.203) < LOD < LOD . were seen in an epidemic of poisoning in Turkey that occurred from 1955 to 1959 when HCB-treated seed grain was diverted for bread production.099) < LOD < LOD .088-.126) .123 (.141) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.225 (.145-.atsdr.081 (.147 (.085) * * . and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.156 (.148-.081-.S.118) < LOD < LOD .186 (. and liver and thyroid cancers (ATSDR.083) < LOD < LOD .163-.157-.102 (.182 (.111) < LOD < LOD .127-.092 (.196) < LOD < LOD . EPA has established a drinking water standard.132) < LOD < LOD .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 * * . More information about external exposure (i.095 (. acute doses produce central nervous system depression and seizures.160 (. very high. EPA at: http://www. Schmid.090 (.092-.171 (. HCB interferes with normal heme synthesis.gov/pesticides/ and from ATSDR at: http://www.123 (.090 (.111-.078 (.099) < LOD < LOD . This condition.097) .102) < LOD < LOD .173) < LOD < LOD . environmental levels) and health effects is available from the U. and many died before 2 years of age (Peters et al.152) < LOD < LOD .072-.088-.073-.163 (. ACGIH has developed workplace exposure limits for HCB. which may vary for some chemicals by year and by individual sample.091-.163) < LOD < LOD .169-.203) < LOD < LOD . and weakness.094 (.090-. thyromegaly.145-. anorexia.120 (.097) < LOD < LOD .179 (..190 (.089-. Infants were exposed transplacentally and through breast milk.

Sala M. 2003)..17:388–399. Seiwert M. As a result of the lower limit of detection in NHANES 2003-2004. Gocmen A. September 2002. HCB detection in serum also was proportional to age..135(4):400404. Link et al. et al. 1989). Reference values updated. Over the past two decades.fda. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.. Food and Drug Administration (FDA).54(3):203-208. Piechotowski I. Lecha M. The metabolism of higher chlorinated benzene isomers. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Glynn et al. Biol Neonate 2002.. Arch Dermatol 1999. IARC Sci Publ 1986. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. August 2008. Zoellner I. Schulz C. et al. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Int J Hyg Environ Health 2002. 4/21/09 Barber JL. Environ Health Perspect 2002. Eskenazi B. April 1982 to 1984. References Agency for Toxic Substances and Disease Registry (ATSDR).58:1185-1201. Available at URL: http://www. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Herrman T. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al.349:144. Schwartz JM.9% of participants had quantifiable levels (Stehr-Green. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Can J Biochem 1976. Laliberte C. Otero R..77:173182.. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Safe A.110(8):835-838. Hexachlorobenzene in the global environment: emissions. Available at URL: http://www. and the geometric mean concentration of HCB in whole blood was 0. Darnerud PO. 2005).44 mg/L. Paepke O. et al. Kohli J. Sweetman AJ. levels.cfsan.81(2):82-85.. Arch Neurol 1982. Ayotte P. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. more HCB levels were quantified. Peters HA. however. van Wijk D.. Ozalla D. et al. Canada). selected elements.. J Exp Sci Environ Epidemiol 2007. but overall. Santiago-Silva M. trends and processes. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Bryan GT. Bradman et al. In Spain. Lawrence River (Quebec. Muckle G. Lackman.atsdr. In the 1976-1980 NHANES subsample.111:349355. FDA total diet study. Organochlorines in Swedish women: determinants of serum concentrations.html.205:297-308. Toxicological profile for hexachlorobenzene update [online]. 1986. Bertram et al. 2002. 2002. Fenster L. Bertram HP. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Barr DB. Krause C. Holland NT. Aune M. 2006). 2002). distribution. Sci Tot Environ 2005. Cripps DJ. Becker K. Jones KC. Herrero C. Lackmann. Granath F. Chemosphere 2005. Atuma S. 1999). 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. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Lepom P. Dallaire F.39(12):744-749.. Gabrio T. HCB levels were directly related to age. 4/21/09 Glynn AW. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Dogramaci I. 2005. In a representative sample of the 1998 German adult population.71(6):1200-1209. Kemper FH. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Link B. 2002) and among children (Link et al. the more recent values in these studies were similar to the lipid adjusted limit of detection in NHANES 1999-2000 and 2001-2002 (Dallaire et al. Environ Health Perspect 2003. dietary intakes of pesticides. Lackmann GM. Gunderson EL. respectively. 2002.gov/ toxprofiles/tp90.gov/~dms/ pesrpts. 2002. Bradman A.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. and other chemicals. Jones D. 2005). Dewailly E. J Assoc Off Anal Chem 1988. Bjerselius R. Biomonitoring of persistent organochlorine pesticides. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Muller C. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.html. Kaus S. only 4..cdc.

Rodamilans M. N Engl J Med 1960. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Demographic and seasonal influences on human serum pesticide residue levels. PA.27:405-421.105(1):78-83. Fourth National Report on Human Exposure to Environmental Chemicals 103 . Environ Health Perspect 1997. To-Figueras J. Barrot C. Santiago-Silva M.Organochlorine Pesticides Schmid R. J Toxicol Environ Health 1989. Otero R.263:397-398. Sala M. Cutaneous porphyria in Turkey. et al. Stehr-Green.

9 (62.9-81. interval) 9.2) 13.6) 16.2-17.70-19.5) 67.5) 11.5 (8.2 (9.80 (<LOD-14.1 (21.87 (9.7 (<LOD-16.68 (<LOD-10.0 (37.6 (33.6) 35.8-87.1 (27.S.1-32.8 (23.7 (53.20-16.7) 10. < LOD means less than the limit of detection.3-56.46-11.3 (42.2) 62.9) 81. 2005). particularly alpha and gamma have been detected widely in air.0-111) 70.9-21.0 (14.1-49. beta. environmental levels declined.1-37.6-89.4) 11. **In survey period 2001-2002.1) 12.9 (30.1 (9.8 (64. The gamma isomer. However.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.9 (26.8) 7.8-19.2 (34.3-85.5) 22. see Data Analysis section) for survey years 99-00.8-16.3) 37. 104 Fourth National Report on Human Exposure to Environmental Chemicals .9-178) 48.4 (16.5) 90th 42.7-96.5-29. 2005).5 (14.4 (52.4 (50.3) 14.0-21.6) 36.9) 17. As pesticide applications of HCH were increasingly restricted or eliminated.9 (32.6 (17.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.5) 16.9 (9.4) 44. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1) 12. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.0) 8.2 (31.6 (16.4 (8.1 (16.1 (11.1 (18. In 2006.66-12.8) 52.7-69.6 (40.4 (12.4-50.8) 27. and 03-04 are 9.7-26.0) 71.Organochlorine Pesticides Hexachlorocyclohexane CAS No. exists in several isomeric forms.3 (42. and 7.7 (29.0-20.3) 34.9 (11.1 (30.9) 15.5 (37.2 (48.4) 901 1067 952 992 1224 1007 Females 11. and sediment as a result of historic production and use. each result has been multiplied by 1.4) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD 21. including alpha. General population Serum beta-Hexachlorocyclohexane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6-42.6-135) 69.0-70.6) 18.7 (30. EPA cancelled agricultural uses of lindane (ATSDR.76.2) 9.0 (33.1-15.5-123) 49.80 (6.1) 71.36.56-12.7 (62.6) 50.7-96.9) 45.8-199) 134 (85. 608-73-1 beta-Hexachlorocyclohexane CAS No.9 (50.0-23.70 (8.8) 95th 68.3) 25.4 (11. See the section “What’s New” at the beginning of this Report for details.7) 56.5 (16. commonly known as lindane.6 (10.2-67.1-27.04-10.70 (6. HCH isomers.8) 12.9-51.9 (40.6 (22.4) 21.0) 7.6-37.8) * * * * * * 15.4-45.6) 653 758 589 1240 1533 1370 20 years and older 10.9-14. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.2-87.3 (26. so they can accumulate in fatty tissues of animals.2-20. containing about 64% alpha and 10%-15% gamma isomers.9-24.0 (35.2) 36.8 (10.89 (<LOD-9.7) 73.0 (19.43 (<LOD-9. water.7-166) 70.0-70.0 (<LOD-12.2) 142 (99.6) 47.4) 10.5 (43.90-8.S.6-47.3-38.2-46.4) < LOD 9.61-12.5) 14.4) 51.6-18.1) 31.7) 97. 319-85-7 gamma-Hexachlorocyclohexane CAS No.5) 40. population from the National Health and Nutrition Examination Survey.2 (29.1-36.S.30-11.6-20. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf. 58-89-9 General Information Hexachlorocyclohexane (HCH).7) 27.8 (21.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16. and have been used either as fungicides or to synthesize other chemicals.7) 23. It is no longer produced or sold in the U.8. gamma.2-52.7 (25.7) 32.2-42.1-16. Lindane has a half-life of about two weeks in soils and water.0) 41.1 (12. 6.9-56.7) 18.0 (8.5528.7-69.4) 27. formerly referred to as benzene hexachloride.2 (50.8 (32.60-13. Technical grade HCH is a mixture of all four isomers.0-34.7 (13.5 (11.1-32.2-55.8 (33. soil.50) 8.2 (18.5 (24. respectively.0) 17.2-98.3) 51. The other isomers can be formed during the synthesis of lindane.8-68. which may vary for some chemicals by year and by individual sample.1 (9.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.4-111) 84.70-12.7) 10.3 (13. HCH isomers are lipophilic.7 (35.90-8.6-14.8 (9. the U.4-73. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.2-22.8-54.8 (17.8) < LOD 10.6-62.0) 35.7-20.8) 39.90) 7. 01-02.3 (62.7) < LOD < LOD < LOD < LOD < LOD < LOD 37. and delta.4) < LOD < LOD < LOD 46.5) 29.1) 13.

32) .350 (. 1971. 2008.078 (. 1977). Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.120 (.260) .220 (.S.294-.089-.191-.250-.37) 1.480 (.110-. tremors. and nephropathy developed (IPCS.280-.081-.140) . 1996.450-. When animals were chronically fed lindane at high doses.250 (.382-.5528.210 (.814) . **In survey period 2001-2002.098 (. Gunderson 1988).090 (.280-.070) . The U.Organochlorine Pesticides exposure to HCH is through the diet. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.120-.230-.290 (.360-.160) . The beta isomer accumulates in fatty tissues and is metabolized more slowly.050) .319) . See the section “What’s New” at the beginning of this Report for details.065 (.191-.086) < LOD < LOD < LOD < LOD < LOD < LOD . resulting in a half-life of about seven years.120) .100 (.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .480 (.620) .221-.057 (<LOD-.091) .310) .110) .840) . 1983).050 (<LOD-.05) .118-.350) .146-.119) . the serum half-life was about 20 hours among children (Ginsburg et al.250-.120 (.050-.048 (<LOD-.331 (.050-. which may vary for some chemicals by year and by individual sample.290 (.680) .290 (..047-. probably by blocking inhibitory neurotransmitters in the central nervous system.120-.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .410) . respectively. ingestion.150-. each result has been multiplied by 1.587) 653 758 589 1240 1533 1370 20 years and older .308-.050 (<LOD-.089) .310) .051 (<LOD-.330 (.222 (..390 (. interval) .470) .120-.220-.450 (.051-.470 (.372 (.100-.069) .170-.190-1.070-. 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.140 (. paresthesias.480) .050 (. Fourth National Report on Human Exposure to Environmental Chemicals 105 .070 (.410-. Saxena et al.160 (.216 (.059-.150) .120 (.077) < LOD . U.390-.290) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD . and seizures. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.560) .057-.420-.062 (. HCH isomers are absorbed after inhalation.103 (.130-.254) 95th .260) .340) . population from the National Health and Nutrition Examination Survey.125) < LOD < LOD < LOD .290) .380 (.320 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.910 (.240-.131-.580 (.103-.200-.442 (.124-.214) .096) .072 (.297-.064 (.056-.580-1.130 (.160-.234 (.140) .700) .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.110) .250 (.260-.080) * * * * * * .244-. 2002)..092 (.150) . Distribution is mainly to fatty tissues.080 (.210 (.144 (.139 (.080-.200-.250 (.190) . hepatic enzyme induction.080-.050-.120) .167 (.070-.100) .100) .270 (.090 (. ataxia.210-.083) .287 (. 1981).404) .S. enlarged livers.180-.174) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.090 (.450) .083 (.460 (. 1986). or dermal exposure. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.410 (.067) .01 (.410) . and FDA has established a bottled water standard and food residue tolerances for lindane. Workers who directly handled HCH have complained of headache.050 (.340-.100 (.067 (.400) ..370-.200 (.175 (.250) .080 (.460) .281 (.210) .501) .620-1. EPA has established a drinking water standard. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.070 (.220-.080-.560 (.064) .400) .220) . Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.058 (<LOD-.040-..110) .065 (.060) .077) < LOD .080) .360) .056-.140) .305) .240 (.300-.310 (.661) 901 1067 952 992 1224 1007 Females .S. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.190) .073-.103) 90th .070-.412 (. OSHA and ACGIH have established workplace standards and guidelines.710) .190-. After dermal application of lindane 1% lotion.050-.173-.510) .100-.690) .068-.150 (.090-. and memory loss (Nigam et al.130) . Rogan.360 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.100-.118 (.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 .600) .521 (.170-. for lindane.330-.057-.570 (.062 (.

html. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. 2004. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al.e.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1998. Kutz et al.S. and 2003-2004.. Additional factors associated with higher beta-HCH levels include rural residence. In populationbased studies of New Zealand adults and German adults and children. aged 9-11 years. 2004) and India (Bhatnagar et al.8. 2004). 1989.. In NHANES 1999-2000. 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.. 01-02. 1991. older age. and 7. 106 Fourth National Report on Human Exposure to Environmental Chemicals .gov/toxpro2. 1971. respectively. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR.epa.atsdr. population from the National Health and Nutrition Examination Survey. respectively.. 1998). 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. which may vary for some chemicals by year and by individual sample. Sturgeon et al. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. Biomonitoring Information Because of its longer half-life.cdc. environmental levels) and health effects is available from the U. 2002. serum levels of lindane were generally below the limits of detection. 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. 1991. Link et al. Kutz et al. and a diet that includes meat (Becker et al. and 03-04 are 14.5.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. 2005.gov/pesticides/ and from ATSDR at: http:// www.5. Radomski et al.. were similar to the 95th percentiles in this Report. 2001-2002. 10.. male sex. In an earlier (1996-1997) sample of German children. Stehr-Green. Becker et al.. More information about external exposure (i. 2005. see Data Analysis section) for Survey years 99-00. the maximum and 95th percentile beta-HCH values.. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. Bates et al.. Stehr-Green..S. 2002).. EPA at: http://www. 1989).

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. A study of Swedish women aged 54 years and older reported a median beta-HCH level that was slightly higher than the geometric mean for women reported in the NHANES 1999-2000 survey period (Glynn et al. which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1986. 2003). the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al.. in this Report (Nigam et al. Survey Geometric mean (95% conf. Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. 1998). Fourth National Report on Human Exposure to Environmental Chemicals 107 .. 1971). respectively. 2005). 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.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Radomski et al.S. 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.Organochlorine Pesticides 2001-2002 survey period (Link et al. In a small study of adults who consumed sport fish from the Great Lakes. population from the National Health and Nutrition Examination Survey.. 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)..

Bull Environ Contam Toxicol 2004. Lowry W. Link B. Saiyed HN. Kaus S. Olson J. Needham LL. Bottimore DP. Rev Environ Contam Toxicol 1991. Lindane. PA. Krause C. Olea-Serrano MF. Cancer Causes and Control 1998.54:1431-1443. and HCB residues in human blood in Ahmedabad. Hanrahan L. Astolfi E. et al. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. et al.cfsan.72:261265. Atuma S. Radomski JL. August 2005. Kashyap R. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Bates MN. gov/toxprofiles/tp43. Rothman N. Krishna Murti CR. Patterson DG Jr. Arch Pediatr Adolesc Med 1996. Majumder SK. Falk C.htm.20(2):186-193. Heinrich R. J Pediatr 1977. Biomonitoring of persistent organochlorine pesticides. 4/21/09 Ginsburg CM.111:349355.96:34-4Food and Drug Administration (FDA). Arch Toxicol 1981. HCH. Cerrillo I. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Environ Res 2004. Karnik AB. Kutty D. Gabrio T. available at URL: http://www.inchem.gov/~dms/pesrpts. August 2008. Brock JW.27:405-421. Angerer J. et al. Metabolism of gammahexachlorocyclohexane in man. Int Arch Occup Environ Health 1986. Wood PH. International Programme on Chemical Safety (IPCS). Visweswariah K. 4/21/09 Kutz FW. Botella B. Zaidi SS. Buckland SJ.106(5):279-289. Sturgeon SR.fda. et al. Bjerselius R. Schulz C. Reisch JS. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Absorption of lindane (g benzene hexachloride) in infants and children. Lepom P. Rivas A. Herrman T.91:998-1000.120:1-82. Rogan WJ. Environ Health Perspect 2003. et al. Chemosphere 2004. Becker K. Zoellner I. and other chemicals. Burse VW. Toxicological profile for hexachlorocyclohexanes update [online]. Garrett N. Occupational exposure to hexachlorocyclohexane. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.9(4):417-424. Deichmann WB. dietary intakes of pesticides. Levels of DDT. Nigam SK. India. Paepke O.52(1):59-67. Glynn AW. Int Arch Occup Environ Health 1983. Saxena MC. Demographic and seasonal influences on human serum pesticide residue levels. Available at URL: http://www. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Int J Hyg Environ Health 2002. Aune M. Siddiqui MKJ.57(4):315-320.71(6):1200-1209. The Great Lakes Consortium. Crespo J. Potischman N. 4/21/09 Anderson HA.atsdr. April 1982 to 1984. Organochlorines in Swedish women: determinants of serum concentrations. Toxicol Appl Pharmacol 1971. Bhatnagar VK. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Exposure of women to organochlorine pesticides in Southern Spain. Placental transfer of pesticides in humans. Needham LL. Olea N. Available at URL: http://www. selected elements.205:297-308. children and newborn infants. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. org/documents/jmpr/jmpmono/2002pr08. Maass R. Bhargava AK. Granath F.58:1185-1201. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.html. VI.cdc. et al. J Assoc Off Anal Chem 1988. Kulkarni PK. Chemosphere 2005. Seiwert M. Raju GS.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).150:981-990. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Brinton LA. Piechotowski I. Pollutants in breast milk. Ellis H. Darnerud PO. Bai KM. et al. Gunderson EL. Needham LL.48:127-134. J Toxicol Environ Health 1989. Rey AA. Stehr-Green. 2002. Environ Health Perspect 1998. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. FDA total diet study.html.

soil.8. Fourth National Report on Human Exposure to Environmental Chemicals 109 . Mirex binds strongly to soil.5-82. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.S.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.2-230) 13.6-305) 15.8 (12.2) 51.6 (<LOD-23. which may vary for some chemicals by year and by individual sample. animals. 01-02.7 (<LOD-47.0-374) 11.5 (<LOD-42. mirex was detected in human adipose samples.1) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 16.3 (15.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6 (<LOD-31. Formerly. water.0 (<LOD-108) < LOD < LOD 50.0) * * * 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 19.8 (<LOD-73. (Kutz et al.70-40.10 (<LOD-15. 10.6) < LOD < LOD < LOD < LOD 71. aquatic organisms. In studies conducted in the 1970’s and 1980’s.. disposal.6 (<LOD-108) 9.0 (14. see Data Analysis section) for Survey years 99-00.S.4 (8.5.1 (13.4-230) 18. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.6. where it was applied directly to soil and by aerial spraying. where it has a half-life of 12 years.3 (15.70 (<LOD-15.5-291) 11. or pesticide application.7) < LOD 66. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. after which it is widely distributed in the body and stored in fat. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and foods. 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. Mirex can cross the placenta and be excreted in breast milk.8) < LOD 15.3) 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.S.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.70-24.5 (<LOD-115) 153 (30. Mirex is absorbed through the skin and from the gastrointestinal tract. and 7. Some states and the U. especially those from persons living in the southeastern U. 2385-85-5 General Information Mirex has not been produced or used in the U. resulting in exposure to newborns and nursing infants. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. 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.5 (9.7 (12.0 (12.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.4) < LOD 15.3-225) 15. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.2 (7. it is a highly persistent chemical in the environment..40 (<LOD-13.4) < LOD 63.S. 1985.7) 8. and 03-04 are 14. Mirex is not metabolized in the body. < LOD means less than the limit of detection. Mirex has been detected in air.Organochlorine Pesticides Mirex CAS No.6) 9. Occupational exposure is limited to workers at sites where mirex contamination is present. since 1977.10-37. respectively.5-425) 40.S. 1995).1 (8. sediments. 1991).1 (<LOD-65.90-29.

The geometric mean mirex levels of the Inuit mothers were 8. 2001-2002.102) < LOD < LOD < LOD < LOD .052-.268) < LOD .140 (<LOD-.470) .090 (<LOD-. Smith. Survey Geometric mean (95% conf. and 4.470) .410 (.090-1. The U.470 (.73) .089-.e.054 (<LOD-.37) .112 (. 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. reproductive toxicity included decreased fertility and testicular damage. EPA has established environmental standards for mirex.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 .053-.106) < LOD .090 (<LOD-. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. 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. as well as in a subsample of NHANES II (1976-1980) participants.079 (<LOD-.093 (.79) .090 (<LOD-. Laboratory animals fed high doses developed liver enlargement and liver tumors.064 (<LOD-.059 (<LOD-. environmental levels) and health effects is available from the ATSDR at: http://www. 2004). population from the National Health and Nutrition Examination Survey. 1995. 1991).S.256 (. 110 Fourth National Report on Human Exposure to Environmental Chemicals .02) .100 (<LOD-.41) .370 (.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 .08 (.450) 1.79) . and 2003-2004 subsamples. In addition.Organochlorine Pesticides exposures are unknown.062-.080-1. 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.077 (<LOD-. 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.106 (.070-1.100 (<LOD-.92) .310 (.220) .110 (<LOD-.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 . More information about external exposure (i. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.cdc. 1989).html..S.7 ng/g of lipid. serum mirex levels were generally below the limits of detection (Stehr-Green.108 (. 2005).090-1.055-. IARC classifies mirex as possibly carcinogenic to humans. 7. In samples obtained between 1994 and 1997. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.090-1.174) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.450 (.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .635) < LOD ..430 (.220 (<LOD-.gov/toxpro2.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .690) .510) < LOD < LOD .atsdr.610) < LOD < LOD < LOD < LOD . Biomonitoring Information In the NHANES 1999-2000.170-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .080-1.8. which may vary for some chemicals by year and by individual sample..170) < LOD .

731-915. New York. Vol. Stroup CR.gov/toxprofiles/ tp66. 1991 pp. Strassman SC. Gilman A. et al. Vena JE. Demographic and seasonal influences on human serum pesticide residue levels. Chashchin V. The human body burden of mirex in the southeastern United States. Inc. Rev Environ Contam Toxicol 1991. Sci Total Environ 2004. Hansen JC. Environ Res 2005. Circumpolar maternal blood contaminant survey. Stehr-Green.atsdr. Watts DL. dichlorodiphenyldichloroethylene. Leininger CC.120:1-82.15:385-394. Carra JS. Academic Press. Smith AG. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Dewailly E. 2 Classes of Pesticides. Kutz FW. Handbook of Pesticide Toxicology. PA. J Toxicol Environ Health 1985. J Toxicol Environ Health 1989. Jr and Laws ER. References Agency for Toxic Substances and Disease Registry (ATSDR).cdc. Wood PH.330:55-70. hexachlorobenzene. Available at URL: http://www. Van Oostdam JC. 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. Odland JO.97(2):178192.Organochlorine Pesticides effect. Fourth National Report on Human Exposure to Environmental Chemicals 111 . August 1995. Olson JR. Kutz FW. 1994-1997 organochlorine compounds. Swanson MK. Chlorinated Hydrocarbon Insecticides. Bottimore DP.27:405-421. Eds. Profiles of ortho-polychlorinated biphenyl congeners. 4/21/09 Bloom MS. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Moysich KB. et al. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Toxicological profile for mirex and chlordecone [online]. Jr.html. In Hayes WJ.

40) < LOD 4.0) 2.9 and 0.0) < LOD 11.20-71.4.71 (<LOD-8.0 (4.57 (<LOD-15.30-27. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.03) 9. and polychlorinated benzenes (Kohil et al.940-3. 1999).0) < LOD 5.63) 18.4.4.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.7) 24.6-trichlorophenol (2.40-18.60 (2. Trichlorophenols are no longer manufactured commercially. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organochlorine Pesticides 2. Both chemicals have been detected in air.20) < LOD 1. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.900-2.4.27) 696 661 521 696 603 939 Limit of detection (LOD.00 (3.40) < LOD 6. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds. 2.0) < LOD 11.0 (8. Such workers would probably Urinary 2.00-8. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.00-3. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.5-trichlorophenol (2.S. including hexachlorobenzene and hexachlorocyclohexanes.0) < LOD 5.9 (<LOD-121) 9. may occur by inhalation or dermal routes. Exposure to trichlorophenols also may result from metabolism of lindane.7. Occupational exposures. Historically.40 (1.27) 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. other organochlorines.30) < LOD 4.5-TCP) and 2.30-44.0) 5.0) 14.42 (<LOD-8. population from the National Health and Nutrition Examination Survey.00-3.60-18.4. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.5TCP and 2.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1. are metabolites of several organochlorine chemicals.40 (2.40 (1.4.0 (3.9.72) < LOD 1..40 (2.40 (2.20 (4.8) 21.50 (.50 (2.80 (2. 1999).4.10-3.71 (<LOD-8.50) < LOD 1.0 (4.00 (2. soils.40 (. EPA. Formation of 2. and sediments.50-16.90-33.60 (.6-Trichlorophenol CAS No.30) < LOD < LOD < LOD < LOD < LOD 1. 2006).0) 2.42 (<LOD-12.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 2. public drinking water systems did not detect 2. 112 Fourth National Report on Human Exposure to Environmental Chemicals . 1976).80 (1.0 (4.980-3.40 (2.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.20) < LOD 90th 5.0) < LOD 5. recent sampling of U. hexachlorobenzene.920-3.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.30-11.30-27.0 (3.30-3.3.30-40.60-8.40) < LOD 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.40 (.0) 2.6-TCP in any of the samples (U.80-41.80) < LOD 1. 95-95-4 2. which may vary for some chemicals by year and by individual sample.20-36.0) < LOD 21.60 (4. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.31 (<LOD-9.6-TCP).6-TCP were used as intermediates in the production of certain pesticides.20) < LOD 5. surface water. < LOD means less than the limit of detection.4.30 (.S.5-Trichlorophenol CAS No.4. however.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .4. 2.980-3.4.19 (<LOD-6.60) < LOD 8.30-27. usually at herbicide production or waste incineration facilities.950 (<LOD-1.50-63.4.40-11.5-trichlorophenol.0) 2.0) 2. 2. Survey Geometric mean (95% conf.0 (5.50 (1.S.50-25.

16 (.53-3.6-TCP level was approximately eight times higher than the corresponding percentile in a small group of 2-6 year old children living near an herbicide manufacturing facility: 33 versus 4 mg/L (Hill et al.93-11.57 (3..37) 16.2) < LOD 5.. Among 6-11 year old children in NHANES 1999-2000.24) < LOD 1.73 (<LOD-8.6-TCP.8) < LOD 9.S. Survey Geometric mean (95% conf.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.24 (3.47-8. 2003).4.78-19.31) < LOD 2.5-TCP or 2.4.6-TCP had increased rates of hepatic tumors. which includes trichlorophenols. environmental levels) and health effects is available from ATSDR at: http://www.32) < LOD 4. Laboratory animals chronically fed high doses of 2.24) < LOD 6.60-3.67 (1.13-13. 2003).24) < LOD 5.90 (4.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). the 95th percentile urinary 2. 7.0 mg/L.57 (<LOD-7.4.6-TCP levels at the 95th percentile were up to eight times higher than 3.4.0) 7. Urinary 2.64 (4. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.6) 4.75 (3. 2004)..83-12.46 (1.1) 2.28-25.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.55 (4.2 (2.29 (1.4.9 (5.57 (<LOD-7.43 (2. Human health effects from 2.gov/toxpro2.74) 11. population from the National Health and Nutrition Examination Survey.4. At lower doses.02-3. 1995) and up to 19 times higher than the 95th percentile value of 1. 1995) were similar.7 (4.e.4.05-8.4. and other chlorinated compounds.69-18.4. Neither 2.8 (5. animals showed hepatocellular abnormalities.00-29.69 (2.6) 4.4) < LOD 3.820-2.49 (1. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.3 (5.5-TCP and limited for 2.4.00-19..19-12.4.9) 12.8) 4. Fourth National Report on Human Exposure to Environmental Chemicals 113 .920-2.00) < LOD 4.53-3.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2. furans.19-4.5-TCP.4) < LOD 3.. as being possibly carcinogenic to humans.1 (<LOD-58.88-16. The 95th percentiles for 2.6-TCP as reasonably anticipated to be a human carcinogen. leukemias.50) < LOD 2.36 (1.20-6.5) < LOD 12.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. IARC classifies combined exposures to polychlorophenols.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 2.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.4.33) < LOD < LOD < LOD < LOD < LOD 2..atsdr.3 mg/L reported in German adults aged 18-69 years (Becker et al.78) < LOD 1. More information about external exposure (i.15) < LOD 2.86 (3.4. However.75 (<LOD-6. the 95th percentile urinary 2.95 (3.44 (. urinary 2. Radon et al.6) 4. In the same 2-6 year old children.16) < LOD 90th 5. 2003.44 (1..43) < LOD 12.78 (3.17) 9.37-11.cdc.24-11.79-4..2) 2.68-4.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .4 (6.980 (<LOD-1. in addition to dioxins.27-17. NTP classifies 2.68 (<LOD-8. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11. 1989).6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.81 (<LOD-9.67 (1.02) < LOD 7.62-20. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.05-17. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples. 1989).. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.html.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. and lymphomas.5) 11.Organochlorine Pesticides be exposed to mixtures of chlorophenols.4) 5.82 (<LOD-32.5-TCP nor 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80 (1.

5-TCP or 2.5-TCP or 2. 1991).30) 4.0 (6.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.10) 6.80-6.4. was about six times lower than the median urinary levels for males in this Report (Radon et al. Mean values of 2. which may vary for some chemicals by year and by individual sample.74-3.89-6.28) 24. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-41.0) 13.30-2.6-TCP exposure and health effects.91-4.23) 2.85 (2.0-43..5 mg/g creatinine) were similar to the limit of detection for 2.5-TCP and to the median 2. for males in NHANES 19992002 (Agramunt et al.5-TCP and 2.33-4. the median urinary 2.32) 3.46-3.85) * 3.40) 2.20-6.70-3.45) < LOD 11.6TCP values.02) 2.0 (13.50 (2.0 (11.4.8-13.4.4.0) 9.0-38.6-TCP than are found in the general population.74 (2.0-50.0) 6.0 (9.0) 10.4.45-9..00 (1.10) 2.40) 2.78 (2.08 (2.8-24.3) 23.0) 15.59-6.70-6.4.4 (10.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.06) * 2.80 (3.1-25.90 (3.7-3.6) 26.79 (5.6-TCP in urine does not mean that the level of 2.3.44) 75th 4.0) 17..0 (14.5-46.0) 7.70 (2.6-TCP level.04) 2.65) 15.4-17.0 (12.0) 13.80 (2. 2003).36 mg/g creatinine.30-33.9 (11.60 (3.00 (4.6-22.0 (16.60-37.8) 32.0) 17.70) 5.24 (2.40 (2.0 (15..52-3. 1998).67) 4.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.4.07 (<LOD-3.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.10 (5.20 (3.66 (8.53) 2.4.12) 2.28) * 2.4.0 (8.72-10. 2004). interval) 2.40-7.0) 11.0 (6.75 (8.84) 2.4 (9.6TCP causes an adverse health effect.80-25.6 (12. Biomonitoring studies on levels of 2.3 (11. population from the National Health and Nutrition Examination Survey.40) 3.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.40-4.0 and 1.20-3.6 (11.6) 21.49 (6.0 (8.32-4.51-12.31 (3.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.9) 694 677 519 696 602 931 Limit of detection (LOD. respectively.0-68.98-11.80) 1.70) 1.58-3.70 (2.4.0 (20.4.0 (14.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4. In harbor workers exposed to chlorophenol-contaminated river silt.40) 4.0) 19. Urinary 2.2) 12.4.3) 20.0-18.90 (4.7-16.60 (3.30-11.0) 7.54) 6.7 (13.01-6.5-TCP level of 0.0-37.0-44.0-38.0 (14.76) 3.4.52 (2.5-TCP or 2.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.92 (2. Survey Geometric mean (95% conf.55-3.56 (3.1) 16.0) 12. < LOD means less than the limit of detection.90-8.4.98-7.57 (<LOD-2. 0.2) 25.78 (2.4.63) 90th 15.6 mg/g creatinine) and 2.90) 2.09-7.0 (6.5-TCP and 2.65 (5.45 (5.0 (7.53) 4.60-3.6-19.31) * 2.6-17.47 (3.18-3.40 (2.80 (2.4.1 (8.0) 19.5-TCP (0.7 mg/L.0) 14.0 (15.95-6.3 (11.00-4. Urinary 2.35-3. Biomonitoring data will also help scientists plan and conduct research about 2.58 (1.67-12.69 (3.3-26.2-0.32) * 3.80-20.95 (4.0) 13.S.95) 3. Finding a measurable amount of 2.4.6-TCP (0. similar to the limit of detection for this Report (Anderson et al.10-3.23-2.0) 14.40-32.7) 21.5-TCP or 2.87-14.70) 3.4.8-15.0) 13.68 (<LOD-2.40-14.36-5.00-21.4 (17.0) 9.0) 10.30-2.9) size 1989 2503 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.40-2.50-5.89 (3.70-6.00 (2.20) 4.23) 3. 114 Fourth National Report on Human Exposure to Environmental Chemicals .80-7.60) < LOD 5.60-21.36 (1.0) 11.10-2. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.14 (2.3) 37.0-54.09) 15.0 (4.20-23.2 (14.99) 6.4 (8.59) 4.9 (13. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.7) 33.70) 5.40-2.60) 6.25-11.9) 13.7 (9.73-9.48-26.26 (2.45 (2.60 (2.8) 18.20 (3.4.8 (9.10-3.3-17.0 (20.1 (10.6-TCP levels that were as much as 450 times higher than the median level among adults in the NHANES 1999-2000 subsample (Pekari et al.

0 (9.82 (8.87-6.65-21.22-9.16-10.78) 90th 12.9-32.51 (2.71 (3.02 (1.60 (4.17) 13.6 (9.70-9.83-6.15 (1.53) * 2.8) 12.08-2.05 (3.6) size 1989 2502 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.3-37.0) 10.58 (4.47-5.00 (2.29-4.0) 8.62-15.6-31.06) 4.43-7.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.33-2.11) 10.7) 25.26-13.59 (2.4 (11.8 (7.27-9.4) 8.82 (3.17-4.73-22.99-2.98 (1.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.22 (<LOD-2.29 (6.1-21.50 (2.56 (7.5 (7.2) 19.50-8.87 (3.5) 9.42 (2.5-28.63) * 4.28-4.55-2.9-64.76) 1.21-11.05 (6.94-13.35 (3.1) 14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7-36.17) 2.81-9.60-2.32 (2.01 (3.52) 2.43 (2.87) * 2.9) 7.5) 12.23 (1.77-4.83-6.4) 9.68) 2. Fourth National Report on Human Exposure to Environmental Chemicals 115 .7) 6.1) 11.S.2 (7.9 (9.33) * 2.38 (2.25-17.5) 11.88) 4.67-17.43 (<LOD-2.18-4.10 (6.0 (6.3 (9.22 (3.9 (9.42) 2.25 (3.8) 21.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.6) 13.76-8.14-2.6 (9.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.88) 5.63 (<LOD-2.65-2.Organochlorine Pesticides Urinary 2.82-2.91 (3.33 (7.0 (11.29-4.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.6 (6.68) 2.63-15.78 (2.04-2.04-16.1 (8.1-32.88) 4.76) 4.9) 8.65) 2.20-2.98) 10.10-9.82) 2.77) 2.2 (12.63 (2.3) 8.9) 8.90 (1.90) 2.53-11.73) 5.75) 75th 4.24 (1.5 (10.25-15.38) 22.9-34.88 (2.54 (2.18-2.6 (10.92) 4.02) 3.91 (7.6) 8.06) 11.2 (13.51-21.6) 12.8 (8. Survey Geometric mean (95% conf.78) 2.88-7.22-2.23) 4.40 (7.87-7.30-2.72-16.00) 4.44 (3.8) 11.76) 2.38-5.6 (12.13 (1.00 (3.56-5.2 (8.14-13.06-2.53 (3.4 (12.5) 8.4.6 (5.91-2.63-13.22 (1.53) 4.49-3.89) 10.25-2. interval) 2.52 (3. population from the National Health and Nutrition Examination Survey.88) * 2.56) < LOD 11.52) 2.41 (3.15 (6.88) 1.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.26 (6.87) 2.46-14.09-3.63) 4.00) 4.10) 4.79-17.89-2.3-23.65) 18.83-5.19-5.5) 11.25 (3.13-6.40 (2.66-4.96) < LOD 4.81) 2.5 (8.9) 19.49) 4.7 (14.8) 19.83 (3.41-6.48-2.9-29.4) 4.32-19.72) 32.52 (5.1 (13.33 (1.95-2.51) 18.6 (22.38 (4.

Szadkowski D. et al. Gregg M.146:83-91.45:440-445. Int Arch Occup Environ Health 1991.cdc. et al.54(3):203-208. Pekari K.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Wegner R. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals .epa. Needham LL.pdf. 4/21/09 Agramunt MC.63:57-62. Seifert B. July 1999. Toxicol Lett 2003. Anderson HA. Fast DM. Heinrich-Ramm R. Domingo A. Baker S. Environ Res 1995. Aitio A.EPA). Pesticide residues in urine of adults living in the United States: reference range concentrations. Shealy DB. Luotamo M. To T. Int J Hyg Environ Health 2003. Jones D. Can J Biochem 1976. Available at URL: http://www. Domingo JL. Radon K. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Corbella J. Toxicological profile for chlorophenols [online]. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Holler JS.18(4):469-474.71:99108. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. December 2006 Draft. Becker K. Olson J. Poschadel B. Available at URL: http://www. U. Hill RH Jr. et al. html. Hill RH Jr. 206:15-24.gov/toxprofiles/tp107. Kohli J.106(5):279-289. Lindroos L. Jarvisalo J.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Environ Health Perspect 1998. Needham LL. Bailey SL. Head SL. Smith SJ. The metabolism of higher chlorinated benzene isomers. Hanrahan L. Kaus S. The Great Lakes Consortium. Burse VW. Seiwert M. Safe A. Schulz C. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Falk C. S. Baur X. Arch Environ Contam Toxicol 1989.atsdr. Am J Ind Med 2004. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. 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]. Urinary excretion of chlorinated phenols in saw-mill workers. Environmental Protection Agency (U.S.

Certain organophosphorus insecticides (e.g. pesticide applicators. and a low persistence in the environment.DimethyldithioDiethylDiethylthio. Although organophosphorus insecticides are still used for insect control on many food crops. less common routes include inhalation and dermal contact. gardeners. chlorpyriphos) are initially metabolized to the more toxic “oxon” form..S.. most residential uses have been phased out in the United States as a result of implementation of the Food Quality Protection Act of 1996. the organophosphorus insecticides have better gastrointestinal than dermal absorption. 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. with usage declining 45% since 1980 (U. Mammalian elimination halflives can range from hours to weeks. EPA. 1993). 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. have accounted for a large share of all insecticides used in the United States. slight to moderate water solubility. which are active against a broad spectrum of insects.g. naled) are also registered for public health applications (e. The thiophosphate type organophosphorus insecticides (e. widely varying degrees of soil leaching or runoff potential. malathion. General population exposure to organophosphorus insecticides may occur by ingesting contaminated food and from hand-to-mouth contact with surfaces containing organophosphorus insecticides. and manufacturers of these insecticides may have greater exposure than the general population.. Most organophosphorus insecticides undergo hydrolysis with excretion of major hydrolytic metabolites in the urine. In general.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Organophosphorus Insecticides: Dialkyl Phosphate Metabolites General Information Organophosphorus insecticides. moderate to high soil binding.Dimethylthio. mosquito control) in the United States. Farm workers. 2004).S. An estimated 73 million pounds of organophosphorus insecticides (70% of all insecticides) were used in the United States in 2001.Diethyldithiophosphate phosphate phosphate phosphate phosphate phosphate (813-79-5) (1112-38-5) (756-80-9) (598-02-7) (2465-65-8) (298-06-6) • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • • Fourth National Report on Human Exposure to Environmental Chemicals 117 . the various organophosphorus insecticides demonstrate low vapor pressures (with some exceptions). EPA. In general.g. Approximately 40 organophosphorus insecticides in a wide variety of formulations are registered for use in the United States by the U. florists.

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

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

71 (2.1) 95th 13.15) 14.50-5.1) 10.0 (9.0) 6. which may vary for some chemicals by year and by individual sample.50) 2.80) 2.26-8.86 (1.56 (4.700-1.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.01) * * 1.758-1.81) 11.02) 4.86-15.30 (2.40-14.2 (14. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30 (2.0 (12.0 (8.72) 5.60-25.2 (7.0-28.80) .32 (.10) < LOD < LOD 4.47) * * 1.3) 17.82-12.599-1.70-14.63) 1.757-2.55-8.39 (8.40-16.10 (2.47) 5.0 (6.00 (5.14) * * . and 0.7 (12.5) 20.96-3.8 (9.27-15.05-7. see Data Analysis section) for Survey years 99-00.81) 1.34-3.40-19.10 (.70-11.623-1.00 (4.79-7.93-24.08-15.13-2.57-7.80) .8) 11.58 (3.10) < LOD .600 (<LOD-1.28) 1.80 (2.90 (1.1.58 (2.1) 13.82) 10.45 (2.58 (5.20 (.0) 11.0) 10.52) * * 1.8 (8. 01-02.61 (3.8) 19.579-1.90) 2.22 (.21 (.98-12.490-2.67) 3.70-23.5-16.55-6.53) 4.00 (1.2 (11.60-18.4 (9.13 (2.10-7.34-7.2) 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 1.38-5.70) < LOD < LOD 75th 3.85 (3.954 (.32) 1.5-17.44-38.50 (2.10 (2.50 (.2 (9.68-7.2) 16.5 (11.8) 7.0 (7.40 (.2.740-2.26 (5.19) 9.2) 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 1.70) .0 (7.290 (<LOD-.8-32.00-7.56-13.04) < LOD 1. respectively.530 (<LOD-2.0-27.94) 3.33 (5.89) 9.80-24.44 (2.21) 9. 0.0 (8.830 (<LOD-3.29) * * 1.90-4.70 (2.4 (9.0) 12.00-27.66) * * 1.1 (10.98-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.35-16.970-2.3-15.0) 10.80) 4.4 (7.95) 5.08 (<LOD-2.40-1.8 (12.9) 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 1.73) * * .10 (.70) < LOD < LOD 1.1-23.860-2.0) 11.3) 14.80) 11.93 (4.0) 6.39 (3.0) 10.51) 2.4) 18.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.8) 7.810-1.0) 5.50-36.0) 7.20-7.9) 14.13 (2.0) 11.02-5.97) 90th 7.2 (9.2 (7.0) 5.56 (6.60) .0 (4.74 (8.00) 3.81) 11.30 (4.9 (8.43-12.7) 11. interval) 1.2) 14.620-1.71-9.90) 3.16) 4.35-11.35-12.60) < LOD < LOD 4.0) 15.46) 10.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0) 10.0) 9.11 (.80) 2.48-7.15-12.2.80) 2.52) 6.97) 8.4) 20.30-4.42-3.12) 4.37 (3.0 (8.60 (1.4) 17.890 (<LOD-2.79 (5.56 (1.290 (<LOD-1.0) 6.91) 4.670-1.4 (7.840-1.750-1.60-11.717-1.99 (5.0 (5.00) 3.27-3.20 (2.30-6.07-10.00-12.50 (4.16 (2.42) .2 (7.00-12.36-4.981 (.3) 16.7 (14.20-4.2-20.955 (.76 (2.17-3.80-4.26-6.9) 8.20 (.S.80) 3.12-19.61) 4.0 (7.70 (4.9-18.6) 7.90-5.00-27.780) < LOD 3.0 (6. 120 Fourth National Report on Human Exposure to Environmental Chemicals .0) 5.20-30.83 (5.60 (5.6) 18.70-19.44-3.23-5.2 (14.80-22.1-17.03 (.40-5.0) 10.0) 11.40-11.94) * * .8 (14.1 (9.5 (8.2) 16.08-2.52-11.74 (8.33-18.00-19.0 (9.0) 20.80 (4. < LOD means less than the limit of detection.20 (.5) 15.0 (7.54 (3. population from the National Health and Nutrition Examination Survey. and 03-04 are 0.20 (.

1 (7.430-1.72) 11.60-9.20-8.75-7.09) 2.46-5.8) 16.45-5.7) 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 .25) 6.960 (<LOD-2.47) * * .820 (.11-6.75 (3.870-2.04 (1.58) * * 1.69) 2.98-22.93-5.87 (1.81 (1.46) 2.1 (8.47 (3.94-9.6 (9.02 (7.43 (.40) < LOD < LOD 75th 2.5) 12.5-13.1 (10.28-9.4 (4.69) 4.7 (10.574-1.996 (.05) .5-20.40) 4.41) .60) * * .8) 6.9 (5.34) < LOD < LOD .9) 12.924 (.24-3.28 (2.6) 11.00-19.55-20.8 (10.633-1.79-3.42 (3.710 (<LOD-1.47 (1.50) 7.69-10.32-12.00-13.80 (7.56) .7) 12.37 (5.54-4.82-14.566-1.15-10.7) 18.549-1.54) .95) 2.2) 13.71) 10.53-11.89-3.1) 4.855 (.02-14.34 (6.03) 2.92-5.0) 7.56) 7.40-5.82-14.6) 8.440 (<LOD-2.510-1.00) 8.68-4.7) 5.01-2.28 (4.37-5.533-1.02-2.818 (.53) 9.30) 2.23) 4.37-3. interval) .03 (2.78 (2.10 (3.88-15.3) 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 1.4) 13.29) * * .608-1.25) < LOD .27) < LOD 2.57-10.890 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (8.40 (3.94-23.04-6.84) 7.920 (.570-1.68) < LOD < LOD 3.960 (.5) 8.54-15.1) 4.83 (7.67) 1.03) 2.87 (3.75 (7.5) 7.34) * * .88) 2.37 (4.98 (3.66 (2.39 (2.500-1.42) 12.38 (1.75) 2.92-2.36) * * 1.90-8.66-15.1 (9.06-2.5) 11.31-14.61 (1.00 (4.45-5.74) 90th 7.3) 5.61-29.47 (3.560-1.932 (.74) 4.14 (3.1 (6.98) .98) .07 (.4) 4.S.94-10.8) 7.79-9.69 (4.80 (2.23 (4.6 (10.890 (<LOD-1.28 (5.57) 4.750 (<LOD-1.54-2.18 (.94-22.03-6.56-13.87-5.83) 8.41) Selected percentiles ( 95% confidence interval) Total * * 50th .37) 9.9 (9.88 (5.4) 4.98) 9.860 (.44 (2.3) 16.21-23.75) 14.9) 11.00-17.40-3.28) 10.780 (<LOD-1.0) 6.6) 9.54-11.40-28.80) 9.66-34.45-11.900 (.29 (2.2 (8.5) 7.76-4.95 (3.7) 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.67-19.80 (6.790 (.85) 2.1) 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. Fourth National Report on Human Exposure to Environmental Chemicals 121 . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2) 5.8) 12.93) 9.64-5.66 (5.19 (4.93-9. population from the National Health and Nutrition Examination Survey.9) 16.53 (6.00 (4.03 (7.10-13.5-16.34 (6.7 (9.05 (1.43) 2.47) 2.71-2.620-1.5-32.94 (4.7 (8.773-1.09 (.90-5.2) 95th 12.9 (9.81-5.2) 5.2) 9.61 (1.2) 7.35 (1.57 (4.67) 4.35) < LOD < LOD 3.02 (2.30 (1.5 (4.62) .84 (5.73 (1.31 (3.3) 12.05 (.40-12.82-26.62-5.09-11.41-12.82-6.13) 4.94 (2.4 (9.98-5.89) * * 1.3) 15.1-15.883 (.2 (10.40-14.26) * * .57 (6.6) 13.650-1.76) < LOD .2) 8.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.85 (6.1 (11.66 (1.77 (6.51-5.38) .56) 4.8) 8.88-10.2 (6.60) 2.52) 4.830-1.540-1.43 (3.9-28.61-13.

9) 16.0) 12.0-19.6) 14.580-2.0) 9.49-4.00 (. population from the National Health and Nutrition Examination Survey.3) 22.0-24.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.00) 8.20 (<LOD-2.88) 10.60 (5.7 (11.60 (2.0-24.46-28.59-3.6) 14.82) 8.7) 22.0 (13.1) 11.00-9.73) 7.27 (3.61 (3.80 (2.3) 14.4 (10.40 (2.61-32.22) 8.0 (9. 01-02.7-21.0) 13.90 (6.9-14.90-9.67-10.5.9 (12.5) 21.7) 15.60 (6.670 (<LOD-1.00-16.40 (2.6 (10.24 (2.80) 5.34-10.35) 4.37 (3.34 (6.0 (15.8-21.9) 95th 14.10 (. 0.63-14.1 (10.670 (<LOD-1.15-6.8) 8.90 (6.75 (3.50) 5.10 (<LOD-1.80) .80-6.0) 13.00) < LOD .90 (2.72) 2.27) 4.29-4.20-8.64) 10.41-5.7) 10.00-4.00) 3.0) 19.9 (7.3 (6.28 (7.0) 12.3 (12.27) .46-4.97-4.67) 3.66-13.0) 9.96) 3.00) 7.50) 3.6-19.95 (5.99 (3.25 (2.7-19.62-17.0 (9.650-1.51) < LOD 1.67) 4.18 (3.8-20.77-14.3) 20.90-15.20) .88) 3.17 (7.20) 3.0 (7.90) 8.70 (8.96) 90th 7.75 (2.53 (3. < LOD means less than the limit of detection.47-6.680 (<LOD-1.4 (14.11-6.50-4.9) 9.30) 3.1 (10.3 (9.84-4.90 (6.3 (9.9-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8-20.70-8.90 (2.5 (8.2 (7.37) 2.80 (2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .5-26.0) 18.0) 11.80 (5.31) 1.22 (6.6-41.4 (10.20) 3.8 (12.0) 7.39-13.0) 14.0-33.0) 14.0 (8.2) 14.95-9.58.06 (2.3) 10.30) 3.7) 16. which may vary for some chemicals by year and by individual sample.5 (9.31-7.740 (<LOD-1.90 (6.2 (9.0) 23.33-11.29) < LOD < LOD < LOD < LOD 3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.04 (3.0 (14.3 (11.01 (2.80-14.0-29. 122 Fourth National Report on Human Exposure to Environmental Chemicals .10-4.8) 9.31-12.00-4.7) 14.41) 3.6) 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 * * * 1.70-5.80-12.81-6.89 (2.790 (<LOD-1.30) < LOD < LOD 4.1-23.6) 11.18) * * * * * * * * 1.45 (3.10-15.5.0) 11.27 (7.70-9.90 (1. and 0.6 (10.670 (<LOD-1.70) 2.77-3.670 (<LOD-1.30) < LOD < LOD .50) .4-17.9) 10.10-10.35 (6.92-17.66) 4.20-4.10) 6.20-18. respectively.22-12.27) 9.00-18.30) 8.80) .89) 2.5 (8.0) 6.74) * * * * * 1.3) 8.60) < LOD < LOD 2.80-3. see Data Analysis section) for Survey years 99-00.90 (2.95 (2.12 (4.24-5.970 (<LOD-2.7 (10.15-2.50-5.8-17.16-1.0 (10.0 (10.22 (6.35-3.8) 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 1.42 (1.58 (1.5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .0 (5.70-9.14 (6.3 (7.8 (12.80-8.0) 12.39 (5.90-15.9-15.52 (6.90-31.40) < LOD < LOD 75th 2.90 (5.78) 5.90) 4.4) 11.00) 3.34-5.S.86-10.6) 18.92) 9.80-4.4) 7. and 03-04 are 0.910 (<LOD-2.70 (1.80-21.34-3.98-9.00-18.

1) 10.30) 7.6) 14.810 (<LOD-1.96-11.9 (9.85-17.590 (<LOD-.3-15.00 (7.6) 6.93-10.89-3.29 (2.7) 12.51-7.940) < LOD < LOD 1.12 (7.33-10.04) 9.78) 4.09-11.00) 2.54) 9.63 (2.91-9.63 (6.2-15.6) 471 576 310 664 821 715 814 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .3) 6.92) 3.5 (11.4-15.89 (3.72-4.29) 3.7 (10.5 (9.2) 12.6) 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 * * * .6) 95th 16.28) 6.34) < LOD < LOD < LOD < LOD 3.5-17.6 (13.25-9.3) 8.06 (<LOD-1.1 (13.77) 3.85-8.29 (5.8) 16.42) 8.06) .00 (<LOD-1.91) 3.2) 12.73 (5.00 (5.6 (13.15 (1.9-17.4-16.2 (9.74-19.760 (<LOD-1.21) * * * * * 1.0 (8.27) 1.93 (2.00 (<LOD-1.58 (4.1 (8.14 (2.0 (11.9 (9.4) 15.75-3.77 (2.92 (5.44-6.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.5 (10.1) 20.27) 5.0 (13.53-8.2) 15.21-21.3) 9.25 (4.0-19.01-5.2) 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.910 (<LOD-1.8) 14.00 (2.28-12.19) 3.87 (3.16 (3.2) 12.4-16.74-4.79-6.5) 13.2) 19.3-17.27-13.89-10.1) 13.97-4.50 (6.4 (11.0 (10.28 (1.7) 9.620 (<LOD-.15) < LOD < LOD 75th 2.86 (3.03 (2.78-10.55 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07 (5.71) < LOD < LOD 2.45) 6.38 (.950) .89 (2.86-3.93 (6.5 (8.07) 2.07-3.23-3.20-3.0-21.54 (7.5) 8.68) .45) 3.6 (12.7 (10.6 (10.5 (15.54-5.70-35.88-7.83 (7.03 (6.30) 8.3-17.0) 14.38) 1.27) * * * * * * * * 1.82-11.973 (.55) 16. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .780-1.7 (11.32) 2.67 (1.43 (2.55) .4) 9.77 (2.7-19.68-19.02-4.69-11.890-2.7) 14.52-3.2) 16.79-9.89-13.37) 3.7) 15.64-11.12) < LOD < LOD 4.34-18.6 (11.16-14.2) 8.78 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.11-3.51-10.68-4.47-9.4) 6.38 (1.09-11.2) 10.8 (8.3 (7.2-30.5) 10.6) 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 1.36 (2.18) 2.99 (4.89) 5.S.93 (<LOD-2.07) 2.6) 12.61 (2.05-3.6) 7.3-34.67 (7.81 (7.2 (9.920 (<LOD-1.8 (10.530-1.7-23.70-2.9-25.38-13. Fourth National Report on Human Exposure to Environmental Chemicals 123 .690 (.4) 7.96-10.37-5.94-14. population from the National Health and Nutrition Examination Survey.86) 9.71 (1.4-18.4) 16.9) 19.8) 11.3) 12.9) 16.6-19.5) 22.95) 90th 8.9 (9.80) 3.6 (11.94 (5.99) 2.89-3.6) 13.50-17.68-10.78 (4.75-3.39-17.42-19.3-21.00 (3.30) 2.00) 8.82-8.72) 4.11 (5.4) 7.30-5.95) 3.850 (<LOD-1.83 (6.4) 7.42) 7.7) 14.41 (7.97) < LOD .27) < LOD .59-3.33) 3.38 (2.32-8.29-2.1 (19.88 (1.95 (2.7 (8.03) 3.48 (2.

580-. 124 Fourth National Report on Human Exposure to Environmental Chemicals .70-7.960-1.730) .353-.57 (1.00) 1.79) .80) 3.80) 3.940) < LOD .14-1.00-2.50 (1.86 (1.73-5.50) 1.20 (2.820 (.10-1.75 (2.31-3.350-.690) .08 (2.94) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.720 (.17) 1.30 (.22 (1.453 (.96-3.47) 2.76-6.690 (.63 (1.83) .340-.570 (<LOD-.89) .16) 1.21) 3.592) * .500 (<LOD-.930) 1.455 (.34) 2.83 (2.09.549 (.49) .36-4.359-.64 (1.960) .25-1.39) 2.77 (1.11-3.740-.90) 2.440-.48 (2.160 (<LOD-.840 (.97 (2.690-1.98-3.47 (1.59-6.26) .260 (<LOD-.390-.27 (3.710) .550 (.01-1.46) 1.490 (<LOD-.00-4.587) * * .90) 2.820 (.42-2.54) .19-1.759) * .459 (.65 (2.690-.15) 2.80) 2.970) .91) 2.80 (2.570 (.20) 2.540 (.04) .30) 4.35) 1.16) 2.382-.620-1.390-.570-1.720-1.50 (1.20-2.710 (.20-1.570 (.22-8. 01-02.30 (.03) 1.94 (3.336-.13) .749 (.700) .27 (2.45-4.98 (2.90-4.880) < LOD .600-1.09 (.95-5.16-3.80) 5.700) .22-3.80 (1.74-5.59-2.449 (.05-3. and 03-04 are 0.280-.560-.98) .880) < LOD 75th .790 (.680-1.29) 1.46-3.49) 2.510 (.210 (<LOD-.60) 2.15) 2.740 (.400) .69-4.30-3.41 (2.00) 2.30) 4.08 (2.78) Sample size 1949 2519 1905 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .670) .750-1.18 (.780) .30-1.657) * * .50-2.70 (1.45 (1.600 (<LOD-.96-5.S.00 (1.592) * 50th .970) 1.10) 3.89-6.20-3.510 (<LOD-.650-.30 (.505 (.37-2.10) 1. which may vary for some chemicals by year and by individual sample.68-5. 0.750) 1.10) 1.467 (.78) . population from the National Health and Nutrition Examination Survey.960) 1.860) < LOD < LOD . respectively.32 (1.680-1.597) * .720-1.73 (1.810) .20 (1.61 (1.34) 2.30-3.94 (2.398-.32-1.570 (<LOD-.343 (.40 (1.20-2.32) 3.450 (<LOD-. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00.460-.31) 95th 2.60-4.76 (1.740-1.710 (.46 (1.38) 1.880 (.20) 3.80) 3.60) 3.585) * * .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.760 (.11-3.303-.83) 1.584) .01) .930-1.33-2.388-.77-2.23-3.57 (2.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.830 (. interval) Selected percentiles ( 95% confidence interval) Total * .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 * .48 (1.31-3.580-1.457 (.79) .01-3.60 (2.30) 2.50 (1.20) 1.980) 1.20 (1.2.73 (2.95) 2.90) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380-.22-3.90 (1.960) .41-5.201-.780 (.04) 1.950) 90th 1.949) .20) 2.910-1.75-2.88) 1.850) < LOD .10-1.1.425 (.910 (.54 (2.30 (1.618) * .380) .50 (1.20 (1.740 (.930) < LOD .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 * .10) 1.70 (1.95 (2.380-.550 (.29-2.910) 1.89) 1.50-2.58 (1.930 (.22-2.80) 2.70 (1.74) 3.46 (2.18 (1.70-2.990-1.86) 3. and 0.20) 1.570) * .45 (1.40 (1.20) 3.17) 1.590-.30) 1.600-.50 (1.83 (2.87-3.05-2.780 (.13) 2.55 (3.800 (.31) 2.45 (2.14 (1.17-4.350-.592-.26 (2.54-2.960 (.83) 2.240 (<LOD-.

92 (1.400-1.840) 1.97 (1.591 (.330-.42 (.71) .28 (1.550-1. Fourth National Report on Human Exposure to Environmental Chemicals 125 .460-1.940-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.05) 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 * .04-5.710 (.310 (<LOD-.65) 2.64 (2.61) 2.36) 3.740) < LOD 1.597) * .910) < LOD .08) 2.87 (2.300 (<LOD-.688) * .930-1.52) 3.91 (1.67 (1.04-1.509 (.58 (1.23) 2.82 (2.580) .550-.11-2.590-1.82) 2.18-2.47-4.70 (3.80) 2.43) 1.79 (1.71 (1.58) 3.66) .820) 1.02-3.950-2.645) .57 (3.790 (.310 (<LOD-.22) 1.72 (2.71) 2.440-1.72 (1.550-.20-7.43) 2.58-6.29-4.520-.710 (.73 (2.510-.30) 3.55 (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 * .43) 2.61-3.305 (.98) 1.67-3.33 (1.08-2.23 (.67) .22) 4.840) 1.448 (.89-3.22-3.88) .310-.393 (.57-2.38 (2.730) .270 (<LOD-.31-1.510 (.390) .72-4.318-.520 (.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.38 (1.22-3.62 (2.530 (.39) 2. interval) Selected percentiles ( 95% confidence interval) Total * .739) * .07) 1.69 (1.67) 1.560-.535 (.20) 1.32) 5.97) 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.630) * .23) 3.24) 4.870) .560-.17) 2.90) 2.05-2.444-.16) 1.75 (2.400) .32) 1.38-3.552 (.470 (<LOD-.250 (<LOD-.17) 2.580 (.03-1.52 (1.45 (2.02-3.60 (1.253-.84-6.05-4.76) 1.95) 1. population from the National Health and Nutrition Examination Survey.05) < LOD .680 (.470) .00 (3.380-1.32) 2.08 (.07) 1.42) .07-3.300-.92) 3.23) 1.580-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30-2.490 (.800) < LOD .870 (.42-6.740) .380) .840) .13 (1.75) 6.S.03-2.00-3.460) .830 (.47 (1.57-4.08-3.590 (.16-2.55-3.94) .77-3.60 (2.460 (.06) 4.540-.980-1.500-.08-3.23) 2.49-4.57 (1.00-1.412-.22 (2.89 (1.47 (1.700 (.14 (2.510 (.550) .61 (3.830) 90th 1.92-8.33) .62 (1.372 (.136-.50) 1.742) * * .447 (.08) 1.88 (1.08 (2.72) 1.06-2.45 (1.640 (.760) .920) .350) .78) 3.750 (.750 (.700 (.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 * .640 (.79) 1.69 (3.25-3.11 (.480-1.61-3.02-6.07-2.99) 2.66 (2.10) 2.485) * * .760) < LOD 75th .07) 1.850) 1.250 (<LOD-.70 (2.64 (2.16-1.53) .77-4.640 (.285-.81) 2.348-.335-.22) .75 (1.09) .05 (1.320-.42-8.720 (.390-1.590) * 50th .08-2.380-.270-.97) 1.49 (1.19 (1.280 (<LOD-.99) 1.44-2.453 (.08-3.720-1.700 (.270-.880) 1.39 (1.08-2.73-3.370-.820) .790) .97 (1.07) 5.17-2.84 (2.22-2.180 (<LOD-.990-1.234 (.710 (.08-3.560 (.403) .32-1.41 (.75-3.67 (1.900) 1.368) * .320-.07 (.32 (.670 (.04) 95th 2.800-1.330 (<LOD-.471-.77 (3.44) 2.230 (<LOD-.377-.63 (1.50 (1.60) 1.515) * * .480) .660-.11) 1.60) .690) < LOD < LOD .20-2.97) 2.34 (1.43 (1.

16) * 1.79 (2.2) 16.13 (1.41 (1. and 0.21 (1.40) < LOD 2.0 (40.1 (25.96) 5.10-13.18) 14.97) 6.13) 12.80) 90th 38.0-41.98 (1.2 (12.0) 3.90-8.61 (1.83 (1.53 (1.0) 20.10) .8-24.30-14.5-27.40-4.0 (25.0 (8.690-3.0-62.1 (10.57-2.23) 9.64-8.1-20.0-43.3 (14.1 (25.48-2.470 (<LOD-1.72 (1.59 (1.0) 32.65 (4.1-40.70) 5.46-6.77 (1.8) 39.70-17.0-41.20) 1.50 (2.81-3.1-46.91 (4.4 (19.50-5.88) 3.78) 9.88) 1.3 (23.8 (26. interval) 1.58) 16.0-260) 34.86 (1.0) 20.5-40.70-6.29-4.0) 3.0-110) 34.94 (1.3 (24.41-4.2) 31.0-39.57-2.0 (17.4.12) 1.2-62.71) 5.7 (12.76 (2.21 (3.83-2.52 (4.76 (2.71 (4.0 (20.1) 95th 48.3 (12.6-54.11 (4.2-80.1 (11.2 (19.0-230) 35.30) 11.4 (15.13 (1.2-33.05-3.45) 2.7-41.5-74.44-7.0) 4.9 (10.67 (1.50-17.1) 18.0-53.0-29.18) 6.20 (2.41) 1.36-2.29-9.48) 5.6 (26.41) 5.0-31.93-3.8) 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 1.6-27.0) 4.90) 11.70 (1.05) 1.59 (1.70 (1.0-39.0 (38.9-21.1) 38.0) 30.41) 1.0-92.8) 62.6 (15.0) 3.7-22.1) 38.2-27.10 (7.10 (1.10 (1.0 (38.0-110) 42.9 (19.02 (2.92-5.80-18.9 (23.29) 2.66-5.5) 30.9 (27.69) 2.0-58.00 (.7 (28.50-2.0) 16.11) 2.0) 16.9-51.23-2.0-69.90 (1.2-39.0) 33.46-2.8 (22.4-22. and 03-04 are 0.53) * 2.79-2.60 (2.20-4.9 (19. population from the National Health and Nutrition Examination Survey.45) 2.80-2.2-47.58-2.0 (26. respectively.9) 48.16) 2.09 (4.0 (21.26 (.0) 4.6 (11.0 (11.0 (19.35-6.70 (7.0) 15.0) 28.78 (1.10) 39.10 (1.8) 32.7) 20.8 (12.8 (12.3) 38.0 (8.50-7.18) 20.71-2.77) 38.4-76.0 (38.64-3.4 (10.6-45.42) 1.830-3.85) * 2.0) 5.75-14.0 (38.26) 75th 11.0) 42.83 (3.0) 13.660-2.3) 33.0-50.46 (.10-4. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0) 17.0) 15.1-47.610 (<LOD-1.7 (12.3) 28.0-53.04) 3.63-6.0) 18.0 (8.30) 4.0) 8.0 (24.1 (22.10 (1.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.00 (.50-20.86-3.27-6.8-21.00-24.53) 1.32 (2.06 (1.0 (38.1 (26.5) 69.6-22.9) 17.0 (32.7) 47.74-2.14) 5.830-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.54 (3.90 (1.6 (9.98) * 2.0) 28.1) 140 (46.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.82 (1.0-47.40) 50th 2.530-4.9) 38. < LOD means less than the limit of detection.49-2.3) 26.0-52.3 (12. which may vary for some chemicals by year and by individual sample.0) 19.17-2. 0.80) < LOD 1.0) 17.3) 31.0 (38.0) 45.25-3.21 (4.81-2.95 (5.83-2.12 (3.S. 01-02. see Data Analysis section) for Survey years 99-00.0 (20.0) 6.70 (.07-5.30 (.5-20.44) Selected percentiles ( 95% confidence interval) Total * 2.44) 3.1-25.92) * 2.79 (1.80) 1.04 (<LOD-2.0 (38.0) 31.5 (24.04-8.0) 3.87-7.0-62.0 (7.61-2.5-45.3 (10.19-2.85 (1.0-58.0-41.5.70) 1.54 (1.0 (13.4) 38.9) 18.4) 19.43-7.0-49.2-26.40-16.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.23-2.0 (6.8) 41. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.600-2.06) * 2.99 (2.48-2.44) 2.18.80) .60) < LOD 1.19) 2.05) * 2.0 (33.31-6.2-27.6) 52.0) 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 2.33 (5.70) 1.40) < LOD 1.1-19.53) 40.0 (37.

S.43) * 2.9) 54.59-15.03-2.38-5.19) 5. Fourth National Report on Human Exposure to Environmental Chemicals 127 .72) 2.1-22.1) 36.91-2.50-5.20) Selected percentiles ( 95% confidence interval) Total * 1.07-2.1) 13.16 (1.5-36.60) 4.6) 3.68 (1.22-3.6) 23.90 (.97 (1.0) 25.68) 47.36-13.79 (2.86) * 2.870-3.19-6.5 (13.88 (1.0 (25.48) 1.2-47. population from the National Health and Nutrition Examination Survey.08 (1.60 (.7) 15.6-32.8) 23.1) 17.71 (1.9-37.52 (1.38 (3.7-38.7 (11.95) 90th 32.0) 10.0) 47.0-118) 29.9 (10.22 (.70-4.7) 95th 51.70 (1.53) 1.39 (1.52-4.0 (14.6) 7.79-17.61 (1.57 (6.02) * 1.33-5.46-22.4 (25.6-38.8-43.27 (6.6) 19.95-16.888-1.64 (1.9-52.9 (7.6 (24.1 (25.46-6.2-38.1 (39.4-34.5) 70.94) 1.0 (23.06) 1.9 (19.19-14.6-51.40-4.76-2.27) 50th 2.41 (2.4 (21.3) 28.38-1.28 (1.17) 2.18-1.8) 3.5 (17.870-3.2 (9.56 (2.930 (<LOD-1.94) 19.88 (1.75 (1.36 (4.1-63.75 (1.5 (41.9-18.61-2.8) 15.4-71.5 (8.88 (4.12) 3.11-2.2) 13.2) 33.82) 1.5 (34.1) 15.2) 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.33) 2.0-40.1) 25.1 (50.66 (1.7-109) 22.6 (11.7 (10.0) 3.2) 36.3 (8.8-37.23-1.83 (.58-17.35) 1.3 (20.30) 28.3 (10.899-2.2-34.36) 10.2) 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 2.3-19.06-1.4) 3.46-5.0 (17.9) 24.18) 3.0) 48.57) 4.3-42.4) 12.3-22.69-18.8) 31.88 (4.7) 61.01 (.62) 4.7) 26.8-26.2 (16.4 (25.5-43.26-4.62 (2.5) 27.43-12.4-39.4 (19.2 (22.4 (9.59-2.80-8.45-1.0 (32.96-16.5-97.20-5.46) 1.12 (1.67 (1.7) 66.9-41.1) 27.7-43.1 (34. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.11) < LOD 1.2 (21.1) 13.3 (9.890-4.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6 (27. interval) 1.2) 13.07) 9.0 (19.09 (5.2 (15.4-67.8-45.67-16.0 (23.7) 23.27-3.14 (.7) 34.54-15.02 (.40-7.9) 3.8 (7.16-2.7-37.71-2.14-8.51) < LOD 1.7-19.9-36.9-95.5-190) 30.9 (26.86) * 3.2) 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 1.750 (<LOD-1.00-16.45 (1.27) 10.1) 25.5 (15.61-22.54-2.58-2.80 (1.18) * 2.2-70.40 (2.22-2.9 (39.26-2.9) 3.50 (2.33) < LOD 1.17-3.84-13.71) 8.4) 12.95 (2.4-21.2) 4.5 (15.0) 13.83) .16 (1.96) 2.6) 112 (40.9) 12.25-3.3) 13.51) .670-1.9 (13.29-5.37-2.4 (5.00) 1.8) 32.08) 1.75-6.63-5.0) 30.00 (4.40 (5.860 (<LOD-1.9) 24.1 (12.21 (4.31) 2.4) 14.0) 952 1187 945 996 1330 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.7-20.16 (1.03) 1.37 (1.5 (6.6) 11.7 (18.06) 75th 9.48 (4.44) 9.0 (39.82 (2.7 (24.1 (33.95-16.4 (12.38) 5.91 (6.680-4.0-71.1) 52.2-28.69-5.7 (18.7) 30.93) 5.24 (1.6-49.94-20.99-4.3-27.2 (8.3 (10.870-3.2) 41.07-2.19) 5.59-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.56) 1.75) * 1.0 (6.4 (11.66 (1.67 (1.00) 6.32 (3.47-17.28) 1.7-47.8) 11.8-34.35) .23) 37.1) 27.47 (1.23) < LOD 2.22 (2.6 (7.66) 8.34) * 1.19 (1.0-70.35 (2.02) 1.55 (2.32-3.15 (.6) 3.43-2.06) 1.1-60.47 (3.67-3.33) 1.

870 (.990 (.210 (.260 (.540) .230-.560 (.430 (.13) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.280) < LOD < LOD < LOD < LOD .110-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.870 (. < LOD means less than the limit of detection.690-1. and 03-04 are 0.430-.380-.390) < LOD < LOD .830 (.320-.870 (.210 (.550) .730) .60) 1.130) .410-1.460 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .10) .099-.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.450 (.290 (<LOD-.190 (.900 (.090 (<LOD-.310 (.15) .870 (.840) .300-1.410-.990) . 0.460-.820 (.360-.230) .320 (.380-.130 (. population from the National Health and Nutrition Examination Survey.03) .650) .850) < LOD .10) .380-.990) .117 (.050-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.720 (.350) < LOD < LOD < LOD < LOD .090 (<LOD-.610-.36) .700-1.140) . 128 Fourth National Report on Human Exposure to Environmental Chemicals .610 (.140-.290) < LOD < LOD < LOD < LOD 90th .830 (.870 (.650-1.840) .240 (<LOD-.640) .10 (.310) < LOD < LOD < LOD < LOD .820 (.780) < LOD 1.470 (.160-.140-.870) < LOD .220 (.660 (.700-1.570) .150) .420-.20) .940 (.540 (<LOD-.770) < LOD 95th .630 (.42) .200) < LOD < LOD .300-.130-.630 (.084-.830) .680-1.740) < LOD .080 (<LOD-.490 (.1.05.120-.120 (<LOD-.30) .530-.560 (.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 * * * * * * .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 * * * * * * * * * .12 (.310) < LOD < LOD < LOD < LOD .350) .32) .640 (.162) * * * * * .680-1.10) .370-.130-.080 (<LOD-.640) .830) < LOD .310-.100 (.450 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .S.400-.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 .540) .160) .42) .700-1. 01-02.650-1.850 (.720) .190 (.140-.090 (<LOD-.650 (.220 (<LOD-.700-1.330-.310 (.410-.650) .770 (.090 (<LOD-.680) .620 (.450 (.090 (<LOD-.58) .1.610 (. respectively.470-1.30) .40) .00) .600 (.860-1.190 (.150 (<LOD-.410) < LOD < LOD < LOD < LOD .090 (<LOD-.680 (.390 (.860) .610-1.170-. which may vary for some chemicals by year and by individual sample.640-1.360-.30) .720-1.850 (. and 0.130) .180) .760) < LOD .120-.171) * * .270 (.730-.160) .370-.130-.440-1.930 (.510-1. see Data Analysis section) for Survey years 99-00.290) < LOD < LOD < LOD < LOD .

230-.500-1.720 (.450) .38) 1.330-.570-.410 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.070 (<LOD-.320 (<LOD-.03 (.490-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.24 (.02-1.140-.650) < LOD .170 (.116 (.66) 1.300-.330 (.940) .100-. Fourth National Report on Human Exposure to Environmental Chemicals 129 .161) * * .990) .670-1.760) .110-.940) .190 (.410-.210 (.290) < LOD < LOD < LOD < LOD 90th .580-1.110) .140-.110) .060-.310) < LOD < LOD < LOD < LOD .360-.00) < LOD .780) < LOD 1.200 (.190 (.370 (<LOD-.300 (.62) 1.740) < LOD 1.170 (.410) < LOD < LOD .570 (.78) .140-.440 (.250-.800-1.390-.880-1.58) 1.410-.580) .540 (.03 (.580) < LOD .860 (.080) .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 .120) .090 (.410 (.860-2.270 (.600) .270) < LOD < LOD < LOD < LOD .580 (.550 (.730) .810 (.220) < LOD < LOD < LOD < LOD .01 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .230 (<LOD-.67) .20) 1.360 (.280) < LOD < LOD < LOD < LOD .640-1.400 (<LOD-.330 (.180-.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 * * * * * * .470 (<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.700 (.970) .510-.240-.110) .29 (.390-.14) 1.650-1.220 (.410) .170) < LOD < LOD .190-.440-1.780 (.140-.360-.150-.330-.700-1.230) < LOD < LOD < LOD < LOD .110) .500) .260) .03 (.36 (1.070 (<LOD-.057-.080 (.860 (.09) .070 (<LOD-.670 (.330-.100 (<LOD-.540) .050 (<LOD-.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 * * * * * * * * * . population from the National Health and Nutrition Examination Survey.730) .550 (.460 (.380-1.12) < LOD .140) .02) .710-1.380-.070 (<LOD-.084-.380 (.700 (.700) .S.660-1.380-.740 (.890 (.380-.360) < LOD < LOD < LOD < LOD .86) .540 (.340-.19 (.960) .140-.720 (.24) .880 (.86) .990) .260-.500 (<LOD-.200 (.560 (.670 (.080 (<LOD-.450 (.120) .610-1.730 (.400) .850 (.300-.570-1.750) < LOD 95th .43) .870) .520-.60) .600-1.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .580 (.03) .111) * * * * * .310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.090 (<LOD-.730) .

12-1.67 (1.30) .83) 2.11) 13.24-7. and 0.20) < LOD < LOD < LOD < LOD < LOD 1.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.800-4.86) 4.32 (1.900 (.0-40.87) 12.50) 2.51 (2.400-1.0 (13.30-7.53-7.40) 2.90-28.0) 2.870) < LOD < LOD .6) 5.36-3.960 (.67) .05-3.0) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.35-10.600 (.00-17.99 (1.53) 20.30) 95th 19.425-1.0) 5.52 (1. < LOD means less than the limit of detection.0) 2.90 (1.40 (1.40-8.48 (2.46 (1.800) 90th 13.30 (.90) .40-7.30 (1.07 (3.33 (4.250 (<LOD-.0) 4.20-17.610 (.29-10.42) 2.0) 5.0 (5.0) 2.90-9.68) 2.07 (3.63) 32.750-1.0) 5.15) 19.16) 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 .18) 1.55-4.45 (2.90-37. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67 (2.0-38.94 (1.691 (.0 (17.90-20.14-5.0) 5.0 (5.52) 5.13 (3.350-.00 (1.07-3.51-8.750-2.30 (2.83-3.30-3.080-1.90) .480-.00) .23-6.35) 11.40-4.30 (1.190-1.20 (1.94-8.10-3.74) 5.620-1.49) 17.97) 20.3) 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 * * * * * * * * * .510-.110 (<LOD-.14) 2.62) 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 * * * * * * .39 (2.47 (3.07-3.40-20.32-9.55-8. and 03-04 are 0.0 (6.70-17.97) 20.0 (17.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.99) 19.00 (.00) 1.28) 1.0-39.840-3.830 (. 01-02.880) 5.53 (2.11) .0) 4.36-3.83-3.85-3.42) .28) .63 (3.87) 5.0 (7.49 (1.10 (3.88-3.82-4.0-38.0) 7.720) 2.59-5.70-3.21-3.0) 2.640 (.0 (3.03 (.640 (.74 (3.60) .360-1.840 (<LOD-1.38-3.0) 2.330 (<LOD-1.40 (1.70-30.15) 14. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.20-4.11 (1.0-44.70-50.0 (4.770 (<LOD-1.890 (.35) 5.0) 2.1.740 (.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10 (3.60) 1.580 (.70) 2.380-.43-4.12) * * * * * * * * .0) 3. population from the National Health and Nutrition Examination Survey.S. 130 Fourth National Report on Human Exposure to Environmental Chemicals .94-3.28-9.0 (5.76 (1.10-9.31-10. which may vary for some chemicals by year and by individual sample.96 (1.770) 2.800) 17.61 (1.0-38.370-.48) 13.910) 2.37) .260-.0 (5.0 (17.21) 3. respectively.90 (2.1.50) .30-6.70-7.07 (1.850) 16.0 (17.99) 11.05 (3. see Data Analysis section) for Survey years 99-00.690 (.20 (1.14) .01) 5.39) .0 (17.49 (1.0) 4. 0.0) 4.00) .20-4.26 (2.590 (.350-.30 (1.90) .80 (4.0 (5.170-1.610) < LOD < LOD < LOD < LOD < LOD 2.52 (1.0-40.0 (4.08.840 (.730 (.00-17.0 (16.960 (<LOD-1.65) 1.10-3.40) 1.05 (2.62-8.66) 4.07) 1.210-1.10 (.31) .

700) < LOD < LOD < LOD < LOD < LOD 1.590) 2.850-3.560 (.03) 2.29 (4.11-5.23-7.48 (4.5 (8.940-4.580 (.770) .81-17.370 (.49-2.88-3.21-3.320-1.69-7.740-1.970-3.390-.53) .360 (.340-.57) 8.27 (2.67-6.37) 4.800-2.01 (1. Fourth National Report on Human Exposure to Environmental Chemicals 131 .30 (4.10 (2.66-47.14-6.56) 2.1) 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.31) .4 (4.04-16.840-3.580-1.41) 18.33-3.57-40.77 (.860-2.59 (1.7 (6.240-.02 (.31) .0 (9.8 (20.48-7.32-6.50) .91-4.650) 90th 10.340 (.44) .430 (<LOD-.1 (7.2-38.580) 1.32) 9. population from the National Health and Nutrition Examination Survey.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.7) 4.14 (1.62 (1.91) 2.5) 2.25-38.270 (<LOD-.89 (2.1 (5.18) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.700) 6.250 (<LOD-.5 (9.430) 1.190-1.02) .56 (1.75) 5.86) .60 (1.260-.96-25.05) .02-4.4-34.8) 1.40-12.8) 7.9) 5.82-11.340-.790) 11.8) 2.690-5.370) < LOD < LOD < LOD < LOD < LOD 1.11) .12 (4.5-40.150 (<LOD-.600 (<LOD-1.48-42. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.51-4.88) 17.1) 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 * * * * * * .71 (2.33-4.90-6.31-18.08) .96-8.22) 2.50) 11.61) 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 .960 (.33 (3.580) 16.660) < LOD < LOD .0) 4.650 (.710 (<LOD-1.88 (.57 (.12-4.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.67) 2.44-11.47-10.9) 6.96) 2.43) .10-3.8) 7.45 (1.85-3.17) 5.29-4.47) 5.330-1.71 (.17 (1.1) 2.28-6.67) 1.83 (4.35 (.670 (.64-4.40-2.00) .820 (.06 (.310-.270-.64) 30.3) 2.9 (11.500 (.7) 5.8) 4.830-3.540 (.57) 1.55) 21.84) 9.25 (1.5) 7.50 (2.86 (3.790 (.73 (4.0 (4.748 (.47) .50 (4.09-3.6) 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 * * * * * * * * * .340-.8) 2.40 (.52 (.25-9.02 (1.07-21.7) 6.620-3.65 (2.22-27.33-5.890 (.88 (2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.630-1.80) 3.47-10.830 (.18) 95th 21.07 (2.56) .97) .38 (2.55) 21.10) 2.4) 2.5 (11.80 (.85 (1.92 (2.7 (12.79 (.820) .15) 9.69) 2.40) 1.00-19.370-1.2 (8.3) 3.53) 27.S.39) 20.31-7.51-44.260-.24) 3.780-4.930) .474-1.03) 16.04 (1.8-33.5) 2.74 (2.730-3.540-1.13 (2.470 (.7) 3.450 (.98 (4.33 (1.55 (3.18) * * * * * * * * .36 (.67 (2.83-11.62-17.41 (4.

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Lancet 1995. National Research Council (NRC).php?record_id=2126&page=1. Robson MG. Tumino R. Buccafusco JJ. Bull Environ Contam Toxicol 1994. Lewis JA. Terry AV Jr.332(1-3):71-80. Occup Environ Med 1995.edu/ openbook. Burcar PJ.68(3):209-227 Maizlish N.12(2):153-172. Jenkins B. Smit LA. low-level organophosphate exposure on delayed recall. Claypoole K. Arch Environ Health 1988. May.nap. Occup Environ Med 2001. Lambert WE. Weisskopf C. Chrislip D. Daniell WE. et al. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Caltabiano LM. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Lasarev M. Russo J. Muniz J. metabolite clearance. gov/oppbead1/pestsales/01pestsales/market_estimates2001. S. Neurotoxicology 2005. Narang A.114(5):691-696. Lu C.S. National Academy of Sciences. Weerasekera G. Berry H. Steenland K.24(1):18-29.30(2):98-103.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. discrimination. A behavioral evaluation of pest control workers with short-term. Spurgeon A. Environmental Protection Agency (U. Effects of chronic. McConnell R. Kidd M.52(2):190-195.43(1):38-45. Vitayavirasak B. Available at URL: http://www. Pedersen L. Barr DB. Lasarev M. Aprea C. Muniz J.2000 and 2001 market estimates. Gladstone EA. Heaton RK. Lancet. Chronic neurological sequelae to organophosphate pesticide poisoning. Nell V. et al. Seiber J. 1/12/09 Peiris-John RJ. Scherer J. Irish RM. Ruberu DK. 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. Keifer M. Pesticides in the Diets of Infants and Children. Effects of long-term organophosphate exposures on neurological symptoms. Neurotoxicol Teratol 1998. Saieva C. Santana J. Hore P.345(8958):11351139. J Occup Environ Med 2002. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides.pdf. Rothlein J. Calvert IA. Arch Environ Health 1975. Stark A. U. Eskenazi B. Stokes L. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Phillips J. Pesticide industry sales and usage . Scand J Work Environ Health 1998. Bravo R. van der Hoek W. Dinoff TM. Rosenstock L. et al. Wickremasinghe AR. Buchanan D. EPA. Schenker M. Keefe TJ. 1991. et al. Washington (DC). Hansen S. Salvini S. 4/7/09 Young JG. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Beach J. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers.113(4):504-508.20(2):115-22. Malathion deposition. Takamiya K. Prendergast MA. Am J Ind Med 1987.58(11):702710. Arch Environ Contam Toxicol 2000.52(10):648-653. Samuels S.338(8761):223-227. et al. J Toxicol Environ Health A 2005. Masala G. low-level exposure to the organophosphate diazinon. 2004. Rohlman D. Savage EP. and spatial learning in monkeys and rats. Petchuay C.S. Sci Total Environ 2004. 1993 [online].38(4):546-563. Jamal GA. Fourth National Report on Human Exposure to Environmental Chemicals 133 . McCauley L. Levy LS. Thompson ML. Frasca G.epa. Ames RG. Bradman A. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa).12(2):134-141. and cholinesterase status of date dusters and harvesters in California. Neurotoxicity among pesticide applicators exposed to organophosphates. EPA). Am J Public Health 1994. Pilkington A. Visuthismajarn P. O’Malley M. London L. Environ Health Perspect 2006. Environ Health Perspect 2005.44(4):352-357.26(2):199-209. Available at URL: http://books. Myers JE. Office of Prevention Pesticides and Toxic Substances. Int J Occup Environ Health 2006. Gillham R. The Pesticide Health Effects Study Group. Mounce LM. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Rodnitzky RL. Washington (DC): U. Rothlein J. vibration sense and tremor among South African farm workers. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Marshall E. Johnson C. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Stephens R.84(5):731-736.

5. For example.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.” 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) 3.6-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 . see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. In addition to reflecting exposure to the parent insecticide. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides. malathion is metabolized to malathion dicarboxylic acid. For general information about the organophosphorus class of insecticides. parathion and methyl parathion are metabolized to para-nitrophenol. the level may reflect exposure to the environmental degradation products of these pesticides.

4 (10. USGS.90 (1.00) 1.S.3 (11..52-12.5. air.39) 4. 2007).26) 7.20-14. staying bound to soil particles.40 (5.90-7. and is infrequently detected in ground water (IPCS.39-2.32) 2.0 (13.7) 9.19-3.01) 1.67 (2.0) 9.90-4.9) 697 660 521 701 602 947 Limit of detection (LOD.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.70 (1.40-26.90 (1.31-2.09 (3.4 and 0.40 (5. For instance.02 (7.50-8.70-11. interval) 1.87-6.71 (6.60-2.81-2.30-5.50-5.5.71 (1.50-2.92 (1.95) 7.31-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.10 (3.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.77 (1.00-8.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.30) 5.0) 10. 1999.8) 10.89 (2.22) 2.21) 3.0) 12. and dust.0 (7.20) 10.77-15.0 (9.24-1.51 (1.35) 2.0) 12.29) 90th 7.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.4.66-4.67 (2.8-15.S.40) 9. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low. 5598-13-0 General Information The chemical 3.3 (10.51) 1.70 (1.88 (1.64) 3.9 (9.38 (3.80-8.61) 75th 3.52-2.13-3.EPA.1) 5.90 (3.60-4.10 (4.10 (1.3 (8.47-13. applied to structures to kill termites.0) 7.30 (2.24-3.60-3.90 (6.55-5.53 (1.50 (2.4-15.60-3.19 (1.96) 3.30 (2.10 (5.74-9.80) 4.7) 13.68-2.0 (7.91) 16.20-11.70-15.37 (4.20 (4.91 (1.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.90 (2.05) 1.EPA.37 (1.67 (1. and sprayed to kill mosquitoes.09 (2.40-10.30-2. 2005).68 (7.25) 3.28-3.0 (7.51-2.0 (10.90) 7.36 (4.72) 2.90-2.22 (1.47) 1.0) 18.10-17.63 (1.44-2.40-13.7) 8. 2002).30-1. 2921-88-2 Chlorpyrifos-methyl CAS No.84) 1.10) 2.9 (7.50-4. After 2001.20-4.9 (10. Estimated intakes from diet and water have not exceeded recommended intake limits.95 (4. in 142 urban homes and preschools in North Carolina.0) 10. dermal.40-2.0) 14.20 (2.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.27 (7.0) 12.57 (2. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.62-2. It also has been applied directly on animals to kill mites.40) 2.76 (1.50 (2.29-1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.98-15.97) 2.04-10.0) 8. Chlorpyrifos is Urinary 3.63 (8. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.60 (4.00-24.0) 11.80 (1.20-16.50 (2.70-16.00) 2.8) 9. and on plants for days to several weeks. Survey Geometric mean (95% conf.30-9.0) 12.37) 5.44-5.3) 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. Approximately 21-24 million pounds per year were used domestically from 1987-1998.47-11.77-6.94 (4.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.86) 4. Fourth National Report on Human Exposure to Environmental Chemicals 135 .80) 12.0) 6.20) 2.80) 2.25) 1.80 (7.1-16.00) 3.2 (10.30) 4.16) 2.61-7. population from the National Health and Nutrition Examination Survey.5-24.44 (3.20) 4.76 (1.70-5.10) 6.6) 7.80-10. Exposure can also result from contact with contaminated surfaces.S.13 (1.17 (1.78 (7.50-2.59-2.50 (1.30 (4.50 (1.7-23.02) 1. although some tolerances for specific food crops have been reduced in the past to avoid exceeding recommended intake limits for total dietary intake in special groups (U.50-14.47-9.99-4.72-4.83) 1.71 (2.32-1.0) 12.9) 11.0) 8.63 (2.70-17.74 (1.43-2.30-11.30-12. and inhalation routes.61 (1.47 (4.0 (7.5 (8.02 (1.59) 2.4 (8.80) 1.20-3.5) 7.90) 3. chlorpyrifos was no longer registered for indoor residential uses in the United States.97-7.3) 8.9-18. The general population may be exposed to chlorpyrifos via oral.66-15.4 (9.60) 5. pre.04-10.79-2.03) 1.46-2.90-8. Approximately 80. 2002).20-2.20) 2.60 (5.40 (6. It has low leachability.0-28.35) 1.77) 1.0) 10.60 (2.45 (1.15 (1.05-5.28) 2.89-2.43-2.97) 4.30) 4. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.000 pounds are used per year.0 (7.70) 1.0) 15.34) 1.97) 7.50-4. but can be detected in streams receiving runoff from application sites.97) 2.and post-construction structural applications for termite control were to be phased out by 2005 (U.

63 (4. Ricceri et al.02) 7. 1984).59) 3.01) 1.89) 4.44-6.11) 7.30-4.21-6.5) 5.98 (6.58 (4.S.32) 1.83-11.19) 6..3) 9. 2006.37 (1. interval) 1.940-1.91) 10.39-1.6-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. Thus.4) 4.22 (4.16) 6. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.24-24.91) 2.19-1.57) 9.00-8.0) 6.73 (1.50 (4.76 (3.06 (5.05-3.66 (1.22-6.65-15.0) 16.00) 1.09-3.85 (2.80-11.93 (1.93 (2.20 (2.47 (1.57-2.35) 1.91) 1.25-12.83) 1.07) 5. cholinergic effects.62-7.36) 1.91 (4.25-11.45-1.09 (1.97) 3.92-2.33-7.09-2. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.1 (7.80-4.EPA.86 (1. Betancourt et al.42 (6.91) 1. Slotkin et al.20-1.06 (1. Urinary 3.69 (1. population from the National Health and Nutrition Examination Survey.56 (4.27-1.12) 1.58-5.97-3. vomiting.43-10.53-5.00-13.86 (1.31-1. Howard et al.44 (5.58 (1.82 (3.28) 2.44 (5.45 (1.03) 1.14-8.42-2.21-1.49 (1. Based on animal data and human cholinesterase monitoring during occupational exposure. TCPy is more persistent in the environment than chlorpyrifos itself (U.90-9.07) 1. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.1-21.47-2.39) 6.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1. resulting in excess acetylcholine at nerve terminals. weakness. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure. TCPy can also occur in the environment from the breakdown of the parent compounds. 2006.64-2.28) 2.93 (4.91-4.43 (4. Metabolic hydrolysis leads to the formation of TCPy. 2005.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.01) 3.82 (2.94-14. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. In pesticide applicators..24 (1.3) 8.41 (1.7) 7.72-2.17-4.97 (2.57) 2.35-1.55 (4.23) 14.33 (5.3) 8.59-2.48 (1.08) 6.09-1. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.51 (1.55 (1.96) 3.95 (1. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.88-8.54 (2.57-2.29 (3.05) 3.22 (6.33 (.24-5.62) 1. 2006b).24) 75th 2.75 (1.71 (1. 2005. and producing acute symptoms such as nausea. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).85-4.58) 1.72) 1.88 (1.3) 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 1.12-1.11 (2.40) 1. paralysis..62) 90th 5. and other metabolites..47 (5.2 (7.95 (3.34-1..38) 3.49-2.1-38.19-2.48 (2.39 (2.66) 1.63 (5.64 (1.06-4.26-14. Roy et al.02 (5.44 (1.01) 99-00 01-02 99-00 01-02 99-00 01-02 3..55) 1.75) 6.56) 2.53 (2.93) 5.30-1.99-8.S.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.98 (7.42 (5. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.31) 1.6) 9.24-1.60-3.83-2.85) 1.80) 3.9 (12. 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.63-2. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.5 (6.24) 5.47 (1.86 (3.05-4.49-2. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.11 (2.88-9.15 (4.46 (2.5.72) 2.85 (3.92 (1.82-4.23-1.01) 3. 2002).79-13.44 (1. and seizures..77) 1.33 (1.99) 1..91-13. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.58 (1.24-4.71) 3.33) 2. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.58) 5.25-1.0) 10.56 (1.19) 3.88-8.68) 6.11-9..88 (1.97) 3.56-2.52 (5.82) 8.14) 1.70-4.66-11. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.85) 4.92) 3.65-11.74) 1.12-3.46 (1. 2006a.88) 6.0) 12.97 (3. neurotransmission.2) 6.54) 5.84-6.91 (3.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .81) 2.81 (3.60 (1.05-8.80-6.94-12.76 (2.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion. Survey Geometric mean (95% conf.22) 1.49-2. Once absorbed.31-4.1 (10.3 (7.05-1.87-3.93) 2.27-7.8) 9. 2005.64-7.00 (7.6) 10.16 (4.39 (4.44 (6.35) 2.68) 1.56) 5. 2000).78 (1.88-10.17-4.

Freeman NC. Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP.63(3):218220. Levels of TCPy in the U.. MacIntosh et al. Carr RL. Haidar S.e.. Fourth National Report on Human Exposure to Environmental Chemicals 137 . In Iowa farm families using several different pesticides. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Burgess SC. but levels were roughly four to six times higher than the geometric means in the U. Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al.S. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al. Biomonitoring Information Urinary TCPy levels reflect recent exposure. 2000). 1992. Barisano A. Eberly LE. 2005. Environ Health Perspect 2005.S.Organophosphorus Insecticides: Specific Metabolites 2004. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. U. 2003.. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. Garabrant D. Barr DB. Following crack-and-crevice application of chlorpyrifos in their homes.. 2001). 2001) and Italy (Aprea et al. In a probability-based sample of 102 Minnesota children aged 3-13 years. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al. Curwin et al. 2005).S. 2005). Toxicol Sci 2006..gov/toxpro2. Slotkin TA. 2004). 2004). Occup Environ Med 2006. 2005). (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. CDC.5. Giordani B. representative subsample of NHANES 19992000 (CDC. Lioy PJ. the weighted population mean of TCPy measurements was approximately three times higher (Adgate. 2005)...Reference values of urinary 3. Whyatt et al.EPA.82(2):305-312. Chlorpyrifos exposure and biological monitoring among manufacturing workers. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al.S. Aprea C. Lotti A. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. 2005). Clayton CA.S. but not chlorpyrifos. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC. Albers JW. 2005.109(6):583-590. et al. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. environmental levels) and health effects is available from ATSDR at: http://www. Perera et al. urinary TCPy levels in children were reported not to have increased (Hore et al. 2005.. Koch et al. Additional information about external exposure (i. et al. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Betancourt AM. Magnaghi S.. Of 482 pregnant women living in an agricultural community. subsamples of NHANES 1999-2000 and 2001-2002 (CDC.epa. Environ Health Perspect 2001. Burns CJ. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect. Meyer A.113(8):1027-1031.. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al.92(2):500-506. the geometric mean urinary TCPy levels were similar in parents and children. 2005).atsdr. 2007). Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. Betta A. population (CDC.. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity.. 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. In Minnesota and South Carolina farmers who used chlorpyrifos. Seidler FJ.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). 2002). 2006). 1999).cdc. References Adgate JL.. et al.. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain.. J AOAC Int 1999. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al. Catenacci G.html and from U. Aldridge JE.. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Berent S.gov/pesticides/. EPA at: http://www.

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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. Bruun D. Sanderson WT.htm. Hill RH Jr. Ryan PB. Tate CA. Environ Health Perspect 2005. J Expo Anal Environ Epidemiol 2005. Ryde IT. Chlorpyrifos. Baker BA. Bradman A. Urinary pesticide concentrations among children.112(10):1116-1124. Toxicol Sci 2006. A longitudinal investigation of selected pesticide metabolites in urine. Howell RJ. National Toxicology Program (NTP). Exposures of preschool children to chlorpyrifos and its degradation product 3. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application.113(2):211-219. Chapman P.114(10):1542-1546. Alexander BH.114(2):260-263. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Brain Res Dev Brain Res 2005. mothers and fathers living in farm and non-farm households in Iowa. Venerosi A. Angerer J. Pesticide residues in urine of adults living in the United States: reference range concentrations.15(3):271-281. Freshour NL.5.93(1):105-113. gov/ntpweb/index.inchem.

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

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

560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.380 (<LOD-. Survey Geometric mean (95% conf.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.670 (<LOD-1. < LOD means less than the limit of detection. 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 .S.2.210) < 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 . population from the National Health and Nutrition Examination Survey.200 (<LOD-.200 (<LOD-. which may vary for some chemicals by year and by individual sample.270) < LOD 659 701 920 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.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 . 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. see Data Analysis section) for Survey year 01-02 is 0. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 141 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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.

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

aerial. diazinon was widely used in residential and garden application. in some pest strips.2 and 0. in the past.45 (<LOD-3. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. an organophosphorus insecticide that is used to control insects on nuts. Prior to 2000. Inhalational and dermal routes of exposure can be significant for pesticide applicators.S. Once absorbed. Fourth National Report on Human Exposure to Environmental Chemicals 143 . 2004). diazinon cannot be sold for residential use. 2007). about 13 million pounds of diazinon were used annually on agricultural sites in the United States. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. USGS. diazinon produced wild bird kills before use restrictions were in place. 2004).S. Most granular formulations. and forage crops. fruits. Diazinon is not well-absorbed through the skin. since 2004.S. and particularly when it was ingested in granular form.49 (<LOD-2. but these uses have been phased out. population from the National Health and Nutrition Examination Survey. 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. Estimated intakes from diet and water do not exceed recommended intake limits (U. 1998). It is toxic to birds.7. 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. Before these restrictions. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. but is rapidly absorbed orally (IPCS. seed and foliar applications are planned to be phased out (U.11) < LOD < LOD < LOD < LOD 454 580 632 829 756 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 894 1191 948 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. 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. It is also used for cattle ear tag applications to control flies and ticks and. vegetable. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. 1998. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection. and other metabolites. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. see Data Analysis section) for Survey years 99-00 and 01-02 are 7.EPA. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No.EPA.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD.

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

Brunet RC.114(2):260-263. Kruse RL.134(1-3):105-113. Carrier G. Toepel K. In 54 Canadian greenhouse workers.epa.. Noisel N. Barr DB. U.org/documents/ehc/ehc/ehc198.pdf. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. The Quality of Our Nation’s Waters. 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. Mason HJ.44(11):2243-2250. Diazinon. Liu F. Barr DB. International Programme on Chemical Safety-INCHEM (IPCS). Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. 2005. Swan SH. Needham LL.gov/circ/2005/1291/. Interim reregistration eligibility decision (IRED. Available at URL: http://www. Anal Bioanal Chem 2003. EPA). Bravo R. Baker SE. 1998. Fenske RA. Pesticides in the Nation’s Streams and Ground Water. Effect of sublethal levels of diazinon: histopathology of liver. Barr DB.. 4/7/09 Lu C. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. March 2006. Bouchard M. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Available at URL: http://pubs.10(6 Pt 2):789-798. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers.37(4):501-507. Available at URL: http://www. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Third National Report on Human Exposure to Environmental Chemicals. Olsson AO.S.gov/ oppsrrd1/REDs/diazinon_ired. Diazinon. Oloffs PC. Nguyen JV. Geological Survey (USGS). Seifert J. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Semen quality in relation to biomarkers of pesticide exposure. Rajendra W. Redmon JB. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al.S. 1/14/09 U. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . May 2004. In a small number of men visiting fertility clinics in Missouri and Minnesota. Environmental Health Criteria 198.htm. Cocker J. Dumas P. 2006). Atlanta (GA).376(6):808-815. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Drobnis EZ. Biochem Pharmacol 1992.S. 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. 2007 [online]. Driskell WJ. Garfitt SJ. Oloffs PC. Pewnim T. Banister E. Environ Health Perspect 2003. 2006). Environmental Protection Agency (U. revised February 15. In 23 children. Sadowski MA. Bull Environ Contam Toxicol 1986.9(2):117-131. et al. Study for Future Families Research Group. EPA 738-R-04-006. Beeson MD.inchem. Toxicol Lett 2002. Centers for Disease Control and Prevention (CDC). Jones K. J Expo Anal Environ Epidemiol 2000. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Ann Occup Hyg 2006.usgs. 1992-2001. Barr DB.111(12):1478-1484. Environ Health Perspect 2006. Swan et al.50(5):505-515. Irish R. References Anthony J. Banister EW.Organophosphorus Insecticides: Specific Metabolites 2005). Drug Chem Toxicol 1986.

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

. but cholinesterase activity was not affected. Additional information about external exposure (i. 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. and it is not considered an animal teratogen or a reproductive toxicant. Flessel et al..S. Of 382 pregnant women living in an agricultural community..gov/pesticides/. 2006). 2000).. 1990).html and from U. IARC considers malathion not classifiable as a human carcinogen. 1996. 2003).S. 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. 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. 1999. 2006). 2004).atsdr. Survey Geometric mean (95% conf. 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.e.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS.. 2001.S. 2006). CDC.S.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. Pluth et al. Giri et al. representative subsample from NHANES 19992000 (Adgate.74 (<LOD-5.5 and 5.EPA.. 2005).. 2002. EPA at: http://www..cdc.epa. 1987. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure.gov/toxpro2. 2005). Malathion itself has not been considered genotoxic (U. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. population from the National Health and Nutrition Examination Survey. Lu et al. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh 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. 1999).. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..EPA. 1993. 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. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Fourth National Report on Human Exposure to Environmental Chemicals 147 . environmental levels) and health effects is available from ATSDR at: http://www. 2005. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. 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. Thomas et al. Toxicity from unprotected bystander exposure during applications is rare (U.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid.S. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. but isomalathion. Human studies of single oral doses between 0.

O’Neill JP. 2005. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. International Programme on Chemical Safety-INCHEM (IPCS). Arch Environ Contam Toxicol 2000. Lu C.gov/oppsrrd1/REDs/ malathion_red. Cancer Res 1996. Hertz-Picciotto I. Erratum in: Toxicol Sci 2003 Aug. The Quality of Our Nation’s Waters. Bouchard M. Brunet RC. and cholinesterase status of date dusters and harvesters in California. Irish R. Available at URL: http://www. Ryan PB. Reregistration eligibility decision (RED) Malathion. Clayton CA. Jaloszynski P. Harris JA. htm. Pesticides in the Nation’s Streams and Ground Water. Dinoff TM. Quintana PJ. EPA). Prasad SB. Gosselin NH. Am J Epidemiol 1990. Trzeciak A.inchem. Goldhaber M. Weltzien E.114(2):260-263.epa. Giri S. Needham LL. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals .73(1):182-94. revised February 15. et al. Eskenazi B. Carrier G. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo.77:1009-1010. metabolite clearance.org/documents/jmpr/jmpmono/v2003pr06. Curl CL. EPA 738-R06-030. A longitudinal investigation of selected pesticide metabolites in urine.22(1):7-17. Fenske RA.pdf. Environ Health Perspect 2004. Atlanta (GA). Mutat Res 2002. Neutra R. Lu C.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Am J Public Health 1987. Szyfter K. Environ Health Perspect 2006. Hooper K.112(10):1116-1124. Eberly LE. U. Lioy PJ. Albertini RJ.S. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. J Expo Anal Environ Epidemiol 1999. Third National Report on Human Exposure to Environmental Chemicals.109(6):583-590.9(5):494-501. Swan SH. Pluth JM. Malathion (addendum). et al. March 2006. Petitti D. Malathion deposition. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Blasiak J. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Samuel O.56(10):2393-2399. Bravo R. Giri A. 1992-2001. Reproductive outcome in women exposed to malathion.usgs. Bradman A. July 2006. Kedan G. Environ Mol Mutagen 1993. J Expo Anal Environ Epidemiol 2005.514(1-2):223231. Toxicol Sci 2003 May. Geological Survey (USGS). Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Barr DB. Available at URL: http://pubs. et al. Dumoulin MJ. Thomas D. Harley K. Centers for Disease Control and Prevention (CDC). Freeman NC. Barr DB.gov/circ/2005/1291/. Mutat Res 1999. Griffith W.445(2):275-283. Environ Health Perspect 2001. Rappaport E. Flessel P.38(4):546-553.S. Genetic toxicity of malathion: a review.132(4):794-795. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Barr DB. 6/1/09 U.S. Krieger RI. 2007 [online]. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Hammerstrom KA.74(2):following table of contents. Grether JK. Available at URL: http://www. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. MacIntosh DL. Toepel K.15(2):164-171. 4/7/09 Kissel JC. Environmental Protection Agency (U. Sharma GD. Nicklas JA. Jewell NP. Barr DB. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers.

8 and 0.20-5. In animal studies. 1977).69) 4. Morgan et al.80) 2. Methyl parathion is not registered for residential use in the United States. In the 1990s. population from the National Health and Nutrition Examination Survey.57) 1.28 (1.21-1. and of the chemical nitrobenzene.940 (<LOD-2. 2007).15-3.S. ethyl parathion.50 (2. Both are toxic to birds.32-1.90-11.70) 2.S.79) 4.910) < LOD < LOD < LOD 1.850) < LOD . 2002.20 (<LOD-2. It had been applied to cotton.37-4. methyl parathion was rapidly absorbed after ingestion.16) < LOD 1.74) 5. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate. Once absorbed.01) 4.00 (2.05) 4.30-3.80 (1. Ethyl parathion.67) < LOD 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30 (1.20) 5. first registered in 1948.26 (1.70) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and eliminated rapidly from the body after absorption (Kramer et al.22-3. was once a restricted-use insecticide with limited applications on certain agricultural crops.37) 2. Fourth National Report on Human Exposure to Environmental Chemicals 149 .S.34 (3.. Methyl Parathion. all registered uses were voluntarily cancelled (U.300-. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70-3.09-1.910) < LOD .70-6.0) 3.80 (2.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .85 (2.40-3.EPA.60 (4.00 (2.50) 2.10 (<LOD-6.70-6.70-6. pulmonary.37-4.70-3.770 (.70 (2. Methyl parathion has low water solubility.860 (<LOD-1.45 (1.60-19.10) 4.70 (3.44) 2. binds tightly to soils resulting in low leachability.19 (.90-9.50) 3.40) 4.50) 1. Many previous registered agricultural uses of methyl parathion have been cancelled (U.298-00-0 Ethyl Parathion CAS No.92-2.92) 5.62 (1. fish.58) 3.. Methyl parathion use is highly restricted.36-1. 2006).48) 90th 2.71 (3. with limited applications in agriculture. Estimated intakes from diet and drinking water have been below recommended limits. peak domestic use was as high as 5-6 million pounds per year.41-4.EPA.20 (2.80 (2.89 (2.0 (3.66 (2.33) 2.990-1.50 (1.0) 4. and oral routes can occur in pesticide and agricultural workers (Muttray et al.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .12) < LOD < LOD 1.01-4.70 (2.10-1. 2003). and aquatic invertebrates.30-5. 2000).50 (1.00) 3.60) 1. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.46 (3.50 (2. which may vary for some chemicals by year and by individual sample.50-9. Given its limited use.10-11.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.700 (<LOD-.0) 3.45) 5.00) 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. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.50) 3.32-1.910) < LOD < LOD .28 (1.70 (2.60-24.32 (1.21 (2.50 (1.72 (3.40) 2. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.0) 2. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.60-5. Increased risk of exposure via dermal. and has a short half-life in soils and on plants.730 (<LOD-.13-1.18-3.40 (1.47) 2. more slowly absorbed through the skin.10) 22.0) 3.60-36.40-4.11-4.70) 2..10 (3. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS. < LOD means less than the limit of detection.61) < LOD 1.01) 695 660 518 679 603 941 Limit of detection (LOD.32-3.37-2.49 (1.27) 2.10 (3.70 (<LOD-3.40) 1.91-3.71 (2.57-4.61) < LOD 1.0) 3.33 (1.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . but by 2003. Survey Geometric mean (95% conf.50 (1.0) 3.790 (<LOD-.40-4.69 (2.28-4.30-16.30 (2. on cereal grains. and to a lesser extent.02-6.1.50-14.11) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.90 (1.67 (1.

13) 4. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS. accidental exposure. Thus.3) 2. 150 Fourth National Report on Human Exposure to Environmental Chemicals . interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.00 (1.79) 1.94-47.23) 1.500) < LOD < LOD .70) 3. environmental levels) and health effects is available from ATSDR at: http://www.1) 2.82) < LOD .15-10.61) 4. ethyl parathion. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.93 (2.720-1. 1995.EPA considers methyl parathion unlikely to be carcinogenic to humans.80 (1. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.690-1.96 (1.80 (1.10 (1.71 (1.970 (.89 (2.88) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organophosphorus Insecticides: Specific Metabolites Metabolites”).4 (3.880 (.33-3.09) 2.e.17) .29) 1.800-1. In large doses. The metabolite.88 (1.13-12.08) < LOD .640) < LOD < LOD 1.05) 4.9) 1. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.25) 1.73 (1..41-2. gov/pesticides/.90 (1.970 (. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.980 (.67-2.11-4. Slotkin et al.60-2.57) 6.440 (<LOD-.790-. EPA at: http://www. 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.26 (1.15) 3.96 (1.78-2.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .71) 1.30) 3.33-3. 1990.56-2. gov/toxpro2.cdc.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 .57-7.04) 1.870) < LOD .89 (2.30-1.S.epa.97 (<LOD-4. does not inhibit acetylcholinesterase enzymes.83 (1.60 (1. resulting in excess acetylcholine at nerve terminals.48-4.97 (2.20) . At high animal doses of methyl parathion.720 (<LOD-.2) 2.01 (..78) 2.00 (1. Additional information about external exposure (i.14-3.. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.850-1.16-4.26) 17.930 (. and other metabolites. Karanth and Pope et al.39 (1.72-2. vomiting.31-3.S. U.39) 1. Orsorio et al. Methyl Parathion..91 (1.67 (3..310-.92 (2.730-1.html and from U. population from the National Health and Nutrition Examination Survey.35-3.37-1.930 (.530) < LOD < LOD < LOD .98-7.01-3.79 (1. but lists ethyl parathion as a possible human carcinogen. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.08 (1. 1995).43) 4.57-2.84) 3.44-3.87 (1. Zurich et al.940 (<LOD-1.17-4. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.7) 3.20 (3.680 (<LOD-1.2) 2..38-3.540) < LOD .07 (1.25 (2.atsdr.20) 3.94-4.55) 2. 1991). Methyl parathion is not considered genotoxic.76-14. and unintentional acute or chronic high-level occupational exposure (Hill et al.830-1.59 (1. Survey Geometric mean (95% conf. weakness.29) 2.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . and producing acute symptoms such as nausea.S. 2006. paralysis.21-21.55 (<LOD-3.04 (2. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion. cholinergic effects.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2003. teratogenic.78-2. In addition to being a metabolite of methyl and ethyl parathion.21) 1. 1978. paranitrophenol. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.08-3..33-6. Jaga and Dharmani.370 (<LOD-.11) 1..82 (2. Lores et al. WHO.840 (.77-7.07) 2.44-3. 2005. 2004).97-10. Parathion and methyl parathion have high acute toxicity in animal testing.91) 1.86 (2.95) 1. 2004).430 (. 2006.31) < LOD .950) < LOD .00) 2.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . and seizures.78 (2. methyl parathion.60) 2.35-3.01 (2.790-1.10) 90th 2.29 (2.400 (<LOD-.

. Lin LI. Guizzetti M. McCann et al.215(3):182-190. 2005. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Neurotoxicol Teratol 2003. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Third National Report on Human Exposure to Environmental Chemicals.. 2002. 1995. J Anal Toxicol 1990. 1999). 2002. McClure PC. oral or dermal administration. J Biomed Sci 2002.112(10):1116-1124. Costa LG. Environ Health Perspect 2002. and levels were similar or slightly lower that those in a small convenience sample of the U. Moseman RF. DiPietro E.htm. Head SL. Environ Res 1995. Role of individual susceptibility in risk assessment of pesticides. Barr JR. general population (CDC.15(2):164-171. 2005. Eskenazi B. Cline RE. Barr DB. Hryhorczuk DO. Wellman SE. In a study of workers who handle parathion. 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. Arch Environ Contam Toxicol 1977. McCann KG. Environ Health Perspect 2002. Kedan G. Gregg M.14(4):213-216. Hetzler HL. Hill RH Jr.S. International Programme on Chemical Safety-INCHEM (IPCS). Baker S. Laboratory investigation of a poisoning epidemic in Sierra Leone. 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... Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Giordano G.9:311-320. population (Olsson et al. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Kissel JC. Runkle KD. Chicago area methyl parathion response. Rev Environ Health 2006. Leng G. Needham LL.5 mg (500 µg)/g creatinine for workers at the end of shift. Occup Environ Med 1999. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Karanth S. ACGIH recommends a BEI of 0. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Hill et al.S.110 Suppl 6:1075-1078. Baker SE. Barr DB. et al.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Moomey CM. Methyl parathion: an organophosphate insecticide not quite forgotten.inchem.110 Suppl 6:1085-1091.. Bradman A.. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Pesticide workers may have much higher levels following pesticide applications.6(2-3):159-173. Harley K. 2005). References Barr DB. J Expo Anal Environ Epidemiol 2005. a range of values several hundred times higher than levels found in the U. Jewell NP. Available at URL: http:// www. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Turner WE. Toxicology 2005. Centers for Disease Control and Prevention (CDC). et al. Clark JM. Pharmacokinetics of methyl parathion: a comparison following single intravenous.21(1):5767. Kramer RE. Pope C. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. A study of 13 children from an agricultural region of Washington State reported median levels that were more than threefold higher than median levels in the NHANES 1999-2000 subsample (Kissel et al. Rockhold RW. Baker RC.33(5):270-276. Ashley DL. Hill RH Jr. Head SL..org/documents/jmpr/jmpmono/v95pr14. Environ Health Perspect 2004. Lewalter J. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Weltzien E. 2002). Atlanta (GA). Shealy DB. 1995). Barr DB. Pathak S.56(7):449553. 4/7/09 Jaga K. Parathion-Methyl (addendum). 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. Slach EF. 2005). 2005. et al. Rubin et al. and many residents were symptomatic (Barr et al. Bailey SL. Alley CC. Pesticide residues in urine of adults living in the United States: reference range concentrations. 2004). Griffith W. et al. Morgan DP. Arch Environ Health 1978.25(5):599-606.71:99108. Bradway DE. et al. Lores EM. CDC. Dharmani C. Curl CL. Lu C.

Letzel S. Monnet-Tschudi F.201(2):97-104. Available at URL: http://www. Available at URL: http://www. March 2006. Olsson AO. EPA).Organophosphorus Insecticides: Specific Metabolites Muttray A. May 2003. Slotkin TA. Dunlop B. Backer G. Available at URL: http://pubs. pdf. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Investigation of a fatality among parathion applicators in California. 5/19/09 Zurich MG. revised February 15.S. 1/12/07 U. 2004. Toxicol Appl Pharmacol 2004.epa. 1/14/09 U. Hill G.110 Suppl 6:1047-1051.gov/oppsrrd1/REDs/factsheets/0155fct. 0153. Ethyl parathion. Toxicol Lett 2006. Rubin C. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Environmental Protection Agency (U. Interim reregistration eligibility decision (IRED) for Methyl Parathion.04/106. Schilter B. Seidler FJ.S. Kieszak S. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County.S. Barr DB.usgs. Sadowski MA. WHO/SDE/WSH/03. Hill RH Jr. Yacovac R. Costa LG. 1995-1996. External and internal exposure of wine growers spraying methyl parathion.D.S. Jung D.20(4):533-546.pdf. Available at URL: http://www. Mengle DC. Osorio AM. Levin ED.E. R. Geological Survey (USGS). EPA). Environmental Protection Agency (U.pdf. U. 6/1/09 World Health Organization (WHO). Esteban E.epa.gov/circ/2005/1291/. 2007 [online]. Tate CA. et al. Ames RG.S. gov/oppsrrd1/REDs/methylparathion_ired.int/water_sanitation_health/dwq/chemicals/ methylparathion. Am J Ind Med 1991. Anal Bioanal Chem 2003. Environ Health Perspect 2006. The Quality of Our Nation’s Waters. Rosenberg J. Ohio. Nguyen JV.162(2-3):219-224. 1992-2001. September 2000.114(10):1542-1546. Facts. Methyl parathion in drinking water. Honegger P.376(6):808-815.who. EPA-738-FOO-009. Case No. Environ Health Perspect 2002. Ryde IT. Pesticides in the Nation’s Streams and Ground Water.

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

15) < LOD .700-1.740 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07) .410 (<LOD-1.850 (.740-1.500 (. population from the National Health and Nutrition Examination Survey.27) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.840) 669 687 929 Limit of detection (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 . 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.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. population from the National Health and Nutrition Examination Survey.64) .94) .700-.300-1.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .770) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .210 (<LOD-.610 (<LOD-1.55) . 154 Fourth National Report on Human Exposure to Environmental Chemicals .210-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .250 (<LOD-. < LOD means less than the limit of detection.S.2.680 (<LOD-.670 (<LOD-1.580-1.470 (.200-.760 (<LOD-.780 (.820) < LOD < LOD . Survey Geometric mean (95% conf.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Survey Geometric mean (95% conf.780 (<LOD-1.21) < LOD .210-. which may vary for some chemicals by year and by individual sample.780 (<LOD-1.780 (.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 01-02 is 0.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .31) .840 (.17 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .S.430 (<LOD-.950) < LOD < LOD 1.

cfsan. Atlanta (GA).inchem. Available at URL: http://www. Total Diet Study: Summary of Residues Found Ordered by Pesticide. Food and Drug Administration (FDA). org/documents/jmpr/jmpmono/v92pr16. Pesticides residues in food: 1992 evaluations Part II Toxicology. Pirimiphos-methyl.Organophosphorus Insecticides: Specific Metabolites References Centers for Disease Control and Prevention (CDC).pdf. 4/7/09 Olsson AO. Barr DB.S. Case No. 4/7/09 International Programme on Chemical Safety-INCHEM (IPCS). Nguyen JV. June 2003. July 2006.htm.gov/~acrobat/tds1byps. Market Baskets 91-3-01-4. Available at URL: http://www. 2535.376(6):808-815.pdf. 850. EPA). Environmental Protection Agency (U. Available at URL: http://www.epa. Anal Bioanal Chem 2003. Finalization of interim registration eligibility decision for pirimiphos-methyl.fda. 1/14/09 Fourth National Report on Human Exposure to Environmental Chemicals 155 . Third National Report on Human Exposure to Environmental Chemicals.S. 2005. Sadowski MA. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. U. gov/oppsrrd1/REDs/pirimiphos-methyl_ired.

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

neurochemical changes in cholinergic. Fredriksson A. and permethrin) in the Hershberger and uterotrophic assays. Yang J. Lazarini et al.atsdr. Generally. 2003. Song L. September 2003.html. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Kim IY. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Guillot TS. Idel H. Environ Health Perspect 1999. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Seth PK. Kunimatsu et al. Bull Environ Contam Toxicol 1999. Wieseler B.27(4):609-614. Shukla Y.. Int J Hyg Environ Health 2002.. Lee SJ.50(2):245-255.62:101-108. Hu JY.27(12):1273-1283. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Xenobiotica 1997. In California. and striatal dopamine levels in male and female rats. Shaw IC. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR.8(1):197-202. Hu et al. Agrawal AK. Ranft U. 2005). Ose K. Caudle WM. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides.gov/toxprofiles/ tp155. Abell AD. Additional information about pesticides is available from U. Moniz AC. J Reprod Dev 2004. dopaminergic.. hypersensitivity. 1991. Okuno Y.. et al. fenvalerate. Kim TS.. Biochem Biophys Res Commun 1998. Kang IH. Kuhn K. Eriksson P. Neurotoxicol Teratol 2001. Garey J. et al. 2001. Garey and Wolff. Chen JH. choreoathetosis.205(6):459-472. Shin JH.. Go V. Bernardi MM. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. et al. Kunimatsu T.8(1):18-21. Leng G. Pogo BG.cdc. 2005). Varoli FM. salivation. Leng G. et al. 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. Adhami VM. and seizures (ATSDR. In developing rodents.23(6):665-673. 2005). on immature and adult mice: changes in behavioral and muscarinic receptor variables. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley.107(3):173-177. EPA at: http://www.211(3):188-197.. Richardson JR. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation.300(3):161-165. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Lazarini CA. Shafer. 2006.gov/pesticides/ and from ATSDR at: http://www. Estrogenicity of pyrethroid insecticide metabolites. 2002). WHO. Toxicological profile for pyrethrins and pyrethroids. Kuhn KH. Neurosci Lett 2001. Wang SL. Toxicol Appl Pharmacol 1991. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Miller GW. Eriksson and Fredriksson. Cruz-Casallas PE. tremor. Neurotoxicol Teratol 2005. Elwan et al. 1998. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Sunami O. Idel H. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Sugiri D. 2002. Kim HS.... 2003. bioallethrin and deltamethrin.gov/toxpro2. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Pyrethroid pesticide-induced alterations in dopamine transporter function. 2005). Zhao RC.251(3):855-859. Toxicol Appl Pharmacol 2006. Elwan MA.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Levsen K.35(2 Pt 1):227-237. Wolff MS. Berger-Preiss E. Yamada T.108(1):78-85. 2003. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. Florio JC. 2006). Pauluhn J. 2000. Spinosa HS. J Environ Monit 2006. References Agency for Toxic Substances and Disease Registry (ATSDR). Estrogenic and antiprogestagenic activities of pyrethroid insecticides. 2003. Go et al. Garey J. 1999.. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Kim et al. Soderlund et al. epa. Bernardi MM.html.S. Regul Toxicol Pharmacol 2002. Leng G. Ray et al. motor activity. McCarthy et al.atsdr. Thomson BM. Effects of prenatal exposure to deltamethrin on forced swimming behavior.. Kamita Y. Lemonica IP. Lewalter J.1/15/09 Aziz MH. 2001. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. cdc. Salzgeber SA.. Neurotoxic effects of two different pyrethroids. Moniz et al. McCarthy AR. 2006. Available from URL: http://www. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. 2002). Leng A. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Wolff MS. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. 2004.

Clark JM. Crofton KM.Pyrethroid Pesticides Ray DE. Sheets LP.S. resmethrin.epa.gov/oppsrrd1/REDs/ factsheets/permethrin_fs.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Laird WJ. Environmental Protection Agency (U. 5/26/09 U. Sargent D. June 2006a. Lesser JE.S. Available at URL: http://pubs. Permethrin. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Toxicology 2002. Meyer DA. Xenobiotica 1992.epa.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. June 2006b. synergies.S. Pyrethroid insecticides: poisoning syndromes.38:95-101. Environ Health Perspect 2005. World Health Organization (WHO). Piccirillo VJ. 1992–2001. Pesticide and Evaluation Scheme.htm. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. 5/26/09 U.who. sumithrin synthetic pyrethroids for mosquito control. 5/26/09 U.S. Soderlund DM. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet).22(8):983-991. pdf. and therapy. Pesticides in the Nation’s Streams and Ground Water. Pyrethroid illnesses in California. EPA). U. 2007.usgs. Rev Environ Contam Toxicol 2006. Mullin LS.S. Reregistration Eligibility Decision for Cypermethrin. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .10.113(2):123-136. O’Malley M. 5/26/09 Woollen BH.htm. Marsh JR. Available at URL: http://whqlibdoc. March 2006. 19962002.gov/oppsrrd1/REDs/cypermethrin_red.gov/ circ/2005/1291/.epa. Environmental Protection Agency (U.171:3-59. 2005. EPA). Shafer TJ.S. Available at URL: http://www.S. Available at URL: http://www. Geological Survey (USGS). Safety of pyrethroids for public health use. Forshaw PJ. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs.pdf. EPA). J Toxicol Clin Toxicol 2000. Spencer J.186:57-72. et al. April 2002. Environmental Protection Agency (U. Available at URL: http://www. Revised February 25.

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

160 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.S. 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.2 and 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00 and 01-02 are 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. population from the National Health and Nutrition Examination Survey. 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. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 161 .S.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.

Spencer J. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Angerer J.Pyrethroid Pesticides References Baker SE. J Expo Anal Environ Epidemiol 2003. Idel H. Sugiri D. Bernard CE. Williams RL. Krieger RI. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Heudorf U. Int J Hyg Environ Health 2006. Leng G.46(3):281-288.13(2):112-119. Drexler H. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Kolossa-Gehring M. Hadnagy W. 2005.209(3):293-299. Heudorf U. Angerer J. et al. Ranft U. Int J Hyg Environ Health 2003. Environ Health Perspect 2001. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int Arch Occup Environ Health 2004. Pyrethroid illnesses in California. Arch Environ Contam Toxicol 2004.206(2):85-92. Berger-Preiss E. Centers for Disease Control and Prevention (CDC). Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Butte W.109(3):213-217. Schulz C. Ball M. Third National Report on Human Exposure to Environmental Chemicals. Heudorf U. Int J Hyg Environ Health 2006. Atlanta (GA). Seiwert M.77(1):67-72. Hoppe HW. Olsson AO. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides.209(3):221-233. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Becker K. O’Malley M. Angerer J. Angerer J. 19962002.186:57-72. Rev Environ Contam Toxicol 2006. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Barr DB.

13 (.68 (.68) . cis-3-(2.330) .700) .340-.460-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.11) .262) * * * < LOD < LOD .110 (<LOD-. but can also reflect exposure to trans-3(2. but it can also reflect exposure to cis-3-(2.460 (.680 (.370-.710-1.440 (.77 (.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.730 (.670 (. 1985.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.. more of the trans-metabolite than Urinary cis-3-(2.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.490-.510 (.160 (.35) .2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.670-2.110-.54) .202 (.180 (.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.730 (.570-.960 (.210-.260 (.740) 1.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin. and ciscyfluthrin.550) .140 (<LOD-.690) . 1999).43) . trans-permethrin.470 (.110-.170 (.180) .610) .770) .2-dichlorovinyl)-2.570 (.340) .200-.580) 1.380-.580-1.490-1.640 (.24) 1.630) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380-.2dichlorovinyl)-2. 1999).400-.44 (. cis-permethrin.900 (. 1985..300-.380 (.460-1. Cyfluthrin.410) .600-1.220-. which may vary for some chemicals by year and by individual sample.340) .32) . < LOD means less than the limit of detection.220-.890 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.510 (.140 (.07 (.530 (.500 (.110-.420-.770-1.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin. cis-cypermethrin.490-1.2-dichlorovinyl)-2.21) .200-.710) .200) < LOD < LOD < LOD .790-1.2-Dichlorovinyl)-2.2-dichlorovinyl)- CAS No.280-.120-.210) .630-.630) . Kuhn et al. transcypermethrin and trans-cyfluthrin.380-.510 (.12 (. Fourth National Report on Human Exposure to Environmental Chemicals 163 .120-.330 (.200 (.880 (.or trans-3-(2.600 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.430-.780) .300-.200-.610) .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 .1.520) .250 (.650-1. Similarly.600) .270-.490-.870) 1.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .790) .120-.350) .950-2.670-1.220-.300 (.210) 90th .28) 671 680 518 701 591 957 Limit of detection (LOD.410) .270 (.35) 1. Survey Geometric mean (95% conf. and trans-cyfluthrin.120-.370 (.2dichlorovinyl)-2.790 (.300 (.and trans-isomers.220-. Kuhn et al.850 (.2-dichlorovinyl)2.230) .270 (. the presence of trans-3-(2.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.160 (<LOD-. 52315-07-8 CAS No.910-5.15) .730 (.280 (.740 (.68) .160 (.50) .08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .08) .270 (.80) .500 (.740-1.68359-37-5 Cypermethrin Permethrin CAS No. Generally.200) .630 (. The presence of cis-3-(2.890 (. Biomonitoring Information Urinary levels of cis.2-dichlorovinyl)-2.670-1.380) .53) .220) .470-1.310) .740-2.680-3.920) 1.200) .155-.150 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .250-. In the body.S.240) .2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. population from the National Health and Nutrition Examination Survey.47 (.820 (.240) .1 and 0. trans-cypermethrin.790-1. ciscypermethrin and cis-cyfluthrin. The chemical trans-3(2.

2003).230-.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.440 (.21) . 2005).220 (.780 (.260 (.680 (.and trans-3(2.420 (.700-2.150-.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.11) .430-1.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC. 2003).540 (.300) .250-.390-.250) 90th ..2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al..380-. 2005).540) . 2001. 2002).Pyrethroid Pesticides 2.920 (.680-1.S.2-dichlorovinyl)-2.290 (.29 (.280 (.450 (.360-1.300-.390 (.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .180 (..430-.470-1. 164 Fourth National Report on Human Exposure to Environmental Chemicals . representative NHANES 2001-2002 subsample (CDC.350 (.350) .230-.830) .12-2.710-3. 2001) showed urinary levels of cis.550 (.430 (.250 (<LOD-.440-.590 (.300 (.170) < LOD < LOD < LOD .270) . 2006.138 (.900 (.250) .250-.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2dichlorovinyl)-2.390-.33 (.840 (. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.11) 1.270-.140-.250-.67 (. Cyfluthrin.370-.260-.104-.200-. 2004.600 (.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.780) 1. the median and 95th percentile of urinary levels of cis-3-(2.510-1.2-dichlorovinyl)-2.320) .120 (.640 (.11 (.560) 1.640-1.290-.170 (. post- Urinary cis-3-(2..370-.130-.33) .280-.49) .190) .450-.380) .640) 1. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.320-.80) .540 (. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.550-1. 2004).810 (.260 (.220) .440-. In the same residents.260 (.290) .750-1.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * . population from the National Health and Nutrition Examination Survey.530 (.12 (.560) . median urinary levels of trans-3-(2..580-1. In a study of volunteers. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.03) 1.380 (. 2005).890 (.and trans-3-(2. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.170 (. In these volunteers. Survey Geometric mean (95% conf.270 (. 2002).300 (..220 (.260) .080-.200-.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.180-.270) . Schettgen et al.240 (<LOD-.450-1.710 (.640-. 2005) In a small group of indoor pest-control operators.2dichlorovinyl)-2. urinary levels of cis-3-(2.750 (.640-1. 2006. 2006) and 1177 urban adults and children (Heudorf et al.2-dichlorovinyl)-2.550-1.230-..530 (.59) .2-dichlorovinyl)-2.400 (.340-.410) ..520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .182) * * * < LOD < LOD .03) size 1951 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th ..550) .230 (.190) . 2006).370-. 2006).680-1. Other studies have provided evidence that urinary levels of cis.2-Dichlorovinyl)-2. Lu et al.150-. urinary trans-3-(2.440 (.340) .2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.24) .300) .S.200 (.890) . Studies in Germany of 396 children and adolescents (Becker et al.190 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.550) .570) .400-1.290) .500 (.340) .700) .11) . 2005).2-dimethylcyclopropane carboxylic acid did not increase.840 (.160 (<LOD-.200) . Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.580) ..150-.250) .31) .880) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700) .59 (1.37) . In a study of urban residents in Germany (Berger-Preiss et al.67) .59) .690-1.210-.590) .800 (.

76-3.63) 1.55-5.20 (.26 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.77) 2.420 (<LOD-.780 (.13) .49-3.700-1.470 (<LOD-.S.40 (1.680-1.410-.410 (<LOD-.5) 2.90) 1.530) .4.56 (1.35) 1.77) 1.66) 691 680 518 690 595 954 Limit of detection (LOD.23 (.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.660) 1.56) 2.59 (1.49-3.01 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.470 (.490 (<LOD-.2dichlorovinyl)-2.580 (.68) 2.39-5.56) 2.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .07-3.94 (1.87 (1.970 (.08-4.68-3.710 (.39 (1.22 (1. 2005).42) 1.42 (2.and trans-3-(2.41 (1.49-5.500 (.20 (.95) 3.19 (2.4 and 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3. trans-Cypermethrin.550 (.89 (2.85) 4.730) .11-1.77 (1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .55-3.14-2.19) 1.760) .820) .43) 2.08-6.41-14.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.480-.03-1.25-3.48) 4.2-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.08) 1. however.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 .25 (1. population from the National Health and Nutrition Examination Survey.55-4. The maximum post-application urinary levels.400-.400 (<LOD-.97-11.62 (1.570) 90th 1.2-dichlorovinyl)-2.490-1.460-.16) 1.12-6.520) .560 (.60-4.560 (.23) 2.03-1.14) 1.91 (1.670) . < LOD means less than the limit of detection.500) .560 (. which may vary for some chemicals by year and by individual sample.910-1.750) .28 (1.840-1.440 (<LOD-.95) 2.27 (1.37 (1.50 (1.17 (.17 (.410 (<LOD-.01) 4.64-4.670) .2-Dichlorovinyl)-2.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .500-.17-1.56 (1.940 (.700) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.20 (.07 (1.460-.830-1.09 (.69) 1.7) 2. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.54 (1.68) 1. 2005).54) 4.800-1.410-.28 (2.14-6. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.69 (1.920-1.63) 1. Urinary trans-3-(2.520-.76-4. Fourth National Report on Human Exposure to Environmental Chemicals 165 .81) 2.2-dichlorovinyl)-2.620) < LOD 2.610) 1.910-1.84 (1. Survey Geometric mean (95% conf.19 (3. Biomonitoring studies on urinary levels of cisor trans-3-(2.10) 2.60) 1.60) .Pyrethroid Pesticides application median urinary levels of summed cis.66) .or trans-3-(2.810-1.68) 1. Finding a measurable amount of cis.68-2.860) .11-2.850-1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.

44) 2.930-1.20 (1.08 (.00) 1.87) 1.820-2.86 (2.56-2.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .70 (.91 (1.15) 3.470 (.22-2.19) .57 (1.56-5.65 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.580) .850) 1.35) 1.13) 1.700 (.55 (2.34-3.19 (1.12-1.61) 1.98 (1. population from the National Health and Nutrition Examination Survey.00) 5.47-2.570 (.31 (2.02-1.45-2.67 (2.74) .560 (.16 (1.65) 1.900 (<LOD-1.800-1.55 (2.670) .800-1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .12 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.780) 90th 1.37 (1.15) 2.15-3.87-3. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.80) 1.15 (1.91-11.33-1.00-5.87 (1. trans-Cypermethrin.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .39 (1.41) 1.700-.34-4.530 (.36 (1.48-2.3) 2.40-2.07-2.720-1.42) 1.74) 2.740) .880 (.31) 1.470-.520 (<LOD-.760 (.07-1.28) 2.11) .91) 1.39) 1.640) .27-2.35 (1.500-.540) .27-2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.530 (<LOD-.440-. Survey Geometric mean (95% conf.S.47-2.15-3.75 (1.580 (.570-.30-3.660) .07-3.750) .56 (1.610-.29) 1.780) .780 (<LOD-.880 (<LOD-1.07) 2.87-8.970 (.42 (.33-2.64 (1.45 (1.87) 1.08 (.22) 1.68) 3.850) .88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.20-2.880-1.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.30-6.570 (<LOD-.730) .26 (1.2-Dichlorovinyl)-2.55 (2.10) 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 .720-1.410-.81 (2.36) 2.07) 2.Pyrethroid Pesticides Urinary trans-3-(2.15-3.47 (1.720 (<LOD-.700 (.60 (1.57) 3.00 (1.480-.60) 2.48 (1.13) .33 (1.00) 1.770) < LOD 2.22-1.850-3.89) 2.31 (.60) 2.

Idel H. Wieseler B. Kolossa-Gehring M. Biological monitoring of workers after the application of insecticidal pyrethroids. Int Arch Occup Environ Health 2003.134(1-3):141-145. Barr DB. Idel H. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Lu C. Berger-Preiss E.209(3):293-299. Ranft U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Hardt J. Leng G. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. et al. Bull Environ Contam Toxicol 1999. Ranft U. Schettgen T. Sugiri D.76(7):492-498. Ball M. Leng G. Third National Report on Human Exposure to Environmental Chemicals. Int Arch Occup Environ Health 2004.Pyrethroid Pesticides References Becker K. Schulz C. Environ Health Perspect 2006. Drexler H. Int J Hyg Environ Health 2002. Atlanta (GA). Environ Health Perspect 2001. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Heudorf U. Levsen K. Bartell S. Heudorf U. Int J Hyg Environ Health 2003.109(3):213-217. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Idel H. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Butte W.68(6):1160-1163.209(3):221-233. Heudorf U.62:101-108. Seiwert M. Leng G. Berger-Preiss E. Angerer J.205(6):459-472. Angerer J. Drexler H. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. George DA. Hoppe HW. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int J Hyg Environ Health 2006. Angerer J. Pearson M.206(2):85-92. 2005. J AOAC 1985. Angerer J. Heudorf U. Bravo R. Angerer J.77(1):67-72.114(9):14191423. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Centers for Disease Control and Prevention (CDC). Permethrin and its two metabolite residues in seven agricultural crops. Int J Hyg Environ Health 2006. Sugiri D. Kuhn K. Hadnagy W. Angerer J.

2005).3-0.2dimethylcyclopropane carboxylic acid formed in the environment.2-dibromovinyl)-2. 168 Fourth National Report on Human Exposure to Environmental Chemicals .2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. 2005). Deltamethrin can degrade to cis-3(2. Thus.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.5 μg/L) than the detection limit (0.. Following residential spraying with deltamethrin for malaria protection in Mexico. Finding a measurable amount of cis-3-(2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. Urinary levels for adults and children in these studies were similar (Heudorf et al.2-dibromovinyl)2. Baker et al.2-dibromovinyl)-2. 2001) showed that urinary levels of cis-3-(2.Pyrethroid Pesticides Deltamethrin CAS No. Studies in Germany of 396 children and adolescents (Becker et al. deltamethrin has been used against mosquitoes that carry malaria. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2-dibromovinyl)-2.S.39 µg/L. In the NHANES 2001-2002 subsample. Biomonitoring Information Urinary levels of cis-3-(2. in some situations replacing the use of DDT.2-dibromovinyl)-2. 2004). 1990). 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. 2001. 52918-63-5 General Information Cis-3-(2.2-dibromovinyl)-2.. 2005).. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.1 μg/L) for the NHANES 2001-2002 subsample (CDC. urinary levels of cis-3-(2.. Outside the U. in detection of cis-3-(2.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate..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. mean peak urinary levels of cis-3-(2. 2006) and 1177 urban adults and children (Heudorf et al.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid of 0.2-dibromovinyl)-2. (2004) reported a geometric mean concentration of cis-3(2.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC..2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.

Survey Geometric mean (95% conf.S. Fourth National Report on Human Exposure to Environmental Chemicals 169 .2-Dibromovinyl)-2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.1.1 and 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.Pyrethroid Pesticides Urinary cis-3-(2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.

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

209(3):293-299. Angerer J. [online] 1990. Schulz C. Butte W. Kolossa-Gehring M. Torres-Dosal A. Angerer J. Third National Report on Human Exposure to Environmental Chemicals. Centers for Disease Control and Prevention (CDC). Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Batres LE. et al. Int J Hyg Environ Health 2006. Fourth National Report on Human Exposure to Environmental Chemicals 171 . toxicokinetics.inchem. Heudorf U. et al. Heudorf U.113(6):782-786. and genotoxicity in exposed children. Int Arch Occup Environ Health 2004.org/documents/ehc/ehc/ ehc97.209(3):221-233. Drexler H. Environ Health Perspect 2001. Deltamethrin. Grimaldo M. International Programme On Chemical Safety (IPCS). Lopez-Guzman OD. Seiwert M. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Carranza C. Hoppe HW.77(1):67-72. Environmental Health Criteria 97.Pyrethroid Pesticides References Becker K. Available at URL: http://www. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. 2005. Heudorf U. Atlanta (GA). 5/26/09 Ortiz-Perez MD. Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Environ Health Perspect 2005.htm. Angerer J. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.109(3):213-217. Ball M. Int J Hyg Environ Health 2006.

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

35) 2.56-5.8) 3.740 (.750) .320) .417 (.160-.265-.940) 1.36) 1.18 (2.670 (.01 (1.45 (2.34) 8.420) .75 (1.292 (.490-.71 (1.52-5.62-8.49 (1.16) 1.384) .25-4.340) .180-.28) 1.35 (2.65 (1.730 (.470-.03 (3.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.273 (.33 (1.04) .16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .373) .29-1.190-.12 (.50 (2.520 (.53) 1.32 (2.240 (.700 (.595) .390) .27-2.86 (1.46) .190-.570-.25-7.33) .387) .820) .34-6.78) 1.41) 3.610) .53-3.89-71.510-.406) .246-.276-.38 (2.33 (2.41 (1.750-1.810) 1.26) 2.820) .760 (.490) .700-1.35) 1.65-2.454 (.25 (2.S.35 (1.320 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.434) .780) 4.630) .12) .13) .345) Selected percentiles ( 95% confidence interval) Sample 95th 4.230 (.238-.1 and 0.02-6.298 (.27-11.190-.48-2.49 (1.73) 1.83-11.30) 3.295) .247-.250 (.321 (.190-.530-.320) .260-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.355) .260 (.560-1.288 (.830-2.76 (1.750) .330) .30 (1.55 (1.69 (1.54) 1.41-2.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .830) 90th 1.590-.49-2.220-.92-3.350-.601) .32-21. Fourth National Report on Human Exposure to Environmental Chemicals 173 .430-. Deltamethrin.18 (1.250-.325 (.560-.288-.05) .42-2.233-.369) .12) 4.226-.300 (.93 (1.26-2.253-.05) 1.340) 1.23 (2.62) 5.45-5.710 (.586) .650 (.25-1.26) 2.43) 3.34 (2.362) .374) 99-00 01-02 99-00 01-02 99-00 01-02 .79) 3.160-.315 (.510-.78 (1.260 (.450 (.72 (1.64) 697 680 524 701 603 957 Limit of detection (LOD.330) .1) 3.60) .49-2.270) .25 (2.04-5.210-.271-.27-2.364) .200-. interval) .740 (.16-1.81 (1.1.1) 3.300 (.800) 1.297 (.51-6.69) 3.507 (.51-3.63-3.240 (.530-.428-.340) 75th .21 (2.46) 2.620-1.200-.39) 2.680 (.840-1. Survey Geometric mean (95% conf.230-.870 (.300 (.850) .230-.266-.960 (.250 (.63 (3.427) .277-.250 (.311 (.570-1.270 (.320) .600 (.52-4.78) 1.41-3.227-.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 .710 (.1) 3.990) .640 (.280 (.320) .560-.32 (1.352-.260 (.230 (.550-.314 (.13 (.353 (.300) .62-6.44) 5.328 (.200-.78) 6.336 (.35) 2.590 (.230-.267 (.314) .90) 1.800 (.360) .440) .292-.370) .850) .290 (.430-.38 (2.14-6. population from the National Health and Nutrition Examination Survey.210-.48-2.30 (.

67 (1.450 (.240 (.460-.930) .312 (.810) 1.677) .13-1.240-.63) 1.534) .730) .09 (.280) .400) .43 (2.S.460-.44) 2.220 (.36 (1.261 (.300-.19-6.550 (.21-4.72 (1.253) .09-2.81 (1.52 (1.09) 3.720 (.590-1.270 (.540 (.480 (.200-.48 (1.440-.67) 1.91) .321-.91) 9.329) .350) .229-.350 (.224-.401) .530-.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .35) 1.550 (.90) 3.270) .03-1.590) .330) 1.640 (.210-.44 (1.25-2.860-1.05-3.49) 1.250) .270 (.330) .150-.43 (1.640 (.410-.261-.240-.73) 1.62) .840-1.51-7.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.370-.49) 3.230) .280 (.0) 3.226-.17 (.330) .240-.80) 4.238-.278) . interval) .610 (.420-.760) .230-.440-.94 (1.200-. Deltamethrin.378 (.02-1.230-.720) 90th 1.280 (.510 (.246 (.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.510 (.216-.03 (.272) .274-.250 (.730) .49 (1.328) .387) .310) .200-.91-4.272 (.83) 1.220-.380 (.330 (.91 (2.11 (.580) .290) .630) .40 (1.440-.95) 1.320) .37) 1.510 (.335-.06-3.07) 2.590) .650) .225-.86 (1.365) 99-00 01-02 99-00 01-02 99-00 01-02 .330) 75th . population from the National Health and Nutrition Examination Survey.750-1.240 (.36-6.10 (2.700-1.83 (1.04 (3.560 (.490 (.39) 1.275 (.380-.43-64.25-5.27) 1.52) 2.250 (.357) .19 (2.316 (.53 (1.423 (.530-.270) .437) .290-.329) .75-8.11 (.88-5.190 (.41) 1.13 (.670) .37 (1.390-.280-.09-2.210 (.43) 1.00) 5.35 (1.590) .32 (2.400-.17-1.270-.930) 1.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .670) 3.190-.227 (.22 (1.240 (.160-.370 (.202-. Survey Geometric mean (95% conf.64-5.04 (.54 (1.96 (1.63-3.16-4.15-2.372) .311 (.35-3.234 (.210 (.740) .02 (2.500) .00) 1.173-.55) 3.280) .299-.300-.730-1.190-.400-.490-.570) .74) 3.67 (1.00) 1.323 (.960-1.290) .19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .84 (1.240-.362 (.62) 1.88) size 1998 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .25) 2.280 (.446) .860-1.274 (.550 (.55 (1.309) .271-.40) 2.240 (.200-.49-2.60) 1.73-4.41-4.410) .309 (.61-2. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.19) 2.490 (.13-1.860 (.60-4.264 (.21 (1.178-.580 (.480-.35) .07-5.

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

350 (.360-.470) .170-.240-.140) .200-.133) * .103) .158 (.260 (.120-.280) . from air and drinking water.350) .160) .260-.090-.270 (.080) . coal-fired plants.190) .119-.190) . ceramics.160) .390) . see Data Analysis section) for Survey years 99-00. Dermal contact with soil.350 (.260 (.230-.130 (.400-.240 (.178) .180-.132 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals .390) .180 (.200 (.080 (<LOD-.240-.400) .108 (.150-. distribution.130) < LOD .130-.100-.410) .350-.300) .120-.140-. and as a fire-retardant in textiles and plastics.300-.115) .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 .137) .240) .137) .115-.146 (.260) .290-.230 (.210 (.430 (.390-.210) .410) .220 (. sheet and pipe metal.280) .280-.280-.270) .112-.117-.130 (.126 (.240 (.154) .430 (.270 (. population from the National Health and Nutrition Examination Survey.330 (.130) .170 (.120 (.320-.130 (.07.119) .080) .310 (.144) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf. respectively.470 (.130-.088-.170) .270) .169 (.190-.230 (.180 (.110-.200 (.130-.184) . The absorption.320-.120 (.120-.370) .110-. to a lesser extent.410-.140) . water.160 (.190) .093 (.140) .220) .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 .150-.600) .150) . or other substances containing antimony is another means of exposure.500) .560) .105 (.114) . castings.095-.109-.130) .230) .220-.240 (. 01-02. and 03-04 are 0.135) * .200-.108-.176 (.140 (.170-.220-.280-.340) .350 (.200 (.180-.145) Selected percentiles ( 95% confidence interval) 50th .130 (.320 (.136) * . People are exposed to antimony primarily through food and. and refuse incinerators that process or release antimony.250-.300 (. and +5.420) .190-.156-.150 (.125 (.200) .120-.330-. Workplace exposures can occur at smelters.390 (.160 (.320-.095 (.150-.070 (<LOD-.190) .220-.190-.200 (.230-.250 (.080-.310 (.164-.250 (.210-.04.230 (.270 (.330-.130-.260 (. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.140) .130 (.141-.130 (.210) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.390) .130-.128 (.180 (.098-.280 (. and excretion of antimony vary depending on its oxidation state.300) .160) .190-.350 (.170-.190) . which may vary for some chemicals by year and by individual sample.350-.200) .160 (.300 (.300) .290 (.130) .079-.120 (. fireworks.132 (.220-.330) .134 (. solder.150) .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 .300-.S.180 (.175 (.130-.390) .250 (. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.120-.180) .240 (.190-.210) .160) .440) .170 (.090 (.117-.154) .130 (.280 (.130 (.190 (.220-. ammunition.170-. and glass.310 (.320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.090) 75th .100-.160-.310) .087-. enamels.160) .134-. and pewter.490) .142 (.160-.340 (.131-.260) .120 (.150 (.120-.320-.190 (.110) . metal bearings.310) .250-.460 (.350-.100) .400) .207) .400) .145 (.330 (.350) .250-.430 (.210 (.440 (.157) .110-.350 (.350) .04.460 (.160-.210-.340 (.270 (.230-.220-.123 (.190 (.490 (.230-.120) .070-. Stibine is a metal hydride form of antimony used in the semiconductor industry.220) 95th .440) .250) .150-.180) .210) .160) .130-.210) .270-.099 (.140) .280-.570) .120) .360 (.230) .330) .230-. It is used in metal alloys.250-. It is also used in paints.400 (. 0.140 (.200 (.143 (.290-.100 (.161) . Antimony can exist in one of four valences in its various chemical and physical forms: -3.120-.154-.220) .120-.330 (.110 (.260-. < LOD means less than the limit of detection.180-.136-.460) .126-.170-.090 (<LOD-.110-.140) .150) . 7440-36-0 General Information Antimony is found in ores or other minerals.180 (.120) .310-.190 (.070 (<LOD-.200-.140 (.120) .320) Total .460 (.160-. interval) .390-.128 (.197) .510) .370-. 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.140 (.180-.090-.470) .330) .280-.320) .190 (.180 (.180-.500) . Antimony enters the environment from natural sources and from its use in industry.330) .280) .360) . storage batteries.100 (.360 (.220 (.Metals Antimony CAS No.310 (.710) . +3.240 (.390-.220) .120-.280) .310-.320 (.120 (.200) .200) .150-.150 (.150) 90th . 0.230) .200-.300-.350) .360) .148-.200 (.530) .400 (.400 (.122 (. and 0.260) .

skin.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 .230) 95th .081) .241-.130) .286 (.167 (.267-.321) .333 (. and ulcers (Werrin.259 (.253 (.140) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.075 (. Inorganic antimony salts irritate the mucous membranes.076-.104-. 1962).181) .30) .178-.117-.207) .140) < LOD .151) .119-.082) .153 (.143) 90th .185-.198) .176 (.310) .163 (.150-.103-.188-.242-.250-.175 (.225) .200-.105-.199-.172-.245) .076-. 1944).280 (.126) .200-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.371 (.405) .098-.185 (.123) .096-.106-.068 (.417) .086) 75th .112 (. Fourth National Report on Human Exposure to Environmental Chemicals 177 .320) .352 (.S.113-.102-.222 (.115 (.317) .727) .145) .117-.119 (.118 (.192 (.098) .143 (.097-.167-.192) ..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 .228 (.099-.189 (.300) .115) .280-.391) .115-.333-.438) .256 (.320 (.164) .146) .192-.238) .131-.170 (.119-..129) * .208 (. 1995).150-.276 (.068-.315) . The toxicity of stibine after acute inhalational exposure is similar to that of arsine.167 (.149) .295 (.117-.087) .357) . and route of exposure (Elinder and Friberg.200) .135) .429) .196 (.338 (.159-.173 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.111 (.430) .193 (.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.269 (.136) .250) .333 (.112-.338 (.213 (. 1953).128-.400 (.233) .164-.257) .235-.148) * .447 (.156 (.485) .095-.099-.123 (. Acute antimony poisoning may cause a metallic taste.124-. resulting in hemolysis with abdominal and back pain (Dernehl et al.281-.089) .161) . Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.107-.244-.131 (.147-.161) .160 (.228-.288 (.267) .130) .121 (. 1973).333-.200-.124) .444) .080 (<LOD-.209 (.156-.333-1.075 (.173-.153-.176-.167 (.195-.239-..108-.116-.187) .250 (.138) * .113-.131) .224 (.069-.320-.147) .135) .. and gastrointestinal symptoms such as vomiting.135 (.236 (.125-.217 (.179-.159-.114 (.373) .124-.069-.227-.333 (.250-.248) .414) .173 (.095-.171) .127 (.471) .079 (<LOD-.308-.194-.124 (.250 (.082) .146-.181) .129 (.111-.364 (.500) .135) .211) .238) .114 (.209) .385 (.114 (.135 (.163 (..195 (.138 (.108-.250-.233-.120 (.139 (.333) .081 (<LOD-.185 (.248-.247) .310) .205-.261) .278) .444) .182 (.154-.152) .181) .204-.107-.144-.176 (.106-. 1954).146-.112 (.133) .115-.209) .318-.152) .080 (.265-. 1958) and occupational exposures (Briegner et al. 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.125 (.266 (.318-.132) .267 (.108-.082 (<LOD-.178 (.391) . abdominal pain.357-. and eyes.164 (.421) . diarrhea. species.173) .121) .241-. myocardium.255) .127) .108 (.120 (.121 (.238 (.380 (.183) .308) .203) .137 (.425) .298 (.139 (. 1986).Metals than for trivalent compounds (Elinder and Friberg.233 (.317) .104-.480) .209-.159-.115 (.230-.317) .138-.271-.085) .149-. and kidney have been demonstrated in high dose animal studies depending on the dose.146-.126 (.278 (.186) .092-.203) .263 (.130 (.071-. Histopathologic inflammatory and degenerative changes in the lung.122 (. 1986).294) Total .208-.741) .129) .272) .126-.120 (.313-.268) .129 (.109-.333-.265 (.193) .138-.250-.206-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.148-.061-.074 (.226 (.277 (.132 (.127) .148-.253-.338) .113) .162-.127) .255-.143) .320 (. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.417) .116 (.343 (.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 .098-.220) .102-.086 (.310 (.077) .084) . liver.225 (.471 (.130) .300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.263-.118 (.229-.107-.214) .100 (.078 (.143) .115 (.188) .364 (.143) Selected percentiles ( 95% confidence interval) 50th . Ming-Hsin et al. interval) .092) .352) .109 (.120 (.134) .127) . 1988.103-.300) .195-.122 (.741 (. population from the National Health and Nutrition Examination Survey.228 (.191 (.109 (.320-.429 (.

Konings J. Minoia C. Schaller KH. indium. Lauwerys R. Int Arch Occup Environ Health 1995. Industrial Medicine and Surgery (Dec. Skulsukai G. Cordasco EM. Pozzoli L.64(2):182-185. Piatnek DA. Centers for Disease Control and Prevention (CDC). J Clin Pathol 1998. Elinder CG. and hydrogen sulfide. Sabbioni E. Antimony. 1998) or compiled reference ranges (Hamilton et al. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. 2004. EPA. population. Ming-Hsin H.521-523. clinical efficacy. Chemotherapy for leishmaniasis: Biochemical mechanisms. or exposure differences. Stone FD. Kiberd B. and a drinking water standard has been established by the U. Kuo-Juie Y. even when exposure levels were below workplace air standards (Bailly et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Bailly R. Alimonti A. Kentner et al. et al. In: Friberg L. Schacke G. Roland H. Iavicoli I. stibine. Cullen A. Van der Venne MT. Yu H-S. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Suchenwirth R..67:119-123. 2nd ed. et al. Pulmonary edema of environmental origin. Chin Med J 1958.13:361-362. Hamilton EI. Industrial antimony poisoning. Handbook on the toxicology of metals. Chest 1973. Matthews T. Dernehl CU. gov/toxpro2. Stead FM. Buchet JP. Ludersdorf et al. Mayer P.10(3):560-586. 26-42. Wu M-T. pp.16: 33-39. which may be due to methodologic. Dezateux et al. Biomonitoring studies on levels of urinary antimony can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of antimony than are found in the general population.S. Lenert G. Liao Y-H et al. Carelli G. Shao-Chi C.html. VI.. Review of elements in blood.48:93-97.. Antimony trioxide is rated by IARC as a possible human carcinogen. Pietra R. Industrial Medicine 1944. 2002. Chia-Yu H. Costeloe K. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Delves HT. Fuchs A. arsenic. Arch Dis Child 1997. Friberg L.. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Rev Infect Dis 1988..59:469-474. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Stasney J.Metals to antimony have been established by OSHA and ACGIH. External and internal antimony exposure in starter battery production.. Gallorini M. Liao Y-H. 1986. Antimony in blood and urine of infants. Caroli S. Ho C-K.76(2):103-115. environmental levels) and health effects is available from ATSDR at: http://www.atsdr. Dezateux C. Cheng-Wei L. Environ Health Perspect 1998.51:238-240.106:33-39. Stocks J. 1998). J Trace Elem Med Biol 2002. Apostoli P. Wade A. and antimony in optoelectronic industry workers. Sabbioni E.. 20012002. 1991. Kentner M. Element reference values in tissues from inhabitants of the European community. Nau CA. Biological monitoring of exposures to aluminum. and 2003-2004. Earlier measurements in general populations (Minoia et al. J Occup Environ Med 2004. Biological assessment of exposure to antimony and lead in the glass-producing industry. gallium. Br J Ind Med 1991. Pilgrim L. 1994) have reported values slightly higher than those in this Report. et al. O’Regan M. Trace element reference values in tissues from inhabitants of the European community I. Gebel TW. 1990. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Sci Total Environ 1994. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al... Leinemann M.. Arsine. respectively. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Semisch CW.46:931-936. Third National Report on Human Exposure to Environmental Chemicals. Ju-Sun P. eds. Briegner H..76:432436. Iavicoli et al. Weltle D.cdc.e. Bolten C. New York: Elsevier. 1998. 1997). Mahieu P. Luedersdorf R. Yang C-Y. Paschal et al. Atlanta (GA). Vouk VB. 2005. Biomonitoring of a worker population exposed to low antimony trioxide levels. Urinary antimony in infancy. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Delves HT. 1995..)1954. HH. Nordberg GF. References Berman JD. Int Arch Occup Environ Health 1987. Petrucci F. Chen J-R.158:165-190. Dunkelberg. 1987). and future strategies. Mayne P. Information about external exposure (i.

Jackson RJ. Sci Total Environ 1990. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Paschal DC. Werrin M. et al.99-108.76(1):53-59. Chemical food poisoning. Antimony poisoning in industry. blood. Environ Res 1998.Metals in urine. Morrow JC.95:89-105. 27:38-45. Ting BG. Pirkle JL. Sampson EJ. Trace metals in urine of United States residents: reference range concentrations. Renes LE. and serum of Italian subjects. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Industrial Hygiene and Occupational Medicine 1953.

copper arsenates.S. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.Metals Arsenic CAS No.6-141) 53.50-14.80-9. the smelting of copper. Although it is still widely used in the United States.6-35.20 (8.70 (6.30 (7.41 (7.90 (7.25-9. Arsenic trioxide is approved to treat acute promyelocytic leukemia.10-10.70) 8. and arsenates (oxidation states of -3.9-46. psoriasis.70-9.2) 46. +3 and +5). arsenites.6 (15.1) 7.9 (17. lead hydrogen arsenate. and other metals.7) 24. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.55 (7.2-93. pesticides. sodium arsenite. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. General population exposure to inorganic arsenic can occur through consumption of drinking water and.5 (23.0 (22.2 (13.2 (41. and play sets. Water sources contain mostly inorganic arsenate.0-19.0-60.9) 68. arsenocholine. grain.9-34.1) 290 725 1542 03-04 03-04 9.80) 6. Various arsenic compounds were used in paint pigments and for tanning animal hides. and.66-8.9-62.4 (7.10) 10.10-7.90) 16.30) 17.0 (11.5 (34. meats. cacodylic acid. and indium arsenides are used in the semiconductor industry.5-41.3-15.2 (12.19-9.90-8.8 (48.9 (8.1) 15. as alloy in metal bearings.6-43.3) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2557 03-04 03-04 03-04 7.2 (51.8) 7.4 (24.1) 1281 1276 03-04 03-04 03-04 9.90 (5.30 (6. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.02-8. or rarely as elemental metalloids (yellow.29 (8.2-20.8) 34.5) 66.80 (5. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.7-83.4) 13. In the last century. lead. black.6 (13.90 (7.1-18.13-8.5 (36. particularly arsenic trioxide.8-61.1 (38. though in some locations arsenite may be prevalent (WHO.90-11. Arsine (AsH3) is a reactive. trimethylarsine oxide. and gray forms).8) 29. it is found in over 200 crystalline or mineral forms.3-111) 78. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.4 (31.5) 41. ocean and fresh waters.8) 33.90-8.12 (6.5-178) 46. referred to as inorganic arsenic compounds.7) 90th 37. Since the 1940s. Survey years 03-04 Geometric mean (95% conf.000 metric tons annually. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.2) 15.2-61.6) 11.8) 7.8-77.4 (26. and foods. In nature.84) 8. The United States no longer produces arsenic from mining but imports about 22. such as arsenopyrite (FeAsS) and realgar (As4S4). Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.10 (6.5) 95th 65.5) 43. mostly for use in wood preservation (ATSDR. retaining walls.40) 7.00-9. gaseous hydride manufactured in small quantities for use in the semiconductor industry.4 (48.0 (14.4) 60.90-14.34-9.5-19.12-10. semiconductors.7 (11.8) 30.3-19. cancers.00 (6.8) 17.1 (32.74. to a lesser extent. solders. were used as treatments for syphilis.5 (40. see Data Analysis section) for Survey year 03-04 is 0. aluminum.97) 8.77) 6.27) 9.7-95. Arsenic is measurable in most soils.9) 21.90) 75th 16.4) 40. and as homicidal poisons.1-40. arsenic as elemental metalloids may be used in some ammunition.0 (43.5 (14. Arsenic trioxide (As2O3.5-52.7) 65.2-17. population from the National Health and Nutrition Examination Survey.6 (9. Before the 20th century. Also. Gallium. and as a cosmetic to lighten complexion.08 (5. 2005). chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. and produce. interval) 8.6 (32. 180 Fourth National Report on Human Exposure to Environmental Chemicals . to a lesser extent. from coal burning. arsenic compounds.4-65.6) 618 722 1074 Limit of detection (LOD. and arsenosugars. alloys.34-10. Arsenic and its compounds have had many uses in the past and present as medicines.57) Selected percentiles ( 95% confidence interval) 50th 7. 2001).84) 8.50 (8.0 (15.90-7.3) 10. and in lead-acid storage battery grids. mental disorders.

3 (24. EPA’s maximum contaminant level (Hughes..2) 15. 2007.1) 8. 2001).35) 7.66-8.3-41.3) 6.40) 8.99-9.0) 14.0-18.7) 95th 50. Survey years 03-04 Geometric mean (95% conf.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . mine tailings).33 (6.28-7. In aquatic organisms.41) 6.3) 9.5-120) 40. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.8) 22. Chowdhury et al.8 (20.2) 90th 30. Inorganic forms of arsenic demonstrate high acute toxicity. age.0 (17.0) 12.S.59) Selected percentiles ( 95% confidence interval) 50th 7.8) 27.25 (6. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.32 (5. Arsenate is reduced in the body to arsenite (oxidation state +3).76 (6.8-32.01) 7.06 (4.1) 24. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.0-38. and folate status (Chen et al.61 (7.8 (27.3-64.10-16. 2006.86-17.. 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.9 (45.51) 75th 14.4 (40. as observed in Bangladesh where millions of people have been exposed. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.10-8. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established. have caused clinical arsenic poisoning.. 2001). Children may have additional exposures from ingestion of contaminated soils (e.7 (25.47 (7.1) 7.58-10.g.64 (7.2-15.30-9. 2006. arsenocholine. 2007. dust.2 (12.2) 40. Gamble et al.8-62.45) 5.1) 6. 2007. 2003. organic arsenic can be converted back to methylated and inorganic arsenic.88) 7.50 (6.66-8. After absorption. 2001).81-9. kelp.07-9.4 (11. 2001).44) 6..7-18.4-64.0) 33.3-62.0) 26. dose level. EPA.6 (10.9) 53. 2001).88 (5.96) 12. Extremely high groundwater arsenic levels.12-10. Smoking tobacco is also a source of inorganic arsenic.7 (9.4) 54. so exposure to the general population is extremely limited.1) 58. In aquatic sediments.3-53. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. 2001.31 (6.9-56.1 (11.04 (5. 2001). but is poorly absorbed dermally (WHO. 2001).4 (26.93-9.7-34. cacodylic acid and monosodium methyl arsenate.S.S.7 (11.11 (5.5) 290 725 1542 03-04 03-04 8. and arsenosugars.7-188) 27. interval) 8.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.5-17. Though modest bioconcentration occurs in some aquatic life.8 (11.4) 32.6) 45.66 (7. though some reduction may occur in the gut prior to absorption. WHO. The semiconductor dopants. Direct exposure to DMA and MMA may result from use of the two pesticides.01) 11. arsenic does not show biomagnification in the food chain (WHO.6 (17.4 (12.8 (21. and contact with CCA-preserved wood structures.18 (5. 1988).0) 1281 1276 03-04 03-04 03-04 8.2-46. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.0-26.38-10. Fish.8 (12.13) 8.4 (24. NRC.44-11. 2001. population from the National Health and Nutrition Examination Survey.1 (14.5) 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 8.33-10. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.8-75.75 (5.3 (27.23-7. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.0) 42. WHO.00 (6. U.93-8. selenium.47 (6.7-35. gallium arsenide and indium arsenide.4 (42. are used in enclosed ultraclean operations within the semiconductor industry..24 (7. Steinmaus et al.1-36.47-6.0 (31. 2001). and some other seafood can contain organic forms of arsenic including arsenobetaine.20-9..75) 13.5 (9.6 (35.6-17. shellfish.04) 7. inorganic arsenic is widely distributed within the body. trimethylarsine oxide (TMAO).9) 13.5) 17.25-9.7-17.0-69. 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. Tseng.7) 28.

30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Although arsenate is reduced in the body to arsenite.S.. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. Cohen et al. apoptosis.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. hyperkeratosis.20 (<LOD-1. 2001). 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. 2001). substitution in phosphate metabolism. 2007).60) 1. NRC. Bredfeldt et al. and endothelial injury (Kumagai and Sumi.80) 1. peripheral vascular disease.EPA.50) 621 725 1078 Limit of detection (LOD. including drinking water sources with elevated arsenic levels (e. can cause peripheral sensorimotor neuropathies.60) 1. WHO. Bangladesh. 2001... 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. 2001. and altered gene expression. gluconeogenesis. and hyperpigmentation of the skin (NRC.S. food residue.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. Studies of arsenic at levels typical of U. 2006) or when exposure occurs in smokers (Chen et al. arsenic trioxide) includes hemorrhagic gastritis with nausea.10 (<LOD-1. < LOD means less than the limit of detection. Survey years 03-04 Geometric mean (95% conf. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. 2007. WHO.. which may vary for some chemicals by year and by individual sample. 2001). including inhibition of numerous enzymes.. The U. 182 Fourth National Report on Human Exposure to Environmental Chemicals . and it also will inhibit succinate dehydrogenase. hepatotoxicity. Cardiac arrhythmias. cell transformations. and by uncoupling oxidative phosphorylation (NRC.10 (<LOD-1. Chronic human intake of arsenic at less than acutely toxic doses.10 (<LOD-1. vomiting. increased oxidative stress. population from the National Health and Nutrition Examination Survey. 2006. drinking water have not been associated with increased cancer rates (Schoen et al. 2006. interference in signal transduction pathways.0. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. and childhood neurodevelopmental effects in observational human studies. hypertension. and production of glutathione may be affected as well.50) 1.20 (<LOD-1. The organic forms of arsenic occurring in seafood have little known toxicity. 2001). WHO. leading to a decrease in adenosine triphosphate energy production. Arsenic has many actions demonstrated in cellular studies.. lung. and diarrhea. NRC. Acutely. and DNA repair inhibition (Cohen et al. 2001). and bladder cancer (IARC. 2007.. renal failure. cytotoxicity. 2004). 2004.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. 2000.. With chronic exposure. 2006. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. Taiwan.S. Such actions may lead to decreased energy production.20 (<LOD-1. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring.g. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al.30) 1. some of these effects may take years to develop. 2004). 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. 1998. see Data Analysis section) for Survey year 03-04 is 1. noncirrhotic portal hypertension.10 (<LOD-1. Chronic elevated arsenic intakes have been associated with diabetes. WHO. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e.g. 2001). Chile). U.20 (<LOD-1. fatty acid oxidation... hematocytopenias. respectively.10 (<LOD-1.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. Chronic arsenic exposure in humans is considered to be a cause of skin. Cellular glucose uptake.EPA has established drinking water.. which can lead to dehydration and shock. Raml et al. but additional or confirmatory research is needed (Kapaj et al.

2004. Shalat et al.. 2007. population (Rubin et al. Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al.69 (<LOD-3... 1986). and were about two-fold lower than those for the U. Offergelt et al.. 2008. and the FDA has established a bottled drinking water standard. 2006). arsenic has been fetotoxic and teratogenic.. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. 2006). urinary arsenic levels have been accepted as a good biomarker of dose (WHO.33 (<LOD-3.. 2006).18 (<LOD-3. environmental levels) and health effects is available from ATSDR at: http://www.. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. In the German Environmental Survey III of 1998. Levels of total urinary arsenic in the U.. 2008).. 2006..html. 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. 2000).75 (<LOD-2.18) 3. 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.50) 1. population from the National Health and Nutrition Examination Survey. 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..cdc. Vahter et al. 2003..19) 3. Fourth National Report on Human Exposure to Environmental Chemicals 183 . Survey years 03-04 Geometric mean (95% conf. DMA produced bladder cancer in some chronic rat studies (Cohen et al. 2001). had decreased since the prior 1990– 1992 survey. 2007. 1999. hand washings from children playing on CCA-treated wood compared to children playing on non-CCA-treated wood playground equipment were slightly to fivefold higher (Kwon et al.41) 3.80 (<LOD-4. Josyula et al. 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. Meza et al.e.61 (<LOD-3. 2004. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al... gov/toxpro2.S.Metals compounds. but generally only at maternally toxic doses (WHO. population in NHANES 2003–2004 (Schulz et al.S. Caldwell et al. Additional information about external exposure (i.S.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 1998. Pellizzari and Clayton. Consequently.33 (<LOD-3.. 2006.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2..04 (<LOD-3.. 2000. In a Nevada town where groundwater levels were naturally elevated. 1999). 2006). although urinary arsenic levels were not associated with CCA contact (Shalat et al. Calderon et al... Valenzuela et al.atsdr.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Pellizzari and Clayton. 2008).S. Compared with this Report. WHO. 2006. Caldwell et al.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. Pellizzari and Clayton 2006). 1992. 2001). 1999. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. Shalat et al.75 (<LOD-2... the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. Though CCA-treated wood contains several thousand times more arsenic than untreated wood.00) 1. 2001). median urinary total arsenic levels in 4052 adults varied with seafood intake. In animal studies.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.

.28) 1.. Blom et al. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. China. 2008.1) 18.. Caldwell et al.g.6.0 (27. Chowdhury et al.6 (11.70 (5. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and.00) 3.2 (6. respectively.600 (.5) 29.4-35. Arsenate.50-6.8 (12. In the late 1980s.70-21.60) 1. Some noncancer effects of arsenic (e.3-39.93) 1.4) 31. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.80 (3. The higher percentiles of total urinary arsenic levels in the U.9 (7. Aposhian et al. Sun et al.871-1.20 (1.45 (1.43-1. For residents of Inner Mongolia.500-1.70-21.7-22. 1985.400-.8 (17. Tseng et al..800-4.40-6. arsenite.10) 8. 2005.3) 95th 35.700-1. population in the NHANES 2003–2004 subsample.20-3.50) 90th 16. Caldwell et al.30 (2.. WHO.7 (21. and TMAO. 2000.5) 292 728 1548 03-04 03-04 1.17-1.66 (1. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.S.Metals other areas of the world (Ahsan et al.29 (1. 2000. Caldwell et al.80 (. Valenzuela et al. 2000. and other factors such as nutrition. After recent seafood ingestion. 2008).00 (. see Data Analysis section) for Survey year 03-04 is 0. 2008).7) 15. arsenobetaine. 2005.00-4. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. when seafood organic arsenic is subtracted). DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. 184 Fourth National Report on Human Exposure to Environmental Chemicals . 2007) with higher levels of arsenic in the drinking water.800) 1.700-1.800-1.20 (4.6. vasospasm. Also.20-25.6 (13.800 (. dermal keratosis. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al. geometric mean levels were about 70-fold higher than for the U. 2007). methylation capacity. Pellizzari and Clayton.1-51.50) .3 (21.30 (1.83) Selected percentiles ( 95% confidence interval) 50th 1.0-23.40) 5.900-1.11-1..2-35.9) 13.7) 13. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.1-94.50) . and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.70) 6. MMA. and TMAO were detected in only 7.70 (3..900 (.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.05) < LOD .19 (. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. 2008). Survey years 03-04 Geometric mean (95% conf.00 (1.1-25. 1990. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. When seafood intake is avoided..4) 23.. 2001). population (Ahsan et al..9 (6.4.20) 18..0) 4. 2003).9-23.6-44.20) 7.S.0) 29.90-29. DMA and MMA. In most human studies. arsenocholine. In the residents of a Chilean town who consumed water with high levels of arsenic.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. with DMA.20-190) 31..e. arsenocholine.00-6. 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.55 (1.3) 35.. interval) 1.3% of a representative sample of the U.5) 32. in NHEXAS 1995–1996.. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.2-38.4 (16. 1..10 (4. 2005.7 (13.3 (9.31-1..40) 75th 5.80) 1.5) 621 725 1078 Limit of detection (LOD. Caceres et al.3) 1284 1284 03-04 03-04 03-04 1..68) . and duration of exposure are also considered important. Individually measurable species resulting from inorganic arsenic exposure are arsenate.0 (26.S.30) 2.62) 2..37 (1.74 (1. population showed a higher contribution of arsenobetaine (Caldwell et al.1) 45.8) 35. 4.10) 4. arsenite.S. Measurable organic arsenic species in this Report are three biologically generated environmental forms.48-2. < LOD means less than the limit of detection.6 (25. These associations are stronger at higher urinary levels.60-3..8-40. which may vary for some chemicals by year and by individual sample.8.30) 10. and 0.5 (14.90-7. 1996.5 (26. population (Sun et al.40-7.800 (.00-12. 2008).20 (. 2008. and two methylated metabolic products. 2006). 2001..00-1.20) 3.80 (4.8-50.80-5. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.20 (2. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.

901-2.7) 9.9-18.5-20. 2008).Metals as with DMA.909-1.1-18.82) Selected percentiles ( 95% confidence interval) 50th 1..36) 2.05) 1.9 (13.8) 29.6 (9.4 (11. 2003.4) 13.40 (1. WHO.5 (18.6-32.28) 1.6 (6.67) 1.91) 90th 16.14 (1.2 (13.5) 17.4-28.67) 4.3 (10. 2008).44 (1. 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.19-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.786-1.638) 1.5) 26.7) 30.80) .43) 14.78-5. 1992.25-7. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.47 (1. Vahter et al.16 (.3-24.83) 8. Fourth National Report on Human Exposure to Environmental Chemicals 185 .531 (.S.6) 19.76-27.65 (1.37-2.68 (1.18-1.6-46. In recent years.61-6.05 (.10 (.50-15.2 (4.72) 12.4) 32.51) 5.54 (1.13-39. 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. Information about the biological exposure indices is provided here for comparison.2 (12. which is below the ACGIH BEI (Caldwell et al..25 (.400-. 2007).29-14. Caldwell et al.1) 26.43) 75th 5. 2001).2 (12. Offergelt et al.5 (18. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0-36. 2006.73-6..88) 2.53 (.64-29.32-7.83) 2.15-1. interval) 1.9 (25.80-153) 17.0 (9.78 (3.3) 1284 1284 03-04 03-04 03-04 1. Survey years 03-04 Geometric mean (95% conf.15-4.30-1..6-29.12) < LOD .4-82. 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.7) 17.. Sun et al. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.9 μg/L.45) 1. The 95th percentile of the U. population from the National Health and Nutrition Examination Survey.62-6.00 (3.79 (1.833-1.21) 5.9) 14.959-1. 2001). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.612-1.9) 32.50-7.4) 292 728 1548 03-04 03-04 1.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.1 (26. 1986.70) 5. population for the sum of inorganic related species was 18.3 (10.51-2..4-21.81 (4.82) 4.55) 1.88 (5.30) 1.47 (2.3) 95th 29. 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.4 (24.4) 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 * * 1.877 (.93 (1..91 (4.00 (1.29 (4. not to imply a safety level for general population exposure..S.1-36.40) 1.15-1.58 (3.39-3.938-1. 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.11 (. 1998.

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

Fourth National Report on Human Exposure to Environmental Chemicals 187 .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. 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. Survey years 03-04 Geometric mean (95% conf.44) 2. Survey years 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.08 (<LOD-4.00 (<LOD-3.00) 1.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3. * 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 1.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.40 (<LOD-1.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00 (<LOD-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2. see Data Analysis section) for Survey year 03-04 is 1.20 (<LOD-1.80) < LOD 621 725 1078 Limit of detection (LOD.95 (<LOD-2.S.S. which may vary for some chemicals by year and by individual sample.

0 (13.9 (11.00-3.0) 10.0 (10.71) 3.60-4.33) 3.73 (3.6) 292 728 1548 03-04 03-04 3.32 (8.00 (5.6 (9.88 (4.00-15.55 (2.84-8.0 (12.69 (3.00 (3. population from the National Health and Nutrition Examination Survey.79 (3.89 (3.00-15.0) 9.11) 4.05) 3.0) 16.31-4.50-15.32-10.00-3.77 (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 3.71-4.0 (12.32 (4.03 (3.9 (7.0 (9.4 (7.00-9.17-6.3 (7.0-16.0) 11.24) 3.0) 17.70-3.00) 7.22) 4.0) 621 725 1078 Limit of detection (LOD.00-5.92) 3.20-4.0) 16.80-6.14) 3.80-5.00 (4.74 (2.57-5.0) 12.82) 3.2) 10.1-15.82-9.1-22.00 (5.05) 5.60-6.45 (8.00 (5.46 (4.1-18.00 (3.00) 3.27-2.00-8.25 (4.78) 4.0 (14.48 (2.24-4.0 (8.00-12.90 (3.86-7.78 (4.00-13.95-6.1 (8.13-4.61-16.27-5.0) 95th 16.00) 3.50 (4.00 (6.34) 3.60-3.45) 8.34-4.37 (2.0-25.34 (3.19) Selected percentiles ( 95% confidence interval) 50th 3.70 (3.69-3.0 (11.42) 3.70) 5.3 (8.80 (4.0) 11.27 (2.80) 7.0 (9.9) 11.06) 5.0) 292 728 1548 03-04 03-04 4.8) 7. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.12-4.00) 75th 6.31) 4.00) 6.00) 6.00-15.00-11.00-4.00 (3.00) 6.08 (2.28) 2.84-18.0 (9.6-18.0-17.00 (7. Survey years 03-04 Geometric mean (95% conf.70-4.17-4.00) 90th 11.00-11.45) 3.71 (4.S.72 (4.14) Selected percentiles ( 95% confidence interval) 50th 3.00-4.65-8.00-4.00) 9.S.7) 12.0) 13.95-4.10) 3.33-4.15) 4.0) 9.00 (7.00) 6.00-4.39-3.0) 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 Sample size 2568 03-04 03-04 03-04 4.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .00-11.00-7.20-12.00 (5.9) 5.0) 13.98) 4.49-4.05) 10.0-19.9) 13. interval) 3.7.34 (3.70-12.69 (3.27 (3.00) 12. interval) 3.71 (3.92-12.17 (2.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00-10.00-7.0 (8.0-16.9) 12.85 (3.73) 6.94) 3.44 (2.97-3.52) 3.5) 95th 13.59 (6.95 (4.37 (3.03-6.5) 12.0) 14.00 (3.69-6.30 (7.67) 9.00) 5.90) 5.90) 2.34-4.0 (10.20) 11.5 (11. Survey years 03-04 Geometric mean (95% conf.00 (6. see Data Analysis section) for Survey year 03-04 is 1.60-7.7-16.30) 3.16 (2.00) 4.74) 90th 9.80) 2.09 (7.91) 75th 5.8) 7.00-22.00-4.00 (3.0) 9.94-3.7) 1284 1284 03-04 03-04 03-04 4.65-6.81 (5.00-7.61-11.00 (6.00-12.0 (10.0 (10.48 (3.44) 5.10) 6.86-21.29-4.11 (3.86 (2.7 (10.38 (3.0-12.12 (3.00 (5.49) 10.00-7.00-4.0-18.0 (13.00 (3.67) 8.3 (8.18 (6.62) 4.16-11.50-5.57 (3.6) 1284 1284 03-04 03-04 03-04 4.00) 4.0) 17.7) 13.16 (4.80-3. population from the National Health and Nutrition Examination Survey.82-5.95-3.0-17.

86 (2.00-2.10 (1.40) 1.40-3.90 (1. Survey years 03-04 Geometric mean (95% conf.00-4.40-3.30 (1.63 (<LOD-1.30) 1.30-1.46-2.70-2.10 (.40) 2.07) 2.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.07-3.90) 1.70-3.816 (<LOD-.20 (1.50) 1.31-3.86 (2.79) 2.90) 2.62) 2.00) 1.90 (2.45) 3.96-2.00 (<LOD-1.00-2.80-2.28 (1.58) 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 1.50 (2.28 (1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80 (1.07 (1.50) 621 725 1077 Limit of detection (LOD.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.57) 95th 2.00) 2.00 (1.S.80) 1.50-2.30-1.50 (<LOD-1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.70-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.43-3.40) 1.70) 2.60 (2.10-3.80 (1.30 (1.20 (1.00-1.77) 1.10) 95th 2.40 (2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.30) 90th 1.18-1.53-2.80) 1.86) 2.80-2.10 (.20 (1.31 (1.900-1.853-1.30) 1.80 (1.00 (<LOD-1. population from the National Health and Nutrition Examination Survey.61-3.88 (1.14-1.40-2.90) 2. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.33 (1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.71-2.60) 1.84-3.30 (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 1.40-2.82-2.33 (1.82-2. population from the National Health and Nutrition Examination Survey.37 (1.60 (1.00) 1. < LOD means less than the limit of detection.18-1.54) 90th 2.61) 2.70-2.60) 2.20-3.53 (1.85) 2.10-1.20) 2.15-1.00 (2.00) 1.20-1.30) 2.20 (1. Survey years 03-04 Geometric mean (95% conf.22) 3.36) 1.11-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 03-04 is 0.S.23) 1.46 (1.30-2.70-2.35-3.20 (1.60-2.9.52 (2.50 (1.85) 1.10 (<LOD-1.80 (1.80 (2.88 (1.20 (1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00) 2.22 (1.05-1. which may vary for some chemicals by year and by individual sample.16 (2.00 (2.86) 3.36 (1.40 (1.81) 1.60) 2.10) 2.93) .10-1.50 (1.00-1.30 (1.88-2.985) 1.34) 2.73-2.17) 2.10 (1.

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

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08 (6.12) 7.31 (2.87-9. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).81-2.59-11. 01-02.56 (2.25 (1.10 (2.71) 1.65 (5. The general population can be exposed to low amounts of barium in air. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.78-2.00-76. such as brazil nuts.75) 2.36-1.50) 1.86 (4.8 (6.20-1.71) 95th 6.54-8.78) 1.64) 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 2.43 (1.56) 4.63 (1.65-8.50 (1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.54) 1. population from the National Health and Nutrition Examination Survey.98) 1.50) 2.4) 9.07 (2.61 (3.28-1.48) 1. Barium compounds are also used commercially in paint.70-2.10-5.88) 7.30 (5.70-6.63) 1.26) 5.29-1.80 (2.08-8. depilatories.10-4.20-5.93 (4. In nature.63 (5.61-8.82-6.60-2.92) 2.82) 1.94-6.11 (3.72) 1.10 (3. fireworks.80) 7.60 (1.69 (1. barium sulfate and barium carbonate).84) 5.61 (5.80-2.40 (1.40) 7.30-3.25-1.90) 2. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.36 (4.63) 1.73-5.50 (3.22-1. Small amounts of barium can be released into the air during mining and other industrial processes.35-1. Fourth National Report on Human Exposure to Environmental Chemicals 193 .95 (4.76-3.44-5.90-13.40 (1.60) 1.56 (6.21 (1.10) 1083 1335 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.77 (3.55-7.10 (4.67) 6.50 (1.09 (1. Barium salts have also been available as rodenticides.22) 6.87-14.49 (1.70) 5.50 (4.14-6. Some barium salts are freely soluble in water.60-6. see Data Analysis section) for Survey years 99-00.38) 2.70) 1.09 (2.12 (2.33 (1.87) 7.40 (5.66 (4.71 (2.50) 2.51) 1.43 (5.39 (1.85 (2.76) 1.93-8.38 (1.11-1.77) 1.12) 6.. are high in barium (Genter.31-2.86 (4.50-6.37-8. such as barium chloride.76 (3.63 (2.60-6.30) 5.12.15-1.53) 2.47-1.45) 7.85) 1.62 (1.35 (1.27 (1.60 (2.51) 2.30) 5.76-2.61 (1.80 (1.04-2.90-2.73 (5.18 (6.30-5.00) 1.48 (6.78) 1.80-5.34) 2.65-1.70-5.01-7.40 (5.90 (6.64-3.20-8.86-4.49) 11.05-2.70 (1.24 (4.20) 2.63 (8.20 (4.49) 2.8) 5.87 (5.63) Total 1.70 (5.54) 2. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.46) 1.50 (1.25-11.50 (1.74-2.15 (1.40-13.90) 4.8) 9.00) 6.49) 4.4) 6.11 (3.90-9. In single dose animal studies.50 (6.26) 2.47-1.05% of the earth’s crust.65-5.40 (5.50-1.39) 4.28) 90th 5.38) 8.73) 3.30 (2.17-1.02 (7.29-5.68 (1.97 (1.15-11.56 (1.32-1.48-4.27) 2.90 (4.78-3. interval) 1.38 (1.54 (6.37) 5. tiles.44-2.10) 3.9) 5.50 (5.54-1.00-8.00 (1.99-5.53-5. and ceramics.00) 1.57 (5. 2001).12 (2.15) 5.48-4.30-1.41) 1.15 (6.46) 1.16 (1.54) 1.00) 4.50-1.60-10. rubber.40) 3.65) 1.49) 8.76-7. soluble forms of barium.70) 4.30) 5.04-6.60) 4.32-7.14 (6.21 (1.54-1.21-8.41-1.77-3.39-1.39) 1.21-2.20 (1.80 (5.4) 7.20-1.70-8.48) 1.20-6.53) 1. and 0.30-2.34 (2.44 (1.62) 1. and food.51 (1.47) 4.35 (2.30 (3. bricks.74) 3.39 (1.75-3.95-6.20-8.27 (1.37 (4.36 (1.96-2.37) 1.80) 6.91) 6.43) 6.30-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80 (1.91 (2.20 (3.30) 8.41-3.54 (2.14-1.26-7.55-3.88) 1.40 (4.61 (1.57-7.52 (1.60-3.34 (1.43 (1.86-5.S.61 (2.72) 4.36-1.88 (5.01 (4.30) 3.18-1.20-1.66) Selected percentiles ( 95% confidence interval) 50th 1.35 (3. Workers employed by industries that make or use barium compounds can be exposed to barium dust. and 03-04 are 0.73 (6. whereas others are practically insoluble (e.29) 5. 0. water.73) 1.80-7.30 (1. it combines with other chemicals such as sulfur or carbon and oxygen.90) 2.70) 3.30 (5.56) 1.59) 3.34 (1.26-1.20-8.12.46-1.49-9.87-3.57) 3.60) 3.35-1.70-2.50 (1.11 (2.65) 3.43) 2.00-3.20-1.85) 1.24-1.10) 5.74-3.70) 1.03 (1.42 (1.22-1.31.g.06-1.60) 1.70) 7.91) 2.71-9.35) 5.49-1.90) 1.40 (1.56 (1.36) 5.Metals Barium CAS No. Certain foods.15-1.70-3.52 (4.65) 1.12-1.80 (1.50 (2.19-1.45 (1. 7440-39-3 Medically.80-3.90 (1.50-6.50 (4.64 (1.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.35-4.30) 2.19) 2. respectively.37-1.62) 1.88) 4.30-1.50) 4.81-2.80 (2.18) 3.50 (4.87-7.80) 1.40) 7.16) 5.32) 8. Barium compounds are used by the oil and gas industries to make drilling muds.24-1.30) 4. glass.82) 2.93-2.06-2.99 (4.62 (1.00 (2.71) 2.72) 75th 3.81-3.87 (6.15 (2.51) 7.2) 6.86) 6.1) 9.

34) 1. water solubility.46) 1.16) 11.00-1.38-1.22-1.77) Total 1.26-1.74 (5.96) 4.65 (2.97-4.59) 2.881 (. 1994.30 (1.00 (3.41 (1.36-1.59) 1.62 (1.29) 1. Toxicity from soluble barium salts is rare.41 (2.703-1.45) 1.47 (5.56) Selected percentiles ( 95% confidence interval) 50th 1. vomiting.76 (4.88 (2.96) 4.12) 2.48 (1.01 (5.84) 2.46 (2.02 (3.50) 1.00 (3.96-6. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.45-6.36 (3.45-1. chemical form.55) .963 (.28-6.48 (1.0) 5.68 (2. 1986).45 (3.33 (5.00 (2.31 (1.59 (1.777-1.754-1.69 (5.54 (1.41) 5.58) 75th 2.51-3.Metals was eliminated primarily in feces and to a lesser extent.46) 2.47-8.26-4.62) 2.16 (1.2) 6. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.36-2.31-1.11-2.69-9.46-22.86 (2.50) 2.60 (1.61) 2.50) 1.38) 1.10-1.27) 7.62 (4.39) 4.26-1.53 (2.31) 5.25-11.65 (5.16-1. weakness.18 (1.37-2.24-6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.36 (5.29-1.74) 1.37-1.05-1.50) 297 368 290 621 762 725 1262 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.03) 3.92) 2.49-1.75-3.905 (.23-1.4) 5. 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.77-5.68) 1.91 (3. interval) 1. Insoluble barium salts.48-3.75-22. Barium is not rated for human carcinogenicity.73) 2.35-1.60 (1.43) 1.72) 6.55-5.76) 2.39 (3.41) 4.62 (2.75) 2.48-5.75) 2. in urine.56 (1.77) 1.99) 1.58-6.52 (3.75) 1. paralysis.75) 1.40-1.97-3.24 (5.34 (1.51) 4.10) 6. 1990).33-4.52-10.39-5.42) 1.66 (1. and route of exposure.10-2.77) 1.45-1.29-7.33) 6.24-1.710-1.76 (2.3) 6.01) 1.31 (4.38 (1.99 (2. NTP.24-6.83) 3. 1984.59 (1.73-4. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.25) 4.82) 1.90-2.08-2.73-2.44 (1.00) 6.87) 1.28-1.06) . 1985.19-1.37 (1.2 (3.4 (5.59-7.96) 7.02) .20 (1.78 (2.38-5.77) 5. Following intravenous injection in animals.55 (1.81-6.22-4.36-1.45 (1.79) 1.15-4.53-21.48-1.48) 2.48 (1. Chronic high doses in animals resulted in kidney damage (McCauley et al. diarrhea.32) 2.04) 5.01 (4.00) 4.30 (1.63-4.28-11.83) 2.51) 6.11) .64 (1.55-6.33 (1.09) 6.89 (2.79-5.21 (1.10 (6.04 (2.76) 2.S.26-1.50 (4.52) 1.80) 4.51 (1.36 (1.33) 1.03-1.56 (1.06) 2.19-1.39 (2.58) 4.91 (3.19-2. are not absorbed when administered.97) 1.18 (1.51) 4.32 (1.99 (4.39-10. hypertension.76) 1.60 (2.36 (1.23-5. Perry et al.24) 3.88 (6.40 (1.58 (4.34-3.68-3.26) 4.55 (1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.29-4.22-2..27 (2.86) 5.98 (2.29 (1.08-1.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.82) 1.43-6.76-3.880-1.60 (5.39-1.25 (1.85-5.38 (1.891 (.47) 1.20-1.921 (.96 (4.34-1.51 (1.3 (6.22-1. 2001).24-3.03) 2.33-1.00) 1.54) 2.96 (4.52-4.32 (1.30) 2.81-6.29 (3.29-3.04) 1.28 (1.14-2.33 (1.00 (5.96) 4.40 (1.00) 4.19-1.915 (..20) 4.47 (2.68 (3.76 (3.13-3.47) 10.52) 2.70) 1.23-2.13-2. 1989).35-3.64 (1.38 (4.64 (1.38-7.60 (2.68 (3.20-2.77) 1.81-7.24-11.56) 4.31-1.02) 4.70) 10.44-2.832-1.55 (5.26-1.37) 2.72) 4. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.28) 5.57) 2.58 (2.00-7.92 (4.63) 1.03) 1.86-7.57-5.80) 3. Symptoms following acute high dose include perioral paresthesias.10) 3.03-1.84 (3.64) 7.38) 4.11) .44-2.68-3.57 (6.46) 3.53) .24-1.72 (2.60) 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 2.59) 1.24 (3.80-6.0) 7.49-1.20-8.28-7.35-1. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.89) 90th 4.39 (2.45) 95th 6.27) 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) 3.52) 7.97 (4. Wones et al.64) 7..45-8.51 (3.49 (1.39-1.38) 1.8) 4.2) 5. and cardiac dysrhythmias.32 (2. The health effects of exposure to barium compounds depend on the dose.58) 1.02-5.39 (2.61 (4.34-5.54) 1.47) 4.31-1.91-2.37 (1.29-4.56-3.36 (3.97 (5.49-1.84-2.42) 1.40 (1.0) 6.32) 2.38 (4.74) 1.42 (4.67-6.57-7.91) 2.49 (1. a benign condition that may occur among barite ore miners.64 (1.54 (2. such as those used in medical radiographic procedures.55 (4.41 (1.71 (5.57-10.47) 1.70) 4. population from the National Health and Nutrition Examination Survey.27-1.27-3.84-5.

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

and 0. aircraft. eating food.170) < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . are mined for commercial recovery of beryllium. and dental bridges. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. 196 Fourth National Report on Human Exposure to Environmental Chemicals . and 03-04 are 0. bertrandite and beryl. and machine-parts industries. and from breathing tobacco smoke. nuclear. 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 . see Data Analysis section) for Survey years 99-00. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and refined beryllium is used in mirrors and special metal alloys for the automobile. Low-level beryllium exposure in the general population can occur through breathing air. near some hazardous waste sites. Beryllium compounds are commercially mined. beryllium is used in instruments.13. electrical. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. computer.13.160) < 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.13. x-ray machines. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton.140 (<LOD-. In studies of laboratory animals. respectively.Metals Beryllium CAS No. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey. coal. the lightest of all metals. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. 01-02. Exposure to beryllium occurs mostly in the workplace. 0. soil. and volcanic dust.130 (<LOD-. Two types of minerals. 7440-41-7 General Information Pure beryllium is a hard gray metal. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames.S. In medicine. or drinking water containing the metal. and can be found in mineral rocks.130 (<LOD-. which may vary for some chemicals by year and by individual sample.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 .

or berylliosis. based upon excess lung and central nervous system cancers in studies of workers. EPA. and drinking water and environmental standards have been established by U. 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. Chronic beryllium disease.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. NTP considers beryllium to be a known human carcinogen. Fourth National Report on Human Exposure to Environmental Chemicals 197 .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 . S. Skin exposure can result in delayed hypersensitivity reactions. including contact dermatitis and subcutaneous nodules.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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. IARC has classified beryllium as a human carcinogen. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response.231 (<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. which produces pneumonitis.333) < LOD < LOD < LOD < LOD 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 2002). respectively. 2003. Maier.281 (<LOD-. 1990).346 (<LOD-. population from the National Health and Nutrition Examination Survey. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. 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 . Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH.S.

Apostoli P. Sci Total Environ 1990.S. Trace metals in urine of United States residents: reference range concentrations. Gallorini M. Maier L. Schaller KH. 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. Sci Total Environ 1994.atsdr.e. Available at URL: http://www. population are lower than levels in workers. A study of 46 elements in urine. 106.htm. which approximate this Report’s limit of detection.. 2001).74:162-166. less than 0. References Apostoli P. Minoia C. Paschal DC. Hamilton EI. Pirkle JL. Hamilton et al. Howerton K. Weston A. McCanlies EC. plasma and urine and a critical evaluation of reference values for the United Kingdom population. 20012002. Levels of beryllium in urine for the U.S. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Ting BG. VI. Sabbioni E. Kriess K. Beryllium [online].inchem. Costa R. Comparison of representative ranges based on U. Ash KO. et al. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. 198 Fourth National Report on Human Exposure to Environmental Chemicals . blood. Pozzoli L.Metals (i. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures.org/documents/ehc/ehc/ ehc106. Genetic and exposure risks for chronic beryllium disease.. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. it is likely that urinary beryllium levels in the U. 0. 3/27/08 Komaromy-Hiller G. Am J Epidemiol 2003.gov/toxpro2. Element reference values in tissues from inhabitants of the European community. Atlanta (GA) 2005. Paschal et al.157:388-398. and the 95th percentile for males in NHANES 2001-2002. 1998). and 2003-2004. Environmental Health Criteria..23:827-839. Minoia et al. International Programme on Chemical Safety (IPCS). Environ Res 1998. Clin Chest Med 2002. HLA-DPB1 and chronic beryllium disease: a HuGE review. and serum of Italian subjects. Centers for Disease Control and Prevention (CDC).158:165-190. Third National Report on Human Exposure to Environmental Chemicals. patient population and literature reference intervals for urinary trace elements. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Sabbioni E. Review of elements in blood.13 μg/L. Andrew M. population were generally undetectable in NHANES 1999-2000. In other studies. Sampson EJ.. 2000.12 to 0. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Jackson RJ. Int Arch Occup Environ Health 2001. 1990.76(1):53-59. Trace element reference values in tissues from inhabitants of the European community I.html. environmental levels) and health effects is available from ATSDR at: http://www. Van der Venne MT. Clin Chim Acta 2000.296(1-2):71-90.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller..S.e.1 μg/L). Given these results. Morrow JC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. They reported urinary beryllium levels ranging from 0. and the fact that most NHANES participant levels were undetectable.cdc. Pietra R. 1990.95:89-105. et al.

500) .386-.00-1.300-.00-1.50 (1.300) .400-.600) .40 (1.600-.50-1.20-1.60) 1.400 (.600-.300 (.400) .300-. 7440-43-9 General Information Cadmium is a soft.600 (.300) 1.500 (.500-.400) .800) .900-1.600) 1.gov/minerals/pubs/commodity/cadmium).60) 1. and 0.300-.600 (.00 (.20) 1. U.500-.00) .50 (1.00-1.70) 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 .400-.20-1.400) .20-1.300) .200 (<LOD-.449) Selected percentiles ( 95% confidence interval) 50th .500 (.400) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-.10 (.50) 1.30 (1.296-.60) 1.362-.3.700) .300-.80 (1.80) 1.400 (. malleable.600 (.500 (.400 (.600) .60 (1.40) 1.20) 95th 1.14.60) Total * .900-1. plastic stabilizers. or copper smelters (U.00-1.40 (1.20 (.10) 1.600) .60 (1.400-.300) .600-1.900-1.304 (.600) .300-.400) < LOD .10) 1.10) 1.600) .400) < LOD .300 (.500-.600 (.600 (.10) 1.800 (.20) .200) .300) . as zinc sulfide) and to a lesser extent.255) .400 (.300-.600 (.30) .70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. lead.900-1.337) .400 (.300-.60 (1.800) .00 (.20) 1.468 (.600) 90th 1.40 (1.300) .00-1.400) .427) * .300 (<LOD-.300-.359-.500) .400) < LOD < LOD < LOD .00-1.300) .300 (.500-.00 (.700) 1.300 (. and incineration of municipal waste materials.400) .500) .500 (.70) 1.500-.30) 1.00) .400 (.300 (.00 (.00-1.00 (.70) 1.20) 1.403 (.900-1.50) 1.403) .500 (.60 (1.513) .300-.00 (1.700) .10 (1.60 (1.40 (1. see Data Analysis section) for Survey years 99-00.900 (.10) 1.800-1.300 (.300-.400-.usgs.00-1.400 (.235 (.412 (.700) . during refining of lead and copper from sulfide ore.421 (.289-.300) .366) * * .600 (.700-1.10) 1.361-.900-1.50) 1.10 (1.300) .10 (1.30-1.300) .424) * .600 (.400 (.400) .395 (.425 (.600 (.10 (1.10 (1.40 (1.10) 1.10 (1.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .344) .420 (.441) * .500-.200 (<LOD-. coatings and plating.304 (.40-1.3. respectively.300-.600) .393 (.500-.400-.90) 1.700-1. and 03-04 are 0.300 (<LOD-.300 (.400 (.400) < LOD .300 (.30-1.367-.500-. Cadmium also may be emitted into the air from zinc.300) .200-. Since 2001.326 (. population from the National Health and Nutrition Examination Survey.300 (<LOD-.00 (.400-.300 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20-1.700) .300-.600) .300-.10 (1.500 (.500) .600 (.300-.50-1.500-. interval) .30-1.400 (.426-.300) .800-1.20 (1.900-1.331) .60-1.309-.400) . which may vary for some chemicals by year and by individual sample.30) 1.200-.300 (.600 (.600) .300 (.400) .700-1.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .313 (.50 (1.400) .500-.00 (.300-.378-.452) .460) . cadmium use has declined in response to environmental concerns (http:// minerals.500) .40 (1.600 (.200 (.500-.50-1.200-.600) .376-.700) .500-.500-.80) 1.600 (.300) .50-1.700) . Other uses include pigment production.40 (1.40-1.400) .900-1.378 (.600 (.300 (.500-.400-. Fourth National Report on Human Exposure to Environmental Chemicals 199 .700) .40) 1.400 (.283 (.500-.20-1.500-.300-.20) 1.500 (.216-.20-1.400 (.900-1.30-1.600-.800 (. 0.400-.300 (.400-.300-.368-.300-.300-.500) .700 (.500-.470) * .10) 1.00 (. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.300) 75th . The predominant commercial use of cadmium is in battery manufacturing.300-.20) 1.200-.S.700) .400) .70) 1.275-.00 (. and nonferrous alloys.30) 1.400) .S.200 (.304-.20) .200-.398) < LOD < LOD < LOD < LOD < LOD < LOD .00 (1.400 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.300 (. EPA.400) .300 (.400-.50 (1.800) 1.400-.300-.900-1.00-1.500) .500 (.200) .Metals Cadmium CAS No.382 (.400 (.20-1.70) 1.00 (.200 (.300) .900 (.20) 1.500 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.400 (.400 (. < LOD means less than the limit of detection.266-. 01-02.20) 1.S.400 (.500-.30-1.20) 1.333 (.

067-.450 (.277 (.394-.500) 90th .313) ..157-.120 (.061-.980 (. Diamond et al.498-.193 (.200 (.330-.38) 1.892 (.445 (.452 (.109 (. 2001).83) 1. For nonsmokers who are not exposed to cadmium in the workplace. **All results are corrected for molybdenum oxide interference in the ICP-MS method.72) 1.886) .17) .223 (.476-.210 (.860) 1.15 (.189-.753-. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.067-.101) . 2003).700-.520-.279 (.226) .246) .170-.255) .203) . 200 Fourth National Report on Human Exposure to Environmental Chemicals .260-.06) .210) .733) .817 (.12-1.848 (.107-.320) .890-1.354) .222) . respectively.820) 1.219 (.306 (. Cadmium absorption may be increased with iron deficiency (Berglund et al.136) .240) .886-1.790 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers. however.30-1. population from the National Health and Nutrition Examination Survey.238-.366-.090) .284) .519) .240-.481) ..214-. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.450 (. copper) and protein.S.445 (.551 (.980) .170-.233) .490) 1.196-.763-.130 (.360) .530) .295) .372) .193-.211-.148) .892-1. ingestion through food is the largest source of exposure.282 (.390 (.22 (1.121 (.470-.255) .366-. potatoes.179-.151-.32 (1.191 (.219 (.190-.230) 75th .20) 1.270 (.260 (.480) .285-.06.25) 1. The kidney is a critical target and shows the earliest sign of cadmium toxicity.717-.126) .38) .299) .393-.280 (.741-1.112-. 2003. 2003).492 (.01 (.705-.230 (.607) .479) .272-.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.109-.229) .34) 1.160) .550 (.610) .115-.15) 1.596) .167-.203 (.077 (. interval) .189-.263) .171-.237-.336) .388-. 2003).281 (.160) .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 .960 (.249) .339) . whose body burdens of cadmium can be approximately twice that of nonsmokers.790 (. calcium.202 (.265) .539) .207-.329 (.810-1. Renal tubular and glomerular damage.211 (.200-.184-.17 (.989-1.57) 1.175 (.426 (. With chronic exposure.209 (.114-.327 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .150-.466 (.17 (.219 (.181 (.261-.02-1.134) . including many food crops such as cereal grains.700-.148-.190-.01) .41 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th . and various seeds.07-1. 01-02.092) .270 (.210) .430-.065-.880) .800-.351-.160 (. 1999.110-.456-.300 (.972 (.310 (.169-.229-.551) .20 (1.233) .183-.128 (.221) .381-.813 (.260-.43) 1.081) .733-.173) . 0.257-. drinking water is a source for cadmium intake.400-.47) 1.430) ..087-.243-.157) ..232) .589 (.390-.48 (1.308) . Horiguchi et al.13 (.Metals 2000).38) .273 (.400-.06.390-.387) .940-1.25 (1.01-1.475 (. rice. wheat.141 (.220 (.493-.820 (.680 (.255) .800 (.818 (.289-.229) .458 (. and 03-04 are 0.192-.633 (.210 (.191-.177-. To a lesser extent.178-.820-1.640) . see Data Analysis section) for Survey years 99-00. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.423-.310) .875 (.04 (.82) 1.436-.440 (.980-1.201 (.686-.362) .300) .20 (1.510-.870) .080 (.235) .200 (..12 (.206) .06-1.730-.806) .855-1.195-.633-1.440-.22 (.817 (.545 (.748-1.19) 1.189) .210 (.490) .077 (.135-.160-.843-1.239 (.890 (.322 (.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 .455 (.326) .977) .153-. and 0.980) . individual values vary and are affected by factors such as dietary intake of essential nutrients (iron. Cadmium in soil is absorbed by plants.17 (.251) .713) .09-1.135 (.290-.559 (.210 (.52 (1.265 (.316 (.100-.04 (.960) 1.227 (.06.198) .220) .623) .980-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.234 (.238) .433-.194-.20 (1.447 (.208-.350 (. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al. Cadmium is absorbed via inhalation and ingestion.510) .36) 1.963-1.192-.249-.230) .530 (.38) 1. 1994).220-.262) .078 (.918-1.700-.507) .204 (.766 (.302 (.03) .253-.24) 1.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.060-.216 (.13) .180 (.232 (.482) .51 (1. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg. 2004a. an inducible metal binding protein.990) .875) .191-.858 (.206 (.10 (1.540) .175 (.28 (1.187 (.283 (.165-.170 (.366) .13-1.231) . Kikuchi et al.74) 1.919) .714-1.210 (.190-.440 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. zinc.15) .061 (<LOD-.241) .202-.412) .462 (.257) .28) 1.839 (.20-1.500) ..150) .140 (.092 (.200-.28-1.836-1.** Survey Geometric mean (95% conf.261-.090) .580) .247) .519) .06-1.220-.199 (.221 (.

At lower environmental exposures.303) .146-.204-.232) .208 (.123-.093 (.617 (.083-..158-.818) .686 (.190 (.266-.168-..783) . 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.873 (.157-.826-1.178) .175-.242) .101) .352) .191) . Olsson et al. 2002.08) .273 (.168-.238-.255-.500-.668-.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 .827) .444-.175 (.433-.071 (.516-.075 (<LOD-. most often a result of occupational exposure (Roels et al.185 (.211 (.404 (.084 (.865 (.830) .716-.253 (.074-.182) .940-1.789 (.757 (.091 (.813-1.288 (.440) .157-.** Survey Geometric mean (95% conf.281) .226) 75th .562-.267 (.137 (.261) .470) .085-.232) .224 (.147 (.212 (.241) .434 (.687 (.767 (.200 (.507-.234) .225) .591 (.296 (.143) .234 (.708-1.229) .247-.176 (. 2004b).343-.719 (.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .473 (.38) .218) .909-1.182) .674-1.247-.143-.147-.431) .181) .191 (.221 (.236-.161-.917) .802 (.143-.490 (.234-.906) .729 (.07 (.476) .779 (. 1996.227-.919 (.126 (..078-.531 (.17) .560-. Staessen et al.209) .140-.783 (.063-. population from the National Health and Nutrition Examination Survey.833-1.197-.209) Selected percentiles ( 95% confidence interval) Sample 95th .104) .792 (.274) 1.412 (.876-1.690 (. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.826-1.650-.181 (. 2000. 1999).304) .769 (.162 (.559-.137-.174-.645-.171-.190 (.02 (.199 (.210 (.159 (.144-.479 (..187-.712 (.300-.185) .830-1.316) .423 (.321) . 1999).106) .607) .154-.331 (.985 (.154 (.207-.240) .222-.173 (.170-.266) .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 .364) .725-1.754) .518) .250) .096) . 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.267 (.09 (.381-.067-.421 (.856) .256-.05) 1.449) .075-.418) .387 (. interval) .311) .07) ..181 (.757) .261-..00 (.192) .135) .929) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate. can result from high dose chronic exposure..189-.470) .201-.173-.175 (.13) .414 (.414-.163) .653) .111-.288) .874-1.690-.219 (.839) .533) .159 (.253) .268 (.187) .979 (.210 (.184-.784) .097) .091 (.293-.438-.196 (.667) .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.336-.239-. 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.289) .220 (.182) .198) .940 (.283 (.176 (.235) .078 (.329 (.700 (.140-.622 (.631) .941 (.240) .263 (.122 (.223) .288-.722-.304-.136-.387-.147-.382-.614) .850) .950) .166 (.350) .205 (..538) .536 (.446) .927-1. 2002.252 (.278) .297) .718 (.090 (.156) .131-.238) .325 (.184) .481 (.170 (.740 (. 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.104) .084-.215 (.206-.795) 1.282 (.316 (.338 (. Horiguchi et al. 2002.716) .931 (.208-.178-.391-.077-.537-.263-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.700) .487 (. Fourth National Report on Human Exposure to Environmental Chemicals 201 .112) .545) .051-. Noonan et al.318 (.727-.270 (.136-.693 (.426-. 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.292) .086 (.202 (.335 (.100 (..247-.177) .12) 1.813-. During the 1950’s and 1960’s.688-. However.438) 90th .16) .107) .207) .184-.S.856 (.098) .691-.091) .491-.210) .678-.663 (.216-.484 (.280 (.388-.219 (.16) 1.06 (.767) .094) .398-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.183) .156 (..850) .199-.884) .818) .308) .917 (.130-.245 (.10) 1.340) .191-.382) .404) .181-.418-.666-.148 (.233 (.647-.441-.432 (.183 (.690-.123-. 2003.085 (.806-1.551) .998) . 2004).04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .440) .113-.289) .163 (.501 (.678 (.228-.261 (.168 (.281) .541) .828) .687-. Jarup et al.423-.630-.156-.962) .377-.225) .194-.308 (.150-.415) .00 (.472) . 1999).696-.221-.

. However. 2003. 2003.. Both IARC and NTP consider cadmium a human carcinogen. respectively...26 and 3. Staessen et al. 2005. Olsson et al. Zhang et al. 2005.. 2002). 1996)... Horiguchi et al. 2004. 2002. 2002.. 2002) and length at birth (Nishijo et al.. Wennberg 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. Becker et al. 2003. 1999). urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.. For NHANES 19992000.. 2004. 2003).. 2005). not to imply a safety level for general population exposure. Salpietro et al.. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. Wilhelm et al. 2000. 1988). data (CDC.1 mg/L (Alfven et al. 2002). Ezaki et al. 2002. 2004). Cadmium can produce lung. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. Ezaki et al. Moriguchi et al.. Information about external exposure (i. 2002. with peak values observed in the fifth to sixth decades (CDC. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH.. Further research is needed to address the public health consequences of such exposure in the United States.. 2000). In adults aged 60 years and older. 2002. 2005.html. Creatinine-corrected urine cadmium values in U. 2004... Olsson et al... Becker et al. respectively... and drinking water and environmental standards have been established by U. 2003... Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. In the typical environmental exposure.cdc. two studies of women in Japan with lower exposures found no correlation between renal tubular effect markers and blood or urine cadmium levels (geometric means were 1. 2003. Occupational standards are provided here for comparison only. 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. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . 2006. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. 1999.. 2000.. In postmenopausal women.e.46 mg/gram of creatinine) (Ezaki et al..atsdr. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. 2002). Jarup et al. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. Wennberg et al. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al.. CDC. 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).S. Olsson et al.. Suwazono et al. 1996. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures. approached these values associated with subclinical changes in renal function and bone mineral density.. as may occur from welding cadmium-alloyed metals..S. Mannino et al. Jarup et al.. Komaromy-Hiller et al.. 2003. Women had higher blood and urine cadmium levels compared to men of similar ages.. 2002. Animal studies have demonstrated reproductive and teratogenic effects. 2006). maternal blood or maternal urine and birth weight (Nishijo et al. 2000.. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. Friedman et al. potentially fatal pneumonitis (Fernandez et al.. Becker et al. 2002). Acute and heavy exposure to airborne dusts and fumes. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. 2006. 1999). has resulted in severe. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. 2002). EPA.. Horiguchi et al. intermediate in former smokers and lower in never-smokers (Becker et al. environmental levels) and health effects is available from ATSDR at: http://www. 2004b). Jin et al. Noonan et al. Staessen et al.. 2004. Staessen et al.gov/ toxpro2.. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. 2006)..Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al.S.. 2004b. 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. 2005..

Cadmium fume inhalation and emphysema. 1999 [online]. Anthropometric. Carlsson MD. Howerton K.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. et al. Fukui Y. Taylor AJ. Neurotoxicology 2003. 206:15-24. Ezaki T. et al. 2005. Lison D. Mascagni P. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Seifert B. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Tsukahara T. Ezaki T. Miyamoto K. population. Comparison of representative ranges based on U. Costa R. Oguma E. Occup Med 1996. Vahter M. Furuki K. Fernandez MA. Miyamoto K. Schulz C. Furuki K. Thayer WC. Machida M. Horiguchi H.354:1508– 1513. et al. ShkiryakNizhnyk AZ. Kaus S. Akesson A. Jarup L. Bregante G. Chiappino G. Darbyshire J. Takebayashi T. Bo M. J Toxicol Environ Health 2003. Okamoto S. Seiwert M. Toffoletto F. Pickering CA. Komaromy-Hiller G. Palomar M. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 4/8/09 Alfven T. Agency for Toxic Substances and Disease Registry (ATSDR). diabetes mellitus. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lundh T. Lepom P. iron deficiency. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Lukyanova EM.cdc. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Stock AL. Becker K. Fourth National Report on Human Exposure to Environmental Chemicals 203 . Nordberg G. Ikeda Y.S. Gadea E. Lancet 1988. Environ Health Perspect 1994.102:83-89. Environ Res 2004. 196:114-123. Nermell B. Consonni D. et al. Uemura T. Chislovska NV.96:353-359.76:186-196. Persson B. et al. Kikuchi Y. Vahter M.59:194-8. Sanz P. Jones RL. Ash KO. Ikeda Y.46:372-374. Environ Health Perspect 2002. Toxicological profile for cadmium update. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002.205:297-308. Nomiyama T. Kaus S.95:20–31. Third National Report on Human Exposure to Environmental Chemicals.148(1-2):11-20. Fukui Y.13(11):1627-1631. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Fatal chemical pneumonitis due to cadmium fumes. et al.gov/toxprofiles/tp5. Fayers PM. Mucha A. Machida M. Environ Res 2006. Alfven T. environmental. Toxicol Lett 2004. Savage-Brown A. Lauwerys R. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Wang H. Clin Chim Acta 2000.66(Pt A):2141-2164. Lancet 1999. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. J Occup Health 2003. Berglund M. Jarup L.1(8587):663-667. Dekio F. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Occup Environ Med 2000.57:668-672. 102:10581066.S. Friedman LS. Zhu G. et al. Elinder CG.atsdr. Sasaki S. Horiguchi H. Bellerup P. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure.296(1-2):71-90. Int J Hyg Environ Health 2003. Hellstrom L. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Moriguchi J. Buchet JP. Centers for Disease Control and Prevention (CDC). Seiwert M. Holguin F. Environ Res 2004b. Atlanta (GA). Moriguchi J. Bernard A. Schulz C. Oguma E.45:43-52. Grubb A. Thorax 2004. Ukai H. Tsukahara T. Greves HM. et al. Diamond GL. Kumagai N. Lidfeldt J. Int Arch Occup Environ Health 2003. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Becker K. Hotz P. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U.000 women in the Japanese general population: a nationwide large-scale survey.110:699-702. Jin T.24:717-724. Comprehensive study of the effects of age. Environ Health Perspect 2005.59:497]. possibly better than b2microglobulin. et al. Serra J. Mannino DM. References Akesson A. Toxicol Appl Pharmacol 2004a. Choudhury H. Krause C. Int J Hyg Environ Health 2002. Available at URL: http://www. Sasaki S. Nerbrand C. Ye T. et al. Davison AG. patient population and literature reference intervals for urinary trace elements. Olfactory function in workers exposed to moderate airborne cadmium levels. Venables KM.html. Kundiev YT. et al.

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07) 4.7 (9.10-7.82) 5.80 (8.71-9. soil.15-8.50 (4. and 03-04 are 0.10-8.62) 4.01) 7.9) 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 4.20) 8.0) 12. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10 (6.00-8. nausea.20-4.64-5.73-5.54) 4.95) 5.00-4.77 (9.52) 7.49) 75th 7. Whether cesium compounds are carcinogenic is unknown.7 (10.97) 4.3) 10.90-12.49) 4.69-6.40-5.86-11.03 (4.4-13.1) 11.70 (8.40 (4.9 (10.13-8.04) 7.08 (7.12-11. interval) 4.0) 11.03 (4.86-12.50) 9.3) 12.99-11.3) 10.8) 11.01-8. although cesium was generally of low toxicity when given to animals.87-7.59) 7.5 (10. see Data Analysis section) for Survey years 99-00.7 (8.59 (5.90) 9.S.60-7.53-11.99-6.17) 4.42) 7.61-6.2) 11.4 (9.9) Total 4.20) 7.79 (4.70 (5.3-15.22-4.05) 5.70-5.60) 7.1-12.4) 9. scintillation counters.80-11.25) 4.84) 5.4) 10.14.47-8.26 (3.90 (4. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.95 (3.00-9.9 (11.80-6.21 (4.60 (8.13 (5.55-11.8 (10.39-4.7) 10.81-14.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70) 7.6 (9.89-5.5-13.84 (4.8) 11.30-5.30 (6.60) 5.55 (7.7) 11.8) 9.43 (5.45-5.0) 11. and high-power gas-ion devices.7 (10.9) 11.20 (6.9) 12.05) 5.74) Selected percentiles ( 95% confidence interval) 50th 4.9 (11.33 (5.71-8.64) 4.36) 3.6 (9.6) 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 4.05-5.32-5.7 (10.84-5.2-13.0) 12.50 (6.84-9.23-4.40-5.31-8.94-4.81 (4.80-13.9) 8.71 (8.40) 5.64) 5.5-16.56-11.40) 7.5) 9. Radioactive 137Cs has been used medically to treat cancer.10-9.1 (9.08-5.3 (8.70 (8.7 (9.00) 6.26-11.77 (9.93 (4.66 (7.60 (7.59-5.40-11.50 (4.03-4.00) 7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00 (7. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite. respectively.40-7.7 (9.55 (4.5) 12.53 (6.94) 4.27-5.86 (7.39) 7.3 (8.60-12.70-8.5 (8.4) 11.56 (4.87 (4. 2004).98 (7.54-11.88 (8.08-5.80-10.64 (4.04 (4.0-13.7-14.08 (6.1) 10.35 (4.3) 9.90) 5.52-9.80 (4. photographic emulsions.83-4.6 (9.96 (6.00-8.38) 5.05-5.3) 10.7 (11.50) 5.87 (4.07-11.3-13.87) 5. and clay.56) 5.0 (9.94 (4.20-7.45-8.42-7.34) 9.3-13.63) 6.32 (3.09) 5.14 (4.5-14.2-13.4) 12.64-10.16-6.20-5.42) 6.8) 12.83) 6.33 (6.4) 10.30) 7.82-4.27) 4.90) 5.77 (4.99) 9.01-6.20-8.33-5.2 (9.13 (7.37) 7.57-5.14. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.90-10.10-5.00-10.80 (8.6) 11.60-6.20) 4.81) 4.61) 7.12-5.74-5.76-6.44 (8.21) 90th 9.92-13.60) 7.1) 9.10 (6.36 (6.6) 10.72) 4.8 (10.80-10.Metals Cesium CAS No.98 (7.2-14.80 (4.47-4.20 (4.80 (8.91 (7. cesium hydroxide is corrosive and irritating at high concentrations.8 (11.26) 7.8) 12. diarrhea.89) 4.59-5.00) 4.74 (4.7) 11.72-7.80-10.87 (4.94 (4.70 (4. Most human exposure to cesium occurs through the diet.1) 9.62 (5.70 (9.29) 4. infrared lamps.36 (3.0) 10.40-11.17 (6.71 (4.10 (8.24) 4.2-12.62 (5.4) 95th 11.63 (4.30) 5.37) 5.1 (10.70) 5.1-12.81) 4.22 (4.20) 5.9 (10. For absorbed cesium salts.7) 10.70 (6. and cardiac arrhythmia (ATSDR.29 (4.5) 10. and 0.5-14.4 (10. population from the National Health and Nutrition Examination Survey.30-10.6 (9.99) 7. and as polymerization catalysts.73-11. 01-02.26) 4.25 (3.60-6.60-7.50 (7.1) 11.12 (4.0) 9.68) 9.9 (11.16-6.46) 7.71-5.67 (4.9 (11.90 (6.1 (11.35 (4.4 (9.49 (5.40) 5. the body half-life is estimated to be 70-109 days based on 137Cs exposures.71) 4.90) 7.43-8.63-4. semiconductors.0 (10.08) 7.70 (6.60-5.40-5.84) 8.68 (7.2.27 (7. Little is known about the health effects of this metal.64) 5.59-5.12) 5.25-5.81) 9.0-15.49 (4.90-12.91-8.1-13.2) 12.97-7.13 (8.8) 12. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.30 (6.80 (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 4.6 (11.99-11.90-10.02 (4.90-8.2 (9. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.8) 9.23) 9.10 (8.50 (4.8-13.70) 5.80) 7.95-4.90-10. 0.35-5.6 (11.50-7.0) 12. Fourth National Report on Human Exposure to Environmental Chemicals 205 . However.77-8.09-5.34 (4.56 (4.97 (7.4) 12.17-6.90) 4.40-5.2-13.32) 4.89) 5.3) 10.

63) 6.8 (9.98 (6.34 (5.39 (5.53 (4.05-3. Minoia et al.50) 4.27-6.44 (4.44) 3.99) 4.17) 9.94 (5.6 (9.2 (8.77 (7.7) 10.20-4.72) 4.53) 6.42 (4.17 (6.9 (9.71 (7.41-4.63 (4. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.30-4.0) Total 4.46) 6. population results shown in this Report (Alimonti et al..3 (9.68) 6.29-3.64) 5.41 (8.97-5.68 (4.41 (5.00-9.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.76-9.79) 6.93-7.70) 6.84-9.51 (3.04-5.96-4.60 (3.43 (8.00-5.3-15.20-4.47) 6.27-4.96) 4. 2004).3 (10.14 (6.9) 10.44 (8.71) 6.02 (5.79-5.28) 8.58 (4.72 (4.46 (7.82-4.30) 10.95-6.95 (5.00-10.64-6.38) 10.11 (5.36-3.46-4.93-9.8) 5.25) 4.70) 7.62) 5.74 (5.08 (6.36-10.20) 5.48) 7.43-6.08) 3. Two small studies of European populations reported urinary cesium levels similar to U.30-4.S.04) 6.65-4.36-6.14) 4.44-9.40-5.47) 7. Using clinically submitted specimens.5) 9.99 (3.00-5.14-4.08 (5.52-5. population.99-9.06 (5.68-11.29) 4.24 (3.49) 3.74-11.79) 4.53) 3.30) 10.43 (4.43 (3.56 (4.28) 7.22) 6.84-7.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.64 (8.00 (8.0) 7.73 (3.5) 9.09) 4.35-7.06 (3.27 (6.78 (3.2) 11.95-12.98) 5.62-8.6) 6.56) 3.41 (4.9 (10.09) 8.03-6.83-6.89-4.61-3.31 (4.7-12.24-10.50) 8.38-7.41) 4.27 (6.18 (7.27) 4.41-7.21-4. and were also roughly similar to those in this Report.47) 6.22 (3.26 (3.81 (4.90 (7.60 (5.04-11.05) 3.54 (5.09 (4.07 (5.50 (6.45 (4.12 (3.38 (3.88-10. 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..82) 7. (2000) found urinary cesium levels that were slightly lower than those reported for the U.08 (3.5) 7.4) 10.95 (3.84-9.66-6.50-5.21 (2.10 (5.60-20. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.18-6.07) 8.91-6.18) 8.85) 4.61 (7.46-8.63 (7.66 (5.75 (7.30 (4.74) 3.67 (5.33-3.07-4.13-9.19-6.2 (8.65 (6.03) 5.87 (5.58-5.84-7.8) 10.96) 4.28 (4.97) 8.85) 5. Komaromy-Hiller et al.90-8.56) 4.13) 7.08) 4.65-3.33 (5.83-7.33-8.83) 8.48-6.77-5.28 (5.51) 4.16-8.40) 6.30 (3.05 (4..91) 5.44-5.20-8.91-9.84-11.10-4.53 (6.35-11.76-6.78 (3.12) 3.06) 4.51 (4.87-4.16-5.95) 8.77) 4.23 (7.43) 8.75-11.37-3.15-4.94) 7.14-6.03) 6.90-3.15 (7.60) 3. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.29) 4.66 (6.04) 5.68) 3.31 (4.3) 9.91) 4.2) 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 3.54 (3. population from the National Health and Nutrition Examination Survey. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.51 (3.24-4.8) 6.10 (3. 2005.59-8.64) 4.02-4.33 (5.05-3.29-3.31-4.26-6.38-12.0 (7.70 (7.78) 4.30 (7.67 (6.26 (4.5 (9.01-8.88-4.18-7.3 (8. 1990).21-3.74) 75th 5.92) 3.63-6.11 (5.72-5.7) 10.79) 9.56) 4.00-4.91) 5.S.35 (4.54 (4.99-4.22-11.3) 11.85-4.16) 5.97-4.38 (3.14) 4.57) 3.10 (3.75 (6.50 (7.99-9.91 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.98) 5.50 (5.42-6.42 (5.67) 5.56-10.21-5.47) 4.58) 3.60-10.91-7.39) 8.29) 5.05) 6.79 (5.10) 7.87) 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 5.13-9.51 (4.64) 9.50) 4.90-8.31-6.91 (5.80) 6.05-4.08-3.41) 9.06) 5.77 (6.19-3.20-4.66 (5.92 (5.55) 4.6 (9.95) 4.87) 5.15-11.00-8.12-6. interval) 4.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .55 (3.50) 4.58 (6.15) 95th 8.00) 6.13 (3.1) 11.78) 4.63-6.47 (7.81 (4.48) 90th 7.14-7.17) 4.37) 4.45-6.27 (8.55-5.35) 3.46 (8.96 (4.63 (6.17-4.08) 4.58) 8.43-11.43 (4.40) 7.16-8.54 (4.25) Selected percentiles ( 95% confidence interval) 50th 4.86 (4.96-4.35 (3.42-4.95) 10.98 (7.59) 4.S.47 (4.68) 4.74 (4.73-4.64 (4.77 (4.51 (7.03-5.07) 8.08-7.39) 5.42-4.

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

39) 1.26-1.850-1.430) .690-.710) 1.500 (.520 (.14-1.398 (.630 (.17 (1.750-.379 (. industry is imported or obtained by recycling scrap metal that contains cobalt.540-. The cobalt used in U.16-1.670-.900) .03 (.03) 1.380 (.355-.640) .28 (1.32-2. automobile airbags.760 (.420) . varnishes.373-.380 (.305-.680) .36) 1.520-. steel-belted radial tires.570 (.15-1.428-.980) .496) . Cobalt is used as a drying agent in paints.16) 1.01 (.60 (1.03 (.316-.850) .373) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.680 (.519 (.50) 1.16 (1.520) .09 (.950 (.790-.07 (.870 (.47) 1.28 (1.417) .37-1.370-.294 (.560 (.350) 75th .300-.424) .460) .920-1.410) .01 (.350-.520-.670 (.950 (.580 (.370) .463-.940 (.352 (.45 (1.590-.480-.410-.24 (1.660) .46 (1.338-.04-1.570) .434 (.03) 1.00) .419) Selected percentiles ( 95% confidence interval) 50th .48) 1.48) 1. seawater.47 (1.24 (.313) .92) 1.960-1.410 (.490-.07-1.73) 1.04 (.28-2.73) 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 .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 .470) .520 (.700) .08.450) .S. It is emitted into the environment from burning coal and oil and car and truck exhaust.450) .418 (.460 (.367 (.32 (1.660) .510) 1.07. shiny.32) 1.460) .270-. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.33-1. hard metal (alloys of cobalt and tungsten carbide).870 (.375 (.330 (.690 (. hard metal or in combination with other elements.740 (.940-1.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.359 (.32 (1.460) .22 (1.380-.393-.09) .360-.810-.600-.550 (.430 (.543) .890) .20 (1.660-.435 (.377-.364-.730) 1.410) .333-.870-1.280-.820 (.564) .17 (.410 (.310-.22) 1.430) .02-1.910-1.291-.50 (1.620-.480 (.950-1.360-.01-2.900) . and magnetic recording media.23) .333-. Usual human exposure is from food sources. population from the National Health and Nutrition Examination Survey.690-.700) .310 (.410 (.327-.300 (. respectively.81) 1.750 (.650 (.540) 1.520 (.285 (. and fertilizers.16-1.19) .600) .860 (.28 (1.610-.15 (1.650-.259-.610 (. 208 Fourth National Report on Human Exposure to Environmental Chemicals .890) 95th 1.710) .530 (.04-1.820 (.530) .770) .520-.06-1.16 (1.580 (.620-. and soil. and kitchenware.890-1.16) 1.47 (1. 01-02.520-.850-1. and 03-04 are 0.334) .390) .394) .630-.370 (.59 (1.800) .270-.12) 1.04) 1.570-.840) .450-.890-1.336-. and 0.Metals Cobalt CAS No.620-.75 (1.523) .750 (.450) .316 (.410-.930 (.950) .08-1.370-.99) 1.405-.550-.81) 1.930-1.331-.04-1.520 (.33 (1.890-1.03) .340) .05) 1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.56) 1.330-.14) .404) .17 (1. Cobalt compounds are used as catalysts in producing oil and gas.44) 1. Cobalt compounds are also used in manufacturing battery electrodes.08) .340 (.03-1.410-.630 (.440-.319) .65) 1.21) 1.26) Total .430 (.680 (.880-1.372) .348-.379 (.460-.580 (.950-1.388-.790) .487) . Cobalt occurs naturally in airborne dust.820 (.398) .431) .670 (.53) 1.386) .420 (.570-.270-.400-.26) 1.800-. interval) .390-.810) .427-.880 (.370-.570) .414) .620) .810) . blue-colored pigments.610) . large appliances.502) . see Data Analysis section) for Survey years 99-00.350-.42) 1.17-1.339 (.515 (.450-.590) .830-1.499 (.530-.465) . and inks.610) .760) .340) .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 .416) .07-1.350 (.16 (.348-.23-2.380-.550) 90th .640) .470 (. It is also a component of porcelain enamel applied to steel bathroom fixtures.583) .540-.05 (.540-.590 (.454 (.680) .52 (1.750 (.06 (.67) 1.320 (.26-2.500) .520) .740-.13) 1.900) .600 (.330) .431) .640) .740-.710 (.590-.480 (.47) 1.06 (.540-.980-1.369 (.450) .790 (.390 (.420) .360-.07.900-1.461 (.920) 1.410 (.452 (.301 (.22-1.670-. 0.469-.850) 1.S.390 (.930) .308-.430 (.380 (.05 (. 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.350-.410 (.650 (.940-1.29 (1. and in synthesizing polyester and other materials.430-.343 (.371 (.670 (.340-.399) .800-.581) .290-.340-.25-1.374 (. diamond-polishing wheels.900-1.460 (.01-1.09 (.68 (1.32) 1.12) 1.390 (.490-.64) 1.

352) .15) 1.329 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.11-1.16) .537 (.500 (. 2003).369 (.361-.435-. 1994).259 (.495 (.348) .352 (.362 (.396) .438) .508-.346 (.669) .471-.368) .949) .272-.60) 1..667-1.481) 90th .990-1. cobalt is excreted predominantly in the urine.339-.33) 1.313-.237-. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.17) . Cobalt is absorbed by oral and pulmonary routes.983) .278-.393-.471 (.353 (.313-.54) 1.19) .00-1.304-.257 (.313-.598 (. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al. with pulmonary clearance half-lives of from one to two years (Hedge et al.259-.33) .10 (.402 (.301-.391 (.28) 1.750-.275-.256-.543) .917) .513-.774 (.960 (.268 (.Metals fabricated from cobalt alloys (Lhotka et al.457) .455 (.463-.895-1.27) 1.821-3.301) .57) 1. 1994.593) .393 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.324-.990) .306 (.380-.829-1.384) .844 (.500-.435 (.740-1.16 (1.362) .757-1.316 (.457-.294-.599) .728 (.857-1.13) 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 209 . or using diamond-polishing wheels that contain cobalt metal. interval) . 1972).282-.824 (.487-.781) 95th 1.33) 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 .534-.23 (1.983-1.360) .06 (.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 .830 (.756 (.323) .630-..561) .44 (.522) .591 (.363) .361 (.733-1.738 (.469-.937 (.10) .296) .376 (.976 (.329-.29) 1.488) .900-1.392 (.00 (.333-.467-.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 .500-.626-.533 (.29) .298 (.547 (.381) .343-.290 (.728) .250) .259) .479-.905) .00 (.630-.29 (1.327 (.694) .792-1. 1979).368) .479) .04-1.515 (. Once absorbed and distributed in the body.804) 1.313 (..29 (1.963-1.574-.911-1.361-. and to a lesser extent.25 (.554 (.27) 1.333-.609) . an essential human nutrient.703-.251-.660-.872 (.361 (.461) .554 (.273 (.760-1.60) 1.349) .452-.372) .335 (.291 (.426 (.848 (.300) .513 (.388 (.00 (.30 (1.708) .955) .750) .932-1.842) .386 (.785) .304) .595) .407) .331-.280-.378-.700 (.468) .723 (.S.704-.388 (.03 (. population from the National Health and Nutrition Examination Survey..12-1.667-1.439) .290 (.457 (.281) .462) .286) .608 (.523 (.444 (.391) Selected percentiles ( 95% confidence interval) 50th .662) .975 (.378 (.434-.616-. in the feces.274-.548 (.503-.00) . refining or processing alloys.50) 1.04 (.449) .404-.433) .297) .847) .691 (.14 (.505) .600-.15 (.938) .594) .792 (.49) 1. using hard metal cutting tools.50) 1.313-..707) .689 (.542 (.368 (.248-.879-1.396) .50 (1.302-.475 (.382-.297-. 1972).471-.324) .309) .333-.278 (.355) .442-.606 (.394) .378-.36) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.700 (.673-.833-1.306) 75th .271 (.400 (.333 (.282 (.563-.421) .12 (.328 (.898 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).736-.955) .963-1.239-.00 (. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.275-. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.851 (.35) .328) .429) 1.11-1.290 (.964 (.738 (.365) .562) .523 (.850-1.248-.24) .419) .634-.781-1.03-1.513) .25 (.417) .826-1.407 (. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.83) 1.310) .560-.963) .615) .611) .02 (.425-.744) 1.326-.319-.365-.562) .343 (.353-.683-. respectively.257-.679-.850 (.929) .753-.895-1.963) .408 (.638-1.585) .352 (.417 (.861-1.861 (.409) .16 (.635 (.313-.328 (.327-.777-..550-.938-1.786-.529 (.334) .10-1.36) 1.10) Total .279) .534 (.737 (.317 (.362-.425) .09) 1.16 (.337 (.289) .303-.234 (.293 (.838 (.314 (.611) .277-. A portion of cobalt retained for long periods is concentrated in the liver.215-.358 (.279 (.829) . Smith et al.487-.552 (.00) .753) 1.344-.342-.73) 1.247 (.647) .644 (.243-.582-.727 (.35) 1.821 (.378-.29 (1.640) .476-.55) . Exposure in the workplace may come from electroplating.428-.337) .632-.387) . Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.296-.449-.581) .952 (.

. 2001. 2003.49:56-67. Grumbein SL.. Lisi. 1994). Krause et al. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations.. 1989). 2001. 1992). A clinical and pathological study of twenty-eight cases. A 1982-1992 surveillance programme on Danish pottery painters. Haseman JK... 1994. Daniel et al. References Alexander CS..S. Cugell DW. Cobalt was once added as a foaming agent to beer.53:395417. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al.. Blood and urinary concentrations as estimators of cobalt exposure. 1998). has been associated with exposure to dusts that contain cobalt. MacDonald et al. 1999). 1990).cdc. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. 1955). Hailey JR. Arch Environ Health 1988.Metals Toxic effects of cobalt have been encountered in workplace settings.43(4):299-303.. 1994. Lauwerys and Hoet. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. environmental levels) and health effects is available from ATSDR at: http://www. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. 1988). Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. 2001). For workers exposed to cobalt in the air.. 4/3/08 Christensen JM. 1985. 2001. Cobalt-beer cardiomyopathy. Am J Med 1972. Available at URL: http://www.S.atsdr. Morgan WKC. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. 1988). Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better.. Iavicoli et al. White and Sabbioni. Shirakawa et al. Poulsen OM. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al.... Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. Centers for Disease Control and Prevention (CDC). “Hard metal” disease. population results in this Report (Kristiansen et al. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. Perkins DG. Toxicol Sci 1999. 1997). 1998). 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. 1993). Information about external exposure (i. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al.... with mean levels that were about 15-20 times higher than in the general U. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L. Swennen et al. 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. population (CDC. Rubin A.50(13):95-104. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary measurements mainly reflect recent exposure.gov/ exposurereport/. 1972).. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al.. 1997. et al.cdc.. Lison et al. 2003). 2006.html. Information about the BEI is provided here for comparison. not to imply that the BEI is a safe level for general population exposure. Linnainmaa and Kiilunen. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen.. Alexandersson R. 2005. usually in combination with tungsten carbide (Cugell et al. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al.e. Sills RC.gov/toxpro2.. 2005 [online]. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect.. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al.. Atlanta (GA). 2005. Thomassen et al. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis. Roycroft JR. 2003. Dunstan et al. Bucher JR.. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . 210 2006. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Sci Total Environ 1994. 1993). although substantial occupational exposures have produced elevated urinary levels for many weeks..

X. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Epidemiological survey of workers exposed to cobalt oxides. Iavicoli I. Roto P. Kraus T. Weyher I. Swennen B. 1985. 3rd ed. Steffan I. Kiilunen M. Bozec C.34:620-626.88(4):443448. Health Phys 1979. Cobalt cardiomyopathy.55(4):269-276. Linnainmaa M. et al. Mutat Res 2003.406:282-296.(1-3):133-139. Int Arch Occup Environ Health 1997.20(1):25-31. Diepgen TL. Lauwerys RB. Meyer zum Buschenfelde K-H. Lison D. De Boeck M. Lison D.148:241-248. Health Phys 1972. Palmroos P. Dunning SP. Thomassen H. Cleland D. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Int Arch Occup Environ Health.150(1-3):167-171. Lisi P.216:253-270. Thabe H. Science 1988. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Occup Environ Med 1994.36:732-734. Boca Raton (FL): Lewis Publishers. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Hammon E. MacDonald SJ. Br J Ind Med 1993.58(10):631-634. Trace element reference values in tissues from inhabitants of the European Union.533:135-152. Dickel H. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Sabbioni E. J Trace Elem Med Biol 2006. Kriss JP. Robinson C. J Bone Joint Surg Br 2005. J Rheumatol 2001. Shirakawa T. Tilley S. Zedda S. et al. Rorabeck CH. Gross RT. and hard metal dust.51(7):447450. Hoher T.50(9):835-842. et al. Biological monitoring of workers exposed to cobalt metal. Unwin P. The release of metals from metal-onmetal surface arthroplasty of the hip. Zweymuller K. Lauwerys R. Dunstan E. Ghat IS. Edmonds CJ. Kuska Y. Mosconi G. Zhuber K. Sanghrajka AP. Smith T. Salvatori S. Ziaee H. Moulin JJ. Lasfargues G. Lauwerys R. Fujimura N. Respiratory health of cobalt production workers. Chess DG. Arch Intern Med 1990. Outcome of occupational asthma due to cobalt hypersensitivity. Buchet JP.45:246-247.95:29-37. Barnaby CF. Wild P. Occupationallyinduced “isolated cobalt sensitization. Romazini S. Cobalt and antimony: genotoxicity and carcinogenicity.21(2):189-195. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Lhotka C. Molders J. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Kusaka Y. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Long-term clearance of inhaled 60Co. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Bunn HF. Chest 1989. Goto S. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Lung cancer risk in hard-metal workers. Weber A. Leghissa P. Hedge AG. Am J Epidemiol 1998. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Stanescu D. J Orthop Res 2003. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. DeSantis V. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Christensen JM. Bourne RB. Peltier A. HoffmannB.48:172-173. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Iversen BS. Co-sensitivity between cobalt and other transition metals. Jarvis JQ. Bacis M. Kirsch-Volders M. Ichikawa Y. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Goto S.69(3):193-200. Pradhan C. J Occup Med 1992. Occup Environ Med 2001. a study of 13 elements in blood and urine of a United Kingdom population. Cannon SR. A report of two cases from mineral assay laboratories and a review of the literature. Heki S. Am J Ind Med 2003.44:124-132. Laippala P. Alessandrelli M. Linna A.150:177-183. and cobalt metals. Buchet JP. White MA. Schaller KH. Kristiansen J. Radulescu M. et al. Sci Total Environ 1994.” Contact Dermatitis 2001. et al. Carnes WH. McMinn DJ. salt. J Bone Joint Surg Br 2006. Salama A. Vitali MT. Absorption and retention of cobalt in man by whole-body counting. Oksa P.204:147-160. Swennen B.22:359367.Metals effects of cobalt. Meier R. et al. Sci Total Environ 1998. Cresti R. Contact Dermatitis 2003. Blunn G. Goldberg MA. Pisati G. Angerer J. Thakker DM.157:117121. Uitti J.242:1412-1415. Sabbioni E. oxides. Schramel P. Sabbioni E. 2001. Zobelein P. Sci Total Environ 1994. Sci Total Environ 1997. Schank M. Clin Orthop Relat Res 2003. Falcone G. Daniel J. Lison D.150. Hoet P.28(5):1121-1128. cobalt salts. Kato M.87(5):628-631. McCalden RW. Szekeres T.

20) 3.10) 2.10-6.90-3.60) 1.30) 2.40) 3.37 (1.40-1. bronze).10 (1.30 (1.50 (1.60-3.52-1.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2. lead was added to gasoline and residential paints and used in soldering the seams of food cans.70 (3.20 (4.30-4.60) 5.55-1.90) 1.50-4.60) 4.25) 1.60 (1.70) 4.50-5. such as lead phosphate and tetraethyl lead.50-3.S.60 (1.40-1.90-4.60-4.60-1.53) 1.60 (4.20) 2.20) 4.60-6.90 (2.40) 1.45 (1.70) 3.900 (.20) .70 (2.70 (1.10-2.43 (1.80-3.50 (2.90) 2.40) 2.96-2.50-1.00-5.40) 5.60 (1.70 (1.37 (1.86) 1.00) 1.10) 1. 7439-92-1 General Information Elemental lead is a soft.30 (1.10-4.75 (1.40) 2.78 (1.87) 1. 01-02.10-2.70) 2.40 (1.80-3.68-1.50 (1.50 (1.56 (1.70 (5.30 (3.80-2.40) 1.80) 1.31) 1.50-1.90) 2.89) 1.23 (1.90-4.20-3.10 (4.66 (1.00) 2.40-1.800-1.60) 3.90-2.70-2.60 (3.40-2.30 (2.50-2.3.40) 1.878-1. dense.20 (2.45-1.52 (1.20) 3.00-4.20 (3.g.40 (2.32-1.Metals Lead CAS No.80 (4.43 (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 1.00-1.10-8.20 (3.00) 4.10-2.50) 4.50 (4.40-4.50-2.70-1.50) 4.60 (3.70) 1.30-1.00) 6.80) 1.90 (2.90) 1.50) 75th 2.50 (4.60 (1.30-1.30) 2.20-1.51) 1.942 (.60-1.60 (3.40-6.80) 1.900 (.00 (2. and 0.09) 1.20 (1.90-6.60 (1.90-2.62) 1.00) 5.50) 5.70) 3.70-4.60-1.90 (1.72) Selected percentiles ( 95% confidence interval) 50th 1.80 (2.90 (3.90 (1. see Data Analysis section) for Survey years 99-00.70 (1.80) 3. interval) 1. antique-molded or cast ornaments.00) 3.36-1.80-4.70-1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.60 (2.20) 1.60) 1.90 (3.40-3.30) 95th 5.00 (1.20 (2.00 (4.70 (2.40-2.50 (2.43) 1.60 (2.80) 2.69 (1.30) 2.40-1.40) 4.60-2.40) Total 1.30-2.00) 4.90-4.60) 1.80 (1.40 (3.00 (6.10-3.40 (1.00) .10 (2.70-3.52-1.55 (1.50) 2.00-4.80-4.80 (5.60) 2.87 (1.25 (1.30-1.30 (2.10) 3.50) 3.50 (1.60) 3. Since lead has been eliminated from gasoline.20 (3.60) 2.50 (3.40-1.50-1.40 (2.60 (1.20-1.00) 2.10) 3.20-4.30 (2.50-2.60 (1.10-1.50 (2. blue-gray metal that occurs naturally in soils and rocks.20 (1. Lead was used in plumbing for centuries and may still be present.00) 1.90 (3.50) 5.90) 2.00 (3. plastics.36-1.10) 1. respectively. 0.30-6.10-2.69) 1.10 (3.10-4.00) 3.30 (2.10) 1. and for radiation shielding. solders.30 (2.25 (1.20) 5.20) 3.30-2.50-5.00-6. leaded glass.37-1.14-1. and 03-04 are 0.70) 1.30-5.10 (1.69) 1.04-1.00-2.20) 4.40-3.60 (2.10-1.20) 90th 3.60 (2.49-1.80) 1.90) 2.90-2.30 (4.20-2.60) 3.70 (1.00-1.20-3. ammunition.60) 1.40) 2.90) 1.20 (1.10 (2.40-5.60) 4.70-6.40-2. Lead has a variety of uses in manufacturing: storage batteries.70) 1.00) 1.90) 3.50) 1.40-1.80) 2.32-1.986) .48) 1.80) 1.50-1. malleable.40-6. the main source of lead exposure for the general U.10-3.36) 1.10) 2.20 (3.80-5.43-1. ceramic glazes.80 (1.80 (1.75) 1.10-2.80) 2.10 (2.10-2.66) 1.60) 5.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70-1.20 (3.80 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.34-1.80-4. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.70-5.30-2.60) 2.60-2.80-3.55-1.946 (.900-1.50-4.71-1.14-1.00) 1.51 (1.10 (1.50) 1.10) 4.14-1.20-3.30-1.60) 2. brass.30 (4.90) 3.80 (3.90 (3.80 (4.60 (3.90 (3.10-3.43) 1.60 (2.50) 1.60) 1.70) 3.10-1.75-1. 212 Fourth National Report on Human Exposure to Environmental Chemicals .83 (1.50) 7.80 (2.50-3.62-1.50) 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 2.80 (1.30 (1.65 (1.10) 3.70-2.75-2. population from the National Health and Nutrition Examination Survey.95) 1.20-2.70) 1. Lead is most often mined from ores or recycled from scrap metal or batteries.77 (1.70) 4.10-3.30 (4.60) 4.60) 4.90-4.20) 3.80-3.00) 2.40 (5.40) 2.10) 5.70) 1.00) 1.S.39) 1.40 (1.91) 1.69 (1.90) 2.50 (3.46 (1.28.30) 1.02) 1.93-2.81) 1.10-6.20 (1.62 (1.3.80 (5.30-2.20-6.30 (1.00 (5.50) 2.50) 1. Before the 1980’s.00-4.70) 4.00 (1.60) 2.22 (1.60-1.60-4. metal alloys (e.70) 4.20 (3.80) 2.50-1.90) 5.40-3.50 (2.01 (1.899-.60) 3. Elemental lead can be combined with other elements to form inorganic and organic compounds.50-2.30-1.90-2.20 (1.30-1.70 (2.40 (1.30) 5.39-1.80 (2.30 (2.70-2.40 (4.50-6.70 (3.17) .00 (4.00) 2.20 (3.19 (1. In the past.12-1.90 (4.30 (2.80 (1.20-3.60 (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.

620 (.30-1.75) 4.700 (.50) 3. 2000).40) 3.70 (2.10-3. and 03-04 are 0.625 (.671-.730 (.636 (.840 (. and contact with soil.800-1.40 (1.674) 1.20-1.20 (1.00-2.731 (.14 (1.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .700-.800) .75) 3.59) 1.10 (1.70) 3.04 (.90 (1.700 (.30-1.80 (1.50-2.700 (.910-.13-3.72) 1.40-3.64) 2.80) 1.960 (.90) 1.677 (.40) 2.70) 1. see Data Analysis section) for Survey years 99-00.80 (2.700) . 1991).00-2. or water contaminated by mining or smelting operations.20 (3.10-5.59-2.50-3.60 (1.800) .729-.40 (1.00) 2.66 (2.600-.749) .44-2.540 (.718) .78-2.90 (2.564 (.40-1.29 (2.73 (1.41) 2.04) .10 (1.10) 2.30) 1.89) 2.70 (2.600) .600-.40) 1. 2007.757-.40 (2. imported children’s trinkets and toys.70-3. lead-based painted surfaces undergoing renovation or demolition.00) .785) .553-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.97) 4.70-2.07-1.86) 1.70) 1.10-1.506-.818) .90 (2.27) 1.700-1.820-1.60 (1.40-1.10 (.20-1. population from the National Health and Nutrition Examination Survey.50 (1. interval) .10-1. Approximately half of the absorbed lead may be incorporated into bone.900 (.20 (2.40-1. 0.970-1.30-1.590 (.40 (1.40-1.40-2.710-1.625-.753 (.900 (.20 (1.50-1.24-1.80) 2.923 (.10 (1.20 (1.22) 1.30) 2.09) 1.20-2.700 (.00 (1.70 (2.02 (.700-.800 (.90-2.30-3.30 (1.31-3.00-1.931) .30) 1. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.70 (2.33-2.800-.31 (1.80 (1.40) 2.86-2.40) 1.661-.790 (.986) .628) 1.80) 1.900) . 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. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery. Fourth National Report on Human Exposure to Environmental Chemicals 213 .558 (.70) 1. stained glass framing.480-.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 1.00-2. pewter utensils and drinking vessels.808 (.20) 1.50 (2.651) .80) 1.70) 3.773) .52 (1.33 (2.00 (1.660) .18-1.50 (2.40 (1.90-4. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead. In the blood.589-.637-.52-1.00) . respectively.10-3.700 (.80) 2.30) .52-1.82 (1.40) 1.Metals occupational (e. and 0. However.900-1. lead-containing folk remedies and cosmetics.20 (2.10-1.10-1.90-2.580-.. CDC.862) .80) 3.60 (1.60-3.560-.605) .00) 2.40) 2.60-2.00 (1.80-3.20) 1.30) 2.78-2.80) 2.1.1.40 (2.10) 1.50) 1.90-2.00 (2.90) 2.50-2.680) .30-1.20 (2.23) .62-4.14 (1.960-1.766 (.700) 1.573 (.17 (1.40 (2.700-.630 (.60 (1.900) . bullet fragments retained in human tissue.21 (2.848 (.900-1.30) 1.960-1.10 (..822-1.50) 1.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.800 (.920 (.595-.86) 95th 2.32 (1.00) .49 (1.941) .695 (.572-.03-2.80) 2.62) Total .20) 1.710-.640 (.10) 2.642 (.S.40) 2.600-.23-4.50-2.535-.00 (1.900) .33.10-3.82 (2.11) 2.50) 2.600 (.60) 2.60-2.641-.11 (1.30) 1.701) .80-2. or after soluble lead compounds are ingested.90 (1.80-2.07 (.50 (2.40) 1.915-1.02) 1.30 (3.27 (1.850 (.815 (.04 (.78-2.20 (1.690) 75th 1.600-. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.40) 1.14-1.857) .00-1.579-.20) .800) .50) 2.20) .900) .60-3.30-5.620) 1.20 (1.795 (.50) 1.04-2.680-.604 (.688 (.800 (.900-1.g.990) 1.00 (.90 (2.833 (.30) 2.90-2.955-1. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.80) 3.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.40 (2.66 (2.650) 1.700-.10) .828) Selected percentiles ( 95% confidence interval) 50th . older plumbing systems with leaded pipes or lead soldered connections.833-1.60 (2.00) .30) 1.800 (.616) . Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.60-1.06) . 01-02.900-1.640-.70) 2.700 (.20 (1.810-1.708-.745-.800) .900) .540-.90-3.900 (.30 (2.00-1.20-1.700-.691-.900) .610 (.10 (.80) 2.04) 2.86 (1. dust.10 (1.738) .12) 90th 2.90) 2.570-.35 (.556-. lead-contaminated dust in indoor firing ranges.800-1.10) .940 (.29) 2.659 (.70 (1.40-5.90 (1.20) .50 (1.00) 1.13) . which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40 (1.591 (.800) .680-.90-3.752 (.526-.990) 2.20-2.613) .579-.600-.920 (. battery and radiator manufacturing) and recreational sources.19 (1.91) 2.03 (1.30-2.500-.935) 1.20) .800-.600 (.600) .10-1.90) 2.

64 (1.12-1.742) .645-.492-.688) .977) 1.862-.702-.43) 2.918 (. 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. scant amounts are lost through sweat.00) .09-1. 2003.94-2.436) .98) 2.47 (2.677 (.03 (.701 (.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 .56-2.793-1.92) 2.718) .31) 1.33) 2.94 (1.63) 1.58) 1.72) . zinc.404 (.98 (1.975-1.85) 1.587-.61) 3.668-.79 (1.15-3.68 (1. abdominal pain.69 (1. For instance.734) .41-1.623 (.696 (.992-1.41) .586-.400) .50) 1.810 (.71 (1.594-.62-1. kidney injury.681-.03) 90th 1.97) 1.56 (1.38 (2.667) .588-. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.404-.670) 1.698) .608-.37-1.14) 1.659-.67-4.03 (1. 1996).01) .701) .851) .33) 1.72-2.10 (1.712 (. Lead can cross the placenta and enter the developing fetal brain.617-.608 (.603 (.63) 4.50-2.893) .25-1.62-3.71-2.33-1.652 (.496 (.61) 1. and through binding to ion channels and regulatory proteins. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.18) .18) 2.618 (.44) 1. O’Flaherty.671 (. Schwartz.27 (1.571-.841-1.66 (1.648 (.31 (1.31 (1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR. In 1991.61) 1.26) Total .720 (.11) 1.561-.07 (.06) 1.03) . and iron.26) 2. Large amounts of lead in the body can cause anemia.19-5.09-1. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.03) 1. The skeleton acts as a storage depot.633 (.72-2.S.85-2.85-2.898) .09) 1..02-1.571-.83) 1.926 (.645-.44 (1.19) 1.914-1. 2004.722 (.56) 3.676) .97) 1.790) . hair. population from the National Health and Nutrition Examination Survey.997-1.25-1.06 (.933) .18) 1.22) 1.61) 1.940 (.50-2. 1995).918-1.04) 2.828) .796-1.53) 1.33 (1.89-2.914 (.24 (1.882-1.05 (.62) 2.38 (2.15-2. BLLs and associated toxic effects differ in children and adults. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.37-1.644) .87) 1.559-. 1995.615 (.742) Selected percentiles ( 95% confidence interval) 50th .963-1.66 (1.64) 95th 2.86 (1.639 (. seizures.61) 1.914 (.428) .11 (.98-2.38 (2.739) .981-1.06 (1.710) . 1993).20-3.720 (.22) .702) .31) 1.01 (.41 (1.43-1.65 (1.17 (. and paralysis.62-2.700-.74 (1.812-1.657) 1.56-3.765) .838) .59-3.65-2.529-.73-2. based on prospective population studies.774 (.. encephalopathy.655-.601-. with lesser amounts eliminated via the feces.0) 3.45 (1.36-2.43 (1.89-5.11 (1.708 (.50 (1.707 (.00 (1.962 (.28) 2.79) 2.639 (.97-18.682) .594-.14 (1.28) .988-1.644 (.11) .938 (.604-.755 (.588-.541-.43 (2.593 (.612-.510-.725) .09-1.746) .46 (2.551-.51) 1.603-.677) .606-.404 (.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 .88) 1.592-.615 (.48 (1.18) 1.623 (.03) 1.07-1.52 (1.460-.569 (.05 (1.17-1.800-.731-.753) .853-1.88 (1.39-1.380-.55 (1.508) .43) 1. 1993. through the inhibition of certain enzymes.04-3.50-1.992-1.75-2.900 (.77) 2.28-1.605-.655) 75th 1.607-.781-1. 1991.408-.55 (1.432 (.88) 2.622 (.828-1.51 (1.638 (.583-.15) 1.11 (.03 (.979 (.667-.920-1.75 (2.82) 1.461) .15) 1.703) .673) .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 .Metals 90% of the body lead burden in most adults.05-1. Staessen et al.677-.08) .79) 1.18 (1.07) .649 (.03-2.758) .639 (.342-. Nash et al.73) 2. 2007).579-.88) 2.641 (.47 (1.83 (2.97 (1. Approximately 70% of lead excretion occurs via the urine.383-. CDC.957-1..722 (.23 (1.52) 1.725) . BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.721 (.40-1. The toxic effects of lead result from its interference with the physiologic actions of calcium.44 (1.31 (2.632 (.946-1.22) 1.990 (.20) .709 (.681-.05-1.50-2.03) 2.00 (.22-2.870 (.698) .535) .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 1.679) 1.49 (1.70 (1.11 (1.679-.375 (.02) 1.08-2.35) 2.639) .20) .03 (.609 (.938-1.730) 1.78-4.635 (.34-1.78 (2.469 (.08) .64) 2.655) .47) 1.667-.64-2.887 (.971 (.933-1.11-1.88-2.46 (1.988 (.654) . and nails (Leggett.603-.917-1.683-.15-2.693 (.53-1. with a half-life of years to decades.10 (.702) .763) .96 (1. interval) .03) .22-1.85 (1.06) .03) 2.66) 2.00 (1.10) 1.876-1.686) .718) 1.658 (.625 (.29 (1.621 (.00 (1.

2005b).0 µg/dL in females (Soldin et al. 2001). 2003. and organic lead compounds not classifiable with respect to human carcinogenicity. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. seizures.atsdr.6%) were lower than those from NHANES 1991-1994.S. including minority race or ethnicity. Borja-Aburto et al.cdc... 2003. 2003). Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8..75 µg/dL in U..e. Telisman et al. the geometric mean BLL was 3. 1995. 1984. usually with BLLs greater than 40 mg/dL. The U. environmental levels) and health effects is available from ATSDR at: http://www..07 µg/dL (Becker et al. Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al.S.S. premature delivery.S. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7. and spontaneous abortion (Baghurst et al.4% of children had BLLs of 10µg/dL or higher (CDC. 1999). adult residents. which is an 84% decline.html. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. More recently. 1998). BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. higher than 100-200 µg/dL). IARC considers inorganic lead compounds probable human carcinogens. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. 1991. Surveillance data reported by U.cdc. 1987. Payton et al. However. 2006).Metals µg/dL or higher as the level of concern in children. 2002).5 per 100. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. EPA. 2007). Information about external exposure (i. lead in women may be associated with hypertension during pregnancy. CDC. Jones et al. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. approximately 11. Both drinking water and ambient air standards for lead have been established by the U. reduce sperm count. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. 1994).xls).S.3 million children tested had BLLs of 10 mg/dL or higher (http://www.000 adults. 2009).. 2006). and decrease fertility (Alexander et al. the prevalence rate has declined annually since 1994 (CDC. 2000).7 µg/dL and 4. 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...9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. 1996.gov/toxpro2. urban residence. Pirkle et al. both the geometric mean (1. and peripheral neuropathy generally occurring at much higher levels (e. 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. 2003.2 µg/dL in males and 3.S.. In NHANES 1999-2002 in children 1-5 years old.4% in NHANES 1999-2004. 2005a). Overall.. High dose occupational lead exposure. Muntner et al. adults in the 1999-2000 NHANES sample. Schwartz. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al.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. BLLs reflect both recent intake and equilibration with stored lead in other tissues. Lanphear et al. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U.. Urine levels may reflect recently absorbed lead.6% in NHANES 1988-1991 to 1. 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...... residing in housing built before the 1950’s.g.. respectively. Bellinger 2005. though there is greater individual variation in urine lead than in blood and greater potential for contamination. adults in the 19992000 NHANES sample (Apostoli et al. with overt encephalopathy.. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. particularly in the skeleton. 1999).21% of approximately 3. Data submitted through state public health programs from 2006 showed that 1. 2005b..gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. and low family income (CDC. 2000). almost double the geometric mean of 1. Korrick et al. when the geometric mean BLL was 2. At low environmental exposures.. may alter sperm morphology. For example.. 1996. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.. Schwartz et al. 1996. Fourth National Report on Human Exposure to Environmental Chemicals 215 . 2002a). In occupationally exposed adults.. Staessen et al. 2002.

Becker K. 2005. Rios C. 2005b. 4/14/09 Alexander BH. N Engl J Med 2003.55(32):876-879. Blood lead reference values: the results of an Italian polycentric study.atsdr.205:297-308. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Lanphear BP. Available at URL: http://www.cdc. JAMA 1996.87:1-471. Hunter DJ. Hu H.115:521-529. van Netten C.123:e376-e385. Ronchi L. Muntner P. Jacobson JL. Korrick SA. Available at URL: http://www.287:1-11. Hernberg S. Scand J Work Environ Health 1984. Am J Epidemiol 1999.113(4):1016-1022. 4/14/09 Centers for Disease Control and Prevention (CDC). CDC. 4/14/09 Centers for Disease Control and Prevention (CDC).htm. Blood lead levels—United States. MMWR Morb Mortal Wkly Rep 2006. Muller CH. Reese YR. Schulz C.html. Ganzi A. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents.54(20):513-516. Mantere P.gov/nceh/lead/publications/ books/plpyc/contents. Blood lead levels measured prospectively and risk of spontaneous abortion. Apostoli P.1542/peds:2007-3608. Preventing Lead Poisoning in Young Children. Krause C. Pirkle JL. Leggett RW. Adult blood lead epidemiology and surveillance—United States. Aug 2007 [online]. Luukkonen R. Birth Defects Research (Part A). Intellectual impairment in children with blood lead concentrations below 10 µg/dL.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. Neri A. Jusko TA. Available at URL: http://www. Hänninen H. Inorganic and Organic Lead Compounds. Managing Elevated Blood Lead Levels Among Young Children.10:43-50. Speizer FE. Kuehnemann TJ. Dietrich K. Baghurst PA.8(3):395-401. Sci Total Environ 2002. Hu H. et al. Available from URL: http://www. Cox C. et al. Henderson CR. Caldwell KL. Public Health Rep 2000. gov/mmwr/preview/mmwrhtml/mm5420a5. Rotnitzky A. Sparrow D. 2002 [online]. Batuman V. Centers for Disease Control and Prevention (CDC). The relationship of bone and blood lead to hypertension. References Agency for Toxic Substances and Disease Registry (ATSDR). A prospective follow-up study on psychological effects in workers exposed to low levels of lead.cdc. Kaus S. et al.gov/nceh/lead/ CaseManagement/caseManage_main. doi:10.275(15):1171-1176. 1988-2004. Available at URL: http://www. Checkoway H. Occup Environ Med 1996. Third National Report on Human Exposure to Environmental Chemicals. Borja-Aburto VH. Bellinger D.26:359-371. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Homa DM. Lead.cdc. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 1999-2002.73:409-420. Lead and hypertension in a sample of middle-aged women. Coresh J. Manton WI. Brody DJ.cdc. Korrick S. IARC Monogr Eval Carcinog Risks Hum 2006. Age-specific kinetic model of lead metal in humans. Teratogen update: lead and pregnancy. Rojas LM. Semen quality of men employed at a lead smelter. Kim R.gov/toxprofiles/tp13. McMichael AJ. Neurotoxicol Teratol 2004.htm. Am J Public Health 1999. Sparrow D.53:411-416. MMWR Morb Mortal Wkly Rep 2005a. JAMA 1996. Blanco J. Atlanta (GA). Seiwert M.htm. Vimpani FB. Neurotoxicol 1987. Weiss ST. Int J Hyg Environ Health 2002. Cox C.101(7):598-616.348:15171526. Aro A. Baj A. Jacobson SW. Wigg NR.82:60-80. 4/14/09 Centers for Disease Control and Prevention (CDC). Hu H. Wager C.275:1177-1181. Roberts RR. Lanphear BP. Environ Res 2000. 2003-2004. Toxicological profile for lead. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. 1991 [online].150(6):590-597. et al. Neurodevelopmental effects of postnatal lead exposure at very low levels. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Environ Health Perspect 1993. Chiodo LM. Robertson EF. Kaufman JD. Payton M. Atlanta (GA). Bavazzano P. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Vupputyuri S. Acquisition and retention of lead by young children. Canfield RL. Ewers TG. Rotnitzky A. Bellinger D.htm. et al. Angle CR. Auinger P. Atlanta.cdc. Lepom P. Cory-Slechta DA. Jones RL. Weiss ST. 4/14/09 Centers for Disease Control and Prevention (CDC). Farias P. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Hertz-Picciotto I. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals .89:330-335. Pediatrics 2009. Pediatrics 2004. Ga. Meyer PA. Stanek KL.gov/mmwr/preview/mmwrhtml/ mm5532a2.

Nash D. blood pressure and cardiovascular disease in men. Smith DR. Rocic B. Soldin OP. Use of endogenous. Schwenk M. Pirkle JL. et al. Schwartz BS.63:1044-1050. Lead. Association of blood lead. et al. Kinetics of lead disposition in humans. Lauwerys RR. Wilhelm M. Hwang KY. lead. Weiss ST. J Hum Hypertens 1995. Physiologically based models for bone-seeking elements.140:821-829. Environ Health Perspect 1996. Brody DJ. Osterloh JD. Hickman T. Payton M. Low-level lead exposure and renal function in the Normative Aging Study. Am J Epidemiol 2001. Pizent A. Hu H.209:301305. cadmium. Hanak B.289(12):1523-1531.Metals results from NHANES III. Rubin R. IV. Lee SS. Sherwin R. Schwartz J. and hypertension in perimenopausal and postmenopausal women. Amery A. cadmium. Lee BK. Int J Hyg Environ Health 2006.108(1):45-53. Flegal AR. Staessen JA. Roels H. Soldin SJ. stable lead isotopes to determine release of lead from the skeleton. Sparrow D. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Semen quality and reproductive endocrine function in relation to biomarkers of lead.S. Telisman S.118:16-29. Blood lead concentrations in children: new ranges.9:303-327. Kaufmann RB. Lustberg M. Cvitkovic P. Paschal DC. blood pressure. Gunter EW. Exposure of the U. Lee GS. Kidney Int 2003. Revised and new reference values for arsenic. zinc. dimercaptosuccinic acidchelatable lead. Gavella M. Low-level lead exposure and blood pressure.153(5):453464.104(1):60-66. and tibia lead with neurobehavioral test scores in South Korean lead workers. Toxicol Appl Pharmacol 1993. 50:31-37. Environ Health Perspect 2000.106:745-750. Clin Chim Acta 2003. JAMA 2003. Stewar WF.327:109-113. Jurasovic J. Schulz D. Arch Environ Health 1995. Kaufmann R. Am J Epidemiol 1994. Environ Health Perspect 1998. O’Flaherty EJ. population to lead: 1991-1994. Blood lead. and copper in men. Magder L. Fourth National Report on Human Exposure to Environmental Chemicals 217 .

285-. and organic forms.80) 3.700 (.689-.02) .60-2. Atmospheric elemental mercury can be deposited on land and water.60 (1..g. interval) .. thimerosal. population from the National Health and Nutrition Examination Survey.500-.300) .80 (3.20 (2.30) 3..20-4. inorganic.60-5. to form inorganic mercury compounds or salts.40-3.419 (. sphygmomanometers and barometers.326 (.Metals Mercury CAS No.20-4.60-6. 1980. solid-waste incineration.80) 1.10-3.80 (1.30) 1.30-2.600) 1.800-1.12) .90) 3.30) 4132 4241 03-04 03-04 03-04 . silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.800-1.40-2. constitutes the main source of dietary mercury exposure in the general population. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.00) 4.300-.60-3. thermostats and switches). elemental mercury is absorbed mainly by inhaling volatilized vapor. electrical lamps.00 (. thermometers.S.60-6.00 (. Accidental spills of elemental mercury. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.50-2.30) 1.900 (. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.703-.2.50) 1.860-1.490 (.877 (. may contain inorganic mercury. see Data Analysis section) for Survey year 03-04 is 0.00 (2.400-. 1993). which can bioaccumulate in aquatic and terrestrial food chains.90-3.50-3. Apart from methyl mercury.90 (1.40) 1.372) . Kingman et al.40-2. mercuric chloride).30) 5.00) 3.00) . with the highest concentrations occurring in the kidneys (Barregard et al.300 (.40 (3.800 (. have often required public health intervention (Zeitz et al.714-. Other major uses include electrical equipment (e.00 (2.20) 2. an organic form of mercury...40) 3. and dental amalgam.900) 75th 1..00) 1.70 (4.30) 3.500 (. After elemental mercury is absorbed. or oxygen. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.90) 90th 3. Survey years 03-04 Geometric mean (95% conf..700) .20-3. which create an episodic potential for volatization and inhalation of mercury vapor. In addition. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements. phenylmercuric acetate) or topical antiseptics (e.781 (. Hursh et al.00 (. and mining and smelting. 2007).50) 5. Some cosmetic skin creams from countries other than the U.80 (1. Also.90 (4.574) .800-1.900) . 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic). predominantly from fish and other seafood.700) .797 (.00) 1. 218 Fourth National Report on Human Exposure to Environmental Chemicals .800-1.776 (.700-. Poorly absorbed from the gastrointestinal tract.800-1.50) 2. The kinetics of the different forms of mercury vary considerably. and is distributed to most tissues.40 (4..472-.g.60 (1.800 (.30-5. 1998.700-. Woods et al.800 (.655-.900) 1.80 (1.90 (1.90) 95th 4.30 (1. such as chlorine (e. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.g.700-.484) .60) 1.672) .30-4.563 (.70 (1.80) 4. 1994.919) .40 (4.500) .00 (1.900) 1. 1999 .40 (3.g.50) 4.903) Selected percentiles ( 95% confidence interval) 50th . Elemental mercury is a shiny.70-2. The ingestion of methyl mercury. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.50-1.00 (. IARC. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).30-6.886) .00-5.10) .800 (.418-.400 (.753-1..363-.500-. merbromin).979 (.00 (2.814 (. and mercury compounds are still used as preservatives (e.500 (.40-1.60 (2.700-.60) 1.00-1.600 (. synthetic organomercury compounds were once used in pharmaceutical applications.60) 2085 2293 3478 Limit of detection (LOD.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 .70) 911 856 2081 4525 03-04 03-04 .40-1. sulfur. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.30 (2.900) 1.700-. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.400-.927) .70 (1.70 (3.S. 2002).

1992).40-2. Methyl mercury is incorporated into growing hair.14.27) .300) .80-3.20) 1.60 (1.70-5.00 (2.00) .7) 4. National Health and Nutrition Examination Survey.700 (.70-5.300) .800-1.820 (.400-. 1973).S.50) 3.50-2. population.500 (.944 (.800) .318 (.200 (.. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .40-2.40) 5.265-.200 (.70) 4.50) 2.919) .800-1. Smith et al.06-1.90 (3..307 (.800) 75th . Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.726-1.800 (.70 (1. 1995. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.700-. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.20-3.30) 1.700) 2. 1999-2002.800-1... Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days..329 (. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.10) 1.700 (.10 (.10) .90) 3.200-. 1993).3) 4.00-6.35 (1.90 (1. 1975.300 (.800) .00) 1.300) .. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith. Myers et al.369) 1.500 (.871-1.30-6. After exposure to elemental mercury.10-1.300) .30 (1.30-2.30 (.. 1994) and then undergoes slow dealkylation to inorganic mercury.50-12. Vahter et al. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.700-. thereafter.00 (2.90) 2.20-2.664-1.00-2.70 (1.700-1. 1969. Fourth National Report on Human Exposure to Environmental Chemicals 219 .10 (1.800 (.700 (. 1984.10 (3.10) .. McDowell et al.300 (...20) .00 (1.300 (.40-1. 1999). 2003).06 (.29) .90 (4..50-3.20-3. Jonsson et al.500-.02 (.10 (1.30 (1.30-6.377 (.200-.30-3.60) 2. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.80) 579 527 370 436 588 806 Limit of detection (LOD.20-3.833 (..60 (2.824) 1..23) .70) 1.697-. Miettinen et al.73) 1.600 (.500-.800) 1. with most elimination occurring through in the feces (Sherlock et al.00-1. 1971).30) 3.50) 1.30-4.30-6.80 (3.00) 4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.90) 90th 1..70 (1.800 (.269-. a measure of accumulated dose (Cernichiari et al.00-2.30 (1.60) 3. 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 (.00) 7.70-6.70-3. Sandborgh-Englund et al. 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.00 (2.374) .300) . 1991.600) .200-.395) . interval) Selected percentiles (95% confidence interval) 50th . 2005). 1990).00) 1.10 (1.01) . 1996).60 (1. Suzuki et al.00) 2.80) 1.10 (.297-.900 (.700-1.30) 1.90) 5.500-.541-.70-3.90 (4. 1992 and 1999..80 (1.00-3. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.40) 1. 2003).200-.407) . The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.20-11.40 (1.90 (1.50 (2.10 (5.343 (.256-. 1993). and a useful marker of exposure in epidemiologic studies (Grandjean et al.60) 1.70) 4.20 (2.299-.00) 6. Excretion occurs by renal and fecal routes.800) 1.50) 1.14 and 0.Metals the tissues to mercurous and mercuric inorganic forms.600) . 1998).40) 2.377) . 1994).300 (.317 (..940) Race/ethnicity (females.30-4.10-3.900 (. 1998).00 (3..900-1. 2004..475) .90) 2. Smith and Farris.60 (3.900 (.40 (1.738-. 1992.60) 1.60 (1.500-1.30-5. Vimy et al.900-1. for both acute and chronic exposures.00-2.825-1. Geometric mean Survey years (95% conf. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.268-...200-.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 . 1994.300) .20 (.667 (. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.20) .30-11.50 (1. 1996.50) 95th 2..500-.0) 4.60 (3.200-. Methyl mercury enters the brain and other tissues (Vahter et al.500-.

600 (.600) .600 (. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. typically after a latent period of weeks to months.600) . pain in the extremities. and cerebral palsy (NRC..800) ..700 (. Sakamoto et al. Factor-Litvak et al.600 (. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. 2002. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.700 (.. 2004). Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. 1987). Survey Geometric mean (95% conf. 2000)... 1995. 220 Fourth National Report on Human Exposure to Environmental Chemicals .500) .700 (. irritability. 1998. anorexia. 1995. sensory impairments. Overt poisoning from methyl mercury primarily affects the central nervous system.. Vupputuri et al.600-.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 . Drexler and Schaller.. dysarthria. 2004.42.500-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700 (.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . DeRouen et al. Smith et al. 2005).. 2005.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . depression.700 (. and progressive constriction of the visual fields.500-. 2004.500-. Once absorbed. 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.. Bellinger et al.Metals may be more efficient for inorganic mercury (Grandjean et al. 2006. Stern 2005.600 (. and sleep disturbance (Bidstrup et al. altered physical growth.500-.600) . particularly irritability.700 (.600) . 2004). Rice. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. insomnia. causing parasthesias. which may vary for some chemicals by year and by individual sample. The constellation of findings may include anorexia. and neurocognitive and behavioral disturbances. limb deformities.500-. the existence of a causal relation is unresolved (Chan and Egeland.600 (.600-.500 (. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al..500-.500-. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. hypertension. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. cerebellar ataxia.600) .800) . 1963)..700) . population from the National Health and Nutrition Examination Survey.700-.500 (<LOD-. 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. gingivitis. In recent epidemiologic studies.500 (<LOD-. dysarthria.600 (.S. 1951. overt signs and symptoms of chronic inhalation may include tremor.. Smith et al.600-.600 (. short-term memory loss. 1983).500 (. 1970... fatigue.600) . 1993). 2006.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .600) . Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. see Data Analysis section) for Survey year 03-04 is 0. Oskarsson et al.700) 2007 2240 3406 Limit of detection (LOD. Rissanen et al. < LOD means less than the limit of detection.700-. ataxia... * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600-. maculopapular rash. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. Salonen et al. 2003).. 2000.500-.600) . 1996). and pinkish discoloration of the hands and feet (Tunnessen et al. Sakamoto et al.600) . hearing impairment.500-. Inorganic mercury exposure usually occurs by ingestion.600 (. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. Acute.700-.. At levels below those that cause acute lung injury. 2000.

24) 1. average age 9. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.23) 2.76-3.520) . 2000). In NHANES 19992002.cdc.S.280-.31) 2.S.447 (. range 40 years to 78 years) had an average total blood mercury concentration of 2.441 (.530-.476 (. However.. 2001. see Data Analysis section) for Survey year 03-04 is 0.07 (.360-.416 (. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.13-2.33 (2. adult women in several ethnic subgroups (Hightower et al.88) 287 722 1529 03-04 03-04 .250) .430) .42) 95th 3.382-.05) 1. A cord blood mercury level of 85 µg/L (lower 95% confidence bound = 58 µg/L) is associated with a 5% increase in the prevalence of an abnormal Boston Naming Test (NRC.555) . Information about external exposure (i.433 (.200 (.350-. 2004.34-3.99-6.55) 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 .00) 1.19 (1.12 (.400 (. Schober et al.78-2. slightly higher total blood mercury levels were found in U.313-.epa. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.52) 2. These distinctions can help interpret mercury blood levels in people.330 (..870-1. who participated in a 1998 representative population survey (Becker et al..S.97) 2. 1995.60 (1.410-. total blood mercury increased with age...85-2. 2009).480 (.770-1.76-3. environmental levels) and health effects is available from the U.88-3.Metals standard for inorganic mercury has been established by U. military veterans (mean age 52.. 1998)..77-2.S.940 (.00 (. EPA at: http://www.340-.78 µg/L for adults and 0.610-1.93 (1.396-. the median concentration of blood mercury was 0..atsdr. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.20 (1. A cohort of 1127 U.29) 1.160-.408) . Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.28) 1.405-. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.870-1.570) . Survey years 03-04 Geometric mean (95% conf... Grandjean et al.480) 75th 1. EPA. particularly methyl mercury.700 (. 2002). average age 33 years. 1998). Mahaffey et al. Over the NHANES 1999-2006 survey periods.67-2.530) .358 (.88 (1. Kingman et al.430 (.360-.254 (.76-4. Fourth National Report on Human Exposure to Environmental Chemicals 221 .330-.26 (1.01 (. total blood mercury geometric mean levels in females aged 16-49 years did not change.14) 90th 2.495 (.534) .440 (.58 µg/L for 4645 adults.46 µg/L for children.03-4. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children. From 1996 through 1998.09 (2.68 (2.530) .8 years.60) 619 713 1066 Limit of detection (LOD.413-. 1997.330-.580) .700-1. 758 children.930-1.960 (.S.840-1.. 2006).18) 2.16 (1. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.67-3. Sanzo et al. and increased slightly in non-Hispanic white children (Caldwell.23) .54 (2.96 (1.330-.61) 1.. Biomonitoring Information In the general population. In Germany the geometric mean for blood mercury was 0.442-.14.gov/mercury and from ATSDR at: http:// www. interval) .30) 3. 2003).08 (1.460 (.16 (.420 (.460) .89) 3.430 (.420 (.406-.66) 3.509) .840-1. Among the three racial/ethnic groups.46) 3.9 years).890 (.63-2. the total blood mercury concentration is due mostly to the dietary intake of organic forms.509) .290-.05) 3.370) .840) 1. and the age-related changes differed across the groups (Caldwell et al.360 (.19 (2.31) 1266 1272 03-04 03-04 03-04 . 2003).90) 2.39-3. During the same survey periods. population from the National Health and Nutrition Examination Survey.08 (1. 2001.e.55 µg/L.96 (1.213-.304) . although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.24 (2. Benes et al.463) .14-2. aged 18 to 69 years. et al.549) . Total blood mercury levels increase with greater fish consumption (Dewailly et al.492) Selected percentiles ( 95% confidence interval) 50th ..60-2..gov/toxprofiles.65) 1. 2009).

196-.30) 1.78-4. 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.276 (. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.619-..588) . mean urinary mercury was 3. 2002).969-1.40-1.56) 1266 1271 03-04 03-04 03-04 .545 (.S.246-.208-.S..25 (.307-.62 (1.11-2.616) .297 (. interval) . women of childbearing age have generally been much lower than these levels (CDC. Langworth et al.06 (.455) .714-1.51-2.587 (.280-.00) 90th 1.400-.447 (.365 (. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.86) 95th 2..88 (1. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.463 (.11) 2. 2006.333-.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .87 (1..04-3.652) .16) 1. 2006). 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.400) .S.32-2.. 2009).03) 2.404-. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.76 (1.79) 1.67 (1.63) 1.65 (1.30) 2.362 (.79 (1. population from the National Health and Nutrition Examination Survey.696 (.225-.480) . 2003). 1998).525 (.535) 1.447-.472-. 1988. Department of Health and Human Services noted that several studies have observed a modest.875-1.00) 286 722 1529 03-04 03-04 .09) 1.391) . Survey years 03-04 Geometric mean (95% conf.88-2.06 (..800-1.532 (.455-.12-3. Urinary mercury levels in recent German (Becker et al.Metals 2000).309-.87) 2. 2009). 2005).255 (. et al. DeRouen et al.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 . Urine mercury and the number of dental amalgams were correlated.77 (2. In the study of U. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.01) 2. not to imply a safety level for general population exposure. 1992).32 (1.1 µg/L..486) Selected percentiles ( 95% confidence interval) 50th .13-2.376-.46-2.498) 75th .67 (1. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.265-.368) .40 (1.909 (.343 (. and Italian (Apostoli et al. Czech (Benes et al. military veterans with dental amalgams.54 (2. a biomarker of perturbation in renal tubular function. and on average.630) .785-1.620-.28 (.275) .392-.347) . et al.S.306 (.39) 1.358) .289) .687) .44) 1.88-2.07) 1.522-.990) .23-2.384 (.476 (.64-2.667-1.970 (.11) 1.385-.964-1.31 (1.768 (. An expert-panel report recently prepared for the U.784) 1. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.443 (.. Levels in U.61) 1.391-.21) 1.485 (. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.13 (1.464 (.508 (. Information about the biological exposure indices is provided here for comparison. the urine mercury increased by approximately 0.599) .1 µg/L for each surface with a dental amalgam (Kingman et al.566) ..S.217 (.35 (1.00 (.417) .. reversible increase in urinary N-acetyl-glucosaminidase.18-1.41-2.301-.537) .455-. 2002) adult population surveys were similar to those in a U.365 (.

32-3.772 (.650 (.77) 1.04-1.631-.92) 3.565 (.99 (2.557-.68 (3.56) 4. 1999-2002.520-.810) .516 (.85) 4.553-.930) .03 (.592 (.24) 6.520-.664) .07) 1.824) . 16-49 years) 99-00 01-02 .97 (1.658 (. 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.92) 2.65-4. Geometric mean (95% conf.710 (.50 (1.719 (.632 (.28 (1.35) .46-4.45) 2.89 (2.723 (.21-3.809) .23-1.51) . National Health and Nutrition Examination Survey.99 (3.540 (.41-6.596 (.97) 2.05 (3.55) 90th 3.605-.636-.62 (3.870) .740 (.426-.53-3.657 (.846) .774) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.03-2.48 (2.35 (1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.56 (1. interval) Selected percentiles (95% confidence interval) Survey years 50th .65) 1.07-2.387-.83-3.32) 2.55-3.650 (.27 (2.41 (1.91 (2.00 (2.742-1.909-1.98 (5.569-.45 (1.47) 1.50 (2.45) 2.42-3.685 (.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.15-1.14-2.37) 1.17) 95th 5. National Health and Nutrition Examination Survey.84 (2.410-.38) 4.06 (.32 (1.69 (1.43-1.09-1.686) .624-.699) 1.639 (.76-5.S.21 (2.18 (3.61-6.03) 1.579-.806) .21 (1.14 and 0.622-.31-1.68-3.39-3.95 (2.44) 3.37 (1.00) 2.61) 1.665) .85-3.540-.07-5.68) 3.790) .27-1.475-.578-.14. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.420-.892) .832-1. Geometric mean Survey years (95% conf.22 (.14-1.59-5.710) 1.502-.42) 90th 2.13-4.92) 4.97) 2.16) 5.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.76) 2.670) 75th 1. interval) Selected percentiles (95% confidence interval) 50th .76 (1.72) 1.655 (.706 (.910) .831) .04-10.45) 95th 3.97) 2.637) .99) 1.56) 3.57-4.14) 3.41 (1.27 (1.77) 2.620 (.831) . 1999-2002.799) .13 (2.79) 1.91-7. population.31 (1.850-1.966) .522 (.94) 1.610-.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .70 (2.606 (.508-.46 (1.3) 5.47) 1.710 (.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .760 (.709) .Metals Urinary Mercury−Females Aged 16-49 Years Old.45-2.05 (2.52) 3.84 (2.87-4.30 (2.615 (.23-1.09-1.25) 2.00 (3.18) 3.16-5.30 (1.22-3.526-.30 (2.656-.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .500-.580 (.501-.582-. population.51 (3. 16-49 years) 99-00 01-02 .30-2.45-3.600 (.24-1.15 (2.69-3.744) 1.560-.709) 75th 1.580-.03 (.46) 3.833) .42) 2.721 (.62 (4.81-6.S.79) 3.10-2.50-4.41 (2.99-2.560 (.724 (.450-.62 (1.81 (3.54) 595 531 381 442 594 826 Limit of detection (LOD.10-4.691) .616-.650) 1.

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Acrodynia: exposure to mercury from fluorescent light bulbs. Turner MD. The kinetics of intravenously administered methyl mercury in man. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Osterloh J. Pediatrics 1987. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Vupputuri S. Environ Health Perspect 2007. Newton G. et al. Environ Res 2005. Woods JS. Allen PV. Bernardo MF. Blood mercury levels in US children and women of childbearing age. Amiano P. Topping G.48(4):221229. Smith AE. Smith PJ. Toxicol Appl Pharmacol 1994. Amurrio A.37:245-252. Sherlock J. Farris FF.98(1):133-142. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Fisher HL. Stern AH.128(2):25125-25126. 226 Fourth National Report on Human Exposure to Environmental Chemicals . et al. Public Health Nutr 2001. Aguinagalde FX. Sinks TH.4(5):981-988. Toxicol Appl Pharmacol 1996. Lind B. Patil LS.Metals Sanzo JM. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Daniels JL.2:117-131. Smith JC. McDowell M.97(2):195-200. Leroux BG.111(12):1465-1470. Arch Environ Health 1993. DeRouen TA. Kaye WE. Toxicol Appl Pharmacol 1994. Am Ind Hyg Assoc J 1970. McMahon KJ. Matsuo N. Hum Toxicol 1984. 1999-2000. Hall LL. Takahashi Y. Goldberg J. Whittle K. Vimy MJ. Effects of occupational exposure to elemental mercury on short term memory. Dorronsoro M.289(13):1667-1674. Langolf GD. Bolger PM. Burbacher T.79:786789. Environ Res 2005. Hislop D. Guo S. Effects of exposure to mercury in the manufacture of chlorine. 1993-1998. Leitao JG. The contribution of dental amalgam to urinary mercury excretion in children. Yoshinaga J. Sandler DP.110:129-132. Stern AH. Mooney TF. Zeitz P. Nakazawa M. Lorscheider FL.258(4 Pt 2):R939-945. Azpiri MA. Orr MF. Methyl mercury pharmacokinetics in man: a reevaluation. The hair-organ relationship in mercury concentration in contemporary Japanese. Suzuki T. Martin MD. Schober SE. Hongo T. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Vahter M. Environ Health Perspect 2003. Shen DD. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Baser M. Smith RG. Longnecker MP. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Tunnessen WW. Br J Ind Med 1983. Smith JC.31:687-700. Jones RL. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Imai H. Am J Physiol 1990. Environ Health Perspect 2002. JAMA 2003.124:221-229.40:413-419.115(10):1527-1531. Friberg L. Vorwald AJ. et al. Mottet NK. Most B.

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.8-90.9-55. WHO.6-82. 1996).0-56.3-75.6-58.9-56.4 (79.7) 45.2 (63.2 (49.. semiconductor and battery industries have begun to use molybdenum.3) 47.7-41. In humans.3) 41.9 (52.5-66.2-59.4) 49. aldehyde dehydrogenase.7-122) 93.4-75. which exert homeostatic regulation over molybdenum balance. urinary excretion over six days CAS No.1-63.3 (47.1) 46.9-82.4) 76.1-52. 0.2) 48.2) 40.3 (53.4) 56.0) 45.7-105) 69.7 (58.7-39.4) 45.7-50.6 (40.0 (42.4 (48.2) 52.4-82.6) 53.8) 48.7 (73.6-111) 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 52.5-65.8 (82. 01-02.0) 60.0) 54.6 (55.6-72.7-91.2 (61.7) 78. and 1.2 (69.8-49.2) 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 (98.7) 46.1) 35.2-53.9 (78.2 (56. inks.1 (34.1-55.5) 44.4 (48.5 (49.0-77.8.9-55.0-65.2) 37.2) 41.6 (43.1) 59.5-52.0-85.0 (76.1-44.1-88.4) 52.3 (71.7 (50.7) 51.9-83. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.3 (55.3-91.2 (40.2-91.5 (41. Compounds of molybdenum are also used as corrosion inhibitors. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.S.0 (81.7-96. 2001.2) 53.3-108) 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 47.6) 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 (99.3 (38.1 (91.6-46.9) 34. respectively.1-48.4-61.8-46.4 (34.6 (55.8 (85.7-84.0-110) 90.3 (55.8) 39. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.2-79.4 (80.9 (73.0-53.5 (37.7-47.5-46.5-52.3 (79.7 (51.2 (38.3) 85.9) 67. and in pigments for ceramics.5 (74.8) 44.5-124) 108 (92. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.5-41.8 (67.4 (72.0-62. population from the National Health and Nutrition Examination survey.0) 55.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.1-59. hydrogenation catalysts.9-85.7 (71. see Data Analysis section) for survey years 99-00.1) 82.Metals Molybdenum or ore deposits.2-59.6-42. lubricants.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.1) 60.5-68.4-52. 7439-98-7 General Information Elemental molybdenum is a silver-white.8-108) 87.9) 62.3) 37. More recently. Fourth National Report on Human Exposure to Environmental Chemicals 227 .3) 83. chemical reagents in hospital laboratories.3-44.0) 62. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.9 (44.5) 80.6-96.3) 65.6 (40.1) 126 (106-147) 109 (94.7-68.8) 75.3-115) 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.2 (55.2-42.2-70.0-101) 82.5-91.2-37. Excretion occurs predominantly via the kidneys.5) 47.4) 42.7) 57. and xanthine oxidase (Kisker et al.6) 93.6-55.1 (38.0 (41.6) 71. 2001).7 (44.2 (49.4) 41.8) 46.0-38.7) 78.7 (45.7-60.8) 40.3 (46. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6 (73.6-62.5 (67.0 (48.0-71.9-109) 97. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.1) 57. At a daily oral molybdenum dose of 24 µg. and 03-04 are 0.8 (42.8-94.0 (43.7 (36.7) 75th 84.5) 80.3 (84.5 (41.5 (48. and paints.9 (32.6) 51.3 (73.1 (71.3 (37.5 (43.7-51.0) 84.7-73.0) 97.2 (83.3) 54.7) 86.7) 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 78.1-52.8.5) 60.5.2) 79.9 (40.9 (33. interval) 45.3-47.7-92.0) 39.5 (81.3 (64. 1997).0 (42.0 (46.6) Selected percentiles ( 95% confidence interval) 50th 50.6) 71.1-51.9 (37.9 (34.5) 85.8-106) 88.7) 77.0-100) 63.7 (37.6 (52.

2-121) 107 (92.0-103) 103 (90.1) 37.8-47.4-118) 172 (131-195) 138 (120-163) 118 (106-134) 780 682 618 546 667 723 760 1132 1074 Non-Hispanic blacks Non-Hispanic whites 228 Fourth National Report on Human Exposure to Environmental Chemicals .6) 39. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.2) 39.9) 40.S.9 (64.2 (36.7-93.5-97.9-41.4) 60.4-76.8) 38.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.2 (33.2-49.2) 42.8 (57.9) 44.7-120) 87.8-47.5 (40.5 (50.7-38.7) 57.4-185) 106 (94.1-45.2-41.3) 64.1 (37.4 (59.2 (43.8-65.7 (77. at daily oral doses of 95 µg and 428 µg.5 (39.2) 37. Biomonitoring Information Molybdenum is an essential element for health.4) 122 (107-133) 109 (99.9 (73.5 (35.0-41.2 (40. and urinary levels reflect intake from all sources.8 (36.5-44.4 (44.1-39.3 (58.4 (53.8 (90.7-44.9-45.6) 39.6 (38.2) 42. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3) 44.5 (39..0) 62.5) 72.9-87.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.4 (37.0-46. 1995). population from the National Health and Nutrition Examination survey.1-43.0-56.3 (71. 2001).0) 39.5 (37.1 (38.8-42.3 (37.1) 40.1 (40.9-42.2-103) 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 42.9) 41. interval) 43.6-61.4) 89.8) 39.1 (38.9 (79.6-76. of the ingested dose (Turnlund et al.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.5-62.1) 101 (83.6) Selected percentiles ( 95% confidence interval) 50th 41.0) 38.1-34.0-120) 85.3) 37.7 (75.1-127) 90.8) 38.9-71.1) 43.S.8) 45.3) 40.3-45.6) 43. 1993).1-38.7) 45.4-120) 101 (84. In industry.1-40. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.5 (80.1 (42.5-60.2-96. Molybdenum is generally considered to be of low human toxicity.4-42.9 (40. EPA.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..1-39.5-45.5) 90th 108 (97.5 (40.0) 44.7-52.3 (37.4-39.0 (80. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.2) 39.5 (34.2-40.3) 56.6 (36.4-107) 85.6 (42.4) 116 (101-126) 104 (88.1-81.3) 57.2 (57.8) 62.5 (78. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.3) 61.2) 58.5) 73.7) 112 (95.9 (39.9-61.6 (71.5 (83.7) 75th 63.3-52. urinary excretion over six days rose to 50% and 67%.7-100) 77.5 (41.7-137) 129 (109-155) 112 (97.1-79.6-45.5 (37.9 (64. 1999).3 (36.3-68.9) 92.6-61.7-43.4) 77.7) 115 (93.4) 58.5-92.5-119) 90.6-41.3-43.1) 65.2 (37. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.0 (58.8-67.3-46. respectively.4) 44.2-65.9 mg/kg/day and established a tolerable upper intake level of 0.6 (59.8) 37.8-46.5 (65.0) 36.8 (37.8) 79.5-99.2-80.7 (66.0) 39.6) 48.4-106) 85.3 (55.8) 71.9 (36.0 (35.0) 88.8) 61.1-43.1 (49.4 (40.2) 43.5 (41.8 (56.9-45.1 (33.2 (52.8-118) 81.3) 41.5 (59.5) 71.9-68.0) 72.4 (67.4 (56. and clinical or epidemiologic evidence of adverse effects is limited. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.2-46.2) 38.7) 62.3-44.5 (79.5 (36. 1961.1-112) 78.9-118) 91.0-133) 119 (88.1 (82.3 (71.9-40..0-46. but available epidemiologic data are scant.9 (49.9) 79.6 (57.5-69. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure. Based on studies finding adverse reproductive effects in rats and mice.1 (54.2-96.4 (78.9) 31.2-47. 1997).6) 36.3 (36.1 (44.2 (73.1) 37. U.1-109) 89.4-66. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.6-88.3 (53.5-70.1-41.6-63.8 (75.4) 61.5-48.5 (54.1-100) 86.1-67.7) 41.4-41.9-117) 57.5 (35.1 (30.3 (83.4 (55.5 (38.5) 63.4) 40.2) 55.8-66.5-46.3) 43.Metals was 18% of the ingested dose.6 (36.4) 48.0) 33.7 (30.2 (69.7-40.8-52.6-63.5-50.3) 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 (50.5 (65.1 (39.3-56.3-59.3 (51.2 (40.2 (40.9-96.7-62.1) 56.7) 42.2) 37.9 (39.3-115) 98.7) 53.5) 60.9 (35.0 (74.4) 47.0-38.5-35.0) 53.03 mg/kg/day in humans (IOM.3-141) 109 (81.8-84.6-78.

van Sprundel MP. Institute of Medicine (IOM). Turci R. Zhurnal Obshchey Biologii 1961. Available at URL: http://ntp. 1996. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. Dietary reference intakes for vitamin A.. Schleyerbach U. Sci Total Environ 1998. 2002. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No.S. edu/openbook. Am J Clin Nutr 1995.216:253-270. White and Sabbioni. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. et al. World Health Organization (WHO). Molybdenum-cofactorcontaining enzymes: structure and mechanism. Weyler JJ. Gatti A. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. and zinc: a report of the Panel on Micronutrients. Third National Report on Human Exposure to Environmental Chemicals. Occupational risk factors of lung cancer: a hospital based case-control study. 16:1313-1319. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Ronchi A.123(1):81-85. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. vanadium. Minoia et al. Christensen JM. Molybdenum 1993 [online]. excretion. vitamin K. 144-154. Turnlund JR. Shmavonyan DM. pp. EPA). 4/14/09 White MA. Food and Nutrition Board. Rees DC. boron. Available at URL: http://books. U. Molybdenum absorption. 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. Sciarra G. Van Meerbeeck JP. iron. J Trace Elem Med Biol 2001. Ann Rev Biochem 1997.php?record_id=10026&page=420. Keyes WR. Washington. (DC): National Academy Press.S.epa. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Minoia C. Rapid Comm Mass Spectrom 2002..gov/index. arsenic.66:233-267.gov/iris/ subst/0425. copper. 2001. X. Occup Environ Med 1999. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Molybdenum in infancy: methodical investigation of urinary excretion. iodine. 4/14/09 Iversen BS. Trace element reference values in tissues from inhabitants of the European Union. Geneva: WHO. Menne C. 56:322-327. manganese. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes.nap. References Centers for Disease Control and Prevention (CDC). Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Available at URL: http://www. Aprea C. Yarovaya GA. Peiffer GL. Analyst 1998. 1998). Sabbioni E.. 420-441. 2005. molybdenum. TR-462.niehs. Environmental Protection Agency (U. silicon. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. 2001).Metals in urine for the U. Schindelin H. Molybdenum. Vermeire PA.22(3):179-191. White MA.htm.nih. nickel. Atlanta (GA). National Toxicology Program (NTP). Sabbioni E. chromium.15(2-3):149-154. Kristiansen J. Droste JHJ. In: Trace elements in human nutrition and health. A study of 13 elements in blood and urine of a United Kingdom population. 1998. Schaub J. 2005). Koval’skiy GA. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces.S. pp. Kisker C. Fourth National Report on Human Exposure to Environmental Chemicals 229 . population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC.62(4):790-796. 4/14/09 Sievers E.

however. Important properties of platinum are resistance to corrosion. 01-02.. carboplatin) in the treatment of cancer. and high catalytic activity. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.S. thick-film circuits printed on ceramic substrates. see Data Analysis section) for Survey years 99-00.. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. respectively. 0.07. cisplatin. and as drugs (e. and 0. which may vary for some chemicals by year and by individual sample. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al.04.g. dental alloys. Platinum compounds are used in electrodes. 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 03-04 are 0. population from the National Health and Nutrition Examination Survey. 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. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples.04. strength at high temperatures. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. jewelry. and iron. 1998). 230 Fourth National Report on Human Exposure to Environmental Chemicals . copper.Metals Platinum CAS No. 7440-06-4 General Information Platinum is a silver-gray. < LOD means less than the limit of detection. as oxidation catalysts in chemical manufacturing. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions.

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

2004. Schierl R. 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. Kuster W. Pethran et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Schierl.4(1):27-36. Pethran A. Angerer J. Iavicoli I.10:63-71. 2004).35:313-321.70(3):205-208. Occup Environ Med 1998.inchem. Ewers U. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. et al. 5th ed. Int Arch Occup Environ Health 2003. 289-380. 1998). Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al.56(3):283-286.S.61(7):636-9. Raab W. Thornton I. pp. Farago ME. Schierl R.htm. Hysell D. Occup Environ Med 2004. 2004) or less than 0.. Seifert B. Huber R. Hauff K.. New York: John Wiley & Sons. osmium. Stilianakis NI. Herr et al. Platinum. Saindelle A. Schierl R. Kaus S. van de Weyer C.04 µg/L) in this Report.Metals the International Programme on Chemical Safety at http:// www. 2003.01 µg/L (Becker et al. 1997. References Becker K. Urinary platinum levels associated with dental gold alloys. Ruff F: Platinum and platinosis. Environ Res 1975a. Ensslin AS. ruthenium. International Programme on Chemical Safety (IPCS). rhodium.. 2003. et al. Parrot JL.htm. population were below the limit of detection (0. et al. Rommelt H. Platinum concentrations in urban road dust and soil. Biomarkers 1999. Blanks R..55(2):138-140. 2003). Fries HG. Hall L.. Czerczak S. Uptake of antineoplastic agents in pharmacy and hospital personnel. Bocca B.005 µg/L (Iavicoli et al. Carelli G. Petrucci F. Environmental Health Criteria 125.. Jankofsky M. Herr CE. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Neuendorf J. Urinary excretion of platinum from platinum-industry workers. Biomonitoring of traffic police officers exposed to airborne platinum. Cohrssen B. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations.123(3):451-454. Kazantzis G.org/documents/ehc/ehc/ehc125. Available at URL: http://www. Saindelle A. Part 1: monitoring of urinary concentrations. Schulz C.. 3/31/08 Moore W Jr.207(1):69-73. Several studies have shown that background concentrations in general populations were usually less than 0. 2000. which elevate urinary platinum by five to twelve-fold (Begerow et al. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Begerow J.. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. In: Bingham E. 1991 [online]. and platinum. Fruhmann G. Powell CH. Nickel. Schulz C. palladium. Seiwert M. 2003. Gromiec JP. Arch Environ Health:1969. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. 1999. Boos KS. Levels of platinum in urine for the U. Pethran A. Gieler U.13(1):24-30. Biomonitoring Information Urinary platinum levels reflect recent exposure. Arch Environ Health 2001.. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Kulka U. eds. Kelly J. Schierl et al. Nowak D. Hebert R. Int J Hyg Environ Health 2004. Environ Health Perspect 1975b.inchem. Br J Pharmacol 1969. Wilhelm et al. Kavanagh P. Hysell D. Patty’s Toxicology. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect.. Alimonti A. Analyst 1998.9:152-158. 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. and in blood and urine in the United Kingdom. Schierl R. Allergy and histamine release due to some platinum salts. Wilhelm M. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Grimm CH. Crocker W. 206:15-24. and gold excretion of patients after insertion of noble-metal dental alloys.19:685-691. J Expo Anal Environ Epidemiol 2003. Senofonte O. Int Arch Occup Environ Health 1997. Turfeld M. Herr et al. et al. 2001). Moore W Jr. Duneman L:Long-term urinary platinum. International Journal of Hygiene and Environmental Health 2003.76(1):5-10.org/documents/ehc/ehc/ ehc125. 1998). palladium. Influences on human internal exposure to environmental platinum. Campbell K. Ruff F: Histamine release by sodium cholorplatinate.

220 (.350-.240-.480) .410) .340) .420) .160-.480) .200 (..330-.134-.410 (.330-.176 (.172 (. 2005).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 .360-.430 (.420-.201 (.170 (.S.250 (.330) .410-.180 (.210 (.690) .225) .172 (.220 (.420) .160 (.178) .300 (.270-.420 (.280) .140-. and 03-04 are 0.160-.520) . 0.460 (.184 (.Metals Thallium depilatory cosmetics. the latter being the current major industrial consumer of thallium in this country.200 (.196) .290-.450 (.201 (. In the past.200 (.147-.170-.150-.197-. population from the National Health and Nutrition Examination Survey.360 (.450 (.173-.370) .290 (.300) .159 (.490) Total . see Data Analysis section) for Survey years 99-00.370-.250-.300) .300) .420) .210) .183) .190 (.160 (.370 (.500) .300 (.350-.350-.430 (. In addition.470) .188) .450 (.170-.370-.500 (.148-. 01-02.165) 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 .370 (. In the United States.590) .220) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.470 (.220) .440 (.420) .440 (.270 (.02.180) 75th .420-.173) .144 (.239) .360 (.260 (.145 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.159 (.179-.290-.390-.200) .480) .430-.480) .490) .240-.162-.160-.450 (.290) .300) .370 (.280) .218) .410 (.360) .202) .290) .400) 95th .350-.270) .200-.230) .320) .172) .290 (.420-.410 (.280-.220) .190 (.170-.170-.330-.153-.430) .160 (.182-.400) .157-.520 (.191 (.390-.206) .218) .400) .390) .440) .290 (.340) .165 (.520) .155 (.420) .440-.330-.510 (.390) .590) .280 (.133-.270 (.197 (.440) .192) Selected percentiles ( 95% confidence interval) 50th .630) .215) .250-.02.320 (.167-.160 (.147-.330) .230) .340-. Fourth National Report on Human Exposure to Environmental Chemicals 233 .280 (.156) .260-.150-.170-.640) .190 (.460-.290) .460) .350-.510) .390 (.150-.290 (. 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.330) .450 (.230-.270 (.220 (.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 .410 (.420) . it has not been specifically mined or refined in the United States since 1984. Human health effects from thallium at low environmental CAS No. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.220 (.450 (.440) .250-.310 (.360 (.170-.250-.400-.160-.175) .400-.220) .290 (.410-.400 (.380-.200-.370) .380 (.185-.170-.470) .220-.158) .310 (.190 (.350 (.230 (.520) .470) .410-.240) .500) .250-.170) .167 (.330-.370 (.450 (.200 (.310-.180-.370 (.320) .410-.196) .350) .350 (.150-.200 (.420) .220 (.210 (.290) 90th .200) .156-. respectively.360-.210-.430) .156) .280) .400) .160-.480) .270 (. Thallium disappears from the blood with a half-life of several days.250 (.170 (.180-.170) .400 (.145-.260-.260) .154-.230) .200) .330) .270-.170) .440 (.260-.159 (.430 (.200) .380-.243) .430-.370 (.330-.230-. however.440 (.400 (.200-.380) .185 (.390 (.500) .280 (.187-.340-.220) .183) .270) .400 (.180-.200) .400 (.167-.250-.217 (.450) .280-.240) .177) .200) .270-.260-.470 (.320) .173) .310 (.217) .240) .490 (.430-.190 (.450 (.02.400-.360-.390-.190 (.240-.400-.300-.300 (. From these and other sources. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.135-.450 (.200-.230) .380 (.149 (.260-.340 (.260 (.560) .340-.320-.410-.370-.250) . 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.147-.150-.360-.430 (.410 (.137-.290 (.350-.250-.202 (.180 (.270 (.202 (. interval) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.181-.410-. and 0.146 (.390) .230-.310) .420-.150-.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400) .330-. thallium was obtained as a by-product of smelting other metals.260 (.370-.410 (.550 (.180) .490) .250-.390) .390-.220) .145-.163) .171 (. representing distribution into other tissues.370 (.400-.350) .490) .170 (.180-.180 (.160 (.190-.200 (.360 (. thallium readily crosses the placenta and also distributes into breast milk.340-.360-.290) .

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

Dolger R. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. 1981. 1985). Brockhaus A. J Soc Occup Med 1985.5 μg/L. Atlanta (GA).. Third National Report on Human Exposure to Environmental Chemicals. Paschal et al. X. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Trace element reference values in tissues from inhabitants of the European community I.48(4):375-389. et al. 2005.. Celier D. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Int Arch Occup Environ Health 1980. Gallorini M. Sci Total Environ 1990. Trace element reference values in tissues from inhabitants of the European Union. Kramer U. Schaller et al. Available at URL: http://www. Soddemann H. 1998. and serum of Italian subjects. Centers for Disease Control and Prevention. 1992 [online].. Environ Res 1998.76(1):53-59. Challeton-de Vathaire C. et al.Metals (CDC. Valentin H. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Sabbioni E. A study of 13 elements in blood and urine of a United Kingdom population.113(1):47-53.gov/toxprofiles/tp54. Schaller KH. White and Sabbioni. Sabbioni E. Apostoli P. Brockhaus et al.47(3):223-231. Manke G. Pietra R.html.cdc. Marcus RL. Pozzoli L. Minoia et al. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Investigation of a working population exposed to thallium. (1981) studied 1. Sci Total Environ 1998. 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. 1998). population) are thought to correspond to workplace exposures at the threshold limit value of 0. 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.atsdr. A study of 46 elements in urine. White MA. Int Arch Occup Environ Health 1981. Pirkle JL. References Agency for Toxic Substances and Disease Registry (ATSDR). Paschal DC. Schmidt M. 1990. Radiat Prot Dosim. Boisson P. Ting BG. Trace metals in urine of United States residents: reference range concentrations. with concentrations ranging up to 76. et al. Ewers U.35(1):4-9. 1980. 2005.S. Investigations of thallium-exposed workers in cement factories.216:253-270. Raithel HJ. Sampson EJ. Morrow JC. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging.1 mg/m3 (Marcus. Cassot G. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al.265 people living near a thallium-emitting cement plant in Germany. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Toxicological profile for thallium. 2005) and are shown with results from NHANES 2003-2004 in this Report. Minoia C. Martin J-C.95:89-105. Wiegand H. 7/15/09 Blanchardon E. Jackson RJ. blood. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust.. Buhlmeyer G.

530 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).080-.060-.090-.250) .060-.410-.073) .150 (.00) .400 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.160 (.160 (.120) .150 (.220-.190 (.070) .270-.130) .140-.170) .220) .470) .090) .520) .230-.105) .080 (.560) . and as catalysts in the petroleum industry. Tungsten is used mainly for producing hard metals.480) Total .180-.062 (.060 (.350) .080 (.430-.300) .S.410 (.440) .170) .091) .069) .090 (.090-.120) .220) .210-. 0.071-.150) .076 (.200) .126) .080) . and 0. and for producing ferrotungsten.070-.056-.300-.380 (.070-.670) .080) 75th .450 (.130) .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 .090-.062 (.200 (.070) .056-.170) . 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust. 236 Fourth National Report on Human Exposure to Environmental Chemicals .270 (.350) .140 (.120-.080) .300 (.080) .180) .300 (.093) .160-.650) .160-.120 (.260) .130 (.122) .340) .081 (.120) .105 (.560) .109) .110 (.110) .160) . Tungsten compounds are used as lubricating agents.360 (.190 (.068) .080 (.110 (.560 (.180-.097-. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.320-. bronzes in pigments.150-.210 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.080 (.084) .400 (.460 (.590) .300 (.450-.290) .310) .100 (.113 (.093 (.500 (.230 (.380-.320 (.430 (.096 (.330-.210 (.330) .190-.160) .800) .290-.360 (.490) .087-.430-.950) .137 (.074-.380-.120-.260-. which are used in rock drills and metal-cutting tools.370 (.360) .060-.570 (.120-.04.510 (.570 (.370-.113 (.400-.04.130-.250-.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 .270-.270-.160-.090-.370 (.123-.160 (.077-.370 (.110-.130) .620 (.290-.130-.090-.130 (.210 (.160 (.060 (.430 (.204) . see Data Analysis section) for Survey years 99-00.460) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.560) .270 (.220) .290) .095-.370) .390) .210 (.080-.790) .400 (.340-.180) .100 (.065-.550) .140-.090) .120-.073-.140) 90th .280 (.092 (. filaments for incandescent lamps.250) .110-.430 (.230-.180) .800) .330) . interval) .140 (.530 (.250) .460 (.340-.310-.230) .350) .050-.100-.180 (.133) .113 (.310-.104) .190-.300) 95th .100) .060-.510-.090-.096-.090) .190-.320 (.120) .190) . Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.230-.107 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.360-.260 (.560) .086 (. which is used in the steel industry.830) .520) .082-.250) . and 03-04 are 0.510-1.100 (.380 (.360-.460) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.111-.340-.090 (.320-.490 (.092) . their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.160-.280 (.070) .290-.640 (.070) .550) .280-.110 (.130-.260 (.270 (.310 (.170) .320) .060 (.071 (.060-.240-.330-.53) .088 (.110 (.060 (.210 (.630) . 01-02.092 (.130-.150 (.070 (.310-.580) .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 .770 (.070 (.370-.550 (.310-.170 (.100) .190-.082 (. mainly as scheelite (CaWO4).080-.310-.093-.082) .130) .470 (.120-.470 (.390 (.430) .620) .100-.110) .250-.200-.810) .073 (.460 (.140 (.230) .Metals Tungsten CAS No.073-.064-.550) .500) .084 (.400) .151) .120-.220 (.270-.050-.060 (.170-.065 (.100) .070-.160 (.050-.090-.100 (.470) .069-.087) .070 (.120) .132) .130) .240 (.060 (.100-.158 (.100) .520) .420-.500 (.090-.101-.058-.04.120) .350 (.260-.180-. population from the National Health and Nutrition Examination Survey.470-. respectively.180) .110-.180-.210) .380) .250) .078-.100) .180 (. Little information is available on the toxicity of tungsten.330 (.170 (.100) Selected percentiles ( 95% confidence interval) 50th .116) .095-.084-.140 (.290 (.076 (.080 (.070-.060-.082 (.088) .066-.350-1.690) .230-. Evidence is lacking for the carcinogenicity of tungsten.420-.620) .070-.400 (.110 (.050-.090 (.113 (.135) .360 (.260-.530 (.380-.380-.090) .101 (.250) .

197 (.074-.301) .106 (.385 (.083 (.136-.315-.431) .299 (.354) .067 (.317) .250-.094-.077-.071 (.286-. or exposure that a control group of non-metal workers had mean levels differences.069-.255 (.168 (.169 (.386) .500) .333-.426) .082) .089 (.067-.279 (.136-.179-.087 (.302-.253-.063-.222-.218 (.146) .197-.091) .439) Total .105 (.605) .431) .436-1.300-.190) .083-.158) .073 (.739) .098-.081 (.091) .098) .497 (.075 (.071 (.797) .094) .154) .091 (.091) .049-.075) .059-.061-.133) .145 (.329-.347 (.333-.077) .308) .339 (.179-.116) .329 (.057-.170-.267) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.071 (.100 (.360 (. 1998).056-.083) .084 (.100) .085-.161) ..261-.275 (.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 . 2001).375) .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 .302-.059 (.301) .453) .062 (.139-.055-.065-.116-.216 (.080 (.174 (.333 (.197) .148) .439 (.184 (.122-.341 (.063-.064-.117 (.215 (. population.S.165) .482 (.201) .130 (.136-.086-.072 (.064-.326) .211 (.070 (.201 (.071) .294 (.199 (.353 (.462) .109 (.098-.074-.300) . Patients with medically-inserted tungsten found at increased levels in drinking water. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.098-.086) .484 (.125 (.063 (.353 (.258 (. population (CDC.091) .082) .071) .153) .436) .108) .075) .053-.S.200-.138) .099-.063-.245-. Using neutron activation analysis to 2000.258-.153-.152-.096) .186 (.200-.167-.333 (.354-..104-.138 (.317-.086) .080-.084 (.412 (.279 (.080-.359 (.079) .167) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.344-.359 (.077) .124-.078-.270 (.122-. Nicolaou et al.075-.057-.082 (.094) .287) .240-.138 (.108-.079) .109-.S. and 2003-2004 (Paschal et al.144 (. interval) .667) .093-.081-.066 (.065) .216-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.880) . Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.150 (.120) .176-.061-.111 (.122 (.167) .174) .058-.383 (.070 (.237) .293 (.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 .130-.214) .667 (.452-..054-.131-.224) .093) .136 (. the residents’ embolization coils showed elevated tungsten levels in Urinary Tungsten (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.103-.164 (.216-.059-.146 (.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 .143-.(Kraus et al.075-.116 (.079) .068 (.358) . similar to those in this Report (Schramel et al.084) .078) .222) .253 (.231-.306) .333 (.237) .074) .333 (.073 (.255-.284) .095-.150-.067 (.554) .133) 90th .215) .065 (.209-.267-.072-.555 (.278-.091 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.217-.300-.073 (.216-.121 (.065-.085 (.203-.237-.339 (.105 (.364 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.081) .158) .231 (.071) .459) .317 (.119 (.176-.068-. measure urinary tungsten.439 (.431) .079) .073 (.056-.083 (.088) .199 (.080 (.158 (.155-.253) 95th .092) .085) .060 (.634 (.066 (.272-.065 (. population from the National Health and Nutrition Examination Survey.208-.148 (.060-.059-.169) .216 (.075 (.107-.300 (.065-.098 (.143 (.255 (.285) .139) .727) .250 (.126-.124 (.090-.198) .119-.333) . Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.381) .054-.158) .071-.340 (.279 (.088) .181 (.151 (.144-.139 (.095) Selected percentiles ( 95% confidence interval) 50th .414) .301) .205-. (1987) found possibly due to methodologic.121-.265 (.061-.426) .465) .078 (.198-.136-.078) .077-. 2005).154) .465) .538) .078 (.188-.167-.484) .250 (.089) .074) 75th .217-.125) .206-.333) .187) .308) . 2001-2002. 1997).083) .087) .100) .084) .823) .133) .180-.392) .060-.074 (.081 (.283) .079 (.582) .146 (.063-.117) .197) .410-.090-.063 (.331-.379 (.157) .28) .079 (.120) .069 (.214-.150-.233-.072-.069 (.086) . 2003.

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

008-.067) .031-.034-.019 (.021 (.037 (.011-.042 (.028 (.021 (.S. and as an aid in electron microscopy and photography.014 (.011) .007) .014 (.022-.027 (.012) .062) .028 (.053) .073) .039) .010) .037) .033) .037) Total .006-.020) . or processing.050) .007-.017 (.028 (.027) .010) .007 (.013 (.009 (.017-.020-.007) 75th .046 (.008 (.006 (.041 (.036 (.007-.008-.013) .008-.026 (.055 (.012 (.040-.017-.013-.009) .008) .013 (.008 (.021 (.038 (.012 (.016-.017) . 0.027) .029-.008) .052 (.027-.023) .044 (.046 (.009 (.054-.013) 90th .009) .064 (. respectively.021) .016) . 01-02.008 (.014 (. and 234U.021) . nuclear fuel.006-.012) .007-.031 (.030 (.024-.016) .028-.010 (.011) .026-.029 (.006-.041 (.047 (.011-.008 (.017-.010) .007 (.018) .027-.038) . Thus.006-.008 (.008 (.033 (.034-.011-.019-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.040) . Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).009-.006-.040 (.007-.010 (. 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.012-.009) .007) .037) .032 (.007-.010-.056) .008-.015 (.017-.007 (.007-.065) .007 (. Since the 1990’s. and 0. population from the National Health and Nutrition Examination Survey.007 (.046 (.009) .039) .010) * .018) .012 (.006-.023) .019-.114 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.011 (. In workplaces that involve uranium mining.007) .046-. interval) .016 (.023-.009-.006 (.008 (.023 (. Variable concentrations of uranium occur naturally in drinking water sources.027 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.066) .040 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 .011 (.024 (.013 (.036) .009-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.023 (.026-.009) .007-.004.008 (.005.015) .028-.009 (.067) .051) .065) .013 (.008 (.013 (.009) .011-.031 (.012 (.009) .014 (.017-.053 (.008 (.017-.007-.013 (.007-.010-. milling.007 (.008) Sample size 2464 2690 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .020-.019-.005-.005-.008 (.015-.004.020-.027) .031 (.036 (.020 (.007 (.023-.010 (.011) .006-.011-.034) .007) .031 (.014 (.008 (.039-.023-.020-.127) .045) .007-.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 .005-. including nuclear weapons.017) .040-.035-. Depleted uranium (DU) refers to uranium in which the proportions of 235U and 234U isotopes have been reduced compared with the proportion in natural uranium.009) .006-.158) .017) .008-.009) Selected percentiles ( 95% confidence interval) 50th .015 (.022-.033 (.025-.072) .024-.027) .009-.021) .013-.016) .007) .011-.007 (.026 (.060 (.012-.015 (. human exposure occurs primarily by inhaling dust and other small particles.015) .008-.007-.031 (.017) .020) .007-.010-.009-.037-.007 (.018 (.005-.010 (.035) .063) .009) .009) .008) .049) .010) .020-.010-.006 (. Uranium has many commercial uses.011) .030) .036-.027-.029-.006-.009-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.007-.009 (.019-.012 (.011) .027 (.006-.026 (.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 .042) .030 (.033-.011) . see Data Analysis section) for Survey years 99-00.021-.009) * .040) .027 (.018-.007 (.010-.018) .013-.010) * .048 (.016-.009) .009 (.022-.007 (.026) .006 (.037) .009-.054) .024-.010) .008 (.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.011-. in some ceramics.010 (.022) .088) .009 (.012) .007-.021-.009 (.030-.016) .043 (.010) .016-.012-.009) .009 (.009) .012 (.009-.008 (.012) .006-.043) .049) . and 03-04 are 0.017 (.023) .008) .279) .008-.016) .054) .008 (.008 (. 235U (about 0.048) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.018) .045) .009 (.007-.036-.007-.006-.005-.036) .017) .022 (.069) .012-.035) .006-.009-.030 (.011) .007-.72%).046 (.023-.008) .046) .016) .010) .010) .009-.013 (.015 (.026) 95th .009 (.050) .012-.023 (.Metals Uranium CAS No.014 (.018 (.007-.008 (.010-.008-.056) .012-.026) .

053) .009) .009 (.010) .010 (.034 (.008-.025-.019) .029) .027 (.024) .007 (.004-.006) .019-.005 (.030 (.004-.018-.063) .039) .048) .028) .010-.010) * .017) .005-.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 . After long term or repeated exposure.016-.006) . Health effects from uranium exposure result from chemical toxicity to the kidney.009) Selected percentiles ( 95% confidence interval) 50th . the half-life of insoluble uranium in the lungs is several years (Durakovic et al.080) . which can occur occasionally from high occupational exposure.013 (.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. population from the National Health and Nutrition Examination Survey.021 (.051 (.013 (. low level exposure. In cases of retained DU shrapnel.007-.006-.009-.032) .020 (.009-.024 (.024-.025-.005-.027 (.020-.010) . about 50% of the absorbed dose is eliminated in the urine within the first 24 hours. 2003).007) .009 (.010-.016 (.011-.015) .005-.012 (.010) .015 (.024) .015 (.011-.022-.008) .015-.024-.027) .019 (.053) .008-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.009) .007-.012-.012) .007) . with much slower elimination from bone.008) .025) 95th .028) .014 (.026 (.007 (.026 (.008) .013 (.051) .S.034 (.029 (.014-.005-.008) . liver.022 (.008-.017 (.017-.011-.019 (. the initial half-life of uranium is about 15 days (Bhattacharyya et al.014) .009) .047) .016) . 1992).006-.006-.014-.006-.007-.050) .007-.029) .006 (.006 (.009-.029 (.013 (.013 (.010 (.015) .018-.007) . where limited absorption occurs (less than 5%).008 (.022 (.014) .017) .012 (.010-.029) .067) .009) * .042-.015) .012 (.009) ..030) .032) . Depending upon the specific compound and solubility. 0.031 (.008) 75th .013 (.007 (.006-.024 (.034-.016-.018-.013 (.011-.011) .020-.043 (.051) .008 (. which represents distribution and excretion.008 (.008) .020) .006-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.009) .059 (.146) .026-.006-.033 (.042) .011-.006-.007 (.007 (. Uranium is eliminated in feces and urine.009-.006-.024-.006-.016) .009) .017-.006-.027-.008-.018-.015 (.006) .006-.033) .015) .034 (.029 (.019) .016) .061) .007 (.018) .013) .035 (.006-.008 (.007 (.016) .009 (.006 (.009) .028 (.021-.028) .025 (.008 (.008-.017-.005-.007 (.005 (.024) .011-.050) .006-.027-.012-.022-.021 (.007 (.019-.008) .013) .035 (.008) .013 (.007 (.020 (.270) .011-.018-.009) .009) .015 (.033 (.014-.024) .022-.012 (.009-.016) .017-.015-.011 (.007-.030 (.009 (.010-.044) .006 (.030) .024 (.039) Total .006-.007 (.006-.058) .008-.1%-6% of an ingested dose may be absorbed.048) ..028-.050 (.013) .007 (.056) .011) * .026 (.006-.008) .025-.010-.013-.007-. 240 Fourth National Report on Human Exposure to Environmental Chemicals .006) .008 (.006-.031-.019 (.006-.034) .016) .Metals impact.012 (.015-.008 (.020-.012 (.012) .017 (.010-.033 (.024) .007-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.045 (.007 (.007-.007-. kidneys.006) .021) .034 (.006 (.011-.014 (.034-.077) .009 (.009-.022 (.020 (.008) .054) .027 (.019-.030 (.021 (.010) .007 (.011 (.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 .013 (.027) .015-.017) .023-.058) .006-. the shrapnel acts as a source of chronic.025-..008 (.026) .005 (.025 (. Inhaled uranium-containing particles are retained in the lungs.007 (.008) .010 (. 2005).018 (.030-.007 (.016-.010-.007 (.013 (.006-.019-.008) .039) .028) .011-.074) .027-.029) .008 (.016-.015-.006-.010 (.051) . After exposure to soluble uranium salts.005 (.007 (.037 (.011) .009) .014) 90th .040 (.041) .007-.011) .019-.027-.010-.010) .022) .008 (.007 (.006-.042) .039) .007 (.010 (.030-.010-.012 (.005-.020-. Radiation risks from exposure to natural uranium are very low.006-.016) .005-. 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.100 (.028 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al. interval) .014) .016) . After inhalation.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 .021 (.012) .010) .034 (.007 (.010-.033 (.006 (.009) .

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

47(6):972-982. Marino R. Washington (DC): NRC. Environ Health Perspect 2002. Health Phys 2004. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Renal effects of uranium in drinking water. Katorza E. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Kidney toxicity of ingested uranium from drinking water. Am J Kidney Dis 2006. Hollriegl V. Salonen L. Inductively coupled plasma mass spectrometry as a simple. Bennett LG.79(1):11-21. Auvinen A. Comparison of representative ranges based on U. Roiz J. U. Squibb K. Gwiazda RH. Charp P. Jarrett JM. Review of elements in blood. Salonen L. VI.91(2):144-153. Roth P. Squibb K. May LM. Van der Venne MT. et al. Cordero S. Paretzke HG. et al. Saha H. McDiarmid MA. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Engelhardt SM. Hancock RG. Radiat Environ Biophys 2005. Mistry K. Sabbioni E. Oeh U.S. Gucer P. Kuwabara J.S.44:29-40. Health Phys 2004. J Toxicol Environ Health A 2004. Health Phys 2002. Environ Res 2004. Komaromy-Hiller G. Wahl W. D’Annibale L. et al. Cremisini C. McDiarmid MA.87:51-56. Saha H. Pekkanen J. Jackson RJ. Paschal DC. Kalinsky V. Human exposure to uranium in groundwater. Andrews WS. Li WB.86:12-18. Heller J. Kurttio P. Pinto V. Tolmachev S. Kane R. Oberbroekling KJ. patient population and literature reference intervals for urinary trace elements. Englehardt SA. Auvinen A. Karpas Z.22–Bioassay at uranium mills. et al. Int Arch Occup Environ Health 2006. Nuclear Regulatory Commission (U.94:319-326. Health Phys 2006. Costa R.67(8-10):697-714. concentration and daily excretion of uranium in urine of Japanese. Uranium daily intake and urinary excretion: a preliminary study in Italy. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF.158:165-190. Health Phys 2003.85:228-235. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Wilson PD. Nuclear Regulatory Commission (NRC) Guide 8. Shelly T.71(6):879-85. Environ Res 1999. Makelainen I. Health Phys 1996. Sampson EJ. Karpas Z.S. Kurttio P. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Orloff KG. Howerton K. Halicz L. Element reference values in tissues from inhabitants of the European community. Smith D. Scott K.110(4):337-342. et al. Lewis BM.296(1-2):71-90. U. Harmionen A. Uranium and thorium in urine of United States residents: reference range concentrations. Hamilton EI. Ough EA. Lorber A. Metcalf S. Komulainen H. Pirkle JL.82(4): 527-532. Clin Chim Acta 2000.S. Oliver M. Ejnik J. Noguchi H. Ash KO. Sci Total Environ 1994. plasma and urine and a critical evaluation of reference values for the United Kingdom population. NRC). Biologic monitoring for urinary uranium in Gulf War I veterans. July 1978. et al. McDiarmid M. Marko R.81:45-51.Metals Galletti M. Ting BG. Biokinetic modeling of uranium in man after injection and ingestion. rapid.

90) 5.40 (4.S.40) 3.0-18.40-6.50-4.0 (11.0 (11.0) 95th 14.20-3.60 (7.90-11.0 (10.0 (9.Perchlorate Perchlorate (Urbansky.30) 6. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.66) 3.50) 6.22-5.50 (5.50) 5.96 (3. and reducing agents. population from the National Health and Nutrition Examination Survey.0 (12.40) 3..0) 8.50-3. 2007).00-5.0 (12.30-7.09) 3.02 (3.0-19.20-12.01 (2.89-3.40-4.40 (3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .46) 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 3.30-6.19 (3.62 (3.90) 6.40) 90th 10. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.80 (7.0) 16.90 (2.40-4. 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.49-3.90 (5.70-3.00) 4.10) 3.65) 3.90-6.10-12.05 (2.60) 5.0) 13. In addition.67-5.0 (8.20 (4.30 (5.0) 11.0) 9.40-7. 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. and electroplating.0-20.40 (5.30-19.70 (3.0) 11.60) 8.60-7. 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.81) Selected percentiles ( 95% confidence interval) 50th 3.0-29.20 (6. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.05 and 0.0 (11.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.40) 6.S.11) 3.76) 4. It is normally found and produced as the anion of a sodium.30-17.0-15.10) 5.60 (4.0-17.0) 13.0 (8.10 (6. Survey years 01-02 03-04 Geometric mean (95% conf.47-4.35 (3.0) 13.EPA.80-4.20 (8. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.0 (13.26 (2. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.00-6.40-11.20 (2.40) 4.0 (9.80-12.0) 8.20 (2.0 (11.80 (3.70-3. Other manufactured uses include fireworks.0 (9.10-4.20 (5.0) 14. 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. laboratory analysis.10 (5.0) 13.00) 3.90-12.70 (3.79 (2.30 (2.0 (9.S.0 (9.40) 3.0 (11.0) 19.10) 3.60 (4.0) 9.0-17.80) 12. 2005).20) 7.20-11.30) 6.0 (9.75-3.10-11.40 (3. but has strong oxidant properties in the presence of concentrated acids.60) 3.51 (3.0 (8. fabric dyeing.40 (8.16) 3.0) 14.0) 10.0-17.00) 5.30 (5.80 (6.0) 9.05.g. matches.10) 5.90 (5.75 (3. potassium.70-11. 1998).93-3.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.90-3.50-11.70-12. and certain plants with high water content (e.56) 3.00) 7.54 (3.0 (12.0 (11.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.0) 13.20-4.03) 3.80) 7. Drinking water.70-9.0-14.20) 3.30-7..80-4.50-7.0) 9.40) 2.39-4.0-23.80) 75th 6.90-9.76 (3.70-7.20 (4.31) 2.29-3.32 (3.19-4.45-4.00) 3.0) 10.40 (5.0) 10.84) 14.70) 3.93-4.0-17. and limited applications in pharmaceutics. 2002).80-8.07-4.60-6.38) 5.10 (7.0) 13.90-9.74-3.50) 5.0) 15. Perchlorate is stable under most environmental and physiological conditions. Perchlorate was added to the U.0 (12.0 (8.0-17.90-11.10-11.68) 4.0 (11.20 (7.0-18.0 (11.08-3. interval) 3.70-5.80-15. milk.30 (2.12) 3. lettuce) can be the main sources of intake for humans (FDA.93 (4.22 (2.50) 3.0-15.40-5.0) 708 617 681 652 1228 1092 Limit of detection (LOD.0 (8.90-10.80) 3.44-4.0) 11. or ammonium salt.0-17.40 (5.90 (4.50) 11.90 (5. certain catalytic metals.00-6.0 (11. leather tanning.80 (3.0 (11.50 (3.87-3. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0) 9.70-6.10-7.20-4.0) 9.70 (3.10 (6.90-3.5 hours and has a small estimated volume of distribution (Crump and Gibbs. 2005).88) 3.51 (3. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.50-4.0) 14.0) 13.50 (8.0 (9.81-16.21 (2.20) 4.0) 12.18-3.0) 13.80-6.40 (4.90 (3.40-13.10) 12.11) 4.0-18.10 (2.0) 15.

10-3.91) 4.0) 4.70-4.6) 20.1-22. NAS.93-7.50) 9.89 (2.6) 12.50-5.47) 2.5 (13.32) 5.20 (7.39-4..0 (11. 2002. Lawrence et al.72 (3.00) 4. dietary iodine intake.50) 6.16-3.0 (9.45-2.0) 7.40) 17.37-13. age.10-7.82 (5.0) 12.35) 3.6-17.EPA.00 (2.83 (5.4) 8.97-5. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.8 (11.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.0) 11.30-10.54 (3.44) 3.53 (2.S.41-9.14 (2.40 (4.0-44.77 (3.56-3.60) 10. and the presence of other substances known to affect thyroid function (e..58) 2.4 (8.19-10.25) 5.25) 5. Also.10 (2.07 (2.60-15. 2005).61 (5. 2006.75) 3.70 (2.30-5.. During gestation and infancy.10 (4.40-10.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.0 (11.70) 2.0) 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 3.22-4.60-5.66) 3..25 (3. thiocyanate.54 (2.51 (3. 2000).60-8.61-10.40 (3.50) 5.08 (3.50-9.00-2. population from the National Health and Nutrition Examination Survey.15-12.90-9.0 (8.10 (4.90-11.37 (4.80) Selected percentiles ( 95% confidence interval) 50th 3.33-6.81-3.30) 5.10) 4.29) 2. Lamm and Doemland. up to 68% RUI has been demonstrated. 2003. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.29-6.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3. 1999.34-3.76-3. In these small short-term experimental studies on males and studies of male perchlorate workers with doses or estimated exposures thousands-fold higher than known environmental exposures. gender. medications).51-4.40) 5.20 (3.3-14.80 (7.98) 3.70) 10.0 (11.30 (3. chronicity of exposure.90-20.26 (3.g. In the U.0) 10. 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.4) 13. interval) 3.02-4.00-11. 2002.12 (6.22-6.30-5.59) 3.20) 8.0) 9.90 (2.0) 13. 2007).S. However.52 (8.0) 14.90-3.60-6. Greer et al.4 (11.20 (4.74) 7.93-5.50 (6.19-6.S.0) 12.70-5.46-4.22 (2.0 (9.7 (11.93-5.10 (1.0-14.1-16.05 (4. levels.EPA.00 (4. Li et al.84) 2.24 (4.50) 2.26) 4.0-14.95 (2.4-16.02) 3.50-3.43) 6.20 (2.46-13. menopausal status.S.00 (6.35 (4.80-3. perchlorate is negative in most genotoxic assays (U.0) 12.90) 5. 2002).60-5.S.1 (11.40) 3.99-3..50 (3.20-9.22-4. in a representative sample of U.60) 8..24-2. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.50) 2.71 (5.10) 13.44-6.40 (7.60-11.0 (9.S. 2005.0-19.60) 3.80-3.61-5.90 (7.87 (7.56 (3.45) 3.1-14.0) 12.3) 11.25) 5.03 (2. 2005).0 (8.30 (6. congenital hypothyroidism is a condition for which nearly all newborn blood is screened. Steinmaus et al.21 (2.30) 3.39 (3.10) 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.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 . although iodine intake was higher than U.5) 8.70-3. nitrate.12-2.0) 9.20-10.73) 3.70 (2.3) 12.S.04-3. Survey years 01-02 03-04 Geometric mean (95% conf.70-15.10) 3.87 (5.80 (4.90-2.39) 2. 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.1 (8.09 (7.20-3.93) 3. levels and sufficient in most participants (Tellez et al.87) 7.4 (10.90-15. 2005.60-11. women with urinary levels of iodine less than 100 micrograms per day. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.90 (4.00-3.87) 2.50) 95th 12. Many factors may be important in consideration of perchlorate action on the thyroid: dose.Perchlorate inhibition (RUI).0) 13.60 (3.00) 9.60-3..80 (7.20) 3.35 (2.89-3. U. 2005).40 (3.0 (10.93-8.18-3.20 (6.0-17.67) 5.20-4. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.52-9.30) 90th 9.10 (6. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.3) 8.30 (5..1-13.46 (3.33 (7.4 (11.2) 8.36 (8.42 (3.3 (10.90 (2.0) 6.76 (3.30) 75th 5.96) 2.87-3.08) 3.60-8.2) 8.1) 8.04-3.86) 4.33-12.64-3..00) 3.09) 3.99 (5.64) 5.20-3..70 (4. 2001.

most of the population is considered to be below the U. Barnard JC. 2005. Valentin-Blasini L. Steinmaus C. Byrd D. Abarca CR. He X. the 95th percentile of NHANES 2001-2002 participants aged 20 years and older have urinary perchlorate levels that are several thousand times less than urinary levels measured during occupational exposure of perchlorate workers (Braverman et al. Goodman G. J Occup Environ Med 2000.. Buffler PA. Tellez RT.113(8):10011008. Osterloh JD.110(9):927-937.113(11):A732. Lawrence J. newborn thyroid function. Thyroid 2001.115(9):1333-1338. Crump KS. CFSAN/Office of Plant & Dairy Foods. Perchlorate in the United States. et al. Deyhle GM. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. 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. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U.17(4):400-407. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.gov/toxpro2. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. References Blount BC. Thyroid 2000. Caldwell KL. Pino S.S.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. National Academy of Sciences (NAS). Primary congenital hypothyroidism. Osterloh JD.atsdr..40(21):6608-6614. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . 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. Blount BC. Cross M. Landingham CB. 6/2/09 Greer MA. Benchmark calculations for perchlorate from three human cohorts. J Clin Endocrinol Metab 2005. (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. Chacon PM. Washington (DC): National Academy Press.41(5):409-411. Lamm S.90(2):700-706.10(8):659-663.html and from ATSDR at: http://www. Pino S. et al. Blount et al. Li Z. Environ Health Perspect 2005.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. population. Braverman LE. Rutherford GW. Blount BC. Health Implications of Perchlorate Ingestion. Lawrence JE. Analysis of relative source contributions to the food chain. Also. Lamm SH. Additional information about exposure and health effects is available from the U.11(3):295. et al. The effect of short-term low-dose perchlorate on various aspects of thyroid function. 2001-2002.html.S. Low dose perchlorate (3 mg daily) and thyroid function.. Richman K. Doemland M. Kirk AB. Howd R. J Occup Environ Med 2003. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. et al.htm. 2005).gov/safewater/ccl/perchlorate/perchlorate. Dyke JV. Crump KS. Jackson WA. Available at URL: http://www.114(12):1865-1871. Mauldin JP.46(5):509. The effect of perchlorate. Erratum in: J Occup Environ Med 2004. Braverman LE.fda. Page Last Updated: 05/28/2009. Environ Sci Technol 2006.EPA at: http://www. Daaboul JJ. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. National Research Council of the National Academies. Food and Drug Administration (FDA). Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Kelsh MA. Magnani B.cdc. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Gibbs JP. May 2007. Braverman LE. Environ Health Perspect 2002. Pirkle JL. Perchlorate Exposure of the US Population. and nitrate on thyroid function in workers exposed to perchlorate long-term. Environ Health Perspect 2006. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Miller MD. Neonatal thyroxine level and perchlorate in drinking water. 2005). Pirkle JL. Greer SE. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. epa. EPA reference dose (Blount et al. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Sesser DE. Li FX. and environmental perchlorate exposure among residents of a Southern California community. J Expo Sci Environ Epidemiol 2007. Skeels MR.42(2):200-205. Valentin-Blasini L. Lamm SH. Lau EC. Environ Health Perspect 2007.S. Erratum in: Environ Health Perspect 2005. Pleus RC. Lamm SH. thiocyanate.45(10):1116-1127. 2007). Dasgupta PK.

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

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

by high protein binding in plasma and other proteins. 2003. in a wide variety of marine and land animals (Kannan et al. 2005.. see Data Analysis section) for Survey year 03-04 is 0. 2006a... 1995. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. heptadecafluoro-1-decanol. 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. 2000.e. 2003a and 2004a). Unlike many organohalogen contaminant chemicals. 2004.. population from the National Health and Nutrition Examination Survey. pancreas. Lau et al. but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). but still can have long residence times in the body. approximately 4. 2006. 2007). Keller et al. which may vary for some chemicals by year and by individual sample...8 years (Olsen et al. 2005). thymus and spleen. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2004. 2004). Bookstaff et al. and β-oxidation of lipids (Kudo et al..4. Prevedouros et al.. 2002. Excepting PFOS and PFOA.. PFCs have been identified in surface coastal and ocean waters (Yamashita et al.. and in offspring. Lau et al. 1990).. U. human toxicokinetics. Olsen et al. environmental fate.. 2005. 2005). Guruge et al. the 8-2 telomer. Some of the effects in animals may be mediated through peroxisomal proliferation.. hepatotoxicity. or effects of other PFCs. Tittlemier et al.S. Kannan et al. but probably include dietary sources (Kannan et al. PFOA is mostly excreted in the urine in animal studies. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins. It is unclear if environmentally degraded telomer products are a major source of other PFCs. 2004..S. endocrine and immune effects... Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 2004. 2005.5 years and for PFOS. 2004). PFOA has been reported to cause liver. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. Taniyasu et al. C5. in part.. 2003). 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. The elimination half-life of PFOA in humans is roughly estimated to be 3.. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. 2007a). peroxisomal proliferation. 2005). For instance. kidney. EPA. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. may metabolize or degrade to PFOA (Dinglasan et al. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. C6. and in human blood and semen (Calafat et al. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. 248 Fourth National Report on Human Exposure to Environmental Chemicals .. growth retardation and delayed sexual maturation (Kennedy et al. Vanden Heuvel et al. 1993). All sources of human exposure are uncertain. 2003).. Survey Geometric mean (95% conf. In some cases. The PFCs often measured in human serum are listed in the table. < LOD means less than the limit of detection.. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver.. there is limited information on the sources. including immunologic effects and tumor induction... but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. C7).

700) . 2003)..600 (.500 (<LOD-1. 2007a.80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th . < LOD means less than the limit of detection. EPA. Olsen et al. development in offspring was stunted and hypothyroxinemia was observed.50) . thyroidal).S. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Fourth National Report on Human Exposure to Environmental Chemicals 249 . 2004. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. and there was no clear evidence of excess all-cause or diseasespecific mortality.00) .80) 640 1454 03-04 03-04 * * < LOD < LOD .500 (.800 (.900 (.10) . and changes in thyroid hormone concentrations (Grasty et al.00 (.. PFOS. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. 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.800) 1. which may vary for some chemicals by year and by individual sample.20) . Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.400-1.700 (. 2003a).500) .300-1.. 2003a. hepatotoxicity.500) . 2004a..S.400 (<LOD-. 2005).500-. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400-.10) * 03-04 03-04 * * < LOD < LOD < LOD .300 (<LOD-. 2003. elderly and children.. population from the National Health and Nutrition Examination Survey.800 (. 2003a. 2003).500-1. reproductive. Survey Geometric mean (95% conf. 2004.. 2001..20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . PFOS...500-1. the potential to estimate risks to humans from animal doses is uncertain.500 (.400 (<LOD-.. 2003a). In such studies..500-1.400-1.. Animal studies of PFOS have demonstrated weight loss. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. Cook et al.500) .400 (<LOD-.400-1. or increased cancer rates (Alexander et al.S.800) 1. In comparing three separate reports on adults.. Harada et al.. Lau et al. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.40) . see Data Analysis section) for Survey year 03-04 is 0. Kennedy et al.500-3. However. 2003). 2007b).800 (.400) .80) 485 538 962 Limit of detection (LOD.3.. U. Fei et al.. 2003a. 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. 1992. At high but non-toxic maternal doses of PFOS. developmental and teratogenic effects were demonstrated in offspring. perfluorohexanesulfonate (PFHxS). A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.400-1. PFOA. 2005). and humans.600 (.900 (.. At doses causing maternal toxicity..S. Olsen et al. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. 2004). Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.900 (.500) .10 (.00) . 2004). and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. 2004b).400-.500-1. 2007). population.800 (.10) .600-2. 1999. monkeys. PFOA. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.500) 90th .300 (<LOD-. U. 2007.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. 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. Olsen et al. 2007b.600 (. 2007a. Thibodeaux et al.108 times higher than background serum levels in humans (Butenoff et al. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al.. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. EPA.300 (<LOD-. 2003. 2003.00) .. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. possibly related to lung immaturity (Lau et al.400-1.

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

Survey Geometric mean (95% conf. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 251 .Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400 (.400 (<LOD-. < LOD means less than the limit of detection.900) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0. which may vary for some chemicals by year and by individual sample.400 (<LOD-.300 (<LOD-.400) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (<LOD-.S. 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th .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 .S.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.500) 485 538 962 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.0. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 1.600 (.300-.600) < LOD .500-.3.

50-6.90 (4.20-1. population from the National Health and Nutrition Examination Survey.05-2.90-19.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.80) 3.30) 3.30 (7.00 (1.721-1.852 (.60 (1.60) 2.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.20) 485 538 962 Limit of detection (LOD.77-2.30-9.90) 1. interval) 1.60) 1.20) .50 (6.90) 1.30) 3.60-4. see Data Analysis section) for Survey year 03-04 is 0.30 (3.10 (4.586-.40 (1.90) 1.0) 8.30-12. 252 Fourth National Report on Human Exposure to Environmental Chemicals .90-2.10-9.00 (5.900 (.90 (1.80-6.10) 6.93 (1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80-4.50) 6.40 (1.30 (1.60 (6.40) 1.00) 2.72) 1.86 (1.60-8.50) 2.80-7.50-10.50 (1.40) 1.10 (1.50 (4. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80) 5.30-6. interval) .60-4.73-2.80-2.90 (2.00) 1.40-1.60-2.44 (2.963 (.09 (.20 (6.70-2.1.40) 640 1454 03-04 03-04 2.900-1.51) 1.10) 75th 1.966 (.0) 1053 1041 03-04 03-04 03-04 1.60-7.26) 2.20-2.10-9.30) 03-04 03-04 .92 (1.80-4.14 (. Survey Geometric mean (95% conf.3.80-8.30 (2.80-7.20) 2.40 (1.10) 4.20 (1.70) 3.10) 75th 3.60 (1.00 (2.70) 13.16) .80-3.20) 1.20 (1.30 (1.5) 8.835-1.30) .6) 7.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.90) 8.01 (1.S.10) 1.90 (1.30-2.56-1.10-5.80-4.27) 1.80) 4.20-1.80-8.40) 640 1454 03-04 03-04 1.600-.700 (. see Data Analysis section) for Survey year 03-04 is 0.40 (1.861 (.20 (1.90 (1.62-2.50 (1.12) .00-1.50 (1.20-1.10 (.70 (1.809) 1.40 (2.50 (2.800 (.900-1.87-2.689 (.60-2.90 (1.00 (1.900-1.984 (.70) 2.10 (.70-2.00-6.00 (1.20-1.30 (2.40) 4.10) 5.80-3.20) 03-04 03-04 2.900-1.912-1.70-6.30 (6.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.00-8.1) 485 538 962 Limit of detection (LOD.900) 1.03) 1.90 (4.40-3.834-1.20 (1.900 (.08) 2.80-12.00 (.900-1.10) 8.60-3.04) .S.50 (6.10) 1.30 (1.67-2.40-1.60) 9.10) 6.90-10.816-1.10) 4.20 (6.50 (4.20-3.60-3.80 (1.90) 3.40) 2.5) 5.00-7.800-1.70) 2.10) 1053 1041 03-04 03-04 03-04 .697-1.72 (1.54) .91) 2.826-1.3 (9.00 (.70) 1.60-2.900-1.30) 3. Survey Geometric mean (95% conf.10 (4.70) 1.60) 3.90) 90th 5.30 (1.80 (1.17 (1.17-1.40) .10 (.50-6.00 (1.50) 2.80) 1. population from the National Health and Nutrition Examination Survey.50-3.00) 3.00) 1.00-1.80) 90th 2.50 (1.42 (1.70-10.60 (1.70-7.700-1.70 (2.70-5.20) 1.80 (4.

4-17.30) 6.3 (35.S.6 (19.7-69.50 (3.20) 7.6) 7.90-12.9 (19.60-9.10) 5.3) 485 538 962 Limit of detection (LOD.40-6.7 (13.90 (7.4-25.60-13.8) 27.0) 485 538 962 Limit of detection (LOD.8) 32.2 (27.35) 3.6-24.9 (13.4-42.9) 22.0) 03-04 03-04 19.1-25.4 (17.4) 20.50-13.96 (3.8-78.20-9.0-16.7-49.8-22.00 (3.1) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 4.6) 42.40) 3.10 (6.4 (19.60 (7.1-35.7-23.90) 6.10-3.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.2) 30.40-10.0) 36.70 (5.10 (3.3-61.9) 9.80 (5.30 (5.20) 10.5) 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 21.70-9.90 (5.50-4.2 (19.4) 640 1454 03-04 03-04 23.1) 15.7 (35.89 (3.2) 45. see Data Analysis section) for Survey year 03-04 is 0.40) 5.0) 21.40-17.65-4.84-3.00 (5.30-5.9-38.3) 28.20) 5.79) 4.40) 90th 7.60 (3.7 (43.37 (2.40-6.9) 27.40-14.20-4.85-4.40) 75th 5. see Data Analysis section) for Survey year 03-04 is 0.1-52. Survey Geometric mean (95% conf.0) 21.60 (6.8-81.2) 640 1454 03-04 03-04 4.70 (3.6) 18.6 (42.3 (44.0-70.20-5.80 (6.60 (6.60) 03-04 03-04 3.0-20.20) 7.2 (28.50) 7.4) 56.1-24.0) 43.20 (4.70-10.30 (3.90-4.90 (7.90-4.1) 57.70-7.5) 1053 1041 03-04 03-04 03-04 14.1 (23.30-8.47-4.5-33.1.60) 8.4) 75th 30.40 (4.4 (19.70-5.8-22.6) 35.7-30.60-6.3) 41.4.50 (4.6) 21.3) 42.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.91) 3.5-23.9-19. Survey Geometric mean (95% conf.53) 3.95 (3.6) 1053 1041 03-04 03-04 03-04 3.00 (5.30) 7.5) 7.60-14.20) 4.2 (18.21-3.7) 39.40 (6.67-4.0 (20.7-33.70) 6. interval) 3.4) 21.80-9.8 (37.6 (44. population from the National Health and Nutrition Examination Survey.99-3. Fourth National Report on Human Exposure to Environmental Chemicals 253 .5) 8.82) 4.7 (19.9 (17.80-12.27) 4.5) 57.5-62.8 (34.30-11.0-66.6-50.2-22.20) 5.2) 30.80) 8.70-7.3 (35.4 (28.1-36.1 (24. interval) 20.7 (43.2 (16.70 (5.5) 32.70) 3.7 (7.18 (3.90 (7.6) 9.1-33.8-30.00) 3.6) 62.30 (3.5 (28.S.4 (23.50-6.8-35.9) 22.7-53.80 (6.9-23.50) 4.3 (28.0) 90th 41.5-21.70) 4.80 (7.6 (35.20 (4.30-6.8 (45. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.07-4.5) 9.5) 18.6-45.7 (35.2-57.1 (19.80-4.9 (22.11 (2.3 (17.10 (3. population from the National Health and Nutrition Examination Survey.0 (27.8-22.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.47 (4.5 (28.5) 19.30-3.60 (5.3-22.60 (4.2 (21.0) 23.8) 46.

300 (.300) .300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300) .200-.300 (.300-.500) . population from the National Health and Nutrition Examination Survey. 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.200-.500) .300-.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (.200-.200-.500) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .400 (<LOD-.300 (.200 (<LOD-.300) . Survey Geometric mean (95% conf.300 (. which may vary for some chemicals by year and by individual sample.S.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 . 254 Fourth National Report on Human Exposure to Environmental Chemicals . see Data Analysis section) for Survey year 03-04 is 0.300-.300 (. see Data Analysis section) for Survey year 03-04 is 0. < LOD means less than the limit of detection.300 (.200-.500) < LOD 485 538 962 Limit of detection (LOD.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf.300 (.S.300-.300) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-.200-.200-. < LOD means less than the limit of detection.200-.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .200-.500) 485 538 962 Limit of detection (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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .300) .300 (.300 (. which may vary for some chemicals by year and by individual sample.2.300 (. population from the National Health and Nutrition Examination Survey.300 (.300) .4.300 (.

50 (1.700 (<LOD-2.700) 90th 1.10) .10-1. Survey Geometric mean (95% conf.50 (1.S.10-1.300-2.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .10-1.800) .60) 485 538 962 Limit of detection (LOD.10) 1.900-1.30 (1.800) . Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.900-1.500 (<LOD-.00) < LOD .80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .10 (1.30 (1.20-1.90) .00 (.80) 1.30) .10-1. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 255 .600 (<LOD-.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.10 (.700 (<LOD-.900 (<LOD-1.3.10 (.10 (. < LOD means less than the limit of detection.900-1.300 (<LOD-.800 (<LOD-.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .70) 1. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf.900) .40) < LOD < LOD .700) 1. < LOD means less than the limit of detection.700) 1.600 (<LOD-1.10) * 03-04 03-04 * * < LOD < LOD .900 (.600 (<LOD-1.400 (<LOD-.10) .00 (.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 .600) .00 (.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th .600 (<LOD-1. see Data Analysis section) for Survey year 03-04 is 0.900) 485 538 962 Limit of detection (LOD.700 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900-1.60) 640 1454 03-04 03-04 * * < LOD < LOD .900) 1.700 (<LOD-.10-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700) .700 (<LOD-.00 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. see Data Analysis section) for Survey year 03-04 is 0.700 (<LOD-. which may vary for some chemicals by year and by individual sample.900-1.700 (<LOD-.900-1.300 (<LOD-1.30) 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 .20) 1.30 (1.30) 1.80) 1.400 (<LOD-1. population from the National Health and Nutrition Examination Survey.6.20 (1.00-1.40) 1.900-1.10) 1.

Needham LL. J Occup Health 2004. Tully JS. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries.68(6):465-471. Taniyasu S. Cook JC. Grasty RC. Herbstman JB. Inoue K. Olsen GW. Kamiyama S. Occup Environ Med 2003. Kumar KS.39(23):9101-9108. Toxicol Sci 2001. Kuklenyik Z. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro.115(11):1596-1602.S. Environ Health Perspect. Ye Y. de Voogt P. Moore RW. Kuklenyik Z. Yoshinaga T. Fei C. The toxicology of perfluorooctanoate.46(2):141-147.and perfluorinated acids. Bignert A. Butenhoff JL. Murray SM. Environ Sci Technol 2005. Fluorotelomer alcohol biodegradation yields poly. Environ Sci Technol 2004. Environ Sci Technol 2004. Corsolini S. Mandel JS. Bandai N. Day RD. Keller JM.60(10):722729. Environ Res 2005. Calafat AM. Hurtt ME. Birth Defects Res B Dev Reprod Toxicol 2003. and perfluorinated contaminants in livers of polar bears from Alaska. Burris JM. Chem Biol Interact 2000.113(2):209-217. Biegel LB. Mandel JH. Peterson RE. Chlorinated. Olsen GW. Loganathan BG. Dinglasan MJ.38(17):4489-4495. Morikawa A. Kannan K. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Toxicol Appl Pharmacol 1995. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Taniyasu S. Holmstrom KE. Saito N. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Reidy JA. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Bookstaff RC. Calafat AM. Guruge KS. Calafat AM. Environ Sci Technol 2005. Biegel LB. Hurtt ME. Reidy JA.179:99-121.104(2):322-333. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Rodricks J. Edwards EA. Polyfluoroalkyl chemicals in the U. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Mandel JH. McLaughlin JK. et al. Harada K. Witter FR. Perfluorinated chemicals in selected residents of the American continent. Environ Sci Technol 2005. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Needham LL. Hurtt ME. Androgenic deficiency in male rats treated with perfluorodecanoic acid.Koizumi A. Needham LL. Mabury SA. Regul Toxicol Pharmacol 2004. Falandysz J.115(11):1670-1676. Rev Environ Contam Toxicol 2003.39(23):9057-9063. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. et al. Olsen J.134(1):18-25.38(10):2857-2864. Apelberg BJ. Cook JC. Tarone RE. Evans TJ. Frame SR. Calafat AM. 2007b. Kawashima Y. and ex vivo studies. Koizumi A. Seneviratne HR.1968--2003. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Yamashita N. et al.99(2):253-261. Kannan K. Mohotti KM.34(4):351-384. Aguilar-Villalobos M. Chemosphere 2006b. Needham LL. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility.7(4):371-377. Watanabe T.Perfluorochemicals References Alexander BH. Ingall GB. Wong LY. Katakura M. Environ Sci Technol 2007a.39(3):363-380. Gaylor DW. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Butenhoff JL. et al. et al. Laane RW.63:490496. Suzuki E. Caudill SP. in vivo. Environ Sci Technol 2006a. Characterization of risk for general population exposure to perfluorooctanoate. Tully JS. Seacat AM. Yun SH. Serum concentrations of 11 polyfluoroalkyl compounds in the U.S. O’Connor JC. Liu RC.39(1):80-84. et al.124(2):119-132. Perkins RG. Lau CS. Fillmann G. Environmental and toxicity effects of perfluoroalkylated substances. Sasaki S. Environ Health Perspect 2007. J Environ Monit 2005. Kannan K.60(1):44-55. The influence of time. Halden RU. Reidy JA. Moore JA. Olsen GW.40:21282134. brominated. Wijeratna S. Frame SR.115(11):1677-1682. et al.41:2237-2242. Kennedy GL Jr. Grey BE. Cook JC. Caudill SP. Rogers JM. Kuklenyik Z. Jarnberg U. Toxicol Appl Pharmacol 1990. Arendt MD. Crit Rev Toxicol 2004. Harada K. Reidy JA. Environ Health Perspect 2007. Kuklenyik Z. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Calafat AM. Yoshinaga T. O’Connor JC. Toxicol Appl Pharmacol 1992. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Inoue K. Yamashita N. Hekster FM. Saito N. Kudo N.

Olsen GW. Yamashita N. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Butenhoff JL.S. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Toxicol Sci 2003. Mar Pollut Bull 2005.68:105–111.41(9):799-806. Hanson RG. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Mandel JH. Horii Y.. Sterchele PF.perfluorohexanesulfonate. EPA). Seymour C.113(5):539-545. Biol Pharm Bull 2003. Olsen GW. Cousins IT. Coordinate induction of acyl-CoA binding protein. Lau C. Rogers JM. Environ Health Perspect 2005. Rogers JM. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Burris JM.) Tittlemier SA. Environ Health Perspect 2003a. Huang HY. Butenhoff JL. et al. fate and transport of perfluorocarboxylates. Environmental Protection Agency (U. J Ag Food Chem 2007. Hansen KJ. Butenhoff JL. Taniyasu S.1177(2):183-190.54(11):1599-1611. II: postnatal evaluation. perfluorooctanoate andother fluorochemicals in human blood.S. Historical comparison of perfluorooctanesulfonate.epa. Kawashima Y. Hansen KJ. 2003a. fish. J Occup Environ Med 1999. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Petrick G.111(16):1892-1901. birds. 2003. Environ Sci Technol 2003. Ehresman DJ. (Erratum in: Toxicol Sci 2004.74(2):369-381. Mandel JH.82(1):359. 2007a. Hanson RG. Ellefson ME. J Children’s Health 2004b. Zobel LR. and perfluorooctanoate in retired fluorochemical production workers. Korzeniowski SH. et al. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Burris JM. Peterson RE. Olsen GW. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations.55:3203-3210. Hanari N. Horii Y. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. van Belle G. et al. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Taniyasu S.2(1):53-76.26(1):47-51. Olsen GW. Reagen WK.115(9):1298-1305.51(8-12):658-668. Washington. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Butenhoff JL. Butenhoff JL.Perfluorochemicals Kudo N. Larson EB.68(1):249-264. Lundberg JK.gov/opptintr/pfoa/pfoara. Mair DC.111(16):1900) Olsen GW. J Occup Environ Med 2003b. Bronson R.40(1):32-44. Chemosphere 2007b. Biochim Biophys Acta 1993. Moisey J. Church TR. (Erratum in: Environ Health Perspect.198(2):231-241. Buck RC.45(3):260-270. Seacat AM. Grey BE. Burris JM. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. and humans from Japan. Lundberg JK. Environ Sci Technol 2006. Toxicol Sci 2002. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Miller JP. Thomford PJ. Environ Health Perspect. Toxicol Sci 2003. Nesbit DJ. et al. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Available from URL: http://www. Chemosphere 2004a. Case MT. I: maternal and prenatal evaluations. and food items prepared in their packaging. Sources. Butenhoff JL.74(2):382-392. The developmental toxicity of perfluoroalkyl acids and their derivatives. Olsen GW. U. Burris JM. fast foods. 1/15/06 Vanden Heuvel JP. et al. Hansen KJ. et al. Rogers JM. Kannan K. Half-life of serum elimination of perfluoroo ctanesulfonate. Thibodeaux JR. Mandel JH. Thibodeaux JR. Helzlsouer KJ. Toxicol Appl Pharmacol 2004. Gamo T. Church TR. Seacat AM. Burris JM. Burlew MM. Barbee BD. Hansen KJ. Richards JH. Pepper K. Prevedouros K. Ehresman DJ. Olsen GW. Stanton ME. A global survey of perfluorinated acids in oceans. Yamashita N. Cao XL et al. Grey BE. Hansen KJ. Kannan K. Olsen GW. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Mandel JH. Froehlich JW.37(12):2634-2639. fish. htm. Lau C. Church TR. Olsen GW.

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

atsdr.. pp. References Agency for Toxic Substances and Disease Registry (ATSDR).cdc. In Staples CA (ed). ovarian abnormalities in the female animals (Jarfelt et al. Dave M. 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. interactions with macromolecules and species differences in metabolism of DEHP. Metabolism of di(2-ethylhexyl) phthalate.gov/toxpro2.. 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. Environ Health Perspect 1997. Cousins IT. 2004. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. 2003.html. 1986). Slakman AR. 227-262. 2000b. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . 105:734-742. and extent of metabolite conjugation to glucuronide (Albro et al. van der Broek PH. 2002). phthalates have been shown to induce peroxisomal proliferation in rodents.Phthalates and metabolites have been tested. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al..cdc. phthalates produced anti-androgenic effects by reducing testosterone production and. Anderson WA. Information about external exposure (i. 2004. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. reducing estrogen production. 2004.html.. In animals. Dirven HA. Part Q: Phthalate Esters. 4/20/09 Albro PW.. Connor C. variation also occurs in the same person during repetitive monitoring (Fromme et al.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Corbett JT. However. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al... NTP-CERHR.. which may be a pathway to the development of liver toxicity and cancers in these animals.45:19-25. Hauser et al.gov/ reports/index. 2004). 2001. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.21:13-34. Evaluation of a recombinant yeast cell estrogen screening assay. Kessler et al.. Pharmacokinetics.gov/ toxprofiles/tp9. 2002). 2003... Matthews HB. Scotter MJ. 2004.805:49-56. Hoppin et al. Environ Health Perspect 1982.html. 2006). High doses of di2-ethylhexyl phthalate (DEHP). Silva MJ. Population estimates of concentrations of specific phthalate metabolites may differ by age.atsdr. Silvapathasundaram S. Rhodes et al. 2000a. Jongeneelen FJ. 2007. and Sertoli cell abnormalities in the male animals and. Needham LL. atsdr.cdc. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis.. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. and race/ethnicity (Silva et al. testicular atrophy. Albro PW and Lavenhar SR. Peck and Albro. 2000c. Available at URL: http://www. Springer. Food Addit Contam 2001. at very high levels. 2007). Assessment of critical exposure pathways.nih. Drug Metab Rev 1989. 2002.e. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. Available at URL: http://www. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. These differences may contribute to species-specific differences in toxicity (ATSDR. McDonnell DP. 2005. but there are known species-related differences in the hydrolysis of diester phthalates. McKee et al. 1982. J Chromatogr B 2004. Biomonitoring studies on levels of phthalate metabolites provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of phthalates than are found in the general population.18(12):10681074. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. Herbert AR.New York. 2001). Vol.. Toxicological profile for di-n-butyl phthalate update [online]. Calafat AM. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. Mackay D. Massey RC. Clark K. Also.gov/toxprofiles/ tp135. Jordan S. Springall C.niehs. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. 1985. Sauer MJ. Lovekamp-Swan and Davis. at higher doses. 2006). 2005). Hauser et al. Schroeder JL.. gender. 2001. dibutyl phthalate (DBP). Castle L. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. 1982). efficiency of intestinal absorption. Coldham NG..html). The Handbook of Environmental Chemistry.3.

Duty S. Yokoyama Y. Liss GM. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Yoshimura M. Int Arch Occup Environ Health 1993.26(8):1219-24. Chahoud I. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004.nih. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Tsukino H. Environ Health Perspect 2004. Hartle RW. Borch J. Brock JW. Reprod Toxicol 2004.16(4):487-493.64(8):555-560. 2000c [online]. Davis BJ. Csanády G. Environ Health Perspect 1997. Lovekamp-Swan T. 2006 [online].niehs. Park S. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Meeker JD. Nielsen J. et al.105:802-811.html. 6/2/09 NTP-CERHR. Ryan L. Filser J. Koch HM. Hanaoka T. 6/2/09 Okubo T. Milligan SR. Calafat AM. Jarfelt K. Singh NP. Gans G. Suzuki T. Drexler H.103:582-587. McKee RH. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Environ Health Perspect 1995.html. gov/chemicals/dehp/dehp-eval.html.gov/chemicals/ phthalates/dbp/dbp-eval. Dalgaard M. Balasubramanian AV.Phthalates in human urine samples. Kalita JC. Environ Health Perspect 2003. 6/2/09 NTP-CERHR. Pan G. Research Triangle Park (NC). Anal Bioanal Chem 2005.19(4):505-515. Boehmer S. Bolte G.niehs. 6/2/09 NTP-CERHR. The estrogenic activity of phthalate esters in vitro. Available at URL: http://cerhr. Brock JW.niehs.22(3):688-695. Giwercman A. Ryan L. Skerfving S. Main KM. Rylander L. Int J Hyg Environ Health 2007.382:10841092. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Available at URL: http://cerhr. Hum Reprod 2007. White R. Jobling S. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Mechanisms of phthalate ester toxicity in the female reproductive system. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Biol Pharm Bull 2003. Henttu P. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. 2000b [online]. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Research Triangle Park (NC). consumer milk. Stringer WT. Available at URL: http://cerhr.nih. Angerer J.25(2):293-302. Silva MJ. Davis BJ. et al.gov/chemicals/dehp/dehp-eval. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Mortensen GK. Meeker JD. et al. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Decreased serum free testosterone in workers exposed to high levels of di-n-butyl phthalate (DBP) and di-2-ethylhexyl 260 Fourth National Report on Human Exposure to Environmental Chemicals . 2000a [online]. Richthoff J. Kano I. Reynolds T. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Zhang S. Parker MG. Silva MJ. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Leffers H.46(11):643-647.112(17):1740]. Akesson B. Hagmar L. David RM. Sumpter JP. Available at URL: http://cerhr.nih.210:21-33. Ladefoged O. Chen Z. Hoppin JA.nih. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Jacobsen H.niehs. Andersson A-M. Research Triangle Park (NC). Harris CA. Hass U. 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Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Peters JM. Zacharewski TR. Rhodes C. Environ Health Perspect 1986. Crit Rev Toxicol 2006.S. Toxicol Sci 1998. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Toxicol Sci 2000. Jackson SJ. Silva MJ. Environ Health Perspect 2004. Albro PW. Batten PL. Abbott BD.58:339349. Reidy JA. Urinary levels of seven phthalate metabolites in the U.114(11):1643-1648. Hodge CC. Matthews JB. Environ Health Perspect 2006. Lambright CR. Orton TC.65:299-308. Wu ZF. Parks LG. et al.Phthalates phthalate (DEHP): a cross-sectional study in China.46:282-293. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Malek NA. Cunningham ML. Clemons JH.45:11-17. et al. Barr DB. Rusyn I. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Environ Health Perspect 1982. Klinefelter GR. Pratt IA.36:459-479. Peck CC. Barlow NJ. Ostby JS. Caudill SP. Fielden MR. Bratt H.112(3):331-338. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. 112(5):A270]. et al. Meek MD.

4) 129 (98.1 (32.4-16.0) 20.8-16. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.0-55.9 (11.0 (34.2) 13.6-17. and 0.6) 29.6-18.0) 16.4) 38.7-16.5) 30.3-130) 122 (88.2) 14.1) 13. 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.2-20.5 (76.8-41. and 03-04 are 0.4) 108 (96.5 (55.7 (13.4 (63.9-87.1 (14.7) 40.6 (32.0) 70.2-17.7-16.8-17.7-15.4) 33.2) 78.4-25.6-72. NTPCERHR.1.2) 14.9-27.3-18.5 (27.6) 16.2) 69.3) 23.1-120) 52.5 (61.5-41.3) 13.0 (14. car care products.1) 68.4) 80.9 (16.0 (27.3-88.6 (13.6-150) 94.9-16.6) 24.2 (11.0-130) 101 (86.4 (32.9) 14.3) 94.6 (41.3) 13.3 (29.2-40. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9-47.3) 37.3.3) 54.1-43.4 (53.1-18.8-121) 79. residents (Blount et al.8 (71.3-21.0 (12.6) 63. particularly male animals (McKee et al.8-17.3-125) Total 15.5 (47.2-39.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.Phthalates Benzylbutyl Phthalate CAS No.0 (23.0-106) 58. because it is not bound to products in which it is incorporated.3 (12.8) 63.9) 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. Food crops take up BzBP. including MBzP.7 (53.3-75.0 (20.5) 15.4-15.6) 95th 103 (94.3 (12.7) 23.4) 65.0) 24. sealants.2) 22.9-14.3 (44. it can be released into the ambient air during use or disposal of the products.8 (14. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.5-40.8 (12. 0.4 (53.8-14.4 (48. some personal care products.0 (33.7 (51.0 (55.1 (13.4-120) 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 13.1 (55.5-18.8-72.2 (19.7-82.6 (21.6) 14.9) 11.5) 82.4) 75th 35.1) 31.4-92.6) 37.6) 13.7-17. vinyl tile.3-161) 99.6 (13.0) 90th 67.5-35.1) 67.4 (10.2-19.1-39. respectively.8 (30.8-18.6-79.9) 14. and to a lesser extent.2-33.0 (11.8-98.0 (30.7-119) 99.3 (22.4 (27.1 (10.6-116) 122 (102-142) 101 (85.4) 12.9-62.8 (50.5-97.6-29.2-115) 113 (91. 2000).1) 32.2-38. interval) 15.1) 14.1 (20.7 (80.8 (80.8 (28. and diet is the major source for general population exposure.2) 66.5) 27.8 (53. 262 Fourth National Report on Human Exposure to Environmental Chemicals .7 (12.4-62.8-13.1 (14.9 (28.0) 33.0) 34.2 (19.1-35. High dose BzBP and its monoester metabolites.6 (53.1) Selected percentiles ( 95% confidence interval) 50th 17.9-49.4) 51.2-116) 122 (102-143) 101 (84.8-76.3 (13.3 (12.5 (57.1) 29.4) 49.2-16.6 (13.6-39.8-35.6) 15.3) 15.3-27.8-133) 89.9 (21.1) 12.0 (15.4) 81.7-170) 169 (134-198) 152 (99.9) 49.6) 35.3) 63.8) 28.5-84.2 (25.7-25.1-61.8) 24. 2001-2002.1) 76.6-38.2-16.1 (19. can produce developmental and reproductive toxicity in rodents.1-15.6 (66.7-13.9) 13.0-85.8 (10.7 (15. 01-02. BzBP can be released into the environment during its production and.5-14. see Data Analysis section) for Survey years 99-00.3 (54.7-14.9) 43.2 (10. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.5-62.8-48.3-74.9-30.5-33.0) 23.4-24.2-183) 101 (78.3-43.4-127) 80.8 (21. and 2003-2004 were generally similar those reported in U.3-34.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7-172) 103 (74.5-36.4) 71.6) 14.1-38.9 (70.2) 17.1 (58.9 (22.3 (29.9) 18.4 (31.9-28.3-12.5-36.2 (47.2) 15.6-92.0 (30.8 (86.1-16.5) 23.6-43.6) 13.3-82.3-18.1-116) 122 (93.6) 50.3 (33.4 (59..0) 32.1 (13.2-155) 91.8) 33.5 (13.S..5 (67.7 (82.9 (12.6-92.7-58.7) 38.5) 65.5) 55. population from the National Health and Nutrition Examination Survey.8) 14.8 (38.6) 25.9 (12.2 (14.1-214) 166 (116-191) 145 (110-213) 88.8 (71.8.4 (32.9 (13.5) 16.0 (15. IARC considers BzBP not classifiable with respect to human carcinogenicity.1-16.2) 12.1-15.8-14.9) 15.6) 35.7-16.0-26. 2004.6-132) 103 (84.5 (26.7-35. 2000).5-94.4) 35.8) 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 16.4 (13.4 (68.7 (70.9-190) 86.7 (11.4) 98.0 (26.6 (12.0 (43.2) 32.6) 67.1-90.8-64.5-25.S.9 (39.3-91.5) 15.4 (10.4) 35.4) 14.3 (30.5 (66.4 (29.6 (13.2 (43.8-16.2-31.2) 33.9) 12.5-145) 138 (106-241) 143 (127-179) 120 (99.

4) 104 (89.8) 56.5-23.3) 36.9 (29.3-64.9) 64.6 (11.4 (11.9) 12. In NHANES 1999-2000.2-78.9-104) 62.5-13.6 (57.1) 24.7-14.8 (46.2) 67.1-14.5) 41.2) 11.3-16.8-64.3) 16.4 (25.9-83.3) 29..4-19.8) 54..7 (13.2 (40.4-79. adolescents compared with adults.1 (21.5 (56.6-40.8-60.4) 17. Weuve et al.6) 25.5) 23.3) 13.2-13.1-120) 77. 2003).9-69.6-86.2 (69.9 (15.9 (43..7-20. 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.9) 12.6 (11..0 (13.7 (21.8 (13.2-21.2) 11.1) 27.8-14.4-18.3-34.3 (23.9 (24. 2007).5) 46.0 (67.1 (34.0) 49.4-27.2-12.0 (49.3) 12.9-28.69-11.7) 46.1 (21.2) 26.4) 21.7-69.6 (51.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.2) 15.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .8 (10.6 (34.7-29.9) 12.3) 18.8 (30.0-109) 65.0) 12.8-80.3) 14.3) 55.3 (15.5-61.8 (49.7-14.9 (12.6 (22.5-26.7) 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 40.4-142) 134 (116-176) 136 (85.5-58.9 (39.5) 10.7-397) 70.8-42.6) 12.6 (14.6) 58..7 (19. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.1 (46.7) 25.9 (51.8) 53.9-14.8-13.7 (11.5-29.2-13.3) 73.0) 13.5-57.5-38. 2007).8-15.9 (15.3-73.1 (18.4 (34.7-15.0) Selected percentiles ( 95% confidence interval) 50th 13.4 (21.2-57.3) 90.1-58.1 (14.5-31.1-79.4) 44.7-61.6-47.9-62.9) 24.9 (10.8) 34.5-58.6-26.6) 13.5 (9.6) 73.9) 11. 2005.4) 13.5 (10.2-15.6) 12.0-53.8) 46.1) 12.4) 14.3) 67.0 (33. population from the National Health and Nutrition Examination Survey.3) 37.8) 108 (75.0 (10. 2002.1 (11.4) 51.8) 33.8-69.1) 39. Hoppin et al.4-17.1 (19.8-34.1-27.0) 60.8) 53.7-31.7 (11.9 (55.7 (38.8-13.1) 23.9 (24.6-81.5 (49.4 (11.8) 68.73-12.0 (62.9 (10. In an annual sample of German university students.2-17.0) 11.3 (13.4) 15.4 (46.2-49.7-20.3) 13.7-12.3-11. 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 (69.7) 38.6-12.0-27. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.4-14.7 (12.7 (18.Phthalates York City (Adibi et al.7 (23.9-23.4-116) 73.4 (33.9 (12.4-90.3 (12.3 (39.S.9 (22.7-19. A small study of African-American women in Washington.6) 53.8-15.8-16.8-173) 195 (121-305) 229 (99.5-26.4) 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. 2003).4 (74.9-13.5 (10.2) 11.0 (12.1 (21. 2005).1) 35.8 (11.8 (69.6 (36.8-39.7 (54.1 (53.8 (12.5 (11.1-12.0 (11.4 (13.1 (15.8) 24. interval) 14.9) 11.8 (50.3 (38.8) 15. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.6 (24.1 (21.7-19.0 (12.3) 89.4) 50.5 (12.5) 16.3) 21.9) 52.7) 19. Hauser et al.7-90.4-14.7 (59.5) 78.1 (41.6) 75th 25..8 (64.8-48.4) 12.4 (63.8) 13.1) 17.0 (41..6 (11..5) 13.4 (12.2 (41.1 (13.4) 13.6) 30.6-20.8-13.7-123) 77.3) 14.3) 13.3 (60. in men attending a Boston infertility clinic (Duty et al.3-38.3 (35.0) 24.0-26.5-79.7-56.1-35.1) 142 (99.5) 20.5-16. 2006).5-99.7-15.1 (23.5) 95th 77.5-213) 49.8) 16. and in a small sample of German residents (Koch et al.0) 24.8) 71.1 (25.7 (14.1) 80.2-26.2-117) 95.4-60.8) 11.6-13.1 (13.8-27.6 (30.4) 90th 50.5-76.3 (24.4 (10.6) 38..5) 17.4-99.1-29.2-51.9) Total 14.4 (11.2 (56.8 (57. 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. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.7 (55. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7 (13.7) 56.2) 12.1 (43.4) 60.4-102) 70. 2004).8-14.1-125) 86.4) 28.1) 24.9 (9. 2004.7) 11. in young Swedish men (Jonsson et al.1-12.6-116) 74.9) 42.5) 14.8) 80.0-51.6-99.7 (11.9-16.2) 32.5 (48.4-15.0 (38.4-42.9) 100 (80.8) 33.4 (26.0 (41.0-48.8) 26.5-42.5 (42..9-115) 57. 2002).0-90.4-23.0-15.4) 25.4 (60.4-93.0) 15.9 (54.6 (30.6 (19. and females compared to males (Silva et al.9-40. 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.95-14.1 (9.8-85.6-15.5 (35.6 (15.9-13.2-15.2 (27.

Davis BJ. Wittassek M. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Jonsson BAG. Barr DB. Environ Health Perspect 2006. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Phthalate monoesters levels in the urine of young children. Brock JW. Chen Z. Silva MJ. et al. Prenatal exposures to phthalates among women in New York City and Krakow. Ryan L. Environ Health Perspect 2004. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. et al. 112(5):A270]. McKee RH. Helm D. Hu H. et al. Schettler T. Duty SM.111(14):1719-1722. 2000 [online].114(9):1424-1431. Pirkle JL. Camann DE. Green RA.68:309-314. Atlanta (GA). Barr D. Environ Health Perspect 2002. Caudill SP. Rylander L. Reprod Toxicol 2004. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Koch HM. Singh NP. et al.93:177-185. Giwercman A. Environ Health Perspect 2003. Ryan L. Baird DD. Needham LL. Sampson EJ. Calafat AM. Hodge CC. Hagmar L.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. 2005. Poland. Available at URL: http://cerhr. Int J Hyg Environ Health 2007.html. Malek NA. NTP-CERHR. Epidemiol 2005. Hauser R. Koch HM.niehs. Rossbach B. et al. Urinary levels of seven phthalate metabolites in the U. Dobler L. Duty S. Caudill SP. Meeker JD. Caudill SP. Reproducibility of urinary phthalate metabolites in first morning urine samples. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.25(2):293-302.S.18(1):122. Levels of seven urinary phthalate metabolites in a human reference population. Research Triangle Park (NC). 4/20/09 Silva MJ. David RM. Butala JH. Hoppin JA. Perera FP. Reidy JA. Sanchez GN. Weuve J. Needham LL. Drexler H. et al.nih. Richthoff J. J Androl 2004. Jedrychowski W. Silva MJ. Wiesmuller GA. et al. Jacek R.210(3-4):319-333. Calafat AM. Angerer J.108(10):979-982. Bull Environ Contam Toxicol 2002.22(3):688-695. Environ Health Perspect 2000. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Brock JW.Phthalates References Adibi JJ. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.110(5):515-518. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Hum Reprod 2007. Environ Res 2003. Third National Report on Human Exposure to Environmental Chemicals. Eckard R. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Silva MJ. Blount BC.112(3):331-338. Hilborn ED. Silva MJ. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Centers for Disease Control and Prevention (CDC). Gans G. Brock JW.16(4):487-493.

0-18.0) 24. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.40-3.7-20. 2001).3. pharmaceutical coatings.50-2.59) 3.11-3..0) 13.5-24.9) 15.30-6.7 (18.0 (19.60 (2.6-20.10) 8.46) 2.00) 4.5 (11.80 (5.5-29.3) 3.85-6.20-2.90-7.00) 10. 2000.5) 23. and also in some printing inks.20-12.8 (9.43) 6. and insecticides.2-14.3-24.70-8.0 (13.56 (5.90-4.80 (2.90-2.30-2.33 (2.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.30-6.80 (3.6 (9.97-7.72-3.4-12.80 (5..70 (5.84) 4. CDC.5) 19. 2005).20 (3.00) 6.50) 7. in a small sample of pregnant women in New York City (Adibi et al.40 (3.4) 22. mostly as MnBP (Anderson et al.46 (2.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.0 (13.40 (7.4) 12.20 (6.60 (8.40 (2.5-16.00-6.3 (13.20-9.9 (16.. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.3) 33.1-17.7) 4.50) 8.2-33.5 (27.40-4.60) 3.1) 16.71 (2.20-12.55 (3. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.0-14.80) 75th 5.90 (6.6 (10. 2003).8) 21.50 (3.30) 10.40-5.. NTP-CERHR.6 (14.7) 15.48 (2. about 65% to 80% of a dose is eliminated in urine within 24 hours.80-5. residents (Blount et al.90 (3.30) 6.00-6. DBP can produce reproductive toxicity in male rodents (McKee et al.0) 12.97) 2.3 (11.60 (5.97) 4.91) 4.73-5.6 (11.7 (17.10) 3.10) 11.30) 2. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.5) 22.56 (3.4 (14.50-4.1-25.00-11. Following oral administration of DBP to humans. Koch et al.3 (16.1 (8..7-31.6 (13.2-22.3-43..50) 18.9-23. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates..20) 7.6-26.90 (4. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.68 (2.50) 2. OSHA has established a workplace air standard for external exposure to DBP.6-34.3 (13.3-48.70 (2.02) 4. population from the National Health and Nutrition Examination Survey.00-9.46 (3. 2007).2 (12.2 (11.3-20. When total DBP metabolites have been measured.5) 25.10-9. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate. interval) 2.3-19.0) 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 2.81 (3. and in a small sample of Japanese adults (Itoh et al.. In addition.40-4.7 (7.44-2.0-38.22 (3.40-3.30 (1.6 (14.50-10.5) 14.6-18.24-8.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.55) 2.4-27.40-17.30 (3.63) 3.8) 40.6) 26.6) 17.30-3.5) 18.80-5. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.70-4.17 (2.56) 3.90-4.70) 3. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.22) 3.70) 5.28-5.0) 9.1) 25.0 and 0.30-13.3 (16.7) 14.5-16.20) 4.10) 2.7 (16. 2000).60-6.30 (4.10-2.30-11.00 (5. Biomonitoring Information Median concentrations reported in the NHANES 19992000.10-9.3-30.66) 2.5 (20.0) 20.56-4.40-12.6) 16.1-12.20 (7.6) 16.50) 5.49-2. 2005. Studies of children found age-related differences in urine MBP levels. in men attending a Boston infertility clinic (Duty et al.1 (13.6 (29.50) 90th 12. they have been referred to as monobutyl phthalate (MBP). 2005).0 (11. 2005).30) 5.50 (6. the median Urinary Mono-isobutyl phthalate (MiBP) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.37) 6.10 (4.40) 5.8) 677 652 703 699 1216 1088 Limit of detection (LOD.5 (17.6 (13.S.96) 3.00) 7.10 (4.S.6) 10.07 (3.00-4.4) 5.2) 5.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.40-9.6-14..00 (7.7 (9.60 (4.00) 4.1-20.2 (8.90 (4.3) 18. 2004. 84-74-2 Di-isobutyl Phthalate CAS No.9-14. 2004.0-25.20-6. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.67 (5.4 (20.17) 4.70-4.3 (19.5 (10.9 (16.40 (2.73 (2.46-5. 2003).90) 12.7 (17.5) 12.9) 10.19-3.30-7.6) 12.6) 17.5) 18.Phthalates Di-n-butyl Phthalate CAS No.50-6.82-3.3 (18.30) 10.1) 22.7) 18. Survey Geometric mean (95% conf.6 (10.7-18.7-31.7) 7. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.26 (2.40 (6.3-18.10 (3. Fourth National Report on Human Exposure to Environmental Chemicals 265 .80 (2. Hauser et al.10) 9.

69 (2.2 (10.51) 2.3 (13.94 (5. 2007).1-12.21) 10.0-18.21 (5. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.17-12.79-8.8-13.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .31 (2. samples from German university students had consistently higher median urine levels of MnBP and MiBP.0 (10. 2005).20-4.37) 3.26-2.6 (8.84 (8.3) 18.58-3.2-13.1) 15.55-6.66) 10.43) 3.47-12.52 (2.35) 3.19 (2.0) 15.0) 11.33 (3.57 (3.18-10.11-2. 2006).22 (2.65-4.73 (5. Weuve et al.8-36.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.46) 3.79 (4.92 (7.51) 15.8 (9.54 (4.81) 4.66 (8.78) 8.76 (3.00-3.82) 4.13 (2.75 (4.6-19. In an analysis of NHANES 1999-2000.65 (4. 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. than adults in NHANES subsamples during the same time period.2 (11. respectively.54 (2.20 (7.30) 2.15-4.18-4.4 (12. Over this time.5-19.45) 3. ranging from more than one-tenth the NHANES median (Itoh et al. 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.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.75 (6.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.6) 13.6 (10.52-20.18) 3.47 (3.95) 10.30 (6.69-7.03 (5.7) 10..38 (6.64-7.53-3.8-18.81) 9. while MnBP declined (Wittassek et al.1-24.1 (11.78-8.93-6.00-3.44 (3.94-12.5 (11.05) 2.04) 7.99) 7.and gender.00-7.6 (15.74-3.9 (15. 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.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 2.62-12.13-6.7 (11.86-4.33 (2.01-2.39) 5.84 (4.9-40.98 (2.91-6.56) 2.57-4.31 (7.64-7.97-2.1) 11. up to four and 13 fold.6) 11. 2004).36-7.53-4.43) 3.81 (3.82 (4.9 (11.08) 75th 4.81 (6.56-4.04) 3.1) 10.42) 2.31) 2.3) 13.17) 90th 8.89) 6.72-7.20-2.4) 7.56) 5.0) 7.46 (2.7) 19.47-5.2) 9.04-5.57 (3.28-13.32 (3.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.6 (8.4-16.67-5.38-10.15) 3.17 (2.9-16.69) 6.29-3.02-10.7) 3.56-15.3 (17.28 (4. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al..33-9.8 (8.27-12.03-11.31) 2.10-5.11 (5. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.1) 4.64-10.2-15.09-2.2) 8.43) 3.07 (2.68) 3.68) 5.25) 5.61-3.1-15.96 (3.1 (10.20 (2.02 (7.5) 13.3) 16.07-5.5) 15.7 (13. 2002..0 (8.46-11.9) 12.52-3.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.6 (9.78) 9.58-4.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.1-25. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.1) 13.20 (2.. An analysis of NHANES 2001-2002 showed similar age.33) 3.74 (4.9 (9.6-19.76-15.08-2.7-28.76-3.4) 15.54) 2.11) 5.7 (21. 2004).8) 10..53-5.80) 7.6 (12. to about two to fourfold higher (Fromme et al.72) 5. 2005).52) 3.89-5.8-18. 2007).68 (2.20-3.80 (3.89 (3.66) 2.26 (2.76-3.32 (7.39-3.94) 6.24) 3.88 (2.S.7) 11.18 (4.99-4.36-2.0 (12.85 (2.2) 24.69) 4.83 (2. Survey Geometric mean (95% conf.8 (10. the students’ median values for MiBP levels remained relatively unchanged.80-3..0) 3.79-6.4) 23.1) 7.34 (3. interval) 2.03-7.62 (6.86) 6.7 (9.18 (1.3) 28.00 (3. Between 1998 and 2003..9-26.14 (4.29-8.66) 4.32) 7.59 (4.5 (9.3) 13. population from the National Health and Nutrition Examination Survey.95-3.51) 5.18) 4.41 (2.65-11.

8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.0 (30.7 (22.0) 31.6-24.3-79.3 (51.7 (70.5) 78.3-96.5) 95.4-25.6 (26.4-44.8) 62.3-60.7-106) 69.8) 23.9) 75.6-31.0 (72.2 (18.9 (20.0 (17.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.5) 36.3 (30.5-47.4 (21.2 (17.3) 40.3-24.5-47.6) 80.4-42.7-121) 97. referred to as monobutyl phthalate (MBP).4 (35.7 (18.6-29.9) 46.9) 21.1 (17.1 (28.2-32.9 (79.5 (74.2 (25.2) 26.9-22.5 (29.1-20.3 (42.9-53.7-92.2) 38.2 (79.8-42.9 (79.5) 34.4 (72.3 (23. Fourth National Report on Human Exposure to Environmental Chemicals 267 .6) 21.0-51.5) 47.1) 23.7) 92.0 (78.3 (30.4 (38.8 (19.4.1-29.5) 19.3) 36.1-27.3-145) 85.6 (48.2-56.0 (18.6) 39.2-63.0-24.1-24.5-43.2-87.0 (45.5) 31.5) 20.7) 52.0-58.9-87.3) 18.7 (28.5) 26.2-21.8-132) 95.4) 20.4 (35.3 (36.5) 24.1.4 (19.5 (28.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.2-114) 73.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.1) 46.5-121) 106 (94.2 (21.2-49.6 (19.1) 25.0 (23.7-124) 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 (16.0-26.1) 31.1-22.4-60.9-92.1 (51.6-44.7-24.6-36.7-53.5 (59.7) 74.7 (43.5-117) 95.2-24.4) 59.0) 20.3-136) 137 (107-162) 119 (90.0-21.4) 64.7-91.4) 52.8) 19.1) 36.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.9-101) 77.0 (20.6 (65.9 (17.2-22.7) 42.8-123) 101 (90.7-20. 01-02.6-113) 108 (90.4) 22.0) 38.7 (51.4 (23.6) 38.S.6) 17.7-42. and 03-04 are 0.8-25.1 (54.0 (15.4 (35.2-159) 92.4-31.1 (16.4-26.0) 84.5) 17. see Data Analysis section) for survey years 99-00.3 (56.1 (21.1 (58.1 (19.0) 117 (104-131) 112 (84. *In the 1999-2000 survey period.9-42.0) 120 (98.7-111) 64.9-22.0 (31.7 (33. 1.2 (74.1 (31.4 (35.8-29.3-67.0) 27.5) 37.9) 29.2 (19.5) 85.2) 68.5 (59.8) 58.3) 24.5) 21. population from the National Health and Nutrition Examination Survey.8) 43.6) 46.5-44.7-42.9-28.6) 35.5-42.7 (19.4-18.6-33.5-53.6 (16.9-114) 116 (97.7 (64.4 (36.1 (36.7) 124 (98.9) 18.4-20.7-117) 118 (108-143) 93.7-34.5) 36.3) 23.8 (57.0) 30.3) 19. interval) 24.6-48.1) 30.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.3) 21.8) 75th 51.6 (44.1 (19. Survey Geometric mean (95% conf.4 (71.2 (21.9.9-33.1) 19.5 (30.6) 71.6 (55.0-73.4 (25.6-37.3-21.0-24.1 (19.6-69.3-40.4 (84.7) 28.2 (75.6 (61.9-79.1) 23.6-49.3 (60.8) 48.2) 90th 98.1-82.5-60.2 (78.7-34.1-51.3-85.3 (17. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.2 (20.6-20.1 (41.1) 47.6-29.7-26.1-92.1-75.1-80.9) 26.2-23.3 (37.6 (32.0 (25.2 (59.6-40.3 (23.0 (36.2) 42.5) 40.1) 20.7 (18.7-127) 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 22.9 (17.1 (19.1 (62.6 (90.1 (18.1) 17. and 0.2-33.1 (26.7 (24.5) 65.2) 32.5-27.9) 71. respectively.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.7 (38.1 (34.2-93.0-32.8-22.6-143) 127 (99.3) 26.1) 23.8-119) 90.0-19.0-19.2 (58.2) 20.3-76.4-159) 107 (84.6) 20.7-116) 95.6 (22.9) 36.2) 62.0) 21.

0-75.8 (13.9 (39.5) 21.0) 53.3 (76.4-61.9) 28.1-62.7-39.5-22.2-27.3) 59.6) 39.5-76.4-76.6-92.5 (14.6-50.9) 52.6) 34.1 (21.3 (17.9 (30.1-83.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.5-41.0 (61.0-38.6-155) 91.0-19.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.5 (18.2-22.0-60.9-100) 86.3-18.1) 44.6 (41.7 (12.4-131) 81.3) 67.8 (33.3 (17.8) 63.3 (19.7-51.5) 39.0) 25.9 (58.2-48.8-43.6 (17.4-24.7-19.4) 15.3) 35.5) 90th 68.4-72.4 (16.6 (31.0) 19.4) 20.8) 20.4 (68.6-44.1) 50.0 (27.5-30.2) 31.4 (56.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.1 (56.9-38.7-37.2 (35.8 (25.0 (70.6 (61.6-128) 96.9) 14.9 (19.8) 30.4 (50.4) 16.8) 35.6) 25.3 (21.1) 35.3) 19.8-24.4-135) 71.7) 36.6 (25.0 (19.4 (20.5 (15.7-23.5) 91.7 (16.1-99.4 (16.7 (60.6) 64.6 (57.4-65.0) 108 (71.1) 21.9) 49.3 (60.5) 134 (93.1 (29.7-80.3-114) 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 17.3 (17.8-32.3) 18.2) 74.3-26.9-26.4 (13.8-24.6) 18.4 (50.1) 17.2-73.0 (16.6-119) 63.1-128) 97.3-21.6-26.4) 53.5-21.9 (37.0) 59.6) 24.4-103) 117 (83.0 (71.3 (52.1 (34.1) 37.5-18.6 (29.1-18.9) 30.7-20.8) 22.3) 33.4 (23.6-19.0) 41.0 (20.1) 20.7-78.3) 19.4 (33.2-86.9-34.7) 19.7 (27.7 (73.6-42.9 (35.3-20.0 (15.3 (16.0 (18.6-22.2 (83.3 (52.6) 24.7 (81.3-23.4-164) 96.2 (19.1) 42.8 (18.6) 38.3) 21.5-37.2) 65.0-17.4) 19.8 (16.7) 42.9-36.6) 83.3 (42.0 (43.9) 62.8 (18.3 (69.4 (45.3-49.7 (19.2-18.8 (17.9) 91.3-17.9 (21.9 (30.0 (69.0-90.3 (24.6-23.4 (37.5-15.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.9-56.9-70.4 (31. 268 Fourth National Report on Human Exposure to Environmental Chemicals .2 (19.5 (64.3 (46.9) 24.1) 22.5-23.4) 15.0) 94.7 (28.2-28.3 (55.4 (18.6 (72.8) 20.4 (31.7-19.6-24.3) 33.2) 159 (102-263) 147 (93. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.0 (52.8) 17.6-27.3-38.7 (57.3 (48.7) 20.6-24.0-41.9 (64.9-68.6-23.6-44.1-99.7 (20.8) 34.8) 75th 38.0 (26.0 (34.5) 17.3-71.0-92.6-32.1) 53.4-34.5-64.3-39.3) 20.9 (16.6 (25.2-108) 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.5-142) 89.8 (50.2-61.5 (30.3-78.3 (71.3-106) 74.4 (17.8) 28.1 (32.0) 35.9) 20.5 (18.8) 13.3) 52.7-28.0) 55.5-142) 81.1 (46.0) 81.1-32.6-16.5 (81.8 (22.1 (15.3-32.6-43.7 (54.9-105) 85.3-21.2-179) 84.0-113) 104 (83.9 (35.0-47.4 (17.0) 26.4-47.5-16.0) 29.7-21.9) 39.9-84.9 (73.8 (18.8) 40.0) 70.2-85.3) 17.9-68.4 (19.2-22.8) 17.8) 17. Survey Geometric mean (95% conf. interval) 22.4) 21.0) 75.9-49.S.0 (18.8-235) 137 (108-198) 88.2-21.4) 51.4 (47.6-74.0 (50.3 (28.4) 62.5) 82.2 (38.7 (14.9 (56.5) 84.1-23.6) 31.1) 61.2-22.6) 65.8 (65.8) 23.2-16.7-26.6) 23.2-106) 64.6-53.0) 28.8) 19.5) 60.8-23.6) 14.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.7-42.6 (27.3-81.6 (74.6-28.5-70.2) 16.9-14. population from the National Health and Nutrition Examination Survey.2 (16.1) 20.4 (53.9) 19.6) 37.1 (61.7 (60.9 (20.2) 21.2) 59.8) 34.3-40.4 (31.1-21.9 (30.7 (43.6 (19.

A biomarker approach to measuring human dietary exposure to certain phthalate diesters.niehs.114(9):1424-1431.208:237-245. Pirkle JL. Caudill SP. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Drexler H. Blount BC. Barr DB. 4/20/09 Silva MJ. Duty S. Giwercman A.16(4):487-493. Jonsson BAG. Boehmer S. Int J Hyg Environ Health 2005.93:177-185. Calafat AM. Itoh H. Brock JW. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Reprod Toxicol 2004. Richthoff J.68:309-314. Angerer J. Caudill SP. Rylander L.22(3):688-695. Available at URL: http://cerhr. Fromme H. et al. et al. Chen Z. Ryan L. Anderson WA. Singh NP. Atlanta (GA). 2005. Hodge CC. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.gov/chemicals/ phthalates/dbp/dbp-eval. Butala JH. McKee RH. Hilborn ED. et al. Silva MJ. Int J Hyg Environ Health 2007. Malek NA. Hauser R.18(1):122. Environ Health Perspect 2000. Koch HM.Phthalates References Adibi JJ. Hum Reprod 2007. Dobler L. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. 112(5):A270]. Prenatal exposures to phthalates among women in New York City and Krakow. Yoshida K. Environ Health Perspect 2003. Sanchez GN. Silva MJ. Castle L. Helm D. Sampson EJ.111(14):1719-1722. Bull Environ Contam Toxicol 2002. Springall C. Calafat AM. Urinary levels of seven phthalate metabolites in the U. Schettler T.210:21-33. Hu H. Centers for Disease Control and Prevention (CDC). NTP-CERHR. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Needham LL. Research Triangle Park (NC). Masunaga S. Epidemiol 2005. Wiesmuller GA.nih. Meeker JD. Brock JW. Silva MJ. Third National Report on Human Exposure to Environmental Chemicals. Green RA. Eckard R.210(3-4):319-33. Perera FP. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Silva MJ. Barr D. Environ Res 2003. Weuve J. Koch HM. Phthalate monoesters levels in the urine of young children. Gans G. Drexler H. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Needham LL. Caudill SP.18(12):10681074. 2000 [online]. J Androl 2004. Duty SM. Scotter MJ. Massey RC. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Environ Health Perspect 2004.112(3):331-338. Angerer J. Koch HM. Int J Hyg Environ Health 2007. Levels of seven urinary phthalate metabolites in a human reference population. Environ Health Perspect 2006. et al. et al. et al. Ryan L.25(2):293-302. Jacek R. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Rossbach B. et al. David RM. Wittassek M. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.html.S. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP).108(10)979-982. Food Addit Contam 2001. Hagmar L. Poland. et al. Reidy JA. Camann DE. Jedrychowski W. Bolte G.

9.3.400) < LOD 1.200-.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 1.300-.400-.400) 1.200-.500) 1.600) .300 (<LOD-.300 (.400 (<LOD-.500) < LOD 1.70 (1. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70 (1.500 (. and polymers.500 (.300-.400 (.200-.400-.70) .300-. including nitrocellulose. resins.600 (.500 (.10 (<LOD-2.200 (<LOD-. and 03-04 are 0. and 0.600) .300-.400-.300-.300 (. Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population. only levels at or above the 90th percentile could be characterized.700) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.500-.00 (<LOD-1. which may vary for some chemicals by year and by individual sample.300) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .10 (<LOD-1.00 (<LOD-1.00) .500) 1.500) < LOD < LOD .10 (<LOD-1. 270 Fourth National Report on Human Exposure to Environmental Chemicals .500 (.400-.700) .500) . < LOD means less than the limit of detection. respectively.400 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.400 (.300 (.00-2.500) .80) .90) .200-.20) .300 (.50) . Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.10 (. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.10) .300-. see Data Analysis section) for Survey years 99-00.900-1.300-.500 (.300) < LOD .700) .500 (.Phthalates Dicyclohexyl Phthalate CAS No. 0.S. In this Report. polyvinyl acetate.300-.300 (.400 (.400 (.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .400 (.600) < LOD .400 (<LOD-.400-.600) .400-.00-3.300) < LOD .300-.300 (. Survey Geometric mean (95% conf.400-. and polyvinyl chloride.400) 1.300 (.600) . 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.500) 1.70) .2.400) < LOD < LOD .500) .200-.200-.50) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) < LOD < LOD .500 (.600) .400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.400 (<LOD-.400 (.500) .500 (.500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .00 (<LOD-1. 01-02.400 (<LOD-. population from the National Health and Nutrition Examination Survey. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.300-.500 (.

620) < LOD .670 (<LOD-.410 (.370 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 271 .420-.290-.770-1.790-1.360-.610 (.00 (<LOD-3.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .16 (<LOD-3.S.590 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.06) .54-6.770-1.630 (<LOD-.660) < LOD < LOD .450 (.490) .770) < LOD 2.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .690-1.330 (.82) .910 (.310) < LOD .950 (.14 (<LOD-3.660) .400-.53) .690) < LOD < LOD .00) .910 (.530-.530-1.18) .380 (.500 (.43 (1.560) 1.53) .770-1.630 (<LOD-.880 (.54) .910 (.22 (<LOD-1.500) 3.220 (<LOD-.12-1.590 (.350-.380-.33) . population from the National Health and Nutrition Examination Survey.800-1.470) 3.82 (1.36-1.710) .34) .06) .11) .05) .33 (<LOD-3.310-.10) .510-.67 (1.450 (.510 (.170-.530) 1.670-1.54 (<LOD-2.740) .910 (.420-.330 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.17) .530 (.500-.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.830) 1.940 (.470 (.250 (.740) < LOD < LOD .240-.390 (. Survey Geometric mean (95% conf.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.400-.270) < LOD .16) .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 1.690 (.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 .74) .260-.480 (.420-.770 (.44) .690) < LOD 2.

9-92. see Data Analysis section) for Survey years 99-00.3 (82..1 (71.3 (74.4.. In contrast. 2001-2002.2. 272 Fourth National Report on Human Exposure to Environmental Chemicals .S. 2007). and 03-04 are 1.7 (70. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. colognes.9 (61.1-93. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. deodorants. 2002).9.7) 71.3-103) 193 (141-256) 184 (148-227) 221 (165-294) 180 (140-221) 181 (152-212) 188 (158-219) 197 (129-249) 183 (142-217) 196 (170-241) 564 (419-818) 479 (387-651) 557 (432-695) 482 (390-590) 498 (441-567) 533 (471-629) 378 (290-730) 451 (315-636) 521 (295-571) 1510 (1050-2150) 1260 (983-1480) 1250 (973-1560) 1340 (1010-1660) 1350 (1060-1660) 1590 (1220-2070) 756 (379-1070) 808 (572-1090) 827 (542-1440) 3260 (1550-4420) 2070 (1470-3050) 2310 (1360-3310) 3480 (2230-4640) 2720 (2160-3670) 2980 (2250-3800) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 179 (149-215) 182 (157-211) 197 (173-224) 178 (154-206) 174 (153-198) 189 (160-225) 154 (119-197) 171 (139-199) 171 (148-201) 174 (138-210) 167 (139-194) 182 (138-219) 523 (372-650) 502 (419-603) 536 (449-654) 425 (350-508) 427 (387-498) 478 (392-564) 1440 (1020-2280) 1450 (1060-2110) 1520 (1210-2070) 988 (880-1230) 1050 (879-1310) 1260 (969-1640) 3500 (2130-4560) 3100 (2110-4390) 2910 (2210-3480) 2230 (1370-3880) 1860 (1490-2500) 2590 (1800-3420) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 181 (157-209) 226 (195-262) 267 (239-298) 322 (275-377) 352 (324-384) 357 (310-412) 152 (133-175) 158 (141-178) 167 (145-193) 174 (146-210) 220 (190-264) 249 (212-307) 306 (256-350) 357 (290-407) 306 (253-414) 134 (108-157) 147 (119-177) 148 (125-175) 441 (390-541) 530 (444-660) 597 (523-688) 789 (635-949) 853 (709-1090) 948 (769-1150) 367 (287-482) 413 (366-451) 418 (366-477)