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CDC Chemical Exposure Fourth Report 2009 Americans

CDC Chemical Exposure Fourth Report 2009 Americans

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Sections

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

2009

Fourth National Report on Human Exposure to Environmental Chemicals

Fourth National Report on Human Exposure to Environmental Chemicals

2009

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

Contents

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

Fourth National Report on Human Exposure to Environmental Chemicals

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Contents

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

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

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Fourth National Report on Human Exposure to Environmental Chemicals

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

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

Fourth National Report on Human Exposure to Environmental Chemicals

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Contents

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

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

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Fourth National Report on Human Exposure to Environmental Chemicals

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

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

Fourth National Report on Human Exposure to Environmental Chemicals

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Contents

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

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

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Fourth National Report on Human Exposure to Environmental Chemicals

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

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

Fourth National Report on Human Exposure to Environmental Chemicals

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Introduction

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

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

• •

• •

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

Fourth National Report on Human Exposure to Environmental Chemicals

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4.4'.2-Dichloroethene trans-1.4.html.4.2-Dichloroethane (Ethylene dichloride) 1.3-Tetramethylbutyl] phenol) Triclosan (2.3. Paradichlorobenzene) 1.2'.cdc.1.5'-Hexabromodiphenyl ether (BDE 153) 2.3.4’. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.1-Trichloroethane (Methyl chloroform) 1.4'-Tetrabromodiphenyl ether (BDE 47) 2.4'.4.1.5.2-Trichloroethane Trichloroethene (Trichloroethylene) m.2’.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. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.4'-Pentabromodiphenyl ether (BDE 85) 2.2'3.4’.4.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.2'.2'.4.6'-Hexabromodiphenyl ether (BDE 154) 2.6-Pentabromodiphenyl ether (BDE 100) 2.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .3.1-Dichloroethane 1.3-Dichlorobenzene (m-Dichlorobenzene) 1.5'.2'.4'-Tribromodiphenyl ether (BDE 28) 2.4'. Table 1.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.5'-Tetrachlorobiphenyl (PCB 49) 2.4.What’s New in this Report What’s New in this Report In this Fourth Report. 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 (2.1.3’. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.5.6.4'.5’.2.2'.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.5-Pentabromodiphenyl ether (BDE 99) 2.2'.4'.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2'.3.1.2-Dichloropropane 2.2'4.6-Heptabromodiphenyl ether (BDE 183) 2.4.5'-Tetrachlorobiphenyl (PCB 44) 2.5.gov/exposurereport/chemical_selection.4.2'.4.4. The process for selection is described at http://www.2-Dichloroethene Dichloromethane (Methylene chloride) 1.3'.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.4'-Tetrabromodiphenyl ether (BDE 66) 2.4-Dichlorobenzene (p-Dichlorobenzene.1-Dichloroethene (Vinylidene chloride) cis-1.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.4.2'.4-Tribromodiphenyl ether (BDE 17) 2.5.2-Dichlorobenzene (o-Dichlorobenzene) 1.

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

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

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

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

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

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

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

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

Animal studies indicate that acrylamide is well absorbed.. gels.9-61. People may be exposed to acrylamide from foods.2) 57.3) 63. Survey Geometric mean (95% conf. and binding agents. In humans.Acrylamide Acrylamide CAS No.2-77.7) 96.1-64.4-76.6) 71.9 (60.5-80.S.S.2-59.0 μg/kg for adults (FAO/ WHO.4 (51.2-114) 163 (147-191) 96. smoking. the main source of exposure is from the diet. pulp and paper production.1 (47. Acrylamide is not thought to accumulate in the body at environmental doses.5) 58. 2005). and in some cosmetics. soil conditioners. but are generally above the U.2-70.7) 54.S.0-66.3 (53.6-65. Polyacrylamides are useful water-compatible polymers used in water treatment.4 (53. 2004). 2006).4) 57.9 (69. FAO/WHO. widely distributed in tissues.2 (58. and an average daily intake is estimated as 0. Tareke et al.8-57. it was discovered that acrylamide is formed when starch-rich foods.9) 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. glycidamide.6 (56. These estimated intakes are hundreds of times lower than occupational exposures. 2004.8 (81.1) 101 (95.7-64.1) 53. 2005).4-60.7 (65.2) 57. ocular and dermal irritation from direct contact with acrylamide containing materials.1) 46. EPA.2 μg/kg/day (U. acrylamide is synthesized and used in the production of polyacrylamide polymer. such as potatoes and some grains. or to glutathione conjugates (Calleman et al.4-89.6-66. in some sealing grouts.7 (58.2 (62. FDA.2-91.0) 57.4-60.1-57. but can covalently bind to form adducts with proteins.4 (54. population from the National Health and Nutrition Examination Survey.6 (81.6) 50.2-93.1 (88. (NTP-CERHR..5 (74.4-83.3-2. as an absorbent in disposable diapers.9-52. Since acrylamide has limited volatility and high water solubility. In 1997.9 (54.7) 73.5 (52. and is either metabolized to the reactive epoxide. see Data Analysis section) for Survey year 03-04 is 3. 2005).0 (57.S.S.8 (52.1-61. and in the synthesis or compounding of dye materials. 2005).0) 85.2-67.4 (54. mineral processing. in permanent press fabrics. 2006.3-71. acrylamide has produced upper airway irritation following inhalation of high levels. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.6-75. 1994). 2005). and cosmetics (NTP-CERHR.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.8 (57. Commercially.0-58. 217 million pounds of acrylamide were produced commercially in the U.9-105) 86..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. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.4) 57.0 (69.2-118) 98.9) 58.6-61.1-64. EPA.3 (55.4) 100 (89.3) 70.5 (44.0 (53. Natural substances in the food are converted to acrylamide.6-108) 61.1) 62. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.8-55.6) 90.6 (51. and from dermal contact with products that contain residual acrylamide. and well below doses known to cause nerve damage or carcinogenicity in animals.3) 86. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.8 (91.0-49.7-60. EPA reference dose of 0.6-104) 82.1 (52. Elimination occurs mainly in the urine as mercapturic acid conjugates. 2002).7-64.0-108) 152 (139-175) 126 (111-142) 108 (86.1) 55.6) 73. are heated at temperatures used for frying and baking. interval) 61.5) 66.1 (83. In the general population.4 (59. Estimated intakes in children are about twice that of adults (DiNovi and Howard. 1990.7 (63.1 (73. 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.0.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.7) 58.7 (55.2 (75. 2005. drinking water.9) 63.9) 75.5 (79.5-85.0 (67.7) 75th 79. Fourth National Report on Human Exposure to Environmental Chemicals 11 . Fennell et al. Recently.

2-90.5-66..2-68. 2005).1 (56. population from the National Health and Nutrition Examination Survey.. and cancer (mammary.4) 53. male germinal cell injury.2) 55.4-65.7 (84.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71. 2006). 2005. adrenal.2 (63. 2005. Puppel et al..3) 59.9-77. fetal death.1) 56.int/ ipcs/food/jecfa/summaries/summary_report_64_final.7) 90. dominant lethality).. presynaptic nerve terminal binding (LoPachin.S.8) 45.9) 59.3) 85. Vesper et al.3) 59. In addition. Axonal degeneration.5) 87.5 (56. U. 2008).2-91..4-59.7) 74.8 (44. 2008). 2002.7 (87.9) 75.9-64. although different analytic methods can affect results.7) 61. and neuronal DNA reactivity (Doerge et al.1) 60. 1997. EPA.4 (56.2 (56. 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.4 (81. Glycidamide has been shown to react with DNA (Doerge et al.8-49..S.0 (80..0-93.3) 59.S. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. probably through its epoxide metabolite..7-86. Klaunig et al. respectively) are markers of integrated acrylamide exposure over the preceding few months. Survey Geometric mean (95% conf.0-62.0-103) 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. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.5 (83.. Puppel et al.0 (75. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).9-62. 2006). 2003..3 (56. 2005).1) 62.. 2005.pdf. Additional information is available from U.4-98. 2004). Maniere et al.5) 75th 85. thyroid. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.6-90. IARC classifies acrylamide as probably carcinogenic to humans..5) 71.2) 87.5-64. 2004. and other sites) (FAO/WHO. EPA. glycidamide (NTP-CERHR. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.4 (61.9) 87.4) 46. U. Schettgen et al. scrotal. 2006) have been demonstrated after acrylamide dosing. reproductive effects (reduced litter size.9-76. 12 Fourth National Report on Human Exposure to Environmental Chemicals . 2001). Rice. 2005.3-101) 95.S.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.0 (52.1-70.9 (58.6-64. 2005). 2005).5-94.1 (82.7 (61. Mucci et al.8) 60. After exposure ceases.who. 2005. 2005.7-64.1-56.5-92.9-78.1 (70.. EPA at: http://www. 2005) have been demonstrated in animals.1 (57. Acrylamide is clastogenic and can produce dominant lethal mutations. 2002.1) 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. 2005..0.4 (51. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al. Vesper 2005) and smoking (Bergmark.0) 118 (103-126) 121 (112-134) 113 (94.7) 60. 2005. NTP-CERHR.6 (90..9) 65. most non-smokers had levels less than about 100 pmol/gram hemoglobin.Acrylamide occupational exposures..4 (90.2) 65.. Schettgen et al. 2006.2 (72. altered gene expression in testicular tissues (Yang et al. AHA levels have been shown to increase with dietary intake (Hagmar et al. Hagmar et al. 2009).7-62. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.8-61. 2005.7 (57. 2005. 2005) and sperm DNA adducts (Xie et al..0 (70. uterine..6-62.9 (81.epa.. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.0) 94. 1997.4-103) 79.6 (66. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.5 (59. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.1 (66.9 (57. 2005.4 (57. see Data Analysis section) for Survey year 03-04 is 4.1-62.8-48.3-78.8 (51.5 (42.4) 83.9-138) 143 (130-159) 96. 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. interval) 59.1-60.

Chicago. Kamendulis LM. July. J Agric Food Chem 2008. Snyder RW. Bjellaas T. Mutat Res 2005. McDaniel LP. Adv Exp Med Biol 2005. Wirfalt E.126(2):361-371. Bridson WE. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Godard T. Rome. Joint FAO/WHO Expert Committee on Food Additives. 1993.56. Hagmar L.561:21-37. Mucci LA. 2004. Adv Exp Med Biol 2005.561:49-62. February.3:406-412. Tornqvist M. 054472. Becher G. Maniere I. Metabolism and hemoglobin adduct formation of acrylamide in humans.pdf. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. [Epub ahead of print] Dybing E.gov/chemicals/ acrylamide/Acrylamide_Monograph. Acrylamide intake through diet and human cancer risk.Toxicol Appl Pharmacol 1994. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Mutat Res 2005. Human exposure and internal dose assessments of acrylamide in food. In another study.580(1-2):157-165. Chem Res Toxicol 1990. Haugen M. Tornqvist M. LoPachin RM.. 1994). Scand J Work Environ Health 2001. et al. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Food and Drug Administration (FDA). 64th Meeting: Summary and Conclusions (FAO/WHO).niehs. Uncertainties. et al. Kautiainen A.27(4):219-226.43:365–410.. Wilson KM. Perez et al. morphological and molecular endpoints in animal models. Toxicol Sci.10(1):78-84. Calleman CJ. He F... Malmberg B. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR).int/ipcs/ food/jecfa/summaries/summary_report_64_final. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Guffroy M. da Costa GG. Calleman CJ. Aprea P. Duale N. Osterman-Golkar S. Magnusson AL. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Toxicol 2005. 2/3/09 Perez HL.fda. Doerge DR. Paulsson B. Farmer PB. National Toxicology Program. 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.pdf. Food Chem. Nordander C. Fennell TR. Toxicol Sci 2005. 6013-6019. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Costa LG. Acrylamide neurotoxicity: neurological. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. 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. Mechanisms of acrylamide induced rodent carcinogenesis. Costa LG. Bergmark E. 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. 2009 Jan 8. 1999). Cheong HK. Yang JS. Calleman CJ. April 13-15. He F. and Research Strategies. et al.580(1-2):131-141. smokers and nonsmokers. Available at URL: http://cerhr. et al. Spicer R.who. The Updated Exposure Assessment for Acrylamide.580(1-2):119-129. NIH Publication No. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Available at URL: http://www. Chem Res Toxicol 1997 Jan. 2/3/09 Klaunig JE. Tian G. Survey data on acrylamide in food: individual food products. Churchwell MI. Granath F. Paulsen JE. 2001. Bruze M. Zhang S. Available at URL: http://www. 8-17 February 2005. Churchwell MI. DiNovi M and Howard D. Hagmar et al.cfsan.120(1):45-54. Axmon A. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Doerge DR. Illinois. 2005. Laurentie M. CFSAN/Office of Plant and Dairy Foods. et al. Wu Y. 2/3/09 Hagmar L.html#u1004. Beland FA. Bergmark E.Acrylamide In occupational settings. Burgess J. 2001). Toxicol Appl Pharmacol 1993. 2006.. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Fennell TR.nih. Andersen M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Bergmark E. gov/~dms/acrydata. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. smoking habits and gender. Rosen I. References Bergmark E. Italy. Twaddle NC.85:447-459. Summer SCJ. Alexander J.

epa. Acrylamide. Weiss T. a carcinogen formed in heated foodstuffs.txt.S. Drexler H. EPA). Reprod Toxicol 2005. Lee SH. Yang HJ. J Agric Food Chem 2008.207(6):531-9.htm. Choi JH.gov/chemfact/s_acryla. Gray JG. Int J Hyg Environ Health 2003. Agudo A. Fu D. et al. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Fueller F. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Smith A. Tornqvist M. Jin Y. Vesper HW. Environmental Protection Agency (U. propylene oxide. Hallmans G. Licea-Perez H. et al. The carcinogenicity of acrylamide. Liu K. Drexler H. Han CH.274(1):59-68. Toxicological effects of acrylamide on rat testicular gene expression profile. Eriksson S. Environmental Protection Agency (U. Ospina M. Schettgen T. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Chae C. Angerer J. Mutat Res 2005. Schettgen T. Mutat Res 2005 Feb 7. Broding HC.163(2):101-8.S.S.epa.206(1):9-14. U. Adv Exp Med Biol 2005. Rossbach B. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure.580(1-2):3-20. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. 2/3/09 Vesper HW. Karlsson P. Benetou V. Ding X. Toxicol Lett 2002. Integrated Risk Information System (IRIS). Letzel S. Marko D. Tjønneland A. EPA).S. Myers GL. Vesper HW. J Agric Food Chem 2002. Available at URL: http://www.56(15):6046-53. Han DU. Kutting B. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Rydberg P. Available at URL: http://www. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Drexler H. Office of Pollution Prevention and Toxics. Ospina M. Hemoglobin adducts of ethylene oxide. Ingham L.Acrylamide glycidamide by gas chromatography-mass spectrometry.580(1-2):71-80. Chemical Summary for Acrylamide. Angerer J. Lee MH. Int J Hyg Environ Health 2004. Sun H.561:89-96. Washington (DC). Toxicol Lett 2006. Slimani N. Tareke E. Liu Y. U. Rice JM. 1994. Meyers T. 2/3/09. Schettgen T.20(6):959-64.19(4):527-34. Rapid Commun Mass Spectrom 2006.gov/iris/subst/0286. revised 1/3/06. Meyers T. Tjaden Z. Anal Biochem 1999.50(17):4998-5006. Analysis of acrylamide. Angerer J. Xie Q.134(1-3):65-70. September. Puppel N.

350-.68) .49) 1.930 (.600-1.21 (.061) < LOD .160) .124 (.080-.88 (.44) 2.505 (.087-. Children exposed to ETS are at increased risk for sudden infant death syndrome.75) 1. Serum Cotinine Metabolite of nicotine (component of tobacco smoke) Geometric mean and selected percentiles of serum concentrations (in ng/mL) for the non-smoking U.63-2.130 (.95) 1.12 (1.164 (.68 (1.302) .17 (1.30) 2.190-. which may vary for some chemicals by year and by individual sample.50-1.990 (.18-3.84-3.080) < LOD .11) .120 (.139) * .23 (2.150) .234) .071) .850 (.300) .68) 2.073) < LOD .02) 1.080-.01 (1.30) 2.060 (.580) . population from the National Health and Nutrition Examination Survey.22) 2.108) * .70-2.120 (.730 (.040 (.89) 1.47-3.131 (.506 (.66) 1.058 (.55 (1.79) 3.210 (.99) 2.080) < LOD < LOD .060 (<LOD-.44 (1.12-4.14) .510 (.130) .81-2.78) 2. stroke.770) .62) 2.620-1.62 (2.88 (1.043-.S.480-.670) .180 (.160) .175 (.32) 1.630 (.790) .120) .140-.92) 1174 1415 1252 1773 1902 1783 3052 3502 3285 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 20 years and older Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 .140 (.70) 2.153-.020-.220-.040-.S.66 (1.23 (.01) 3. 2004).100-.42-4.17 (.690 (.02 (. 83% of measurements had an LOD of 0.93) .063) .94) 1.54) 1.820) .02) 1.32-2.770) .090-.070 (<LOD-.990) .110 (..110) .071 (.99) 2.350 (. DHHS.5% nicotine by weight (Kozlowski et al.77 (1.050-.260-1.110-.950 (.20) 1.50-4.96) 2.920 (. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.075 (.360) .23 (1.188) .63 (2.710 (.050 (<LOD-.120-.060 (.059-.163 (.066-.050 (<LOD-.090-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.120 (.370-.180) .15 (2.470-.047-. 1998).110 (.110) .92 (1.310) .086 (.350-.190-.084) . cardiovascular disease.540 (.148-.28) .057-.050) .16) .800 (.060) .160-.42 (1.040 (.260) 1.910-1.621-1.66-3.49) 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.09-2.060-.087 (.052 (<LOD-. acute respiratory illness.060-.080-.030 (.20-2.53 (1.167 (. acute respiratory infections.580-1.080 (.76 (1.726) .312) .280 (.S.21-1.180 (.120 (.14) .533-. maternal exposure during pregnancy can result in lower birth weight. and various other disorders (U.310-1.54 (1.310) 90th 1.089) Age group 3-11 years 99-00 01-02** 03-04 .43 (1.83-2.60-2.087) < LOD < LOD .310-1.53-4. Fourth National Report on Human Exposure to Environmental Chemicals 15 .660) .060 (<LOD-. and 0.17) .160 (.066) . see Data Analysis section) for Survey years 99-00.160 (.45) 1.48-2. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.120 (.Cotinine Cotinine CAS No.220) . ear problems. 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.104-.520 (.080 (.48-3. and 17% had an LOD of 0.19) .070) .050) .54 (1.015 ng/mL.49) 1.77 (2.65 (1. emphysema.05) 1.20) .630 (.740-1.137-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * . Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.620 (.180) .240 (.059-.030-.142-.110 (.144 (.080-.068) .110-.077) .308 (.070) 75th . respectively.062 (.14-1.040 (.320) .570 (.997-3.106-.34 (1.87-3.126) . ** In the 2001-2002 survey period.110 (.154-.770-1. 2004).047-.00) .213) . The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.230 (.12) 1.500 (.30) * .230) .140-.15) 2.111-. and 03-04 are 0.21-1.050 (.094) .066 (.00) 1.05.198) * .137 (.39) 3.050 (<LOD-.050 (<LOD-.33-2.076-.50 (1.19-2.26-1.630 (.19) 1.120-.77 (1.12 (2.38-2.55-2.060-.068) .180) .54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .04 (1.44 (2.840) 3.150) .540-.428-.40) .20 (1. DHHS.030-.35 (2.190-.410) .32-2.090-.950-1.430-1.164 (. Survey Geometric mean (95% conf.50) 3.052 (<LOD-.450-.110 (.960-1.050-.580 (.200) 1.216 (.070) .625) .570-1.740-1.015.115-.163) .09-3.160 (.077) .053 (<LOD-.860 (.180) .180) .193) .480-1.400-.220) .145) .088-.201) .96 (1.23-2.05 ng/mL.39 (1.140 (. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP. 2006).070-. Cigarettes contain about 1.09-3.85 (1.96-4.20 (.110-.054 (.57) 2.197) .28-1.44) 2.187) .030-.040-. < LOD means less than the limit of detection. and exacerbated asthma (U.900-1.

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

Epidemiol Rev 1996. Mowery PD. Exposure of the U. 1999. Third National Report on Human Exposure to Environmental Chemicals. National Center for Chronic Disease Prevention and Health Promotion.57(1):79115. Benowitz NL. Trends in the exposure of nonsmokers in the U. Pirkle JL.291(3):1196-1203. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Sosnoff CS. 1999-2002. Coordinating Center for Health Promotion.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. June. 1988-1991. Jacob P III. U. Pirkle JL. Available at URL: http://monographs.cancer. U. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Dollery CT. Benowitz NL. Environ Health Perspect 2006. Kira S. Benowitz NL.S. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 .S. JAMA 1998. National Toxicology Program (NTP). J Pharmacol Exp Ther 1999. Aiba M. U. 1988-1991. Pharmacol Rev 2005.S. Curtin LR.114(6):853-858. Bernert JT. JAMA 1998.S Department of Health and Human Services (U. Etzel RA. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Richter PA. Tob Control 1998. Int Arch Occup Environ Health 1991. Benowitz NL. Kozlowski LT. Tobacco related exposures. Respiratory nicotine absorption in non-smoking females during passive smoking. Centers for Disease Control and Prevention. Smoking and Tobacco Control Monograph 10 [online].56:483-493.fr/ENG/Monographs/ allmonos90. Giovino G. Houseman TH. International Agency for Research on Cancer.S.gov/ntp/roc/eleventh/profiles/ s176toba.php. Office on Smoking and Health [online] 2006. Strauss WJ. 4/13/09 Iwase A. Centers for Disease Control. Vogler GP. Schwartz SS. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Brody DJ.pdf. 11th ed. BMJ 1975. 1991. Department of Heath and Human Services. Jarvis MJ. Summary of Data Reported and Evaluation [online] 1986. et al. 4/13/09 U. Metabolism and disposition kinetics of nicotine. IARC Monogr Eval Carcinog Risks Hum. Giovino GA.S. Tobacco Smoke. Caraballo R. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. National Institute for Occupational Safety and Hygiene (NIOSH). Pollack HA. Atlanta (GA): 2005. In Report on Carcinogens. available at URL: http://mtn. iarc. and the United States. the United Kingdom. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults.gov/tcrb/monographs/10/. Perez-Stable EJ. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Clin Pharmacol Ther 1994.gov/library/ secondhandsmoke/. Flegal KM. Vol 83. Cotinine as a biomarker of environmental tobacco smoke exposure. Jacob III P.18:188-204.pdf. Ethnic differences in N-glucuronidation of nicotine and cotinine. Summary of Data Reported and Evaluation [online] 2004. Absorption and metabolism of nicotine from cigarettes. Soliman S. Herrera B. population to secondhand smoke: 1988-2002. Tobacco Smoke and Involuntary Smoking. [online]. Jacob P.iarc.cdc. IARC Monogr Eval Carcinog Risks Hum. Bernert JT. References Armitage AK. Caudill SP.15:302-307.94(2):314-320. Hukkanen J.63:139-43. Pechacek TF. JAMA 1996. Turner DM.S.nih. Available at URL: http://monographs. Schober SE. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Tob Control 2006. Brody DJ. Pickett MA.surgeongeneral. 4/13/09 International Agency for Research on Cancer. Pechacek TF.niosh. Mehta NY.7:369-375. 4/13/09 Centers for Disease Control and Prevention (CDC). et al. Herrera B. Available at URL: http:// cancercontrol. 4/13/09 Perez-Stable EJ. Maurer KR. Available at URL: http://www. Lewis PJ. Am J Public Health 2004. cigarette smokers: the Third National Health and Nutrition Examination Survey. DHHS). Department of Heath and Human Services. Coordinating Center for Health Promotion. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Warner K.4:313-316. Centers for Disease Control and Prevention. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary.S. 4/13/09 National Cancer Institute (NCI). Modin G.280:152-156.php. Jacob P III.niehs.gov/eid/rmca/critdocs/ criteriadoc/33. DHHS). Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Benowitz NL.fr/ENG/Monographs/allmonos90. 2004. George CF. Fong I.275:1233-1240. Nicotine metabolism and intake in black and white smokers. Available at URL: http://ntp.S Department of Health and Human Services (U. Sweeney CT. Racial/ethnic differences in serum cotinine levels among adult U. Vol 38.280:135-140.

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

have been reported as result of self-poisoning by ingestion or excessive dermal application.EPA at: http://www.100-.560) < LOD .S. 1995. Sudakin and Trevathan.100-.S.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2003). There are over 225 insect repellents brands containing DEET. 1998). including seizures and encephalopathy.190) < LOD .140-.130-. which may vary for some chemicals by year and by individual sample..100-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. Survey Geometric mean (95% conf.210 (..gov/pesticides/.S.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 .N-Diethyl-meta-toluamide (DEET) CAS No.180 (.140 (. Fourth National Report on Human Exposure to Environmental Chemicals 19 .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 . DEET is not genotoxic.110-. About 3-8% of dermally applied DEET is absorbed. 2002). but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. population from the National Health and Nutrition Examination Survey.130-.110 (<LOD-.140) < LOD .160) < LOD .110-. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.1.100 (<LOD-. 2002).130) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . One survey detected DEET in 74% of sampled streams in the U.. 2005). 134-62-3 General Information N. Its use is recommended for prevention of several vector-borne diseases.170 (.110 (<LOD-.120-. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.120-. EPA. DEET can be applied to clothing and the skin to repel biting insects. < LOD means less than the limit of detection.449 and 0. DEET has low acute toxicity.100-.520) < LOD .EPA.240) < LOD .epa. DEET is not registered for use on agricultural commodities. 1998).140) < LOD .180) < LOD . 2003). (U.180 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.110 (. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.130-.270) 688 678 518 700 598 956 Limit of detection (LOD.250) < LOD .220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .130 (. DEET is not a developmental or reproductive toxicant in animals (U.S.170 (.140) < LOD .220 (.110 (.150) < LOD . Urinary N.N.130-.100-. After absorption. (Kolpin et al.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.130 (. Neurological effects in humans.S.S. and it has not been rated by IARC or NTP with respect to human carcinogenicity. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.N-Diethyl-meta-toluamide (DEET) N.130 (.110 (.180 (.110 (. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.EPA.100-. Additional information is available from U.130) < LOD . and they range in concentration from 4% to 100%. DEET is also used in combination with dermal sun screens (U.

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 .93) < LOD .330 (.250) < LOD .370-. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.190 (.390-.S. In this survey period.410 (.200 (. 20 Fourth National Report on Human Exposure to Environmental Chemicals .270) < LOD . Biomonitoring studies on levels of DEET provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEET than are found in the general population.290-.410 (.480 (.140-. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.190 (<LOD-.370) < LOD ...230-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1992).350) < LOD .640 (.320 (.500 (.270-.410-.250 (.250-.170-.130 (<LOD-. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.630) < LOD .270 (.S.190-.230-.330 (. Survey Geometric mean (95% conf.280 (.270 (<LOD-.230) < 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 .N.440) < LOD .320) < LOD . 2007). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240-.150) < LOD .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.350) < LOD .300 (.240) < LOD .150-.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Urinary N.280-1.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .580) 964 1191 1013 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .190 (.490) < LOD . Urinary DEET levels as high as 5. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC. population from the National Health and Nutrition Examination Survey.350-. 2005). representative subsamples from NHANES 2001-2002.

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

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

2/4/09 Ouchi K. MacLusky. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP).niehs. Chung MK.102(19):7014-7019. and Hajszan. Lynch BS. 2/4/09 Fujimaki K. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Available at URL: http://ecb..14(2):149-157. Reidy JA. Available at URL: http://cerhr. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. and other organic wastewater contaminants in U. Koh WS. Watanabe C. National Institutes of Health. Furukawa M. Fujii S.pdf . Han SS. Sottas CM.35(2 Pt 1):238-254. National Institute of Environmental Health Sciences. bisphenol A glucuronide. Environ Sci Technol 2002. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Belgium. Calafat AM. Human Health. Twomey K.jrc. 1999-2000: a national reconnaissance. Yang M. Gray GM. Environ Health Perspect 2005. Tyl RW. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Regul Toxicol Pharmacol 2002. Barber LB.S.116(1):39-44.Environmental Phenols References Akingbemi BT. Rubin C. Klinefelter GR. Occup Environ Med 2002.nih.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. 4. and Hardy MP.137(3):353-362.pdf. Marr MC. Caudill SP. Toxicol Sci 2002. Brussels. November 26.. Bisphenol A.145:592-603. Biochem Biophys Res Commun 2003. 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. September. McConnell EE.Scientific Committee on Toxicity. Proc Natl Acad Sci USA 2005. Cohen JT. C. Bradley S. Watanabe S. Needham LL. Available at URL: http://cerhr. Kawamura N. August 2001. Barr DB.eu/ health/ph_risk/committees/sct/documents/out156_en. Serizawa S.pdf . Hughes C. 2002.. Kolpin DW. Ispra. Joskow R. Barr JR. Arakawa C. Howdeshell KL. 2/4/09 European Commission. Ye X. Ema M. Tsugane S. Szigeti-Buck. T. Available at URL: http://ntp.S. Shin HC. Imai H. Calafat AM. Pharmaceuticals. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. niehs. et al.149:988-994. Kim YH. 2007. European Commission. K. Leranth. 5: 505-523. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Kuklenyik Z. Calafat AM. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Zacharewski TR. Park S. Pyo MY.59(9):625-628. Ekong J. Brine DR. 2008. Hlywka JJ. In vitro and in vivo interactions of bisphenol A and its metabolite.pdf. Life Sci 2001.36(6):1202-1211. DirectorateGeneral Health and Consumer Protection.nih. Yoshinaga J. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Cunha G. Timms BG. streams. J Am Dent Assoc 2006. Hum Ecol Risk Assess 2004. Meyer MT. Endocrinology 2004.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. et al. Hara K. NC.113(4):391-395.gov/chemicals/bisphenol/bisphenol. Richter CA. Myers CB. Kim CS. Ikka T. vom Saal FS. niehs. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. An evaluation of the possible carcinogenicity of bisphenol A to humans. Haighton LA.europa. Reprod Toxicol 2001. Matthews JB. Gender differences in the levels of bisphenol A metabolites in urine.10:875-921. with estrogen receptors alpha and beta. Ecotoxicity and the Environment (CSTEE). N. Hanaoka T. Endocrinology 2008. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. National Toxicology Program. Cha SW. Needham LL.pdf.780(2):365-370. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. hormones. Italy. Rat two-generation reproductive toxicity study of bisphenol A. Nippon Eiseigaku Zasshi 2004. Munro IC.gov/chemicals/bisphenol/BPAFinalEPVF112607.J. Han SY. Rhomberg et al. 2003.69(22):2611-2625.68(1):121-146. Thomas BF.S. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Research Triangle Park. et al. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.nih. May 22.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. Keimowitz AR. Kroes R. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Kiguchi M. Thurman EM. Chem Res Toxicol 2001. Harazono A. U. Exposure of the U. Zaugg SD.59(4):403-408. Doull J. Koulova AI. Furlong ET. Kim JC. Joint Research Centre Institute of Health and Consumer Protection. Wong LY. Needham LL. Environ Health Perspect 2008. Barton L. Available at URL: http://ec.312(2):441-448. Reidy JA. Department of Health and Human Services. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection.

Csanady GA. Biological monitoring of bisphenol a in a Korean population. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Nagel SC. III.147(6 Suppl):S56-69. Vom Saal FS. Environ Res 2007. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Sheldon LS. Lordo RA.113(8):926-33. Hughes C. An observational study of the potential exposures of preschool children to pentachlorophenol. Kawamoto T.44(4):546-51. Lee SM. Chuang JC. Endocrinology 2006. bisphenol-A. Environ Health Perspect 2005. Dekant W. Morgan MK. and nonylphenol at home and daycare. Chang SS. Jang JY. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. et al. Wilson NK. Kim SY.40(7):905-12. Witorsch RJ. Filser JG. Food Chem Toxicol 2002. Colnot T. Large effects from small exposures. Yang M. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature.Environmental Phenols Volkel W.15:12811287. Chem Res Toxicol 2002. Welshons WV.103(1):9-20. Arch Environ Contam Toxicol 2003. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. vom Saal FS.

Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.30) 1.600-1. and through manufacturing waste streams (Warhurst. In rats. Disposition in humans has not been studied sufficiently.500) . and impaired spermatogenesis (e.600) .50) .70 (1.600-1. have demonstrated estrogenic effects particularly when injected at high doses in animals. and the polyethoxy chain may consist of up to 50 ethoxy units. 2004). 1997. Saito et al.500) ..80 (1. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. population from the National Health and Nutrition Examination Survey.60) 613 652 1092 Limit of detection (LOD.600-1. Less frequently.500-1.300 (<LOD-.. 1995.20) 314 715 1488 03-04 03-04 * * . to shorter chain alkylphenol ethoxylates.Environmental Phenols 4-tert-Octylphenol CAS No. 1996).. see Data Analysis section) for Survey year 03-04 is 0.10-2.30 (1..90) 2.40) 1. 34 Fourth National Report on Human Exposure to Environmental Chemicals .20-2.40) 2.700-1.30-2. In 1999-2000. Several alkylphenols. textiles.477) .20-2. pesticides. impaired steroidogenesis. orally administered 4-tert-octylphenol was well absorbed.300-. streams in 30 states (Kolpin et al. 2000.40) * 03-04 03-04 03-04 .10 (.200-..268-. the various alkylphenols have also been used as emulsifiers and modifiers in paints.S.00 (.900 (.60) .30 (1.300 (<LOD-.600-1. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams. 2003.60-3. Bian et al.3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.30) 90th 1.30) 2.500) . is used to manufacture alkylphenol ethoxylates. and from contact with some personal care products and detergents. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.10 (1.10 (.400) 1. testicular atrophy.80) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50) 1.300 (<LOD-..50-2.900 (. altered estrus cycles and reproductive outcomes.900 (.20) 2. Indoor and to a lesser extent. 2002). including 4-tert-octylphenol.30 (1.20-2.50 (1.70 (1..1. an alkylphenol.g. During the 1980s and 1990s.60-3.60-3.300 (<LOD-.60-3. 2006. which may vary for some chemicals by year and by individual sample. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).80 (1. Blake and Boockfor.369 (. Ying et al. did not bioaccumulate..70 (1.60) 1. 2002). The alkylphenol ethoxylates enter the environment through human use of products containing them.60-3. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.00 (.357 (.30 (. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.20-2.80 (1.600) .500 (.40 (1.299-. which are anionic surfactants used in detergents.600-1.50) 1. In the 1990s.507) * < LOD .00) 1229 1288 03-04 03-04 03-04 * .40) 1. The alkylphenols can bioaccumulate in some fish.50-3.90) 2. and was quickly eliminated from the blood (Certa et al.400 (.497) * . outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.200-.2.500-1.300 (<LOD-. leading to inhalation as another potential exposure route (Rudel et al.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.600) 1.20-2..50) .00 (1.900 (.60-3.S.10) 2.50) 1.20) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th . industrial cleaners.5% of 139 U. over 500.800-1.40) 2.20-2.10) 1.500) 75th .30 (1. altered neonatal sexual development. Survey Geometric mean (95% conf. 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. Katsuda et al. Laws et al.400 (. and some personal care products. Urinary 4-tert-Octylphenol (4-[1. and to alkylphenoxycarboxylates. 140-66-9 General Information 4-tert-Octyphenol. fish) and drinking water.400 (. 4-octylphenol monoethoxylate was detected in 43.389 (. and some of their degradation products are toxic to aquatic life.600) . 2000.20) 1.274-..000 tons of alkylphenol ethoxylates were produced annually worldwide. < LOD means less than the limit of detection. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.600-1.70 (1.g.900 (. through sewage.300-.20 (1. and emulsifiers.

207-. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.14) 314 713 1487 03-04 03-04 * * .280-.00) 2.43) 1.270 (.620) .. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.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 .59 (1. Nagao et al.269 (.384) * .85 (1. Survey Geometric mean (95% conf. at lower or environmentally relevant doses (Blake et al.400) . Biomonitoring studies on levels of 4-tert-octylphenol provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 4-tert-octylphenol than are found in the general population.40-4.06 (2.25-2.Environmental Phenols Myllymaki et al. nonylphenol.370 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 35 .25) 90th 1.41) .1.65-3.S.890-2.435 (..11) 2.160-. Kawaguchi et al. In a small number of adult Japanese volunteers.460 (.31-2. Tyl et al. population from the National Health and Nutrition Examination Survey. 1999). 2004).29) 2.420) .67-2.470-1.40 (1.00) 2. 2003. Sweeney et al.71) 2.380 (<LOD-.17 (.81 (1.S.450) 1.68-2.00) 1.450) .15) 1.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.640-1.20 (1.73) 2.50 (2.500-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.610) .10-2.910 (.349) * < LOD .00 (.78 (1.33) 3. 2001). It is unclear if estrogenic or other effects occur in animals through oral dosing.730-1.03 (1.54) * 03-04 03-04 03-04 .78) 1228 1286 03-04 03-04 03-04 * . Calafat et al. 2004.560) .337-. IARC and NTP have not rated octylphenol.18-4. 2005.850 (.860 (.31 (1.36-3. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.630-1. or their corresponding ethoxylates with respect to human carcinogenicity.410 (.740 (.3.320 (<LOD-.62 (1..96-4.00 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.25) 2.170-.550-1. representative subsample of NHANES 2003-2004. 4-tert-Octylphenol is not considered directly genotoxic.02-4.11) 1.59) 1. 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.570) .43) 1.53-3. 2001.22) .24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.540-1.620-1.68) 2.08) 1.276 (.05-2..03 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary 4-tert-Octylphenol (4-[1.62) .270 (.11-2..470-1. 2000.64 (.300 (<LOD-.76 (2.270-. Yoshida et al.770 (.43-3.62 (1.03-6.530) .78) 3.260 (<LOD-.740 (.199-..470) 75th .33 (2.60 (1.

Yoshimura S.36(6):1202-1211. Ono H.18(1):43-51. Pharmaceuticals. Regul Toxicol Pharmacol 1999. McCoy GL. Blake CA. Raychoudhury SS.37(20):4543-53. Environ Sci Technol 2002. et al. prolactin. alkylphenols.S. Warhurst AM. testis size. Yoshimura Y. Inoue K. Reprod Toxicol 2001. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats.121(1):21-33. Estrogenic activity of octylphenol. polybrominated diphenyl ethers. Inoue K. Nicol L. Myers CB. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Okada F. Sakui N. Toxicol Sci 2000. Taya K. Meyer MT. Kolpin DW. Food Chem Toxicol 2006. Muller AM. Bolt HM. 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.57(2):255-266. Bodman GJ. Izumi S. streams. Wiegand HJ. Yoshida M. Kawaguchi M. Xu L. Yoshida M.folliclestimulating hormone. Toppari J. and other organic wastewater contaminants in U. and other endocrine-disrupting compounds in indoor air and dust. Indoor Air 2004. Ferrell JM. Chen J. Kawaguchi M. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Toxicol Lett 2001. Nair-Menon JU. Haavisto TE. Paranko J. nonylphenol. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.uk/resource/reports/ethoxylates_alkylphenols. Nagao T. Taya K. Roche JF.44(8):1355-1361. Camann DE. Tyl RW. et al. Exposure of the U. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Nakagomi M. Maekawa A. Environ Health Perspect 2008. Boockfor FR. Boockfor FR. Furlong ET. 1999-2000: a national reconnaissance. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol.15(6):683-692. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Laws SC. 2/4/09 Ying GG.207(1):59-68. Spengler JD. Takenaka A.30(2 Pt 1):81-95. Environ Int 2002. Ye X. Williams B. An environmental assessment of alkylphenol ethoxylates and alkylphenols. and testosterone. Katsuda S. Brooks AN. Ito R.pdf. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry.116(1):39-44. Reprod Toxicol 2004. Available at URL: http:// www. Watanabe G. Qian J.foe. Needham LL. Environ Sci Technol 2003. 2003.28(3):215-226. Toxicol Appl Pharmacol 2000. Rudel RA.141(7):2667-2673. Endocrinology 2000. and sertoli cell number.54(1):154-167.799(1):119-125. Certa H. Anal Chim Acta 486:41-50. Zaugg SD. 1995. hormones. Thurman EM.71(1-2):112-122. bisphenol A and methoxychlor in rats. Marr MC. Karjalainen M. Arch Toxicol 1996. Kookana R.14(5):325-332. Myllymaki SA. Watanabe G. Makino T. Blake CA. Katsuda S. Usumi K. Takai N. et al. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Carey SA. Sweeney T. Barber LB. Calafat AM. et al. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Cooper RL. Wang X. Seto H. Saito I. Fail PA. Onuki A. Indoor air pollution by alkylphenols in Tokyo. Toxicol Appl Pharmacol 2005.co. Wong LY. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Biol Reprod 1997. Saito Y. Brody JG. Two-generation reproduction study with para-tert-octylphenol in rats. Reidy JA. Song L.Environmental Phenols References Bian Q. Phthalates. Horie M.S. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Fedtke N. Korn LR.165(3):217-226. Maekawa A. Seely JC. Millette CF. Brine DR. pesticides.

and wound disinfection solutions. Calafat et al.. Fourth National Report on Human Exposure to Environmental Chemicals 37 .. streams sampled in 30 states (Kolpin et al. representative subsample of NHANES 2003-2004.2 µg/L was comparable to the median level (8.. General population exposure results from dermal and oral use of products containing triclosan. Triclosan is not considered teratogenic at maternally toxic doses. Some reports show endocrine effects are observed in amphibians and fish (Foran et al. acne medications. Lyman and Furia. Biomonitoring studies on levels of triclosan provide physicians and public health officials with a reference values so that they can determine whether people have been exposed to higher levels of triclosan than are found in the general population. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al. 2004).Environmental Phenols Triclosan CAS No.S. 2007. Calafat et al. and has also been impregnated into some kitchen utensils.. toys. Veldhoen et al. a process that can result in the formation of small amounts of 2. 1976. 2007). 2000).. but not by race/ethnicity and sex. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent. 1996. (Sandborgh-Englund et al. 2000. 2008).. Biomonitoring Information Urinary triclosan levels reflect recent exposure.6% of 139 U.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al. 2002). 1969). 2005. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. it has low acute toxicity.8-dichlorodibenzo-p-dioxin (Aranami et al.. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. Triclosan has been added to soaps. It can be photochemically and biologically degraded.. In animal studies.. IARC and NTP do not have ratings with respect to human carcinogenicity. Triclosan can be absorbed across skin into the blood stream.. In a U. toothpastes.S. mouthwashes. It acts by inhibiting bacterial fatty acid synthesis. Triclosan enters the aquatic environment mainly through residential wastewaters. In the body it is conjugated to glucuronides and sulfates (Bodey et al.. Moss et al.. the median urinary triclosan level of 7. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. In animal and human studies. 1987). deodorants. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard. triclosan was found in 57. Triclosan formulations may rarely cause skin irritation. Matsumura et al. and medical devices.. 2007).. 2008 has shown higher levels during the third decade of life and among people with the highest household income. 2007. young girls.. Triclosan has a low bioaccumulation potential in fish. 2006). In 1999-2000. Mezcua et al. In a study of 90 U. 1988.

89-11.2 (13.0-15.7 (9.S.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.6-20.2) 13.2-14.2) 12.3 (26.4) 7. interval) 13.6-111) 33.8-112) 30.6) 39. population from the National Health and Nutrition Examination Survey.3-67.9 (33.8) 116 (39.94 (7.20 (7.54 (8.6-65.1 (45.5) 66.90-10.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6) 10.2) 9.86-12.1) 14.0) 49.0) 9.0 (34.4-18.48 (8.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.74 (5.32-14.30-14.1) 9.55 (4.8) 14.6 (12.10-9.80 (5.0-19.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.40-11.1-39.1) 50.7) 10.3) 6.50-10.70-16.50) 10.9 (50.0-213) 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 .38-18.20-10.7) 123 (36. see Data Analysis section) for Survey year 03-04 is 2.3) 10.4 (32.4) 51.8-127) 37.8) 7.21 (6.7 (11.6 (10.1) Selected percentiles ( 95% confidence interval) Sample 95th 368 (294-463) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.7 (14.9) 8.3.2 (11.2 (25.6) 90th 212 (172-241) 03-04 03-04 03-04 9.92-12.10) 84.4) 90th 249 (188-304) 03-04 03-04 03-04 8.4 (38.1) 9.00 (4.6) 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 9.8-63.8 (21.18 (5.8) 9.29-12.3 (9.7 (28.1) 13.22-10.2-58.7) 292 (151-432) 132 (78.5-86.0 (11. Survey Geometric mean (95% conf.60 (8.9) 32.8-60.5) 13.3) 47.9-61.4. interval) 12.11-11.3 (8.6 (30.1) 7.6-14.0 (26.1) 9.20-11.5) 20.4-19.0-15.2-46.6) 31. Survey Geometric mean (95% conf.93 (7.S.20-13.9) 7.0 (36.2 (10.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.7 (39.3-31.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 (8.4) 25.1) 11.Environmental Phenols Urinary Triclosan (2.16 (6.45-10.9-236) 193 (90.6-37.82 (8.72-13.4 (11.3-15.4) 357 (225-456) 203 (87.1 (15.8-85.0 (8.9) 75th 47.0) 65. population from the National Health and Nutrition Examination Survey.4) 317 (231-433) 144 (96.6-14. Urinary Triclosan (2.4.1) 9.48-10.20 (7.6 (9.0-73.40-17.5) 11.4) 73.2-58.43-13.4 (12.2 (37.6) 12.9 (11.9 (8.3-35.5-14.45 (5.00-8.60 (6.2 (27.45-13.5 (11.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.3 (11.4) 75th 43.6-15.

Matsumura N. Ekstrand J.24(3):209-218. Bodey GP. Aranami K. Photolytic degradation of triclosan in freshwater and seawater. Hirano M. Percutaneous penetration and dermal metabolism of triclosan (2.7/2. Larson EL. Kaneshima H. Williams FM. Gomez MJ. Hong HC. Shiratsuchi H. Leonard PA. Environ Health Perspect 2007. Food Chem Toxicol 2000.17(5):637-644. streams.28(9):1748-1751.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples.4. J Toxicol Environ Health A 2006.83(1):84. Biol Pharm Bull 2005. 4. The oral retention and antiplaque efficacy of triclosan in human volunteers. Lyman FL.38(2):64-71. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. 1999-2000: a national reconnaissance. hormones. Veldhoen N. Hernando MD. Chelimo C. Urinary concentrations of triclosan in the U. Ye X.. Toxicology of 2. Odham G. Arch Environ Contam Toxicol 1988. Mezcua M. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis).116(3):303-307. Ishibashi H. Barber LB. Meyer MT. Anal Chim Acta 1004. Environ Sci Technol 2002. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Pinney SM.67(4):532-537.S. et al. Wong LY. Furia T. Wigmore H. 4’-trichloro-2’-hydroxydiphenyl ether. Watanabe N. Triclosan: applications and safety. Bhargava HN. Pharmaceuticals. Levy SB. Wolff MS. Gilbert RJ. Fernandez-Alba AR. et al. Katsura E. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Moss T. J Invest Dermatol 1976. Erratum in: Aquat Toxicol 2007.115:116-121.36(6):1202-1211. Kolpin DW. Sandborgh-Englund G.524:241-247. Pilot study of urinary biomarkers of phytoestrogens. Kanetoshi A. population: 2003-2004. Foran CM. Reidy JA.69(20):1861-1873. Ebersole R. Windham G. and other organic wastewater contaminants in U. Bennett ER. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Mar Environ Res 2000. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Nagao Y. phthalates.66:1052-1056. Skirrow RC. Zaugg SD. et al. Adolfsson-Erici M.45 Suppl 2:S137-S147.80(3):217-227. Gunderson MP. Aquat Toxicol 2006. Br J Clin Pharmacol 1987. Teitelbaum SL. Am J Infect Control 1996. Furlong ET. Okui T. Needham LL. Clapson DJ. Thurman EM.50(1-5):153-156.23(5):579-583. Evidence of 2.4’-trichloro-2’hydroxydiphenyl ether). Pharmacokinetics of triclosan following oral ingestion in humans. and phenols in girls. Aguera A. Calafat AM. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Readman JW. Howes D.38(4):361370. et al. Britton JA. IMS Ind Med Surg 1969. Osachoff H.Environmental Phenols References Aiello AE. Benson WH. Chemosphere 2007. Environ Health Perspect 2008. Ferrer I.S. Ogawa H. Williams PE.

70) 2.33-2.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .37) .48-2.75) 2. with repeated or chronic exposure.47-5. and dermal contact with PCP-treated products. herbicide.10 (1.350-.630 (.350) 90th .67) 1. population from the National Health and Nutrition Examination Survey.350 (.350) < LOD . PCP has been detected in soils.350-.00) 1.350 (.350-.73 (1.350) < LOD .350) < LOD . PCP is distributed to most tissues and is not extensively metabolized.390 (..64) 1. 40 Fourth National Report on Human Exposure to Environmental Chemicals .350-1. the elimination half-life may be a week or more (Uhl et al.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .60) 1. Kohli et al.00 (.350-.58-2..30 (. PCP cannot be used on wood in residential or agricultural buildings.350-.01 (<LOD-1.76) 1.94 (1.350 (..90 (1.54-2.990-2.350) < LOD .65 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.350) < LOD .350-2.350 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.23 (.350) < LOD < LOD 75th .350) . 1997). To-Figueras et al.25 and 0.350 (.42) 696 680 521 696 603 951 Limit of detection (LOD.37 (.650 (.350 (.350-1.350-.480-2.350) < LOD .60) 1. water and sediments because of the large amounts that were produced and used historically.53) size 1994 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .350-. and possibly of lindane (IPCS.58-2.350 (.350 (.350-.650) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08-3.5.350-. along with small amounts of tetrachlorohydroquinone and conjugates.960) 1. Survey Geometric mean (95% conf. are eliminated in the urine.350-2.350-.91 (1.. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation. < LOD means less than the limit of detection. PCP is absorbed rapidly and well by all exposure routes.00) 2. Acute.350 (.770 (.48 (. and metabolic acidosis were observed in CAS No.350) < LOD . General population exposure to PCP may occur by inhalation of contaminated air. air. PCP is eliminated over a few days (Braun et al.500-2. After absorption.350-. other polychlorinated benzenes.350-2.350-.350) < LOD .30 (.30) 1. bactericide.09) .90) 2.10 (.350-1.350-.680-1. plants.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .350) < LOD .350-.98 (1.350-.510-3.350 (.47-3.350-1.860-2.980 (.45-2.62 (. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.350) < LOD .350-2.30) 1.350 (.00) 1.350 (. 1979).890 (.10) 1. utility poles and fence posts).350) < LOD .350 (.350-2. mollusicide.18 (<LOD-1.530) 1.350 (..10 (<LOD-1.350-.40 (. 1976.350 (.350 (.350) < LOD .10) 1.32 (.350-.350-.04) 1.350) < LOD .350 (.350 (. Human exposure to PCP has become less common. Effects including hyperthermia. The parent compound and conjugates. Since 1984.350) < LOD .660 (.350-.890-1. 2002.350 (. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.90) 1. algaecide and insecticide.g.350) < LOD .S.78) 1. After a single dose. and it is used primarily as a preservative for wood to be used outdoors (e.350 (.80) . PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.S.990 (<LOD-2.350-.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. hypertension.350-.94 (1.390 (. 1986). In the environment.83 (2.70) .30) .65 (.76) .350 (.350) < LOD . PCP use in the U.850-2. PCP is degraded by sunlight and metabolized rapidly by microorganisms.50) 1.510-5.350-. and animals. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. so it is relatively non-persistent.590-1.30 (1. has been restricted. ingestion of contaminated food or water.51) 1.33) . which may vary for some chemicals by year and by individual sample.

830) < LOD .320 (.360 (.08 and 5.30 (. 2003).36) .400 (.40) 1. or skin absorption.590) < LOD .30) 1.56) 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.html.19) 2.260 (.300 (.75 (<LOD-2. children in the 1980’s.560-. OSHA has established an occupational standard.300 (. van Raaij et al.700-2.330-. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2. 1991).35-2.52) 1.78) 1. chronically administered high doses of PCP were hepatotoxic. EPA at: http://www.320) < LOD < LOD 75th .950-1.630 (.570 (.560) < LOD .380-.850 (.240-.00-1. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.S.epa.67-2.900-1.30) 1.35) 1.09 (<LOD-2. respectively) (Seifert et al.500-1.57 (1.370 (.430) < LOD .95) 3.34 (.92) 1. 2004.29-3..08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.gov/ toxpro2.26 (1. population from the National Health and Nutrition Examination Survey.52 (<LOD-1.40) 1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .340-.55) 1.35-2.25) 1.990 (.950-1.280) < LOD . environmental levels) and health effects is available from the U. In a small sample of U.250 (.94 (1..40-2.16 (. inhalation.560) < LOD .21-2.320) < LOD .67-3.220-.16-1.S. 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. 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.0 mg/L.780) < LOD .19) 2.760 (.gov/ pesticides/ and from ATSDR at: http://www.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . The U.73 (1. Death can result from seizures and cardiovascular collapse.220-.650 (.40) 1.67 (1.610 (. carcinogenic.910-1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.500 (.25-2.10-2.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.84-4.440 (. Fourth National Report on Human Exposure to Environmental Chemicals 41 .cdc.67 (1.9 mg/L. 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 (4.78) 1.e.25 (1.300 (.S. Pentachlorophenol is not mutagenic or teratogenic.6 and 14.290-.75) 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. respectively) (Becker et al.84) 1.18 (1.00-1.270-.79) 1. In animals.83 (1.82 (1.360-.67-3.atsdr. More information about external exposure (i.06) 1.82) 1.94 (1.67 (1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .19) 2.590-1.13 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.800) < LOD 1.06-3.490) < LOD .710-1.730) < LOD ..800-1.67 (1.52 (1.350) < LOD .290) < LOD . EPA has developed standards for PCP in drinking water and the environment.18) .21 (.650) 90th 1.920 (.48-2.Fungicides adults and children severely exposed to PCP through ingestion.90) 1.52 (<LOD-1.320) < LOD .250 (.35) 1.S.. 1995). 1989).10 (1.430-.270-.84 (1.51) 1.06 (.67 (1..57 (.26 (1.09) size 1994 2527 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .EPA. Survey Geometric mean (95% conf.69 (1..310-..94-3.580-.650 (.25-2.290-.420) < LOD . 2003). 1989).310) < LOD .25 (1.30-2.510-.00) 1. 2000). Among adults in the NHANES 1999-2000 subsample.40) 1.470 (. and the FDA has established a standard for bottled water.19 (1.950-1.09-1.25-1.780-1.510-.11) 2.500-. In NHANES 2001-2002 subsamples..40) 1. and adversely affected thyroid function (U.

Schulz C. Seifert B. Can J Biochem 1976. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Jones D. Blau GE. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Gregg M. Bragt PC. Arch Environ Contam Toxicol 1989. et al. Arch Environ Contam Toxicol 1989.org/documents/jmpr/jmpmono/2002pr08.58:182-186.S.inchem. Sala M. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Schulz C. Chenoweth MB. Dev Toxicol Environ Sci 1979. htm. g o v / f d m s p u b l i c / c o m p o n e n t / main?main=DocketDetail&d=EPA-HQ-OPP-2004-0402. Safe A. Smith SJ. et al. Shealy DB. Toxicology 1991: 67(1):107-16. van den Berg KJ. urine. Needham LL. Notten WR.S. Phillips DL.105(1):78-83. Available at URL: h t t p : / / w w w.10:552-65. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. International Programme on Chemical Safety (IPCS). Hill RH Jr. Hill RH Jr. Holler JS. Seiwert M. To T. available at URL: http://www. 11/30/2004. Seifert B. Seiwert M. house dust. Santiago-Silva M. Becker K. Baker S. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Braun WH.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. drinking water and indoor air. Uhl S. Fast DM.4:289296. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Barrot C. 206:15-24. Schmid P. Biomonitoring studies on levels of PCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of PCP than are found in the general population. 4/21/09 van Raaij JA. 2002. Krause C. hair. Environ Res 1995. Head SL. Bailey SL. Helm D. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. PCP: Human Risk Characterization [online].18(4):469-474. Needham LL.54(3):203-208. To-Figueras J. U. Lindane. Otero R. References Becker K. Pesticide residues in urine of adults living in the United States: reference range concentrations. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. The metabolism of higher chlorinated benzene isomers. Hill RH. Schlatter C. Environmental Protection Agency (U.71:99108. Cline RE. Environ Health Perspect 1997. Engel R. Kaus S. J Expo Anal Environ Epidemiol 2000. Pharmacokinetics of pentachlorophenol in man. Arch Toxicol 1986.18:475-481. et al. Rodamilans M. Int J Hyg Environ Health 2003. r e g u l a t i o n s . 4/21/09 Kohli J. EPA).

sodium ortho-phenylphenate (SOPP).40-2. Timchalk et al.389-.402-.60 (1.696) * .20) < LOD 2.S.50-3.570-1.500-2.85) 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 . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.80) 1.00 (1.466 (.820 (.50) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.890) 1.88) 1.50) < LOD .410-.540-2. fungicides.10 (1.493 (.80-3. interval) . Available evidence suggests that OPP does not accumulate in the body.00 (1.450 (<LOD-.790) 2. and sanitizers.770 (.742) * .349-. General population exposure can occur via dermal.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .20 (1.00) < LOD .50-2.17 (.10 (1.690) < LOD .580-1. but OPP and SOPP are still used on pears and citrus (U. 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.600) < LOD 75th .386-. 2002.EPA.19 (.470 (<LOD-.20) < LOD 1.20-3. Workers who manufacture.90) 2.710-2. Both have been used in agriculture to control fungal and bacterial growth on stored crops.497 (.50) .670) 2.830 (. Cnubben et al.30) < LOD . it was used in home sanitizers for surfaces.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .610-1.10) 2. formulate.508 (.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.890 (. SOPP is applied topically to the crop and then rinsed off.630) < LOD .22 (. 1998). and as a wood preservative. Most agricultural food applications have been revoked.80 (2.970 (.10-1.50 (1. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.570-.389-.90) .Fungicides ortho-Phenylphenol CAS No.20 (1.636) * . OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al. on ornamental plants and turfs. 2006). Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.450 (<LOD-.30) < LOD 1.90) 1.30-2. leaving the chemical residue OPP.80) 1.370-.760-2.60 (1. Estimated human intakes have been below recommended intake limits (U.836) * .3.370-.638) * .930 (.600) < LOD 1. EPA. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.750-2.07 (. < LOD means less than the limit of detection.60 (1.800-3. OPP is still used as a disinfectant fungicide for industrial applications.600) < LOD .10) .EPA.570 (.00 (1.621) * .S.490 (<LOD-.20) 2.509 (. such as fruits and vegetables.40 (.85) 2.550-1.600-1.490 (<LOD-.690-1. or apply these chemicals may be more highly exposed than the general population.740 (..50-4. OPP is considered to be moderately toxic after acute oral doses in animal studies.570-2. 90-43-7 General Information Ortho-phenylphenol (OPP.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 ..50) < LOD .390-. however.30-7.10) 1.40-5. Fourth National Report on Human Exposure to Environmental Chemicals 43 . small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.27 (.20-2.3 and 0. In the past.40-7.00) .433-.520 (.40-5. 1989).370-.567 (.600-1.350-1.. whereas SOPP is not volatile and is more water soluble. Survey Geometric mean (95% conf. 2006).33 (.10) .560-8.552 (. Both chemicals degrade within hours to weeks in the environment (U.S.780) < LOD .50 (1. 2006). inhalational.840-1.450 (<LOD-.00-2.50) < LOD .28 (.490 (<LOD-.00) .76) 1.14 (<LOD-3.90) .61) 2.890 (.640) < LOD .30) 1.850 (.570 (.496 (.28-3.34) 1. and it has limited water solubility. population from the National Health and Nutrition Examination Survey.03) 1.09) 2.10) .624) * .490 (<LOD-.30) < LOD 90th 1.S.880-2. are antimicrobial agents used as bacteriostats. or 2-phenylphenol) and its water-soluble salt. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.22) 2.645) * .480-1.90 (1.498 (.610 (.20 (.00 (1.950) < LOD .590-2.10) 1.60-3.600) < LOD . 1998.770 (. which may vary for some chemicals by year and by individual sample.90 (1.860 (.600-1.02) 1. OPP is volatile.490 (<LOD-. 2006).23) 695 680 520 695 603 953 Limit of detection (LOD.60-2.50 (1.30 (1.10-2.92 (.364-. in paints.420 (<LOD-.710) 3.

900) < LOD .18) 2.00 (1.97 (2.360 (<LOD-.860 (. Murata et al.84 (1. 2002.61 (1.270-.62) .750-2.32) 1. IARC has classified SOPP as a possible human carcinogen.38) 1.4) 3.910-1.361-. Ito et al.. Volunteers exposed to 0.970) 1. Bomhard et al.11 (.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.780 (.620-1.508) * .01) 1.656) * . 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.496 (. 1997.590) * .24-2. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel. 2000.29) 1. Biomonitoring Information Urinary OPP levels reflect recent exposure. leading to production of two metabolites.780-14.27) < LOD .93) .21) 1.12) < LOD 1.86 (1.11 (..640-1.880-1. 1992.17 (. 1984.666) * .455-.93) .81) 1.791) * .550-.89 (1.06 (1. reproductive.09-3.403-.47) .38-3.514 (.560-2. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .S.980 (<LOD-1.EPA 2006). Zhao et al.09 (1.311-.444 (.990) < LOD .380 (..93 (1.480-. Smith et al.484) * .07) 2.59) .329-.353-.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 .17) 2.470) < LOD .02 (.810) < LOD ..670 (.08-1.00 (.750 (.810-1..96 (1..25-6.46) < LOD 1. but no neurologic. Detectable levels were seen in over half the U.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .EPA 2006).S.860 (.61 (. and it has classified OPP as not classifiable with respect to human carcinogenicity. less likely.75 (1.78 (2.420 (<LOD-.05-2. 2005.32) 3.26) 1.440 (. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.58) 2.43-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.248-.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.40-13. by possible genotoxic mechanisms (Hagiwara et al.S.453 (.64 (2.510 (<LOD-.61 (2.385 (.91 (1.38) 2. CDC. Pathak and Roy. population from the National Health and Nutrition Examination Survey.770-2.550) < LOD .gov/pesticides/.910 (<LOD-1.44 (1.610) < LOD 1. In high dose animal studies.28 (<LOD-4. OPP was not found to be mutagenic.580) < LOD .Fungicides anemia. or.17 (.11) < LOD 90th 1.600-1. 1999. Brusick. 2005).52 (..38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .670 (. or developmental toxicity was observed (Bomhard et al.750 (.51-3.473) * .59) 1.568) * . 44 Fourth National Report on Human Exposure to Environmental Chemicals .410 (<LOD-.43 (1.650-1.382 (.21 (.580-1.88-4.04-4.510-.06-5.560) < LOD 75th .53) 1.29) 1.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.500) < LOD . U.910 (.69 (1. 1993.620-1.. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.epa. interval) .570) < LOD 1.343 (. 2002.291-.33-2.24-2. Kwok et al.96 (1. 1984.410 (<LOD-.28 (2. Additional information is available from U.840 (.06-4.43-2.74 (1.96-4. 1998.13) 1.900-1.800-1.. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated..670) < LOD . 1999. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.420 (<LOD-.31) < LOD .0) 1.93) 1. 2005).08) 1.S.08-2.11) 4.11-1. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.980 (.43) 3. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect. U.950) < LOD .550 (.20) < LOD 3. 1986).75 (1. Nakagawa et al.301-.320 (<LOD-.EPA at: http:// www.12-2.690 (.940-2.33) .21-2.470 (<LOD-.460-. 2002).S.96) 1.09-6.

Christenson WR. Hagiwara A. St John MK. Inoue S. Comparative metabolism of orthophenylphenol in mouse. Moriya K. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Brendler-Schwaab SY. Centers for Disease Control and Prevention (CDC). March 1986. Hakkert BC. Gierthy J. 2005. Meuling WJ. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Cano M. Toxicol Appl Pharmacol 1998. Richter M. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers.50(11):3351-3358. National Toxicology Program (NTP). 4/9/09. Atlanta (GA).703(12):97-104. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Zhao S. Cnubben NH. Bartels MJ. Eadon G. Ito N. Stanley JS. Roberts AL. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Elliott GR. Kawanishi S. Sangha G. EPA 739 R-06004. Identification of SARA compounds in adipose tissue. Shibata M. 4/13/09 Onstot JD.22(10):809-814. Turteltaub KW. Hagiwara A. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Kwok ES. 90-43-7) in Swiss CD-1 mice (dermal studies). Fourth National Report on Human Exposure to Environmental Chemicals 45 . Hum Exp Toxicol 1998. Ito N. Nakagawa Y. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Herbold BA..286(2):309-319. Murata M. Brusick D. Selim S. 1989. van de Sandt JJ. Environ Mol Mutagen 2005. J Agric Food Chem 2006. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. Christenson WR.20(5):851-857. Mutat Res 1993. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Bromig KH. Bartels MJ.35(2 Pt 1):198-208.EPA). Bomhard EM.159(1):18-24. Crit Rev Toxicol 2002. Third National Report on Human Exposure to Environmental Chemicals. et al. Eastmond DA. Environmental Protection Agency (U. Coelhan M. Brzak KA. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Arnold LL. Pathak DN. Available at URL: http://www. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol.gov/oppsrrd1/REDs/ phenylphenol_red.74(2):61-71. J Chromatogr B Biomed Sci Appl 1997. Bartels MJ. Bormett GA. Xenobiotica 1998. U.28(6):579594.45(5):460-481.32(6):551-625. Bartels MJ.pdf. Environmental Protection Agency (U. The carcinogenicity of the biocide ortho-phenylphenol. Vogel JS. Toxicol Appl Pharmacol 1999. Smith RA.Fungicides References Appel KE. Imaida K. EPA-560/5-89-003.S. Fukushima S.niehs. Drugs.17(8):411-417.150(2):402-413. Moldeus P. EPA).gov/ntp/htdocs/LT_ rpts/tr301. Glas K. Sangha GK. Roy D. Shirai T. Timchalk C. Mendrala AL. McNett DA. J Agric Food Chem 2002. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. et al. Regul Toxicol Pharmacol 2002.nih. Timchalk C.S. IARC Sci Publ 1984. 2006. Arch Toxicol 2000. Freyberger A. Tayama S. Available at URL: http://ntp.epa.(56):399-407. July 28.pdf. Food Chem Toxicol 1984. Buchholz BA.43(7):14311437. Moore GA. O-phenylphenol and its sodium and potassium salts: a toxicological assessment.S. Leser KH. Biochem Pharmacol 1992.S. U. Fukushima S. rat and man. Hirose M. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Narang A. Office of Toxic Substances. Carcinogenesis 1999.54(16):5731-5735.

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

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

population from the National Health and Nutrition Examination Survey.S. population from the National Health and Nutrition Examination Survey. < 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.Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. see Data Analysis section) for Survey year 01-02 is 0. which may vary for some chemicals by year and by individual sample. 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.1. 48 Fourth National Report on Human Exposure to Environmental Chemicals . 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. Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.

Environ Health Perspect 2003. et al. Kinney PL. Tinwell H.24(10):1003-1012.S.EPA): http://pmep. Sanderson WT. epa.Herbicides References Ashby J. Whyatt RM. Centers for Disease Control and Prevention (CDC). Green T. Environmental Protection Agency (U. Comparative metabolism and elimination of acetanilide compounds by rat. J Expo Anal Environ Epidemiol 2005.37(4):10881093. Deddens JA. Kier L. and other herbicides in rivers. J Agri Food Chem 1989.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Environ Sci Technol 2005. Alavanja MC.39(17):6561-6574.15(9):702-735.html. 2000. Environ Health Perspect 2000. Davison KL.cce.pdf. Furlong ET.S. Hsiao JJ. Curwin BD. et al.248(2-3):115-122. Hladik ML. Larsen GL. Casida JE. Linhart SM. Wratten SJ. Occurrence of sulfonylurea. Battaglin WA. EPA 738-R-00-009.11(4):353359.111(5):749-756. Federal Register: January 24. Reynolds SJ. Volume 65. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Peter CJ. Feil VJ. Lefevre PA. Coleman S. Available at URL: http://www.17(6):559-566. Camann DE. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Number 15.S. Ward EM. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. acetochlor.cornell. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Thurman EM. Sci Total Environ 2000. Rose RL. Roberts AL. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. 2005. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. U. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Hines CJ. et al. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Sci Total Environ 2000. Bravo R. EPA). Striley CA. Atlanta (GA). Hein MJ. imidazolinone. Barr DB. Environmental Protection Agency (U. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor.108(12):1151-1157. Jefferies PR. Wilson AG. Olsson AO. Barr DB. March 2006. 1998.S. 5/30/06. Third National Report on Human Exposure to Environmental Chemicals.S. pages 3682-3690. Acetochlor (Harness) Pesticide Petition Filing 1/00. Andrews HF. Linderman R. J Expo Sci Environ Epidemiol 2007. Hum Exp Toxicol 1996. Xenobiotica 1994.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Quistad GB. Dialkylquinonimines validated as in vivo metabolites of alachlor.248(2-3):123-133. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Kolpin DW. Barr DB. Hodgson E. and metolachlor herbicides in rats. sulfonamide. EPA).15(6):500-508. Available at URL(non U. reservoirs and ground water in the Midwestern United States. 5/30/06 U. Burkhardt MR. Feng PCC. Heederik D. Barr JR. Chem Res Toxicol 1998.

.EPA. 2003). though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. but shows little bioaccumulation. IPCS. 1996. 1998. 1996. whereas 60% of applicators had detectable amounts. It is absorbed by plants and inhibits plant protein synthesis. General population exposure to alachlor may occur through consumption of contaminated food or drinking water.EPA. 1995). Since the late 1980s alachlor use has been declining. 1998). Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. alachlor has demonstrated hepatotoxicity.. as measured through conversion to deethylamine. Alachlor has low potential for acute toxicity. EPA at: http://www. USGS. formulators. Hines et al. 1999 and 2007. 1995. hemosiderosis. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. but has not shown developmental or reproductive toxicity in mammalian systems (U. 2003). Tessier and Clark. the dermal exposure route is potentially significant for applicators.EPA. In animals. and uveal degeneration. 2005). 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.S. 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. 2000. Hladik et al. but not likely at low doses. 1998). 1994. WHO. WHO. Additional information about is available from U. mean values of urinary concentrations of alachlor metabolites.S. In a study of applicators and workers exposed to alachlor. 1996).EPA.EPA. In animal studies. corn cropland was treated with alachlor. (2003) showed that 2. Alachlor has a soil half-life of a few weeks. U.. 1998. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. WHO. but another metabolic pathway can produce 2. 2000. stomach. 1989. about 20-25% of the U. 2003).. the latter may account for some observed effects (Davison et al. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. 2005.. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure..1 to 1. Estimated human intakes have been below recommended limits (U. WHO. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine.1 mg/L at various collection times (Sanderson et al. Hill et al.. Feng and Wratten. mercapturate conjugates were predominant metabolites. 1998). 1997.6-diethylaniline and its reactive metabolite..Herbicides Alachlor CAS No. 50 Fourth National Report on Human Exposure to Environmental Chemicals .gov/pesticides/. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. In 1993-1995. NTP and IARC do not have ratings regarding human carcinogenicity. Alachlor itself is not considered mutagenic. Because it can be absorbed through skin.S. 2003). In chronic animal testing. U. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al.. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. ranged from 0.S. 1998.EPA considers alachlor to be a probable human carcinogen at high doses. soybeans. 1999. and field workers. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. peanuts and other crops. 1988.S.epa. Jefferies et al.S.S. 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. U. Kolpin et al. and on non-crop land for general weed control. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. U.S. including corn.

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

47(6):503-517. Reregistration Eligibility Decision (RED) Alachlor. 4/2/09 U. 2003. World Health Organization. Lau H. Striley CA. An evaluation of the carcinogenic potential of the herbicide alachlor to man.php. Alachlor in Drinking-water. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. World Health Organization (WHO). Atlanta (GA). Sci Total Environ 2000. Martens MA.248(2-3):123-133. Casida JE. ALACHLOR. Supplemental Technical Information (available on-line only). Xenobiotica 1994.org/documents/pds/pds/pest86_e. Hum Exp Toxicol. March 2006. EPA).gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Feil VJ. Hines CJ. Thake DC. Roberts AL. imidazolinone.S. Environ Health Perspect 2003. Erratum in: Life Sci 1989. Hull RD. revised February 15. 1997. Environmental Protection Agency (U. Sanderson WT.S.inchem. Life Sci 1988.56(9):883-889. Geneva. Geological Survey (USGS).43(25):2087-94. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Sacramento. Deddens JA. Clark JM. Tessier DM.htm. 2/27/09 U. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor.24(10):1003-1012. 1998. EPA 738R-98-020. Dialkylquinonimines validated as in vivo metabolites of alachlor. 2/27/09 Jefferies PR. Casida JE. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. and other herbicides in rivers. 1992-2001. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Thurman EM. Quistad GB.pdf. Kier LD. Shealy DB. Thelin GP.S. Burkhardt MR. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Heydens WF. Driskell WJ. Bull Environ Contam Toxicol 1996. Am Ind Hyg Assoc J 1995. 1996. Background document for development of WHO Guidelines for Drinking-water Quality. acetochlor. et al. Hines CJ. Whyatt RM. Larsen GL.gov/oppsrrd1/ REDs/0063. No.S. Furlong ET. Casida JE.Herbicides References Battaglin WA. Camann DE. DNA adduct formation by alachlor metabolites. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Available at URL: http://www. Kolpin DW. 2007. California. Davison KL.11(4):353359. Brown MA. December 1998. Available at URL: http:// www. Quistad GB. Mutat Res. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. 2005.111(5):749-756. Available at URL: http://www. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor.44(18):1325. Centers for Disease Control and Prevention (CDC). Biagini RE. Feng PCC. reservoirs and ground water in the Midwestern United States.usgs. who. Peter CJ. Barr JR.248(2-3):115-122. Third National Report on Human Exposure to Environmental Chemicals. Linhart SM. Kinney PL. Wilson AG. WHO/ FAO Data Sheets on Pesticides.43(9):2504-2512.18(6):363-391. Occurrence of sulfonylurea. J Agri Food Chem 1989. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Hill RH Jr.37(4):10881093. Kimmel EC. Jefferies PR. Comparative metabolism and elimination of acetanilide compounds by rat. Hill AB. 1999. Ann Occup Hyg 2003. et al. 86. International Programme on Chemical Safety (IPCS). Kolpin DW. Tolos W.395(2-3):159-171. Circular 1291. 1999. MacKenzie B.pdf. Wratten SJ. Geological Survey (USGS).39(17):6561-6574. Sci Total Environ 2000. Hsiao JJ. 98-4245 (by Barbash JE. Hladik ML. Chem Res Toxicol 1998. Barr DB. Environ Sci Technol 2005. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. J Ag Food Chem 1995.epa. U.56(6):853-859.int/water_sanitation_health/dwq/chemicals/en/alachlor. and metolachlor herbicides in rats. Henningsen G. Biagini R. sulfonamide. Shoemaker DA. Brown KK. Available at URL: http://water. Gilliom RJ). Andrews HF. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.

S. It is also used as a non-selective herbicide. which have half-lives of several months. metabolized. Atrazine has limited water solubility and is not tightly bound to soil. 1912-24-9 General Information Atrazine is a widely used chlorotriazine herbicide that acts against broadleaf and grassy weeds.EPA.S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1878 2477 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 449 568 639 809 790 1100 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 919 1162 959 1315 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 676 498 684 550 918 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample. In soils.S. For the general population. 1993).and post-emergence to agricultural land for crops such as corn and sorghum. Applicators of atrazine may be exposed dermally and by inhalation. Catenacci et al.. it is one of the more commonly detected pesticides in surface and ground waters (USGS. 2005.S.. glutathione conjugation appeared to be the major route of biotransformation. all of which act by inhibiting plant photosynthesis. Hayes et al. Survey Geometric mean (95% conf. atrazine is slowly degraded to dealkylated products.Herbicides Atrazine CAS No. 2003a). but estimates of seasonal intakes from drinking water in a small number of communities have exceeded the recommended limits (U. and cyanazine. U. It has little toxicity in birds and moderate toxicity in some fish and aquatic invertebrates. 2003b).. < LOD means less than the limit of detection. 1990).EPA. 2003b). drinking water is an infrequent source of atrazine exposure. 1996. atrazine use has progressively been restricted in an effort to reduce surface and ground water contamination. Atrazine was first registered as an herbicide in 1958. Fourth National Report on Human Exposure to Environmental Chemicals 53 . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. More than 70 million pounds have been applied annually in recent years.EPA. 2007). 2002.3. Timchalk et al. Atrazine mercapturate products accounted for a major proportion of human urinary metabolites (Lucas et al. with about 75% of corn cropland receiving treatment. 1993.. Atrazine is applied pre. and then eliminated in the urine over a few days (Bradway et al. Bacteria and plants can metabolize atrazine to hydroxyatrazine.791 and 0. Atrazine may alter the sexual development of frogs at environmental levels (Gammon et al. 1982. population from the National Health and Nutrition Examination Survey.. Related chlorotriazine herbicides include simazine. Urinary Atrazine mercapturate Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. The dealkylated chloroatrazine metabolites. U. Atrazine does not bioaccumulate. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Atrazine is well absorbed orally.. resulting in atrazine mercapturate and N-dealkylation products (IPCS. As a result. propazine. In regions where atrazine is used. In animals and humans. but it is leachable into ground and surface waters.

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

References Adgate JL. 3/11/09 Laws SC. In the NHANES 2001-2002 subsample. Toxicol Sci 2003.43(2):155-167. Lucas AD. Mendoza M. Gillis JH. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Hermaphroditic. Barr DB.64(9):672-678. Aldous CN. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Ann Occup Hyg 2003. Chen H.. Maroni M. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Laws SC. Hines CJ. Stoker TE. Barr DB. Moseman RF. Biagini RE.. Bersani M. 82. Curwin BD. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Eldridge JC. Toxicological profile for atrazine. Eldridge JC.61(4):331-355. Sanborn JR. Toxicol Sci 2000. Schmid J. Wetzel LT. Collins A. Simpkins JW.atsdr. 3/11/09 Arcury TA.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. In small studies of Maryland residents in 19951996 (MacIntosh et al. et al. Tapia J. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Catenacci G.99(8):5476-5480. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Stoker TE. Toxicol Lett 1993. Barr DB. 2001 [online]. Barbieri F.47(6):503-517. et al. 1996. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.115(8):1254-1260. Tyrey L. Sanderson WT. Seiber JN. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products.76(1):190-200. Pfeifer KF. 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.gov/toxprofiles/tp153.109(6):583-590. Lee M. Cooper RL. A risk assessment of atrazine use in California: human health and ecological aspects. Lioy PJ. 2005). Stoker TE.69(2):217-222. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). 1993)..inchem. Noriega N. Atlanta (GA).org/documents/pds/pds/pest82_e. 2007). The geometric mean of urinary atrazine mercapturate was 1. Cooper RL. Extrom PC. Breckenridge CB. Freeman NC. Goodrow MH. atrazine was detected in only four children (Arcury et al. McElroy WK.. Vonk A. Available at URL: http:// www. In a study of 60 farm worker children. Proc Natl Acad Sci USA 2002. Carr WC Jr. Deddens JA. Geneva. Wetzel LT. Striley CA. In a small number of field workers. Ferrell JM.. 2000). Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.html. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Jones AD. et al. Environ Health Perspect 2001. Ferioli A. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect..58(2):366-376. Bradway DE. Hein MJ. Brown KK. Pest Manag Sci 2005.30(2):244-247. Stevens JT. World Health Organization. Hayes TB. Centers for Disease Control and Prevention (CDC). Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.15(6):500-508.43(2):155-167. J Expo Anal Environ Epidemiol 2005. Steroids 1999. Quandt SA. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Shoemaker DA. International Programme on Chemical Safety (IPCS). ATRAZINE. Gillis JH. J Toxicol Environ Health 1994. 2005. levels of atrazine mercapturate were generally not detectable (CDC. Perry et al.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al.htm. Agency for Toxic Substances and Disease Registry (ATSDR). et al. et al. Goldman JM. Saiz SG. 2003. Cooper RL.. Eberly LE. Reynolds SJ.cdc. J Agric Food Chem 1982. Available at URL: http://www. WHO/ FAO Data Sheets on Pesticides. Biological monitoring of human exposure to atrazine. J Toxicol Environ Health 1994. 2005). Toxicol Sci 2000. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Gammon DW. Clayton CA. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Fleenor-Heyser DG. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Ferrell JM. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Environ Health Perspect 2007. Blewett C. No. 2001). Grzywacz JG. Heederik D. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Third National Report on Human Exposure to Environmental Chemicals. Stuart AA.53(2):297-307. diamino-S-chlorotriazine and hydroxyatrazine. et al. Cottica D.

Delzell E. Office of Prevention.9(5):494-501. Hammerstrom KA. Available at URL: http://water. Environmental Protection Agency (U. Interim Reregistration Eligibility Decision For Atrazine. Geological Survey (USGS). Lansbergen GW. MacIntosh DL.S. EPA Office of Pesticide Programs. A longitudinal investigation of selected pesticide metabolites in urine. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Toxicol Appl Pharmacol 2004. March 2006. 6/1/09 U. J Toxicol Environ Health A 1999.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Washington (DC). Ann Epidemiol 2000. Cooper RL. Stoker TE. Breckenridge CB.10(7):479. Sathiakumar N. Perry M. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Kastl PE. 1992-2001. Available at URL: http://www.61(1):27-40. Crit Rev Toxicol 1997. Laws SC. U. Available at URL: http://www. Stoker TE. Dryzga MD. Langvardt PW. Ryan PB. Stevens JT. EPA). 0062. May 2003a.epa. Singzoni B. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .pdf.58(1):50-59.S. Sanderson JT. A review of epidemiologic studies of triazine herbicides and cancer. Guidici DL.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Supplemental Technical Information (available on-line only). Dagenhart D. Pesticides and Toxic Substances. Circular 1291.S. J Expo Anal Environ Epidemiol 1999. White paper on potential developmental effects of atrazine on amphibians. Toxicol Appl Pharmacol 2002.php.epa. Cooper RL. Laws SC. Environmental Fate and Effects Division. Guidici DL. Toxicology 1990. A risk characterization for atrazine: oncogenicity profile. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. 2003b. Tortorelli J. Wood C. Rayner JL. Case No. Environmental Protection Agency (U.usgs. EPA). The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. 3/11/09 U.gov/oppsrrd1/REDs/ atrazine_ired.67(2):198-206. Boerma J. Osborne DW. 2007. Timchalk C.27(6):599612. Chem Res Toxicol 1993. Fenton SE.S.182(1):44-54.56(2):69-109.195(1):23-34. van den Berg M. Pesticides in the Nation’s Streams and Ground Water.Herbicides development of a biomarker of exposure.6(1):107-116. Wetzel L. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Needham LL. Toxicol Sci 2000. Toxicol Sci 2002. Christiani D. revised February 15.pdf.S. The Quality of Our Nation’s Waters.

890 (.4-D can be applied either as an aqueous salt or as oil-soluble esters.560-1. General population exposure to 2.560-.420-.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.80) 1. 1974. headache. 2..400) < LOD . renal and hepatic injury.930-1.330 (.910) < LOD .310) < LOD .730 (.27 (1. abdominal pain. by direct contact with agricultural and residential areas after applications. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.21) 1.690 (.210 (<LOD-.420) < LOD .13) < LOD .4-D were used in the U.250 (<LOD-. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.70) 1.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .43) 1.550-1.952 and 0.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . in 2001 (U.05-2. Sauerhoff et al.55 (1.27 (.660) 1.08) < LOD . 94-75-7 General Information Widely used throughout the United States.690 (.40) 1. Recent estimates of chronic intakes of 2. 2004). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4-D have been below recommended intake limits (U.10) < LOD 1.S.30 (<LOD-2.EPA.310 (..890) < LOD .490 (. hypotension.24 (.20 (. 1989. nausea.EPA in 1948.07 (. agricultural. 4-D. It is not well absorbed through the skin.740 (.S. 2007).48) < LOD 1.32 (1.S. It was first registered with U.60) 1. It is poorly bound in soils.680-1.490) < LOD < LOD < LOD .20 (<LOD-1. it acts as a plant growth hormone.320) 90th .350) < LOD < LOD < LOD .230-.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .10 (<LOD-1.. with a half-life of several days to several weeks.910) 1.4-D) controls broadleaf weeds in residential. and mecoprop). Kohli et al. 2005).02-1.4-Dichlorophenoxyacetic Acid CAS No.370-.4-D may occur during residential applications. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. Similar to other chlorophenoxy herbicides.810-1.Herbicides 2. but at higher levels they are herbicidal.4-D has low acute toxicity.10 (<LOD-1. Human health effects from 2. 1977).210-.03) 695 659 520 668 589 892 Limit of detection (LOD.260 (<LOD-.4-D or exposed for prolonged periods.S.00-2.760 (.S.690-1.230 (<LOD-. dizziness. and by consuming food or drinking water contaminated with 2.27-2. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 57 .EPA.4-D is rapidly absorbed via oral and inhalation routes.440-1.2.960-1. At low levels. 2. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.540-.250 (<LOD-. and aquatic environments.4-dichlorophenoxyacetic acid (2. As much as 62 million pounds of 2.16) < LOD .670-1.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. the chlorophenoxy herbicide 2.37) size 1977 2413 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD . Once absorbed. It is rarely detected in ground waters (USGS. and delayed Urinary 2. myotonia.66) < LOD 1. MCPA.22) < LOD .410) < LOD .51 (1. these herbicides can enhance plant growth. 2. 2.930 (.610 (.610-. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.690 (.

U.S.740 (. 1980.610-.990-1.17 (.19) .580-. Biomonitoring Information Urinary levels of 2. 58 Fourth National Report on Human Exposure to Environmental Chemicals . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. population from the National Health and Nutrition Examination Survey.380 (<LOD-.4-D reflect recent exposure. Pearce and McLean. 2005).620-.550-.350 (<LOD-.680) < LOD .700 (. 2004). liver.73) .270-. 2.41 (1.330-. 1995.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .4-D levels were detectable in less than a quarter of the individuals studied. Additional information is available from U.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 . Acute high doses administered to laboratory animals produced ataxia.16) 1. 2001.. Average post-application urinary levels of 2.480 (.340 (. 1996. 2005.S. 1985. 2005).4-D does not have significant reproductive.670 (<LOD-1.890-1. Hill et al.720 (. 1992). 1989).780 (. 2002.24) 1.380) < LOD .13 (..660) < LOD .14 (. 2.. CDC. The acid and salt forms of 2.epa.35) < LOD . 2002. 2005). 2005).39) < LOD 1. population (Hill et al.EPA. Epidemiological studies have reported associations of several types of cancer. 1996.. eyes. 2. 1996.S. Frank et al.570) < LOD ..32 (<LOD-2.S.08 (. other exposures.590 (<LOD-1.930-1. thyroid.790) 1.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.490 (. developmental.780) ...380-. IPCS. or to contaminants in the herbicide formulations (specifically 2. U. and evidence of histological injury to the kidneys. 2005. Post-application levels in farmers and home gardeners were dependent on Urinary 2. 1995).27-1. Kutz et al.S.05) . Survey Geometric mean (95% conf. In previous samples of the U.EPA.610-. 2003. 2005. 2006.920) < LOD 1.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. and of adults and children (Baker et al. It is unclear whether these associations are related to the chlorophenoxy herbicides.340-. myotonia. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.640 (. urinary 2.4-D production plant workers and a few forestry workers spraying 2.890) < LOD 1.780-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.08 (.S.560-..13 (.590 (<LOD-1. in small samples of children (Hill et al..390) < LOD < LOD < LOD . 2005. Knopp et al.660 (.820-1. U.470) < LOD .790) < LOD . such as soft tissue sarcoma and non-Hodgkin’s lymphoma.810-1.56) . adrenals and gonads (NTP. U.670 (. or teratogenic effects in chronic rodent studies (Charles et al.EPA at: http://www.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .7.4-D are eye irritants.810-1.850) < LOD .670 (.410) 90th .410) < LOD 1.380 (<LOD-.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .520-.Herbicides neuropathy (Bradberry et al. IPCS.980) < LOD 1. 1994). IPCS.EPA.EPA 2005).410) < LOD < LOD < LOD .gov/pesticides/. 2000).3.410 (<LOD-.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. Kolmodin-Hedman and Erne..560-.S. IOM. 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.440 (.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.270 (<LOD-. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.08 (.

Sanderson WT. Crit Rev Toxicol 2002. Garabrant DH. Scand J Work Environ Health 2005. 2003. Hanley TR Jr. International Programme on Chemical Safety-INCHEM (IPCS).4-dichlorophenoxyacetic acid in man.. National Toxicology Program (NTP). Developmental toxicity studies in rats and rabbits on 2. Forestry workers involved in aerial application of 2. Acquavella JF.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 2.4-D than levels found in the general population.4-D). the number of acres to which it was applied (Curwin et al. 2005.php?record_id=10603. Baker BA. References Arbuckle TE.4-D. Chapman P.4-D and 2. Available at URL: http:// www. Beeson MD. Alexander BH.10(6 Pt 2):789-798.32(4):233-257. Updated March 7. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC.S.4. Murphy RS.4:318-321. Baker S. Survival and Growth Curves from NTP Toxicity Studies.4-D in urine does not mean that the level of the 2. Bailey SL. Biomonitoring of herbicides in Ontario farm applicators. Centers for Disease Control and Prevention (CDC). Shealy DB. Arnold EK.31 Suppl 1:90-97. Hill RH Jr. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Arch Toxicol Suppl 1980.org/documents/jmpr/jmpmono/v96pr04. Occup Environ Med 1994.31(2):121-125. Biomonitoring studies of 2. Absorption and excretion of 2. Driskell WJ.4-D were highest in the farmers who applied the 2.60(1):121-131.nih. Tandon JS. Sircar KP. 2005). Barr DB. et al. J Environ Sci Health B 1992.. Exposure of homeowners and bystanders to 2. Kutz FW. Finding a measurable amount of 2. Veterans and Agent Orange: update 2002. Environ Res 1995. Biomonitoring for farm families in the farm family exposure study. Atlanta (GA). Mandel JS. Campbell RA.4-D will result in an adverse health effect. Honeycutt R. J Expo Anal Environ Epidemiol 2000.Herbicides the time since application. 2005).5-T). Bus JS. Reynolds SJ. Review of 2. Harris SA. Arch Environ Contam Toxicol 1989. Heederik D. Available at URL: http://ntp. and the use of protective clothing or equipment (Arbuckle et al. Mandel et al. Smith SJ. Assessment of exposure to 2. the amount of pesticide applied. Head SL.4-. To T. Brody D. Erne K. Selected pesticide residues and metabolites in urine from a survey of the U. Tables. general population. Kohli JD. Philbert MA. et al.4:427-435. Baker SE.4-Dichlorophenoxyacetic Acid). 3/17/09 Institute of Medicine (IOM). Available at URL: http:// www. geometric mean urinary levels of 2.4:97-100.71(2):99-108. Washington (DC): National Academies Press..niehs.. Cook BT.4-dichlorophenoxyacetic acid (2. 3/17/09 Knopp D. Dichlorophenoxyacetic acid. Arch Environ Contam Toxicol 1985. J Toxicol Environ Health 1992.15(6):500-508. Ripley BD. Hill RH Jr. Pesticides residues in food: 1996 evaluations Part II Toxicology. Barr DB.18(4):469-474. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. TOX-63 Peroxisone Project (2.31 Suppl 1:98-104. Frank R. 2. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Dhar MM. Cole DC. Carter-Pokras OD. Estimation of occupational exposure to phenoxy acids (2. Gupta BN. Fast DM. et al. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .4-D) epidemiology and toxicology. Toxicol Sci 2001.gov/index. Ritter L.edu/catalog. Pesticide residues in urine of adults living in the United States: reference range concentrations.nap.51(3):152-159.4-D): exposure and urinary excretion. TOX-63: TOXICITY REPORT CURVES. In farm families.27(1):23-38. Kolmodin-Hedman B.inchem. Khanna RN. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Needham LL. Curwin BD. Third National Report on Human Exposure to Environmental Chemicals. Stephenson GR. Sirons G J. Solomon KR. van Ravenzwaay B. Board on Health Promotion and Disease Prevention. 914. Xenobiotica 1974. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Gregg M. Vet Hum Toxicol 1989.htm.37(2):277-291.4 dichlorophenoxyacetic acid (2. 2006. J Expo Anal Environ Epidemiol 2005 Nov. 1992). Harris et al. Wilson RD. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.4-dichlorophenoxyacetic acid and its forms. Holler JS.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Beasley VR. Hein MJ. 2005. Scand J Work Environ Health 2005. Needham LL. 2005 Charles JM.4-dichlorophenoxyacetic acid (2.

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

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

62 Fourth National Report on Human Exposure to Environmental Chemicals .S. population from the National Health and Nutrition Examination Survey.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.670 (<LOD-. Survey Geometric mean (95% conf.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. see Data Analysis section) for Survey year 01-02 is 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 830 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-. 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 . Survey Geometric mean (95% conf.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .240) 679 701 957 Limit of detection (LOD. Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. which may vary for some chemicals by year and by individual sample.S.440 (<LOD-.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2.200 (<LOD-. < LOD means less than the limit of detection.

1999.11(4):353359. 1998. Davison KL.php. Andrews HF. 2007. Sanderson WT. EPA). Environ Health Perspect 2003. Pesticides in U. Barr JR. Jefferies PR.gov/oppsrrd1/ REDs/0001. California. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Casida JE.111(5):749-756. Linderman R. Atlanta (GA).S. Environmental Protection Agency (U. Gilliom RJ). Burkhardt MR.39(17):6561-6574. streams and groundwater. World Health Organization (WHO). March 2006. Coleman S. et al. Hsiao JJ. Available at URL: http://www. 6/1/09 Whyatt RM. Reynolds SJ. Wratten SJ. Dialkylquinonimines validated as in vivo metabolites of alachlor. Biagini RE. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. acetochlor. and metolachlor herbicides in rats. usgs. Supplemental Technical Information (available on-line only). Geological Survey (USGS). Rose RL. Chem Res Toxicol 1998. 98-4245 (by Barbash JE.108(12):1151-1157. reservoirs and ground water in the Midwestern United States. Quistad GB. and other herbicides in rivers. Hein MJ. April 1995.15(6):500-508. Linhart SM. Sci Total Environ 2000. Comparative metabolism and elimination of acetanilide compounds by rat.S. Furlong ET. Occurrence of sulfonylurea. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.248(2-3):123-133. 2005. Kolpin DW.S. Brown KK. Reregistration Eligibility Decision (RED) Metolachlor. Ann Occup Hyg 2003. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Alavanja MC. Barr DB. et al. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Heederik D.pdf.epa. sulfonamide. Available at URL: http://water. Sci Total Environ 2000. Gillion. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.37(4):10881093. Centers for Disease Control and Prevention (CDC).S. Thurman EM. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://water. Barr DB.ESTfeature_gilliom. revised February 15. Hladik ML. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Shoemaker DA. Kinney PL. U. R. Environ Sci Technol 2005.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.int/water_sanitation_health/dwq/chemicals/ metolachlor. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. 4/2/09 U. Peter CJ. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.248(2-3):115-122. 1992-2001. Ward EM. Roberts AL. Camann DE.usgs. Xenobiotica 1994. Environ Sci Technol 2007. 3/26/09 U.pdf 3/30/09 Hines CJ.who. Available at URL: http://water. Hodgson E. J Agri Food Chem 1989. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.41:3409-3414. Feil VJ. Curwin BD. Thelin GP. 2003.Herbicides References Battaglin WA. Environ Health Perspect 2000. Larsen GL. J Expo Anal Environ Epidemiol 2005. Geological Survey (USGS).html. Available at URL: http://www.gov/nawqa/pnsp/pubs/files/051507. Sacramento. Metolachlor in Drinkingwater. Circular 1291. Kolpin DW. Feng PCC.24(10):1003-1012. imidazolinone.S. EPA 738R-95-006. Deddens JA. Striley CA.gov/nawqa/ pnsp/pubs/wrir984245/text.47(6):503-517.usgs. Background document for development of WHO Guidelines for Drinking-water Quality.pdf.

4.2 and 0.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.4. but higher levels are herbicidal. the general population is unlikely to be exposed to it. with an elimination half-life of approximately 19 hours (Arnold et al.4. and concern about contamination with 2. At low levels. Epidemiological studies have reported associations of several types of cancer. Mohammad and St. and delayed neuropathy (Bradberry et al.7.5-T was once applied as either an aqueous salt or as an oil-soluble ester.4. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. Given the commercial unavailability of 2. 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. dizziness.4.4-D were used as defoliants in the Vietnam War (e.5-T is eliminated mostly unchanged in the urine. nausea. it is not well absorbed through the skin.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4..5-T. ranging from several weeks to many months. headache.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. Nelson et al.5-T use as a herbicide in 1985.. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.4. 2. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2.4. < LOD means less than the limit of detection. The half-life of 2. Ester forms of 2. 2004). renal and hepatic injury. 1992..S. 2.4. 2007). Agent Orange).4. 1989. which may vary for some chemicals by year and by individual sample. myotonia. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.5-T degrades to 2. 1974). 1986.4.. 93-76-5 General Information 2.4..5-trichlorophenol and other degradates..4. abdominal pain.5-T and 2. Chlorophenoxy herbicides act as plant growth hormones.5-T has been rarely detected in ground waters (USGS. Although 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. these herbicides can enhance plant growth.3.5-Trichlorophenoxyacetic acid (2.4. Omer.4.1. Kohli et al. Human health effects from 2. 2.5-T in soil varies with conditions. hypotension.5-T (Holson et al. 64 Fourth National Report on Human Exposure to Environmental Chemicals .4. Once absorbed into the body.5-Trichlorophenoxyacetic Acid CAS No.g.Herbicides 2.5T is rapidly absorbed via oral and inhalation routes. 1992).

2005).4. 2003.EPA at: http://www. Mean urinary levels of 2.Herbicides or contaminated herbicides.4. in which urinary levels of 2. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. Finding a measurable amount of 2. Biomonitoring studies on 2.3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. Urinary 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. similar to results of NHANES II (19761980).4. Fourth National Report on Human Exposure to Environmental Chemicals 65 . 1980).epa. U. 2002.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.4.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.. 2.5-T does not mean that the level will result in an adverse health effect. population from the National Health and Nutrition Examination Survey.7. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.gov/pesticides/. other exposures.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.5-T also were below the limit of detection (Kutz et al.S.5-T were generally below the limit of detection. IOM.4. Additional information is available from U.4.4. or to contaminants in the herbicide formulations (specifically 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. 2005.5-T itself is not mutagenic.5-T than levels found in the general population. Pearce and McLean.5-T reflect recent exposure.EPA. 2004). IPCS.S. 1996. 1992).4. Survey Geometric mean (95% conf. Biomonitoring Information Urinary levels of 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. It is unclear whether these associations are related to the chlorophenoxy herbicides. urinary levels of 2.

Mohammad FK. Arch Int Pharmacodyn Ther 1974. Scand J Work Environ Health 2005. Neurobehav Toxicol Teratol 1986.4. Environmental Protection Agency (U. Pesticide industry sales and usage . Available at URL: http://www. Nelson CJ. 3/17/09 Institute of Medicine (IOM).5-trichlorophenoxyacetic acid (2.23(2):65-73. Sircar KP.4-. Murphy RS.19(2):298-306. Absorption and excretion of 2.4. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.org/documents/jmpr/jmpmono/v96pr04.epa. discussion 5-7. International Programme on Chemical Safety-INCHEM (IPCS).4. Proudfoot AT.5-T in four-way outcross mice. Multireplicated dose-response studies with technical and analytical grades of 2. Cook BT.4.5-trichlorophenoxyacetic acid (2. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Vet Hum Toxicol 1989. II. Holson JF.EPA).inchem.4.5-T).5-T). Agricultural exposures and non-Hodgkin’s lymphoma. Washington (DC): National Academies Press.htm. Fundam Appl Toxicol 1992. Arch Toxicol Suppl 1980. Review of 2. gov/oppbead1/pestsales/01pestsales/market_estimates2001. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .31 Suppl 1:1825.4:318-21.EPA. Gaines TB. Estimation of occupational exposure to phenoxy acids (2. Pesticides residues in food: 1996 evaluations Part II Toxicology.5-t mixture.4-D) epidemiology and toxicology. Toxicol Rev 2004. U. Gupta BN. S.edu/catalog. Brody D. Dhar MM.nap. 3/17/09 Kohli JD.31(2):121-125.4-D and 2.19(2):286-297. general population. LaBorde JB. Gaylor DW. Behavioral and developmental effects in rats following in utero exposure to 2. Tandon JS. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice.4-dichlorophenoxyacetic acid (2. 2004. Veterans and Agent Orange: update 2002. Centers for Disease Control and Prevention (CDC). Available at URL: http:// www.S. Vale JA. Beasley VR. Dichlorophenoxyacetic acid. Selected pesticide residues and metabolites in urine from a survey of the U.32(4):233-257. et al. Garabrant DH.S. Erne K. Nelson CJ.4. Kolmodin-Hedman B.pdf. Gaines TB. McLean D.5-T). Third National Report on Human Exposure to Environmental Chemicals.4. McCallum WF. 2005. Poisoning due to chlorophenoxy herbicides. Sheehan DM. 914.Herbicides References Arnold EK. Developmental toxicity of 2. Washington (DC): U. Board on Health Promotion and Disease Prevention. 2. Office of Prevention Pesticides and Toxic Substances.8(5):551-60. 2003. Developmental toxicity of 2. Available at URL: http:// www. Philbert MA. 210:250-255.4-D/2. Khanna RN. Kutz FW. Carter-Pokras OD.4. St Omer VE. J Toxicol Environ Health 1992. et al. Wolff GL. Crit Rev Toxicol 2002. Bradberry SM. May. I. Fundam Appl Toxicol 1992.S. Pearce N.2000 and 2001 market estimates. Atlanta (GA). LaBorde JB. Holson JF.37(2):277-91.php?record_id=10603.5-trichlorophenoxy acetic acid in man.

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

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

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

1) < LOD 9.070-.060) .054-.048 (<LOD-.1 (13.077 (.100) .150 (.8) 15. Survey years 01-02 03-04 Geometric mean (95% conf.080 (.147 (.5) 19.109-.50) 15.7-22.120-.063-.0 (10.180) .1) 15.80-9.130 (.110-.2) 14. see Data Analysis section) for survey years 01-02 and 03-04 are 10.110 (.140) .8-17.4-18.108-.60-10.9 (14.3 (18.180) .4) 14.6-33.100-.0-25.049-.4) 19. < LOD means less than the limit of detection.9 (13.70 (7.50 (8.4) 539 456 484 487 980 885 Limits of detection (LOD.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.138) .6 (14.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.8 (18.149) .3-21.1) 15.090-.80 (<LOD-10.110) .062 (.00 (8.112) 95th .8-24.064 (.090-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1-18.1-16.10 (<LOD-16.6-24.30 (8.070 (<LOD-. population from the National Health and Nutrition Examination Survey.160 (.062-.90) 90th 15.8-17.139 (. Fourth National Report on Human Exposure to Environmental Chemicals 79 .2) 11.8 (11.0-21.0 (10.100-.086-.1 (18.5) 21.5 (16.160 (.00-14.30 (8.4 (12.096-.1-24.7-19.053 (<LOD-.0) < LOD 9. Serum Dieldrin (whole weight) Also a Metabolite of Aldrin Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.6) 19.5 (<LOD-11.140 (.80-10.2) 15.5-17.5) 15.7 (15.109-.075) < LOD .1-19. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD 9.139 (.064) 90th .4) < LOD < LOD 16.102 (. which may vary for some chemicals by year and by individual sample.090 (. population from the National Health and Nutrition Examination Survey.7) 15.073-.9-23.4-17.9 (12.1) 10.6) 16.7 (14.0) 19.4) 21.138 (.190) .150 (.3 (18.2) 12.0 (11.109 (.8) < LOD 8.103 (.7 (<LOD-15.113 (.6) 9.5 and 7.070) .130-.5-17.130-.059 (.112-.9 (12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-15.8-25.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .080-.103 (.1) 13.1) 14.120 (.4 (12.089 (.117) < LOD .098 (.9-38.110 (.090-.140-.4) 20.110) .056-.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 8.40-9.4) 95th 20.120 (.084-.158) .8.069) < LOD < LOD . 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 . Survey years 01-02 03-04 Geometric mean (95% conf.090 (<LOD-.3 (19.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .110 (.6 (15.093) .0 (15.130) .9 (13.062 (.120 (.3 (14.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.100) .190) .3 (13.170) .130) .2-15.088-.6 (15.100 (.1) 20.9-22.120) .130) .124) .8 (9.242) .100-.8-19.083-.160) .116) .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.054-.6-24.101) . which may vary for some chemicals by year and by individual sample.054-.40-10.147) 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 .0) 21.058) < LOD .130-.080) .055 (.S.077-.S.8) 14.

1991. Brock JW. Teta MJ. Soto AM. Garrett N. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.html.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Corrigan FM. Facca A.66(4):229-234. Serrano FO. Kitzazwa M. Sanchez-Ramos J. Jorgensen T. Academic Press. Song S. 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 Bates MN. Priestly BG. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Olea N. Wienburg CL. McIntosh LJ. VT.9:1357-1367.352:1816-1820. Edwards JW. plasma dieldrin. Aldrin and Dieldrin [online]. 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.cdc. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. 2007 [online]. Available at URL: http://www.59:229-234. Li AA.64-65 Spec. Cox. Kanthasamy A. Eds. Basit A. 15. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Ellis H. Narahashi T. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Mink PJ. Chlorinated Hydrocarbon Insecticides. Hartvig HB.27:405-421. Kanthasamy AG. toxicology. Andersen A. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Part A 2000. Cancer Epidemiol Biomarkers Prev 2000. Fernandez MG. August 2008. Stehr-Green. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Effect of occupational exposure to aldrin on urinary D-glucaric acid.usgs.gov/~dms/ pesrpts. Turner W. No:429-436.gov/ circ/2005/1291/. J Toxicol Environ Health 1989. Demographic and seasonal influences on human serum pesticide residue levels. Vol. are nonestrogenic in transfected HeLa cells. Handbook of Pesticide Toxicology. 1989. Toxicological profile for aldrin/dieldrin [online]. Schulte P. Anantharam V.54:1431-1443. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. J Toxicol Environ Health. Jr. Sonnenschein C. Buckland SJ. bioaccumulation. Inc. Patterson DG Jr.fda. 1992-2001. et al. Pesticides in the Nation’s Stream and Ground Water. Environmental Health Criteria 91. Carlson JN. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Organochlorine exposure and risk of breast cancer. 4/21/09 Jorgenson JL. Lancet 1998. either singly or in combination. PA.109(Supp1):113-139. Int Arch Occup Environ Health 1994. Available at URL: http://www.cfsan. Shore RF.91(1):122-126. and lymphocyte sister chromatid exchange. Rosellini RA. Reprod Toxicol 2000. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Food and Drug Administration (FDA). In Hayes WJ. Chapin RE. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Toxicol Lett 1992. Chemosphere 2004. Mann D.htm. Roy ML. Daniel SE. Finley B.103(Suppl 7):113-122. United States Geological Survey (USGS).gov/toxprofiles/ tp1. Six high-priority organochlorine pesticides. Grajewski B. Exp Neurol 1998.26:701-719.atsdr. September 2002. 4/21/09 Hoyer AP. Smith AG. J Occup Environ Med 2005. Needham LL.150:263-271. Available at URL: http://www. Neurotoxicol 2005. Chung KL. Mumtaz MM. Patterson DG Jr. et al. David VL. Frey JM.html. New York. Environ Health Perspect 1995. Psychopharmacology (Berl) 1987.47:1059-1087. 6/1/09 Ward EM. Grandjean P. Organochlorine insecticides in substantia nigra in Parkinson’s disease. International Programme on Chemical Safety (IPCS). Revised Feb. Available at URL: http://pubs. 2 Classes of Pesticides. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. 731-915. References Agency for Toxic Substances and Disease Registry (ATSDR). Tully DB. Ginsburg KS.org/documents/ehc/ ehc/ehc91.inchem. Jr and Laws ER. Environ Health Perspect 2001. and epidemiology in the United States. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.14:95-102. pp.

1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.6-45.4 (22.7-70.1 (25.2-56.1) < LOD < LOD < LOD < LOD < LOD 8.7-12.9 (11.4 (10.8-23.5) 37. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.8.5-41. and 7.0) 37.5) < LOD < LOD 9.8 (10.3 (27.2) < LOD 11.70 (<LOD-10.S.3 (20.2 (41.8-43.4) < LOD < LOD < LOD 23.89-10. buildings.4) 12.4) < LOD 11. fish.0-67.5-44.6 (9. chlordane was used to kill termites and other insects on agricultural crops.6 (25. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-32.2-49.7) 42.2-28.5-13.2 (10. 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.20-11.0-13.8-33.6) 48.2) 46. 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. which may vary for some chemicals by year and by individual sample.9 (15.4-21.8 (17.7-56.9 (36.6) 9.3-43.8-73. in addition to trace amounts of numerous other related compounds (ATSDR.6 (9.8) 44.6) 49.8-42.3 (26. 2007).90 (8. Until 1988.4 (30.1-65.9 (17.9) 10.1 (27.1-25.5) 21.7 (10.4) 22.4 (31.1) 16.0 (20.82-11.3) 37.10-18. Since 1992.9) 23.2) 36.8 (40.9) 36.4 (35.5 (8.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7 (43.6 (16.0) 27.5 (41.9-42.8-20.7) 28.5-42.9) 11.9) 47.1-50.9 (29. Survey Geometric mean (95% conf.1 (<LOD-12.4-40.0-25.10 (8.37 (8. Consequently.9-38.9) 13.0 (<LOD-12.0-61.5) 56.3 (9.S.5) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 11.3) 10.1) 22.6-24.4) 18.10-11.63 (8. 01-02.4) 29.6) 23.7) 19.7) 9.2) 22.3) 10.5-38.3-49.4 (<LOD-12. respectively.5 (33. 2007).0 (26.69-10..7 (<LOD-32.9 (11.6) < LOD 11.3 (25.5 (34.3) 18.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.74 (<LOD-10.1) * 11.0 (32.8 (17.2) 33.1 (16.7 (34.2) * 12. Chlordane is not currently produced or used in the U.2) 34.2 (37. foods high in fat such as meat.6) 9.1-19.6) 39. 1994).2) 37.7 (<LOD-13.9 (18.2 (9.5) 44.0) 75th 20.8 (18.3-24.1) 30.5) < LOD < LOD < LOD < LOD 13. < LOD means less than the limit of detection.7-25.0-18.2 (39.1 (44.6) 8.9) 17.9) 11.6) 11.1 (20.7-14.6-24.7 (42.9) 39.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.0) 41.8) 52.20-10.1-51.7 (32. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.8-32.4 (30.9-21.8-61.3-32.9) 37.8) 27.1 (40.1 (<LOD-12.5-65.7-39.3) 41.9) 23.7) 35.2) < LOD 11. and dairy products are the usual sources of exposure to these chemicals in the general population.9-40.6-53.1) 90th 34.0) 21. Fourth National Report on Human Exposure to Environmental Chemicals 81 .2-26.3) 18.5 (31.9-21.6-12.9 (21.6 (43. the technical grade product of each chemical contains 10%-20% of the other chemical.6) 20.6-18.2-49.0 (16.5) 9.0) 31. see Data Analysis section) for Survey years 99-00.1) 30.9 (26.9 (15.4-51. and in soil.1 (<LOD-12.4) 37.5.7 (19.5-43.7 (17.8-31.5-40. heptachlor use has been limited to treatment of fire ants near power transformers. 57-74-9 Heptachlor CAS No.9 (31.0) 20.8) 18.1-25.5. As a result of the manufacturing process.7 (34.6) 48.0-33.Organochlorine Pesticides Chlordane CAS No. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.36-11. 1994.3 (28.4-45.1-15. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.0 (37. 10.30-11. and 03-04 are 14.5) 38.3 (11.1) * 11.2 (21.8) 53.9) 31. 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.3-45.3-45.3 (21.5) 10.2 (28.4-14.8-33.2-21. from the early 1950’s until the mid-1980’s.8 (10.1 (17.20 (<LOD-11.5 (<LOD-12.5-47.8) 52.7) 19.8 (42.1 (11.3 (<LOD-19.1 (15.4) 39.0-12.2 (36. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.9 (26. Technical grade chlordane had contained 7% trans-nonachlor. population from the National Health and Nutrition Examination Survey.6) 36.S. lawns.7) 31.

and breast milk is a major excretion route in lactating women.271 (.320 (.077) .170-.058-.430) . FDA established allowable residues of chlordane. EPA has established environmental criteria for chlordane and heptachlor.115 (. 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.S.058-.170) .560) .146) < LOD < LOD .250 (. 2006).115-. 1977a.260 (.090-.100 (<LOD-.320) .260 (.148-.057) * .231) .090) . heptachlor.350 (.269 (.076) < LOD . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.190-.065-.073) < LOD < LOD < LOD < LOD .199-. 1996.240) .510) .230-.200-.207 (.149 (.063 (.270 (.130 (.207) .290-.320 (. 1991.290) .450) .240-.140 (.200 (.370 (.280) .079) < LOD < LOD < LOD .070 (<LOD-.310) .350 (.074-.180-.180) .373) .133) 90th . Chlordane and heptachlor are absorbed after oral.200-.160 (.050 (<LOD-.120-.075 (.150) .240-. Survey Geometric mean (95% conf.130-..430) .106-.227) < LOD .087-.070-.300) .250 (.148) .070 (<LOD-.068) .250-. to heptachlor. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.225 (.110-.130 (.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 * * * * .146) .Organochlorine Pesticides (Dallaire et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th . The U.063 (.100 (.210 (.210-.077) .310-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.063 (.080 (.070-.300 (. and inhalation exposure.110 (<LOD-. neonatal mortality.258 (.063) * .213) * . Rogan.300) . Takahashi et al.091) . population from the National Health and Nutrition Examination Survey.287) .300) .066-.140 (.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .070 (<LOD-.063 (.048-.080 (. 2001.080) .253-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1981). high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.047 (<LOD-.204 (.073 (.208 (.150 (.380) .260-.370 (.223) .140-. The major metabolite of heptachlor is heptachlor epoxide.150 (. 1986). Acute.302) .066-. In laboratory animal studies.092) . 1991).280-.240 (.057-.070-.280-.066 (. which may vary for some chemicals by year and by individual sample.230 (.. 2007).130 (.083) .104-.140) .128 (.290-.180-. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS. 2007.136) .083 (. Shindell and Ulrich. and heptachlor epoxide in foods and bottled water.082 (.230 (.057 (.150 (.108-. IARC.090) .140 (.310) .300-.053-.340) .120-.050-.286 (.063-.290) .230) . and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.190-.270 (.440) .070 (. Le Marchand et al. characterized by seizures and paralysis.348) .120 (.245-.. and alterations in immune function of offspring.170) .077) .320 (.130) .280-. 1986).230-. Elimination of all these chemicals from the body occurs over months to years. Smith.140-.200-.077) .300) .130-.410) .270 (.310 (.080) .320) .400) .126 (. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.061-.100-.230-.246-.216-.064) < LOD .070) < LOD < LOD < LOD < LOD < LOD .160) .315 (.062) < LOD .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .242-.120-.112 (.069 (<LOD-.130) .286 (.053-.170) .S. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.258-.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.058 (.049 (<LOD-.210 (. 1977b.290-.170) .350) .126) .119 (.280 (.165-.066 (<LOD-.130-.056 (. dermal.450) . OSHA has established occupational exposure criteria.060 (<LOD-.067 (.260 (.071 (.055-. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.070) .080) . 82 Fourth National Report on Human Exposure to Environmental Chemicals .150-.068-.220-.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .160) .068) 75th .160) .170) .203-.320 (.280 (.168-.180) .140 (.400) . and the U. which is also persistent in the body (ATSDR.130-.189-.079) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.S.340) .370 (. 2002.130-..063) .310) .330 (.290 (.220-.190-.220 (.189 (.104) .100-.070 (<LOD-.360) . chronic doses of heptachlor have produced liver enlargement and injury.

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

6 (13.9-16.6 (8.2 (18.3) 18.6-21.8 (<LOD-23.8) 20.1-38.3 (13.2 (<LOD-25.5) < LOD 14.9-23.2) 26.8 (15.6 (12.7 (16. and 7.3) 23.5 (11.2-16.0 (15.2 (<LOD-16.8) 19.4) 21.3 (<LOD-25.5 (<LOD-32.40) 15.1-15. 84 Fourth National Report on Human Exposure to Environmental Chemicals .2) 20.3) 18.0-54.8 (13.6-17.8-46. see Data Analysis section) for Survey years 99-00.8) 21.0-17.9-29.1) 13.6) 13.2-27.2-27.7 (10.2) 15.6 (16.7-19.S.9-25.6 (14.6 (11.3) 16.4 (<LOD-54.1 (16.6) 14. 01-02.8) 13.90 (<LOD-9.5 (18.9) * * * 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 8.6) 22.7-18.4 (15.0 (11. < LOD means less than the limit of detection.20 (<LOD-9.8-24.4 (11.3) 10.5 (<LOD-21.0) 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 13.8) 14.8) 16.7 (13.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.2-17.8 (18.1-16.3) 18.8 (13.3) 22.2) 13. 10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6) < LOD < LOD < LOD 27.0-19.1) 20.4 (11.1 (19.8-23.8. population from the National Health and Nutrition Examination Survey. and 03-04 are 14. respectively.9 (12.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.50) < LOD < LOD < LOD 17.5 (10. which may vary for some chemicals by year and by individual sample.9 (15.5.8-24.4 (<LOD-19.5) 19.0-17.0) 13.6.2 (<LOD-62.9) 15.6 (<LOD-27.1) 23.5 (11.3-18. Survey Geometric mean (95% conf.8) 19.1-29.6 (16. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.10-13.8-24.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7-25.0-16.8) 13.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.8) 14.3) 27.8 (18.4) 18.8) 15.9-29.

100-.190) .077-.107-.150 (.063) < LOD < LOD < LOD .140-.130) .100-.S.110) .190) .097) < LOD .130 (<LOD-.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 .113) .090-.180 (<LOD-.063) .057 (<LOD-.200) .090 (.240) .180) .128 (.149) .270) .069 (.104) .120 (.117) .126 (.135 (.135 (.111-.170) .110 (<LOD-.110-.106-.200) .100 (.110 (<LOD-.100 (<LOD-.087 (.130-.120-.180 (.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.200 (.190) .120) .170) .140) .101 (.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.173) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .090-.161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .170 (<LOD-.120) .098 (.110 (.111) .070-.150 (<LOD-.076-.113-.170 (.094 (.140) . which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th .082-.150 (.133 (.170 (.180) .096 (.110 (.108) .380) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120 (<LOD-.100 (.190 (.108-.055 (<LOD-.170) .180) .071-. population from the National Health and Nutrition Examination Survey.100 (.116) < LOD < LOD < LOD . Survey Geometric mean (95% conf.090-.130-.157) .130-.120 (<LOD-.101 (.110) .053-.180) .100 (.067-.090-.090-.110-.220) .170 (.090-.090 (<LOD-.074-.310) .108) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .077-.130 (.130-.310) . Fourth National Report on Human Exposure to Environmental Chemicals 85 .130) .094 (.

0-24.3 (45.3-86.6) 56.0 (16.4-22.6-19.8) 19.6) 56.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.6 (16. < LOD means less than the limit of detection.0 (60.9-35.1) 17.9 (66.5) 26.7 (16.3-21.7-160) 86.1) 62.0-23.3) 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.2 (15.7) 73.6-54.7) 17.8 (26.8 (13.0-59.5.5) 20.6-22.4) 59.2) 30.5) 14.5) 9.0-38.7 (30.1-20.3-57.4-52.3-32.1 (47.0) 75th 31.4 (16. 10.4) 20.8) 47.0-93.7) 28.6 (52.3) 18.4) 107 (84.2 (60.2-16.3) 30.2-21.3-50.1-16.6 (12.8-21. which may vary for some chemicals by year and by individual sample.S.9-89.2) 19.9 (47.8 (28.7 (11.6) 10.4) 16.7-20.5-20.7 (18.6 (<LOD-14.0 (62.0 (42.4) 19.7-23.4-67.1) 14.4 (11.7-32.5-69.9-22.1 (10.2 (7.2-18.8 (12. respectively.8 (<LOD-20.2-18.7-35.8-110) 59.8-67.9) 51.8-129) 74.5-111) 68.8-19.4 (45.0 (15.3) 16. and 7.8 (42.1) 17.7 (13.1) 16.0 (13.2 (14.8-41.7-21.8 (15.0) 33.6) 25.7-29.2-23.2 (36.7-77.1 (22.6) 13.1-18.3 (56.9 (51.3-30.1) 18.8-90.8 (71.6 (56.5) 19.3) 19.1) 78.0-20.0-37. population from the National Health and Nutrition Examination Survey.1-34.9 (51.8-90.8-77.9) 14.7 (74.9 (28.8 (16.1) 17.5) 36.9 (19.9 (16.1) 30.6) 54.1) 17.0 (29.2) 34.8 (19.0) < LOD < LOD 8.6) 34.7) 52.5) 14.0-93.8 (17.86-13.2 (59.3 (17.6-66.3) 18.5-36.0-23.5) 48.8-19.9 (29.6-20.3) 15.6) 84.1) 17.5-87.1-22.2 (19.9) < LOD < LOD < LOD 20.6) 82.8 (45.8 (30.5) 30.1-126) 67.1) 17.1) 32.6 (56.8 (11.0-68.8 (28.9-69.1-51.4-23.5) 78.9-45.1 (65.3 (16.9) 14.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.8-16.9-40.1) 18.1-55.3) 32.0 (16.0 (19.5) 77.9) 51.3) 36.7 (59.8) 51.0) 49.8.2) 17.7) 78.5) 35.4-18.7-22.10 (<LOD-11.4-62.7) 15.2) 59.9-20. 86 Fourth National Report on Human Exposure to Environmental Chemicals .2) 39.0 (48.1 (48.4) 55.2-37.2-17.2) < LOD 10.8) 80. and 03-04 are 14.4 (67.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.0-22.5 (15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (50.1-34.2-88.2 (14.5 (44.70 (<LOD-12.4 (12.1 (17.1) 17.3 (14.0) 13.9 (<LOD-14.0 (14.9-58.0-123) 74.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.3-58.5-17.5-19.9-65.7) 59.8 (28.7) 56.3-74.7-38.5 (13.2) 20.0 (15.9 (36.8 (26.5 (15.0) 18.6 (32.0) 19.4 (28.3 (58.1) 31.5-95.7) 78.5) 90th 55.9-64.6-88.5.6-82.1-16.7 (28.2 (26.0) 40.8 (49.7-34.2 (64.5 (45.3) 30.8-16. Survey Geometric mean (95% conf. 01-02. see Data Analysis section) for Survey years 99-00.4-35.4 (30.8-79.1 (41.4) 48.8 (13.3 (14.1) 78.6 (57.7 (59.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.8 (26.3) 25.9-65.0 (42.3-39.3 (49.7-113) 68.5 (25.3) 32.2 (25.0-143) 112 (68.6 (15.0-113) 68.1-28.7) 35.5) 22.6) 60.9 (15. interval) 18.7 (35.2 (27.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.7-17.7-18.9 (15.4-36.0 (13.7) 14.9-36.

100-.350 (.085-.220 (.098 (.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .210 (.110-.590 (.310-.520) .317 (.559) .092 (.060 (<LOD-.540) .390 (.460) .099-.099-.060) .190-.520 (.081 (.210) .112 (.270-.370 (.130) .090-.301-.930) .122) .120 (.071 (<LOD-.080-.470 (.090 (.340) .091) . Survey Geometric mean (95% conf.286-.684) .430-.089 (.062 (.116 (.104-.090) .080-.279-.470 (.210) .450) .092 (.290-.210-.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.220 (.158-.205 (.110 (.100 (.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.170 (.087 (.830) .461 (.100-.395) .590 (.047-.240) .400-.110 (.125 (.093-.220) .105 (.084-.490) .272-.367) .150) .093-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .150) .090-.191 (.131) .180-.130) .080) .830) .180-.390) .573 (.060-.630) .078-.520 (.120 (.310-.210 (.111 (. which may vary for some chemicals by year and by individual sample.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .234) .094 (.397-.098-.510 (.S.110 (.161) .232) .091-.106 (.122) .210-.250) .360-.161-.120) .330-.090-.240 (.680 (.120) .260) .190-.680) .054-.090 (<LOD-.430-.590) .130) .177-.120-.500) .180-.320-.310-.470-.458 (.690) .120) .400) .106 (.160-.108) 75th .340-.041 (<LOD-.068-.130 (.097) .300) .119) Selected percentiles ( 95% confidence interval) Sample 95th .840) .240) .340-.141) .080-.400 (.120 (.343 (.400-.470-.135 (.220 (.130) .098 (.190-.104 (.310 (.080-.490 (.460) .124) .110 (.116-.061-.420) .090-.510-.130) .390 (.600 (.490 (.260) .460-.630) .183 (.096) .430-.110 (.080 (.210) .242) .390) .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 .127) < LOD < LOD .100-.470 (.400 (.310) .497-.186-.098) .093-.20) .240-.220 (.134) .417 (.140) .113) .410-.190-.640 (.651) .109 (.390 (.220 (. interval) .355 (.960) .160 (.580 (.093) .330-.210 (.202 (.280) .129) .173-.190-.069) .119) < LOD < LOD < LOD .690) .285-.330 (.405) .125) .141) .440-.440) .090-.126) .240) .117) . Fourth National Report on Human Exposure to Environmental Chemicals 87 .108) .120) .085-.130) .079-.409-.070 (.069-.082) .420 (.100 (.250) .300-.096-.220 (.081-.085-.580 (.090-.220 (.103 (.800) .096-.250) .395-.600) .288 (.110 (.211) 90th .111-.410-1.310-.594) .237) .324 (.130) .095-.128 (.490-.390-.130 (.114) .565) .480) .109 (.116) .371) .350-.186 (.327 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120-.630) .171-.380 (.106 (.230 (.112 (.320-.220 (.100-.055 (<LOD-.360-.079-.103 (.237) .288-.190-.580 (. population from the National Health and Nutrition Examination Survey.110) .108 (.120-.078 (.113) < LOD .370 (.145-.414 (.760 (.390 (.550 (.

Chashchin V. New York. Royce W. May 1994. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Bjerselius R.atsdr.org/documents/iarc/ vol79/79-12.pdf. JAMA 1988. Bioassay of heptachlor for possible carcinogenicity.htm. International Agency for Research on Cancer (IARC). Lawrence River (Quebec.html. Environ Health Perspect 2003. Chlorinated Hydrocarbon Insecticides. LeMarchand L. Hansen JC. 1963-1967.pdf. Bioassay of chlordane for possible carcinogenicity.150:981-990. Baker DB. 4/21/09 Baker DB.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Hawaii Med J 1991. Jr and Laws ER. Sci Total Environ 2004. Available at URL: http://ntp. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Van Oostdam JC. Smith AG. Bull Environ Contam Toxicol 1981:27:506-511.atsdr. Willman E. 1979-1980. Chlordane and heptachlor [online]. In Hayes WJ.nih.330:55-70. August 2007.niehs.cdc. Hertz-Picciotto I. Barker J. 2006.110:617-624.html.gov/ntp/ htdocs/LT_rpts/tr009. Dendle WH. Tartter P. Wong L.9:1-109. Vol.html. Eds. Dewailly E.8:1-123. National Toxicology Program (NTP). Charles MJ. Available at URL: http://www.htm. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii.gov/ntp/ htdocs/LT_rpts/tr008. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Voorspoels S. Glynn AW. Wohlleb JC.41:145–148. 2001. Darnerud PO. Distribution of polychlorinated biphenyls. J Occup Med 1986. Canada). Bleiweiss IJ.cdc. Gilman A. Keller JA.inchem. Concise International Chemical Assessment Document 70 Heptachlor [online].50(3):108-118.259(3):374-377. Senie R. Organochloride pesticide residues in human milk in Hawaii. Granath F. Drews K. KalubaSkotarczak A. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Poland. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Siegel BZ. Arch Pediatr Adolesc Med 1996. Lulek J. Stehr-Green P. 79. maternal serum and milk from Wielkopolska region. 4/21/09 Dallaire F. Vol. 2 Classes of Pesticides. Takei G. 6/1/09 National Toxicology Program (NTP). Natl Cancer Inst Carcinog Tech Rep Ser 1977a.heptachlor.Summaries & Evaluations. Arch Environ Health. Aune M. 1994-1997 organochlorine compounds. Ayotte P. Muckle G. Available at URL: http://www. Odland JO. Kolonel LN. Brower S. Toxicological profile for heptachlor and heptachlor epoxide [online]. Covaci A. et al. gov/toxprofiles/tp12. A Report to the Hawaii Heptachlor Research and Education Foundation. Saidein D. Dewailly E. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. et al. Available at URL: http://www. Jr. et al.niehs. Atuma S. Available at URL: http://www. 1993.28:497501. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. 731-915. Mortality of workers employed in the manufacture of chlordane: an update. 1991 pp.org/ documents/cicads/cicads/cicad70. Jaraczewska K.nih. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Berkowitz GS. Shindell S and Ulrich S. Circumpolar maternal blood contaminant survey.84:151-161. Available at URL: http://www. Handbook of Pesticide Toxicology. International Agency for Research on Cancer (IARC) . Organochlorines in Swedish women: determinants of serum concentrations. Pollutants in breast milk.org/site/foundation/ research/projects2. Academic Press. Loo S. Wolff MS. Laliberte C. et al. Available at URL: http://ntp. 6/1/09 Rogan WJ.gov/toxprofiles/tp31.110(8):835-838. Environ Res 2000. Environ Health Perspect 2002.111:349355. 4/21/09 James RA. Takahashi W. 1986. Inc. Toxicological profile for chlordane [online]. 9/25/07 International Programme in Chemical Safety (IPCS). Environ Health Perspect 2002. Organochlorine exposures and breast cancer risk in New York City women. Head SL. Sci Tot Environ 2006.372:20-31.inchem.

5 (14. Smith. and trace amounts of several related compounds.2 (11.0 (18.8-23. which may vary for some chemicals by year and by individual sample.3-16.0 (10.1-27. DDT usually refers to the technical product.0-27.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.S.3 (27. 1991). population from the National Health and Nutrition Examination Survey.7-16. although DDT and DDE intakes have decreased over time (FDA.4.0 (21.0 (18.00 (<LOD-10. Food imported from countries that still use DDT may contain the chemical or its residues.1 (23. or dermal exposure. particularly for endemic vector and malaria control.0) 40. as well as in plant and animal tissues. DDT is converted in the environment to other more stable chemical forms.0-15.9 (<LOD-20.5 (23.4 (23.9 (10.4) < LOD 17.p’-DDT (65%-80%).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. air.8. fish.6 (9.3) 21.5 (23. DDT was used at one time as a treatment for head and body lice. Fourth National Report on Human Exposure to Environmental Chemicals 89 .50-11. 1991).2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. and dairy products.8-26. 1988).8-17. In the general U.1) 31.8) 30.1-71.5-54. DDT and DDE can cross the placenta. DDT is converted to DDE and several other metabolites.4) < LOD < LOD < LOD 61.7 (19. 2008.1) 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 12.9) 29.1’-(2.7) < LOD 18.2) 30.8) 36.6 (25.2-65.8-39. depending on conditions.0) 20.3) 21.2) 155 (59. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (<LOD-12.5) 23.p’-DDD (4% or less).10-13. 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.3) 22.3 (<LOD-21. < LOD means less than the limit of detection. when virtually all use of it was banned. Gunderson. DDT can be absorbed after ingestion.S.70 (8.9-34.2 (<LOD-40.S. which is a mixture containing p.8) 15.2-95.3-236) 24.2) < LOD < LOD 9. These chemicals are highly persistent in soil.9) 17. particularly meat.5 (15. The biodegradation half-life of DDT in soil varies from 2 to 15 years.3 (<LOD-31. sediments.0-53.9 (21.5) 25. 2002.6 (31.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. continues to be the primary source of DDT exposure.7 (15. after World War II until 1972.0-155) 83.1 (33.p’-DDT (15%-21%).9 (10. and 03-04 are 20. Only a small proportion of DDT is metabolized and excreted (Smith.6 (<LOD-25. It was produced and used in the U.9-28. Survey Geometric mean (95% conf.0-37.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11. 17. including 1. In the body.6-33. It is still used in some countries. inhalation. o.3-590) 293 (104-541) 48. population.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) 28.5-36.5) < LOD < LOD 9. respectively. food.0) 26.9) 14.9 (10. and water. see Data Analysis section) for Survey years 99-00.1’-dichloro-(2.90 (<LOD-12. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.6 (22.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.0-35.7.7) 12. resulting in fetal exposure. 01-02. p.9) < LOD < LOD 9. Both Serum p. and 7.1 (<LOD-39. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.0) 19.2-bis(p-chlorophenyl) ethane (DDD).

150-.240 (. 2006). premature delivery..120-. 2002. accidental exposures. 2004. 1956).530 (. Hayes et al. 1997).128 (.075) 1.170-. reproductive organ abnormalities. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.140-.. and duration of lactation. 90 Fourth National Report on Human Exposure to Environmental Chemicals ..313 (. tremor.061) < LOD < LOD < LOD . fertility..00 (. In high dose.p’-DDE can produce anti-androgenic effects (Gray et al.048 (<LOD-. 2006. lung cancer.106) . Beard..343) < LOD . Jusko et al. and o. In laboratory animals. and altered behavior after neonatal exposure (Eriksson and Talts.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 .150 (<LOD-. have not been consistently demonstrated (Beard..106-..S.180) .220) .112 (. 1998). 2006. polychlorinated biphenyls.230) .400 (.180 (.190 (. 2002.180) .069) .160-.080-.203) .059-.190-1.570-4.189) 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 .074-.p’-DDD and p.087 (.105-.078 (. which may vary for some chemicals by year and by individual sample.34) .120 (<LOD-.130 (<LOD-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.098-.146 (.180 (.250 (. 2002. and seizures.142 (. 2001). and leukemia have also been inconclusive (ADSDR.170) .530) ...051 (<LOD-. DDT may bind to estrogen receptors (Chen et al.g.627) .095) < LOD . Animal studies reported reduced fertility.063 (<LOD-.079) < LOD < LOD . Snedeker.130 (<LOD-. Longnecker et al.189-. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.150 (<LOD-. 2006).330-4.240) .26) 1.054-..130-.068-. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.420) .140) . 2001).. Gladen and Rogan.084 (.065-.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .180-.130 (<LOD-. population from the National Health and Nutrition Examination Survey.220) .62 (.106) < LOD < LOD . Mariussen and Fonnum. 2001).. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. other organochlorines. Gray et al.290) .143) < LOD < LOD .200 (.400) .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. 2002. interval) Selected percentiles ( 95% confidence interval) Sample 95th .078-.Organochlorine Pesticides chemicals are excreted in breast milk.170 (.150) .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. Calle et al.01) .250-1.201 (. 2000. 2006). overt signs of acute human toxicity include vomiting. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.132-. 1996). Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.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 .190 (. Studies of DDT exposure and pancreatic cancer. 2006. 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.071 (.108 (. Survey Geometric mean (95% conf. dioxins and furans).00) .260) .064 (. 1995. Reproductive effects in humans affecting birth weight. 2001). Jusko et al. resulting in exposure to nursing infants (Rogan. A workplace standard for DDT has been established by Serum p.114-.150-.071-.146 (.086 (.230) .

S. Survey Geometric mean (95% conf. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. Compared to females in the NHANES 1999-2000 subsample.Organochlorine Pesticides OSHA and a guidance established by ACGIH. 2005).atsdr. Heudorf et al. 2004). mean serum levels of DDT and DDE in the U.gov/ pestcides/ and from ATSDR at: http://www.e.html. 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. IARC classifies DDT (p.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.S.. Biomonitoring Information DDE persists in the body longer than DDT. 2002. 1989). 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.cdc. In general. Fourth National Report on Human Exposure to Environmental Chemicals 91 . 2004). Declining DDE levels over time have also been observed in the German population.. and 7. In a population-based sample of men and women from eastern Slovakia. for males and females in the NHANES 19992000 subsample (Pavuk et al.7-119) 113 (100-140) 93... Median DDE levels among a population-based sample of Swedish women in 19961997 were similar to females in the NHANES 1999-2000 subsample (Glynn et al. respectively. see Data Analysis section) for Survey years 99-00.6.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. 1991). 1998.gov/ toxpro2.epa. 2003).. Link et al. 8. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. NTP considers DDT as being reasonably anticipated to be a human carcinogen. respectively. Stehr-Green. population declined by about fivefold to tenfold..3.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.. EPA at: http://www. Since the 1970’s.8. compared to levels observed in this Report (Anderson et al. More information about external exposure (i.6 (81.. population from the National Health and Nutrition Examination Survey.S. 2002. environmental levels) and health effects is available from the U. Smith. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. and 03-04 are 18. 2003. 01-02.p’-DDT) as a possible human carcinogen.

39-2.8 (13.97-4.46 (1.8) 15. Serum p. 1989).11-1.41-12.02-8.1) 7.32-1.10) 2.68) 2.p’-DDT.6) 9.516 (.25-16.1 (9.14 (1. Finding a measurable amount of p.5) 7.68-4.38 (1.419-.35) 1.51 (1.25-14.80 (2.32) 1.85-10.66-2. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE than are found in the general population.53) 7.84-3.41 (1.57-3.37-16.19-14.81 (1.78 (4.81) 11.10) .57 (3.21) 90th 7.68 (2..52 (1.39) 1.66) 1.5) 22.27) 3. serum levels of o.60-13. 309 versus 268 ng/g lipid.71) 12.75) 6.83 (1.25) 8.76) 1.05) 1.488-.870 (.81-5.40-4.890-1.69) 8. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.0 (12.22 (7.64) 3. less than one percent had detectable serum levels of o.04-1.p’-DDT (Stehr-Green.38 (1.75 (4.5) 5.49 (6.75) 1.91) 3.75) 2.26-10.28) 1.25 (.54-7.31 (1.05 (3.965-1.3-43.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.3) 13.49) 8.00) 7.81 (7.2) 19.56-3.66-17.23 (7.45 (1.15-4.56-6.07) 1.56) 2.51-15.7-20.18) 1.5) 16.77 (1.520 (.6 (17.01) 1.03-4.3 (9.600) .61 (1.24 (1.9-17.7-19.9 (26.2) 26.43-4.53-15.4 (8.13 (1.430-. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.726) .00 (6.55-9.3) 10.14) 2.00-1.2 (9.01-1.54 (1.72) 1.53) 1.96) 1.6 (8.6) 9.71 (6.46-2.57-2.51) 3.70) 1.84 (3. 1971)..611-1.385-.11 (2.07 (5.64-2.50-17.91-3.91 (6.92) 1.18-1.49 (1.1) 40.34 (7.47) 3.66) 4.51-49.72) 1.14) 2.69 (1.994-2. In a subsample of NHANES II (19761980) participants.S.45 (1.860 ng/L) and DDE (about 14. 1991).6) 11.43-4.56-2.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.8 (9.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.18-1. interval) 1.4) 13.18-4.2 (6.0 (9.51) 1.01-11.93 (7.4) 9.4 (12.58) 1.59 (4.p’-DDT.65) 1.9) 7.8 (13.06) 1.16-1.635) 1.7) 9.0) 2.50 (2.71 (5.6) 12.51-8.59 (1.561 (.32-1.62-6. 2004).32 (1..24) 1.66-4.63 (1.27-1.69) 4.82 (1.97 (3. 2005).88-35.534-. Survey Geometric mean (95% conf. 2004)..6) 9.7-48.5) 10.04 (6.33-1. In the NHANES 1999-2000.6) 9.31-12.87 (5.32-9.63 (1.8 (14. population from the National Health and Nutrition Examination Survey.9) 5.26) 3.p'-Dichlorodiphenyldichloroethene (DDE) (whole weight) Metabolite of Dichlorodiphenyltrichloroethane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.70-3.09-1.52 (3.557) 1.01-15. or p.75 (8.12 (.30 (1.48-4.2-32.26 (1.77 (1.10-1.66) 3.680-1.71) 32.730) .99) 1.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.590 (.49 (1.6) 13.91-2.2 (19.58) 1.82) 1.43 (5.54) 8.26-2.p’-DDT were below the limits of detection.57-13.58) 75th 3.9-38.25 (1.456 (.37-1.40 (3.65 (1.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.01) 1.6) 8.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .34-11.92 (3.2 (9.12-1.14-9.3 (8.13) 4.85-4.22-1.20 (.48 (6.36-2.32 (1.963-1.14-1.76 (2.4-19.820-1.92 (3.06) 3.01-1.00 (.57 (1.646) .76-3.59) 3.0) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites 92 Fourth National Report on Human Exposure to Environmental Chemicals .16 (2.59 (1.25) 1.623 (.34) 6.36 (3.37 (1.500-.59) 6.34) 2.63-15.57 (1.37-4.30-1. A small study of Indian men with background exposure reported mean serum DDT and DDE levels that were around fiftyfold higher than the 95th percentile for DDT and tenfold to twentyfold higher than the geometric mean DDE levels among males in this Report (Bhatnagar et al.88 (2.19) 4.80) 3.01-5.03-1.69 (.31-2.57) 2. 2001-2002 and 2003-2004 subsamples.8-90.69 (2.53 (2.6 (7.44) 1.13-2.Organochlorine Pesticides nearby agriculture (Botella et al.07) 1. High mean levels of whole blood DDT (about 3.39 (3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.55 (2.36-1.7) 13.46 (1. considerably higher than levels in this Report (Smith.63 (6.80) 1.36-11.22) .02 (2.9 (15.81-18.87-16.96) .18 (6.3) 16.37-10.80) 1.02) 1.36) 3.79) 4.85 (1.76) 1.40-8.24-17.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.21) 3.34-3.40-4.01-11.66) 1.12 (6.39-1.7 (8.17-3.796 (.7) 16.17 (3.29 (1.18-3.30-1.4) 14.10-5.90) 22. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.6 (9.61-2.1 (8.43-8. o.90-8.47 (1.30 (1.52-6.1) 12.

and 7. < LOD means less than the limit of detection.S.7. which may vary for some chemicals by year and by individual sample.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.8. population from the National Health and Nutrition Examination Survey. respectively. 01-02. see Data Analysis section) for Survey years 99-00. Survey Geometric mean (95% conf. * 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 93 . 17.4. 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. and 03-04 are 20.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. which may vary for some chemicals by year and by individual sample.Organochlorine Pesticides Serum o. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. 94 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.p'-Dichlorodiphenyltrichloroethane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. Survey Geometric mean (95% conf.

a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Levels of DDT. Bjerselius R. Aune M.1-dichloro2. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Thun MJ. Gladen BC. Rogan WJ. Wolf CJ. Brock JW. Toxicological profile for DDT. Organochlorines in Swedish women: determinants of serum concentrations. Falk C. Lambright C. Environ Res 2004.cdc. Hanrahan L. et al. selected elements. and dichloro(diphenyl)ethylene (DDE). and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Calle EE. Beard J. Swanson MK. Botella B. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.85:504508. Maternal serum level of 1. Effects of environmental antiandrogens on reproductive development in experimental animals.358:110-114. Jr. Hediger ML. Drexler H. et al. Environ Health Perspect 2004. FDA total diet study. Gray LE Jr. Brock JW. Bates MN. Vorojeikina DP. Durham WF. Ostby J.21(1-2)37-48. Talts U. Bhatnagar VK. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Seiwert M. DDT and human health. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Needham LL. Exposure of women to organochlorine pesticides in Southern Spain. and polythelia among male offspring. Klebanoff MA. Katz SH.53(8):1161-1172. Buckland SJ. April 1982 to 1984. Link B. Koepsell TD. DDE and shortened duration of lactation in a northern Mexican town. Moysich KB. Patterson DG Jr. Gunderson EL. Heudorf U. JAMA 1956. hexachlorobenzene. Am J Epidemiol 2002. Herrman T. Food and Drug Administration (FDA).111:349355. et al. Chemosphere 2004. Granath F.206:485-491. Crespo J. Bull Environ Contam Toxicol 2004.atsdr. Lepom P. Int J Hyg Environ Health 2003. Becker K. Olea N. Barr DB. Am J Public Health 1995. et al. Arnold SF. Vena JE. J Assoc Off Anal Chem 1988. Saiyed HN. Zoellner I. Lancet 2001. Bloom MS. Ellis H. Environ Res 2005. Profiles of ortho-polychlorinated biphenyl congeners. Zhou H. Biomonitoring of persistent organochlorine pesticides. Notides AC. Olea-Serrano MF.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Olson JR. lindane (g-HCH). Krause C. Gray KA. Kashyap R. Rivas A. Olson J.54:1431-1443. Cueto C. 4/21/09 Anderson HA. Kaus S. Longnecker MP. Needham LL. Darnerud PO.. Klebanoff MA. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. hypospadias. Zaidi SS. et al.106(5):279-289.7(3):248-264. Environ Health Perspect 1998.112(17):1761-1767. Furr J.fda.205:297-308. et al. et al. Baker RJ. Frumkin H. Biochem Pharmacol 1997. Zhou H.72:261265. Burse VW.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Hurd C. Henley SJ. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males.17(6):692-700. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Garrett N. Jr.71(6):1200-1209. Available at URL: http://www. Glynn AW. Hayes WJ. India.cfsan. Hum Reprod Updat 2001. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Available at URL: http://www. September 2002. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Environ Health Perspect 2003. Schulz C. and DDD [online]. August 2008. Savitz DA. et al.155(4):313-322.96:34-40. Organochlorines and breast cancer risk. Angerer J. Paepke O. The Great Lakes Consortium. Klebanoff MA. Chemosphere 2005. Maternal DDT exposures in relation to fetal and 5-year growth.gov/ toxprofiles/tp35. Atuma S. Davis MD.58:1185-1201. Greenfield TA. Fourth National Report on Human Exposure to Environmental Chemicals 95 . dichlorodiphenyldichloroethylene. Epidemiology 2006.97(2):178192. et al. HCH.162:890-897. Charles MJ. Longnecker MP. Cerrillo I.gov/~dms/ pesrpts. 4/21/09 Gladen BC. Int J Hyg Environ Health 2002. Gabrio T. CA Cancer J Clin 2002. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Chen CW.html. dietary intakes of pesticides. Sci Tot Environ 2006. Neurotoxicol 2000. Kulkarni PK. DDE. and other chemicals. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Willman EJ. Eriksson P.355:7889. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Needham LL. and HCB residues in human blood in Ahmedabad. Parks L.html.52:301-309. Jusko TA. Piechotowski I.

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

endrin can persist for years..40 (<LOD-6. At high doses.Organochlorine Pesticides Endrin CAS No. have been cancelled by the U. Depending on soil conditions. Kavlock et al. 1992).S.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. 72-20-8 General Information Endrin. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals.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. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. < LOD means less than the limit of detection. Endrin is absorbed rapidly after ingestion.S.S. is no longer manufactured in the U. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. anti-12hydroxyendrin. In the body.8. 1991). which may vary for some chemicals by year and by individual sample. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. Survey Geometric mean (95% conf.20 (<LOD-5. Hepatic effects of endrin exposure have included necrosis.50) < LOD 5. total diet surveys (FDA. 1996.10 (<LOD-5. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. rodenticide and avicide. Endrin was not widely used as a termiticide. IPCS. 1981). Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. 1992). or discarded.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. and inflammation (Smith. unless the dose is high and the exposure is very recent.30) < LOD 5.20 (<LOD-5.40-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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. Over time.. 2008). 1979. unlike aldrin and dieldrin. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. endrin usually is not detected in serum of exposed individuals. Smith. a stereoisomer of dieldrin. All uses of the pesticide in the U. 1987). Because it is metabolized so rapidly.30 (<LOD-6. 1991). Endrin was used as an insecticide. Endrin has been detected in soils. 1992). Endrin does not accumulate in body tissues (IPCS. see Data Analysis section) for Survey years 01-02 and 03-04 are 5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. Ketoendrin is a major photodegradation product (IPCS.60 (5.. largely the result of historical agricultural application or run off from contaminated soils (ATSDR.S. and occasionally at low levels in sediment and surface waters. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 97 . inhalation or dermal exposure routes. An epidemic of acute endrin poisoning.10 (<LOD-5.50) < LOD < LOD < LOD 5. 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..S. 1992. EPA. or from contact with contaminated soils and sediments in areas where endrin was applied. fatty infiltration. endrin has been detected with declining frequency in U. endrin is converted rapidly to its major metabolite. manufactured.09 and 7.

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

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

3-22.0 (14. 1997).9-20.7 (15.5-15.3-26.8) < LOD < LOD 27. and accumulates in fatty tissues where it persists for years.9) < LOD < LOD 20.9) < LOD < LOD 20.0-16.2) < LOD < LOD 29. see Data Analysis section) for Survey years 99-00.6) < LOD < LOD 24. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.8 (15. 31.9-32.7-15.6 (23.4.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.2 (24. distributes widely throughout the body.5-14.7-26.3 (12.0) < LOD < LOD 15.4.7) * * 14. Therefore. The general population may be exposed to HCB through diet.2-31.6) < LOD < LOD 26. and 03-04 are 118.9) < LOD < LOD 19.6-19.3) 24. respectively. or game taken from areas with HCB contamination.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 * * 16.9) < LOD < LOD 16.2 (17.0-28.6-trichlorophenol (2. HCB is well absorbed after oral administration.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.4) < LOD < LOD 33. measuring HCB in serum is a specific indicator of exposure to the parent Serum Hexachlorobenzene (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.4) < LOD < LOD 23.5-TCP) and 2.1 (13.8 (26. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.3 (16.5) < LOD < LOD 18. Survey Geometric mean (95% conf.6) < LOD < LOD 26.9 (25.9-15.3 (22.5 (13.1 (17.7 (19.7 (27.2-15. population from the National Health and Nutrition Examination Survey. breast milk is an additional route of elimination in nursing women. The FDA dietary surveys have shown that over time. 2005).2) < LOD < LOD 13. HCB is slowly metabolized.7-21.0) < LOD < LOD 24. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.6-44. 2002).S.2-15.7 (15.2 (14. and sediment (Barber et al.3-20.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6-26.1) * * 15. primarily as a fungicide and seed treatment until the U.6) < LOD < LOD 25. particularly by consuming fish.5-14. EPA cancelled its use in 1984. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.0.4) < LOD < LOD 22.8. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR. 2.4-16.8 (22.1-16.4) < LOD < LOD 19.0-19.1) < LOD < LOD 15.3 (14. 2008.6-TCP) (To-Figueras et al. Although it is not manufactured as an end-product in the U. and elimination occurs by renal and fecal routes.5 (14.0 (18.5-trichlorophenol (2. 1976).3) < LOD < LOD 20.4.4.2 (14.6) < LOD < LOD 14.3 (20.6 (21.7-16.Organochlorine Pesticides Hexachlorobenzene CAS No.4 (18.6-32. Gunderson.0-25.. Urinary metabolites include pentachlorophenol (PCP). 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.0) * * 15. 01-02. and foods with a high fat content.S.5-15.9-17.7-22.4 (22.9) < LOD < LOD 15.1 (14.9-30. and 7..4 (18.0) < LOD < LOD 15. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.5 (13.3) * * 15.S.4 (11.9 (23. wildfowl. and has been detected in soil.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.6 (24.5-18.5-33.8-15..6-33.4) < LOD < LOD 14. which may vary for some chemicals by year and by individual sample.S.1 (14.0 (18.7-30.7-29.4-15.9) 19.2 (13. 100 Fourth National Report on Human Exposure to Environmental Chemicals .3 (22.7) < LOD < LOD 75th < LOD < LOD 90th * * 15. 1988). water.0 (25.9 (14.1-20.7-16.9 (25..7) < LOD < LOD 24.4) < LOD < LOD 18. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.3) < LOD < LOD 29. < LOD means less than the limit of detection.9-24. air.9) < LOD < LOD 28. HCB has been detected in fewer foods since the 1980s (FDA.

179 (. as well as hypertrichosis.114-.072-. and many died before 2 years of age (Peters et al.090 (.176-.115 (.163) < LOD < LOD .175) < LOD < LOD .145-. immunologic abnormalities.088-. More information about external exposure (i.160 (.122) < LOD < LOD .152) < LOD < LOD .088-.095 (.141) < LOD < LOD . and the FDA has established a bottled water standard for HCB.gov/pesticides/ and from ATSDR at: http://www.081-.069) * * . anorexia.113-.171 (.107) < LOD < LOD . This condition. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.e.104 (.099) < LOD < LOD .111-.130) < LOD < LOD . population from the National Health and Nutrition Examination Survey.225 (.092 (.090 (.126) .157 (. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.097) .107-.148-.121 (.088-.132) < LOD < LOD .S.094 (.123 (. reproductive and developmental toxicities.095-. 1960).092 (.083) < LOD < LOD .gov/toxpro2.129) < LOD < LOD .167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .cdc.078 (.Organochlorine Pesticides chemical.079 (.258) < LOD < LOD .125 (.089-.099) < LOD < LOD .073-.086-. acute doses produce central nervous system depression and seizures.S. 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.114-.176) < LOD < LOD . 2002). In humans. 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. EPA has established a drinking water standard.163 (.102) < LOD < LOD .081 (.191 (.epa.099) < LOD < LOD .167 (.077-.091-.118-.174-.069) < LOD < LOD .100) < LOD < LOD .086-.156 (.085-.092 (. Survey Geometric mean (95% conf.062-.109) * * .111) < LOD < LOD .118) < LOD < LOD .082-. HCB interferes with normal heme synthesis. Fourth National Report on Human Exposure to Environmental Chemicals 101 .095 (.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. Infants were exposed transplacentally and through breast milk. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.097) < LOD < LOD . The U.143-.118-. thyromegaly. very high.155) < LOD < LOD . Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Chronic feeding studies in animals have demonstrated kidney injury.095) < LOD < LOD 75th < LOD < LOD 90th * * . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .120 (.089-.064 (.157-.186 (. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.182 (.147 (.145-.092-. and weakness.. EPA at: http://www.095) * * .212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .203) < LOD < LOD .135-.196) < LOD < LOD .090-. With chronic exposure.123 (.190 (.203) < LOD < LOD . and liver and thyroid cancers (ATSDR.090 (. Biomonitoring Information Serum concentrations reflect the body burden of HCB.S. environmental levels) and health effects is available from the U. ACGIH has developed workplace exposure limits for HCB.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 * * .065 (. 1982.140 (. Schmid.060-.102 (.127-.169-.087 (.123 (.147-.atsdr. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen. which may vary for some chemicals by year and by individual sample.173) < LOD < LOD .097 (.086) < LOD < LOD .094) < LOD < LOD . arthritis.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 * * ..159-.098 (.html.085) * * .163-.178-.

Atuma S. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene.html. Hexachlorobenzene in the global environment: emissions.110(8):835-838. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. 2002).. Available at URL: http://www. 2006). lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002.205:297-308. Aune M. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Link B. Darnerud PO.58:1185-1201. Arch Dermatol 1999. Glynn et al. 2002. 4/21/09 Barber JL. The metabolism of higher chlorinated benzene isomers. 1989)..349:144. Ayotte P.. Arch Neurol 1982.71(6):1200-1209. 1999). Over the past two decades. August 2008. Bryan GT. Canada). Biol Neonate 2002. Bradman et al.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. 4/21/09 Glynn AW.54(3):203-208. 2005)..17:388–399.gov/~dms/ pesrpts. HCB detection in serum also was proportional to age. Environ Health Perspect 2003.. Ozalla D. Gunderson EL. Dewailly E.cfsan. but overall. Lackman. 2003). Toxicological profile for hexachlorobenzene update [online]. Gocmen A. and the geometric mean concentration of HCB in whole blood was 0. Schwartz JM. Bradman A. Krause C. Barr DB. Jones D. Food and Drug Administration (FDA). et al. Fenster L. Zoellner I. 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.111:349355. et al. however. In a representative sample of the 1998 German adult population. Holland NT.. In the 1976-1980 NHANES subsample. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al.9% of participants had quantifiable levels (Stehr-Green. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher.. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Sweetman AJ. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2002. Sci Tot Environ 2005. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.. Sala M. Link et al. HCB levels were directly related to age. Bertram et al.cdc. et al. selected elements. van Wijk D.atsdr. 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. 1986. Kohli J.44 mg/L. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Piechotowski I. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. FDA total diet study. Becker K. 2002. only 4. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Reference values updated. levels. 102 Fourth National Report on Human Exposure to Environmental Chemicals . German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Kaus S. In Spain. Can J Biochem 1976. Biomonitoring of persistent organochlorine pesticides.77:173182. Muckle G. Available at URL: http://www. Lepom P. Chemosphere 2005.html. September 2002.81(2):82-85. and other chemicals. Kemper FH.. April 1982 to 1984. J Assoc Off Anal Chem 1988. 2005). Muller C. 2002. dietary intakes of pesticides. Granath F. Safe A.gov/ toxprofiles/tp90. J Exp Sci Environ Epidemiol 2007. Environ Health Perspect 2002. Cripps DJ. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Otero R. Gabrio T.39(12):744-749. Santiago-Silva M. Herrman T. References Agency for Toxic Substances and Disease Registry (ATSDR). Lackmann GM. 2002) and among children (Link et al. 2005. Int J Hyg Environ Health 2002. Lecha M. Lackmann. Seiwert M. IARC Sci Publ 1986.. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Peters HA. Dallaire F. Paepke O. et al. As a result of the lower limit of detection in NHANES 2003-2004. more HCB levels were quantified. Dogramaci I. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. distribution. Organochlorines in Swedish women: determinants of serum concentrations. trends and processes. Herrero C. Laliberte C. Lawrence River (Quebec.fda. Eskenazi B. Bertram HP. Bjerselius R.135(4):400404.. Schulz C. respectively. Jones KC.

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

2 (18.5528.8-19.9 (9.3 (26.1 (16.89 (<LOD-9.4 (11.3) 14. HCH isomers.43 (<LOD-9.3) 37.2-42. Lindane has a half-life of about two weeks in soils and water.1-37.6 (22.6 (40.4) 44.90) 7. 01-02. formerly referred to as benzene hexachloride.2 (29.7) 23.S.5) 40.1-32.1 (9. see Data Analysis section) for survey years 99-00.7-20.5 (11. EPA cancelled agricultural uses of lindane (ATSDR.3-56.4-111) 84. containing about 64% alpha and 10%-15% gamma isomers. respectively.2 (50.3 (13.2) 9.1) 12.5 (43.6 (16.8 (21.0 (33.S. 104 Fourth National Report on Human Exposure to Environmental Chemicals . particularly alpha and gamma have been detected widely in air.0 (37.0-70.4-73.6-18. water.4) < LOD 9.0) 41.8) < LOD 10.5 (24.1 (18.4 (50. and sediment as a result of historic production and use. **In survey period 2001-2002. 2005).8) 7.36.1-16.8.9 (62.1-49.9 (50.9 (30. 2005).4) < LOD < LOD < LOD 46.7) 97.1 (27.3 (42.2 (48. soil.5 (8.8) 95th 68. each result has been multiplied by 1.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.5) 67.5) 11.3 (62.1) 31.6) 36.7) 10.0) 71. Technical grade HCH is a mixture of all four isomers.7 (53.0 (8.5) 16. The gamma isomer.8 (64.0-111) 70.4) 21.3) 51.6) 18.2-87.9) 81. The other isomers can be formed during the synthesis of lindane.1-36.9-81.8) * * * * * * 15.6) 16.1-15.2-55.7) 56.0) 7.7-96. interval) 9. and delta.70 (6.80 (<LOD-14.3) 34.5) 22.0-21.4) 51.6-135) 69.4 (12.0) 17. HCH isomers are lipophilic.5) 90th 42.5 (14. so they can accumulate in fatty tissues of animals. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.8) 12.1 (12. beta. and 7.2-22. 58-89-9 General Information Hexachlorocyclohexane (HCH).3) 25.7 (29. which may vary for some chemicals by year and by individual sample.8 (32.80 (6.1 (11.1) 71.6-47.9-24.8 (33.70 (8.6) 47.8-199) 134 (85.2-17.8 (23.0 (<LOD-12.4) 901 1067 952 992 1224 1007 Females 11.9 (26.6) 50.7-69.90-8.5 (37.S.6 (17. In 2006.6-42.7 (35.4) 11.0 (19.5-29.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.90-8.2 (9.6) 653 758 589 1240 1533 1370 20 years and older 10.56-12.2-46. 6.9) 45.2-98.30-11.6) 35.6 (33.7 (25.8 (10.3 (42.1) 13.0-34.1) 12.4 (52.4) 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 21.8 (17.0-20.4-50.5) 29.9 (40.6-20. gamma. 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.2-52.6-37.7) 10. < LOD means less than the limit of detection.3-38.70-12.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.9-21.7 (13.7-26. exists in several isomeric forms.0) 8.8-87. It is no longer produced or sold in the U.1 (30.2 (34.1-27. and 03-04 are 9.1 (9.0 (35. and have been used either as fungicides or to synthesize other chemicals.60-13.8) 27.04-10. the U.2 (31.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.50) 8.9 (11.0 (14.6-89.5 (16.Organochlorine Pesticides Hexachlorocyclohexane CAS No.4 (16.7) 18.7-166) 70.2-67.70-19.0-23. See the section “What’s New” at the beginning of this Report for details.0-70.7 (30.2) 36.9 (32.5) 14. including alpha.9-51.8) 39. However.9-14.8 (9.7-96.8-16.4) 27.1 (21.2) 62.7 (<LOD-16.3-85.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.0) 35.7) 27.5-123) 49.8-54.2) 142 (99.1-32.46-11.6-62.66-12. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.4-45.87 (9.9-178) 48.68 (<LOD-10.9-56.7 (62.61-12. commonly known as lindane.8-68.4) 10.2) 13.76.20-16.2-20. environmental levels declined.7) 73. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.6 (10. As pesticide applications of HCH were increasingly restricted or eliminated.9) 17.4 (8. 608-73-1 beta-Hexachlorocyclohexane CAS No.6-14.7) 32.7-69. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 319-85-7 gamma-Hexachlorocyclohexane CAS No.8) 52. population from the National Health and Nutrition Examination Survey.9) 15.

2002).382-.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .131-.412 (..281 (.01 (.120-.050-.098 (.410) .100 (.096) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .350) . 1981).092 (.050 (<LOD-.370-..250 (.360) . or dermal exposure. ingestion.580-1.460 (.150) . 1983).139 (. each result has been multiplied by 1.057-.056-.160-. respectively.118-.140) .280-.308-.460) .190-1.200 (.067 (.050 (.175 (.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 . enlarged livers. population from the National Health and Nutrition Examination Survey.072 (.070-.442 (.068-.480 (.100) .587) 653 758 589 1240 1533 1370 20 years and older .661) 901 1067 952 992 1224 1007 Females .320 (.100-.210 (.380 (.120) .5528.083 (.167 (.210) .080-. and seizures.170-.067) .305) .260) . which may vary for some chemicals by year and by individual sample. 1996.150 (. **In survey period 2001-2002.191-.220) .190-.160) .089) . 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. Gunderson 1988). The U.170-.047-.064 (.250 (.290) .340) .600) .220 (.070 (.220-.390 (.280-.404) .051 (<LOD-. 1977).144 (.080-.400) . Distribution is mainly to fatty tissues. and nephropathy developed (IPCS.400) . Rogan. the serum half-life was about 20 hours among children (Ginsburg et al.077) < LOD .220-.081-.250 (.230-.100-.450-.570 (.222 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.090 (.331 (.S. When animals were chronically fed lindane at high doses.062 (.120 (.090-.260-.110) .056-.150) .057-.069) .470) .700) .37) 1.090 (.058 (<LOD-. and memory loss (Nigam et al.360 (. OSHA and ACGIH have established workplace standards and guidelines.330 (.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .130) .32) .051-.150-.310) .070-.340-.501) .065 (.910 (.290) .297-. The beta isomer accumulates in fatty tissues and is metabolized more slowly.240-. After dermal application of lindane 1% lotion.450 (.140) .040-.480 (. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.050-.470 (.120-.210 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.191-.174) .130 (. 2008.086) < LOD < LOD < LOD < LOD < LOD < LOD .160 (..065 (.290 (.103-. Saxena et al.110) .690) .580 (.124-.521 (. HCH isomers are absorbed after inhalation. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.048 (<LOD-.210-. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.077) < LOD .250) . 1986).080 (.089-.120-.360-.710) .310 (.180-. resulting in a half-life of about seven years.216 (.244-.080-.120 (.057 (<LOD-.270 (.073-. tremors.560 (.260) .294-.070 (.059-.840) .620) .173-. paresthesias. for lindane. 1971.250-.480) .05) .110) .060) .200-.330-.510) .070-.091) ..410 (.319) . ataxia. and FDA has established a bottled water standard and food residue tolerances for lindane. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.560) . U.050) .120 (.300-.290 (.814) .190) .140) .080) * * * * * * .234 (.250-.620-1.120) .118 (. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.050-.420-.372 (.140 (.287 (.290 (.221-.125) < LOD < LOD < LOD .S.240 (.050-. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways. interval) .S. EPA has established a drinking water standard.100) .080 (.062 (.146-.083) . probably by blocking inhibitory neurotransmitters in the central nervous system.064) .119) .190) .254) 95th .110-.130-.410-.Organochlorine Pesticides exposure to HCH is through the diet..214) .450) . hepatic enzyme induction.070) .050 (.390-.680) .310) .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.050 (<LOD-.350 (.078 (. See the section “What’s New” at the beginning of this Report for details.410) . from 6% of samples in 1982-1984 to 2% in 1994 (FDA.100 (.100-.103) 90th . Fourth National Report on Human Exposure to Environmental Chemicals 105 .200-.090 (.103 (.080) . Workers who directly handled HCH have complained of headache.

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

1971). In a small study of adults who consumed sport fish from the Great Lakes. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al. 2003). 1986. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 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.S. 1998). in this Report (Nigam et al.. Beta-HCH and lindane levels in workers involved in HCH production have been more than 1000-fold higher than the 95th percentile and limit of detection (lipid adjusted). Radomski et al. respectively.Organochlorine Pesticides 2001-2002 survey period (Link et al.. Fourth National Report on Human Exposure to Environmental Chemicals 107 . 2005). population from the National Health and Nutrition Examination Survey. 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. Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biomonitoring studies on levels of HCH isomers provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of HCH isomers than are found in the general population.. Survey Geometric mean (95% conf. 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. which may vary for some chemicals by year and by individual sample..

India. 108 Fourth National Report on Human Exposure to Environmental Chemicals . J Toxicol Environ Health 1989. J Assoc Off Anal Chem 1988. Atuma S. Piechotowski I. gov/toxprofiles/tp43. Granath F. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Patterson DG Jr.91:998-1000. 2002. et al.9(4):417-424. Arch Toxicol 1981.96:34-4Food and Drug Administration (FDA). Garrett N. Needham LL.54:1431-1443. Herrman T. PA. Brinton LA. Deichmann WB. Exposure of women to organochlorine pesticides in Southern Spain. Rivas A. Raju GS. et al. Lowry W. Arch Pediatr Adolesc Med 1996. Rogan WJ. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Cerrillo I. International Programme on Chemical Safety (IPCS). and other chemicals. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Brock JW. Demographic and seasonal influences on human serum pesticide residue levels. Siddiqui MKJ. Crespo J. Bates MN. Chemosphere 2005.111:349355. Buckland SJ. Bhatnagar VK.html. Astolfi E. Saiyed HN. Falk C. FDA total diet study. Kutty D. Link B. and HCB residues in human blood in Ahmedabad.57(4):315-320. Kulkarni PK. Environ Health Perspect 2003. Bull Environ Contam Toxicol 2004. Saxena MC. The Great Lakes Consortium.205:297-308. et al. Olson J.58:1185-1201. 4/21/09 Ginsburg CM. Darnerud PO. et al. Needham LL. J Pediatr 1977. Majumder SK. Cancer Causes and Control 1998. Angerer J. August 2005. Available at URL: http://www. et al.120:1-82. Zoellner I.fda. selected elements. 4/21/09 Anderson HA. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Environ Health Perspect 1998. Lindane. Int J Hyg Environ Health 2002. April 1982 to 1984. Toxicol Appl Pharmacol 1971. Bhargava AK.inchem. Nigam SK. Int Arch Occup Environ Health 1986. Radomski JL. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Olea-Serrano MF. Potischman N. Toxicological profile for hexachlorocyclohexanes update [online]. org/documents/jmpr/jmpmono/2002pr08. Krause C. Available at URL: http://www. Int Arch Occup Environ Health 1983.150:981-990. Metabolism of gammahexachlorocyclohexane in man. Bjerselius R.27:405-421. Paepke O. Rothman N.cfsan. Occupational exposure to hexachlorocyclohexane.106(5):279-289. Karnik AB. Kaus S. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Pollutants in breast milk. Bai KM. et al.cdc.gov/~dms/pesrpts. Ellis H. Aune M. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. available at URL: http://www. Levels of DDT. Chemosphere 2004. Krishna Murti CR. Burse VW. Seiwert M.20(2):186-193. Olea N. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Becker K. Placental transfer of pesticides in humans. Needham LL. Glynn AW. Maass R.72:261265. VI. Environ Res 2004. children and newborn infants. Lepom P. Reisch JS.atsdr. HCH. dietary intakes of pesticides.52(1):59-67. Bottimore DP. Biomonitoring of persistent organochlorine pesticides. Sturgeon SR. Stehr-Green. Gabrio T. Kashyap R. Botella B. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Hanrahan L. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Wood PH. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.71(6):1200-1209. et al. Organochlorines in Swedish women: determinants of serum concentrations. Heinrich R.html. Rey AA. 4/21/09 Kutz FW. Gunderson EL. Visweswariah K. Schulz C. Zaidi SS. Absorption of lindane (g benzene hexachloride) in infants and children. August 2008.48:127-134.htm. Rev Environ Contam Toxicol 1991.

6 (<LOD-31. which may vary for some chemicals by year and by individual sample.8. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. respectively. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. water.S.4) < LOD 15.3 (15. Mirex can cross the placenta and be excreted in breast milk.Organochlorine Pesticides Mirex CAS No. Mirex is not metabolized in the body. Fourth National Report on Human Exposure to Environmental Chemicals 109 .0-374) 11.1 (13.70-40.1 (<LOD-65. Some states and the U.5-291) 11. where it was applied directly to soil and by aerial spraying.S.S. where it has a half-life of 12 years.5. 1995).4-230) 18.0 (<LOD-108) < LOD < LOD 50. and foods. 1991). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3 (15. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. Formerly. animals. 01-02.5-82. 1985.5 (<LOD-42.4) < LOD 63. and 03-04 are 14. 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.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.0) * * * 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. especially those from persons living in the southeastern U. population from the National Health and Nutrition Examination Survey.5 (9.5-425) 40.6 (<LOD-108) 9.7) < LOD 66.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. after which it is widely distributed in the body and stored in fat.2-230) 13.7 (<LOD-47.0 (14. < LOD means less than the limit of detection. or pesticide application. Occupational exposure is limited to workers at sites where mirex contamination is present.7 (12.0 (12.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.. it is a highly persistent chemical in the environment.8 (12.8 (<LOD-73.6.6 (<LOD-23. Survey Geometric mean (95% conf.70 (<LOD-15. 2385-85-5 General Information Mirex has not been produced or used in the U. (Kutz et al. sediments.2 (7.10-37. 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.7) 8.70-24.1) 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. see Data Analysis section) for Survey years 99-00.6-305) 15. In studies conducted in the 1970’s and 1980’s. 10.2) 51.3) 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. mirex was detected in human adipose samples. soil.. since 1977.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.6) 9. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. disposal.3-225) 15. Mirex binds strongly to soil. Mirex is absorbed through the skin and from the gastrointestinal tract. and 7.10 (<LOD-15. aquatic organisms. Mirex has been detected in air.90-29.4 (8.5 (<LOD-115) 153 (30.6) < LOD < LOD < LOD < LOD 71.1 (8.40 (<LOD-13.S.S.8) < LOD 15. resulting in exposure to newborns and nursing infants.

100 (<LOD-.635) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .79) .450 (. and 2003-2004 subsamples.41) .106 (.310 (.08 (.92) .080-1.053-.080-1.140 (<LOD-. environmental levels) and health effects is available from the ATSDR at: http://www.370 (.054 (<LOD-. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.090 (<LOD-.062-. The geometric mean mirex levels of the Inuit mothers were 8.079 (<LOD-. 1989). In addition.510) < LOD < LOD .055-.html.690) .059 (<LOD-. IARC classifies mirex as possibly carcinogenic to humans.108 (. 7..112 (. 1991).8. 2005).090-1.077 (<LOD-.Organochlorine Pesticides exposures are unknown.610) < LOD < LOD < LOD < LOD . Smith. 2001-2002.052-.268) < LOD .73) . population from the National Health and Nutrition Examination Survey.470) .430 (. 2004).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 . Survey Geometric mean (95% conf.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .450) 1.S.7 ng/g of lipid. as well as in a subsample of NHANES II (1976-1980) participants. serum mirex levels were generally below the limits of detection (Stehr-Green.410 (.090 (<LOD-. 110 Fourth National Report on Human Exposure to Environmental Chemicals .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.070-1.e.S. 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. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue. EPA has established environmental standards for mirex.110 (<LOD-..470 (.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 . Biomonitoring Information In the NHANES 1999-2000.170-3.106) < LOD .37) .090-1.220 (<LOD-. which may vary for some chemicals by year and by individual sample. reproductive toxicity included decreased fertility and testicular damage.gov/toxpro2.089-. In samples obtained between 1994 and 1997.064 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .cdc. More information about external exposure (i.170) < LOD .256 (. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.102) < LOD < LOD < LOD < LOD .220) .79) . 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. 1995.atsdr. The U.090 (<LOD-.. which is approximately twofold to threefold lower than the 90th percentile for females in the NHANES 20012002 subsample but similar to 95th percentile for females in the NHANES 2003-2004 subsample (Van Oostdam et al.470) .093 (.100 (<LOD-. and 4. Laboratory animals fed high doses developed liver enlargement and liver tumors.02) . 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.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 .090-1.

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

which may vary for some chemicals by year and by individual sample.42 (<LOD-8. 2.40) < LOD 1.27) 696 661 521 696 603 939 Limit of detection (LOD.980-3.40 (.00-8.40) < LOD 6.8) 21.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. 1999).50-16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50-63.30-44.0) 2.6-Trichlorophenol CAS No.20) < LOD 90th 5.90-33. may occur by inhalation or dermal routes. Such workers would probably Urinary 2.10-3.03) 9.50) < LOD 1.980-3.30 (.0) 5. and sediments. 2.0) 2.40 (2.40-11.50-25.57 (<LOD-15.0) 2. hexachlorobenzene.40 (2. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.60 (2. recent sampling of U.S.40 (2.7.40 (1.00-3.6-trichlorophenol (2.0 (4.30-27.40 (2.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR. 1976).4. Formation of 2.4.00 (2.S.5-trichlorophenol (2.00 (3. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.0) < LOD 21.20 (4. 2006).71 (<LOD-8.0 (8. 1999).20) < LOD 1.S.80 (1. are metabolites of several organochlorine chemicals.60) < LOD 8.0) < LOD 11.0) < LOD 11. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Historically.0) 2.900-2. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.4.30-3. Both chemicals have been detected in air.0) 2.20) < LOD 5.940-3.40) < LOD 4.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . < LOD means less than the limit of detection.71 (<LOD-8.4.4.4.6-TCP).60 (4.7) 24. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.30-40.27) 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. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.0 (3.31 (<LOD-9. and polychlorinated benzenes (Kohil et al..9 and 0.0) < LOD 5. other organochlorines.3. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.30-27.80) < LOD 1.0) < LOD 5. population from the National Health and Nutrition Examination Survey. 95-95-4 2.9 (<LOD-121) 9.60 (.0 (4.42 (<LOD-12.20-71.950 (<LOD-1.30) < LOD 4. Trichlorophenols are no longer manufactured commercially.5-Trichlorophenol CAS No.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4.40 (1.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.6-TCP were used as intermediates in the production of certain pesticides.40 (.30-11.920-3.30-27.50 (2.40-18. surface water.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.50 (1.19 (<LOD-6.0) < LOD 5.50 (.0 (4. usually at herbicide production or waste incineration facilities.9.72) < LOD 1.0) 2.0 (5.63) 18.5TCP and 2. EPA. 2. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.0 (3.4.00-3.4.6-TCP in any of the samples (U. Survey Geometric mean (95% conf.60-18.4.20-36.Organochlorine Pesticides 2. Exposure to trichlorophenols also may result from metabolism of lindane. public drinking water systems did not detect 2.60-8.4.0) 14.30) < LOD < LOD < LOD < LOD < LOD 1. soils.5-trichlorophenol.4.80 (2.5-TCP) and 2. including hexachlorobenzene and hexachlorocyclohexanes.80-41. 112 Fourth National Report on Human Exposure to Environmental Chemicals . however. Occupational exposures.

S.1 (<LOD-58. 1995) were similar. At lower doses.Organochlorine Pesticides be exposed to mixtures of chlorophenols.53-3.e.57 (<LOD-7. 1989). More information about external exposure (i.05-8.69-18.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al. animals showed hepatocellular abnormalities.24) < LOD 5.19-4. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.9) 12..00-29..7 (4.00-19.67 (1.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .9 (5.gov/toxpro2.4..00) < LOD 4.73 (<LOD-8.24) < LOD 6. environmental levels) and health effects is available from ATSDR at: http://www. which includes trichlorophenols.27-17.37-11.6-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.57 (3.50) < LOD 2.5-TCP and limited for 2.5) 11.5-TCP nor 2.93-11.32) < LOD 4. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.8) < LOD 9. Urinary 2.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.820-2.4.html..4. Neither 2. urinary 2.6) 4.4.80 (1. 1989).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.49 (1.4.02) < LOD 7.44 (.55 (4..33) < LOD < LOD < LOD < LOD < LOD 2.83-12. 2003).3 mg/L reported in German adults aged 18-69 years (Becker et al.3 (5.29 (1.69 (2.6) 4.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11. the 95th percentile urinary 2. Survey Geometric mean (95% conf. 2003).4) 5.53-3. 1995) and up to 19 times higher than the 95th percentile value of 1.47-8.980 (<LOD-1.86 (3.75 (3.6-TCP had increased rates of hepatic tumors.0 mg/L.15) < LOD 2.2) 2. in addition to dioxins.4.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.0) 7.2) < LOD 5.5) < LOD 12.79-4.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.43 (2.16) < LOD 90th 5.6) 4.4.1) 2.90 (4. and lymphomas.88-16.4.6-TCP as reasonably anticipated to be a human carcinogen.20-6.8) 4. Laboratory animals chronically fed high doses of 2.4.81 (<LOD-9.75 (<LOD-6. and other chlorinated compounds.4 (6.36 (1.6-TCP levels at the 95th percentile were up to eight times higher than 3. 7. 2004).5-TCP. Human health effects from 2.4) < LOD 3.4.60-3. Radon et al.24 (3. NTP classifies 2. population from the National Health and Nutrition Examination Survey. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.78-19.17) 9. the 95th percentile urinary 2.78 (3. furans. In the same 2-6 year old children.44 (1.64 (4.2 (2..4) < LOD 3.46 (1.11) 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 2.05-17. Among 6-11 year old children in NHANES 1999-2000.24-11. IARC classifies combined exposures to polychlorophenols..920-2.74) 11.5-TCP or 2.68-4.82 (<LOD-32.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.19-12. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.atsdr.16 (.6-TCP. Fourth National Report on Human Exposure to Environmental Chemicals 113 .95 (3.28-25.02-3. 2003.31) < LOD 2.24) < LOD 1.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. leukemias.78) < LOD 1.. However.4.cdc.8 (5.57 (<LOD-7.62-20.43) < LOD 12. as being possibly carcinogenic to humans.4.67 (1.37) 16.68 (<LOD-8.13-13. The 95th percentiles for 2.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).

5 mg/g creatinine) were similar to the limit of detection for 2.4.49 (6.0 (20.32) 3.90-8.40) 3.0-44.23) 2.74-3.72-10.70 (2.6TCP causes an adverse health effect. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.54) 6.66 (8. 2003).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.10 (5.3-17.00 (4. Biomonitoring studies on levels of 2.9 (13.68 (<LOD-2.40-2.30-2.89 (3. interval) 2.70) 5.00-21.3 (11.0-43.6 (12.0) 13.1) 16.6) 26.6-TCP level.8-13.58 (1.40) 2.4.0) 19.09-7.89-6.4.5-TCP and to the median 2.3) 37.36-5.40) 2.20 (3.28) 24.80 (3.95 (4.65 (5.45) < LOD 11.4.56 (3.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.07 (<LOD-3.23-2.00-4.65) 15.0 (6.30-2.30) 4.67) 4.00 (2.8-24.92 (2.23) 3. which may vary for some chemicals by year and by individual sample.0 (12.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 20.60 (3.57 (<LOD-2.0) 17.0 (11.9 (11.2-0.67-12.4-17.45 (5.0) 13.40-14. 1998).7 (9.20) 4.85 (2.80-6.36 mg/g creatinine.91-4.0 (8.6-TCP (0.80-20.4..0-50.90 (4. Urinary 2.12) 2.6-TCP than are found in the general population.10-3.90) 2.4.0 (14. respectively.69 (3. In harbor workers exposed to chlorophenol-contaminated river silt.6) 21.0-18.60 (2.0 (4.98-7.32-4.5-46.52-3.6-TCP exposure and health effects.26 (2.4.0 (6.4.76) 3.0-41.5-TCP or 2.40-4.31) * 2.0) 13.0-54.8 (9.5-TCP or 2.51-12.5-TCP or 2.70-6. population from the National Health and Nutrition Examination Survey.0 (20.0 (14.7-16.55-3.60-3.00 (1.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.0 (14.25-11.4.4.06) * 2..4.47 (3. for males in NHANES 19992002 (Agramunt et al.95-6.31 (3. Survey Geometric mean (95% conf.4.40 (2.4.99) 6.10) 6.87-14.70-6.24 (2.4.30-33. was about six times lower than the median urinary levels for males in this Report (Radon et al.3) 23.70 (2.7-3. Mean values of 2.0) 17.63) 90th 15.50 (2. 0.4. < LOD means less than the limit of detection.0) 9.0) 14.09) 15.0-37.3-26.0) 11. 1991).08 (2.0) 15.80 (2.53) 4. Urinary 2.90 (3. 114 Fourth National Report on Human Exposure to Environmental Chemicals . 2004).6-19.7) 33.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.35-3.60-37.84) 2.50-5.59-6.0 and 1.2 (14.2) 12.4.1 (8. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.59) 4.60) 6.4.20 (3.75 (8.0) 11.52 (2. Biomonitoring data will also help scientists plan and conduct research about 2.44) 75th 4.7 mg/L.4.9) 13.95) 3.78 (2.40) 4.70) 1.8) 32.78 (2.60-21.0 (6.0 (15.0) 10.20-23. the median urinary 2.40-7.4 (10.4 (8.70-3.0-38.0) 9.30-11.4.0) 6.0-68.80-7.80) 1. Finding a measurable amount of 2.48-26.40 (2.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.73-9.0 (13.0 (8.7) 21..0) 10.20-3.10-3.45-9.0) 7.58-3.4 (9.5-TCP level of 0.0 (7.7 (13.5-TCP and 2.6-17.5-TCP and 2.S.70) 5.32) * 3.80 (2.5-TCP (0.40-2.9) 694 677 519 696 602 931 Limit of detection (LOD.0 (9.0 (16.0) 14.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4. similar to the limit of detection for this Report (Anderson et al.6-TCP in urine does not mean that the level of 2.40-32.9) 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 2.46-3.1-25.02) 2.3 (11.0) 7.85) * 3.20-6.6TCP values.8) 18.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 19.33-4.01-6.79 (5.80-25.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.0) 12.60 (3.10) 2.0 (15.4 (17.28) * 2.6 mg/g creatinine) and 2.0-38.3.0) 13.8-15.53) 2.98-11.60) < LOD 5.45 (2.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.6 (11.36 (1.6-22.18-3.70) 3.4.74 (2.1 (10.5-TCP or 2.10-2.14 (2.2) 25.04) 2.

79-17.38 (2.17) 13.73-22.20-2.48-2.6) 12.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.38-5.47-5.82 (3.52) 2.58 (4.4) 9.26-13.88) * 2.65) 18.88) 5.91-2.09-3.78) 90th 12.51 (2.1 (8.56) < LOD 11.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.38 (4.4.4) 4.00 (3.9 (9.15 (1.88) 4.29-4.8 (7.25 (3.8 (8.8) 19.99-2.6 (9.53-11.9 (9.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.25-2.76-8.87) * 2.95-2.05 (6.6 (9.83-5.75) 75th 4.4) 8.0 (9.22 (3.6 (12.23 (1.10-9.68) 2.6 (22.42) 2.42 (2.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.83-6.7-36.17) 2.29 (6.27-9.63) * 4. population from the National Health and Nutrition Examination Survey.4 (11.15 (6.49-3.82 (8.43 (2.18-2.53 (3.6) 8.10 (6.88) 1.04-2.25-17. Survey Geometric mean (95% conf.9-32.43 (<LOD-2.8) 21.87) 2.23) 4.9) 7.6 (5.0 (11.6) 13.68) 2.3-37.33-2.1) 11.29-4.51-21.06-2.32 (2. interval) 2.3 (9.73) 5. Fourth National Report on Human Exposure to Environmental Chemicals 115 .66-4.43-7.1-21.32-19.1-32.94-13.04-16.46-14.2 (12.06) 11.78) 2.5) 9.56-5.63 (<LOD-2.17-4.13 (1.50-8.7) 25.00) 4.63-15.62-15.33) * 2.38) 22.26 (6.22-9.50 (2.00 (2.49) 4.1 (13.87-7.6 (6.18-4.67-17.72-16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 8.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.90) 2.02) 3.98 (1.81-9.24 (1.40 (2.51) 18.22 (1.82) 2.76) 4.5 (8.9) 8.88) 4.33 (7.77-4.87-6.19-5.01 (3.16-10.91 (7.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.92) 4.0) 8.22 (<LOD-2.2 (13.59 (2.63 (2.S.9) 19.5) 12.65-2.28-4.71 (3.13-6.65-21.2 (8.6 (10.54 (2.91 (3.89-2.63-13.87 (3.96) < LOD 4.5) 11.88 (2.00) 4.30-2.9-34.8) 12.83 (3.6-31.76) 1.22-2.41-6.5) 11.44 (3.77) 2.9) 8.2) 19.55-2.63) 4.78 (2.Organochlorine Pesticides Urinary 2.98) 10.7 (14.82-2.11) 10.25-15.83-6.02 (1.25 (3.33 (1.06) 4.0 (6.60 (4.5 (10.7) 6.0) 10.53) 4.9-64.14-2.89) 10.8) 11.88-7.90 (1.3-23.65) 2.5-28.4 (12.21-11.52 (5.53) * 2.08-2.9-29.6) 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 2.41 (3.76) 2.56 (7.10) 4.52 (3.5 (7.1) 14.60-2.72) 32.81) 2.70-9.40 (7.05 (3.14-13.2 (7.5) 8.35 (3.52) 2.

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

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

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

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

16 (2.20 (2.0) 7.0 (4.840-1.98-5.86-15.290 (<LOD-1.35-12.8) 11.70) .2 (11.890 (<LOD-2.0) 15.290 (<LOD-.757-2.33 (5.86 (1.15-12.0-27.82) 10.26 (5.40 (.70 (4.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.S.03 (.80) .0) 11.2.8 (14.56-13.93-24.13 (2.0) 10.600 (<LOD-1.56 (6.00-27.11 (.0) 5.10 (.72) 5.26-6.8 (9.10 (2.52-11.70-14. < LOD means less than the limit of detection.3) 17.05-7.10-7.30 (4.2 (9.34-3.52) * * 1.50) 2.717-1.28) 1.21) 9.15) 14.37 (3.2 (14.0 (12.8 (12.80-22. 0.80) .4 (7.67) 3.14) * * .2 (7.13-2.26-8.60 (5.12) 4.52) 6.35-11.10) < LOD < LOD 4.02) 4.90 (1.07-10.0-28.90-4.58 (2.80) 4.1.530 (<LOD-2.47) * * 1.8) 7.0) 6.00-19.3-15.89) 9.73) * * .50 (2.20 (.19) 9.46) 10.80-24. 120 Fourth National Report on Human Exposure to Environmental Chemicals .9) 8.53) 4.42-3.3) 16.80 (2.70) < LOD < LOD 1.40-16.44 (2.81) 1.0) 6.758-1.1) 13.00 (4.54 (3.32) 1.43-12.55-6.76 (2.981 (.70-23.79-7.5) 15.740-2.82-12.0) 9.9 (8.71-9.0 (8.9) 14.33-18.08-15.80 (4.970-2.90) 3.13 (2.45 (2.700-1.00-7.830 (<LOD-3.0) 10.44-3.63) 1.955 (.20-30.4) 17.2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5-16.40-1.40-14.0) 5.56 (1.81) 11.57-7.20 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.750-1.50-5.0 (6.30 (2.4 (9.2 (7.00 (5.60-11.4 (9.68-7. and 0.0 (7.80) 11.599-1.27-15.10) < LOD .66) * * 1.810-1.2) 471 576 308 664 822 701 814 1122 922 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.0 (5.00 (1.00-27.620-1.00-12.44-38.00) 3.0) 11.04) < LOD 1.55-8.10 (2.623-1.74 (8. and 03-04 are 0.780) < LOD 3.2) 16.50 (4.2) 16.51) 2.6) 7.85 (3.0 (8.29) * * 1.17-3.579-1.0) 10.99 (5.21 (.95) 5.79 (5.30-4.98-12.7) 11. population from the National Health and Nutrition Examination Survey.5 (8.61 (3.16) 4. interval) 1.56 (4.58 (3.2 (9.60) .48-7.01) * * 1.10 (.8) 19.94) * * .5 (11.40-11.8 (8.954 (.860-2.1-17.4) 18. which may vary for some chemicals by year and by individual sample.40-19.0) 5.1-23.20-7.70-11.60 (1.91) 4.9-18.0 (7.47) 5.80) 2.0) 6.81) 11.8) 7.90) 2.670-1.30 (2.30-6.3) 14. see Data Analysis section) for Survey years 99-00.93 (4.74 (8.71 (2.4) 20.2) 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 1.90-5.0) 12.38-5.39 (8.490-2.39 (3.1) 95th 13.20 (.1) 10.97) 8.70 (2. 01-02.2 (14.0 (6.00) 3.20 (.7 (14.70) < LOD < LOD 75th 3.0) 11.50-36.2-20.0 (8.70-19.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80) 3.0) 10.2) 14.40-5.8-32.80) 2.0) 11.80) 2.0) 20.1 (10.34-7.83 (5.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.60-25.4 (7.80-4.22 (. respectively.2 (7.0 (7.08-2.0 (7.02-5.94) 3.97) 90th 7.0 (9.1 (9.0 (9.36-4.7 (12.32 (.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 1.12-19.60-18.0) 10.23-5.00-12.27-3.61) 4.5) 20.5-17.42) .50 (.08 (<LOD-2.96-3.20-4.35-16.58 (5.60) < LOD < LOD 4.6) 18.

6) 9.1 (9.7) 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 .61 (1.67-19.34 (6.03) 2.1 (8.60-9.3) 15.900 (.38) .10-13.47 (1.56) .3) 12.608-1.82-6.870-2.883 (.40 (3.47) * * .43) 2.00) 8.98) .26) * * .50) 7.64-5.6) 11.890 (<LOD-1.31-14.4) 4.58) * * 1.94 (2.54-4.56-13.82-14.8 (10.54-11.5-16.60) * * .18 (.04-6.43 (.54-2.24-3.860 (.94-9.38 (1.818 (.7) 18.79-3.5) 11.79-9.35) < LOD < LOD 3.93) 9.540-1.57-10.81-5.40-12.5) 12.37) 9.28 (5.37 (4.41-12.9 (5.09-11. Fourth National Report on Human Exposure to Environmental Chemicals 121 .02 (2.7) 672 678 472 509 695 577 595 948 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.1 (11.00 (4.66 (2.5-13.05) .9 (9.650-1.5-20.87 (1.570-1.6 (10.8) 8.89-3.90-8.93-9.3) 16.66-15.54-15.07 (.37 (5.1 (10.74) 90th 7.960 (<LOD-2.1-15.00 (4.6 (9.2) 5.68) < LOD < LOD 3.54) .53) 9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.28) 10.7) 12.53 (6.40) 4.84) 7.72) 11.21-23.03) 2.28 (2. population from the National Health and Nutrition Examination Survey.57 (6.920 (.00-19.47 (3.89) * * 1.3) 5.23 (4.0 (8.76) < LOD .83 (7.94 (4.574-1.42) 12.560-1.780 (<LOD-1. interval) .84 (5.5) 7.66-34.88-10.39 (2.40-5.7 (8.76-4.67) 1.57 (4.566-1.830-1.74) 4.633-1.61-13.03 (2.2) 9.61-29.52) 4.0) 7.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.1 (7.95 (3.94-10.92-5.02-2.60) 2.03-6.549-1.25) 6.81 (1.82-26.35 (1.1 (6.80 (6.4 (9.5-32.2 (10.92-2.510-1.00-17.5) 7.773-1.440 (<LOD-2.01-2.98) .20-8.83) 8.4) 4.6) 13.41) .51-5.37-3.40-28.8) 12.93-5.56) 7.09 (.94-22.0) 6.924 (.1) 4.68-4.28-9.75 (3.15-10.75) 2.430-1.75 (7.4) 13.30 (1.19 (4.14 (3.34 (6.533-1.7 (10.71-2.80) 9.S.69) 4.69 (4.29) * * .62-5.13) 4.05 (.57) 4.02 (7.40) < LOD < LOD 75th 2.98) 9.820 (.11-6.43 (3.4 (4.960 (.44 (2.3) 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 1.40-14.09) 2.9-28.30) 2.32-12.02-14.31 (3.42 (3.25) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.05 (1.34) < LOD < LOD .2) 5.41) Selected percentiles ( 95% confidence interval) Total * * 50th .45-5.78 (2.790 (.47) 2.40-3.73 (1.9) 12.28 (4.66 (5.27) < LOD 2.00-13.06-2.996 (.710 (<LOD-1.750 (<LOD-1.87-5.61 (1.9) 11.45-11.36) * * 1.46-5.90-5.8) 16.71) 10.45-5.69-10.2 (6.88) 2.77 (6.2) 95th 12.47 (3.8) 7.500-1.69) 2.85 (6.80 (2.10 (3.85) 2.88 (5.03 (7.855 (.55-20.82-14.23) 4.46) 2.95) 2.9 (9.1) 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 1.67) 4.890 (<LOD-1.98-5.7 (9.66 (1.34) * * .2 (8.8) 6.1) 4.2) 7.6) 8.98 (3.620-1.2) 13.56) 4.7) 5.04 (1.29 (2.5) 8.80 (7.94-23.88-15.2) 8.9) 16.62) .932 (.37-5.53-11.75-7.87 (3.5 (4.98-22.75) 14.

66) 4.5.60) < LOD < LOD 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.22) 8.11-6.96) 3.14 (6.00) < LOD .670 (<LOD-1.88) 3.90 (6.75 (2.63-14.8-20.67) 3.6 (10.6 (10.12 (4.20) .92) 9.90 (6.29-4.39-13.30) < LOD < LOD 4.75 (3.80) . which may vary for some chemicals by year and by individual sample.60 (6.8 (12.53 (3.90 (2.17 (7.0 (10.7) 16.80-12.06 (2.90-15. population from the National Health and Nutrition Examination Survey.7-21.10 (<LOD-1.740 (<LOD-1.4 (14.5 (8.0) 19.10 (.0 (5.10-10.9) 95th 14.90 (6.790 (<LOD-1.46-28.10-15.00-4.910 (<LOD-2.58.50-4.42 (1. 01-02.3 (9.7) 10.8-17. 0.2) 14. and 0.0 (14. 122 Fourth National Report on Human Exposure to Environmental Chemicals .52 (6.67-10.80-21.0) 13.8 (12.90-9.0) 18.27 (7.70-5.0) 9.95 (5.40) < LOD < LOD 75th 2.6) 14.3) 20.82) 8.680 (<LOD-1.41-5.27) .01 (2.22-12.70-8.3 (6.0) 11.9 (12.31) 1.47-6.20-4.90 (1.4 (10.3) 14.70-9.78) 5.3 (11.0 (15.50-5.46-4.30) < LOD < LOD .9 (7.1-23.S.72) 2.59-3.0) 14.62-17.73) 7.50) 3.0-24.89 (2.0) 11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.74) * * * * * 1.20-8.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80 (2.0) 7.15-6.90 (5.00) 7.4 (10.90) 8.18 (3.3 (12.0) 12.80-14.670 (<LOD-1.1) 11.7 (10.61 (3. < LOD means less than the limit of detection.51) < LOD 1.16-1.8) 8.0 (8.22 (6.90) 4.6-19.90-15.970 (<LOD-2.6-41.4-17.5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .5 (8.0-24.3) 22.8) 9.7) 14.37 (3.8-20.31-7.37) 2.00-16.41) 3.35 (6.7) 15.70) 2.77-3.650-1.34-5.10) 6.0) 12.70-9.00-9.7-19.67) 4.0-33.49-4.80) .4) 7.88) 10.5 (9.30) 8.00) 3.04 (3.45 (3.80 (5.9) 16.00-18.0) 13.7 (11.0 (9.0) 9.98-9.4) 11.97-4. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .31-12.25 (2.24-5.35) 4.670 (<LOD-1.95 (2.0-19.58 (1.22 (6.80 (2.96) 90th 7.3) 8.95-9.3 (9.90 (2.30) 3.1 (10.15-2.20 (<LOD-2.00-18.9-15.2 (7.86-10.9-14.00-4.40 (2.90-31. respectively.27) 9.6) 14.28 (7.30) 3.80-8.50) 5.1 (10.70 (1.5.90 (6.20) 3.66-13.9-17.89) 2.99 (3.0 (13.80-4.80-3.0) 12.6) 11.84-4.90 (2.92-17.5-26.77-14.24 (2.60 (2.20) 3.40 (2.3) 10.64) 10.60 (5.6) 18.27 (3.00) 3.0) 23.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 6. and 03-04 are 0.34 (6.9) 9.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.35-3.0) 14.29) < LOD < LOD < LOD < LOD 3.39 (5.20-18.2 (9.7) 22.0-29.61-32.00 (.70 (8.50) .34-10.27) 4.580-2. see Data Analysis section) for Survey years 99-00.3 (7.0 (9.80-6.0 (7.33-11.10-4.5) 21.8) 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 1.80) 5.18) * * * * * * * * 1.00) 8.81-6.9) 10.670 (<LOD-1.34-3.8-21.0 (10.

5) 22.6 (11.43 (2.82-8.01-5.00 (7.91-9.27) 5.23-3.5) 8.7 (8.29 (2.3 (7.32) 2.8 (10.89-10.06 (<LOD-1.74-4.4-18.3-17.6) 13.6) 12.16 (3.00 (3.29 (5.38 (1.07-3.590 (<LOD-.6 (13.5) 10.530-1.50-17.7 (11.75-3.37-5.87 (3.3-21.4) 7.5-17.5) 13.67 (1.7) 14.89) 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.9 (9.1) 13.21-21.2 (9.27) < LOD .34-18.55) .2) 16.45) 6.94 (5.79-9.00 (<LOD-1.61 (2.3) 9.30) 7.4) 7.3-34.47-9.890-2.36 (2.5 (15.27-13.1) 10.78 (4.73 (5.05-3.52-3.810 (<LOD-1.42) 8.2) 12.2) 15.4) 9.7-23.1 (19.50 (6.85-8.86) 9.63 (6.03 (6.54-5.37) 3.45) 3.6) 14.38 (.83 (6.7 (10.6 (10.4-15.1 (8.9 (9.58 (4.3) 6.15 (1.89-13.3) 12.95 (2.0 (8.28) 6.9) 19.33) 3.70-2.70-35.12) < LOD < LOD 4.93 (2.38) 1.54) 9.7-19.20-3.51-10.77) 3.81 (7.03) 3.89-3.4 (11.83 (7.59-3.75-3.89 (2.67 (7.86 (3.6) 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 1.760 (<LOD-1.42-19.93 (6.30) 2.32-8.2 (9.00 (<LOD-1.2) 10.30) 8.78-10.55 (2.7) 9. 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.12 (7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8) 14.88-7.3) 8.00) 8.2) 12.0-19.4-16.780-1.38-13.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.72) 4.18) 2.64-11.25 (4.78 (6.97) < LOD .89-3.85-17.53-8.0-21.42) 7.29) 3.6-19.33-10.4) 6.71) < LOD < LOD 2.850 (<LOD-1.5 (9.99) 2.86-3.80) 3.44-6.02-4.27) * * * * * * * * 1.21) * * * * * 1.6) 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 * * * * * * .16-14.2-15.06) .69-11.63 (2.S.910 (<LOD-1.690 (.8) 16.11-3.41 (7.96-10.8) 11.00) 2.9) 16.00 (5.6) 7.95) 90th 8.95) 3. Fourth National Report on Human Exposure to Environmental Chemicals 123 .92 (5.48 (2.38 (2.7 (10.3-15.27) 1.03 (2.09-11.3-17.74-19.94-14.940) < LOD < LOD 1.93-10.0) 14.973 (.6 (12.97-4.11 (5.6 (11.68-10.68) .7) 14.0 (13.00 (2.9-25.8 (8.96-11.4) 16.7) 15.29-2.4-16.15) < LOD < LOD 75th 2.4) 15.28 (1.93 (<LOD-2.19) 3.07 (5.51-7.6 (13. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .5 (11.68-4.1) 20.620 (<LOD-.28-12.34) < LOD < LOD < LOD < LOD 3.5 (8.5 (10.2) 19.04) 9.9 (9.78) 4.1 (13.2-30.92) 3.9-17.82-11.2) 12.77 (2.54 (7.88 (1.91) 3.89 (3.71 (1.0 (10.0 (11.6) 6.72-4.07) 2.2) 8.6) 95th 16.6) 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 * * * .99 (4.07) 2.55) 16.30-5.79-6.39-17.25-9.77 (2.09-11.950) .4) 7.68-19.14 (2.7) 12.920 (<LOD-1.

27 (2.89) 471 575 296 664 822 690 814 1122 919 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .650-.75 (2.79) .830 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.800 (.690-.25-1.46) 1.95) 2.18 (.74) 3.710) .80) 5.41-5.00) 2.94 (2.80) 2.48 (1.440-.20-1. respectively.343 (.94) .730) .449 (.31-3.690 (.580-.340-.940) < LOD .96-5.32) 3.60 (2.2.90) 3.54-2.10) 1.50 (1.83 (2.930 (.20 (1.21) 3.467 (.47 (1.820 (.30) 1.31) 2.500 (<LOD-.89) 1.05-3.73 (2.810) .90) 2.30 (.780 (.74-5.04) .949) .10) 3.38) 1.587) * * .50 (1.49) 2.79) .46 (1.00-4.S.59-6.690-1.380-.600-1.10) 1.64 (1.88) 1.01-3.22 (1. interval) Selected percentiles ( 95% confidence interval) Total * .40 (1.570 (.30-3.46 (2.09 (.970) .950) 90th 1.27 (3.457 (.96-3.80) 3.210 (<LOD-.05-2.70 (1.160 (<LOD-.240 (<LOD-.63 (1.590-.49) .960) .820 (.30) 4.60-4.83) 2.600 (<LOD-.29-2.29) 1.22-8.50 (1.570) * .83) .13) .790 (.17) 1.850) < LOD .670) .22-3.22-3.459 (.15) 2.450 (<LOD-.16) 1.20-2.30-1.33-2.94 (3.620-1.592) * .86) 3.45 (1.30-3.89) .08 (2.45-4.740 (.20 (1.740-1.597) * .760 (.87-3.75-2.11-3.26 (2.54 (2. population from the National Health and Nutrition Examination Survey.380) .95 (2.400) .17-4.930-1.16-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.32 (1.600-.540 (.20-3.70-7.73-5.690) .98 (2.388-.48 (2.47) 2.740-.280-.60) 3.60) 2.505 (.880) < LOD 75th .00 (1.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.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.618) * .69-4.930) 1.83) 1.30 (.76 (1. and 0.22-2.910) 1.1.700) .390-.584) .41 (2.260 (<LOD-.960) 1.980) 1.55 (3.30) 4.425 (.570 (.15) 2.990-1.570 (<LOD-.40 (1.749 (.720-1. < LOD means less than the limit of detection.91) 2.95-5.80) 3.16) 2.720-1.61 (1.77-2.510 (.720 (.86 (1.80) 3.04) 1.57 (2.592-.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 * .20) 1.78) 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 * . 124 Fourth National Report on Human Exposure to Environmental Chemicals .10-1.13) 2.65 (2.59-2.710 (.680-1.68-5.10) 1.560-.860) < LOD < LOD .710 (.89-6.740 (.382-.580-1.11-3.960-1.31-3.910 (.80 (1.01) .78) .83 (2.20) 3.490 (<LOD-.45 (1.80) 2.970) 1.380-.570 (<LOD-.09.14-1.03) 1.50 (1.840 (.20 (1.34) 2.42-2.453 (.50) 1.20 (2.46-3.455 (.97 (2.00-2.680-1.98) . see Data Analysis section) for Survey years 99-00.780) .960) .759) * . and 03-04 are 0.353-.350-.76-6.880 (.17) 1.750-1.30 (1.700) .26) .90-4.550 (.750) 1.98-3.70 (1.30) 2.57 (1.20) 3.570-1. 0.585) * * .70-2.37-2.36-4.19-1.549 (.910-1.73 (1. 01-02.80 (2.08 (2.460-.34) 2.359-.50-2.14 (1.930) < LOD .20) 2.592) * 50th .303-.50-2.550 (.657) * * .70 (1.23-3.45 (2.90) 2.77 (1.54) .18 (1.880) < LOD .960 (. which may vary for some chemicals by year and by individual sample.35) 1.30 (.32-1.31) 95th 2.01-1.20) 2.90 (1.510 (<LOD-.350-.20) 1.00) 1.780 (.398-.58 (1.10-1.336-.390-.50 (1.20-2.201-.39) 2.

00-1.688) * .79) 1.79 (1.530 (.75-3.485) * * .300 (<LOD-.92-8.33 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.720 (.61) 2.710 (.07) 1.460-1.310 (<LOD-.250 (<LOD-.520-.320-.380-.49 (1.590-1.71 (1.73 (2.42-8.97) 1.285-.43) 1.310 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.95) 1.52 (1.08-3.67) .33) .17-2.04) 95th 2.393 (.453 (.03-2. Fourth National Report on Human Exposure to Environmental Chemicals 125 .82 (2.22-2.60 (2.16-1.05-2.58) 3.17) 2.08-2.44) 2.64 (2.36) 3.61-3.800) < LOD .06) 4.17) 2.550-.480) .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 * .400-1.550) .47-4.70 (3.06-2.444-.70 (2.07) 5.234 (.560 (.412-.77-4.23 (.62 (2.71) .84-6.57 (1.60) .20-7.72) 1.23) 1.11-2.300-.930-1.44-2.710 (.591 (.742) * * .43 (1.91 (1.950-2.84 (2.460) .42-6.22) .630) * .22-3.880) 1.92) 3.66 (2.28 (1.19 (1.560-.67 (1.67-3.43) 2.00 (3.72 (2.390-1.47 (1.740) < LOD 1.820) .840) .75 (2.02-6.550-1.39) 2.447 (.77-3.253-.500-.490 (.760) .08-2.75 (1.850) 1.71) 2.22) 1.330-.23) 2.32) 1.30-2.20) 1.540-.60) 1.900) 1.45 (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 * .02-3.830 (.08-2.08-3.72-4.700 (.380) .560-.750 (.50) 1.730) .16) 1.31-1.840) 1.840) 1.67 (1.82) 2.230 (<LOD-.08-3.98) 1.870 (.710 (.73-3.08) 2.552 (.550-.55-3.42) .52) 3.57-2.270-.58 (1.76) 1.980-1.368) * .310-.910) < LOD .11) 1.47 (1.510 (.400) .23) 3.509 (.30) 3.87 (2.99) 2.790 (.18-2.77 (3.08 (.640 (.740) .23) 2.55 (1.590) * 50th .318-.270-.470) .05 (1.88 (1.03-1.22-3.61-3.41 (.403) .870) .280 (<LOD-.38 (2.05) 1.89 (1.53) .680 (.597) * .25-3.66) .61 (3.32 (.480-1.510-.38-3.330 (<LOD-.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.590 (.32) 2.04-5.57-4.72 (1.57 (3.830) 90th 1.370-.460 (.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.390) .05-4.470 (<LOD-.32-1.471-.535 (.20-2.94) .07) 1.49-4.750 (.08) 1.940-1.43) 2.50 (1.580) .24) 4.136-.08 (2. population from the National Health and Nutrition Examination Survey.75) 6.670 (.42 (.65) 2.67) 1.335-.22) 4.S.320-.377-.920) .58-6.69 (3.13 (1.820) 1.305 (.78) 3.64 (2.700 (.380-1.98) 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 * .520 (. interval) Selected percentiles ( 95% confidence interval) Total * .38 (1.760) < LOD 75th .790) .90) 2.22 (2.10) 2.80) 2.448 (.39 (1.348-.660-.690) < LOD < LOD .97) 2.515) * * .440-1.32) 5.34 (1.62 (1.16-2.92 (1.88) .09) .45 (2.04-1.270 (<LOD-.645) .372 (.63 (1.29-4.350) .69 (1.580-.07 (.81) 2.60 (1.640 (.00-3.580 (.700 (.07-2.14 (2.05) < LOD .08-3.720-1.02-3.97 (1.800-1.739) * .99) 1.640 (.11 (.180 (<LOD-.07) 1.97 (1.89-3.510 (.250 (<LOD-.07-3.990-1.

50-17.0) 45.98 (1.9 (19.77) 38.5) 69.0-53.5.8) 32.2-39.6-54.92-5.66-5. which may vary for some chemicals by year and by individual sample.0-41.54 (1.9) 48.10-4.0-47.1-25.20 (2.0) 16.9) 38.0 (13.0 (20.8) 62.9-51.0 (6.07-5.4) 19.3 (23.63-6.13 (1.0-39.06 (1.70 (7.600-2.0) 28.2-47.64-3.5-20.2-26.9) 18.30-14.5-74.2-27. and 0.0) 15.0 (11.10-13.0-58.71) 5.0) 31.5-40.90) 11.11) 2.0-52.0 (38.54 (3.7 (12.0) 3.3) 38.27-6.90 (1.10 (1.10 (1.76 (2.10 (7.0) 4.6-45.0-110) 34. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80-18.85) * 2. population from the National Health and Nutrition Examination Survey.41) 5.70 (1.45) 2.0 (7.3) 33.99 (2.1) 140 (46.470 (<LOD-1. see Data Analysis section) for Survey years 99-00.33 (5.0-62.53 (1.4-22. and 03-04 are 0.80) 90th 38.57-2.10) .1) 95th 48.00 (.0 (38.8 (22.50 (2.72 (1.0-58.7-22.21 (3.0-41.30 (.18.75-14.8 (12.86-3.0-49.0 (38.8) 41.8-24.0 (38.57-2.58) 16.79 (2.02 (2.16) * 1.20-4.79 (1.0 (21.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.23-2.71-2.48-2.60 (2.13 (1.4-76.04 (<LOD-2.88) 1.0-92.6-22.8-21.5-45.50-20.2) 16.70-17.8 (12.48-2.26) 75th 11.94 (1.830-4.05-3.0 (20. 01-02.0) 3.5-27.80) 1.76 (2.2 (12.0) 6.0) 32.48) 5.0) 3.0 (32.91 (4.45) 2.69) 2.0 (38.70 (1.0) 33.4.0 (26.0) 20.05) 1.42) 1.7 (12.29) 2.30) 11.25-3.40-4.1) 38.88) 3.1 (10.52 (4.6 (11.0) 5.44-7.0) 4.12 (3.41-4.21 (1.50-2.1) 38.70) 5.70 (.64-8.0 (38.0 (8.0-41.00 (.32 (2.74-2.690-3.0-43.0) 30.0) 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 2.44) 3.0-62.7-41.44) Selected percentiles ( 95% confidence interval) Total * 2.46 (.0 (8. interval) 1.0) 8.3 (14.0-110) 42.0 (19.0) 4.20) 1.1-47.81-2.8) 39.0 (8.0) 18.2-27.6 (15.3) 28.7) 20.1 (22.0-39.97) 6.1 (26.0 (33.49-2. 126 Fourth National Report on Human Exposure to Environmental Chemicals .11 (4.1-40.19) 2.0-50.0) 3.70) 1.23-2.1-46.83 (3.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.S.40) < LOD 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. < LOD means less than the limit of detection.10 (1.80) < LOD 1.4 (15.53) * 2.6) 52.2-80.46-6.0 (37.70-6.0) 15.0) 19.3 (12.83-2.13) 12.96) 5.0) 42.1-19.43-7.0) 16.18) 6.530-4.21 (4.0-31.86 (1.83 (1.04) 3.50-7.50-5.0 (40.6 (26.53) 40.1 (11.70) 1.2 (19.26 (.3 (10.9-21.67 (1.0-29.660-2.41) 1.41) 1.19-2.2-33.30) 4.9 (10.65 (4.29-9.3 (12.0) 17.80) .0 (38.830-3.18) 20.1) 18.29-4.90-8.77 (1.5 (24.0 (25.1 (25.2) 31.0) 13.10 (1.16) 2.95 (5.44) 2.1-20.0) 20.8 (26.78) 9. 0.4 (19.0) 17.12) 1.59 (1.0 (17.36-2.0-53.83-2.3) 26.53) 1.71 (4.61 (1.82 (1.92) * 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6-27.98) * 2.78 (1.2-62.9) 17.04-8.40) < LOD 2.4) 38.79-2.9 (19.87-7.31-6.7 (28. respectively.90 (1.35-6.41 (1.05) * 2.7) 47.93-3.3 (24.85 (1.59 (1.6 (9.23) 9.17-2.61-2.3) 31.10) 39.9 (23.0 (24.06) * 2.0) 28.80-2.8) 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 1.46-2.00-24.40-16.14) 5.18) 14.09 (4.60) < LOD 1.610 (<LOD-1.58-2.4 (10.0-69.5) 30.0-230) 35.81-3.40) 50th 2.1 (25.9 (27.0-260) 34.

56 (2.12 (1.27 (6.4 (12.29-5.79 (2.20) Selected percentiles ( 95% confidence interval) Total * 1.6-49.9-95.680-4.1) 13.40 (2.870-3.76-2.7-43.8) 23.7) 34.4 (11.2 (15.38 (3.62) 4.35) 1.5-43.72) 2.28) 1.86) * 2.95-16.5-190) 30.5 (34.01 (.1-60.899-2.7-47.1) 25.71 (1.4-71.33-5.14 (.90 (.0 (23.9-41.4-39.15 (.86) * 3.1) 13.1 (50.8-26.6) 19.0) 47.4 (25. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.97 (1.96-16.6) 3.5 (41.2) 41.1-22.3-19.2) 471 575 310 664 821 715 813 1121 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.6) 7.2) 33.3-27.53) 1.6) 23.5-97.3 (8.50-5.64 (1.870-3.95) 90th 32.11-2.99-4.27-3.1) 17.58-17.59-2.56) 1.0 (32.3 (10.33) 1.25-3.88 (4.69-5.30) 28.36) 10.3) 28.1) 27.4 (21.16-2.03-2.8) 3.50 (2.69-18.75 (1.9) 12.33) < LOD 1.S.40-7.0) 48.67-16.54-15.0) 30.1) 36.02) 1.8-37.890-4.19) 5.888-1.00-16.8-43.9-18.9) 24.41 (2.06) 1.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.46-5.4) 3.6) 112 (40.5 (6.9-52.36 (4.57 (6.16 (1.40-4. population from the National Health and Nutrition Examination Survey.7-19.08) 1.19-14.16 (1.5 (13.0 (25.19-6.870-3.2 (9.6) 11.38-1.9 (19.82) 1.1) 27.9 (10.4) 12.0) 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 1.0 (6.1) 15.47-17.7 (18.9-37.70-4.7 (18.3) 13.3 (9.4-21.17-3.6-51.0) 10.4-34.80-8.2-38.23) 37.34) * 1.63-5.32-3.5 (8.8-45.84-13.8) 11.75) * 1.4 (19.60) 4.3 (20.62 (2.17) 2.55 (2.88 (4.71) 8.61-22.43-2.8 (7.0 (14.860 (<LOD-1.45 (1.24 (1.22-3.46-6.58-2.2 (21.9) 54.14-8.3 (10.0 (39.4) 14.67 (1.44) 9.5 (17.6) 3.5 (15.02) * 1.2) 36.9 (7.93) 5.68 (1.9-36.23-1.66 (1.31) 2.67-3.91-2.2-34.88 (1.1 (39.12) 3.57) 4.03) 1.7) 30.0-70.94) 19.22 (.38-5. interval) 1.43) * 2.52 (1.0 (23.2 (16.91 (6.28 (1.54-2.0) 3.51) < LOD 1.2-70.94) 1.0-118) 29.06) 1.46-22.27) 50th 2.7 (11.18-1.9) 3.1 (33.7) 66.1 (34.75-6.02 (.7) 23.19) 5.2) 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.16 (1.930 (<LOD-1.1-63.39 (1.45-1.06) 75th 9.18) * 2.6 (27.2) 13.00) 1.0 (19.2-47. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.08 (1.83) .22 (2.07) 9.82 (2.0) 25.4 (9.46) 1.96) 2.9 (39.59-2.47 (1.7 (24.59-15.60 (.21 (4.7-38.6 (24.8) 15.43-12.68) 47.7) 26.26-2.6-38.5) 70.1) 52.07-2.47 (3.3-42.750 (<LOD-1.20-5.18) 3.51) .07-2.19 (1.8) 31.2) 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 2.4-67.5-36.7) 95th 51.06-1.8-34.48 (4.22-2.2) 13.7 (10.2 (8.6-32.09 (5.1 (25.61 (1.5 (15.7-20.1 (12.0) 13.7) 15.2-28.75 (1.71-2.38) 5.94-20.83 (.4 (25.70 (1.2) 4.6 (11.79-17.66 (1.33) 2.40 (5.95 (2.11) < LOD 1.27) 10.67 (1.7-109) 22.0-40.48) 1.52-4.61-2.35 (2.00 (4.66) 8.1) 25.7-37.36-13.88 (1.9) 24. Fourth National Report on Human Exposure to Environmental Chemicals 127 .8) 32.23) < LOD 2.32 (3.7) 61.9 (13.0 (17.4) 12.26-4.9 (26.37 (1.9) 3.3-22.670-1.4 (5.0-71.80 (1.95-16.6 (7.37-2.5) 27.2 (22.35) .00) 6.

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 .650-1.32) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130-.150 (<LOD-.1.170-.870 (.430 (.360-.13) .860) .03) .270 (.30) .140-.470-1.720) .090 (<LOD-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.450 (.140) .10 (.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 * * * * * * * * * .460 (.400-.370-.30) .230-.1.410) < LOD < LOD < LOD < LOD .20) .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 * * * * * * .350) .600 (.650 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.100 (.090 (<LOD-.12 (.760) < LOD .160) .540 (<LOD-.700-1.310) < LOD < LOD < LOD < LOD .00) .610-1.560 (.310-.150) .120 (<LOD-.680) . see Data Analysis section) for Survey years 99-00.690-1.162) * * * * * .720 (.650) .210 (.870 (. respectively.640) .220 (.640 (.680-1.680-1. 0.420-. and 03-04 are 0.130 (.540) . and 0.930 (.510-1.160) .310 (.870 (.730) .840) .310) < LOD < LOD < LOD < LOD .700-1.140-.430-.380-.830 (.117 (.130) .660 (.990 (.830) .770) < LOD 95th .650-1.630 (.830 (.10) .440-1.60) 1.830) < LOD .320-.370-.610 (.620 (. population from the National Health and Nutrition Examination Survey.350) < LOD < LOD < LOD < LOD .680 (.570) .240 (<LOD-.900 (.630 (.780) < LOD 1.220 (<LOD-.640-1.390) < LOD < LOD .080 (<LOD-.090 (<LOD-.700-1.110-.099-.820 (.850) < LOD .190 (.610-.15) .42) .10) .05.410-1.410-.230) . < LOD means less than the limit of detection.130) .080 (<LOD-.190 (.840) .280) < LOD < LOD < LOD < LOD .390 (.S.290) < LOD < LOD < LOD < LOD .090 (<LOD-.870 (.730-.200) < LOD < LOD .530-.540) .460-.850 (.720-1.050-.260 (. 01-02.380-.300-.130-.650) .470 (.450 (.090 (<LOD-.58) . 128 Fourth National Report on Human Exposure to Environmental Chemicals .30) .300-1.290) < LOD < LOD < LOD < LOD 90th .490 (.180) .740) < LOD . which may vary for some chemicals by year and by individual sample.210 (.410-.870) < LOD .860-1.330-.320 (.290 (<LOD-.610 (.990) .120-.140-.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .550) .084-.360-.190 (.171) * * .380-.40) .820 (.850 (.10) .450 (.700-1.120-.870 (.560 (.940 (.990) .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.42) .130-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .090 (<LOD-.160-.310 (.640) .36) .770 (.

410 (.500-1.190 (.190-.570 (.450 (.410-.550 (.080) .700 (.780) < LOD 1.190 (.86) .570-.700-1.110) .310) < LOD < LOD < LOD < LOD .09) .560 (.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .380-.740) < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.330-.890 (.00) < LOD .330-.03) .510-.360) < LOD < LOD < LOD < LOD .110) .110) .20) 1.540) .720 (.340-.750) < LOD 95th .24 (.330 (.800-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.940) .390-.140) .300-.520-.360-.161) * * .410 (.570-1.111) * * * * * .057-.960) .070 (<LOD-.730) .86) .360-.084-.19 (.860 (.110) .580 (.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 * * * * * * .380-.140-.78) .390-.500 (<LOD-.400 (<LOD-.220) < LOD < LOD < LOD < LOD .02) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .730) .62) 1.110-.170) < LOD < LOD .410) < LOD < LOD .080 (<LOD-.940) .080 (.440-1.760) .670 (.700 (.380 (.230-.410-.720 (.100 (<LOD-.120) .220 (.260-.610-1.02-1.600-1.990) .450) .230) < LOD < LOD < LOD < LOD .66) 1. Fourth National Report on Human Exposure to Environmental Chemicals 129 .060-.330-.116 (.660-1.170 (.36 (1.270 (.580-1.330 (.12) < LOD .580) .880 (.810 (.300-.260) .670-1.360 (.150-.380-.580 (.24) .29 (.240-.400) .03 (.880-1.490-1.870) .070 (<LOD-.140-.290) < LOD < LOD < LOD < LOD 90th .540 (.230 (<LOD-.140-.860 (.200 (.990) .550 (.14) 1.200 (.300 (.170 (.650) < LOD .180-.090 (<LOD-.640-1.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.280) < LOD < LOD < LOD < LOD .120) .03 (.780 (.03 (.270) < LOD < LOD < LOD < LOD .440 (.730) .740 (.460 (.580) < LOD .050 (<LOD-.540 (.01 (.60) .850 (. population from the National Health and Nutrition Examination Survey.380-1.470 (<LOD-.070 (<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 * * * * * * * * * .43) .250-.S.670 (.410) .140-.970) .700) .600) .860-2.500) .370 (<LOD-.100-.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 .730 (.67) .58) 1.38) 1.090 (.710-1.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.140-.320 (<LOD-.210 (.650-1.070 (<LOD-.

99) 11.0 (5.28) .52) 5.40) 2.42) 2.90-9.170-1.59-5.50) 2.770 (<LOD-1.15) 19.74 (3.52 (1.900 (.620-1. and 0.99 (1. 01-02.76 (1.750-1.63 (3.36-3.49) 17.0) 4.0) 2.110 (<LOD-.35) 11.03 (.0) 2.24-7.51-8.55-8.52 (1.691 (.425-1.39 (2.05 (3.840 (.0) 2.0) 5.66) 4.61 (1.60) .55-4.080-1.50) .0-38.20-4.0) 7.0) 5.07) 1.0) 4.330 (<LOD-1.74) 5.70) 2.30 (1.1.87) 12.33 (4.07 (3.30 (1.62) 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 * * * * * * .08.90-20.0-38.0 (13.90) .00 (.960 (<LOD-1.10 (3.910) 2.S.48 (2.480-.0 (6.0 (5.49 (1.70-30.360-1.190-1.70-17.0) 4.20-17.400-1.90 (1.67) .370-.90-37.97) 20.70-3.0 (5.65) 1.87) 5.14) 2.0) 2.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.83) 2.30 (.53) 20.20-4.13 (3.610) < LOD < LOD < LOD < LOD < LOD 2.770) 2.960 (. population from the National Health and Nutrition Examination Survey.60) 1.82-4.31) .70-7.640 (.00) .94-3.42) .830 (.37) .10 (.51 (2.750-2.250 (<LOD-.610 (.11) . and 03-04 are 0. 0.740 (.35) 5.43-4.0-39.49 (1.00) .97) 20.18) 1.40-7.0 (7.0 (16.40) 1.10-3.99) 19.00-17.00) 1.88-3.07 (3.0-38. which may vary for some chemicals by year and by individual sample.10 (3.12) * * * * * * * * .11 (1.890 (.05 (2.840-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40-20.850) 16.0) 5.3) 952 1187 935 997 1331 995 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .0 (17.0-40.840 (<LOD-1.210-1.35-10.07-3.0 (5.30-3.0) 2.800) 17.0-44.0 (3.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.580 (.83-3.0) 3.23-6.0 (4.0 (17.90) .0 (17.31-10. see Data Analysis section) for Survey years 99-00.880) 5.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.21) 3.21-3.38-3.53 (2.720) 2.20 (1.640 (.28) 1.70-50.870) < LOD < LOD .0-40.10-3.260-.45 (2.350-.40 (1.690 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-9.36-3.6) 5. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.30) .40 (1.26 (2.16) 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 .07 (1.05-3.39) .90) .800) 90th 13.40-4.94 (1.68) 2.0) 2.40-8.85-3.32-9.30) 95th 19.0) 5.0) 4.30 (1.0 (5.46 (1.48) 13.730 (.600 (.590 (.67 (1.1.47 (3.11) 13.07-3.90-28.53-7.0 (4.67 (2.62-8.63) 32.14-5.96 (1. respectively.28-9. 130 Fourth National Report on Human Exposure to Environmental Chemicals .380-.800-4.350-.30-6.14) .83-3.15) 14.00 (1.30 (2.20 (1.80 (4.90 (2.30-7.0 (17.0 (17.32 (1.00-17.94-8.12-1. < LOD means less than the limit of detection.01) 5.86) 4.0) 2.510-.20) < LOD < LOD < LOD < LOD < LOD 1.29-10.

12-4.52 (.40-2.8) 7.4) 2.28-6.700) 6.690-5.61) 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 .66-47.18) 95th 21.620-3.02 (1.310-.18) 1.24) 3.340 (.320-1.8 (20.580 (.25 (1.64) 30.600 (<LOD-1.56) .59 (1.10-3.55) 21.930) .5 (8.33-5.67-6.1) 2.650) 90th 10.8) 1.44-11.47) .820 (.75) 5.82-11.580) 16.360 (.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.97) .8) 2.81-17.90-6.850-3.7 (12.470 (.36 (.55) 21.13 (2.05) .57 (.5) 7.71 (2.55 (3.41 (4.3) 3.790) 11.03) 16.9) 6.7) 3.49-2.940-4.18) * * * * * * * * .35 (.51-4.330-1.73 (4.340-.07-21.51-44.92 (2.69-7.80) 3.47-10.370-1.1 (5.91) 2.00-19.88 (.02 (.33-4.17) 5.1 (7.6) 952 1187 934 997 1330 993 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .08) .77 (.540 (.700) < LOD < LOD < LOD < LOD < LOD 1.260-.790 (.33-3.670 (.630-1.48-42.85-3.7) 6.7) 4.04-16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07 (2.40) 1.32-6.01 (1.02) .270-.83-11.09-3.50) .960 (.474-1.31) .33 (1.15) 9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.48-7.27 (2.67) 2.57) 1.89 (2.11-5.29-4.32) 9.10) 2.25-9.43) .830-3.91-4.340-.430 (<LOD-.14-6.770) .02-4.71 (.40-12.650 (.500 (.69) 2.730-3.240-.45 (1.88 (2.21-3.57-40.7) 5.890 (.0 (9.22-27.50 (4.370) < LOD < LOD < LOD < LOD < LOD 1.84) 9.86) .23-7.780-4.14 (1.5) 2.9) 5.340-.3) 2.62-17.580-1.580) 1.41) 18.540-1. Fourth National Report on Human Exposure to Environmental Chemicals 131 .29 (4.48 (4.590) 2.50) 11.430) 1.30 (4.31-7.970-3.31) .65 (2.660) < LOD < LOD .39) 20.5) 2.50 (2.04 (1.830 (.47-10.56) 2.53) .38 (2.67) 1.47) 5.80 (.96-25.7 (6.22) 2.2-38.8) 4.0) 4.44) .86 (3.96-8.88) 17.450 (.S.390-.4-34.85 (1.31-18.67 (2.2 (8.12 (4.840-3.79 (.62 (1.150 (<LOD-.270 (<LOD-.5 (11.260-.9 (11.06 (.74 (2.98 (4.560 (.820) .190-1.40 (.0 (4.800-2.64-4.96) 2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.860-2.370 (.53) 27.8) 2.11) .00) .56 (1.03) 2.33 (3.25-38.740-1.37) 4.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.5-40.88-3. population from the National Health and Nutrition Examination Survey.10 (2.5 (9.1) 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 * * * * * * .8) 7.748 (.17 (1.8-33.57) 8.710 (<LOD-1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.83 (4.250 (<LOD-.60 (1.4 (4.

Denley HV. and incidental exposure to organophosphate pesticides using urine alkyl phosphate and phenolic metabolite measurements. Fenske RA. Hansen S. Amr MM. Regul Toxicol Pharmacol 2003. J Occup Environ Med 2004. Reprod Toxicol 1998a. and neuropsychological study of sheep farmers and dippers exposed to organophosphate pesticides. Bradman A. Environ Res 2001. Environ Health Perspect 2003. Astroff AB. Farahat FM. Fenske RA.113(12):1802-1807. Keifer MC.111(3):377382. Jamal GA. Miller M. et al. et al. neurophysiological. Urinary excretion of alkylphosphates in the general population (Italy). Eigenberg DA. Fisker-Andersen J. Toxicol Ind Health 1998b.16(5):417-426. Lu C. Shebl MM. Kipen H. Mathieu L. J Expo Sci Environ Epidemiol 2006. Grzywacz JG. Aprea C. Daniell W. Am J Ind Med 2006. Environ Health Perspect 2003. Anger WK. Curl CL. Hawk R. Barnhart S. Lu C. Ann NY Acad Sci 1997. Temporal association of children’s pesticide exposure and agricultural spraying: report of a longitudinal biological monitoring study. J Toxicol Environ Health 1981. Chen W. Organophosphorus pesticide exposure of urban and suburban preschool children with organic and conventional diets. Long-term use of organophosphates and neuropsychological performance. Garrison RP.12(6):619-645. Young AD. Surveillance of occupational. A clinical neurological. Krieger RI. Gillham RA.14(6):869-889. Vaughan TL. Sciarra G. Astroff AB. The relationship between maternal and fetal effects following maternal organophosphate exposure during gestation in the rat. Bradman A. Garabrant DH. Blanchard O. Buchanan D. Boccalon P. Peterson JC. J Expo Anal Environ Epidemiol 2005.837:257-268. Farahat TM. Arch Environ Health 1998.7(5):715-731.37(3):382-395. Castorina R. Occup Environ Med 2003.111(13):1640-1648. Novelli MT. Kissel JC. Heudorf U.110(8):829-833. Eaton DL.38(1):91-97. Neurobehavioural effects among workers occupationally exposed to organophosphorous pesticides. Koch D. Duggan A. Giordani B. Sci Total Environ 1996. Fiedler N.46(4):367-378. Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals. Environmental and biological monitoring of exposure to organophosphorus pesticides: application to occupationally and non-occupationally exposed adult populations. Checkoway H. Correlation of urinary pesticide metabolite excretion with estimated dermal contact in the course of occupational exposure to Guthion. et al. Charnley G. Environ Res 1992. Bouvier G. Berent S. Neuropsychological performance among agricultural pesticide applicators. et al. Curl CL. Bravo R. Kissel JC. Lunghini L. Chukwudebe A. Harnly ME. Curl CL. Cumulative organophosphate pesticide exposure and risk assessment among pregnant women living in an agricultural community: a case study from the CHAMACOS cohort.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites References Albers JW. Occup Environ Med 2002. Costa LG. Jolley L.108:521-525. Fenske RA. Robinson LR. Leffingwell JT. Strambi M.59(1):217-228. 86:80-87. Kedan G. Castorina R. et al. Environ Health Perspect 2000. Quandt SA.49(9):751-760. Neurophysiological function in farm workers exposed to organophosphate pesticides. Elgethun K. Sartorelli E. et al. Arcury TA. Davis SW. McKone TE. Greenhalgh R. The effect of the 14-day agricultural restricted entry interval on azinphosmethyl exposures in a group of apple thinners in Washington State. Barr DB. Eskenazi B. Freshwater KJ. Fenske RA.60(4):279-286. Eskenazi B.59(7):434-441. Richardson RJ. Kelly-McNeil K. Davies JE. Barr DB. Sartorelli P. Momas I. Biologic monitoring of exposure to organophosphorus pesticides in 195 Italian children. Barr DB. Franklin CA.53(1):714. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Abdelrasoul GM.32(5):487-496. Barr DB. Chevrier J.177:37-41. Schweitzer SJ. Pilkington A. The effects of occupational exposure to chlorpyrifos on the neurologic examination of central nervous system function: a prospective cohort study. Environ Health Perspect 2005. Metabolites of organophosphorous insecticides in urine specimens from inhabitants of a residential area. Abdel-Azis M.15(2):164-171. Centers for Disease Control and Prevention (CDC). Aprea C. 2005. Griffith W. Environ Health Perspect 2002. 132 Fourth National Report on Human Exposure to Environmental Chemicals . Regul Toxicol Pharmacol 2003. Orsi D. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies. Di-alkyl phosphate biomonitoring data: assessing cumulative exposure to organophosphate pesticides. Organophosphorus pesticide urinary metabolite levels of children in farmworker households in eastern North Carolina. Am J Ind Med 1997. Bozzi N. Engel LS. accidental. Demers P. Seta N. Angerer J. Organophosphate urinary metabolite levels during pregnancy and after delivery in women living in an agricultural community. Fenske R.

52(10):648-653. discrimination. low-level organophosphate exposure on delayed recall. Occup Environ Med 2001. Rothlein J. Pilkington A. Lu C. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Jamal GA. Environmental Protection Agency (U. et al. Eskenazi B. Terry AV Jr. Petchuay C. Effects of long-term organophosphate exposures on neurological symptoms. Tumino R. Pesticide industry sales and usage . Lancet.2000 and 2001 market estimates. Available at URL: http://www.38(4):546-563. National Research Council (NRC). Lewis JA. Stark A. Seiber J.S. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Ruberu DK. Neurotoxicol Teratol 1998. Nell V. Mounce LM.84(5):731-736. Schenker M. S. Claypoole K. Weerasekera G. Keefe TJ. Gladstone EA. 4/7/09 Young JG. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Steenland K. May. Scand J Work Environ Health 1998. Washington (DC). Beach J. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function.edu/ openbook.24(1):18-29. Santana J. Lambert WE. Arch Environ Health 1988. Rodnitzky RL.S.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI.44(4):352-357. London L.php?record_id=2126&page=1. and spatial learning in monkeys and rats. Hansen S. Narang A. vibration sense and tremor among South African farm workers.pdf. Muniz J. Neuropsychological effects of long-term exposure to organophosphates in sheep dip.345(8958):11351139. Effects of chronic. Pedersen L. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Bravo R. Neurotoxicity among pesticide applicators exposed to organophosphates. The Pesticide Health Effects Study Group. Calvert IA. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments.26(2):199-209. Buchanan D. metabolite clearance. Am J Ind Med 1987. Int J Occup Environ Health 2006. Chronic neurological sequelae to organophosphate pesticide poisoning. 1991. Irish RM. A behavioral evaluation of pest control workers with short-term. Hore P.68(3):209-227 Maizlish N. 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. Frasca G. et al. Dinoff TM. Burcar PJ. Phillips J. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Lancet 1995. Myers JE. van der Hoek W. Ames RG. Visuthismajarn P. J Toxicol Environ Health A 2005. et al. Russo J.12(2):153-172. Neurotoxicology 2005.epa. EPA. Washington (DC): U. et al. Pesticides in the Diets of Infants and Children. low-level exposure to the organophosphate diazinon. Office of Prevention Pesticides and Toxic Substances. Occup Environ Med 1995. Chrislip D.332(1-3):71-80. Rothlein J.58(11):702710.30(2):98-103. Rosenstock L.nap. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Environ Health Perspect 2006. Bull Environ Contam Toxicol 1994. National Academy of Sciences. Thompson ML. Robson MG. Berry H.20(2):115-22. Masala G. Johnson C. and cholinesterase status of date dusters and harvesters in California. EPA). Keifer M. Buccafusco JJ.338(8761):223-227. Marshall E. Sci Total Environ 2004.43(1):38-45. Savage EP. J Occup Environ Med 2002. Lasarev M. O’Malley M. Arch Environ Health 1975. Prendergast MA. Arch Environ Contam Toxicol 2000. Salvini S. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Muniz J. Kidd M. Samuels S. Weisskopf C. Rohlman D.52(2):190-195. Occupational exposure to organophosphate pesticides: a neurobehavioral study.113(4):504-508. Stokes L. U.114(5):691-696. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Levy LS. Aprea C. Caltabiano LM. Daniell WE. Smit LA. Stephens R. 1993 [online]. Available at URL: http://books. Scherer J. Jenkins B. Saieva C. 1/12/09 Peiris-John RJ. McCauley L. Vitayavirasak B. Takamiya K. Bradman A. Spurgeon A. Malathion deposition. Lasarev M. Am J Public Health 1994. 2004. McConnell R. Gillham R. Barr DB. Environ Health Perspect 2005. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers.12(2):134-141. Wickremasinghe AR. Heaton RK. et al.

For general information about the organophosphorus class of insecticides. For example. In addition to reflecting exposure to the parent insecticide. parathion and methyl parathion are metabolized to para-nitrophenol. the level may reflect exposure to the environmental degradation products of these pesticides.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. malathion is metabolized to malathion dicarboxylic acid.” 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) 3.5. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides.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 .

4-15.5-24. 2921-88-2 Chlorpyrifos-methyl CAS No.02 (1.13-3.24-3.70-5.95 (4.51-2.31-2.0 (7.S.80 (1.20-2.71 (1.00-24. 2002).91) 16.92 (1. but can be detected in streams receiving runoff from application sites.44 (3.80) 12.53 (1.76 (1.10) 6.0 (7.94 (4.80 (7.3) 8.97) 2.61) 75th 3.8) 10.10 (4.09 (3.0) 8.0) 10.0-28. The general population may be exposed to chlorpyrifos via oral.78 (7.70-16.88 (1. Survey Geometric mean (95% conf.26) 7.67 (1.27 (7.81-2.70-11.0) 12.5) 7.0 (9. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.72-4.20 (4.5 (8.44-5.3 (8.87-6.89-2.57 (2.19 (1.90-7.0) 12.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.47-9.22) 2.30) 4. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.37) 5.70) 1.32) 2.3 (10.30-1.51) 1.00) 3.43-2.79-2.34) 1. It has low leachability. dermal. interval) 1.13 (1..25) 1.10 (3.16) 2.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.61-7.90 (2. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.90-2.90-8.32-1.50-14.24-1.S.59) 2.50 (1.20-11.39-2.3 (11.47) 1.40 (5.10) 2.50 (2.30-9.and post-construction structural applications for termite control were to be phased out by 2005 (U.01) 1. 2007).30 (2.67 (2.0) 6.29) 90th 7.50-5.9 (10.71 (2.50 (1. 1999.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1. air.30-11.59-2.50-2.40-10.20-3.02 (7.2 (10.4 and 0.60-2.77-15.97) 4.60-3.47-11.05) 1.25) 3.74 (1.39) 4.0) 10.63 (8.0) 12. 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.37 (4.55-5.50 (2.0 (10.70-17.40-26.0 (7.96) 3. and sprayed to kill mosquitoes.68-2.61 (1. staying bound to soil particles. 2005).89 (2.51 (1.50-4.64) 3.8) 9.31-2.EPA.40-2. Approximately 21-24 million pounds per year were used domestically from 1987-1998.4 (8.80) 4.4 (9.60) 5.20-16.72) 2. Approximately 80.80-10. Estimated intakes from diet and water have not exceeded recommended intake limits.50 (2.76 (1.9 (7.09 (2. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.0) 7.29-1.91 (1.20) 4.1) 5.35) 2.77) 1.38 (3.0) 11.97) 2.44-2. and dust.0) 15.0 (13. Chlorpyrifos is Urinary 3.6) 7.67 (2.40-13.17 (1.05-5.0 (7.37 (1.10-17.7) 13.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.63 (2.99-4. After 2001.9-18. and is infrequently detected in ground water (IPCS.1-16.19-3. in 142 urban homes and preschools in North Carolina. and inhalation routes.30-2.5.00) 2.02) 1.20-4.74-9.S.20 (2.04-10.40) 9.47-13.95) 7.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.00) 1.90 (1.84) 1.80) 1.52-2.8-15.63 (1.60-4.0 (7. chlorpyrifos was no longer registered for indoor residential uses in the United States.62-2.15 (1.77-6.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.0) 9.30-12.30 (2.86) 4.97) 7.30-5.60 (5.77 (1.70 (1.28-3.90 (1.00-8. Fourth National Report on Human Exposure to Environmental Chemicals 135 .20) 10.10 (5.0) 12.52-12.68 (7. USGS.80) 2.97-7.9) 697 660 521 701 602 947 Limit of detection (LOD.71 (6.EPA. Exposure can also result from contact with contaminated surfaces.000 pounds are used per year.22 (1. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.40) 2.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1. It also has been applied directly on animals to kill mites. 5598-13-0 General Information The chemical 3.66-4.45 (1.03) 1.0) 10.80-8.0) 14.98-15.35) 1.46-2. and on plants for days to several weeks.0) 12.70-15. population from the National Health and Nutrition Examination Survey.50-4. pre. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.0) 18. applied to structures to kill termites.60 (2.66-15.30) 5.28) 2.21) 3.90 (3.83) 1.7) 8.30 (4.9) 11.36 (4.60-3.90) 3.4 (10.5.60 (4.43-2.04-10.10 (1.7) 9.50-8.4.90 (6.0) 8. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.14) Selected percentiles ( 95% confidence interval) Sample 95th 10. 2002).40 (6.90) 7.7-23. For instance.20) 2.20-14.70 (1.9 (9.30) 4.50-2.20) 2.40 (5.90-4.47 (4.

paralysis.48 (1.35-1.39) 6.40) 1. 2006. resulting in excess acetylcholine at nerve terminals.93 (2.52 (5. Thus.93) 5.24-5. 2005..77) 1. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.88-10.38) 3.00-13.33-7. 2006b).46 (1.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.17-4.91-4.7) 7.36) 1.45-1.12-3.33 (5.58 (1.05-4.00 (7.97) 3.82 (2. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.65-15.32) 1.14-8.05-1. 2006a.06-4.47 (1.58) 5.64 (1.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.45 (1.95 (1.57) 9.37 (1.28) 2.6-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. Ricceri et al.20-1.74) 1.56 (1. and other metabolites.07) 1.64-7.05) 3.44 (5.02 (5.63 (5.16) 6. interval) 1.96) 3.44-6.54) 5.3) 8.54 (2. weakness.91-13.33) 2.01) 3.19-2. The metabolite TCPy does not inhibit acetylcholinesterase enzymes. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.80-11.28) 2.20 (2.46 (2.9 (12.86 (3.92-2. 2005.6) 10.91 (4.35) 1.80) 3.EPA. Survey Geometric mean (95% conf.68) 1.60 (1.14) 1. and producing acute symptoms such as nausea.59) 3.92 (1.99) 1.88) 6. TCPy is more persistent in the environment than chlorpyrifos itself (U.55 (4.S.68) 6.15 (4.09-3.19) 6.72-2..83) 1.62) 90th 5.24 (1.43-10.62-7.82) 8. 2005.57) 2.88 (1.71) 3.98 (6.39 (2.58 (1.80-6.23-1.57-2.99-8.5 (6.95 (3.82 (3.81 (3. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.25-1.1 (10. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.55 (1.8) 9. cholinergic effects.S.49-2.44 (5.88-9.30-4.39 (4. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure. vomiting.94-12.69 (1. and seizures.4) 4.56 (4. neurotransmission.16 (4.21-6. Betancourt et al.57-2.19) 3.59-2.44 (6.42 (5.31) 1.6) 9. population from the National Health and Nutrition Examination Survey.42 (6. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.5) 5.09-1.85-4.56) 5.09 (1.27-7.78 (1.24-24.72) 2.49 (1.0) 16.88 (1.87-3. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.65-11.97 (2.75 (1.90-9.2 (7. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.80-4.31-1.29 (3.76 (2.83-2.33 (1.91) 1.81) 2..11 (2.58-5.01) 3.34-1.. Slotkin et al.53-5.97) 3. Once absorbed.25-11.93 (1.71 (1.84-6.940-1.07) 5.98 (7.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .11 (2.63 (4.33 (.24) 5.66 (1.56) 2.43 (4.23) 14.00) 1.51 (1.47 (5.85) 4.91 (3.91) 10.63-2.97 (3. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.85 (2.11-9. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.12-1.79-13.83-11.91) 2.41 (1. Roy et al.91) 1.22 (4. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).22 (6.01) 1.60-3.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.0) 10.49-2..26-14.97-3.3) 8.17-4. Metabolic hydrolysis leads to the formation of TCPy.24) 75th 2.02) 7..47 (1.47-2.25-12.56-2..93 (4.58) 1..64-2.09-2.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.88-8.27-1.39-1.55) 1.62) 1.2) 6.1 (7. 2002).93) 2.19-1.06 (1.22-6. 1984).82-4.66-11.48 (2.08) 6.86 (1.35) 2.92) 3. Two observational studies of pregnant women and their offspring exposed to chlorpyrifos at environmental levels have found inconsistent relationships with birth outcomes of weight and length (Eskenazi et al.05-3.0) 12.50 (4.44 (1.49-2.3) size 1994 2508 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.44 (1. Urinary 3.94-14.21-1.24-1.5.85 (3.42-2.1-38.75) 6.1-21.66) 1. 2000).12) 1.0) 6.3 (7.31-4. In pesticide applicators. 2006.58 (4.76 (3.53 (2.03) 1.00-8.22) 1.24-4.11) 7. Based on animal data and human cholinesterase monitoring during occupational exposure.89) 4.73 (1.05-8.85) 1.06 (5. TCPy can also occur in the environment from the breakdown of the parent compounds. Howard et al.30-1.3) 9..70-4.72) 1.86 (1.88-8.

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

et al. U. Third National Report on Human Exposure to Environmental Chemicals. Mandel JS. Available at URL: http://ntp. Tate CA. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application. Croghan CW. Bradman A. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Environ Health Perspect 2006a. Meeker JD. 4/7/09 Koch HM. Roy TS. Wartenberg D. Ann Occup Hyg 2007. Chlorpyrifos: pharmacokinetics in human volunteers. Ryan L. Barr DB. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures.155(1):71-80.114(10):1542-1546. Ryde IT.10(4):327-340.207(2):112-124.9(5):494-501. Sharma V. Barr DB.111(2):201-205. Bravo R. MacIntosh DL. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. et al. Zhang J.93(1):105-113. Seidler FJ. Freshour NL. Biomonitoring for farm families in the farm family exposure study. Chlorpyrifos. Fortuna S. Weltzien E. 2005. Bravo R. Environmental Protection Agency (U. J Expo Anal Environ Epidemiol 2005. Ricceri L. Bruun D. Dick RB. Bennett DH. 4/7/09 Perera FP. Jett DA. Hore P. Barr D.6-trichloro 2-pyridinol in their everyday environments. Available at URL: http://www.114(2):260-263. Camann D. Yang D. EPA). Environ Health Perspect 2006b. Baker S. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Needham LL. Environmental Health Criteria 198. Brain Res Dev Brain Res 2005. Seidler FJ. Jewell NP. J Expo Anal Environ Epidemiol 1999. et al. Hardt J. Executive summary of safety and toxicity information.114(5):746-751. Bailey SL. Environ Health Perspect 2000.113(2):211-219.niehs. Toxicol Appl Pharmacol 1984. Baker BA. Ryan PB. Bucelli R. Environ Health Perspect 2003. et al.inchem.51(1):53-65. Sanderson WT. Rick DL. et al. Howard AS. Cometa MF. Jones PA. Rauh V. Morgan MK. Kromhout H. Head SL. J Expo Anal Environ Epidemiol 2005. February 5.nih. Heederik D.31 Suppl 1:98-104. Lorenzini P. Shealy DB. Fenske RA.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC).71:99108.5. Pesticide residues in urine of adults living in the United States: reference range concentrations. Environ Health Perspect 2004. et al.org/documents/jmpr/jmpmono/ v99pr03. Howell RJ. Reid TM. Angerer J. mothers and fathers living in farm and non-farm households in Iowa. Int J Hyg Environ Health 2001. Lioy PJ.15(3):271-281. Slotkin TA.6-trichloro-2-pyridinol. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect 2005. Honeycutt R. Tsai WY. Chrislip DW.htm. Hines CJ. Robertson GL. et al. Toxicol Sci 2006. Neurologic function among termiticide applicators exposed to chlorpyrifos. Hill RH Jr. Pellizzari E. Sheldon LS. et al. Alexander BH. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Seidler FJ. Exposures of preschool children to chlorpyrifos and its degradation product 3. Levin ED. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.204(2-3):175-180. International Programme on Chemical Safety-INCHEM (IPCS). Edwards RD. 1999. 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. Toepel K. Freeman N. Gurunathan S. Chapman P. Environ Res 1995. Adgate JL.5. gov/ntpweb/index. Irish R. Eskenazi B. 2921-882. Slotkin TA. Freeman N. 1992. Environ Health Perspect 2006. Herrick RF. J Expo Anal Environ Epidemiol 2000. chlorpyrifos. Levin ED. Striley C.S. Interim registration eligibility decision for chlorpyrifos. Capone F.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Kinney P. A longitudinal investigation of selected pesticide metabolites in urine. Nolan RJ. Toxicol Appl Pharmacol 2005. Barr DB. Chuang JC.S. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Lu C. Hammerstrom KA. Scand J Work Environ Health 2005. Venerosi A. Urinary pesticide concentrations among children. Ozkaynak H. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Slotkin TA. Steenland K. Hein MJ.73:8-15. Harley K. Curwin BD. Robson M. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. National Toxicology Program (NTP).108(4):293-300. Acquavella JF. et al. Saunders JH. Gregg M. Atlanta (GA).112(10):1116-1124.15(4):297-309. Lein PJ. et al.

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

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

Survey Geometric mean (95% conf.210) < LOD < LOD 567 815 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1312 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.200 (<LOD-.380 (<LOD-. see Data Analysis section) for Survey year 01-02 is 0. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.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.270) < LOD 659 701 920 Limit of detection (LOD. Survey Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. 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.670 (<LOD-1.27) < 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 .S. Fourth National Report on Human Exposure to Environmental Chemicals 141 . 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.

Environmental Protection Agency (U. Centers for Disease Control and Prevention (CDC). 2005.12(6):619-645. Atlanta (GA). Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. EPA).pdf. September 2000.gov/oppsrrd1/ REDs/0018tred. Eigenberg DA. 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.epa. Available at URL: http://www. Anal Bioanal Chem 2003. Freshwater KJ. Sadowski MA.376(6):808-815.S. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. Reprod Toxicol 1998. EPA 738-R-00-010. Olsson AO. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . Barr DB. U. Nguyen JV.S.

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

1998). At high doses. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.gov/pesticides/.. 2003). Seifert and Pewnim. or reproductive toxicant (IPCS. respectively (Baker et al. 2002). and indoor applications have been documented. cholinergic effects. 1986. 1992). although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1.EPA considers diazinon unlikely to be carcinogenic in humans.45 and 1. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. 1998). subsamples of NHANES 1999-2000 and 20012002. and producing acute symptoms such as nausea.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. in the 2001-2002 subsample (CDC. respectively. Diazinon has moderate acute toxicity in animal studies.e.html and from U. 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.. population from the National Health and Nutrition Examination Survey. and seizures. resulting in excess acetylcholine at nerve terminals. Diazinon is not considered to be a mutagen. environmental levels) and health effects is available from ATSDR at: http://www. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. diazinon does not accumulate in tissues (IPCS.. Intoxications in humans from intentional overdose. vomiting. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Survey Geometric mean (95% conf... diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.49 μg/L. 1986 Rajendra et al.S.cdc. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. In animals..epa.72 (<LOD-4.76 (<LOD-3.S.S. Olsson et al. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. In two nonrandom samples of United States adults and children. In addition to being a human metabolite of diazinon.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 1.48) < LOD < LOD 644 678 484 699 554 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. The U.atsdr. Thus. 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.gov/toxpro2. 2000. 144 Fourth National Report on Human Exposure to Environmental Chemicals . In the U. animal carcinogen. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants.S. Additional information about external exposure (i. paralysis. agricultural. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. EPA at: http://www. weakness.

March 2006.gov/circ/2005/1291/.inchem.44(11):2243-2250. Sadowski MA. Brunet RC.S.111(12):1478-1484. Barr DB. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Environmental Protection Agency (U.9(2):117-131. 1992-2001. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Fenske RA. Dumas P. Driskell WJ. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Pesticides in the Nation’s Streams and Ground Water. Drug Chem Toxicol 1986.Organophosphorus Insecticides: Specific Metabolites 2005).pdf. Semen quality in relation to biomarkers of pesticide exposure. 1/14/09 U. Third National Report on Human Exposure to Environmental Chemicals. 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. Kruse RL. Rajendra W.10(6 Pt 2):789-798.epa. Available at URL: http://www. Oloffs PC.376(6):808-815. Noisel N. The Quality of Our Nation’s Waters. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. May 2004. References Anthony J.usgs. Ann Occup Hyg 2006. Beeson MD.. revised February 15. 4/7/09 Lu C.. 1998. Barr DB. 2006). Barr DB. Mason HJ. Geological Survey (USGS). Anal Bioanal Chem 2003. Environ Health Perspect 2003. EPA). 2007 [online]. Bull Environ Contam Toxicol 1986. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Banister E. Swan SH. Available at URL: http://pubs. Barr DB. Nguyen JV.114(2):260-263. Diazinon. et al. 2006). Bravo R. Effect of sublethal levels of diazinon: histopathology of liver. Oloffs PC. Drobnis EZ. Available at URL: http://www. Banister EW. Cocker J. Study for Future Families Research Group. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. 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.50(5):505-515. Liu F. Swan et al. Diazinon.S.gov/ oppsrrd1/REDs/diazinon_ired. Pewnim T. Olsson AO.htm. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Seifert J. Environ Health Perspect 2006. Jones K.S. Carrier G. Toxicol Lett 2002. Centers for Disease Control and Prevention (CDC). Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. J Expo Anal Environ Epidemiol 2000. EPA 738-R-04-006.134(1-3):105-113. In 54 Canadian greenhouse workers. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . International Programme on Chemical Safety-INCHEM (IPCS). (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. 2005. U. Interim reregistration eligibility decision (IRED. Needham LL. Irish R. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biochem Pharmacol 1992. Baker SE. Environmental Health Criteria 198. In 23 children. Atlanta (GA). urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Bouchard M.37(4):501-507.org/documents/ehc/ehc/ehc198. Toepel K. In a small number of men visiting fertility clinics in Missouri and Minnesota. Redmon JB. Garfitt SJ.

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

epa. EPA at: http://www. Giri et al.S.. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. 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. Human studies of single oral doses between 0. 2005). Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. 1987. 2005. Of 382 pregnant women living in an agricultural community.S. Survey Geometric mean (95% conf. 2004). population from the National Health and Nutrition Examination Survey.cdc. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. Pluth et al.EPA. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample.S. 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. Additional information about external exposure (i... Lu et al..5 and 5. but isomalathion.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. representative subsample from NHANES 19992000 (Adgate. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC.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. 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.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.gov/toxpro2. Fourth National Report on Human Exposure to Environmental Chemicals 147 . 2006). Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al.. 1990).EPA. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2006).html and from U. Malathion itself has not been considered genotoxic (U. 2000).Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. 30% had detectable levels of malathion dicarboxylic acid at a detection limit about tenfold lower than the detection limit in the NHANES 1999-2000 analyses (Eskenazi et al. Toxicity from unprotected bystander exposure during applications is rare (U. 1999. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid.. Thomas et al.74 (<LOD-5. 1999).S. 2002. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. IARC considers malathion not classifiable as a human carcinogen. Flessel et al. 1996. 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. 2005). 1993. CDC. but cholinesterase activity was not affected. 2003). 2006).gov/pesticides/. 2001. environmental levels) and health effects is available from ATSDR at: http://www..atsdr.e.

Third National Report on Human Exposure to Environmental Chemicals. Dinoff TM. Jaloszynski P.112(10):1116-1124. Quintana PJ.114(2):260-263.77:1009-1010. EPA). and cholinesterase status of date dusters and harvesters in California. EPA 738-R06-030. Barr DB. Available at URL: http://www. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight.epa. Available at URL: http://www. Atlanta (GA). Reproductive outcome in women exposed to malathion. Carrier G. Harris JA. Curl CL. Trzeciak A.usgs.22(1):7-17.S. Albertini RJ.9(5):494-501. Barr DB. Bravo R. Toepel K. Brunet RC. 4/7/09 Kissel JC. Samuel O.74(2):following table of contents.38(4):546-553. Malathion (addendum).Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Needham LL. Eskenazi B. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Clayton CA. htm.pdf. et al.445(2):275-283. Environ Health Perspect 2004. Hertz-Picciotto I. 2005. Flessel P. Mutat Res 2002. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Toxicol Sci 2003 May. Hammerstrom KA. Giri S.gov/circ/2005/1291/. Grether JK. et al. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Thomas D. Mutat Res 1999. Eberly LE. Am J Public Health 1987. Nicklas JA. Lu C. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.15(2):164-171. metabolite clearance. Malathion deposition. et al. Arch Environ Contam Toxicol 2000. Weltzien E. Available at URL: http://pubs. Bradman A. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. 1992-2001. Genetic toxicity of malathion: a review. U. July 2006.514(1-2):223231. A longitudinal investigation of selected pesticide metabolites in urine. Environ Health Perspect 2006. March 2006.S. Pluth JM.109(6):583-590.56(10):2393-2399. Am J Epidemiol 1990. Gosselin NH. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals .132(4):794-795. Petitti D.org/documents/jmpr/jmpmono/v2003pr06. Ryan PB. The Quality of Our Nation’s Waters. 2007 [online]. Centers for Disease Control and Prevention (CDC). Prasad SB. Geological Survey (USGS). Erratum in: Toxicol Sci 2003 Aug. Pesticides in the Nation’s Streams and Ground Water. International Programme on Chemical Safety-INCHEM (IPCS). Szyfter K.gov/oppsrrd1/REDs/ malathion_red. Griffith W. revised February 15. MacIntosh DL. Barr DB. Dumoulin MJ. Fenske RA. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Giri A. Lioy PJ. 6/1/09 U. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Freeman NC. Bouchard M. Lu C. Environmental Protection Agency (U. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Kedan G. Krieger RI.inchem. Swan SH. Barr DB. J Expo Anal Environ Epidemiol 1999. O’Neill JP. Harley K. Sharma GD. Neutra R. J Expo Anal Environ Epidemiol 2005. Environ Health Perspect 2001. Hooper K. Cancer Res 1996.73(1):182-94. Irish R.S. Blasiak J. Goldhaber M. Rappaport E. Environ Mol Mutagen 1993. Reregistration eligibility decision (RED) Malathion. Jewell NP.

0) 3.90-9.70-3. Fourth National Report on Human Exposure to Environmental Chemicals 149 .50) 3.60-24.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .01-4.60) 1.50 (1.EPA.49 (1. peak domestic use was as high as 5-6 million pounds per year.70-3.70-6. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.91-3.01) 4.37-4.40-3.40) 2. and has a short half-life in soils and on plants.10 (3.30 (2.69) 4.0) 3. Survey Geometric mean (95% conf.34 (3.41-4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.37-2. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.61) < LOD 1.50-14.01) 695 660 518 679 603 941 Limit of detection (LOD.62 (1. 2006).57-4.00) 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. Estimated intakes from diet and drinking water have been below recommended limits. first registered in 1948.60 (4.69 (2.30 (1. Methyl parathion use is highly restricted.11) 2.90 (1.40 (1. Once absorbed.30-5.72 (3. methyl parathion was rapidly absorbed after ingestion.67 (1.70-6.730 (<LOD-.32-1. Given its limited use.S.28-4.0) 2.18-3.66 (2.45) 5.00 (2.61) < LOD 1.33 (1.0) 3.12) < LOD < LOD 1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion. Many previous registered agricultural uses of methyl parathion have been cancelled (U.910) < LOD .79) 4.990-1.92) 5. and of the chemical nitrobenzene.37-4.300-. on cereal grains.85 (2.32-1.48) 90th 2.770 (.80 (2. and oral routes can occur in pesticide and agricultural workers (Muttray et al.13-1.50 (2.22-3.28 (1.21 (2. but by 2003.89 (2. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. ethyl parathion.50) 2. < LOD means less than the limit of detection.20) 5. Methyl Parathion.70) 2. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.05) 4. all registered uses were voluntarily cancelled (U.940 (<LOD-2. was once a restricted-use insecticide with limited applications on certain agricultural crops.20 (2. and to a lesser extent. Both are toxic to birds.74) 5.32 (1.910) < LOD < LOD .92-2. 1977). population from the National Health and Nutrition Examination Survey.71 (2.. and aquatic invertebrates.10) 22. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.70 (2. 2000).47) 2.30-16.. Morgan et al.20 (<LOD-2.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .11-4. binds tightly to soils resulting in low leachability.60-5.70) 2.0) 3. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8 and 0. In the 1990s.298-00-0 Ethyl Parathion CAS No.10) 4.45 (1.70-6.57) 1.40-4.50 (1.00 (2.40) 4.28 (1.02-6.850) < LOD .50 (2.27) 2. and eliminated rapidly from the body after absorption (Kramer et al. In animal studies. It had been applied to cotton.36-1.26 (1.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.33) 2.70 (<LOD-3.. more slowly absorbed through the skin.71 (3.44) 2.67) < LOD 1. Methyl parathion has low water solubility.60-19. 2003).0) 3.40) 1.0 (3.10-1. with limited applications in agriculture.790 (<LOD-.37) 2.50-9.700 (<LOD-.46 (3.16) < LOD 1. fish.90-11.860 (<LOD-1.50 (1.70 (2.S. 2002.00) 3.80 (2. Ethyl parathion.58) 3. 2007).1. which may vary for some chemicals by year and by individual sample.15-3.910) < LOD < LOD < LOD 1.20-5.0) 4.50) 1.30-3.80) 2.60-36.50) 3.70) 2.32-3.80 (1.10 (3. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.70 (3. Increased risk of exposure via dermal. Methyl parathion is not registered for residential use in the United States.09-1.21-1.10 (<LOD-6.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .19 (.50 (1.40-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-11. pulmonary.EPA.S.70 (2.

ethyl parathion.11-4.EPA considers methyl parathion unlikely to be carcinogenic to humans.cdc.20) .39 (1.97-10.530) < LOD < LOD < LOD .72-2..78-2. The metabolite.97 (<LOD-4.500) < LOD < LOD . 1995. In addition to being a metabolite of methyl and ethyl parathion. 2005. gov/pesticides/. and other metabolites.730-1.05) 4. EPA at: http://www.13) 4.400 (<LOD-.88 (1.29 (2.540) < LOD .89 (2. 1991).01-3. Slotkin et al.48-4.. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.55) 2. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.73 (1.830-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. weakness.720 (<LOD-.89 (2.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . paranitrophenol.440 (<LOD-. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.44-3.15) 3. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.04) 1.31) < LOD . and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Methyl parathion is not considered genotoxic.37-1.31-3.10 (1. Thus.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Karanth and Pope et al.83 (1. 1995).29) 2.67-2.97 (2.44-3..11) 1.82) < LOD . 150 Fourth National Report on Human Exposure to Environmental Chemicals . 2004).08 (1.430 (. methyl parathion. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.39) 1. environmental levels) and health effects is available from ATSDR at: http://www.04 (2.57) 6.91 (1.680 (<LOD-1. Methyl Parathion. accidental exposure.atsdr.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .14-3.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.00 (1.17-4. and producing acute symptoms such as nausea.16-4.S.60-2.08-3.950) < LOD .30) 3. does not inhibit acetylcholinesterase enzymes.29) 1.970 (.80 (1. Lores et al.4 (3.33-6.84) 3.970 (.17) .23) 1.41-2.70) 3.790-1.310-.96 (1.870) < LOD .78-2.25 (2.33-3. and unintentional acute or chronic high-level occupational exposure (Hill et al.67 (3.640) < LOD < LOD 1. Recent in vitro and in vivo animal studies suggest that parathion may have additional neuronal and glial cell effects at lower doses (Guizzetti et al.3) 2.80 (1.77-7.87 (1.79) 1.20 (3. 1990. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion. 1978.59 (1.00) 2. Zurich et al.00 (1.9) 1.23) 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 .56-2.38-3. U.55 (<LOD-3.21-21..08) < LOD .880 (.13-12. WHO.720-1.01 (2.2) 2. population from the National Health and Nutrition Examination Survey. vomiting.76-14.1) 2. 2006.98-7. Additional information about external exposure (i. but lists ethyl parathion as a possible human carcinogen.79 (1.690-1.26) 17.7) 3.25) 1.07) 2. At high animal doses of methyl parathion.370 (<LOD-.94-4.86 (2.95) 1. Jaga and Dharmani.21) 1..90 (1.e.S.93 (2.30-1. 2006.35-3. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.82 (2.35-3.09) 2.940 (<LOD-1.2) 2.Organophosphorus Insecticides: Specific Metabolites Metabolites”).800-1. Parathion and methyl parathion have high acute toxicity in animal testing. 2003.92 (2.26 (1.78) 2.61) 4.15-10. teratogenic.96 (1. In large doses.980 (.S. 2004). paralysis. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.57-2. gov/toxpro2.71 (1.60 (1. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens..930 (..94-47.07 (1.html and from U. resulting in excess acetylcholine at nerve terminals.790-. Survey Geometric mean (95% conf.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .57-7.91) 1. and seizures.01 (.71) 1. cholinergic effects.930 (.88) 1.78 (2.33-3.epa. Orsorio et al.850-1.20) 3.10) 90th 2.43) 4.840 (.60) 2.

Head SL. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Hill RH Jr.21(1):5767.15(2):164-171. Hetzler HL.org/documents/jmpr/jmpmono/v95pr14. Guizzetti M. Barr DB. Clark JM. 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. Laboratory investigation of a poisoning epidemic in Sierra Leone. Baker SE. Toxicology 2005. J Anal Toxicol 1990. Giordano G. 2005). 2002).71:99108. et al. Kedan G. general population (CDC. and levels were similar or slightly lower that those in a small convenience sample of the U. Baker S. Griffith W. Hill et al. McClure PC. Available at URL: http:// www.. Morgan DP. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect...215(3):182-190. Bailey SL. McCann KG. Turner WE. Curl CL. Wellman SE. Hryhorczuk DO.htm. In a study of workers who handle parathion. McCann et al. Lores EM.S. Arch Environ Contam Toxicol 1977.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure.. Lin LI. Pathak S. Leng G. Environ Health Perspect 2004. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Head SL. 4/7/09 Jaga K. Baker RC..inchem. Third National Report on Human Exposure to Environmental Chemicals. Rockhold RW. 2002. et al. Environ Health Perspect 2002. Costa LG. Barr JR. ACGIH recommends a BEI of 0. Parathion-Methyl (addendum). 2005. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. 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. Shealy DB. 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.6(2-3):159-173. a range of values several hundred times higher than levels found in the U. 1999). J Expo Anal Environ Epidemiol 2005. Atlanta (GA).112(10):1116-1124.S. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Lewalter J. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.. 1995. Environ Health Perspect 2002. oral or dermal administration. Bradway DE. Bradman A.. Chicago area methyl parathion response. Gregg M. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Karanth S.56(7):449553. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Environ Res 1995. CDC. Weltzien E. Rev Environ Health 2006. and many residents were symptomatic (Barr et al. Centers for Disease Control and Prevention (CDC). Hill RH Jr. Neurotoxicol Teratol 2003. et al. Children and adults living in residences where methyl parathion was applied indoors had urinary levels of para-nitrophenol which were several hundred times higher than those in the NHANES 19992000 subsample.5 mg (500 µg)/g creatinine for workers at the end of shift. Moseman RF. Jewell NP. 2005.110 Suppl 6:1085-1091. Pesticide residues in urine of adults living in the United States: reference range concentrations. population (Olsson et al. Runkle KD. Eskenazi B. Needham LL. et al. Arch Environ Health 1978. Barr DB. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Occup Environ Med 1999. Lu C. Moomey CM. J Biomed Sci 2002. Slach EF. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Rubin et al. 2002. Dharmani C. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Cline RE. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine.25(5):599-606. 2004). Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. References Barr DB. Ashley DL. Pesticide workers may have much higher levels following pesticide applications. 1995).33(5):270-276. 2005). Kramer RE. Pope C.14(4):213-216. Alley CC. International Programme on Chemical Safety-INCHEM (IPCS). et al.110 Suppl 6:1075-1078. Barr DB. DiPietro E. Methyl parathion: an organophosphate insecticide not quite forgotten.9:311-320. 2005. Role of individual susceptibility in risk assessment of pesticides. Harley K. Kissel JC.

2004.E. Schilter B.201(2):97-104.usgs. Honegger P. Hill RH Jr. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos.110 Suppl 6:1047-1051.gov/circ/2005/1291/. September 2000.S. Ethyl parathion. WHO/SDE/WSH/03. Toxicol Appl Pharmacol 2004. Toxicol Lett 2006. Pesticides in the Nation’s Streams and Ground Water.epa. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. revised February 15. May 2003. Case No. External and internal exposure of wine growers spraying methyl parathion. Rubin C.epa. March 2006.D. Rosenberg J. Osorio AM.162(2-3):219-224. 1992-2001. Environmental Protection Agency (U.S. Seidler FJ. Investigation of a fatality among parathion applicators in California.376(6):808-815. Slotkin TA. Environmental Protection Agency (U. EPA). Yacovac R. Levin ED. Environ Health Perspect 2006. Methyl parathion in drinking water.gov/oppsrrd1/REDs/factsheets/0155fct.114(10):1542-1546. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Barr DB. Available at URL: http://www.Organophosphorus Insecticides: Specific Metabolites Muttray A. 1995-1996. Available at URL: http://www. Hill G. Ames RG. 0153. Available at URL: http://www.pdf. Jung D. 2007 [online]. Olsson AO. Costa LG. Mengle DC. Sadowski MA. EPA-738-FOO-009. Geological Survey (USGS). Letzel S. Anal Bioanal Chem 2003. Backer G.20(4):533-546. Ohio. Facts. Tate CA. 1/14/09 U. Available at URL: http://pubs.S.04/106. Environ Health Perspect 2002. Nguyen JV. pdf. Am J Ind Med 1991.S. et al. Kieszak S. gov/oppsrrd1/REDs/methylparathion_ired.S. Esteban E. Monnet-Tschudi F. 6/1/09 World Health Organization (WHO).pdf. R. The Quality of Our Nation’s Waters.who. 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. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. U. 5/19/09 Zurich MG. Dunlop B.int/water_sanitation_health/dwq/chemicals/ methylparathion. EPA). 152 Fourth National Report on Human Exposure to Environmental Chemicals . 1/12/07 U. Ryde IT.

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

680 (<LOD-.07) .780 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .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 .740 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700-1.610 (<LOD-1.210-1. 154 Fourth National Report on Human Exposure to Environmental Chemicals .55) .470 (.670 (<LOD-1.780 (<LOD-1.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .210-.580-1. Survey Geometric mean (95% conf.770) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .950) < LOD < LOD 1.780 (<LOD-1.780 (.27) .840) 669 687 929 Limit of detection (LOD.410 (<LOD-1.94) . population from the National Health and Nutrition Examination Survey.S.Organophosphorus Insecticides: Specific Metabolites Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.200-. see Data Analysis section) for Survey year 01-02 is 0.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2.820) < LOD < LOD . which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th .760 (<LOD-.210 (<LOD-. Survey Geometric mean (95% conf.840 (.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .15) < LOD .250 (<LOD-.500 (.430 (<LOD-.850 (.700-.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .64) .21) < LOD .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .31) .300-1. Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one (creatinine corrected) Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection.740-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.17 (.S.

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

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

Lazarini et al. et al. Hu et al. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Kim TS. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. hypersensitivity. 2002. Int J Hyg Environ Health 2002.108(1):78-85.gov/pesticides/ and from ATSDR at: http://www. In California.62:101-108. September 2003. cdc. J Environ Monit 2006. McCarthy et al. Toxicological profile for pyrethrins and pyrethroids.. Bull Environ Contam Toxicol 1999. et al. 2002). motor activity.27(12):1273-1283. et al. Agrawal AK.8(1):18-21. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Available from URL: http://www. Pyrethroid pesticide-induced alterations in dopamine transporter function. EPA at: http://www. 2005).atsdr. Pogo BG. Toxicol Appl Pharmacol 1991. Wang SL. McCarthy AR. 1991. Guillot TS. epa.. Generally. Go V. Song L. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz 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. 2003. Adhami VM.. Biochem Biophys Res Commun 1998. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Cruz-Casallas PE. 2003. Idel H.. Bernardi MM. 2001. Ose K. J Reprod Dev 2004. Kim HS.205(6):459-472. Florio JC. Lazarini CA. Kang IH. 2005). Effects of prenatal exposure to deltamethrin on forced swimming behavior. Lee SJ. Shin JH. Richardson JR.gov/toxpro2. 2006. In developing rodents. 2004. choreoathetosis.. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.. Eriksson and Fredriksson. Thomson BM. Leng A. Bernardi MM. Eriksson P.. neurochemical changes in cholinergic. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate.23(6):665-673. dopaminergic.35(2 Pt 1):227-237. Caudle WM.. Go et al. Kuhn KH. Levsen K. Leng G. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. 2001..cdc. bioallethrin and deltamethrin. Regul Toxicol Pharmacol 2002. Garey J.8(1):197-202. 1998. and striatal dopamine levels in male and female rats. Garey and Wolff. Seth PK. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity..211(3):188-197. Sunami O. 2006. 2005). Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides.50(2):245-255. tremor. Additional information about pesticides is available from U. Elwan MA. Shaw IC. Soderlund et al. Leng G. and permethrin) in the Hershberger and uterotrophic assays. Spinosa HS. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. WHO. Shafer. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Wieseler B. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Yamada T. Idel H. Neurotoxicol Teratol 2005. Kunimatsu T. 2002). Lewalter J. salivation. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Lemonica IP. 2005). Kamita Y. Shukla Y.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Toxicol Appl Pharmacol 2006. Abell AD. Miller GW. Wolff MS. 2006). Fredriksson A. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. 2003. and seizures (ATSDR. 1999. Kuhn K.107(3):173-177. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. References Agency for Toxic Substances and Disease Registry (ATSDR). Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Zhao RC.300(3):161-165. Leng G.html..html. Elwan et al. Chen JH. Neurotoxicol Teratol 2001. Kim et al. on immature and adult mice: changes in behavioral and muscarinic receptor variables.. Hu JY. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Kunimatsu et al. Neurotoxic effects of two different pyrethroids. Pauluhn J. 2003. Garey J. Ranft U. Xenobiotica 1997. Salzgeber SA. fenvalerate. Wolff MS.gov/toxprofiles/ tp155.251(3):855-859. Berger-Preiss E. Okuno Y. Neurosci Lett 2001. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Yang J. Environ Health Perspect 1999. Ray et al. et al.1/15/09 Aziz MH.27(4):609-614. 2000. Estrogenicity of pyrethroid insecticide metabolites. Sugiri D. Moniz AC. Kim IY.atsdr. Varoli FM.. Moniz et al.S.

Permethrin. Pesticide and Evaluation Scheme.epa. Safety of pyrethroids for public health use. U. Sheets LP.usgs. resmethrin. Soderlund DM. June 2006b. Revised February 25.epa. Marsh JR.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005.htm. EPA).186:57-72.38:95-101. Sargent D.Pyrethroid Pesticides Ray DE. Spencer J. O’Malley M. EPA). April 2002. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. World Health Organization (WHO). Shafer TJ. Pyrethroid insecticides: poisoning syndromes. Pyrethroid illnesses in California. Environmental Protection Agency (U.S. Toxicology 2002. Forshaw PJ. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . 1992–2001. Available at URL: http://www.S. Piccirillo VJ. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Geological Survey (USGS). Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. Lesser JE. March 2006.22(8):983-991.gov/ circ/2005/1291/. Environmental Protection Agency (U. June 2006a. Laird WJ.S. Xenobiotica 1992. and therapy. Available at URL: http://pubs.10. 5/26/09 U.pdf. synergies. Meyer DA. Environmental Protection Agency (U. Crofton KM.gov/oppsrrd1/REDs/cypermethrin_red. Available at URL: http://whqlibdoc.epa.who. et al.S. Clark JM. Environ Health Perspect 2005. 2005.113(2):123-136. 5/26/09 Woollen BH. 19962002. EPA).gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes.S. 5/26/09 U. Available at URL: http://www.htm. Reregistration Eligibility Decision for Cypermethrin. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). Pesticides in the Nation’s Streams and Ground Water. pdf. 2007.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Available at URL: http://www. 5/26/09 U. sumithrin synthetic pyrethroids for mosquito control.S. Rev Environ Contam Toxicol 2006.S.171:3-59. Mullin LS. J Toxicol Clin Toxicol 2000.

In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Urinary levels for adults and children in these studies were similar (Heudorf et al. Leng et al. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002.S. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. 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.Pyrethroid Pesticides Cyfluthrin CAS No. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. Baker et al. 2005.68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin.S. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0.... 2003).. 2003). Thus. Cyfluthrin is rapidly metabolized and eliminated from the body. 2006). 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 . 2004). 2001.2 μg/L) in the U..95 µg/L. 2006) and 1177 urban adults and children (Heudorf et al. 2005)... but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. Seven individuals participating in floor exercises on cyfluthrin treated carpet demonstrated a rise in the urinary excretion of 4-fluoro-3-phenoxybenzoic acid in the 72 hours following the activity (Williams et al. 2001) showed that urinary levels of 4-fluoro-3-phenoxybenzoic acid at the 95th percentile ranged from either slightly higher or lower than the detection limit in the U. most of which were dermal and respiratory irritations (Spencer and O’Malley. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. representative 2001-2002 NHANES subsample (CDC. representative subsample in NHANES 2001-2002 (CDC. Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. Finding a measurable amount of 4-fluoro-3-phenoxybenzoic acid in urine does not mean that the level will result in an adverse health effect. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. Following an indoor application exposure. 2005). Studies in Germany of 396 children and adolescents (Becker et al. 2003). In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 160 Fourth National Report on Human Exposure to Environmental Chemicals .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. < LOD means less than the limit of detection. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.2 and 0. which may vary for some chemicals by year and by individual sample.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 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. * 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. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 161 .Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid (creatinine corrected) Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

Olsson AO. Angerer J. Drexler H. Hoppe HW. O’Malley M. Heudorf U. Hadnagy W. Rev Environ Contam Toxicol 2006. Centers for Disease Control and Prevention (CDC). Spencer J. Berger-Preiss E. Ranft U. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Seiwert M.209(3):293-299. Schulz C. 19962002.109(3):213-217. Int J Hyg Environ Health 2006. Angerer J. Heudorf U. Environ Health Perspect 2001.77(1):67-72.209(3):221-233. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. J Expo Anal Environ Epidemiol 2003. Human exposure to indoor residential cyfluthrin residues during a structured activity program. 2005. Atlanta (GA). Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides.46(3):281-288. Int J Hyg Environ Health 2003. Pyrethroid illnesses in California. Angerer J. Sugiri D. Ball M. et al. Arch Environ Contam Toxicol 2004. Heudorf U. Butte W. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.Pyrethroid Pesticides References Baker SE. Williams RL. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int Arch Occup Environ Health 2004.186:57-72. Angerer J. Int J Hyg Environ Health 2006. Leng G.13(2):112-119. Third National Report on Human Exposure to Environmental Chemicals. Kolossa-Gehring M. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Bernard CE. Krieger RI. Barr DB.206(2):85-92. Becker K. Idel H.

410) .110-.510 (.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.13 (.300-.200-.630 (.160 (.600 (. The presence of cis-3-(2.330 (.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 .52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.520) .380) .07 (. Cyfluthrin.68359-37-5 Cypermethrin Permethrin CAS No.530 (.490-.2-dichlorovinyl)2.170 (.120-.202 (.780) .2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.900 (.12 (.710) .370 (.340) .690) .230) .740-1.880 (. Fourth National Report on Human Exposure to Environmental Chemicals 163 .200) < LOD < LOD < LOD .77 (. transcypermethrin and trans-cyfluthrin.240) .460-.180 (.580-1. 1985. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.1 and 0.420-.S.210-.54) .670-1.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.250 (. population from the National Health and Nutrition Examination Survey.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .or trans-3-(2.670-2.53) . and trans-cyfluthrin.262) * * * < LOD < LOD .08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .890 (.210) 90th .110 (<LOD-.380-.200) . 1999).300 (.740 (.280 (.180) .110-.80) .490-.770-1.680 (.650-1.150 (.460 (.570 (.310) .120-. 1999).50) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.340-.670-1.2-dichlorovinyl)-2.08) .340) .700) .155-.44 (.160 (.300-.600) ..500 (.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.270 (.280-.630) .350) .15) .1.2-dichlorovinyl)- CAS No. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-dichlorovinyl)-2.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . Similarly.850 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. ciscypermethrin and cis-cyfluthrin.730 (.730 (.550) .790 (.21) . In the body. Kuhn et al.580) 1.24) 1.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.790-1.68 (. cis-permethrin. trans-permethrin.2-Dichlorovinyl)-2.380-.11) ..920) 1.200) .890 (.200 (.680-3.510 (. 1985.68) .200-.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.260 (.200-.35) .120-. Kuhn et al. and ciscyfluthrin. but can also reflect exposure to trans-3(2.600-1. cis-3-(2.430-.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.790) .670 (.270-.28) 671 680 518 701 591 957 Limit of detection (LOD. more of the trans-metabolite than Urinary cis-3-(2.460-1. the presence of trans-3-(2.870) 1.2-dichlorovinyl)-2.270 (.630) .68) .610) . Generally.770) .330) .220-. but it can also reflect exposure to cis-3-(2.270 (.300 (.120-.370-.910-5.630-. < LOD means less than the limit of detection.500 (.470 (.490-1.380-.710-1.490-1.740) 1.43) . Biomonitoring Information Urinary levels of cis.250-.740-2.210) .2dichlorovinyl)-2.220) . Survey Geometric mean (95% conf.570-.and trans-isomers.440 (. cis-cypermethrin.790-1.220-.240) .380 (.47 (.470-1. The chemical trans-3(2.820 (.400-. trans-cypermethrin.410) .960 (.950-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.140 (.110-.140 (<LOD-.32) .220-. which may vary for some chemicals by year and by individual sample.2dichlorovinyl)-2. 52315-07-8 CAS No.730 (.510 (.640 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.220-.160 (<LOD-.35) 1.610) .

550 (.12-2. Studies in Germany of 396 children and adolescents (Becker et al.170 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.260) .190) .520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . 2005) In a small group of indoor pest-control operators.290) .59) .390-.450-.430-.380) . representative NHANES 2001-2002 subsample (CDC.190) .150-. 2005).2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.190 (.67) . In the same residents.560) .250) .340) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.700-2.690-1.31) .580-1.680-1.104-.21) .540 (. population from the National Health and Nutrition Examination Survey.24) .430 (.440 (.. urinary levels of cis-3-(2.830) .840 (. the median and 95th percentile of urinary levels of cis-3-(2.890 (.2-Dichlorovinyl)-2.260 (.and trans-3(2. 2003).270 (.350 (.200) .250) 90th .500 (.680 (. 2005). 2004).220) .540) .230 (.230-.370-. Other studies have provided evidence that urinary levels of cis. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.810 (.750 (.440-.430-1.2dichlorovinyl)-2.350) ..700) .640-.230-..S.150-.11) .33 (.180-.290) .530 (.750-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.640-1. 2006.320) . 2006)..880) ..080-.59) .49) .2dichlorovinyl)-2.33) .37) .710 (.920 (.260 (.370-.440-. Survey Geometric mean (95% conf.420 (. Cyfluthrin. Lu et al. median urinary levels of trans-3-(2.570) .440 (.370-.450 (..150-.320-.220 (. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.200-.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al. In a study of volunteers.300-.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.170) < LOD < LOD < LOD ..260-.510-1.300) . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.250-.270-.300 (.540 (.S.2-dichlorovinyl)-2.2-dichlorovinyl)-2.890) .780 (.11) .67 (. 2002).2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U. urinary trans-3-(2. 2006) and 1177 urban adults and children (Heudorf et al.550) .390-.590) .290 (.130-.300 (..08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .450-1. 2003).300) .580) .250-..840 (.230-.280-.03) 1.640 (.80) .680-1.340) .780) 1.400-1..250-.560) 1.2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid did not increase.220 (.182) * * * < LOD < LOD .280 (.470-1.11) 1. 2005). 2004. 2001. In these volunteers. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.Pyrethroid Pesticides 2.11 (.. 164 Fourth National Report on Human Exposure to Environmental Chemicals . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. post- Urinary cis-3-(2.2-dichlorovinyl)-2.270) .14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.380-.710-3.530 (.900 (.240 (<LOD-.138 (.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .29 (.550-1.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.340-. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.260 (. 2006.700) .2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.250) . 2006).120 (.600 (.180 (. 2002).360-1.400 (.640-1.200-.200 (.59 (1.210-.170 (.12 (.800 (.550) .290-.270) .390 (.380 (. 2005).2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.590 (.250 (<LOD-. In a study of urban residents in Germany (Berger-Preiss et al.640) 1.550-1.03) size 1951 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .410) . Schettgen et al. 2001) showed urinary levels of cis.160 (<LOD-.140-.and trans-3-(2.

810-1.or trans-3-(2.55-3.60) 1.730) . 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.68) 1.01) 4.19) 1.500 (.400-.56 (1.68-3.43) 2.910-1.14-2.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .860) .14) 1.440 (<LOD-.42 (2.35) 1. Biomonitoring studies on urinary levels of cisor trans-3-(2.17-1.48) 4.49-3.84 (1.28 (1.17 (.28 (2.26 (.7) 2.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .910-1.85) 4.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.400 (<LOD-. < LOD means less than the limit of detection.410-.11-1.760) .60) . Urinary trans-3-(2.550 (.660) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.410-.970 (.620) < LOD 2.94 (1.670) .77) 1.520) .77) 2.850-1.750) .S.97-11.37 (1.70) size 1976 2525 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .49-3.13) .520-.76-3. however.55-4.03-1.19 (3. which may vary for some chemicals by year and by individual sample.69 (1.Pyrethroid Pesticides application median urinary levels of summed cis.800-1.54) 4.940 (.560 (.14-6.41 (1.95) 3.25-3.56 (1.580 (.50 (1.420 (<LOD-.12-6.17 (.40 (1.500-.530) .2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.41-14.820) .09 (.5) 2.10) 2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.and trans-3-(2.19 (2.23) 2.16) 1.470 (<LOD-.03-1.08) 1.710 (. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.23 (.69) 1.500) .4 and 0.59 (1.700) .56) 2.4.60-4.66) 691 680 518 690 595 954 Limit of detection (LOD.20 (.56) 2.2-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.95) 2.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .49-5.2dichlorovinyl)-2. trans-Cypermethrin.81) 2.560 (.39-5.01 (1.89 (2.560 (. 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.20 (.39 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.2-dichlorovinyl)-2.77 (1.780 (.07 (1.08-4.700-1.490-1. Finding a measurable amount of cis.66) . Fourth National Report on Human Exposure to Environmental Chemicals 165 .2-dichlorovinyl)-2.64-4.25 (1.2-Dichlorovinyl)-2.20 (.68) 1.680-1.68-2.830-1.840-1.490 (<LOD-.42) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.68) 2.54 (1. 2005).460-.670) . 2005).87 (1. Survey Geometric mean (95% conf.08-6.91 (1.480-.920-1.63) 1. The maximum post-application urinary levels.460-.11-2.55-5.570) 90th 1.22 (1.90) 1.410 (<LOD-.470 (.610) 1.27 (1.07-3.410 (<LOD-.62 (1.63) 1.76-4.

55 (2.500-.880 (<LOD-1.740) .570 (<LOD-.80) 1.530 (.08 (.720-1.48-2.07-2.19 (1.820-2.44) 2.31 (.20-2.64 (1.57 (1.86 (2.570 (.530 (<LOD-.33-1.800-1.410-.540) .15-3.780 (<LOD-.87) 1.37 (1.60) 2.12 (.15-3.750) .39 (1.45-2. 166 Fourth National Report on Human Exposure to Environmental Chemicals .56-2.610-.67 (2.02-1.13) .34-3.670) . population from the National Health and Nutrition Examination Survey.36 (1.57) 3.22-1. Survey Geometric mean (95% conf.780) .07-3.89) 2.440-.35) 1.520 (<LOD-.720 (<LOD-.19) .11) .850) .700-.47 (1.91) 1.87-8.08 (.13) 1.780) 90th 1.12-1.470-.S.580) .470 (.60 (1.720-1.45 (1.61) 1.87) 1.74) .07-1.Pyrethroid Pesticides Urinary trans-3-(2.640) .00) 5.65 (2.22) 1.60) 2. trans-Cypermethrin.33 (1.580 (.880 (.00-5.730) .55 (2.70 (.29) 1.00) 1.31) 1.660) .930-1.570-.700 (.74) 2.560 (.39) 1.760 (.970 (.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .35 (1.15 (1.36) 2.15-3.16 (1.00) 1.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.56 (1.34-4.27-2.770) < LOD 2.47-2.56-5.07) 2.28) 2.47-2.26 (1.900 (<LOD-1.850) 1.480-.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 .88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.75 (1. * 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 2.81 (2.91-11.30-3.87 (1.33-2.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .3) 2.91 (1.30-6.700 (.2-Dichlorovinyl)-2.07) 2.48 (1.00 (1.20 (1.55 (2.880-1.87-3.42) 1.31 (2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.41) 1.65) 1.800-1.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.15) 3.850-3.15) 2.40-2.98 (1.68) 3.42 (.27-2.22-2.

Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Hardt J. Centers for Disease Control and Prevention (CDC). Heudorf U. Kuhn K. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Angerer J. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Levsen K. Seiwert M. Atlanta (GA). Kolossa-Gehring M. Permethrin and its two metabolite residues in seven agricultural crops. Heudorf U. Schettgen T. Leng G. Angerer J.109(3):213-217. Int J Hyg Environ Health 2002. George DA.206(2):85-92. Bull Environ Contam Toxicol 1999. Leng G.134(1-3):141-145. Hadnagy W. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.209(3):221-233. Heudorf U. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Butte W.68(6):1160-1163. Hoppe HW. Angerer J. Idel H. Biological monitoring of workers after the application of insecticidal pyrethroids. Bravo R. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Drexler H. Berger-Preiss E. Int J Hyg Environ Health 2003.209(3):293-299. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Ball M. Environ Health Perspect 2001. Ranft U.62:101-108. Third National Report on Human Exposure to Environmental Chemicals. Lu C. Sugiri D. et al. Barr DB. Schulz C. Angerer J. Bartell S. Angerer J. Environ Health Perspect 2006. Int J Hyg Environ Health 2006. Leng G. Wieseler B.114(9):14191423.76(7):492-498.Pyrethroid Pesticides References Becker K. 2005. Int Arch Occup Environ Health 2004.77(1):67-72. Idel H. Ranft U. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Berger-Preiss E. Drexler H. Pearson M. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Heudorf U. Int Arch Occup Environ Health 2003. Sugiri D.205(6):459-472. J AOAC 1985. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Int J Hyg Environ Health 2006. Idel H. Angerer J.

2-dibromovinyl)2. (2004) reported a geometric mean concentration of cis-3(2. Urinary levels for adults and children in these studies were similar (Heudorf et al.2-dibromovinyl)-2.2-dibromovinyl)-2. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population.2-dimethylcyclopropane carboxylic acid in the environment (IPCS. 1990). urinary levels of cis-3-(2.2-dibromovinyl)-2.2-dibromovinyl)-2.. 168 Fourth National Report on Human Exposure to Environmental Chemicals . The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample.. In the NHANES 2001-2002 subsample. 2001) showed that urinary levels of cis-3-(2. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.Pyrethroid Pesticides Deltamethrin CAS No. 2001.2-dibromovinyl)-2.1 μg/L) for the NHANES 2001-2002 subsample (CDC. Baker et al.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.39 µg/L.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. in detection of cis-3-(2.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Following residential spraying with deltamethrin for malaria protection in Mexico.2dimethylcyclopropane carboxylic acid formed in the environment. 2006) and 1177 urban adults and children (Heudorf et al.5 μg/L) than the detection limit (0. 52918-63-5 General Information Cis-3-(2.2-dibromovinyl)-2. Outside the U. Deltamethrin can degrade to cis-3(2. Studies in Germany of 396 children and adolescents (Becker et al.. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 2005).2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al. in some situations replacing the use of DDT. 2005). Thus. Finding a measurable amount of cis-3-(2. deltamethrin has been used against mosquitoes that carry malaria.3-0. 2005).2-dibromovinyl)-2.2-dibromovinyl)-2. mean peak urinary levels of cis-3-(2..2-dimethylcyclopropane carboxylic acid of 0. Biomonitoring Information Urinary levels of cis-3-(2.S.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.. 2004)..2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 and 0.1. 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. Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 169 .Pyrethroid Pesticides Urinary cis-3-(2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.2-Dibromovinyl)-2. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.

Pyrethroid Pesticides Urinary cis-3-(2.S. * 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. population from the National Health and Nutrition Examination Survey.2-Dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 170 Fourth National Report on Human Exposure to Environmental Chemicals . Survey Geometric mean (95% conf.

Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Angerer J.109(3):213-217. Centers for Disease Control and Prevention (CDC). Batres LE.Pyrethroid Pesticides References Becker K. Int J Hyg Environ Health 2006. Third National Report on Human Exposure to Environmental Chemicals. Ball M. Butte W. Angerer J. Heudorf U. Environmental Health Criteria 97. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Lopez-Guzman OD. Angerer J. International Programme On Chemical Safety (IPCS).inchem. Heudorf U. Atlanta (GA). Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.htm. Kolossa-Gehring M.77(1):67-72. Schulz C. Available at URL: http://www. Deltamethrin. Grimaldo M. 5/26/09 Ortiz-Perez MD. Hoppe HW. Int J Hyg Environ Health 2006.113(6):782-786. Heudorf U. [online] 1990. 2005.209(3):221-233. Int Arch Occup Environ Health 2004.org/documents/ehc/ehc/ ehc97. Torres-Dosal A. Environ Health Perspect 2001. Seiwert M. Drexler H. Environ Health Perspect 2005. Fourth National Report on Human Exposure to Environmental Chemicals 171 . et al. Angerer J.209(3):293-299. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Carranza C. and genotoxicity in exposed children. et al. toxicokinetics. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.

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

53) 1.41 (1.81 (1.276-.315 (.45 (2.640 (.700-1.710 (.750) .210-.430-.570-.320) .850) .34) 8.595) .69) 3.48-2.49 (1.240 (.38 (2.63 (3.65 (1.430-.370) .41-2.250 (.35) 2.250 (.62-8.8) 3.32 (2.33) .69 (1.490-.190-.05) 1.490) .600 (.28) 1.72 (1.62-6.325 (.314 (.160-.330) .940) 1.266-.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.601) .780) 4.12) 4.78 (1.55 (1.39) 2.277-.16) 1.260 (.27-2.364) .570-1.297 (.292 (.740 (.290 (.75 (1.65-2.292-.271-.21 (2.750-1.25 (2.78) 6.427) .1) 3.800) 1.12) .590-.13 (.260 (.250 (.240 (.620-1.86 (1.267 (.507 (.32 (1.454 (.760 (.270) .260-.260 (.73) 1.49 (1.64) 697 680 524 701 603 957 Limit of detection (LOD.428-.233-.870 (.417 (.650 (.35 (1.820) .25-7.510-.230-.46) .295) .93 (1.960 (.41-3.200-.560-.340) .230 (.200-.680 (.530-.12 (.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .23 (2.60) .434) .30) 3.190-.320) .16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .353 (.26-2.300 (. Fourth National Report on Human Exposure to Environmental Chemicals 173 .300 (.300 (.30 (1.05) .62) 5.373) .590 (.280 (.180-.1) 3.34-6.700 (.288-.314) .49-2.355) .350-.1 and 0.43) 3.1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.440) .30 (.320) .33 (1.374) 99-00 01-02 99-00 01-02 99-00 01-02 .S.800 (.230-.253-.25-4.288 (.51-3.18 (1.610) .530-.79) 3.25) 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 .352-.71 (1.362) .328 (.740 (.36) 1.406) .510-.02-6.33 (2.1) 3.840-1.01 (1.238-.200-.560-1.220-.336 (.710 (.92-3. Survey Geometric mean (95% conf.26) 2.03 (3.360) .160-.990) .270 (.387) .04-5.51-6.340) 1.369) .27-11.46) 2.35 (2.320) .330) .29-1. Deltamethrin.42-2.830-2. interval) .35) 1.273 (.34 (2.32-21.27-2.450 (.384) .190-.630) .54) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.340) 75th .420) .560-.730 (.89-71.25 (2.300) .298 (.210-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.50 (2.52-4.311 (.250-.78) 1.45-5.550-.586) .470-.76 (1.750) .246-.670 (.16-1.53-3.320 (.26) 2.820) .18 (2.227-.265-.04) .52-5.850) .190-.830) 90th 1.83-11.25-1.14-6.247-.78) 1.321 (.390) .230 (.63-3.13) .226-.41) 3.49-2.810) 1.35) 2.38 (2.44) 5.520 (.56-5. population from the National Health and Nutrition Examination Survey.48-2.230-.90) 1.

510 (.40 (1.07) 2.53 (1.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .40) 2.173-.43-64.490-.370-.330) 75th .380 (.309) .229-.90) 3.230) .35) 1.55) 3.200-.329) .240 (.63) 1.460-.323 (.10 (2.19 (2.190 (.13 (.41) 1.380-.550 (.270 (.225-.04 (.91) 9.329) .446) .401) .750-1.62) .09-2.460-.72 (1.230-.670) 3.730) .81 (1.730-1.95) 1.44) 2.27) 1.330) .230-.321-.17-1.224-.570) . population from the National Health and Nutrition Examination Survey.74) 3.84 (1.275 (.240 (.210 (.390-.86 (1.280) .420-.178-.250 (.19-6.61-2.44 (1.960-1.311 (.91-4.280) .270-.490 (.240-.330) 1.63-3.510 (.227 (.09) 3.423 (.150-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.309 (.810) 1.330 (.261 (.80) 4.370 (.75-8.32 (2.860-1.312 (.200-.83) 1.43 (2.03 (.220 (.250 (.240-.03-1.290-.630) .410) .310) .271-.357) . Survey Geometric mean (95% conf.250) .290) .02 (2.362 (.67 (1.440-.220-.677) .200-.48 (1.00) 1.15-2.246 (.91) .25-2.590-1.41-4.11 (.62) 1.210-.240-.55 (1.25-5.350 (.300-.450 (.16-4.270) .49-2.860-1.510 (.96 (1.290) .09-2.270 (.550 (.05-3.13-1. interval) .299-.160-.234 (.21 (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 .365) 99-00 01-02 99-00 01-02 99-00 01-02 .280-.94 (1.610 (.36-6.240 (.202-.590) .440-.17 (.52 (1.530-.316 (.36 (1.270) .35-3.700-1.13-1.720) 90th 1.274 (.00) 1.238-.88-5.335-.35) .06-3. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.328) .240-.02-1.730) .43) 1.760) .21-4.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.278) .590) .378 (.560 (.52) 2.64-5.07-5.67) 1.280 (.19) 2.650) .350) .35 (1.49) 3.540 (.216-.25) 2.00) 5.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .500) .640 (.37 (1.387) .280 (.200-.550 (.49) 1.11 (.440-.22 (1.91 (2.226-.300-.320) .400-.400-.330) .534) .39) 1.54 (1.280 (.590) .83 (1.253) .240 (.S.670) .372) .60-4.0) 3.49 (1.580 (. Deltamethrin.190-.930) .67 (1.210 (.37) 1.264 (.272) .04 (3.437) .930) 1.60) 1.272 (.860 (.43 (1.190-.640 (.480-.400) .261-.580) .840-1.490 (.480 (.73) 1.09 (.530-.274-.740) .73-4.51-7.410-.720 (.

Sugiri D. Bravo R. Levsen K. Int J Hyg Environ Health 2006. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. toxicokinetics. Sugiri D. urban cohort. Atlanta (GA). GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Ortiz-Perez MD. Pearson M. Carranza C.111(1):79-84. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation.Pyrethroid Pesticides References Baker SE. Obel J. Kolossa-Gehring M. Idel H. and genotoxicity in exposed children. Lopez-Guzman OD. Leng G. Hardt J. Int J Hyg Environ Health 2002.206(2):85-92. Int Arch Occup Environ Health 2003. Batres LE. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Angerer J. Third National Report on Human Exposure to Environmental Chemicals. Lu C. Centers for Disease Control and Prevention (CDC). Angerer J. Hadnagy W. Barr DB. 2005. Environ Health Perspect 2006. Grimaldo M. Hoppe HW. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence.46(3):281-288. Biological monitoring of workers after the application of insecticidal pyrethroids.205(6):459-472. Godbold J. Int J Hyg Environ Health 2003. Seiwert M. Environ Health Perspect 2005. Environ Health Perspect 2003. Ball M. Ranft U. Idel H. Torres-Dosal A. Barr DB. Ranft U.209(3):221-233. Exposure to indoor pesticides during pregnancy in a multiethnic. Becker K. Lapinski R. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Liu Z. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Berkowitz GS. Leng G. et al. Olsson AO. et al. et al.76(7):492-498. Berger-Preiss E.113(6):782-786. Berger-Preiss E. Arch Environ Contam Toxicol 2004. Deych E.114(9):14191423. Bartell S.

161) .460 (.150) .280-.310 (.110-.460 (.260 (.100 (.320) Total .154-.087-.200 (.112-.220) .600) .122 (.300-.350) .190-.210) .280-.260 (.126 (.250 (.220-.330 (.154) .110-. castings. from air and drinking water. ceramics.100-.120) .120-.140) .100 (.207) .220-.120) .137) .108-.164-.180 (.320-.200) .210) .095 (.117-.095-.200) . and as a fire-retardant in textiles and plastics.114) .140) .210) .260) .280) .160 (. coal-fired plants.140 (.170 (.270 (.158 (.360) .080-. distribution. see Data Analysis section) for Survey years 99-00.120-.240) .300-.300) .136) * .115-.230) .140) .300 (.135) * .260 (.280) .190-.350-.390) .320) .400) .320 (.130) .200 (.180) .120-.200) .130 (.230 (.200 (.160) .210 (.144) .093 (.170-. Dermal contact with soil.280) . 7440-36-0 General Information Antimony is found in ores or other minerals.130 (.120 (.130) < LOD .330) .150-.160) .300 (.270) .120-.170 (.310-. which may vary for some chemicals by year and by individual sample. enamels.330 (.110-.180-.240 (.340 (.310) .170-.290-.125 (.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 .184) .137) .128 (.115) .070 (<LOD-.190) .134-.130-.230-.130 (.190 (.120 (. and excretion of antimony vary depending on its oxidation state.130 (.470 (.430 (.250) .390) .410-.360) .150 (.090 (<LOD-.04.280-.080) .098-.470) .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.240 (.400-.130) .320-.190-.500) .150-.108 (. Antimony enters the environment from natural sources and from its use in industry.160-.150) 90th . People are exposed to antimony primarily through food and.220-.190) .330) 1132 1335 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .170-. < LOD means less than the limit of detection.570) .180-.260-.170) .350 (. 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.180-.230) . and 0.230 (.132 (.330) . and refuse incinerators that process or release antimony.150-.123 (.320 (.220) 95th .120-.103) . Antimony can exist in one of four valences in its various chemical and physical forms: -3.120 (.170-.176 (.280 (. and pewter.440) .240 (.560) .300) .180) .330 (.169 (.420) .110) . and 03-04 are 0.490 (.200 (.390 (.390) . respectively.310) .250-.090 (.180-.160) .099 (.410) .320-.141-.270 (.300) .130-.210-.270) .130 (.500) .210 (.128 (.410) .350) .160) .143 (.160 (.120) .130-.280-.350-.510) .330-.210-.130-.190 (.430 (.100-.200) .230-.350 (.190-.400 (.110-.180 (.360 (.175 (.240 (.160-.350) .150 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals .180 (.350-.490) .350 (.119-.310 (.160-.400 (.180 (.230-.260-.240-.Metals Antimony CAS No.119) .350 (.370) .140 (.220-.310 (.140) .180 (.210) .440 (.120-.180 (.140) .460 (.290-.090-.132 (.250-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.220-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.290 (.140 (.200 (.270-.190 (.160) .080 (<LOD-. interval) .131-.280 (.440) . or other substances containing antimony is another means of exposure.200-.120 (.156-.090) 75th .170-.330) .070 (<LOD-.178) .130 (.250-.150-.04.350 (.320-.250 (.190-.190) .220) .180-.136-. 0.130-.240 (.130-.220) .154) .230-.S. Workplace exposures can occur at smelters.220 (.150) .140-.360 (.370-. and glass.160) . Stibine is a metal hydride form of antimony used in the semiconductor industry.130 (.148-. The absorption.250 (.090-.260) .220-.142 (.310-.400) .360-.340) .190) .088-. ammunition.250-.400 (.120-.133) * .100) .330-. fireworks.190 (.120-.260) .270 (.140) .120-. solder.134 (. and +5.390) . It is also used in paints.390-.200-.080) .197) .390-.105 (.330) .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 .190 (.280-.160-.120) .110 (.430 (.146 (.079-.460) . metal bearings.145 (.120 (.200-.200 (. 0. water.340 (.710) .145) Selected percentiles ( 95% confidence interval) 50th . to a lesser extent.070-.230) .130) .220 (.210) .150 (.270 (.140 (.470) . Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications. population from the National Health and Nutrition Examination Survey.157) .280) .117-.109-.300-.230-.07. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.400) .150-.310 (.350) . It is used in metal alloys.200-. storage batteries. 01-02.230 (.190) .126-.130-.130 (. +3.160 (.390-. sheet and pipe metal.240-.530) .150) .

140) .152) .154-.200-.127) .333 (.097-. resulting in hemolysis with abdominal and back pain (Dernehl et al.087) .122 (.135) .116-.250 (. Fourth National Report on Human Exposure to Environmental Chemicals 177 .114 (.236 (.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 . diarrhea.352) .164-.741 (.135 (.069-.160 (.139 (. Histopathologic inflammatory and degenerative changes in the lung.125-.076-.118 (.099-. 1958) and occupational exposures (Briegner et al.245) .121 (.115 (.124-.131) .222 (.444) .143 (.104-.150-.148-.077) .120 (.480) .250) .268) .317) .120 (.117-.116 (.265 (.182 (.727) .129) .250-.313-.187) .315) .310) .084) .200-. species..119-.444) .164) .124 (.191 (.281-.103-.205-.126 (.115-.080 (.267-.102-.111-.089) .129 (.195-.373) .192 (.250-.200) .114 (.417) .171) .068-.132 (.188-.146-. interval) .308-.207) .149) .127) .333-.255) .181) .153 (.146-.294) Total .176-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.120 (.286 (.320) .098-.276 (.107-.178-.152) .144-.119-.150-.156 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.259 (. and ulcers (Werrin. 1986).148) * .298 (. 1962).172-.235-.106-.196 (. and route of exposure (Elinder and Friberg.253-.148-.167-.242-.176 (.146-.208-.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 .133) .153-.086) 75th .107-.228 (. Ming-Hsin et al.131 (.130 (.120 (.178 (.741) .175 (.130) .137 (.134) .181) .317) .173 (. and gastrointestinal symptoms such as vomiting.320-.333-. skin.250 (.119 (.121 (.228-.163 (.085) . and kidney have been demonstrated in high dose animal studies depending on the dose. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.138 (.192-.217 (.159-.429) .146) .265-.167 (.278 (.485) .343 (.320-.357-. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.112 (.Metals than for trivalent compounds (Elinder and Friberg.123 (.320 (.209 (.147-.318-. 1988.136) .167 (.333-1.261) .092) .203) . The toxicity of stibine after acute inhalational exposure is similar to that of arsine.127) .357) .170 (.256 (.300) .098-.30) .069-.199-.310) .162-.118 (.226 (.193) .250-.267) .167 (.438) .132) .111 (.229-.075 (.189 (.115) . liver.112 (.271-.206-.114 (.277 (.391) .209) .115 (.320 (.117-.122 (.417) .338) .214) .115-.200-.107-.266 (.317) .124-.129 (.147) .105-.193 (.333) .173 (.130) .185 (. 1995). 1944).126) .108 (.267 (.108-.385 (.414) .225 (.082) .127 (.135 (.300) .078 (.159-.185-. 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.124) .126-.131-.156-.098) .253 (.238 (.075 (.068 (..400 (.263-.195 (.280-.113) .117-.181) .220) .209) .. and eyes.269 (.208 (.109 (.405) . Inorganic antimony salts irritate the mucous membranes.138) * . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.081) .471) .179-.447 (.228 (.143) Selected percentiles ( 95% confidence interval) 50th .161) .194-.143) 90th .333 (.074 (.076-. abdominal pain.500) .471 (.135) . Acute antimony poisoning may cause a metallic taste.308) .164 (.129) * . 1953).352 (.159-.161) . 1973).380 (.127) .295 (.128-.109-.429 (.099-.185 (.338 (.391) .108-.233 (.238) ..233-.138-. 1954).183) .123) .135) .095-.278) .239-. population from the National Health and Nutrition Examination Survey.248-.248) .338 (.103-.257) .130) .230-.145) .071-.204-.318-.195-.104-.250-.163 (.080 (<LOD-.S.333 (.241-.176 (.188) .364 (.125 (..425) .227-.173-. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.095-.280 (.113-.115 (.112-.364 (.143) .139 (.272) .081 (<LOD-.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 .263 (.247) .321) .300 (.100 (.113-.173) .241-.109 (.203) .371 (.333-.149-.086 (.061-.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.225) .430) .310 (.244-.092-.213 (.079 (<LOD-.108-.255-.186) .421) .230) 95th . 1986).198) . myocardium.192) .224 (.082 (<LOD-.106-.082) .238) .102-.140) < LOD .209-.288 (.121) .211) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.151) .143) .233) .096-.138-.

2nd ed. Sabbioni E. Cordasco EM. et al. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. Br J Ind Med 1991. Kiberd B. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Antimony in blood and urine of infants. Friberg L. Skulsukai G.48:93-97. Antimony trioxide is rated by IARC as a possible human carcinogen. Mayer P. Fuchs A.76:432436. 1987).158:165-190.. Industrial antimony poisoning. Lauwerys R. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Chen J-R. Third National Report on Human Exposure to Environmental Chemicals. J Clin Pathol 1998. Mahieu P. Liao Y-H. and future strategies. Urinary antimony in infancy. Briegner H. Sci Total Environ 1994. Nau CA. O’Regan M. Review of elements in blood. J Trace Elem Med Biol 2002. and a drinking water standard has been established by the U. Minoia C. Delves HT. gallium. 1990. Centers for Disease Control and Prevention (CDC). environmental levels) and health effects is available from ATSDR at: http://www. Dezateux et al. eds. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Stasney J. Biomonitoring Information Levels of urinary antimony reflect recent exposure. gov/toxpro2. Ming-Hsin H. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals .. Mayne P.. Roland H. pp. indium.. Pilgrim L. Stocks J. Chemotherapy for leishmaniasis: Biochemical mechanisms. or exposure differences. Petrucci F. 20012002. Buchet JP. Paschal et al. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Nordberg GF.106:33-39. Chest 1973. Rev Infect Dis 1988. 1998. Weltle D. Schaller KH. Sabbioni E. Biological monitoring of exposures to aluminum. Trace element reference values in tissues from inhabitants of the European community I. Kentner M. Biomonitoring of a worker population exposed to low antimony trioxide levels. Industrial Medicine 1944. 1986.521-523... Cheng-Wei L. Semisch CW. respectively. Information about external exposure (i. Cullen A. Stone FD.. et al. In: Friberg L. and hydrogen sulfide. Schacke G.51:238-240. Carelli G. External and internal antimony exposure in starter battery production. Environ Health Perspect 1998. Liao Y-H et al. and antimony in optoelectronic industry workers. Element reference values in tissues from inhabitants of the European community. Industrial Medicine and Surgery (Dec. 1994) have reported values slightly higher than those in this Report.)1954. Delves HT. Ju-Sun P. clinical efficacy. Van der Venne MT. stibine. and 2003-2004. Pozzoli L.. Yu H-S. Kuo-Juie Y. Vouk VB.cdc. Luedersdorf R. 2002. arsenic. Pulmonary edema of environmental origin. 1997).html. Yang C-Y. Elinder CG.S.64(2):182-185. References Berman JD. Chin Med J 1958. Bolten C. Dunkelberg. 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. 1991. even when exposure levels were below workplace air standards (Bailly et al. Atlanta (GA). Kentner et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Costeloe K. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Caroli S.59:469-474.13:361-362.Metals to antimony have been established by OSHA and ACGIH.e. Arch Dis Child 1997. Shao-Chi C. Matthews T.. Piatnek DA. Stead FM.46:931-936. Arsine. Hamilton EI. 1998). Dezateux C. Iavicoli I.67:119-123. Gallorini M. Antimony. 1998) or compiled reference ranges (Hamilton et al. Leinemann M. VI. Chia-Yu H. New York: Elsevier. Wu M-T. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Pietra R. Dernehl CU. Ho C-K. 1995. Alimonti A.. 2004.. et al. 26-42. Biological assessment of exposure to antimony and lead in the glass-producing industry.76(2):103-115.10(3):560-586. Apostoli P. Handbook on the toxicology of metals. Iavicoli et al.. population.atsdr. J Occup Environ Med 2004. Wade A. Lenert G. Int Arch Occup Environ Health 1995. HH. EPA. Ludersdorf et al.16: 33-39. Suchenwirth R. Gebel TW. Int Arch Occup Environ Health 1987. Bailly R. Konings J. Earlier measurements in general populations (Minoia et al. which may be due to methodologic. 2005.

Werrin M.76(1):53-59. Pirkle JL.99-108.95:89-105. Antimony poisoning in industry. Fourth National Report on Human Exposure to Environmental Chemicals 179 . et al. Sci Total Environ 1990. and serum of Italian subjects. Quarterly Bulletin of the Association of Food and Drug Officials 1962. Morrow JC. Trace metals in urine of United States residents: reference range concentrations. Ting BG. Jackson RJ. Industrial Hygiene and Occupational Medicine 1953.Metals in urine. Chemical food poisoning. Renes LE. Environ Res 1998. blood. Sampson EJ. 27:38-45. Paschal DC.

1) 15. and other metals.0 (22.84) 8.27) 9. retaining walls. +3 and +5). to a lesser extent.13-8.0-19.70 (6. alloys.00 (6. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.90-7.4 (31.6-141) 53.80 (5.S.7) 65.57) Selected percentiles ( 95% confidence interval) 50th 7. black.0 (15.6-43. sodium arsenite. see Data Analysis section) for Survey year 03-04 is 0.41 (7.9-34. meats.4-65.5 (23.02-8. Water sources contain mostly inorganic arsenate.0 (11. and play sets.55 (7. the smelting of copper.0 (14. such as arsenopyrite (FeAsS) and realgar (As4S4). and. cacodylic acid.10-7.7) 90th 37.8-77.80) 6. and produce. General population exposure to inorganic arsenic can occur through consumption of drinking water and. lead.3-15.77) 6.4 (48.7-83. 2001). and as a cosmetic to lighten complexion. particularly arsenic trioxide. interval) 8.90-14. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.8-61.10-10.30 (7.5 (14.66-8. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.1-40.5 (40.3) 10. Survey years 03-04 Geometric mean (95% conf.5-19.9 (8. Gallium.90 (7.5) 41.19-9. from coal burning.10) 10.90 (5. and in lead-acid storage battery grids.1) 290 725 1542 03-04 03-04 9. and gray forms).9) 21. Arsenic is measurable in most soils. and indium arsenides are used in the semiconductor industry. referred to as inorganic arsenic compounds.9) 68. Arsenic and its compounds have had many uses in the past and present as medicines.Metals Arsenic CAS No. copper arsenates.7) 24.4) 60.30 (6.2 (41. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. Various arsenic compounds were used in paint pigments and for tanning animal hides. In nature. and foods.90) 75th 16.50 (8.1-18. 180 Fourth National Report on Human Exposure to Environmental Chemicals . ocean and fresh waters.5-52.90 (7. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. arsenocholine. mental disorders. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.2-17. Arsenic trioxide (As2O3.6-35.84) 8.6) 11. as alloy in metal bearings.8) 33.2-93. The United States no longer produces arsenic from mining but imports about 22.0-60.2 (12. aluminum.2-20. Although it is still widely used in the United States.1 (32.9-46.90-8.70-9.5) 43.5) 66.9-62.00-9. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. arsenic compounds.4 (24. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.12-10.29 (8.1) 7.10 (6.4) 13.8) 30. arsenic as elemental metalloids may be used in some ammunition.6 (9.20 (8.6 (15. or rarely as elemental metalloids (yellow.25-9.90-8.4 (26. population from the National Health and Nutrition Examination Survey. Since the 1940s.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 7.8 (48.2) 15.5 (34. Before the 20th century.90) 16. though in some locations arsenite may be prevalent (WHO.5-41.80-9. and arsenates (oxidation states of -3. 2005).3-19. psoriasis. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. semiconductors.1) 1281 1276 03-04 03-04 03-04 9. arsenites. Arsenic trioxide is approved to treat acute promyelocytic leukemia.34-9. In the last century.5 (36.8) 29.70) 8. pesticides.6) 618 722 1074 Limit of detection (LOD.34-10. solders.5) 95th 65.2 (13.7 (11. were used as treatments for syphilis.6 (32.8) 7.8) 34. Also.000 metric tons annually. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.90-11.9 (17. mostly for use in wood preservation (ATSDR.6 (13.7-95. and as homicidal poisons.12 (6. Arsine (AsH3) is a reactive.0 (43.3-111) 78. grain.30) 17.97) 8.1 (38. cancers. trimethylarsine oxide.2-61.8) 7. lead hydrogen arsenate.5-178) 46.74.40) 7.08 (5. it is found in over 200 crystalline or mineral forms.4 (7. and arsenosugars.4) 40.2 (51. to a lesser extent.8) 17.50-14. gaseous hydride manufactured in small quantities for use in the semiconductor industry.2) 46.

2-46. EPA.7-34.93-9.10-16.9) 13. 2001).. 2006.4 (11.2) 40.31 (6.86-17.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.88) 7.9-56.0-18.8-75.3-62.3-53. are used in enclosed ultraclean operations within the semiconductor industry. gallium arsenide and indium arsenide.45) 5. 2001).8 (20.4 (26.20-9.33 (6. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. The semiconductor dopants.04 (5. Fish. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.33-10. 2001.1) 6.8 (27. Direct exposure to DMA and MMA may result from use of the two pesticides.4 (24..5-17. selenium.44) 6.8-32.7-188) 27.96) 12.3) 9.8 (12. In aquatic sediments.4-64.4 (12.32 (5.9) 53.0) 1281 1276 03-04 03-04 03-04 8.7 (11. Children may have additional exposures from ingestion of contaminated soils (e.0-38. inorganic arsenic is widely distributed within the body.44-11.7-18.8) 22.6) 45. 2001).66-8.S.01) 11.4) 54.S.0) 42.2) 15.0-26. Smoking tobacco is also a source of inorganic arsenic.75 (5.2-15. Gamble et al. Steinmaus et al.8 (21.6 (10.7) 28.. After absorption. cacodylic acid and monosodium methyl arsenate.58-10.3-41. dose level. arsenocholine.2 (12.25-9. WHO.13) 8.5) 290 725 1542 03-04 03-04 8.11 (5. Inorganic forms of arsenic demonstrate high acute toxicity. 2001).7 (25.4) 32.2) 90th 30.01) 7.4 (42.75) 13.3-64.88 (5. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.1) 58.S. interval) 8. Chowdhury et al.4 (40.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .5-120) 40. 2001).10-8. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.0) 33.07-9.5 (9.23-7.24 (7.8-62. and contact with CCA-preserved wood structures.38-10.66 (7. arsenic does not show biomagnification in the food chain (WHO.61 (7. NRC. as observed in Bangladesh where millions of people have been exposed. though some reduction may occur in the gut prior to absorption.59) Selected percentiles ( 95% confidence interval) 50th 7.8) 27. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.7-35.g.0) 12. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.04) 7. 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.6-17. 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.93-8.0 (17. WHO. Though modest bioconcentration occurs in some aquatic life.51) 75th 14. kelp.3) 6. Tseng. 2001.9 (45.47 (7. have caused clinical arsenic poisoning. 2007.1) 24..00 (6.47 (6. organic arsenic can be converted back to methylated and inorganic arsenic.41) 6. Arsenate is reduced in the body to arsenite (oxidation state +3).0-69.1-36..3 (27.76 (6.7 (9. 2001).12-10.81-9. 2003. 2006. and folate status (Chen et al.1 (11. dust.1) 8. mine tailings). and arsenosugars.35) 7.7-17. age.18 (5.3 (24.6 (17. and some other seafood can contain organic forms of arsenic including arsenobetaine.0 (31.50 (6. Survey years 03-04 Geometric mean (95% conf..99-9.1 (14.28-7.25 (6. 2007. Extremely high groundwater arsenic levels.0) 26. In aquatic organisms.47-6. population from the National Health and Nutrition Examination Survey. 2001). EPA’s maximum contaminant level (Hughes. 1988). trimethylarsine oxide (TMAO). so exposure to the general population is extremely limited. 2007.5) 17. shellfish.8 (11.1) 7.6 (35.5) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2557 03-04 03-04 03-04 8.06 (4.64 (7.40) 8.0) 14.30-9. U. 2001). but is poorly absorbed dermally (WHO.7) 95th 50.66-8.

. 2006) or when exposure occurs in smokers (Chen et al. 2004). cell transformations. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. 2001. 2000. 1998. Survey years 03-04 Geometric mean (95% conf. WHO. 2001).0.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Cohen et al. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. hematocytopenias. leading to a decrease in adenosine triphosphate energy production.. increased oxidative stress. fatty acid oxidation.. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al.20 (<LOD-1.g. WHO. and diarrhea. 2001). and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. see Data Analysis section) for Survey year 03-04 is 1. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. some of these effects may take years to develop. noncirrhotic portal hypertension. 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 1.10 (<LOD-1. and it also will inhibit succinate dehydrogenase. With chronic exposure.60) 1. 2001).S... hepatotoxicity.S. 2001. gluconeogenesis.10 (<LOD-1. The organic forms of arsenic occurring in seafood have little known toxicity.60) 1. respectively.. Acutely. NRC.. which can lead to dehydration and shock. hyperkeratosis.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.20 (<LOD-1. apoptosis. 2004.30) 1. vomiting. 2004).EPA. Chronic elevated arsenic intakes have been associated with diabetes. The U.20 (<LOD-1.10 (<LOD-1. Chronic arsenic exposure in humans is considered to be a cause of skin. Chile)..10 (<LOD-1.. food residue. 2006. including drinking water sources with elevated arsenic levels (e. Cellular glucose uptake. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2007).S.50) 1.10 (<LOD-1. drinking water have not been associated with increased cancer rates (Schoen et al. 2001).Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. WHO. but additional or confirmatory research is needed (Kapaj et al.. NRC. Raml et al. can cause peripheral sensorimotor neuropathies. Bredfeldt et al. Chronic human intake of arsenic at less than acutely toxic doses. population from the National Health and Nutrition Examination Survey. and altered gene expression. arsenic trioxide) includes hemorrhagic gastritis with nausea. 2001). interference in signal transduction pathways. 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.80) 1..g. Although arsenate is reduced in the body to arsenite. lung. renal failure. 2007. Arsenic has many actions demonstrated in cellular studies. cytotoxicity. peripheral vascular disease. Cardiac arrhythmias. Taiwan. hypertension. and hyperpigmentation of the skin (NRC. including inhibition of numerous enzymes.S.20 (<LOD-1.EPA has established drinking water. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. and DNA repair inhibition (Cohen et al. 2006. Studies of arsenic at levels typical of U. and endothelial injury (Kumagai and Sumi. 2006. substitution in phosphate metabolism. 2001). Bangladesh. WHO. 182 Fourth National Report on Human Exposure to Environmental Chemicals . The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. and by uncoupling oxidative phosphorylation (NRC. and bladder cancer (IARC. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e.50) 621 725 1078 Limit of detection (LOD. Such actions may lead to decreased energy production. U. and childhood neurodevelopmental effects in observational human studies. 2007.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.. and production of glutathione may be affected as well.

Levels of total urinary arsenic in the U. 2007. In the German Environmental Survey III of 1998. 1992. Pellizzari and Clayton 2006).70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 2006.50) 1... urinary arsenic levels have been accepted as a good biomarker of dose (WHO. but generally only at maternally toxic doses (WHO. 1998. 2006. Josyula et al... Survey years 03-04 Geometric mean (95% conf.e.S. 1986). 2004. Shalat et al..41) 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) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. Caldwell et al. environmental levels) and health effects is available from ATSDR at: http://www... 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. 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. 2006)..Metals compounds. population (Rubin et al. Offergelt et al.html.75 (<LOD-2.75 (<LOD-2. Valenzuela et al.. Additional information about external exposure (i. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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. Calderon et al. 2008. 2001). 2008). 2008). 2003.80 (<LOD-4. In a Nevada town where groundwater levels were naturally elevated.S. In animal studies. Though CCA-treated wood contains several thousand times more arsenic than untreated wood.atsdr. 2004.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.S.61 (<LOD-3.. although urinary arsenic levels were not associated with CCA contact (Shalat et al.00) 1.. DMA produced bladder cancer in some chronic rat studies (Cohen et al.19) 3. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. arsenic has been fetotoxic and teratogenic. Vahter et al..04 (<LOD-3..cdc. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.. 2001)..18) 3.18 (<LOD-3.33 (<LOD-3. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3. Compared with this Report. 1999). had decreased since the prior 1990– 1992 survey. median urinary total arsenic levels in 4052 adults varied with seafood intake. Pellizzari and Clayton. gov/toxpro2. Shalat et al.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. and the FDA has established a bottled drinking water standard. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. 2006). 2006. 2006). 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. * 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. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al... higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al.33 (<LOD-3.. WHO. population in NHANES 2003–2004 (Schulz et al. 2000)..... 2006). Fourth National Report on Human Exposure to Environmental Chemicals 183 . 1999. Caldwell et al. Meza et al. 2000. 2007. Pellizzari and Clayton. Consequently.69 (<LOD-3.. 2001). and were about two-fold lower than those for the U. 1999.

vasospasm.9) 13.31-1. Survey years 03-04 Geometric mean (95% conf.900 (.40) 75th 5.9-23. 2008.37 (1. geometric mean levels were about 70-fold higher than for the U.20 (4.20) 18. Arsenate.90-7. Tseng et al.11-1.30) 2.1-25.S.e. Caldwell et al.30) 10.4.7) 13.00 (1.6 (11. interval) 1. 1990.60-3. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004. In the late 1980s..40-6.10) 8. Pellizzari and Clayton. 2007).20 (.00-6.2-38..Metals other areas of the world (Ahsan et al.20-25.80 (4. In most human studies.62) 2.8. After recent seafood ingestion. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. arsenocholine.3 (21.70 (5. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.700-1.40-7. 2007) with higher levels of arsenic in the drinking water.20) 3.800 (.90-29.4-35.S.00) 3.9 (7.7 (21.S. 2008).800) 1.6. methylation capacity. population (Ahsan et al.60) 1. Caldwell et al.29 (1. 184 Fourth National Report on Human Exposure to Environmental Chemicals .4) 23.3) 95th 35.50) . Chowdhury et al. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. Blom et al.00-1.6) 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 * * 1.55 (1.3% of a representative sample of the U.0) 4.S.05) < LOD .6-44.6 (25. and TMAO were detected in only 7.3 (9. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.20 (2. 2005..17-1. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. respectively.. in NHEXAS 1995–1996. dermal keratosis.28) 1. 2000.. arsenite. Individually measurable species resulting from inorganic arsenic exposure are arsenate. and two methylated metabolic products.40) 5.93) 1.8-50.871-1. DMA and MMA.70-21. 2001..0-23.00-12.8-40. Caldwell et al.800 (. 2000. 1. 4.2-35. 2008)..50) 90th 16.. WHO. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.1) 18..19 (.45 (1.70 (3.900-1. Some noncancer effects of arsenic (e. MMA. China. and other factors such as nutrition.9 (6..83) Selected percentiles ( 95% confidence interval) 50th 1.6 (13.3) 1284 1284 03-04 03-04 03-04 1.1-94.7) 15.700-1.66 (1.5 (26. 2003)..80) 1. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.8) 35.5) 29. Valenzuela et al. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.50) .80 (. Measurable organic arsenic species in this Report are three biologically generated environmental forms.1-51..8 (17. population in the NHANES 2003–2004 subsample.0 (26..8 (12.5) 292 728 1548 03-04 03-04 1. and 0.4 (16. 2005.30 (2. 1996. 2008). with DMA. When seafood intake is avoided.400-.70-21. 2008.10) 4.20-190) 31. 2008). population (Sun et al. < LOD means less than the limit of detection.20) 7.. arsenocholine. 2001).600 (.800-1... Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic. 1985. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. The higher percentiles of total urinary arsenic levels in the U. arsenite. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70) 6.43-1. Sun et al.6. These associations are stronger at higher urinary levels. arsenobetaine. population showed a higher contribution of arsenobetaine (Caldwell et al..10 (4.3-39.5) 621 725 1078 Limit of detection (LOD. which may vary for some chemicals by year and by individual sample. Also. In the residents of a Chilean town who consumed water with high levels of arsenic.S.0) 29.00 (.5) 32. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.3) 35. 2005. For residents of Inner Mongolia. see Data Analysis section) for Survey year 03-04 is 0.5 (14.. and duration of exposure are also considered important.20 (1. Caceres et al.74 (1.80 (3.1) 45..68) .7-22.7 (13.50-6.30 (1. population from the National Health and Nutrition Examination Survey. when seafood organic arsenic is subtracted). 2000.800-4.0 (27. Aposhian et al.500-1.g. 2006).2 (6. and TMAO.00-4. 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. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.4) 31..48-2.80-5.20-3.

72) 12.4) 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 * * 1.6-32.73-6.70) 5. Sun et al. population for the sum of inorganic related species was 18.76-27.00 (1.47 (1.37-2.1 (26.14 (1.43) 14..S.6-29.0-36. 2008). population from the National Health and Nutrition Examination Survey.5) 26.4-21.68 (1.83) 8.80) .2 (12.82) 4.1-36. 2007).30-1.6 (9.50-15.19-2..3) 1284 1284 03-04 03-04 03-04 1.4-82.79 (1.61-6.959-1.7) 17.5-20.5 (18. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.64-29.43) 75th 5.6-46.786-1.4 (24. Offergelt et al.12) < LOD .51) 5.5 (18.05 (.9) 32.29 (4.53 (. 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..15-4.6) 19.40 (1.45) 1. The 95th percentile of the U.938-1.7) 9.3-24.5) 17.4 (11.91) 90th 16..30) 1.7) 30. 1992.18-1. 2003. In recent years.3 (10.54 (1.16 (. interval) 1.55) 1.36) 2. Information about the biological exposure indices is provided here for comparison.05) 1. Caldwell et al. 2006. 1986.21) 5.67) 4.58 (3.9 μg/L.3) 95th 29.2 (13.40) 1.9 (25.78 (3.4) 32.78-5. 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.400-.6 (6.81 (4.877 (. The American Conference of Governmental Industrial Hygienists (ACGIH) provides an occupational biologic effect index (BEI) for urinary inorganic arsenic plus metabolites equal to 35 μg/L (ACGIH.Metals as with DMA. 2008).833-1.93 (1. not to imply a safety level for general population exposure.9) 14.25 (.25-7.62-6. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al. 2001).2 (12.638) 1.65 (1.47 (2.15-1..1) 26.1-18.80-153) 17.4) 292 728 1548 03-04 03-04 1..88 (5. Vahter et al. which is below the ACGIH BEI (Caldwell et al.11 (.82) Selected percentiles ( 95% confidence interval) 50th 1.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.39-3.3 (10.. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. 2001).91 (4.13-39.00 (3..51-2.909-1.28) 1.83) 2.9-18.4-28.4) 13.901-2.9 (13. WHO. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2 (4.15-1.67) 1.612-1.0 (9. Survey years 03-04 Geometric mean (95% conf.531 (.88) 2. Fourth National Report on Human Exposure to Environmental Chemicals 185 . 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.44 (1.50-7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (. 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.8) 29.29-14.32-7. 1998.

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

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 3.00) 1.08 (<LOD-4. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey years 03-04 Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey years 03-04 Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2. which may vary for some chemicals by year and by individual sample.40 (<LOD-1. < LOD means less than the limit of detection.80) < LOD 621 725 1078 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 187 .00 (<LOD-2.S.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. population from the National Health and Nutrition Examination Survey.95 (<LOD-2.00 (<LOD-3.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (<LOD-1. population from the National Health and Nutrition Examination Survey. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.44) 2.S.

9) 11.50-15.05) 3.0-17.00 (5.0) 292 728 1548 03-04 03-04 4.73 (3.0-16.10) 3.S.00 (3.06) 5.34-4.00) 90th 11.37 (2.0) 621 725 1078 Limit of detection (LOD.98) 4.05) 5.0 (13.22) 4.0 (9.80) 7.17 (2.50-5. interval) 3.32-10.00-4.0) 17.19) Selected percentiles ( 95% confidence interval) 50th 3. interval) 3.00-5.91) 75th 5.0 (10.65-6.90 (3.33) 3.82-5.6) 1284 1284 03-04 03-04 03-04 4.00-4.00) 6.69 (3.27-2.00 (3.9) 13.45) 8.77 (3.61-16.0) 11.60-6.00) 12.00-11.59 (6.48 (2.00-13. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00) 6. Survey years 03-04 Geometric mean (95% conf.9) 5.17-6.9) 12.20-4.0-18.00 (3.05) 10.79 (3.60-7.57 (3.9 (7.0 (14.00-11.90) 5.88 (4.80) 2.5) 95th 13.70-3.0 (11.71-4.00-4.45 (8.34) 3.37 (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 4.00-15.8) 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 3.18 (6.6-18.0) 13.16 (4.7) 1284 1284 03-04 03-04 03-04 4.0 (8.33-4.11) 4.03-6.0) 16.39-3.00-10.0-16.89 (3.3 (8.10) 6.16-11.27-5.00-7.1-18.65-8.92) 3.69-6.17-4.20) 11.7-16.00 (4.8) 7.00) 3. population from the National Health and Nutrition Examination Survey.13-4.86 (2.34-4.5 (11.14) Selected percentiles ( 95% confidence interval) 50th 3.3 (8.71) 3.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00) 9.16 (2.08 (2.49) 10.00 (5.00-7.0) 9.69-3.00-15.82-9.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .80-6.8) 7.78) 4.15) 4.0 (13.0 (10.00-7.95 (4.00 (7.00-11.24) 3.48 (3.1 (8.00-22.00) 5.74 (2.0-17.74) 90th 9.S.00-4.95-6.81 (5.45) 3.70) 5.70 (3.00 (6.0) 12.00 (3.86-7.71 (4.3 (7.50 (4.00 (5.4 (7.03 (3.20-12.0-12.73) 6.00) 3.60-4.32 (8.00-8.67) 9.2) 10.30 (7.80 (4.49-4.0) 11.31-4.34 (3.7) 13.6 (9.7 (10.84-18.00-12.00 (7.29-4.82) 3.6) 292 728 1548 03-04 03-04 3.00 (3.0 (12.00 (5.90) 2.55 (2.46 (4.1-22.0) 13.5) 12.25 (4.0) 95th 16.0-25.9 (11.95-4.14) 3.44 (2.42) 3.0) 9.70-4.11 (3.00-9.00-3.94) 3.0) 9.97-3.00 (6.7.24-4.86-21.0 (12.1-15.00) 7.34 (3.0) 17.0) 10.09 (7.0 (8.28) 2.92-12.00-4. see Data Analysis section) for Survey year 03-04 is 1.00 (5.0 (10.67) 8.62) 4.00) 4.0 (10.95-3.60-3.69 (3.0) 16.80-5.72 (4.00) 75th 6. Survey years 03-04 Geometric mean (95% conf.27 (2.00-12.57-5.27 (3.00 (6.32 (4.0 (9.00) 4.30) 3.00-3.00-15.38 (3.00-7.7) 12.71 (3.94-3. population from the National Health and Nutrition Examination Survey.0 (9.80-3.00 (3.00-4.61-11.0) 14.0-19.12 (3.31) 4.85 (3.00) 6.78 (4.52) 3.44) 5.12-4.00) 6.70-12.84-8.

36 (1.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.70-2.40 (1.70-2.46 (1.34) 2.00 (<LOD-1.10 (.80) 1.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.90) 1.20) 2.96-2.18-1.40 (2.93) .40) 1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.37 (1.80 (1.71-2.30-1.10) 2.58) 2.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.86 (2.90) 2.50 (1.50-2.80 (2.00 (1.10 (<LOD-1.43-3.70) 2. population from the National Health and Nutrition Examination Survey.57) 95th 2. Survey years 03-04 Geometric mean (95% conf.22) 3.85) 1.16 (2.88 (1.80) 1.50 (<LOD-1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.17) 2.00-1.73-2.30 (1.10-1.11-1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .00-4.60) 2.84-3.30-1.00) 1.45) 3.30) 90th 1.31-3.60-2.81) 1.10-3.07) 2.10) 95th 2.00) 2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.80 (1.20-3.53 (1.70-3.46-2.80-2.60) 2.14-1.20 (1.88 (1.52 (2.53-2.05-1.15-1.10-1.40-2.23) 1.20 (1.50 (2.30) 1.40) 1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.50 (1.86 (2.61-3.00 (2.79) 2.90 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.33 (1.60 (2.10 (1.90 (1.00-2.50) 621 725 1077 Limit of detection (LOD.22 (1.70-2.62) 2.60) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20 (1.07 (1. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.00 (<LOD-1.40) 2.00) 1.80 (1.50) 1.10 (.90) 2.82-2.63 (<LOD-1.853-1.80-2.88-2.28 (1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 0.40-3.60 (1.36) 1.900-1.00) 2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.00-1.S.10 (1.80 (1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.35-3.28 (1.30 (2.9.61) 2. population from the National Health and Nutrition Examination Survey.30 (1.816 (<LOD-.77) 1.86) 2.30 (1.31 (1.07-3.86) 3.20-1.33 (1.985) 1. Survey years 03-04 Geometric mean (95% conf.20 (1.S. which may vary for some chemicals by year and by individual sample.40-3.82-2.54) 90th 2.20 (1.20 (1.70-2.85) 2.00 (2.30) 2.40-2.30) 1.00-2.30-2.18-1.00) 1.

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

Aposhian HV.89:145-151. et al. Monomethylarsonous acid induces transformation of human bladder cells. Moore LE. Biomarkers of exposure: a case study with inorganic arsenic. September 2005 [online]. including Arsenic. Poplin GS. Lewis AS. Hsu LI. Bolgiano D. Eblin KE. Amigo H. J Environ Sci Health A Tox Hazard Subst Environ Eng 2003. Linderholm H. Ingested arsenic. Lagerkvist B. Chowdhury UK. Needham LL. Environ Health Perspect 1990. Hsueh YM. Cebrian Garcia ME. Montesinos N. Coble K. MMA(V). 8/7/07. Crit Rev Toxicol 2006. J Health Popul Nutr 2006. A prospective study of blood selenium levels and the risk of arsenic-related premalignant skin lesions.html. Associations between drinking water and urinary arsenic levels and skin lesions in Bangladesh. Wu MM. The effect of variable environmental arsenic contamination on urinary concentrations of arsenic species. Updated September 2004 [online]. Int Arch Occup Environ Health 1998.13(3):211-218. Hysong TA. Norin H. Annu Rev Pharmacol Toxicol 2007. Environ Health Perspect 1996. Sengupta MK. Environ Health Perspect 1999. van Belle G. Razniewska G. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans. Concentrations of the sunscreen agent benzophenone-3 in residents of the United States: National Health and Nutrition Examination Survey 2003-2004. Toxicological profile for arsenic.116(7):893-897. Burbacher T. Biggs ML.107(8):663-667.13(8):693697. J Expo Anal Environ Epidemiol 2003. et al. placebocontrolled folic acid-supplementation trial in Bangladesh. Zheng Y. House dust and inorganic urinary arsenic in two Arizona mining towns. et al.84(5):1093-1101.fr/ENG/Monographs/vol84/ volume84. Occurrence of monomethylarsonous acid in urine of humans exposed to inorganic arsenic. Jagadish B. transcription factor. Reidy JA. Caceres DD. Volume 84. Thomas DJ. Peterson H. Atalah E. International Agency for Research on Cancer (IARC).42(12):1195-1201. Christakopoulos A.292(24):2984-2990. Gamble MV. Arsenic methylation patterns before and after changing from high to lower concentrations of arsenic in drinking water. Methylated arsenicals: the implications of metabolism and carcinogenicity studies in rodents to human risk assessment. Chanda CR. Arsenic exposure to smelter workers. arsenate. Stute M. Available at: http://www.36(2):99-133. Le XC. Jakubowski M. Human health effects from chronic arsenic poisoning--a review. Calafat AM. Moldeus P. Scand J Work Environ Health 1985. Reduction in urinary arsenic with bottled-water intervention. Kalman DA. Sumi D. Graziano JH. 8/7/08 Ahsan H. Chiou HY.atsdr.114(11):1790-1796.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Toxicol Appl Pharmacol 2006. Bhattacharya P.gov/toxpro2. Environ Res 2005. Josyula AB. Matczak W.pdf. Arsenic: signal transduction. Exposure to inorganic arsenic in drinking water and total urinary arsenic concentration in a Chilean population. Beck BD. Liu X. cigarette smoking. Chem Res Toxicol 2000. Some Drinking-water Disinfectants and Contaminants. Am J Clin Nutr 2006. et al. Blom S. Roy S.41(10):2399-2428. Burgess JL.216(1):69-79. et al. Trzcinka-Ochocka M. J Occup Environ Med 2000. Ye X. Thor H. et al. Lodh D. Ryhage R.47:243-262. Hughes MF.38(1):87-113. Hopenhayn-Rich C. Eldan M. Fourth National Report on Human Exposure to Environmental Chemicals 191 . Folate and arsenic metabolism: a double-blind. Biological monitoring of occupational exposure to arsenic by determining urinary content of inorganic arsenic and its methylated metabolites. Kurzius-Spencer M. Gandolfi AJ. Loomis D.71 Suppl:S29-32. Summary of Data Reported and Evaluation. Healy SM. Kumagai Y.104(11):1200-1207. Hughes J.8(2):119-127. Bredfeldt TG. Ahsan H.98(2):151-159.11(4):265-269. Parvez F. Chen CL. Excretion of arsenic in urine as a function of exposure to arsenic in drinking water. and biotransformation involved in cellular response and toxicity. Ilievski V. Mash EA. Wong LY. JAMA 2004. Smith AH. Gurzau A. Cancer Epidemiol Biomarkers Prev 2007. Slavkovich V. Perrin M. 7th edition. J Environ Sci Health A Tox Hazard Subst Environ Eng 2006. Pino P. et al. Liber K. and lung cancer risk: a follow-up study in arseniasis-endemic areas in Taiwan. Chen Y. Pattern of excretion of arsenic compounds [arsenite. Slavkovich V. J Appl Toxicol 1988. Cellular metabolism of arsenocholine. Arnold LL. Environ Health Perspect 2008. Parvez F.16(2):207-213. Pilsner JR. Environ Health Perspect 2006. Kapaj S. Schreinemachers D. Cohen SM. American Conference of Government Industrial Hygienists (ACGIH). Calderon RL.iarc. Hudgens E. Hall M. Clinical and neurophysiological studies. Documentation of biological exposure indices. McClellen H. Hysong TA. Rahman A. Le XC. Kalman DA. van Geen A.24(3):298304. et al. Cincinnati (OH): ACGIH Worldwide. Available at URL: http://monographs. DMA(V)] in urine of children compared to adults from an arsenic exposed area in Bangladesh. Lu X. Rahman MM. Sandstrom M. Chen SY. Sturup S.cdc. O’Rourke MK. Gurzau ES. 2001.

Toxicol Appl Pharmacol 2005. Vahter M. pp. Lewis Publishers. Meza MM. Arsenic in drinking water-2001 update. Jimenez M. Calderon-Aranda ES. Marshall G. Holmes AK. Rumpler A. and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. J Anal Toxicol 2006. Environmental Protection Agency (U. Huang YL. Schulz C.30(5):293-301. Assessing the measurement precision of various arsenic forms and arsenic exposure in the National Human Exposure Assessment Survey (NHEXAS). Arsenic exposure. Seifert B. 8/8/07 192 Fourth National Report on Human Exposure to Environmental Chemicals . Belson MG. Smith AH. J Toxicol Environ Health A 2007. Xu Y. Flanders WD. Friberg L. Burgess JL. Toxicity of dimethylmonothioarsinic acid toward human epidermoid carcinoma A431 cells. Arsenic.Metals Kwon E.S. Jones RL. 2nd ed.222(3):374-380.K. Moore LE.gov/iris/subst/0278. Wang Z. et al. Sun G. urinary arsenic speciation. Tseng CH. Kieszak SM. EPA).gov/safewater/arsenic/regulations_factsheet. Ibata K. In:Industrial Chemical Exposure.114(2):220-227. Borja-Aburto VH.115(4):648-652. Buchet JP. 3rd Ed.S. Environmental Health Criteria 224. Environ Health Perspect 2006. and metabolism of arsenic. Rubin CS. Buckley BT. Geneva 2001. Li X.96(2):119126. Tseng CH. Boeckx M. Erratum in: Toxicol Appl Pharmacol 2006. urinary arsenic metabolites and human diseases: current perspective. Chem Res Toxicol 2007. Twenty years of the German Environmental Survey (GerES): human biomonitoring--temporal and spatial (West Germany/East Germany) differences in population exposure. Environmental Protection Agency (U. 1998 [online]. Available at URL: http://www. Int J Hyg Environ Health 2007. U. Fleming LE. 2001.htm.113(3):250-254. et al. Arsenic and Arsenic Compounds.367(1):80-88. Liaw J. Arsenic on the hands of children after playing in playgrounds.114(8):1293-1296. Becker K. Mexico. Valenzuela OL. Arsenic. Li L. Lauwerys RR. A pilot study of children’s exposure to CCAtreated wood from playground equipment. Shalat SL. et al. Integrated Risk Information System. Hoet P. Toxicol Appl Pharmacol 2007. Zhang H. Fact Sheet: Drinking Water Standard for Arsenic. Environ Health Perspect 2007. Genetic polymorphisms in MTHFR 677 and 1298. Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers. Available at URL: http://www. Roels H. Increased mortality from lung cancer and bronchiectasis in young adults after exposure to arsenic in utero and in early childhood. Solo-Gabriele HM. Guidelines for Biological Monitoring. Lauwerys R.49(6):387-393. GSTM1 and T1. Int Arch Occup Environ Health 1986. Arsenic methylation. Naranmandura H. inorganic. et al.S.S. Sonora. et al. Morton J. Environ Health Perspect 2006. Francesconi KA. Nevada. National Research Council (NRC). Garcia-Vargas GG. Urinary arsenic metabolites in children and adults exposed to arsenic in drinking water in Inner Mongolia. Available at URL: http://www. January 2001 [online]. Sci Total Environ 2006. Li B. Environ Health Perspect 2004. 8/7/07. Gandolfi AJ. Conrad A. Sun X. Arsenic drinking water exposure and urinary excretion among adults in the Yaqui Valley. Mason H.25(1):1-22. Arsenic in Drinking Water. Washington (DC) National Academy Press. EPA 815-F-00-015. Br J Ind Med 1992. Rahnster B. Vahter M. Huang YK. html.115(1):151-157. using a routine LC-ICP-MS method. Steinmaus C.112(14):1375-1380. CruzGonzalez MB. Seiwert M. Nolinder P. Rey OA. Biggs ML. Suzuki KT. Kopplin MJ. EPA). Thio-dimethylarsinate is a common metabolite in urine samples from arsenic-exposed women in Bangladesh. World Health Organization (WHO). Kalman D. Yang MH.20(8):1120-1125. Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites. Fok N. Kolossa-Gehring M.70(2):159-170. Boca Raton (FL).epa. Ferreccio C. Raml R. 2001. Pellizzari ED. Ochi T.epa. Yuan Y. Jin Y. et al.inchem.htm. Lu X.211(2):175. Offergelt JA.org/documents/ehc/ ehc/ehc224. von Ehrenstein O. Environ Res 2004. Clayton CA.57(2):79-91. Chung CJ. Urinary trivalent methylated arsenic species in a population chronically exposed to inorganic arsenic. Garcia-Montalvo EA. Jhangri GS.36-37. Chen CJ. Black K.210(3-4):271-297. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 2007. Environ Health Perspect 2005. 8/7/07 U. Speciation of arsenic compounds in urine from occupationally unexposed and exposed persons in the U. China. et al. Nygren A. Goessler W. Environ Health Perspect 2007. Shipp M. Investigating childhood leukemia in Churchill County.206(3):299-308.

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 1.82-6.54 (6.09 (2.19) 2.84) 5.87-9.05% of the earth’s crust.75) 2. barium sulfate and barium carbonate).40 (1.47-1.20-1.50) 2.21-2.66) Selected percentiles ( 95% confidence interval) 50th 1.37-8.57 (5.26-7.48-4.49) 4.73 (6.49) 8.74-2.15) 5.50) 1. such as brazil nuts.20-8. Workers employed by industries that make or use barium compounds can be exposed to barium dust.68 (1. fireworks.g.76-7.21 (1.50) 4.93 (4.20 (4.90) 1.39 (1. Some barium salts are freely soluble in water.37-1.65-8.61 (1.50 (1.90) 2.55-3.73) 1.33 (1.93-8.78-2.77) 1.50 (6.4) 7.30-1.35 (1. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. In nature.S.21 (1. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).54-8.72) 75th 3.26) 2.20-1.42 (1.71) 2.40 (1.36-1.50 (4.46) 1.24-1.20) 2.4) 9.70-5. and ceramics. respectively.70-6.50-6.71) 95th 6.05-2.00 (1.74) 3.12.18) 3.38 (1.63 (8. interval) 1.61 (2. are high in barium (Genter.12) 6.71 (2.60-3.92) 2.20-1.30 (2.11 (3.50 (1.00) 4.10 (3. 0.90-9.80-7.51 (1.15-11.41-1.86-4. and food.87-3.29-5.81-3.56 (2.20-1.48) 1.30-2.91) 2.64-3.50 (2. population from the National Health and Nutrition Examination Survey.11 (2.40 (1.18 (6.37) 5. and 0.95 (4.62 (1.40 (4.35-4.24-1.50-6.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.35 (3.35-1.30 (5.10-5.25-1.30) 4.61 (5.10-4.39-1.22) 6.95-6.88) 4.60) 3.10) 5.25-11. it combines with other chemicals such as sulfur or carbon and oxygen.00-8.86 (4.56 (6.65-1.37) 1.70-3.80 (5.65) 1. 7440-39-3 Medically.27 (1.16 (1.80 (1.80 (1.70) 3.78) 1.46) 1.15-1.30) 5.52 (1. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.91) 6.02 (7.48) 1.41) 1. soluble forms of barium.98) 1.62 (1.50-1.80) 1.49 (1.67) 6.63 (2.70) 1.87) 7.08 (6.77-3.59-11.00) 6. see Data Analysis section) for Survey years 99-00.71-9. tiles.86 (4.80 (2.18-1.43) 2.17-1.30) 5.46-1.81-2.80-2.11-1.56) 1.70-8.53-5.10 (2. 01-02.61 (3.12) 7.32-1.49-1.38) 2.26-1.30-1.80 (1.00-76.60) 1.49) 2.00-3.00) 1.14-6.12.63) 1.43 (5.39) 1.40) 7.53) 2.50) 2. Barium compounds are also used commercially in paint.10 (4.31 (2.85) 1.73 (5.45 (1.01 (4.94-6.80) 6.54) 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 2.49-9.60 (1.54) 1.60) 4.50 (4. and 03-04 are 0.00) 1.54-1.20-6.27) 2.50 (1.52 (4.90 (4.80-5.90-2.21-8.51) 1.50-1.63) Total 1.60-6.65-5.70-2.55-7.36-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.35 (2.99-5.90 (1.77 (3.90) 2.54 (2.47) 4. whereas others are practically insoluble (e.86-5.85 (2.88) 7.64 (1.14 (6.56) 4. Small amounts of barium can be released into the air during mining and other industrial processes.40) 3.70) 1.1) 9.60) 1.47-1.60-10.40 (5.62) 1.30 (5.15 (6.31-2.19-1.20 (1.70 (1.44-2.01-7.32-7.34 (1.63 (1.78) 1.40-13.53) 1.08-8.45) 7.4) 6.76 (3.2) 6.50 (3.93-2.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.63 (5..8) 9. depilatories.76-3.09 (1.72) 4.40 (5.26) 5.20-8.15 (2.73) 3.82) 1.48-4. In single dose animal studies.87 (5.14-1. bricks.90 (6.30 (3.22-1.51) 2.50 (5.38 (1.85) 1.28-1.44 (1.70) 7.12-1.80-3. Fourth National Report on Human Exposure to Environmental Chemicals 193 .61 (1.11 (3.41-3.30) 5.60-6.48 (6.56 (1.70) 4.63) 1.30-5.72) 1.70-2.65) 3.71) 1.78-3. glass.87-14.50 (1.60 (2.99 (4.76) 1.28) 90th 5.00 (2.96-2.39) 4.20-5.43) 6.30 (1.12 (2.8) 5.34) 2.75-3.36) 5.62) 1.43 (1. water.57) 3.30-3.90) 4.35) 5. rubber.15-1.30) 8.29) 5.04-2.70) 5.9) 5.76-2.61-8.36 (1.29-1.37 (4.20 (3.30) 3.80 (2. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.65) 1.22-1.54-1.39 (1.73-5.34 (2. Certain foods.24 (4.36 (4. 2001).88) 1.69 (1.57-7.66 (4.44-5.81-2.Metals Barium CAS No.8 (6.87 (6.27 (1.20-8.30-2.30) 2.35-1.49) 11.86) 6.04-6.16) 5.40 (5.50 (1.43 (1.07 (2.50 (4.70 (5.90-13.54) 2.15 (1.06-1.74-3.34 (1.06-2.38) 8. Barium compounds are used by the oil and gas industries to make drilling muds.32) 8.97 (1.51) 7.60-2.59) 3.10) 3.12 (2.03 (1.31.91 (2.65 (5. such as barium chloride. Barium salts have also been available as rodenticides.82) 2.88 (5.56 (1.87-7.80) 7.25 (1. The general population can be exposed to low amounts of barium in air.40) 7.

83) 2.96) 7.23-1. Insoluble barium salts.27-3.13-3.Metals was eliminated primarily in feces and to a lesser extent.10) 6.29 (3.43-6.54) 2.59 (1.65 (2.39-5.62) 2.40 (1.38-5.75-3.29-1.65 (5.75) 1.84-5.75) 2.00) 4.50) 1.38 (4.73) 2.99 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00-1. vomiting.58 (2.91-2.68 (2.47) 10.3) 6.31 (4.98 (2.72) 4.22-1.02) 4.62 (2.13-2.2) 5.78 (2.52-4.33) 1.26-4.46) 2.38-7.60 (1. 1990).29 (1.32) 2.36-2.88 (6.35-1.99 (2.52-10.22-1.04 (2.52) 1.39 (2.48-5.36 (3.47 (2.01) 1.14-2.80-6.10 (6.44-2.35-3.41) 4.58-6.92) 2. Following intravenous injection in animals.91) 2.80) 4.36 (5.30 (1.76 (4.40 (1.00-7.16 (1.51) 6.20-1.37 (1.2 (3.54 (1.21 (1.48) 2. 1985.20) 4.48 (1.01 (5. Barium is not rated for human carcinogenicity.75) 1.31 (1.73-4.61 (4. interval) 1.00 (3..0) 7.703-1.27-1.64 (1. 1984.70) 10.68) 1.06) .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 2.68-3.38) 1.08-2.22-2.31) 5.60 (5. water solubility.37 (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 1.28-11.80) 3.84) 2.71 (5. weakness.42) 1.24-11.32) 2.36 (3.921 (.41) 5.90-2.59) 1.57-10.84-2.96) 4.82) 1.29-7. such as those used in medical radiographic procedures.97-3.45-1.02-5.77) 5.60 (2.51 (3.2) 6.00 (2.16) 11.89 (2.4) 5.34-1.48 (1.39-10.36-1.56 (1.86) 5.57-5.40 (1.24-1.18 (1.29-4.41 (2.64) 7.24-1.49 (1.39-1.45-6.45) 1.77) Total 1.754-1.56 (1.37) 2.777-1.915 (.96) 4.00) 4.51 (1.68) 3..47-8.31-1.69-9.891 (.28-6.00 (3.40-1.36 (1.58) 4.59 (1.47) 1. Wones et al. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.03) 2.55 (5.91 (3.28-1.87) 1.76 (3.24-6.96) 4.18 (1.57 (6.29-3.06) 2. 1986).22-4.48-1.0) 6.10) 3.83) 3.67-6.55 (1. Perry et al.00) 6.29) 1.77) 1.81-6. Chronic high doses in animals resulted in kidney damage (McCauley et al.53) .46) 3.96 (4.62 (1.24-6.39 (2.905 (.34) 1.3 (6.32 (1.38-1.01 (4.04) 1.49 (1.76) 2.72) 6.20-8.99) 1.41 (1.48 (1.64 (1.47) 4.76 (2..59) 1. diarrhea.54 (2.43) 1. NTP. are not absorbed when administered.24 (5.46 (2.05-1.68 (3.03) 3.46-22.41 (1.81-7.55 (1.36-1.64) 7.25) 4.91 (3.70) 1.19-1.70) 4.56-3.55-6.44 (1.74) 1.53 (2.38 (1.51) 4.31-1. 2001).76) 1.49-1.45 (3.19-1.03-1.00 (5.49-1.63-4. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis. 1989).26-1.36 (1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.00) 1.86 (2.45-8.97 (5.86-7.97) 1.42) 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. Symptoms following acute high dose include perioral paresthesias.0) 5.19-1.50 (4.69 (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.64 (1.03-1.11) . and route of exposure.4 (5.19-2.08-1.26-1.97-4.57-7.58) 75th 2.880-1.38) 4.51-3.55) .50) 1.51) 4.28) 5.81-6.11) .28 (1.74 (5. 1994.11-2.881 (.30) 2.53-21. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.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 .34-5.26) 4.24) 3.61) 2.62 (4.57) 2.58) 1.42 (4.77) 1.45-1.03) 1.79) 1.39-1.23-5.46) 1.34-3.74) 1.77) 1.02) . paralysis.16-1.96-6.8) 4.15-4.34 (1. population from the National Health and Nutrition Examination Survey.S.24 (3.26-1.58 (4.59) 2. in urine.89) 90th 4.25 (1.29-4.710-1.85-5.37-1.37-2.56) Selected percentiles ( 95% confidence interval) 50th 1.47) 1.44-2.27 (2.33 (1.56) 4.76-3.47 (5.33 (5.963 (.33-4.52) 2.96 (4.23-2.39) 4.38 (4.79-5.64 (1.33-1. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.28-7.12) 2.66 (1.60 (2.55 (4.10-2.73-2.76) 2.68-3.75-22.84 (3.72 (2.63) 1.68 (3. a benign condition that may occur among barite ore miners.97 (4.38) 1.09) 6.77-5.832-1.04) 5.39 (3.52 (3. and cardiac dysrhythmias.60 (1.35-1.02 (3.59-7.88 (2.54) 1.31-1.27) 7.20 (1.51 (1.39 (2.92 (4.75) 2. Toxicity from soluble barium salts is rare.45) 95th 6.32 (2.33) 6.25-11.55-5.49-1.38 (1. chemical form. The health effects of exposure to barium compounds depend on the dose.26-1.20-2.48-3. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.50) 2. hypertension.82) 1.33 (1.32 (1.52) 7.45 (1.30 (1.24-3.10-1.

technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no. Weltle D. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. and a drinking water standard has been established by U. Levy. In: Calabrese EJ. References Brenniman GR. Pozzoli L. 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. eds. 231-249. Centers for Disease Control and Prevention (CDC). et al. Gallorini M. strontium. Ting BG. et al.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Howerton K. Biomonitoring Information Levels of urinary barium reflect recent exposure.85:355-359.. 1984. barium.niehs.95:89-105. patient population and literature reference intervals for urinary trace elements. 1985. 221-252 Komaromy-Hiller G. Trace element reference values in tissues from inhabitants of the European community I. Powell C. 1994. the welders had no obvious adverse clinical effects (Zschiesche et al. PS.. A study of 46 elements in urine. Sampson EJ.S.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. blood. Environ Res 1998.gov/toxpro2. 1989. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. In: Inorganics in drinking water and cardiovascular disease. 2000) to levels in NHANES 1999-2000 and 2001-2002.cdc. Fourth National Report on Human Exposure to Environmental Chemicals 195 . Available at URL: http://ntp. Reeves AL.niehs. Epidemiological study of barium in Illinois drinking water supplies.64(1):13-23. 5th ed. 1986.197210.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. Morrow JC. Sabbioni E. 2nd Ed. Clin Chim Acta 2000. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies). Princeton NJ: Princeton Scientific Publications. New York: Elsevier. Advances in modern toxicology. Third National Report on Human Exposure to Environmental Chemicals. In Friberg L. Minoia C. Frohman. 1990. ed. [online]. p. Jackson RJ. Jr. 2005. Vol 2: Specific Metals. 2005. Stadler BL. Calabrese EJ. pp. Int Arch Occup Environ Health 1992. eds.. Perry EF. EPA. and radium In: Bingham A. Kopp SJ. Inc.76(1):53-59. calcium. 2001. et al. Paschal et al.e. Environ Health Perspect 1990. Wones RG. Handbook on the Toxicology of Metals. Information about external exposure (i. Minoia et al. 1998).html?charset=iso-88591&url=http%3A//ntp. Zschiesche W. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding... 84-94. p. Apostoli P. Perry HM. NTP. Comparison of representative ranges based on U. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Sci Total Environ 1990. Magnesium. Nordberg GF. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report.gov/ntp/htdocs/LT_rpts/tr432. Princeton (NJ): Princeton Scientific Publications. Trace metals in urine of United States residents: reference range concentrations. 2001-2002. Atlanta (GA).28(3):373-388. Lack of effect of drinking water barium on cardiovascular risk factor.296(1-2):71-90. Vouk VB.S. environmental levels) and health effects is available from ATSDR at: http://www. Genter MB.. Pietra R. et al. LA. J Toxicol Environ Health.nih.nih. New York: John Wiley & Sons. McCauley PT. and serum of Italian subjects.. ed. p.atsdr. Barium. Laurie RD. National Toxicology Program (NTP). and 2003-2004 (CDC. Costa R. Schaller KH. Exposure to soluble barium compounds: an interventional study in arc welders. Investigations into the effect of drinking water barium on rats. Douglas BH. 4/8/09 Paschal DC. Ash KO. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Cohressen B.. Pirkle JL.gov:8080/cs.html. 1992). Patty’s toxicology.

130 (<LOD-. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. In medicine. 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 . and dental bridges. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. computer. aircraft. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames.130 (<LOD-. In studies of laboratory animals. see Data Analysis section) for Survey years 99-00. electrical. x-ray machines. the lightest of all metals.13. Two types of minerals. and machine-parts industries. and 0.13. which may vary for some chemicals by year and by individual sample. soil. Low-level beryllium exposure in the general population can occur through breathing air. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 7440-41-7 General Information Pure beryllium is a hard gray metal. and 03-04 are 0.150) < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 01-02.160) < 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. coal. and refined beryllium is used in mirrors and special metal alloys for the automobile. Beryllium compounds are commercially mined. are mined for commercial recovery of beryllium. bertrandite and beryl. and from breathing tobacco smoke. 196 Fourth National Report on Human Exposure to Environmental Chemicals . inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes.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 . respectively. near some hazardous waste sites. 0. nuclear.S. population from the National Health and Nutrition Examination Survey. or drinking water containing the metal.13. and volcanic dust. eating food. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.140 (<LOD-. beryllium is used in instruments.Metals Beryllium CAS No. < LOD means less than the limit of detection. and can be found in mineral rocks. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. Exposure to beryllium occurs mostly in the workplace.

Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. Fourth National Report on Human Exposure to Environmental Chemicals 197 . Maier. NTP considers beryllium to be a known human carcinogen. Skin exposure can result in delayed hypersensitivity reactions. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. S. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. and drinking water and environmental standards have been established by U. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. 2002). population from the National Health and Nutrition Examination Survey.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 . including contact dermatitis and subcutaneous nodules. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . EPA.S. 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.231 (<LOD-. 2003.281 (<LOD-. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al.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. Chronic beryllium disease. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. 1990). based upon excess lung and central nervous system cancers in studies of workers.346 (<LOD-. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. IARC has classified beryllium as a human carcinogen. which produces pneumonitis. respectively. or berylliosis.

gov/toxpro2.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. Beryllium [online]. and serum of Italian subjects. Trace element reference values in tissues from inhabitants of the European community I. Ting BG. 1990. Atlanta (GA) 2005. Gallorini M. Jackson RJ.76(1):53-59. In other studies. 20012002.e. Sabbioni E.org/documents/ehc/ehc/ ehc106. Pirkle JL. patient population and literature reference intervals for urinary trace elements. blood. and the 95th percentile for males in NHANES 2001-2002. and the fact that most NHANES participant levels were undetectable.S. A study of 46 elements in urine.S. 2000.Metals (i.. Hamilton et al. population were generally undetectable in NHANES 1999-2000. Comparison of representative ranges based on U. Hamilton EI.. Maier L. 1990. Kriess K. Review of elements in blood. Paschal DC.12 to 0. References Apostoli P. Pozzoli L. Weston A. it is likely that urinary beryllium levels in the U.157:388-398. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure..158:165-190. Van der Venne MT. less than 0.296(1-2):71-90. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Pietra R. Centers for Disease Control and Prevention (CDC). Morrow JC. Genetic and exposure risks for chronic beryllium disease. Sampson EJ. 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. Environmental Health Criteria. which approximate this Report’s limit of detection. 2001). 1998). Sabbioni E.e. 3/27/08 Komaromy-Hiller G. Levels of beryllium in urine for the U. Environ Res 1998.. McCanlies EC. International Programme on Chemical Safety (IPCS). Schaller KH. 0. Minoia C. Andrew M. Element reference values in tissues from inhabitants of the European community. Howerton K. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. plasma and urine and a critical evaluation of reference values for the United Kingdom population. HLA-DPB1 and chronic beryllium disease: a HuGE review.S. Third National Report on Human Exposure to Environmental Chemicals.inchem.95:89-105.1 μg/L).html. They reported urinary beryllium levels ranging from 0. and 2003-2004.74:162-166. Apostoli P. Available at URL: http://www. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Clin Chim Acta 2000. Am J Epidemiol 2003. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Costa R. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. environmental levels) and health effects is available from ATSDR at: http://www. 106.cdc. VI. Paschal et al. et al.atsdr. Clin Chest Med 2002..23:827-839. Trace metals in urine of United States residents: reference range concentrations. Given these results. Int Arch Occup Environ Health 2001. population are lower than levels in workers.13 μg/L. et al. Minoia et al. Ash KO. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Sci Total Environ 1994. Sci Total Environ 1990.htm.

20-1.200-.10) 1.300 (.304 (.30) 1.00 (.30-1. Cadmium also may be emitted into the air from zinc.300 (<LOD-.700) .382 (.400) .10 (1.300-.200-.500-.800 (.300) .00) .S.700) .600 (.700) .300) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .400 (.10) 1.300-.300-.50 (1.40 (1.420 (.500-.500-.424) * .300-.367-.30-1. and incineration of municipal waste materials.300) .500 (.500-.500 (.20) 1.400) < LOD .60 (1.300-.800-1. during refining of lead and copper from sulfide ore.800-1. Other uses include pigment production.266-.90) 1. lead.200 (.400) .378-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20) 95th 1.400 (.60-1.00-1.500-.700) 1.255) . and 0.10 (1.80) 1.300-.900-1.600 (. and 03-04 are 0. coatings and plating.00-1.403 (.600) 1.470) * .362-.500-. or copper smelters (U.200 (.300-.40-1.40) 1.00 (1.80 (1.393 (.500 (.300 (<LOD-.10) 1.30 (1.20-1.333 (.300 (.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.700) .400-.00 (.600) .300-.50-1.400-.600) .00-1. and nonferrous alloys.235 (.400) < LOD < LOD < LOD .3.400 (.400-.20) 1.600 (.20) .600) .900-1.900 (.300 (.60) 1.70) 1.400 (.70) 1.400 (. interval) .900-1.00 (. cadmium use has declined in response to environmental concerns (http:// minerals. as zinc sulfide) and to a lesser extent.513) .30) .441) * .400 (.200) .300-.600 (.300) .20-1.366) * * .500-.331) .300 (.10) 1.00-1.500-.400) .60 (1. Since 2001.40-1.600 (.600) .14.500-.300-.600 (.20) 1.300-.gov/minerals/pubs/commodity/cadmium). 0.20 (.50 (1.60 (1.427) * .900 (.600) .216-.400 (.40 (1.500-.304-. The predominant commercial use of cadmium is in battery manufacturing.20) 1.400-.300 (.S.400) < LOD .500) .300 (. malleable.900-1.usgs.00-1.20) 1.400) .800) 1.300-.00 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.412 (.30-1.300-.300-.275-.20) 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 .400 (.300 (.368-.300 (<LOD-.376-.300-.300) .400) .900-1.421 (.200 (.300 (. 01-02.395 (.300-.300) .700 (.600 (.400) .500) .500 (.300-. see Data Analysis section) for Survey years 99-00.00 (.20) 1. 7440-43-9 General Information Cadmium is a soft.40) 1. plastic stabilizers.20-1.600) .500) .600 (.800) .700) .400-.300 (<LOD-.300) 1.400-.400-.00 (.361-.600 (.600-.449) Selected percentiles ( 95% confidence interval) 50th .20) . U.500-.700) .600) 90th 1.800 (.700-1.400) .300-.359-.403) .50-1.600 (.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 * * * * * * .500 (.300-.900-1.10 (1.400) .296-.398) < LOD < LOD < LOD < LOD < LOD < LOD .30) 1.500) .00-1.500) .50) 1.400) . Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.400) .700-1.40 (1.600 (.40 (1.00 (.500) .400 (.426-.10) 1.400) < LOD .00 (.900-1.300) .468 (.70) 1.400 (.00 (.300) .400-.600) .337) .50-1.200) .20-1.300) .60) 1.50 (1.300 (.700) .00-1.600 (.10 (1.300 (.700-1.3.80) 1.50) 1.600) .00) . Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.900-1.60 (1.30-1.200 (<LOD-.50) 1.10) 1.60) Total * .500 (.400 (.50-1.S.20) 1.400 (.500-.30) 1.378 (.300 (.200-.900-1.452) .300) 75th .60 (1.500-.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 (.300) .20 (1.00 (1.900-1.40 (1.50 (1.400) . which may vary for some chemicals by year and by individual sample.600-1.386-.500) .300 (.304 (.10 (.283 (.326 (.400-.20-1.300) .400-.600-.500-.500 (.40 (1.200 (<LOD-. < LOD means less than the limit of detection.300 (.30-1. respectively.500-.00 (.700) .60) 1.400) .20-1.00-1.500 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .70) 1.400 (.10 (1.10 (1.300) .400 (.309-.500-. EPA.10 (1.00-1.400 (.460) .600 (.300-.800) .10) 1.313 (.400) .500 (.300-.10) 1.400-.500-.200-.400) .500-.344) .200-.289-.600-.600) .600 (.400 (.40 (1.Metals Cadmium CAS No.300-.425 (.300 (. population from the National Health and Nutrition Examination Survey.

394-.229-.610) .077 (.880) .918-1.300 (.192-.239 (.115-.189) .208-.283 (. 1994).13) .090) . Renal tubular and glomerular damage. however.310) .320) .22 (1. Cadmium is absorbed via inhalation and ingestion.480) .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 .977) .393-.238) .28 (1.203 (.240-.233) .272-.109-. interval) .061-.178-.607) .Metals 2000). Kikuchi et al.173) . copper) and protein..** Survey Geometric mean (95% conf.817 (.510) . and 0.243-.255) .06.175 (.229) .060-.700-. 1999.067-.196-.423-.17) .200-. an inducible metal binding protein.390 (.03) .220) .38) .839 (.372) .34) 1.226) .201 (.748-1.17 (.107-. potatoes.260 (.366) .766 (. wheat.282 (.456-.41 (.230) 75th .940-1.235) .733-.24) 1.270 (.077 (.980) .206 (.875) .445 (.848 (.810-1.135 (.633-1.28-1.232 (.790 (.151-.251) .265) . cadmium accumulates in the liver and kidneys where it is bound to metallothionein.092 (.12-1.640) .530 (.860) 1. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.109 (.10 (1.209 (.818 (.202-. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.090) .273 (.83) 1.234 (.01 (. 200 Fourth National Report on Human Exposure to Environmental Chemicals .551 (.06.169-.263) .238-.101) .247) .01-1.440-.157) .963-1.13-1.387) .316 (.281 (.207-.189-.230 (.189-.366-.336) .48 (1.211-.730-.20 (1.284) .110-. 2001).15) 1.141 (. 01-02.06.479) .551) . rice.261-.210 (.190-.200 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.400-.302 (.150) .170 (. Diamond et al.680 (.175 (.308) .813 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .450 (.52 (1.25) 1.241) .135-.20-1.179-.261-.204 (.458 (. see Data Analysis section) for Survey years 99-00.519) .790 (.47) 1.295) .26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .221 (.313) .482) .219 (.390-.126) ..430) .858 (.32 (1.195-.15) .160) .253-.550 (.733) .980) .220-.980-1.170-.15 (.289-.112-.470-. 2004a.100-.220 (. To a lesser extent.476-.989-1.153-.257-.210 (.596) . 2003).843-1.219 (.510-.462 (.20 (1.38) .545 (.171-.148) .28) 1.191-.890-1. ingestion through food is the largest source of exposure.210) .S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.25 (1.06) . a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.713) .232) .260-.194-.700-. Horiguchi et al.114-.183-.246) .210 (..22 (. For nonsmokers who are not exposed to cadmium in the workplace.960) 1.700-.440 (.450 (.890 (. drinking water is a source for cadmium intake.067-.972 (.327 (.623) .447 (.339) .455 (.381-.200-.20 (1.980-1.199 (.078 (.350 (.165-.277 (.51 (1.892-1.220-.200 (. zinc.820) 1.140 (.280 (.300) .237-.481) . 2003). 0..157-.919) .17 (.43) 1.400-.13 (.306 (.229) .087-.211 (.202 (.227 (.231) .128 (.191-.210 (.540) .06-1.210 (.255) . Cadmium absorption may be increased with iron deficiency (Berglund et al.492 (.800-. The kidney is a critical target and shows the earliest sign of cadmium toxicity. respectively.362) .886-1.980 (.255) .498-.519) .310 (.240) .130 (.520-.38) 1.187 (.82) 1.06-1.262) .466 (.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.326) .249) .04 (.17 (. With chronic exposure.04 (.892 (.181 (.38) 1.490) .875 (.150-.633 (. and 03-04 are 0.490) 1.214-.190-.500) 90th .436-.160) .806) .285-.74) 1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR. population from the National Health and Nutrition Examination Survey. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.092) .20) 1.07-1.452 (.686-.170-..219 (.230) .065-.206) .136) .366-.705-.203) .09-1.445 (.222) .299) .30-1.820 (.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.855-1.19) 1.121 (. including many food crops such as cereal grains.02-1.36) 1.177-.493-.360) . Inhalation of cigarette smoke is a predominant source of exposure in smokers.080 (.539) .530) .753-.72) 1.081) .061 (<LOD-.193 (.426 (.330-.388-.433-.233) .354) .12 (.475 (.01) .440 (. 2003).507) .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 .148-.279 (.198) .589 (.817 (. Cadmium in soil is absorbed by plants.763-.57) 1.800 (.249-.184-.390-.990) .717-.257) .223 (.270 (.412) .180 (.160-.260-.559 (.820-1.221) .329 (.500) . About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.351-.167-.134) .870) .216 (.886) .714-1. 2003.120 (.192-.741-1.191 (.322 (. calcium.290-..193-.190-.265 (.430-.960 (.210) .160 (.836-1. and various seeds. whose body burdens of cadmium can be approximately twice that of nonsmokers.580) .

247-.209) Selected percentiles ( 95% confidence interval) Sample 95th .173 (.479 (.163) .176 (.387 (.421 (.438) 90th .112) .184-.404 (.288) .663 (.140-.700) .170-.232) . most often a result of occupational exposure (Roels et al.950) .12) 1.266) .199-.097) . 2004b).481 (.283 (.238) .137-.194-.783) .16) .137 (.135) ..221 (.438-.227-.826-1.630-. can result from high dose chronic exposure.434 (.098) .148 (.418-.288 (.10) 1.08) 780 682 614 546 667 717 760 1132 1070 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 * Not calculated: proportion of results below limit of detection was too high to provide a valid result.931 (.296 (.234 (.156-.559-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.096) .215 (.261-.245 (.850) .690-.678 (.206-.653) .998) .234-.083-. At lower environmental exposures.181 (.441-.311) .175-.247-.06 (.123-.873 (. 2003. However.136-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.779 (.077-.085 (.830-1.175 (.219 (.687 (.331 (.136-.352) .754) ..917) .219 (.833-1.533) .210 (.414 (.130-.415) .182) .647-.927-1.185) .537-..281) .431) .818) .126 (.281) .218) .202 (.07 (.696-.941 (.207-.09 (.718 (.818) .13) . 2002.253) .304) .144-.329 (.303) . interval) .161-.147 (.00 (.472) .325 (.274) 1.398-.159 (.484 (. 2000.221-.690 (.500-.631) .38) .412 (.123-.150-.470) .433-.201-.767) .085-.263-.909-1.190 (.536 (.700 (.687-. Staessen et al.229) .645-.490 (.07) . two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.387-.282 (.181-.388-.300-.184) .740 (.985 (.929) .268 (.100 (.143-.940 (.143-.184-.273 (.192) ..107) .470) . 1999).091) .288-.828) .178) .198) .232) .122 (.190 (.919 (.850) .191-.444-.168 (.162 (.545) .783 (.182) .531 (.591 (. 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.876-1.233 (.487 (.212 (.289) .792 (.104) .067-.308) .208-.091 (.111-. 1996.668-.906) .104) .113-.106) .183 (.518) .207) .147-.729 (.209) .350) .140-.234) .789 (.476) .171-.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .078-.154 (.418) .090 (.297) .304-.813-.667) .247-.263 (.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 .856 (.289) .293-..491-.158-.166 (.02 (.187-.674-1.210) .143) .084-.191) .560-.813-1.078 (.757) .321) .767 (.** Survey Geometric mean (95% conf.266-..17) .826-1.204-..686 (. Jarup et al.223) .131-.364) .185 (..075 (<LOD-.261) .538) .154-.316) .156) .432 (. 1999).318 (.839) .343-.501 (.440) .693 (.255-.678-. Fourth National Report on Human Exposure to Environmental Chemicals 201 .757 (.183) .225) .830) .226) 75th .377-.196 (.423-.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 .216-.253 (.228-.173-.722-.391-.607) .211 (.242) .225) .191 (.181) .308 (.181 (.261 (.159 (.622 (.220 (.178-.256-.094) .236-.267 (.404) .335 (.051-.240) .795) 1.08) . 2002. Noonan et al.865 (.280 (. Horiguchi et al.063-.727-.712 (. 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.174-.235) .239-.205 (.086 (. Olsson et al.170 (.806-1.827) .168-.874-1.147-.666-.241) .16) 1.962) .177) . 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.690-.176 (. 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.200 (.208 (.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.156 (.074-..292) .278) .884) .507-.979 (.157-.182) .541) .382) .101) .716) . 1999).940-1.381-.238-.725-1.224 (.650-..551) .708-1.473 (.769 (.784) .691-.075-.614) .562-.146-.252 (.250) .084 (.516-.240) .316 (.449) . population from the National Health and Nutrition Examination Survey. 2002.187) .S.197-.446) .414-. During the 1950’s and 1960’s.267 (.157-.802 (.222-.336-.688-.093 (.175 (.091 (.270 (.05) 1.189-.719 (.163 (.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .071 (.340) .423 (.426-.00 (.168-.338 (.617 (.856) . 2004).382-. 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.210 (.199 (.917 (.440) .716-.

respectively.. Women had higher blood and urine cadmium levels compared to men of similar ages. data (CDC. 2005).. Jarup et al. 2002). 2003.1 mg/L (Alfven et al.e... Jarup et al.html. Komaromy-Hiller et al. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. Information about external exposure (i. 2000. maternal blood or maternal urine and birth weight (Nishijo et al. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. environmental levels) and health effects is available from ATSDR at: http://www.. Animal studies have demonstrated reproductive and teratogenic effects. 2004. 2002. Staessen et al.. Cadmium can produce lung. and drinking water and environmental standards have been established by U. potentially fatal pneumonitis (Fernandez et al. For NHANES 19992000.. 2005. Becker et al. 2004. Ezaki et al. Zhang et al.. 2000.. not to imply a safety level for general population exposure. 2005.cdc.46 mg/gram of creatinine) (Ezaki et al... 2006. 2003. EPA. 2002). pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies... Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. 2003)... 1999).S.. 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. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. 1999. However.. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.. 2006. 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). Staessen et al...atsdr. 2003. 2002).. Wilhelm et al. In adults aged 60 years and older. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures... Mannino et al. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1.. Horiguchi et al. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity.. Staessen et al. approached these values associated with subclinical changes in renal function and bone mineral density. Wennberg et al. Creatinine-corrected urine cadmium values in U. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. 2002. Becker 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. Occupational standards are provided here for comparison only. 2004). 2006). Noonan et al. 2005. 1999).. 2003. Acute and heavy exposure to airborne dusts and fumes. 2005. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. 2002).. Salpietro et al. 2004b).. 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. 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. Suwazono et al.S. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals .. Becker et al. CDC.. 2002. Both IARC and NTP consider cadmium a human carcinogen. has resulted in severe.gov/ toxpro2. In the typical environmental exposure. Olsson et al. Further research is needed to address the public health consequences of such exposure in the United States. 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. 2006). Ezaki et al. 2004.. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. Horiguchi et al. respectively.. Friedman et al. 2002. as may occur from welding cadmium-alloyed metals. intermediate in former smokers and lower in never-smokers (Becker et al. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. 1988). 2002) and length at birth (Nishijo et al. 2003. 2000. Moriguchi et al.. 2002. 2002).. In postmenopausal women. 2004b. with peak values observed in the fifth to sixth decades (CDC..S.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al.. 2000).. Jin et al.. Olsson et al.. 2004.26 and 3. 2003.. 1996). 2002. Olsson et al. 1996.

Lancet 1988. Machida M. Gadea E. Kikuchi Y. Olfactory function in workers exposed to moderate airborne cadmium levels. 196:114-123. Miyamoto K. Occup Med 1996. Toffoletto F. Mannino DM.S.102:83-89. Holguin F. Nermell B. Fatal chemical pneumonitis due to cadmium fumes. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Schulz C. Lundh T. et al. Davison AG. Furuki K. Alfven T. Consonni D. Jarup L. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Tsukahara T. Chiappino G. Bellerup P. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria.354:1508– 1513. Becker K. Comparison of representative ranges based on U.57:668-672. et al.atsdr. Ikeda Y. Mucha A. Vahter M. Toxicol Lett 2004. Nordberg G. population. Tsukahara T. 2005. Bo M. Seifert B.148(1-2):11-20. Buchet JP. Kumagai N. Pickering CA.13(11):1627-1631.95:20–31. Lauwerys R. possibly better than b2microglobulin. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Sasaki S. Choudhury H. Int J Hyg Environ Health 2002. Lukyanova EM. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study.76:186-196. Oguma E. iron deficiency. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Environ Res 2006. Horiguchi H. Environ Health Perspect 1994. Environ Res 2004. Carlsson MD. Krause C. Anthropometric. Grubb A. Serra J.96:353-359. Occup Environ Med 2000. Miyamoto K. Palomar M. Chislovska NV. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Hotz P. Third National Report on Human Exposure to Environmental Chemicals.000 women in the Japanese general population: a nationwide large-scale survey. et al. Nomiyama T. Toxicol Appl Pharmacol 2004a.S. Oguma E. Ezaki T.110:699-702. et al. Furuki K. et al. Seiwert M.59:194-8. Environ Health Perspect 2005. Atlanta (GA).html. Lancet 1999. Thorax 2004. ShkiryakNizhnyk AZ.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. Hellstrom L.296(1-2):71-90. Ezaki T. Mascagni P. Komaromy-Hiller G. et al. Fukui Y. Schulz C. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Environ Health Perspect 2002. Int J Hyg Environ Health 2003. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. 206:15-24.24:717-724. J Toxicol Environ Health 2003. 102:10581066. et al. Greves HM. Darbyshire J. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Moriguchi J. Seiwert M. Dekio F. Persson B. Toxicological profile for cadmium update. Lidfeldt J. References Akesson A. et al. Horiguchi H. Machida M.45:43-52. Sanz P. Fourth National Report on Human Exposure to Environmental Chemicals 203 .59:497]. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Environ Res 2004b. diabetes mellitus. Ikeda Y. Savage-Brown A. Zhu G. et al. Available at URL: http://www. Agency for Toxic Substances and Disease Registry (ATSDR). Jarup L. Taylor AJ. Ye T. Kundiev YT. Bernard A. Berglund M.205:297-308. J Occup Health 2003. Diamond GL. 1999 [online]. Ash KO. Fukui Y. Nerbrand C. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Becker K. Costa R. environmental. patient population and literature reference intervals for urinary trace elements.gov/toxprofiles/tp5.66(Pt A):2141-2164. Okamoto S. Kaus S. Lison D. Neurotoxicology 2003. Fayers PM. Thayer WC. Ukai H. Fernandez MA. Clin Chim Acta 2000. Uemura T. Bregante G. Wang H. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Comprehensive study of the effects of age.cdc. Takebayashi T. Centers for Disease Control and Prevention (CDC). Akesson A. Vahter M. Kaus S. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. et al. Elinder CG. Stock AL. 4/8/09 Alfven T. Friedman LS. Moriguchi J. Cadmium fume inhalation and emphysema. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. et al. Int Arch Occup Environ Health 2003. Sasaki S. Howerton K. Lepom P. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Venables KM. Jin T.46:372-374.1(8587):663-667. Jones RL.

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

23-4.5-13.92-13.5-14.94 (4.20) 5.99-11.0) 12.40) 5.10 (8.70 (9. interval) 4.0 (9.60-7.70 (8.15-8.07) 4.50) 5. 0.20 (4.9) Total 4.25-5. semiconductors.Metals Cesium CAS No.6 (9.40-5.29 (4.60-12. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00) 7.13 (8.64 (4.64-5.84) 8.90-8.36) 3.2-13.82) 5.61) 7.4) 12.8) 11.60) 5. However.49) 75th 7.20-4.8-13.0 (10.81) 4.31-8.7) 10.5) 10.64) 4.7 (8.9 (11.80-11. although cesium was generally of low toxicity when given to animals.4 (10.71-5.50 (4.44 (8. Most human exposure to cesium occurs through the diet.93 (4.74) Selected percentiles ( 95% confidence interval) 50th 4.2.30 (6.12-5. and high-power gas-ion devices.70-8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.99) 7.40) 7.34) 9.16-6.90) 9.49) 4.94 (4.3) 9.30-5.80 (8.42) 7.26) 4.62) 4.54-11.26-11.30 (6.77 (9.05) 5.12) 5.03-4.71-9.08 (6.94-4.46) 7.5-14. and cardiac arrhythmia (ATSDR.0) 11. population from the National Health and Nutrition Examination Survey.53 (6.84-5.73-11.89-5.0) 10.5 (8. diarrhea.40) 5.70 (6.4) 9.8) 11.1 (11.4) 10. For absorbed cesium salts.7 (10.32) 4.72) 4. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.94) 4.13-8. see Data Analysis section) for Survey years 99-00.6 (9.50) 9.64-10.55-11.8) 12.63 (4. Radioactive 137Cs has been used medically to treat cancer.95 (3.50-7.4 (9.6 (11.10-5.60-5.16-6.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4.05-5.7-14.00) 6.81 (4.10-7.37) 5.71-8.45-5.52-9.1 (9. nausea.05-5.59-5.81) 4.1) 9.3 (8.45-8.32 (3.7) 11. Fourth National Report on Human Exposure to Environmental Chemicals 205 .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 4.36 (6.57-5.8) 12.2-13.00-8.64) 5.4) 95th 11.33 (5.77 (4.20 (6. and 0.36 (3.25) 4.7 (9.01) 7.50 (4. 2004).5) 12.33 (6. and 03-04 are 0.6) 10. scintillation counters.87 (4.27-5.50 (7.54) 4. and as polymerization catalysts.71 (4.84) 5.40-5.71 (8.55 (4.47-8.90-12.30) 5.76-6.2-14.42) 6.70 (8.32-5.37) 7.86 (7. the body half-life is estimated to be 70-109 days based on 137Cs exposures.13 (5.6 (9.13 (7.99-6.9) 11.74-5.20-5.87 (4.9 (10.6 (9.07-11.0) 12.77 (9.26 (3.4) 10.60) 7.8) 9.00) 4.17 (6.90 (4.90-10.95-4.39) 7.50 (6.86-11.0) 11.1) 10.5-16.35 (4.1-13.2-13.87) 5.02 (4.3) 10.80-13.8 (10.26) 7.87-7.4-13.20-7.40-5.80 (4.12-11. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.42-7.68 (7.30) 7.80 (8.80) 7.90-12.97) 4.10 (6.17-6.40-5.0) 12. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4) 11.80-10.61-6.00-10.98 (7.53-11.82-4.30-10.83) 6.5) 9. cesium hydroxide is corrosive and irritating at high concentrations.56) 5.59-5.8) 9.63-4.9) 12.1-12.97-7.70) 5.21 (4.90-10.89) 5.03 (4.35-5.89) 4.00-9.70 (6.39-4.90) 5.74 (4. respectively.80-10.03 (4. 01-02.10-9.70-5.1 (10.3) 10.14.49 (4.2) 11.3-15.10 (8.3) 10.05) 5.60 (8.0-13.80 (8.49 (5.60-6. soil. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.80 (4.04) 7.59) 7.40-7.40 (4.21) 90th 9.43 (5. infrared lamps.72-7.84-9. photographic emulsions.95) 5.5 (10.20) 7.2) 12.2 (9.69-6.66 (7.00 (7.0) 9.22 (4.99-11.10 (6.00-8.29) 4.91 (7.7) 11.60-7.9 (11.62 (5.20-8.83-4.34 (4.98 (7.59 (5.96 (6.59-5.80 (4.70) 7.35 (4.27) 4.25 (3.67 (4.91-8.7 (10.1) 11.81) 9.1) 9.2 (9.70) 5.40-11.01-8.43-8.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80-10.20) 8.10-8.3-13.7 (11.17) 4.52) 7.90) 7.90-10.70 (5.80-6.9) 8.23) 9.3-13.08-5.86-12.2-12.08) 7.8 (11.50 (4.S.20) 4.01-6.90) 4.0-15.3 (8.9 (10.24) 4.27 (7.70 (4.64) 5.81-14.47-4.9 (11. and clay.7 (10.56 (4.77-8.60) 7.6 (11.38) 5.73-5.1) 11.90 (6.90) 5.99) 9.14.68) 9.3) 12.1-12.33-5.84 (4.7 (9.97 (7.71) 4.40-11.09) 5.6) 11.87 (4.7) 10. Whether cesium compounds are carcinogenic is unknown.08-5.4) 12.79 (4.7 (9.8 (10.62 (5.04 (4.4 (9.22-4.12 (4.3) 10.08 (7.00-4.56 (4.55 (7.60-6.63) 6.88 (8.6) 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 4.14 (4.9 (11.09-5.60 (7. Little is known about the health effects of this metal.8) 12.56-11.

3 (10.90-8.53) 6.60 (5.17-4.91 (5.09) 4.71) 6.27 (6.60 (3.87) 5.58) 8.8) 5.24-10. population.13-9.84-7.25) 4.19-6.95 (5.14-6.77 (4.64 (4.9 (9.50 (7.3) 1226 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 3.95) 10.48) 90th 7.66 (5.74 (4.94 (5.3) 11.59-8.26 (3.50) 8.92 (5.21-4.33-3.87-4..20-4.60) 3.5) 7.41-4.5 (9.8 (9.22-11.43) 8.95) 8.00-4.S.8) 10.22 (3.92) 3.14) 4.43-6.04) 6.04) 5.49) 3.61 (7.98 (6.85-4.87) Sample size 2464 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.78) 4.87 (5.9 (10.00) 6.51 (4.30) 10.72-5.44 (8.48) 7.71 (7.63-6.05-3.78 (3. 2004).82) 7.83) 8.91-7.91-9.38 (3.23 (7.03) 6.04-5.27 (6.21 (2.84-9.41 (8.10-4.00-8. population from the National Health and Nutrition Examination Survey.84-11.60-10.89-4.77 (6.21-5.17) 9.14) 4.5) 9.55) 4.31 (4.63) 6.04-11.54 (4.41 (4.42 (5.96 (4.24-4.35-11.15-11.39 (5.22) 6.07) 8.99-4.85) 4.74) 75th 5.64) 9.58-5.74 (5.76-6.05) 3.74) 3.02-4.00 (8.70) 6.30 (3. population results shown in this Report (Alimonti et al.66 (6.10 (3.35) 3.2 (8.57) 3.96-4.14 (6.3-15.55-5.51 (4.7) 10.97-5.50) 4.98 (7.40-5.30) 10.05) 6.51) 4.45 (4.47) 6.41) 9.84-9.99 (3.47) 4.83-7.70 (7.42-4.93-9.83-6.75 (6.20-8.08 (5.40) 6.26 (4.06 (5.17 (6.17) 4.56) 4.50) 4.08) 3.79-5.42-4.95) 4.46-4.46 (8.12) 3.45-6.53 (4.0 (7.35-7.77) 4.43 (3.63-6.11 (5.68) 3.8) 6.96-4.38 (3.20-4.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .20-4.07 (5.25) Selected percentiles ( 95% confidence interval) 50th 4.63 (7.50 (6.46-8.37) 4.43 (4.29) 5.36-6. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.33-8.35 (3.6) 6.38-7. 1990).16-5.33 (5.65 (6.16-8.62) 5.64) 4.19-3.4) 10.95-6.7) 10.29) 4. Komaromy-Hiller et al.27-4.72) 4.30-4.63 (4.14-4.07) 8.53 (6.50) 4.59) 4.41-7.63 (6. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.50-5.08 (6.13-9.15 (7.90-3.79) 6.60-20.43 (8.28 (5.S.64 (8.12-6.93-7.47 (7.97-4.68) 4.81 (4.16-8.85) 5.09) 8.01-8.44-5.24 (3.38) 10.36-3.88-4.42 (4.68 (4.74-11.78 (3.06) 5.3 (9.28) 7.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure. 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.03-5.51 (3.26-6.51 (3.70) 7.58 (4.06) 4.65-3.36-10.44 (4.18-7.13 (3.00-10.77 (7.77-5.58 (6.90 (7. interval) 4.64) 5.08 (3.05-4.79) 9.03-6.18 (7.00-5.41) 4.09 (4.30 (7.54 (3.05 (4.42-6.47) 7.18) 8. Using clinically submitted specimens.02 (5.10 (3.84-7.75 (7.58) 3.29-3.0) Total 4.6 (9.56-10.54 (5.27-6.55 (3.99-9.08-7.28 (4.44) 3.30-4.96) 4.76-9.98) 5.47) 6.35 (4.79 (5.29) 4.97) 8.2 (8.91) 4.47 (4.46) 6.S.03) 5.30 (4.15) 95th 8.86 (4.20) 5.34 (5.00-5.12 (3.67 (6.43 (4.61-3.7-12.2) 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 3.15-4.38-12.14-7.10) 7.95-12.40) 7.56 (4.27) 4.16) 5.05-3.91 (5.81 (4.1) 11.73-4.3) 9.90-8.37-3.08) 4.52-5.56) 3.18-6.99-9.54 (4.82-4.98) 5.75-11.66-6.78) 4.10 (5.21-3.07-4.39) 8.56) 4. (2000) found urinary cesium levels that were slightly lower than those reported for the U.27 (8.91) 5.62-8.73 (3.65-4.6 (9.00-9.88-10.95 (3.08) 4..64-6.39) 5. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.06 (3.9) 10.67 (5.31-6.48-6.31-4.46 (7.53) 3.2) 11.31 (4.11 (5. Two small studies of European populations reported urinary cesium levels similar to U.13) 7.43-11.80) 6.50 (5.51 (7..41 (5.91-6.68-11. and were also roughly similar to those in this Report.72 (4.28) 8. 2005.33 (5.66 (5.0) 7.91) 5.3 (8.99) 4.44-9.96) 4.08-3. Minoia et al.94) 7.67) 5.5) 9.79) 4.29-3.68) 6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.

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

390 (.580 (.950) . seawater.460) .540-.610-.790 (.950-1.44) 1.S.640) .16) 1.600 (.431) .870-1.980) .850-1.500) .650 (.410 (.380 (.463-.564) .334) .393-.930) .373) .405-.680 (. 208 Fourth National Report on Human Exposure to Environmental Chemicals .Metals Cobalt CAS No.300 (. 0.487) .700) .950-1.650-.24 (.860 (.540-.520 (.350-. hard metal (alloys of cobalt and tungsten carbide).380 (.60 (1.530 (.380-.07.890-1.810-.570) .416) .470) .08-1.710) .410-.331-.980-1. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.32 (1.520 (.24 (1.68 (1.620-.499 (.890-1.410 (.910-1.434 (.420 (.367 (.500 (.450-. Cobalt compounds are also used in manufacturing battery electrodes.410 (. and fertilizers.01-1.520) .690-.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 .47) 1.590 (.75 (1.03) 1.414) .660) . Usual human exposure is from food sources.04 (.03-1.410) .03 (.480 (.04-1.04) 1. and soil.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 .17 (. steel-belted radial tires. varnishes.350-.29 (1.81) 1.550-.610 (.316-.09 (.450) .570-.340) .750 (.550 (.32-2.330 (.25-1.580 (. and 0.590) .340-.379 (.07-1.540-.690 (.480-.550) 90th .338-.280-.820 (.570-.460) .65) 1.47) 1.04-1.336-.430 (.350-.900) .09 (.940-1.900-1.496) .37-1.28 (1.520 (.294 (.360-.940-1.450) .47 (1. blue-colored pigments.310 (.47 (1.23-2. and inks.900) .32) 1.370) .13) 1.20 (1. automobile airbags.19) .440-.333-.348-.450) .370 (.359 (. see Data Analysis section) for Survey years 99-00.650 (.73) 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .530-.369 (.379 (.06 (.600) .36) 1.394) .520-.410 (.410-.540) 1.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.870 (.259-.740 (.670-. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.08) .680 (.313) .319) .820 (.398 (.840) .352 (.22-1.820 (.12) 1.350) 75th .380 (.520-.454 (. Cobalt is used as a drying agent in paints.519 (.930 (.880 (.92) 1.750 (.374 (.17 (1.26) 1.26) Total .790) .600-. Cobalt occurs naturally in airborne dust.410-.430 (.17-1.800) .760 (.28 (1.710) 1.45 (1.410 (.450) .340 (.371 (.950 (.630 (.330) .890-1.850) .270-. It is also a component of porcelain enamel applied to steel bathroom fixtures. hard metal or in combination with other elements.583) .810) . It is emitted into the environment from burning coal and oil and car and truck exhaust.06 (.22 (1.800-.291-.33 (1.580 (. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.400-.900-1.16 (1.520-.388-. 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.02-1.320 (.32 (1.850) 1.427-.48) 1.301 (.418 (.333-.469-.81) 1.364-.14-1.490-.460 (.26-1.285 (.50) 1.419) Selected percentiles ( 95% confidence interval) 50th .410) .300-.16 (1.53) 1.520-.05) 1.01-2.21) 1.620) .830-1.610) .08. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.530) .620-.740-.417) .305-.800-.64) 1.14) .380-.880-1.660) .560 (.373-.790-. and kitchenware.690-.16) 1.850-1.12) 1.375 (.355-.465) .386) .56) 1.398) .17 (1.03) .308-.370-.428-.343 (.59 (1. Cobalt compounds are used as catalysts in producing oil and gas.399) .67) 1.502) .07.42) 1.730) 1.480 (.510) 1.52 (1.15 (1.750 (.460-.750-.390) .16-1.22) 1.350 (. interval) .950 (.05 (.520) .920-1.16 (.348-. respectively.16-1.431) .26-2.50 (1.670-.670 (.28 (1.404) .680) .310-.680) .360-.960-1.640) .430 (. shiny.590-.890) .470 (.07-1.23) . population from the National Health and Nutrition Examination Survey.05 (.370-.340-.630-.99) 1.870 (. and magnetic recording media.03 (.430) .39) 1.28-2.04-1. and 03-04 are 0.73) 1.581) . industry is imported or obtained by recycling scrap metal that contains cobalt.09) .520 (.339 (.340) .900) .270-.430) . The cobalt used in U.330-.670 (. and in synthesizing polyester and other materials.S.430-.920) 1.630 (.01 (. large appliances.490-.316 (.00) .890) 95th 1.46 (1.03) 1.33-1.377-.420) .660-. diamond-polishing wheels.460 (.740-.460) .420) .06-1.370-.270-.540-. 01-02.940 (.461 (.515 (.570) .372) .810) .590-.452 (.523) .390 (.710 (.930-1.424) .435 (.48) 1.390 (.670 (.640) .15-1.360-.290-.07 (.760) .01 (.770) .570 (.327-.610) .32) 1.543) .620-.450-.700) .390-.

35) .15) 1.329-..386 (.277-.737 (.647) .562) .593) .838 (.368) . 1994.297-.304) .963) .339-.358 (.479) .467-. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).753) 1.343 (.462) . and to a lesser extent.744) 1.280-.365) . 1972). 1994).279) .976 (.29) .335 (.660-.449-. Cobalt is absorbed by oral and pulmonary routes.830 (.353-.469-.29) 1.476-.425-. 2003).679-.15 (.777-.355) .487-.861 (.842) .703-.929) .616-.421) .407) .317 (.632-.314 (.740-1.606 (.548 (.275-.481) 90th .471-.900-1.471-.309) .938-1.10) .905) .963-1.750) .463-.298 (.286) .30 (1.00 (.291 (.554 (.785) .274-.368 (.426 (.278-..12 (.25 (.11-1.615) .990) . Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.781) 95th 1.792-1.50) 1.57) 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 .33) 1. in the feces.36) 1.343-.04-1.738 (. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.542 (.952 (.S.300) .500-.404-.513) .547 (.14 (.281) .917) .380-. using hard metal cutting tools.872 (.29 (1.83) 1.360) .392 (.282-.35) 1.313 (.895-1.294-.522) .290 (.503-.346 (.611) .500-.879-1.756 (.363) . Exposure in the workplace may come from electroplating.495 (.391 (.03-1.328 (.365-.60) 1.728 (.215-.630-.707) .376 (..723 (.327-.23 (1.368) .361 (.932-1.829) .388 (.505) .378-.55) .353 (.960 (.523 (. A portion of cobalt retained for long periods is concentrated in the liver.829-1.911-1.382-.361 (.352 (.352) .362) .316 (.955) .608 (.533 (.324-.391) Selected percentiles ( 95% confidence interval) 50th .44 (.16 (.29 (1.600-.25 (.326-. interval) .319-.259 (.452-. with pulmonary clearance half-lives of from one to two years (Hedge et al.331-.11-1.239-.955) .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 .73) 1. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.407 (. refining or processing alloys.03 (.983-1.750-.50 (1.247 (.500 (..667-1.461) .00 (.396) .10) Total .689 (.594) .349) .387) .378-.Metals fabricated from cobalt alloys (Lhotka et al.289) . Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.786-.333-.19) .348) .313-.599) .16 (1.694) .634-.667-1.479-.417 (.400 (.333 (.396) .272-.561) .560-.691 (.352 (.475 (.00 (.847) .963-1.781-1.16 (.248-.251-.301-.409) .595) .662) . cobalt is excreted predominantly in the urine.243-.439) .328 (. or using diamond-polishing wheels that contain cobalt metal.29 (1.306 (.857-1.428-.313-.361-.00 (.393-.10-1.429) 1.550-.821 (.293 (.12-1.324) .275-. respectively. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.393 (.362-.303-.611) .585) .313-.234 (.313-.638-1. Once absorbed and distributed in the body.895-1.457 (.449) .328) .342-.673-.471 (.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 .513-.534-.256-.851 (.760-1.975 (.898 (.304-.468) .644 (.402 (.753-.457) .273 (.333-.938) .369 (.306) 75th .296) .434-.334) .268 (.708) .457-.36) 1.278 (.736-.861-1.438) .282 (.344-.24) .728) .733-1.433) .257-. population from the National Health and Nutrition Examination Survey.337) .361-.333-.419) .362 (.455 (.257 (.388 (. an essential human nutrient.06 (.609) .16) .290 (. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.543) .630-.844 (.591 (.757-1.04 (.384) .582-.738 (.804) 1.417) .700 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.435 (.10 (.259) .297) .50) 1.552 (.529 (.250) .640) .378 (.54) 1.271 (.983) .00) .28) 1. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.488) .279 (.425) . 1972).323) .442-.296-.523 (.435-.381) .850-1.534 (.963) .683-.248-.310) .635 (.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 .562) .826-1.598 (.372) .408 (.700 (.290 (.824 (.33) .313-.27) 1.792 (.301) .394) .60) 1.378-. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.821-3.833-1.563-.626-..513 (.949) .17) .337 (.237-.937 (. 1979).669) .774 (. Smith et al.848 (.581) .09) 1.00) .850 (.27) 1.537 (.554 (.487-.444 (.329 (.49) 1.990-1.964 (.727 (.259-.327 (.574-.302-.508-..02 (.704-.00-1.515 (.

cdc. 1990). has been associated with exposure to dusts that contain cobalt. 1989). The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. Cobalt-beer cardiomyopathy. Cobalt was once added as a foaming agent to beer. 1994. Thomassen et al. Perkins DG. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L.e. 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. Lison et al. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population..49:56-67.. population (CDC. A 1982-1992 surveillance programme on Danish pottery painters. Toxicol Sci 1999. Available at URL: http://www. 2005. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 2003... The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . 2003). Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. Lisi. Third National Report on Human Exposure to Environmental Chemicals.. 2001. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. population results in this Report (Kristiansen et al. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. Bucher JR. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al... White and Sabbioni.S. Roycroft JR. 1985. 210 2006. Morgan WKC. 2003.. Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. environmental levels) and health effects is available from ATSDR at: http://www. Lauwerys and Hoet. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. 1994)... not to imply that the BEI is a safe level for general population exposure. 2001.. Atlanta (GA). 1955). Linnainmaa and Kiilunen... Iavicoli et al.atsdr. although substantial occupational exposures have produced elevated urinary levels for many weeks.. Krause et al. 1998). 1997. References Alexander CS. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al... Cugell DW. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. Hailey JR. Daniel et al. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. Shirakawa et al. Urinary measurements mainly reflect recent exposure. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. Blood and urinary concentrations as estimators of cobalt exposure. 2001. 1998).cdc. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect. 1992). Swennen et al. Dunstan et al.. 1994.gov/ exposurereport/.html. A clinical and pathological study of twenty-eight cases. Poulsen OM. Am J Med 1972. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. Information about external exposure (i.. Centers for Disease Control and Prevention (CDC). 2005 [online].. with mean levels that were about 15-20 times higher than in the general U. Rubin A.. Sci Total Environ 1994. 1988). 1972). Grumbein SL. 1999). 2005. 2006. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al. an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis. Alexandersson R.53:395417. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. 1993).S.. “Hard metal” disease. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. et al. 4/3/08 Christensen JM... Haseman JK.. Sills RC. Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al.gov/toxpro2.43(4):299-303. Information about the BEI is provided here for comparison. For workers exposed to cobalt in the air. MacDonald et al. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al. 1997). 1988). usually in combination with tungsten carbide (Cugell et al. Arch Environ Health 1988.50(13):95-104. 1993). A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al.Metals Toxic effects of cobalt have been encountered in workplace settings. 2001).

Dunning SP. Mutat Res 2003. Oksa P. Thakker DM. Sci Total Environ 1998. Cobalt and antimony: genotoxicity and carcinogenicity. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Kiilunen M. X. Respiratory health of cobalt production workers. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Fujimura N. Bozec C.55(4):269-276. Dickel H. Goto S. Roto P. Jarvis JQ.533:135-152. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Int Arch Occup Environ Health 1997. Sabbioni E. Lison D. The release of metals from metal-onmetal surface arthroplasty of the hip. Sabbioni E. Boca Raton (FL): Lewis Publishers.216:253-270. Zobelein P. Lhotka C. Goldberg MA. Weber A. Schaller KH. Kusaka Y. Zedda S. Kristiansen J. Int Arch Occup Environ Health. HoffmannB. Am J Ind Med 2003.48:172-173. 1985. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. DeSantis V. Moulin JJ.406:282-296. Chess DG. Peltier A. Ichikawa Y. Christensen JM. Alessandrelli M. Edmonds CJ. Absorption and retention of cobalt in man by whole-body counting. Gross RT. J Trace Elem Med Biol 2006. Cleland D.150. Blunn G. Chest 1989. Arch Intern Med 1990.28(5):1121-1128. Ziaee H.51(7):447450. Kirsch-Volders M. Bacis M. Sanghrajka AP. Stanescu D.88(4):443448. Wild P. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Zweymuller K. Zhuber K. Smith T. Health Phys 1979. et al. Buchet JP. Steffan I. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Industrial Chemical Exposure: Guidelines for Biological Monitoring. J Bone Joint Surg Br 2006. Science 1988. De Boeck M.50(9):835-842. Schank M. Occupationallyinduced “isolated cobalt sensitization. and cobalt metals.204:147-160.Metals effects of cobalt. Occup Environ Med 1994. Salama A. McMinn DJ. Ghat IS. Hoet P. Radulescu M. Biological monitoring of workers exposed to cobalt metal. MacDonald SJ.20(1):25-31. J Orthop Res 2003.95:29-37. et al. J Occup Med 1992. Trace element reference values in tissues from inhabitants of the European Union.22:359367. Falcone G. Iavicoli I.21(2):189-195. Linnainmaa M. Cresti R. salt. Rorabeck CH.34:620-626. Cannon SR. Meier R. McCalden RW. J Bone Joint Surg Br 2005. White MA.36:732-734. Barnaby CF. Bunn HF. Palmroos P. Robinson C. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Sci Total Environ 1997. Hedge AG. Long-term clearance of inhaled 60Co. Unwin P. Lison D. Kriss JP. Outcome of occupational asthma due to cobalt hypersensitivity. a study of 13 elements in blood and urine of a United Kingdom population. Leghissa P. J Rheumatol 2001. cobalt salts. Thabe H. Contact Dermatitis 2003. Sabbioni E. Goto S. Carnes WH. Lisi P. Buchet JP. Molders J. Meyer zum Buschenfelde K-H. Pradhan C. Kuska Y.45:246-247. Thomassen H. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Diepgen TL. et al. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Linna A. Cobalt cardiomyopathy. oxides. Uitti J. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Lauwerys R.69(3):193-200. Dunstan E. Salvatori S. Br J Ind Med 1993. Schramel P. Sci Total Environ 1994. Laippala P. Am J Epidemiol 1998.157:117121. Epidemiological survey of workers exposed to cobalt oxides. Sci Total Environ 1994. Fourth National Report on Human Exposure to Environmental Chemicals 211 .87(5):628-631. Swennen B. et al. Pisati G. 2001. Romazini S. Clin Orthop Relat Res 2003. et al. Heki S. Hoher T. Kato M. Hammon E.148:241-248. Co-sensitivity between cobalt and other transition metals. Shirakawa T. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Angerer J. Lasfargues G. Bourne RB. Lauwerys R. et al. Occup Environ Med 2001. Lung cancer risk in hard-metal workers. 3rd ed. Lison D.58(10):631-634.44:124-132.150:177-183. Daniel J.” Contact Dermatitis 2001. Vitali MT. Mosconi G. Lauwerys RB. Szekeres T. Swennen B. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial.150(1-3):167-171. Kraus T. Health Phys 1972. Tilley S.242:1412-1415. and hard metal dust. A report of two cases from mineral assay laboratories and a review of the literature. Weyher I.(1-3):133-139. Iversen BS.

00 (2.50-3.00) 2.80 (4.75-1.36-1.20) 3.80) 2.78 (1.40) 1.50) 3.30-2.10-2.90-4.80 (1.20-3.70) 1.70 (1. blue-gray metal that occurs naturally in soils and rocks.10-2.90) 2.80-5.20 (2.80) 1.80 (2.40) 2.10) 4.45-1.70 (3.83 (1.30) 1.50 (4.g.80 (1.S.10-1.50) 2.50 (2.50 (1.52-1.90 (4.20 (1. ammunition.20-4.00-6.37-1.49-1.10-2.12-1.10) 3.10-3.10-6.20-2.80 (3.60 (1.00) .75-2.10 (1.30 (2.50-3.10) 3. antique-molded or cast ornaments.70) 4.60) 1.10-3.40 (2.93-2.71-1.17) .00) 5.69) 1.20-6.60 (3.10-3.80 (5.40) 4.90) 2.50) 1.60) 4.60-3.70 (2.70-2.60 (3.60-4.40-1. 7439-92-1 General Information Elemental lead is a soft.87 (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 2.50-4.43-1.30) 95th 5.80-4.70-5.70 (1.60 (2. 212 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.30-2.40-3.50) 5.40-2.36-1.90 (2. interval) 1. and for radiation shielding.40) Total 1.52-1.90 (3.90) 2. metal alloys (e. brass.50 (1.50) 4.60 (1.00-4.25 (1.80-3.20-3.00) 6.30 (2.30 (3.90 (1.90-3.30-1.30 (4.50-1.60) 3.10 (2.51) 1.S.30 (2.70) 3.80 (5.00) 1.20 (2.50-1.40-1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.10-4.80 (1.10) 5.10 (2. Before the 1980’s.36) 1. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.946 (.32-1.39-1.80-4.20) 4.00 (3.30-1.30 (2.60 (2.10-6.20 (3.10) 1.51 (1.70) 4.50) 1.80-3.986) .86) 1.10-4.00 (4.80) 1.90-6.20 (3.60-1.10 (4.50-1. Lead is most often mined from ores or recycled from scrap metal or batteries.70) 1.00-5.40-3.60-4.70-1.20) 1.60) 3.40-2.70 (1.60 (1.37 (1.50) 1.00) 1.43 (1.80-2.40 (4.30 (1.10-2.30-4.66) 1.899-.65 (1.04-1.00) 2.60 (1.30-1.00 (5.90) 2.40-4.43 (1.40) 3.91) 1.60) 3.70 (2.96-2.20) 4.60) 1.10 (2.25) 1.48) 1.70 (5.66 (1.37 (1.02) 1.40 (2.50) 2.20 (1.55-1.90) 1. 0.50 (1.69 (1.28.50-5.75) 1.20 (3.56 (1.60 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.19 (1.10 (1.20-2.50-2.39) 1.40-1.70-3.09) 1.34-1.60) 1.60 (1.60 (3.70-2.20) 5. solders.80) 3.80 (1.20) 2.40-1.30 (2.50-2.20 (3.80 (1.00 (6.40 (1.90) 2.800-1.20-1.60-2. plastics.60) 1.942 (.60 (3.20) 3.20 (3.30 (1.10) 3.45 (1.80-3.40) 2.00-1.70-1.00 (4. Elemental lead can be combined with other elements to form inorganic and organic compounds.10-3.25 (1.60 (1.50 (2.90-4.60) 2.60) 4.50 (3.90-4.01 (1.00) 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 1.70 (2.40 (1.90) 1.80-4. and 0.50 (2.20) 3.90-4. respectively.50-4. bronze).90-2. malleable.60) 4. Lead was used in plumbing for centuries and may still be present.90 (1.50) 75th 2.60 (4.00) 2.68-1.40) 1.30-5.80 (1.20) 90th 3.60) 4.20 (1.80) 2.90 (3.23 (1.10) 1.00-4. 01-02.40-6.00) 2.14-1.10) 2.60-1.89) 1.00 (1.40) 2.50) 7.70-6.62-1.Metals Lead CAS No.60) 5.90) 3. the main source of lead exposure for the general U.70 (1.900-1.60) 2.10-2.50 (2.30 (1. such as lead phosphate and tetraethyl lead.62 (1.32-1.80) 2.20 (1.00-1.30-1.81) 1.20 (1.70) 2.90) 1.50 (1.55 (1.50 (3.80-3.10-1.20 (3.30-1.60) 5.90-2.40-1.60) 2.30 (2.30-1.60) 2.70-1.10 (1.50 (4. leaded glass.70-2.72) Selected percentiles ( 95% confidence interval) 50th 1.80 (2.90 (2.10-1.60-1.70) 3.20 (4.69 (1.40 (3.70) 1.3.55-1.50 (2.40-2.90-2.50) 4.00) 1.30 (4.10-2.70) 4.20) .90 (3.40) 2.20) 3.30-6.40-5.70) 4.10) 2.60 (1.80) 1.70) 3. population was aerosolized lead emitted from combustion engines that used leaded gasoline.40 (1.20-3.00 (1.00) 4.60-1. In the past.22 (1.00) 1.43) 1. Since lead has been eliminated from gasoline.10-8.50-1.40-6.53) 1.14-1.878-1.40) 5.52 (1.30) 2.40 (1.87) 1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.80) 1.90) 3.00-2.00) 4. ceramic glazes.20-3.60) 3.50-1.62) 1.20 (3.90 (3.50) 5.00) 3. dense.40 (5.30 (2.50-2.77 (1.70 (3.43) 1. and 03-04 are 0.60-6.46 (1.31) 1.70-4.30) 2.60 (2.60-2.30-2.00-4.30-2.10) 1.40-1.80) 2.50-5.40) 1.900 (.20-1.80) 1. Lead has a variety of uses in manufacturing: storage batteries.60) 2.30) 2.60) 1.30 (1.50) 1.80 (2.60 (2.90 (3.10 (3.30) 5.90) 5.50-6.30 (4.14-1.70) 1.00) 3.75 (1.70) 1.80 (4.95) 1.3.90-2.900 (.60 (2. lead was added to gasoline and residential paints and used in soldering the seams of food cans.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. see Data Analysis section) for Survey years 99-00.50-2.69) 1.40-3.

64) 2.560-.00-2.840 (.30-3.20 (1.90-2.757-.50-2.40 (2.616) .20-1.90 (1. Approximately half of the absorbed lead may be incorporated into bone.40) 2.80) 3.40) 2.09) 1.535-.595-.600 (.40-1.60-1.30) 1.60-3.90 (1.620 (.50) 1.00) 2.20) 1.674) 1.75) 4.50 (1.59) 1.30) 2.940 (.70 (2.80-2.558 (.33 (2.600-. 1991).80) 3.90 (2.480-.23-4.66 (2.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.00-1.30-1.651) .600-.620) 1.691-.04-2.03 (1.90-2.900 (.833 (.700-.20 (1.40-1.00) .40) 1.62) Total .800 (.11 (1.800-.60 (1.700 (.40) 1.35 (.625 (. imported children’s trinkets and toys.60-2.90) 1.900) .60) 2.589-.80) 1.730 (.790 (.990) 1.10-3.960-1.604 (.00) . 0.680-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20) 1.749) .600) .30) 1.91) 2.630 (.04) 2.30-1.10 (1.49 (1.89) 2.900-1.20) .800-1.564 (. bullet fragments retained in human tissue.80) 1.04) .80) 1.20) 1.915-1.29) 2.60 (1.62-4.580-.S.20 (2.40) 1.660) . CDC.506-.90) 2.40 (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 .900-1.526-.848 (.900) .572-.11) 2.600-.671-.70 (2. In the blood. and 03-04 are 0.700 (.78-2.90-4.795 (.27 (1.822-1.80) 2.70) 1.40 (1.700 (.00-2.14-1. and contact with soil.570-.810-1.50-2.40-2.40-3.640-.86-2.640 (.90-2.50 (2.625-.97) 4.808 (.52 (1.20-2.70-2.650) 1.27) 1.920 (.10) 2.00) 2.800) .818) .30-5.02) 1.30 (1.677 (.13) .59-2.80) 2.20-1.745-. battery and radiator manufacturing) and recreational sources.800) .573 (.600) . absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.40) 2.30) .70) 3.20 (2.10-3.800-.731 (. lead-containing folk remedies and cosmetics.78-2.50-3.10-1.700-.12) 90th 2. interval) .52-1.753 (. lead-contaminated dust in indoor firing ranges.14 (1.900) .700-1.10-1. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.910-.23) .21 (2.700) .80) 2.20) .766 (.40 (1.800) .857) .60 (2. see Data Analysis section) for Survey years 99-00.04 (.20-1.579-.72) 1.20) .82 (2.50) 1.1.32 (1.935) 1.688 (.82 (1.18-1.50) 3.700-.10-1.80 (2. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.40 (1.60 (1.800) .700-.600-.40 (2. stained glass framing.900 (.00 (1. older plumbing systems with leaded pipes or lead soldered connections.960-1.22) 1.20 (1. Fourth National Report on Human Exposure to Environmental Chemicals 213 .556-.636 (.60-3.02 (.10) . pewter utensils and drinking vessels.70) 2.641-.30-2.900-1.680-. or water contaminated by mining or smelting operations.10-1.600 (.40-1.800-1.07 (. respectively.13-3.73 (1.86) 1. However.50 (2.628) 1.815 (.70) 1.990) 2.00 (1.862) .20) .718) .40 (2.70) 1.30-1.752 (.955-1.800 (.10-1.24-1.00) .10-5.785) .80 (1. 2007.33-2.90-2.701) .30 (3.80) 2.44-2.40) 1.10) 2.10 (1.00 (.540 (.40-5. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.661-.923 (.700) 1.613) .10) .30) 2.659 (.19 (1.80) 2.605) .52-1.10 (1.590 (.10 (1.500-. lead-based painted surfaces undergoing renovation or demolition.90) 2.773) .986) .700 (.30) 1.40) 3.800) .60 (1.591 (.10-3. 01-02.14 (1.50) 1.970-1.86 (1.710-1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.00 (2.75) 3.66 (2.20-2.50) 2.800 (.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. or after soluble lead compounds are ingested.900-1.40 (1.710-.10 (. dust.833-1.695 (.30) 1.600-.30) 2.03-2. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.820-1.90 (2..20 (1.04 (.708-.00-1.900) .90 (1.29 (2.700 (.70 (2.07-1.637-.00-1.40) 2.900 (.10 (.960 (.90 (2.20 (1.00-2.553-.86) 95th 2.50 (1.931) .41) 2.30-1.920 (.50-1.31 (1.50-2.10 (.729-.00 (1.33.690) 75th 1.Metals occupational (e.30 (2.540-.800 (.80-2.20 (3.680) .20 (1.900) .00 (1.1.17 (1.40) 1. and 0.00) 1.579-.90-3.941) .78-2.70 (2.40 (2..610 (. 2000).g.00) .40-1. Absorption of ingested lead can be as much as five times greater in children than adults and even greater when intakes of dietary minerals are deficient. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.60-2.700-.642 (.700 (.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90) 2.10) 1.31-3.70 (1.900) .90-3.50 (2.80 (1.738) .80-3.828) Selected percentiles ( 95% confidence interval) 50th .70) 3.20 (2.70-3.50) 2.850 (.06) .30) 1.

720 (.933) .97-18.742) Selected percentiles ( 95% confidence interval) 50th .342-.508) .85-2. encephalopathy.712 (.78-4.05 (1.50-1.579-.615 (.62-2.632 (.718) .644 (.87) 1.56-2. abdominal pain.649 (. kidney injury.10 (1.03) 2. scant amounts are lost through sweat.400) .28) .492-.708 (.612-. and paralysis.28-1.0) 3.Metals 90% of the body lead burden in most adults.638 (.383-.28) 2.09) 1.33 (1.61) 3.82) 1.94 (1.14) 1. The skeleton acts as a storage depot.46 (1.721 (. CDC.583-.88) 2.70 (1.898) .47 (1. 2007).24 (1.75 (2.670) 1.33) 2.561-.683-.88) 1.47) 1.428) .22-2.608-.645-.05 (.730) 1.34-1.940 (.64-2.658 (. Staessen et al.03) 1. The toxic effects of lead result from its interference with the physiologic actions of calcium.05-1.01) .61) 1.07-1. and nails (Leggett.68 (1.725) .862-.673) .693 (.22-1.51 (1.53) 1.734) .701) . 1993.43 (1.73) 2.510-.96 (1.98 (1.11 (.74 (1.03 (.667-.26) Total .722 (. 1993).918-1.09-1.33) 1. through the inhibition of certain enzymes.18) . BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.696 (.603 (.00 (.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 .29 (1.19) 1.677-.00 (1.828-1.55 (1.61) 1.605-.41) .79) 1.43-1.870 (.667) .85 (1.593 (.56-3.926 (.88) 2.639 (.47 (2.917-1.853-1.607-.62) 2.02-1.461) .618 (. 2004.63) 4.22) 1.588-. Schwartz.655) 75th 1.603-.10) 1.00) . O’Flaherty.22) .569 (. population from the National Health and Nutrition Examination Survey.20) .559-.702) .703) .535) .78 (2.709 (.742) .06) 1.38 (2. 1991.635 (.657) 1.828) .667-.43 (2.88-2.876-1.03 (.15-2.668-.677) .06 (. based on prospective population studies.66) 2.688) . Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.73-2.681-.15) 1.31 (1.66 (1.774 (.677 (.15-3.07) ..17-1.03) 90th 1.65-2.79 (1..06 (1.587-.981-1.75-2.49 (1.681-.64) 2.25-1. the Centers for Disease Control and Prevention (CDC) established a BLL of 10 Urinary Lead (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.25-1.98) 2.979 (.66 (1.10 (.718) 1.645-.97) 1.701 (.404 (.380-.51) 1.938-1.702) .11 (1.633 (. 1995).56 (1. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.755 (.11) .36-2.793-1.03) .37-1.541-.50) 1.03 (1.990 (.790) .07 (.S.655-.01 (.50 (1.38 (2.914 (.946-1.882-1.710) .622 (.746) . 1995.838) .639 (.800-.89-5.15-2.962 (.18) 1.812-1.58) 1.725) .20) .758) .432 (.61) 1.436) .841-1.731-. interval) .89-2.05-1.62-3.39-1.592-.19-5.64 (1.88 (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.31) 1.375 (.957-1.72-2.781-1.03) 1.50-2.38 (2.65 (1.18) 2.604-.71-2.918 (.469 (.652 (.765) .11 (1. zinc.659-.992-1.623 (.83 (2.31) 1.963-1. 1996).52 (1.460-.72-2.496 (.639 (.00 (1. Nash et al. For instance.623 (.571-.08) .641 (.648 (.31 (1.85-2.23 (1.551-.938 (.722 (.404-. with lesser amounts eliminated via the feces.686) .67-4.94-2.887 (.. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.11-1.739) .753) .594-.09-1.644) . In 1991.50-2.44) 1.988-1.22) 1.639) .59-3.404 (.893) .11) 1.45 (1.571-.920-1.654) .26) 2. seizures.69 (1.46 (2.608 (.33-1.55 (1.971 (. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.603-.763) .98-2.08) .03-2.85) 1.977) 1.20) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .851) .52) 1. 2003.64) 95th 2.41-1.671 (.41 (1.09-1.06) .720 (.702-.31 (2.975-1. with a half-life of years to decades.72) .63) 1.18) 1.40-1.707 (.655) .04-3.621 (.997-1. BLLs and associated toxic effects differ in children and adults.586-.606-.17 (.992-1.86 (1.92) 2.97 (1.44 (1.601-.04) 2.08-2.44 (1.609 (.53-1.12-1.79) 2.698) .914-1.14 (1.48 (1.914 (.408-.77) 2.615 (.810 (.56) 3.933-1.35) 2.15) 1.00 (1.83) 1.37-1.50-2. Large amounts of lead in the body can cause anemia.679-.529-.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 1.682) . and iron.11 (.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 .679) 1.796-1.27 (1.61) 1.03) .700-.625 (.43) 2.03 (. Lead can cross the placenta and enter the developing fetal brain. and through binding to ion channels and regulatory proteins.698) . hair.97) 1.988 (.62-1.20-3.588-.676) .43) 1. Approximately 70% of lead excretion occurs via the urine.71 (1.900 (.18 (1.02) 1.03) 2.617-.594-.

75 µg/dL in U. More recently. BLLs reflect both recent intake and equilibration with stored lead in other tissues. Pirkle et al. 2005a).5 per 100. when the geometric mean BLL was 2. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. Data submitted through state public health programs from 2006 showed that 1. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al.. 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. the geometric mean BLL was 3..6%) were lower than those from NHANES 1991-1994. the prevalence rate has declined annually since 1994 (CDC.S. Muntner et al.html.21% of approximately 3. 2003. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.07 µg/dL (Becker et al..3 million children tested had BLLs of 10 mg/dL or higher (http://www.S. and peripheral neuropathy generally occurring at much higher levels (e..e. In NHANES 1999-2002 in children 1-5 years old. EPA.cdc. almost double the geometric mean of 1.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample.. and low family income (CDC. including minority race or ethnicity.. 2000).4% in NHANES 1999-2004.S. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. 2005b. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. usually with BLLs greater than 40 mg/dL. 1996. and organic lead compounds not classifiable with respect to human carcinogenicity. High dose occupational lead exposure. particularly in the skeleton. 1999).atsdr. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. 1996. Payton et al. Korrick et al... adults in the 19992000 NHANES sample (Apostoli et al. 2002).2 µg/dL in males and 3.0 µg/dL in females (Soldin et al. Staessen et al. Bellinger 2005.... IARC considers inorganic lead compounds probable human carcinogens. 1995. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. Lanphear et al. respectively. 1984. Schwartz et al..g. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. and decrease fertility (Alexander et al. though there is greater individual variation in urine lead than in blood and greater potential for contamination.xls). For example.gov/toxpro2.Metals µg/dL or higher as the level of concern in children. Information about external exposure (i. Jones et al. Both drinking water and ambient air standards for lead have been established by the U.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. Urine levels may reflect recently absorbed lead. However.. Surveillance data reported by U. which is an 84% decline. 2007)..000 adults. 2003. urban residence. 1987. residing in housing built before the 1950’s. Borja-Aburto et al. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. reduce sperm count. with overt encephalopathy.. In occupationally exposed adults. Telisman et al. The U.4% of children had BLLs of 10µg/dL or higher (CDC. 2002a). adult population has similar or slightly lower BLLs than adults in other developed nations (CDC.. adult residents. 2003).gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. 2001). Schwartz. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.. 2005b). Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. adults in the 1999-2000 NHANES sample.S. 1996. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. 2009).. lead in women may be associated with hypertension during pregnancy.. CDC. 1994). both the geometric mean (1.. higher than 100-200 µg/dL).7 µg/dL and 4. 2006). 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. 1991. Results of studies of adults with either occupational or environmental lead exposure have shown consistent associations between increased BLLs and increased blood pressure (Nash et al.S.cdc. may alter sperm morphology. At low environmental exposures. 2002. 2006). 2003. 2000)..6% in NHANES 1988-1991 to 1. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. environmental levels) and health effects is available from ATSDR at: http://www.S. approximately 11. Fourth National Report on Human Exposure to Environmental Chemicals 215 . Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al.. Overall. 1998). 1999). premature delivery. and spontaneous abortion (Baghurst et al. seizures.. 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.

Sci Total Environ 2002. Public Health Rep 2000. Dietrich K. Hertz-Picciotto I. 1999-2002. Hernberg S.cdc. 4/14/09 Centers for Disease Control and Prevention (CDC). CDC. Korrick S. Mantere P.cdc.150(6):590-597. Neurodevelopmental effects of postnatal lead exposure at very low levels. Auinger P. Wigg NR. Chiodo LM. References Agency for Toxic Substances and Disease Registry (ATSDR). A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Vimpani FB. Teratogen update: lead and pregnancy. Hunter DJ.8(3):395-401. et al. Lead. 1991 [online]. Korrick SA. Hu H.53:411-416. Luukkonen R. 4/14/09 Centers for Disease Control and Prevention (CDC).gov/toxprofiles/tp13.htm. IARC Monogr Eval Carcinog Risks Hum 2006. Available at URL: http://www. Pirkle JL. Lepom P. Scand J Work Environ Health 1984. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. et al. et al. Weiss ST. Available at URL: http://www. Farias P. et al. Aro A.htm.htm. Robertson EF. Rios C. 4/14/09 Alexander BH. 2003-2004.87:1-471. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.cdc.cdc. Am J Epidemiol 1999. Stanek KL. Jacobson JL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Caldwell KL. Kaufman JD. Reese YR. 2005. Baj A. et al. Atlanta (GA). Blood lead levels—United States. Cox C. Pediatrics 2004. Int J Hyg Environ Health 2002. Muntner P. JAMA 1996. Weiss ST. gov/mmwr/preview/mmwrhtml/mm5420a5. Rotnitzky A. Lanphear BP. Adult blood lead epidemiology and surveillance—United States. van Netten C.115:521-529. Leggett RW. Ronchi L. Speizer FE.275:1177-1181. Occup Environ Med 1996.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.html. Ga.205:297-308. Available at URL: http://www. Available at URL: http://www. Rojas LM. Roberts RR. Blood lead reference values: the results of an Italian polycentric study. Managing Elevated Blood Lead Levels Among Young Children. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Age-specific kinetic model of lead metal in humans. Ewers TG. Schulz C. Homa DM. The relationship of bone and blood lead to hypertension. Checkoway H. Aug 2007 [online]. Brody DJ. Pediatrics 2009. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Blanco J. Bellinger D. Toxicological profile for lead.54(20):513-516. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Sparrow D.gov/nceh/lead/publications/ books/plpyc/contents. N Engl J Med 2003.htm. Environ Health Perspect 1993.123:e376-e385.gov/mmwr/preview/mmwrhtml/ mm5532a2. 4/14/09 Centers for Disease Control and Prevention (CDC). Coresh J. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention.26:359-371. Semen quality of men employed at a lead smelter. Becker K. Krause C.89:330-335.atsdr. Apostoli P. Bavazzano P. Am J Public Health 1999. Henderson CR. Lanphear BP. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Muller CH. 1988-2004. Seiwert M. Baghurst PA. Blood lead levels measured prospectively and risk of spontaneous abortion. Angle CR.gov/nceh/lead/ CaseManagement/caseManage_main. Centers for Disease Control and Prevention (CDC). 2005b. Hu H. 2002 [online]. Meyer PA. Vupputyuri S. Canfield RL. Kaus S. Atlanta.287:1-11. Cory-Slechta DA. Jones RL. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Sparrow D. Wager C.1542/peds:2007-3608. JAMA 1996. Neri A. Jacobson SW. Bellinger D. Ganzi A. Kuehnemann TJ.cdc. Borja-Aburto VH. Atlanta (GA). Lead and hypertension in a sample of middle-aged women. Hu H. doi:10. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Rotnitzky A. Jusko TA.73:409-420.55(32):876-879. Neurotoxicol 1987. Available from URL: http://www. Hänninen H. Cox C. McMichael AJ.101(7):598-616. Manton WI.82:60-80. Kim R. Inorganic and Organic Lead Compounds. Third National Report on Human Exposure to Environmental Chemicals. Environ Res 2000. Preventing Lead Poisoning in Young Children.10:43-50. Batuman V. MMWR Morb Mortal Wkly Rep 2005a. MMWR Morb Mortal Wkly Rep 2006.348:15171526.113(4):1016-1022. 4/14/09 Centers for Disease Control and Prevention (CDC). Birth Defects Research (Part A). Acquisition and retention of lead by young children. Payton M.275(15):1171-1176. Neurotoxicol Teratol 2004.

Jurasovic J. Lee SS. Payton M.289(12):1523-1531. zinc. Roels H. Weiss ST. Paschal DC. Stewar WF. Brody DJ. Kinetics of lead disposition in humans.140:821-829.106:745-750. Smith DR. Low-level lead exposure and blood pressure. Am J Epidemiol 1994. Flegal AR. Staessen JA. Environ Health Perspect 1996. dimercaptosuccinic acidchelatable lead. Pirkle JL. Lustberg M. Rocic B. Schulz D. Revised and new reference values for arsenic. 50:31-37.9:303-327. Lee GS. Lee BK. Gunter EW. Kaufmann R. Hwang KY. Fourth National Report on Human Exposure to Environmental Chemicals 217 . O’Flaherty EJ. Am J Epidemiol 2001. Toxicol Appl Pharmacol 1993. Hanak B. Use of endogenous. Kaufmann RB. Nash D. stable lead isotopes to determine release of lead from the skeleton. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Wilhelm M. and hypertension in perimenopausal and postmenopausal women. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Hu H.S. Osterloh JD. Amery A. JAMA 2003. blood pressure.327:109-113.63:1044-1050. population to lead: 1991-1994. Schwartz BS. cadmium. IV. Magder L. Soldin SJ. et al. Sparrow D. Schwartz J. Association of blood lead. Telisman S. Arch Environ Health 1995. blood pressure and cardiovascular disease in men.118:16-29.209:301305. Lead. Blood lead. Clin Chim Acta 2003. et al. Gavella M. and copper in men. Low-level lead exposure and renal function in the Normative Aging Study.153(5):453464. J Hum Hypertens 1995.104(1):60-66. Rubin R. Environ Health Perspect 2000. Blood lead concentrations in children: new ranges. Environ Health Perspect 1998. Physiologically based models for bone-seeking elements. lead. Exposure of the U. Hickman T. Schwenk M. Lauwerys RR. Sherwin R. Soldin OP. Pizent A. Int J Hyg Environ Health 2006.108(1):45-53.Metals results from NHANES III. Cvitkovic P. and tibia lead with neurobehavioral test scores in South Korean lead workers. Kidney Int 2003. cadmium.

70 (4. 1998.90-3. inorganic. may contain inorganic mercury.50-3.40-1. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal). electrical lamps. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.2.00 (2.60 (1.g. and organic forms..800-1.472-. constitutes the main source of dietary mercury exposure in the general population.00-1.70 (1.600) 1.60 (1. or oxygen.02) .40) 3.30) 1.00) 4.40 (3.700-. Accidental spills of elemental mercury.714-.30-5. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.20 (2.40 (4.00) 1.800-1. and mining and smelting. 1994. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.40-2.80 (1.40-3.753-1.50) 1.60-6.g. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.00) 1.80) 1.80) 3.90) 95th 4. 1993). solid-waste incineration. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.500 (.. elemental mercury is absorbed mainly by inhaling volatilized vapor.Metals Mercury CAS No. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.70 (3. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.00) ..00-5.50) 5. mercuric chloride).80) 4. see Data Analysis section) for Survey year 03-04 is 0.781 (.00 (1.40-2.g. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.90) 90th 3. After elemental mercury is absorbed.20-3.600 (. merbromin). IARC.700 (.700-.877 (.10) .60-3. The ingestion of methyl mercury.300 (. predominantly from fish and other seafood.40) 1.80 (3.60) 1.860-1.800 (.372) . Elemental mercury is a shiny. with the highest concentrations occurring in the kidneys (Barregard et al. Survey years 03-04 Geometric mean (95% conf.400 (. have often required public health intervention (Zeitz et al.903) Selected percentiles ( 95% confidence interval) 50th .797 (. to form inorganic mercury compounds or salts.60-2.10-3.800-1.672) . 1999 . population from the National Health and Nutrition Examination Survey. 1980.563 (.20-4.00 (.900) 1.418-.800 (. and is distributed to most tissues.979 (. such as chlorine (e.300) .500-. Kingman et al.30) 4132 4241 03-04 03-04 03-04 .500) . Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach. which create an episodic potential for volatization and inhalation of mercury vapor.30 (2. 218 Fourth National Report on Human Exposure to Environmental Chemicals .90) 3.70-2.700) .886) .919) .90 (1. sphygmomanometers and barometers. 2002).00 (. Woods et al.S.776 (.927) ..285-.800 (.80 (1..900) 75th 1.800-1.12) .900) .00 (. an organic form of mercury. thermostats and switches). Some cosmetic skin creams from countries other than the U.40-1. 2007).900) 1. which can bioaccumulate in aquatic and terrestrial food chains.703-. Atmospheric elemental mercury can be deposited on land and water. Poorly absorbed from the gastrointestinal tract.363-.500 (..40 (3. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.900) 1.30) 3.50-1.30) 3.60-5.484) . Other major uses include electrical equipment (e.400-.80 (1.689-. synthetic organomercury compounds were once used in pharmaceutical applications.00) 3. sulfur. Hursh et al.30) 5.490 (. phenylmercuric acetate) or topical antiseptics (e.900 (. The kinetics of the different forms of mercury vary considerably.655-. thimerosal.30-2.800-1.90 (1.40 (4. In addition..70 (1.500-..70) 911 856 2081 4525 03-04 03-04 .800 (. Apart from methyl mercury.419 (..700) .50) Total Age group 1-5 years 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 8373 03-04 03-04 03-04 03-04 .30-4. thermometers.g.700-. and dental amalgam.400-.814 (.30) 1.30 (1.574) .50-2. and mercury compounds are still used as preservatives (e.50) 2.20-4.60-6.00 (.700-.50) 4. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).30-6.300-.20) 2.60 (2.00 (2.00 (2.60) 2085 2293 3478 Limit of detection (LOD.60) 1.326 (.S. interval) . Also.90 (4.700-.

Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.29) . 2004.40-2.10-1. interval) Selected percentiles (95% confidence interval) 50th .10) .30) 3.50) 1.500-.200-. Geometric mean Survey years (95% conf.60 (1.50) 3.30 (1.. Methyl mercury is incorporated into growing hair.10) .800) 75th .Metals the tissues to mercurous and mercuric inorganic forms.30-6.700 (. 1991.940) Race/ethnicity (females.200-.700-. 1996.871-1.600 (. 1999-2002.35 (1.01) .300 (.820 (..10 (.60 (1. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.80 (3.944 (.00) 7.80-3.30) 1.265-.300) .200-.10 (1.60) 1.664-1. Myers et al.825-1....00-2.300 (. 2003)..90) 5. 1994). and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.297-.00 (3.307 (.73) 1.00 (1. 1994) and then undergoes slow dealkylation to inorganic mercury..300) . 1998).10-3.00-1.50 (2. Jonsson et al.7) 4.90) 2.377 (.300) .10) 1.90 (1.30-6.200 (.06 (.900 (.70) 4.329 (. 1992). 1969.30-4.900 (. 1973).20-11.700 (.407) .500-1.475) . population.70 (1. 1993).600) .27) .60 (3.80) 579 527 370 436 588 806 Limit of detection (LOD.70 (1. 1995. 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.299-.90 (1.700) 2. 1996).10 (1.500 (. for both acute and chronic exposures.800-1.726-1.60 (3. 2005).20-3.00) 4.800 (. a measure of accumulated dose (Cernichiari et al. Smith and Farris.40) 1.0) 4. 1975....00) 6.400-.70-3.70-5.00) 1.00 (2. Smith et al.50-12.700-1.50 (1.800) . McDowell et al. After exposure to elemental mercury. Methyl mercury enters the brain and other tissues (Vahter et al.60) 2..700-.800) 1. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.14.00 (2. Vahter et al..30 (.90 (3.30-6.50-3.00-3.374) .10 (5.300) . and the newborn’s levels decline gradually over several weeks (Bjornberg et al.40 (1.00-2.60 (2.30-5.500-..300 (.343 (. 2003).395) .700 (.90) 2.70-6. Miettinen et al.00-2. 1990).200-.02 (.S.30-11.10 (1.256-.60) 3.200-.50) 2.70-3.700-1. Excretion occurs by renal and fecal routes.40-2.50-2. Fourth National Report on Human Exposure to Environmental Chemicals 219 ..200 (.300) .20) .500 (.20) 1.600) .20 (2. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.50) 1.300 (..10 (. 1984.90 (4.90) 90th 1.20 (.919) .14 and 0.833 (. 1971).20-3.00) .. 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..90 (4.. with most elimination occurring through in the feces (Sherlock et al.800-1.800) 1.40 (1.900-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al. Suzuki et al.300) .20-3.50) 95th 2.23) .377) .80) 1.20) .00 (2. Sandborgh-Englund et al.06-1.268-..70) 4. and a useful marker of exposure in epidemiologic studies (Grandjean et al.318 (.40-1.738-..369) 1.500-. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .30) 1.800 (. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.200-.3) 4.30-2.80 (1. 1998). 1992. Vimy et al.10 (3.800 (..00-6.824) 1. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.00) 1.500-. 1993).500-.30 (1.90) 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 .90) 3.40) 2. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al. 1999).900 (. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.667 (.30-4.800) ..70 (1. 1992 and 1999.700 (.697-.70-5.00) 2.800-1. National Health and Nutrition Examination Survey. thereafter.317 (.20-2.70) 1. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.60 (1.40) 5.30 (1. 1994. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.30-3.541-.60) 1.900-1.269-.

. 1983). particularly irritability. altered physical growth. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 2006. 2002. dysarthria.S. 1963).500 (<LOD-.700 (. 1998..500-. 2005).. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.600) .700) 2007 2240 3406 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. 2004.700) 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 .. hearing impairment.600-. limb deformities. Oskarsson et al.600 (.42.500 (. Salonen et al.600-. Inorganic mercury exposure usually occurs by ingestion. 2004). 2003). causing parasthesias. fatigue.500-. high-dose exposure to elemental mercury vapor may cause severe pneumonitis.600) . Rissanen et al. Rice. 2004.700-.. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.. and pinkish discoloration of the hands and feet (Tunnessen et al. and cerebral palsy (NRC. 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. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. ataxia. 1951.. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. 1987).600-. 2006. anorexia.600 (.600 (.700 (. 1995. maculopapular rash.600) .. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. Stern 2005. 1993). and progressive constriction of the visual fields.800) . 1995.600 (. overt signs and symptoms of chronic inhalation may include tremor. DeRouen et al.. 2004).600) .500-.500-. sensory impairments. which may vary for some chemicals by year and by individual sample..600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500-.600) . gingivitis.600) . 2000). cerebellar ataxia.500 (. hypertension.500-.600 (. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. The health effects of mercury are diverse and can depend on the form of the mercury to which a person is exposed and the dose and the duration of exposure. Factor-Litvak et al.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . Sakamoto et al. Smith et al.. In recent epidemiologic studies. Vupputuri et al..500-..Metals may be more efficient for inorganic mercury (Grandjean et al. dysarthria.500) . Survey Geometric mean (95% conf.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . The constellation of findings may include anorexia. insomnia.500-. Bellinger et al. typically after a latent period of weeks to months.600) .600) .700 (. pain in the extremities. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.800) .. 2005. and neurocognitive and behavioral disturbances. short-term memory loss.600) .700-. the existence of a causal relation is unresolved (Chan and Egeland.700) .500 (<LOD-.. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. 220 Fourth National Report on Human Exposure to Environmental Chemicals .700 (. 1970. 1996).500-. Overt poisoning from methyl mercury primarily affects the central nervous system.700-. Sakamoto et al. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. irritability.600-. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis.600 (.600 (.600 (. Once absorbed. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease. depression.700 (. Smith et al. see Data Analysis section) for Survey year 03-04 is 0. 2000.700 (.. Acute... Drexler and Schaller. At levels below those that cause acute lung injury. 2000. and sleep disturbance (Bidstrup et al.

Schober et al.960 (. Kingman et al.cdc. 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. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.65) 1. Information about external exposure (i.495 (.S.. 1998).13-2.29) 1.400 (.epa.330-.gov/toxprofiles. range 40 years to 78 years) had an average total blood mercury concentration of 2. total blood mercury increased with age..08 (1.420 (. Biomonitoring Information In the general population.24) 1.360-.88 (1.S. 1997.280-. 2009)..480 (. 1998).570) .430) . Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2003).93 (1. adult women in several ethnic subgroups (Hightower et al..460 (. 758 children. These distinctions can help interpret mercury blood levels in people. who participated in a 1998 representative population survey (Becker et al.14) 90th 2.408) .360-.330-.480) 75th 1.S. 2000). Grandjean et al.840) 1.atsdr.12 (.442-.31) 1266 1272 03-04 03-04 03-04 . aged 18 to 69 years.. Mahaffey et al.23) 2. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.441 (.96 (1.254 (. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.370) .20 (1.01 (. particularly methyl mercury.66) 3. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.88) 287 722 1529 03-04 03-04 .39-3.30) 3.63-2.05) 3.509) .304) .555) . However.549) . In Germany the geometric mean for blood mercury was 0.840-1.290-.433 (.67-3.14-2..530) .. 2001. 2003). the total blood mercury concentration is due mostly to the dietary intake of organic forms.358 (.88-3.24 (2.420 (.76-4.14.840-1.19 (2. 2006). 1995. In NHANES 19992002. Benes et al.580) .. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children. interval) .34-3.54 (2.S.60) 619 713 1066 Limit of detection (LOD. 2009).31) 2.78 µg/L for adults and 0.. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.940 (.. Sanzo et al.77-2.520) .430 (.03-4.60-2. 2004.534) .28) 1. From 1996 through 1998.07 (.870-1.350-. see Data Analysis section) for Survey year 03-04 is 0.770-1..61) 1. Fourth National Report on Human Exposure to Environmental Chemicals 221 .160-. 2001.18) 2.09 (2..413-. EPA at: http://www.33 (2. Among the three racial/ethnic groups. During the same survey periods. and the age-related changes differed across the groups (Caldwell et al.55 µg/L.19 (1.90) 2.440 (. and increased slightly in non-Hispanic white children (Caldwell. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.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 .89) 3.05) 1.382-.46) 3.00 (.68 (2.9 years).405-.76-3.460) .46 µg/L for children.00) 1.42) 95th 3. Total blood mercury levels increase with greater fish consumption (Dewailly et al. Survey years 03-04 Geometric mean (95% conf.26 (1.700-1. total blood mercury geometric mean levels in females aged 16-49 years did not change.Metals standard for inorganic mercury has been established by U.416 (. average age 9.340-.360 (. 2002). slightly higher total blood mercury levels were found in U.509) .16 (1.97) 2.23) .60 (1.530) .476 (.250) .85-2.58 µg/L for 4645 adults. military veterans (mean age 52.410-. the median concentration of blood mercury was 0. environmental levels) and health effects is available from the U.67-2.16 (.99-6. population from the National Health and Nutrition Examination Survey.313-.447 (.930-1.S.406-.463) .870-1.8 years. Over the NHANES 1999-2006 survey periods.gov/mercury and from ATSDR at: http:// www.396-.52) 2. Urinary mercury consists mostly of inorganic mercury (Cianciola et al. et al. A cohort of 1127 U.492) Selected percentiles ( 95% confidence interval) 50th .e.96 (1.213-..890 (.200 (.08 (1..330 (.530-.76-3. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.430 (. average age 33 years.330-. EPA.78-2.610-1.700 (.

79 (1.13-2.217 (.464 (.Metals 2000).00 (.909 (. Czech (Benes et al. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.77 (2.88 (1.208-.362 (.09) 1.280-.S.64-2. Biomonitoring studies provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of mercury than are found in the general population. 2009).297 (.522-.61) 1.00) 286 722 1529 03-04 03-04 . In the study of U.56) 1266 1271 03-04 03-04 03-04 .03) 2.85) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2537 03-04 03-04 03-04 .28 (. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell. DeRouen et al.714-1.498) 75th . Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.67 (1.32 (1.40 (1.404-.06 (. population from the National Health and Nutrition Examination Survey.343 (. 1998).545 (.687) .1 µg/L for each surface with a dental amalgam (Kingman et al.616) . The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.301-.255 (.. a biomarker of perturbation in renal tubular function. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.23-2.00) 90th 1.667-1.41-2.11-2.06 (.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .31 (1. women of childbearing age have generally been much lower than these levels (CDC.969-1. Department of Health and Human Services noted that several studies have observed a modest.275) .63) 1.620-.32-2.. and Italian (Apostoli et al.86) 95th 2.447-. Urine mercury and the number of dental amalgams were correlated.525 (. Langworth et al. Urinary mercury levels in recent German (Becker et al. Information about the biological exposure indices is provided here for comparison.384 (. 2006).76 (1.54 (2.970 (. 2002)..463 (. 2003).79) 1.1 µg/L.365 (.11) 1.87 (1.630) .485 (..990) .196-.307-.358) . 2005).04-3.443 (. reversible increase in urinary N-acetyl-glucosaminidase.368) . Levels in U.39) 1.65 (1.30) 2.44) 1.768 (. 1988.455-.40-1..391-. 2006.365 (.476 (.S.455-.25 (.508 (.566) .480) .455) . 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.537) . 1992).18-1.400-.652) .246-. et al.01) 2.12-3.30) 1.276 (. 2002) adult population surveys were similar to those in a U. et al.696 (.289) .11) 2.800-1.S..619-. and on average... 2009). military veterans with dental amalgams.599) .535) 1. interval) .333-.347) .784) 1. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.51-2.225-.385-.587 (. the urine mercury increased by approximately 0.13 (1.78-4. An expert-panel report recently prepared for the U. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.785-1. mean urinary mercury was 3.16) 1. not to imply a safety level for general population exposure.07) 1.88-2.447 (.21) 1.588) .472-. Survey years 03-04 Geometric mean (95% conf.417) .391) .486) Selected percentiles ( 95% confidence interval) 50th .67 (1.87) 2.46-2.309-.400) .265-.964-1..88-2. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.532 (..875-1.306 (.S.S.376-.62 (1.392-.35 (1.

48 (2.616-.10-2.501-.596 (.97 (1.57-4.21 (2.831) .S.50 (2.540 (.54) 595 531 381 442 594 826 Limit of detection (LOD.23-1.637) .65-4.41 (1. population.76-5.706 (.760 (.724 (.772 (.97) 2.560-.68 (3.72) 1.790) .51) .98 (5.92) 2.579-.475-.87-4.94) 1.450-.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .25) 2.09-1.28 (1.99) 1.500-.774) .870) .46) 3. National Health and Nutrition Examination Survey.38) 4.650 (.32 (1.909-1.522 (.50-4.686) .636-.721 (.582-.04-10.540-.806) .553-.79) 3.45-3.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .526-.00 (3.55) 90th 3. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old. 1999-2002.00 (2.639 (.13-4.740 (.15 (2.62 (3.592 (.21 (1.15-1.710 (.631-.892) . 16-49 years) 99-00 01-02 .16) 5.27 (1.85-3.22-3.84 (2.557-.21-3.16-5.97) 2.76) 2.39-3.420-.809) .53-3.622-.670) 75th 1.17) 95th 5.14-2.81 (3.41 (1.709) 75th 1.37) 1. 16-49 years) 99-00 01-02 .650) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.910) .665) .810) .18 (3.723 (.31 (1. Geometric mean (95% conf.32-3.516 (.50 (1.719 (.31-1.62 (4.578-.710) 1.30 (1.14) 3.81-6.742-1.656-.30 (2.99-2.76 (1. interval) Selected percentiles (95% confidence interval) Survey years 50th .97) 2.508-.92) 3. population.14-1.14 and 0.560 (.35 (1.699) 1.709) .387-.41-6.47) 1.47) 1.18) 3.91 (2.84 (2.580 (.658 (.624-.45) 2.07-5.43-1.27 (2.77) 1.46-4.22 (.59-5.426-.930) .657 (.03 (.615 (.56 (1.30 (2.91-7.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.37 (1.69 (1.42-3.00) 2.51 (3.565 (.23-1.85) 4.56) 4.83-3.13 (2.03 (.691) .68) 3.685 (. National Health and Nutrition Examination Survey.710 (.45) 95th 3.03) 1.35) .99 (3.605-.664) .79) 1.99 (2.580-.27-1.04-1.65) 1.77) 2.03-2.06 (.744) 1. interval) Selected percentiles (95% confidence interval) 50th .45) 2.14.32) 2.05 (2.56) 3.62 (1.92) 4.S.07) 1.832-1.55-3.44) 3.606 (.61-6.610-.41 (2.24-1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.520-.30-2.09-1.410-.600 (.52) 3.42) 90th 2.Metals Urinary Mercury−Females Aged 16-49 Years Old. Geometric mean Survey years (95% conf.42) 2.61) 1.46 (1.68-3.655 (.833) .966) .10-4.89 (2.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .45-2.24) 6.824) .620 (.07-2.632 (.69-3.850-1.650 (.799) .95 (2.520-.3) 5.45 (1.502-.831) .569-.846) .70 (2.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females. 1999-2002. 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.05 (3.

Metals References Aberg B. Becker K. Chan JM. Fish consumption. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. Gagliardi T.289:1324.149:301-305. Cortesi I. Schuzt A. Arch Environ Health 2001. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure. Jacobs D. 224 Fourth National Report on Human Exposure to Environmental Chemicals .33:1-9. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. and lead. Bernardo M. Woods JS. Drexler H. Tissue levels of mercury determined in a deceased worker after occupational exposure. Kline J. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Levallois P. and Se in blood of the population in the Czech Republic. Mortensen ME.72:169-173. Lancet 1951. Arch Environ Health 1969.111:719-723. Caudill SP. Barregard L. Roels H. Tavares M. DeRouen TA. Arch Environ Health 1992. Impact of maternal seafood diet on fetal exposure to mercury. JAMA 2006. Jarvholm B. Barregard L. Krause C. 2007 TLVs and BEIs. Hasselgren G. Cernichiari E. Apostoli P. JAMA 2006. Cox C. McKinlay S. Cent Eur J Public Health 2000. Biennow M. Seiwert M. The concentration levels of Cd. mercury exposure.16(4):705-710. Int J Epidemiol 2004. Schulz C. Weihe P. Vahter M. Int Arch Occup Environ Health 1988. Chronic mercury poisoning in men repairing direct-current meters. Videro T. Sallsten G. Grandjean P.295(15):17841792. Nutr Rev 2004. Cejchanova M. population: 19992006. Elia G.61:65-69. Weber JP. Am J Epidemiol 1999.47(3):185-195. Neurotoxicology 1995. Sallsten G. Kaus S. Skerfving S. Cernichiari E. Hultberg B. Factor-Litvak P. et al. Budtz-Jorgensen E. Bernard AM. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. et al. Int JHyg Environ Health 2002.50:17-27. Myers GJ. Martin MD. et al. Cianciola ME. Ayotte P. Health effects of dental amalgam exposure: a retrospective cohort study. and heart diseases. Bates MN. Lepom P. Greitz U. Subrt P. Cutress T. Cardenas A. Grandjean P. Barregard L. White RF. Daniel D. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Marsh DO. J Toxicol Environ Health 1997. Berglund B. Int Arch Occup Environ Health 1999. Becker K. Attewell R. Niklasson B. Schulz C. Sallsten G.. Jorgensen PJ.2:856-861. Total blood mercury concentrations in the U. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Smid J. Trachtenberg F. Schutz A. Castro-Caldas A. Seifert B.77(2):124-129. Application to workers exposed to mercury vapour. Leroux BG. Arch Environ Health 1992. Harvey DG. 206:15-24.62(2):68-72. Fawcett J. Martins IP. Bjornberg KA. Third National Report on Human Exposure to Environmental Chemicals. Geier J. Garrett N. Spevackova V. Drago I. Lapham LW. Sci Total Environ 2002. Barregard L. Jorgensen PJ.113(10):1381-1385. Benes B. Int J Hyg Environ Health 2009. et al. Kinetics of mercury in blood and urine after brief occupational exposure. Begg M. Clarkson T.212:588-598. Cernichiari E. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo). Br J Ind Med 1993. Townes BD. Cerna M. et al. 2005. Cu. et al.S.205:297-308.8(2):117-119. Markers of early renal changes induced by industrial pollutants. Lebel G. Kaus S. Metabolism of methyl mercury (203Hg) compounds in man. Jones RL.7(3):176-184.295(15):1775-1783. Bonnell JA. Snihs JO. Assessment of reference values for mercury in urine: the results of an Italian polycentric study. Buchet JP. Leitão J. Locket S. Zn. Kjellstrom T. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Lauwerys RR. Seiwert M. et al.19:478-484. 52:19-33. Centers for Disease Control and Prevention (CDC). Barbon R. Mangili A. Ekman L. Brewer R. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices.56(4):350-357. Hg. Mercury derived from dental amalgams and neuropsychologic function. Bellinger DC. Persson G. Enzymuria in workers exposed to inorganic mercury. Egeland FM. Echeverria D. Sandborgh-englund B. Rosenbaum G. Bidstrup PL. Pb. Conradi N. Environ Res 1998. Environ Health Perspect 2003. Martin MD. Schaller KH. Atlanta (GA). Dewailly E. Bruneau S. Debes F. Cincinnati (OH): Signature Publications. selenium. Osterloh JD. Weihe P. Falk R. Int J Hyg Environ Health 2003. Aposian HV. Caldwell KL. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Luis H. ACGIH. I. Environ Health Perspect 2005. Woods JS.

Environ Health Perspect 2004. Myers GJ.5:252-257. Mercury concentrations in urine and whole blood associated with amalgam exposure in a US military population. Tillander M. Cernichari. Schultz A. Sallsten G. Matsumoto S.51(3):234-241. Rissanen K. Renal and immunological effects of occupational exposure to inorganic mercury. Volume 58. Ann Intern Med 1963. Korolainen A. Sandborgh-Englund G. Korpela H. Circulation 1995. Voutilainen S. KajiwaraY. Allen J.5:214-219. IARC Monographs on the Evaluation of Risks to Humans. Nakano A. National Research Council (NRC). The distribution and biological half-time of 203 Hg in the human body according to a modified whole-body counting technique. Hursh JB. Pellizzari E. docosahexenoic acid and docosapentaenoic acid. Ceulemans E. cardiovascular. Murata K. Yasutake A. Barregard L. Schutz A. and the risk of acute coronary events— The Kuopio Ischaemic Heart Disease Risk Factor Study. Elinder CG. Schutz A. Seppanen K. Fourth National Report on Human Exposure to Environmental Chemicals 225 . Satoh H. Patterson DG Jr. and the risk of myocardial infarction and coronary. Bolger PM. Hattula T. and multiracial groups. Ekstrand J.361:1686-1692. arsenic.iarc. J Dent Res 1998. The effect of ethanol on the fate of mercury vapor inhaled by man. et al. Miettinen JK.59(5):692-706. Mehaffey KR. Nakai K. 1993. Declining risk of methylmercury exposure to infants during lactation. Nakamoto S. McDowell MA.13:496-501. lipid peroxidation. Cox C. Fish oil-derived fatty acids. et al. Hernandez GT.php. Environ Res 1995.71(1):29-38. Osterloh J. Rahola T. Prenatal methylmercury exposure from ocean fish consumption in the Seychelles child development study. 7/15/09 Jonsson F. children and women of childbearing age: reference range data from NHANES 1999-2000. Environ Health Perspect 2004. Ann Clin Res 1971.103:2766-2679. Intake of mercury from fish. et al. Hair mercury levels in U. Rice DC. Arch Toxicol 1996. Ohlin B. Lauwerys RR. Halbach S.112(5):562-570.48:247-53. Kingman A. Langworth S. Shamlaye CF. Environ Health Perspect 2006. Available at URL: http:// monographs. O’Hare A. J Pharmacol Exp Ther 1980. Fernando R. Burse VW. Weihe P. Washington (DC). Blood organic mercury and dietary intake: National Health and Nutrition Examination Survey. Langworth S.50(9):814-821. Acute mercurial intoxication treated by hemodialysis. Environ Res 2002. J Dent Res 1998. Kubota M. Environ Sci Technol 2004. Boeckx M. Kolff WJ. Oskarsson A. Br J Ind Med 1991. Elimination of free and protein-bound ionic mercury (203Hg2+) in man. Toxicological effects of methylmercury.S.77(4):615-624. Lagerkvist BJ. Skerfving S. Clickner RP. and Exposures in the Glass Manufacturing industry. National Academy Press. Sampson EJ.112(11):1165-1171. Blood mercury reporting in NHANES: Identifying Asian. Rahola T. Urinary excretion of mercury after occupational exposure to mercury vapor and influence of the chelating agent meso-2. Dillon CF.77(3):461-467. 2000. Miettinen JK. Native American. and any death in eastern Finnish men. Hattula T. Roels HA. Greenwood MR. Hightower JM.70(5):310-314. Hum Exp Toxicol 1994.38:3860-3863.3dimercaptosuccinic acid (DMSA). methylmercury transport across the placenta via neutral amino acid carrier. Brown LJ. Lakka TA. Demuth S. Circulation 2000. Ann Clin Res 1973. et al. Rissanen T. Akagi H. Salonen JT. Pacific Islander. Mercury.155(2):161-168. Kauhanen J. A compartmental model for the kinetics of mercury vapor in humans. Needham LL. Environ Physiol Biochem 1975. Elimination of 203Hg-methyl mercury in man. Decrease in mercury concentration in blood after long term exposure: a kinetic study of chloralkali workers. Toxicol Appl Pharmacol 1999. Nyyssonen K. Bodurow CC. Clarkson TW.3(2):116-122. Sakamoto M.91:645655.fr/ENG/Monographs/vol58/index.95:406-13. Kubota M. Environ Res 2004. Arch Environ Health 1996. Hallen IP. Amalgam tooth fillings and man’s mercury burden. Palumbo D. Relation of a seafood diet to mercury.214(3):520-527. and polychlorinated biphenyl and other organochlorine concentrations in human milk.49(6):394-401. International Agency for Research on Cancer (IARC). Davidson PW. Sakamoto M. Elinder CG. Beryllium. Hattula T.Metals Grandjean P. Cadmium. selenium. Lancet 2003. Maternal and fetal mercury and n-3 polyunsaturated fatty acids as a risk and benefit of fish consumption to fetus. Br J Ind Med 1993. Kantola M.90:185-189. Sundquist KG. Liu XJ. The US EPA reference dose for methyl mercury: sources of uncertainty. Johanson G. Nyyssonen K. Mercury in biological fluids after amalgam removal. Sandborgh-Englund G. Total and inorganic mercury in breast milk and blood in relation to fish consumption and amalgam fillings in lactating women. 1999 and 2000.114(2):173-175. Vesterberg O. Hirayama K. Adachi T. Salonen JT. Br J Ind Med 1992. Seto DS. Albertini T. Rahola T. Sanchez-Sicilia L.

37:245-252. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Kaye WE. McDowell M. Imai H.258(4 Pt 2):R939-945. Amiano P. DeRouen TA. Vahter M. Orr MF. Goldberg J. Leroux BG. Effects of occupational exposure to elemental mercury on short term memory. Daniels JL.110:129-132. Most B. Toxicol Appl Pharmacol 1994. Environ Health Perspect 2002. Yoshinaga J. Vorwald AJ. Lorscheider FL. Bolger PM. Sherlock J. Suzuki T. Takahashi Y. Hislop D. Schober SE. Allen PV. Baser M. Matsuo N. Aguinagalde FX. Sinks TH. Azpiri MA. Jones RL. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Effects of exposure to mercury in the manufacture of chlorine. Langolf GD. Friberg L.2:117-131.48(4):221229. Arch Environ Health 1993. Vimy MJ. Fisher HL. Smith JC. Smith PJ. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. 1993-1998. Farris FF. Toxicol Appl Pharmacol 1996. The hair-organ relationship in mercury concentration in contemporary Japanese. Lind B. Woods JS. Martin MD.97(2):195-200. Methyl mercury pharmacokinetics in man: a reevaluation. Environ Res 2005. Environ Health Perspect 2007. Environ Health Perspect 2003. Topping G.98(1):133-142. Stern AH. Smith AE. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Acrodynia: exposure to mercury from fluorescent light bulbs. JAMA 2003. Smith RG. Osterloh J. Turner MD. Vupputuri S. McMahon KJ.124:221-229.289(13):1667-1674. Patil LS. Nakazawa M. et al. Guo S. Tunnessen WW. Mooney TF. Public Health Nutr 2001. Stern AH. Newton G. Amurrio A.Metals Sanzo JM.128(2):25125-25126.115(10):1527-1531. Burbacher T. Whittle K. 1999-2000. Hall LL. Am J Physiol 1990. The kinetics of intravenously administered methyl mercury in man. Toxicol Appl Pharmacol 1994. Mottet NK. Hum Toxicol 1984. Dorronsoro M.4(5):981-988. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Pediatrics 1987. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Environ Res 2005. Sandler DP. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Smith JC. et al. Leitao JG. Am Ind Hyg Assoc J 1970.111(12):1465-1470. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. The contribution of dental amalgam to urinary mercury excretion in children. Br J Ind Med 1983. Longnecker MP.31:687-700. Shen DD.79:786789. Bernardo MF. Hongo T. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Blood mercury levels in US children and women of childbearing age. Zeitz P.40:413-419. et al.

5 (74.8 (67.9-82.4 (34.0 (48. 7439-98-7 General Information Elemental molybdenum is a silver-white.0-110) 90.0 (43.6-111) 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 52.5-41.3-115) 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.4) 49.1-44.0-100) 63.9 (40.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.8) 40. Fourth National Report on Human Exposure to Environmental Chemicals 227 .2 (49.7 (36. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.6) Selected percentiles ( 95% confidence interval) 50th 50.4) 41.3) 41.7 (50.0 (42.5 (37.1) 57.5) 44.2) 48.3 (38.5) 80.9 (73.7) 46.2 (69.4) 56. and 03-04 are 0.6 (73.5-124) 108 (92.7-84.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.3) 85.0) 84. population from the National Health and Nutrition Examination survey.9 (44. Compounds of molybdenum are also used as corrosion inhibitors.4-82.6) 71.3 (55.5-68.4 (48.1-52.7) 51.7 (73.7) 86.9 (52.4 (48.0-53.5 (41.1) 60.2-79.7-68.2 (49.8-94.3 (55.7 (37.1 (34.5 (43.2) 37.3 (73. 2001.4) 76.3 (84.3 (64.5-66. More recently.2-53.9-55.3-91.2-37.1) 126 (106-147) 109 (94.3 (47.8-108) 87.1-63.6-82. 2001).7-92.0 (42.9 (37.9 (32.1 (71.7-50.5 (41. and in pigments for ceramics.2) 79.9-85.5) 47.0-56.7) 77.2-91.0 (46.3-44.9 (78.8.0) 55.6-58.6 (43.0-65.7 (51.7) 45.0 (41.2-59.0-85.7) 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. 01-02.1) 59. inks.6) 51.6) 93.3 (71.3-47. In humans.0-38. lubricants.8) 46. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.0) 97.4-75.4 (80. interval) 45.2 (38.6-72.2-42.1) 46.3 (79.5-52.9-55.7 (45.5-65.5-91.9-56.8 (82.1-48. hydrogenation catalysts. which exert homeostatic regulation over molybdenum balance.3 (46.4-52.8-106) 88.2-59.8.5 (49.0-77.8 (85.2) 41.0) 62.7-91.7-105) 69.2) 40. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.9 (33.2 (83. 0.3) 54.6 (40.5 (81.0) 54.3-75.0-62.4) 45.8) 39.8-46.4 (72.2) 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 (98.0 (76.0 (81.2 (40.7-47.7-96.9-83. aldehyde dehydrogenase.7-60.2) 52.8) 48.1) 35.1 (91.3-108) 215 (161-278) 169 (145-194) 148 (136-163) 154 (132-180) 158 (130-177) 127 (114-139) 1121 1335 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 47.2 (55.3) 65.1-88. 1996).9) 67.5 (67. and paints.3) 47. and xanthine oxidase (Kisker et al.6) 53.9) 62.6) 71. semiconductor and battery industries have begun to use molybdenum.1 (38.8-49. 1997).5-52.7-41.7 (44.4) 42.3 (53.6 (55.4-61.4) 52.7-122) 93. At a daily oral molybdenum dose of 24 µg.5.6 (55. The recommended dietary allowance for adult men and women is 45 µg/day (IOM. respectively.8) 75.9-109) 97.2) 53.3) 83. see Data Analysis section) for survey years 99-00. Excretion occurs predominantly via the kidneys.1-52. urinary excretion over six days CAS No..1-55.8-90.0) 60. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.1-51. WHO.5) 85.7 (58.5) 60.9) 34.4 (79.6-96.7-51.6) 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) 37.0-71.7-73.7) 78. Molybdenum occurs in natural waters and may be present in concentrations of several hundred micrograms per liter or higher in ground and surface water near mining operations Urinary Molybdenum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5 (48.9 (34.0) 39.6 (52.7 (71.6 (40.7) 78.5) 80.8 (42.2 (61.1-59.Metals Molybdenum or ore deposits.S. and 1.6-46.2-70.2 (56.5-46.0-101) 82.2 (63.6-62.3 (37.8) 44.0) 45.7) 57.6-42.7) 75th 84.7-39. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. chemical reagents in hospital laboratories.1) 82.6-55.

4-120) 101 (84. but available epidemiologic data are scant.9) 41. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.0) 39.5 (59.5) 90th 108 (97.1 (40.6 (59.4 (37.3 (51.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.Metals was 18% of the ingested dose.8-47.9-40.4 (78.4) 116 (101-126) 104 (88.2) 39.6) 36.7 (75.2-65.1 (49.0) 88. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.6-61.1-43.0) 72.2-47.4) 44.2) 43.0 (35. U.5 (41.6-45.9 (36.7) 42.4-66.1 (39.0-46.8) 38.8-47.6 (42. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.0-120) 85.3) 56.5 (54.0-41.6-88.8 (36.2 (33.3 (53.8-65.2) 55. respectively.5 (80.5-46.1-81.8) 38.4 (67.5 (40. 2001). EPA.3-52.8-84.6) 43.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.0-103) 103 (90.3 (36.2-96.7) 41.5-70. and clinical or epidemiologic evidence of adverse effects is limited.2 (50.8-67.2-103) 131 (112-179) 123 (107-155) 118 (100-139) 152 (122-181) 136 (117-169) 122 (115-142) 1121 1334 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 42.1-39.0 (74.7-120) 87.6 (57.2 (43.5 (65.5-92.3) 43..2-40.5 (65.1-127) 90.4) 47.5-119) 90.3-115) 98.1-38.1-34. 1995)..4 (59.0) 53.2) 42.2 (57.6) 39.8-42.5-60. Based on studies finding adverse reproductive effects in rats and mice.5-45.9) 79.5-97.9) 40.5-48.7-62.9-96.7-44.6-76.7 (66.4) 122 (107-133) 109 (99.1) 37.3-44.7-38.5 (83. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.2-49.3) 37.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.1) 101 (83.7) 57.1-43.5 (39. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5-35.0) 62.7-43.2) 37.1 (44.9-87.0-38.2-41.3-102) 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 40.2-121) 107 (92.3-43.8 (90.0 (80.3 (83.8) 79.9-41.8 (56.9 (40.5-99.9 (79.5) 60.0 (58.0) 33. In industry.6 (71.5 (50.2-46.1-79.3-68.5-44.8 (57.8) 71.1 (82.S.0-133) 119 (88.3) 61.3 (58.0) 36.4 (44.2 (73.9) 44.5) 71.1 (37.1-67.4 (40. 1993).4-39.7) 112 (95.5 (37.2 (52.5) 72.7-52.9 (64.5 (40. 1997).5 (79.6 (36.4-106) 85.9 (35.8-52.5 (39.4) 77.4-118) 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 .7) 75th 63.2) 39.S.7-93.4) 58.3-141) 109 (81.4-107) 85. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.1 (30.6) Selected percentiles ( 95% confidence interval) 50th 41.1 (54.6) 39.6-61.9-71.3 (37.4 (53.5 (41.9) 92.4) 89.1-40.4) 61.3 (37. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.7) 62.7) 115 (93.8) 37.4-42.1) 37.9 (39. Biomonitoring Information Molybdenum is an essential element for health.9-45.8) 62.6) 48.2) 42.8 (37.2 (40.0-56.5-62.7) 53.1-112) 78.1-45.9 (39.5 (35.7 (77.9 (73.2) 37. 1999).4-41. at daily oral doses of 95 µg and 428 µg.2 (36.8-118) 81.7-40.9 (49.9 mg/kg/day and established a tolerable upper intake level of 0.1 (33.5) 73.6-63. interval) 43.3) 41.4) 40.4 (55.8) 45.9 (64.6 (36.8) 61.5-69.9-45.9) 31.3-45.9-61.3 (55.2 (37.8) 39.4-76.7-137) 129 (109-155) 112 (97. urinary excretion over six days rose to 50% and 67%.6-63.0) 39.1 (38.9-117) 57.6 (38.8-66.3) 44.0-46.3) 57. population from the National Health and Nutrition Examination survey.1-39.2) 38.2 (69.7-100) 77. 1961.3) 40.1 (38.5) 63.3-59.1) 65.8-46. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.03 mg/kg/day in humans (IOM.9-118) 91.4) 48.2-80.7) 45.1 (42.1) 56.1-100) 86.9-42.1) 43.5 (35. Molybdenum is generally considered to be of low human toxicity.8 (75.4 (56.2) 58.6-41.5 (34.2 (40.1-41.4) 60.5-50.0) 44.7 (30. and urinary levels reflect intake from all sources.1) 40.2-96.4-185) 106 (94.6-78.3-46.3-56.3 (71.0) 38. of the ingested dose (Turnlund et al.3 (36.5 (37.3) 64.5 (38.5 (36.2 (40.5 (78..1-109) 89.3 (71.9-68.

Minoia et al.S. 16:1313-1319. 1996. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. iron. National Toxicology Program (NTP). population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. World Health Organization (WHO). Keyes WR.S. Schindelin H. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. X. Geneva: WHO. vitamin K. van Sprundel MP. Dietary reference intakes for vitamin A. 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. copper. 2005. 1998). Peiffer GL. J Trace Elem Med Biol 2001. Sciarra G..S.66:233-267. Kristiansen J. Droste JHJ. pp. Van Meerbeeck JP. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Molybdenum.22(3):179-191. Schleyerbach U. manganese. Institute of Medicine (IOM). 56:322-327. Available at URL: http://ntp. 144-154. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes.nap. 1998. Rapid Comm Mass Spectrom 2002. Sabbioni E. (DC): National Academy Press. Trace element reference values in tissues from inhabitants of the European Union. Gatti A. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. pp. iodine. Environmental Protection Agency (U.niehs.. edu/openbook.nih. Aprea C. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. 4/14/09 Iversen BS. White MA. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8.Metals in urine for the U. 2005). chromium. Sci Total Environ 1998. 420-441. Schaub J. U. Koval’skiy GA. Rees DC. Yarovaya GA. Zhurnal Obshchey Biologii 1961.62(4):790-796. 4/14/09 Sievers E. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Menne C.gov/index. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Molybdenum absorption. TR-462. A study of 13 elements in blood and urine of a United Kingdom population. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Kisker C. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Occup Environ Med 1999. Molybdenum-cofactorcontaining enzymes: structure and mechanism. 4/14/09 White MA. 2001. Weyler JJ.. 2001). References Centers for Disease Control and Prevention (CDC).gov/iris/ subst/0425. Turnlund JR. et al.123(1):81-85. Minoia C. Available at URL: http://books. Am J Clin Nutr 1995. Ann Rev Biochem 1997. Available at URL: http://www. nickel. and zinc: a report of the Panel on Micronutrients. Vermeire PA. EPA). Third National Report on Human Exposure to Environmental Chemicals. Shmavonyan DM.php?record_id=10026&page=420. Washington. Analyst 1998. Ronchi A. White and Sabbioni. Occupational risk factors of lung cancer: a hospital based case-control study.epa. boron. excretion. Atlanta (GA).htm. Molybdenum in infancy: methodical investigation of urinary excretion. vanadium. silicon. Christensen JM. arsenic. 2002. Food and Nutrition Board.216:253-270. In: Trace elements in human nutrition and health. molybdenum. Molybdenum 1993 [online].15(2-3):149-154. Turci R. Sabbioni E.

0. and high catalytic activity. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. Platinum compounds are used in electrodes. jewelry. 7440-06-4 General Information Platinum is a silver-gray. and iron. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. dental alloys. cisplatin. 1998). < LOD means less than the limit of detection. and 03-04 are 0. thick-film circuits printed on ceramic substrates. Important properties of platinum are resistance to corrosion. 230 Fourth National Report on Human Exposure to Environmental Chemicals . 01-02. and 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. respectively.g. the ambient air concentrations of platinum associated with its use in automotive engine catalytic converters are estimated to be thousands of times lower than occupational exposure limits. see Data Analysis section) for Survey years 99-00.04. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.04. population from the National Health and Nutrition Examination Survey. carboplatin) in the treatment of cancer.S. 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. however.. copper..07. which may vary for some chemicals by year and by individual sample. strength at high temperatures. and as drugs (e.Metals Platinum CAS No. as oxidation catalysts in chemical manufacturing.

. 1975b). Toxicity is determined by the type of compound (e. halogenated salts) encountered in occupational settings can cause platinum salt hypersensitivity with symptoms that include bronchitis and asthma after inhalational exposure and contact dermatitis after skin exposure. platinum metal and insoluble salts are very poorly absorbed (<1% of a dose) and cleared from the body within a week after a single dose.Metals doses or at biomonitored levels from low environmental exposures are unknown.. 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. inhalational. Saindelle et al. Platinum metal and insoluble salts can produce eye irritation. Most absorbed platinum accumulates in the kidneys and is excreted in urine (Moore et al. The carcinogenicity of other platinum compounds remains uncertain. 1969). 1969.e. or recommended for the metal form by NIOSH (Czerczak and Gromiec. The pharmaceutical cisplatin is an animal carcinogen and reasonably anticipated to be a human carcinogen as determined by NTP. 2000). Platinum metal is biologically inert.. 1975a. whereas soluble platinum compounds (e. route of exposure (e. metallic. Animals exposed to cholorplatinate salts used in industry have demonstrated severe hypersensitivity with asthma-like symptoms and anaphylactic shock (Parrot et al.. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.g.. or organometallic). oral). cutaneous.S. Workplace air standards for external exposure are established for soluble salts of platinum by OSHA and ACGIH. Fourth National Report on Human Exposure to Environmental Chemicals 231 . 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. Information about external exposure (i.. When ingested or inhaled. inorganic salt.g.. and duration of exposure. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.g. population from the National Health and Nutrition Examination Survey. intravenous medicinal use.

Kaus S. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Ruff F: Histamine release by sodium cholorplatinate. Campbell K. Platinum concentrations in urban road dust and soil.. rhodium. Raab W. Iavicoli I. which elevate urinary platinum by five to twelve-fold (Begerow et al. 2003). Schierl R. Available at URL: http://www. Carelli G. Schierl R. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. pp. Part 1: monitoring of urinary concentrations. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Fries HG.. Wilhelm et al. Turfeld M. Schierl R. Grimm CH.10:63-71. Cohrssen B.org/documents/ehc/ehc/ehc125. ruthenium.. Czerczak S. Several studies have shown that background concentrations in general populations were usually less than 0. Thornton I. 2003. J Expo Anal Environ Epidemiol 2003. Kulka U. osmium. Gieler U. Environ Res 1975a. Allergy and histamine release due to some platinum salts. Urinary platinum levels associated with dental gold alloys. Saindelle A. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Kazantzis G. Biomarkers 1999. Schierl R. eds. Begerow J. Schulz C.123(3):451-454. population were below the limit of detection (0. 2003. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. 1998). Angerer J. et al. Saindelle A. Herr CE.005 µg/L (Iavicoli et al. Br J Pharmacol 1969. Schierl. 206:15-24. 2003.04 µg/L) in this Report. Nowak D. Kuster W. Nickel. Rommelt H. References Becker K. Analyst 1998. New York: John Wiley & Sons. 1997. Alimonti A. Platinum. Int Arch Occup Environ Health 1997. Schulz C. Parrot JL..13(1):24-30. Jankofsky M.. Bocca B.htm. Stilianakis NI.70(3):205-208. palladium. Moore W Jr. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Pethran et al. Occup Environ Med 2004. Farago ME. Arch Environ Health 2001. Patty’s Toxicology. Crocker W. Boos KS.. et al. et al. 2004) or less than 0.35:313-321. 2004).. Levels of platinum in urine for the U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Wilhelm M. Ewers U. Hauff K.01 µg/L (Becker et al.org/documents/ehc/ehc/ ehc125. Blanks R. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. and platinum..61(7):636-9. Duneman L:Long-term urinary platinum. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. et al. and gold excretion of patients after insertion of noble-metal dental alloys. 5th ed.htm. 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. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. 3/31/08 Moore W Jr.Metals the International Programme on Chemical Safety at http:// www. 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. 1991 [online]. Int J Hyg Environ Health 2004. Hysell D.inchem.55(2):138-140. Biomonitoring Information Urinary platinum levels reflect recent exposure. Arch Environ Health:1969.76(1):5-10. Uptake of antineoplastic agents in pharmacy and hospital personnel. 2000. Pethran A. Kavanagh P. Seiwert M.9:152-158. Seifert B. Hysell D. Ruff F: Platinum and platinosis. 2004. Int Arch Occup Environ Health 2003. Hebert R. Influences on human internal exposure to environmental platinum. Gromiec JP. Neuendorf J.4(1):27-36.19:685-691. Hall L. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Fruhmann G.S. International Journal of Hygiene and Environmental Health 2003. 289-380. van de Weyer C. and in blood and urine in the United Kingdom. Huber R. 1998). 1999. Kelly J. Environmental Health Criteria 125. Pethran A. Urinary excretion of platinum from platinum-industry workers.. Herr et al.inchem. Biomonitoring of traffic police officers exposed to airborne platinum. Powell CH.. palladium. In: Bingham E. Environ Health Perspect 1975b. 2001). Schierl et al. Ensslin AS.207(1):69-73. International Programme on Chemical Safety (IPCS). Senofonte O.56(3):283-286. Petrucci F. Herr et al. Occup Environ Med 1998.

410 (.360-.134-.290-.470) .320) .180 (.170) .196) .330) .159 (.220 (.340-.160-.217 (.160 (.350) .260) .280) .520 (. respectively.450 (. Fourth National Report on Human Exposure to Environmental Chemicals 233 .160 (. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.400) .300 (.150-.280 (.220 (.206) .420-.340) .171 (.196) .02.340) .370-.450 (.202) .S.470 (.390 (.218) .400 (.440) .250 (.201 (.270 (.360-.159 (.290) 90th .450 (.145-.290 (.180) 75th .270) .310) .190 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.510) .167-.192) Selected percentiles ( 95% confidence interval) 50th .350 (.270 (.260-.200-.330-.240-.370-.200) .02.137-. In the past.145-.250-.260-.430) .200 (.167-.173) .390) .197 (.220) .360-.400-.260-.400) .200-.520) .170-.149 (.290 (.190-.340-.280) .200 (.210 (.360-.280-.160 (.230 (.176 (. In the United States.170) . 01-02.200) .200 (.135-.400 (.160-. Thallium disappears from the blood with a half-life of several days.340 (.156) .170-.480) .175) .173) .197-.300) .500 (.390-.210-.260-.300-.400 (.167 (.320) .340-.350-.150-.460-.270 (.240) . Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.450) .640) .350-.177) .450 (.410-.250-.200) .450 (.550 (.280 (.250-.330) .380 (.260 (.183) .147-.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 .320) .159 (.230) .390) .500) .184 (.163) .310 (.330-.360) .330-.170) .200) .155 (.240-.290) . and 0.220) .170 (.140-. it has not been specifically mined or refined in the United States since 1984.320 (.420) .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 .170 (.350-. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.200 (.210) .410 (.280) .200-.470) .150-.188) .410-.145 (.380) .260-.400) 95th .230-.350-.310 (.250-.380 (.220-.690) .230-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.350 (.191 (.360 (.225) .240) .290-.200) .220 (.460) .430) .390-.490) .200 (.02.520) .470 (.390-. population from the National Health and Nutrition Examination Survey.270) .250 (..170-.370 (.630) .420) .160-.210 (.590) .172) .370 (.500) .510 (. interval) .220 (.440) .250-.410-.165 (.360 (.400) .270 (.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 . From these and other sources.187-.180-.410-.490) .300) .270-.201 (.400-.380-.290) .400-. see Data Analysis section) for Survey years 99-00.370 (.160 (.290 (.180-.370 (. Human health effects from thallium at low environmental CAS No.420-.202 (.270 (.250) .350-.220) .390) .490) .154-.170-.180 (.420) .460 (.160-.410-.200-.420) .190 (.420) .440 (.Metals Thallium depilatory cosmetics.330-.290 (.230) .185-.182-.310-.147-.370 (.430 (.480) . the latter being the current major industrial consumer of thallium in this country.590) .170 (.148-.300 (.180) .185 (.190 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.170-.243) .240) .280 (.430 (.156) .560) .170-.147-.190 (.480) . however.290) .260 (.370) .480) .450 (.400-.450 (.350-.430-.180 (.144 (.470) .150-.400) .250-.360 (. 0.420-.370-.202 (.217) .330) .320-.220) .440-.370) .330-.240-.300 (.440 (.420) .146 (.310 (.270-.500) .490 (.380-.440 (.160-.370 (.150-. representing distribution into other tissues.300) .157-.520) .260 (.153-.360 (.410 (.360-.340-.178) .450 (.330) . thallium was obtained as a by-product of smelting other metals.160 (.250-.290) . thallium readily crosses the placenta and also distributes into breast milk.150-.480) .410) .162-.410 (.330-.156-.230-.400 (.180-.230) .270-.430 (.450 (.300) .370 (.390 (. In addition.440 (.280-.400 (.400-.220 (.430-.183) .218) .158) .220) .420-.220) .410-.390) .350) .172 (.430-.181-.290 (.180-.330-.190 (.440) .200 (.410 (.215) . 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.133-.239) .200) .420 (.173-.430 (.190 (.370-.170-.172 (.290 (.420) . and 03-04 are 0.250-.410 (.179-. 2005).490) Total .390-.230) .

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

Gallorini M. Pirkle JL. 2005. Pietra R. Available at URL: http://www. Investigations of thallium-exposed workers in cement factories. Sci Total Environ 1998. 1992 [online]. Martin J-C. Valentin H.35(1):4-9. 1990. Schaller KH. White and Sabbioni.cdc.47(3):223-231. 1981. Soddemann H. Cassot G. Int Arch Occup Environ Health 1981.. J Soc Occup Med 1985. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1998. Boisson P. et al. et al. Ting BG.1 mg/m3 (Marcus. Radiat Prot Dosim. Kramer U. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Apostoli P. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Trace element reference values in tissues from inhabitants of the European Union. Morrow JC. A study of 13 elements in blood and urine of a United Kingdom population. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Ewers U. Marcus RL. blood. Environ Res 1998.gov/toxprofiles/tp54. Trace metals in urine of United States residents: reference range concentrations. Minoia et al. Brockhaus et al.5 μg/L. White MA. X. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. References Agency for Toxic Substances and Disease Registry (ATSDR).76(1):53-59. Investigation of a working population exposed to thallium.. Minoia C.95:89-105.216:253-270.html. Sci Total Environ 1990. Sabbioni E. 1980. Centers for Disease Control and Prevention. Schaller et al. Sabbioni E. 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. A study of 46 elements in urine. Wiegand H. Celier D. et al.. Atlanta (GA).S. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Jackson RJ. Paschal et al. with concentrations ranging up to 76.Metals (CDC. 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. Sampson EJ. Third National Report on Human Exposure to Environmental Chemicals. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. and serum of Italian subjects. Toxicological profile for thallium.atsdr. Buhlmeyer G. Int Arch Occup Environ Health 1980. Dolger R. 7/15/09 Blanchardon E.113(1):47-53. Raithel HJ. Pozzoli L. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Challeton-de Vathaire C.. 2005) and are shown with results from NHANES 2003-2004 in this Report.265 people living near a thallium-emitting cement plant in Germany. Paschal DC. 1998). Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. 1985). Manke G. Schmidt M. (1981) studied 1. 2005. Trace element reference values in tissues from inhabitants of the European community I.48(4):375-389. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Brockhaus A.

330-. mainly as scheelite (CaWO4).300-.260 (.350) .290 (.120-.180) .220) .470 (.460 (.130-.097-.340-.110 (.073) .280 (. interval) .086 (.116) .120) .120-.270-.570 (.060-.100-.170) .250-.380-.180-.500 (.280 (.310-.200 (.300) 95th .104) .170) .450 (. Evidence is lacking for the carcinogenicity of tungsten.080 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.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 .090 (.550 (.090-.670) . Little information is available on the toxicity of tungsten.270 (.790) .090) .070 (.151) .320 (.380-.120 (.140 (.300 (.130 (.470 (.056-.260-.430 (.230-.080 (.120-.082) .220) .130) .690) . which is used in the steel industry.160-.160 (.160 (.570 (.109) .340) .100) .090-.370) .056-.300) .350 (.380) .360) .088 (.060 (.310-.Metals Tungsten CAS No. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.060 (.560) .080 (.520) . which are used in rock drills and metal-cutting tools.070-.110-.150 (.070) .460 (.076 (.100 (. and 03-04 are 0.070) . and 0.080-.290-.560) .082 (.320 (.070-.250) . Occupational exposure is from dusts released during grinding or drilling of hard metals.470) .190-.300 (. bronzes in pigments.180) .330-.180-. 01-02.210) .113 (.100) .340-.060 (.260) .770 (.150 (.470) .240-.100) . and for producing ferrotungsten.100 (.060-.530 (.070-.210 (.122) .140 (.290-.330) .200) .092 (.330 (. filaments for incandescent lamps.180-.060-.410-.170 (.064-.110 (.00) .096 (.230-.620) .158 (. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone. and as catalysts in the petroleum industry.810) .100 (.430 (.100-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.550) .190-.100) .350-1.220) .440) .095-.060 (.210-.470-.065-.550) .093-.160 (.230 (.230-.620) .420-.340-.100) .160) .120) .320-.113 (.410 (.060 (.087-.400 (.190 (. population from the National Health and Nutrition Examination Survey.190 (.110-.360-.076 (.084-.250) .400 (.310) .370 (.950) .050-.400) .060-.250) .250) .140) 90th .113 (.210 (.091) .560) .100-.084) .160-.180) .095-.069-.170) .150 (.092) .101 (. see Data Analysis section) for Survey years 99-00.062 (.350) .080) .090-.135) .110) .620 (.510-1.420-.100) Selected percentiles ( 95% confidence interval) 50th .380-.220-.190) .370 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.230) .390) .132) .320) .360 (.800) .270-.093 (.080 (.550) .080) 75th .101-.830) .050-.490 (.100 (.360 (.080-.050-.087) .090-.070) .074-.160 (.210 (.250) .260 (.081 (.310-.120) .460) .430-.260-.068) .320-.380 (.170) .310 (.380-.070-.077-.490) .150-.430-.073-.360-.107 (.133) .170 (.073 (.090) .070-.580) .082 (.560) .310-.200-.204) .04.180 (.04.113 (. 0.090-.800) . Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water. 236 Fourth National Report on Human Exposure to Environmental Chemicals .140-.260-.430 (.110) .071-.630) .190-.080 (.500 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.170-.069) .460) .S.058-.110 (.088) .650) .120) .070) .160-.300 (.250) .110 (.140-.270-.480) Total .310-.130-.430) .090 (.520) .105 (.062 (.330) .090-.073-.290) .400 (.080) .370-.230-.04.080-.160 (.530 (.130) .510-.070 (.640 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).130-.520) .090 (.066-.290) .092 (.060-.160) .210 (.126) .130-.140 (.065 (.53) .280-.270 (.230) .080) .120) .140 (.120-.360 (.530 (.160-.180-.130) .450-.090) .590) .120-.137 (.130) . Tungsten is used mainly for producing hard metals.071 (.110 (.060-. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.130) .400-.123-.120-.070 (.500) .460 (.120) . respectively.290-.270-.240 (.150) .180) .084 (.250-.096-.210 (.370-.093) .090-.090-.390 (.090) .350) .060 (.560 (.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 .180 (.510 (.370 (.220 (.082-.110-. Tungsten compounds are used as lubricating agents.190-.078-.270 (.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 .111-.380 (.050-.400 (.105) .130 (.

078 (.079) .122-.146 (.065-.111 (.077-.301) .208-.188-.056-.431) .184 (.088) .186 (.197) .081) .255 (. similar to those in this Report (Schramel et al.133) .823) .122-.061-.339 (.237) .063-.060-.136-.082) .099-.057-.453) .150-.167) .098-.084) . population.333) .075 (.381) .167-.091) . population (CDC.108) .059-.359 (.412 (.094-.364 (.078-.080-.068 (.086) .125) .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.329-.121-.216-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.333) .299 (.287) .158) .353 (.293 (.205-.199 (.131-.080 (.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 .414) . 1997).085-.333 (.222) .078) .061-.250 (.150 (.065 (.087) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.091 (.S.217-.174) .217-.144 (.(Kraus et al.197-.072-.071) .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 .095) Selected percentiles ( 95% confidence interval) 50th .199 (.071) .727) .329 (.085 (.059-.462) .222-..086-.083-.339 (. measure urinary tungsten.436) .056-.170-.294 (.347 (.605) .452-.739) .333-.143 (.S.158) .209-.153) .465) . 2003.146) .083 (.174 (.306) .333-.120) .201) .077-.431) .138) .216-. 2001).065-.139) .064-.079) .317 (.054-.107-.055-.105 (.385 (.358) . Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.302-.484 (.086) .439 (.133) .098) .104-.071-.265 (.096) .379 (.302-.105 (.078 (.S.066 (.341 (.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 .150-.383 (.167) .240-.078) .333 (.206-.283) .091) .169 (.253) 95th .165) .359 (.116-. 2005).079 (.275 (. (1987) found possibly due to methodologic.125 (.261-.116) .126-.075) .200-.187) .203-.119 (.301) .068-.253-.122 (. 2001-2002.308) .497 (.121 (.060 (.198-.059 (.153-.431) .093) .258-.255-.124-.079) .073 (.109 (.333 (.098-.080-.555 (.081 (.124 (.069 (.151 (.148) .169) .095-.057-.279 (.074 (.326) . population from the National Health and Nutrition Examination Survey.176-..354-.077) .272-.091) .308) .091 (.426) .144-.089 (.216 (.218 (.059-.214) .154) .250-.083) .237) .436-1.065) .074) .216 (.176-.582) .064-.063 (.181 (.139 (.180-.084 (.069 (.136 (.087 (.075 (.333 (.315-.224) .465) .075-.081 (.211 (.250 (.088) .130 (.360 (.344-.133) 90th . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.152-.108-.092) .079 (.100 (.161) .179-. 1998).093-.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 . and 2003-2004 (Paschal et al.286-.054-.164 (.103-.071) .410-.063-.063 (.157) ..136-.053-.073 (.300-.216-.179-.267-.201 (.100) .080 (.081-.061-.214-.089) .28) .130-.148 (.245-.098 (.069-.062 (.079) .136-.231-.094) .426) .197 (.300) . or exposure that a control group of non-metal workers had mean levels differences.482 (.085) .117) .300 (.284) .634 (.066 (.143-.279 (.072-.231 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.167-.484) .500) .060-.270 (.074-.667 (.138 (.067 (.074) 75th .073 (.083) .190) .082) .082 (.554) .168 (.797) .098-.233-.086) .317) .067-.667) .146 (.071 (.279 (.353 (.117 (.071 (.136-.067 (. 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.090-.063-.109-.070 (.072 (.106 (.198) .084 (.255 (.331-.154) .258 (.538) .340 (.065-.392) .880) . Patients with medically-inserted tungsten found at increased levels in drinking water.070 (. Nicolaou et al.049-.138 (.083 (.065 (.075) .439 (.063-.278-.074-.155-.077) .119-.091) .200-.267) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.215) .253 (. interval) .145 (.215 (.090-.094) .116 (.197) .071 (.317-.120) .100) .084) .285) .139-.073 (. Using neutron activation analysis to 2000.158 (.354) .459) .075-.058-.300-.301) .237-.158) .386) .439) Total .375) .

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

022-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.114 (.013-.008 (.008) .014 (.010) .008 (.022 (.007 (.006 (.046 (.007-.065) .009) .007) .024-.020-.010-.022-.044 (.014 (.025-.051) .006 (.018) .012 (.006-.012 (.009) * .007 (.005-.026-.007-.011-. see Data Analysis section) for Survey years 99-00.026 (.023 (.017-.021) .009) .007-.009 (.009) Selected percentiles ( 95% confidence interval) 50th .007-.036 (.021-.007) .088) .032 (.008 (.008 (.005.024-.064 (.021 (.073) . milling. respectively.034) . 235U (about 0.028 (.026) 95th .053) . population from the National Health and Nutrition Examination Survey.017-.008 (.015 (.007 (.011-.009-.040 (.033) .007 (.031 (.008 (.022-.007-.009 (.008) .009-.012) .042 (.027) .012-.014 (.009 (.027 (. Thus.016) .009 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. in some ceramics.063) .009) .007-.009) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.008 (. and 234U.024 (.030 (.056) .020) .031 (.021) .008 (.009 (.023) .026 (.010) .007-.041 (.039) .012-.027 (. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.007) 75th .013 (.008-.023-.007-.009) .014 (.011-.016) .006 (.009 (.008) .007-.017) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.018 (.008 (. Fourth National Report on Human Exposure to Environmental Chemicals 239 .031 (.019-.016-.007-.015) .015 (.014 (.011) .021-.015 (.008-. 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.028-.017) .037) .010) .012 (. and 0.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.031 (.008-.005-.007 (.036 (.036-.040-. Since the 1990’s.027-.013-.021 (.007-.037 (.030 (.042) .006-.031-.018) .022) .007-.039) .010) * .027-.036) .008 (.035-.010-.007) .047 (.S.055 (.006-.019-. or processing.009-.049) .017-.010 (.013 (.006-.015 (.006-.046 (. and 03-04 are 0.Metals Uranium CAS No.007 (.010) .018) .012) .007 (.067) .019 (.038 (.017-.009-.067) .007) .009) .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 .040 (.018) .013 (. In workplaces that involve uranium mining.045) .050) .008-.016) .010-.030-.023) .011) .009 (.008-.066) .026) .011) .037-.035) .035) .011) .030) .158) .008 (.009-.008 (.010-.010 (.037) . interval) .056) .006-.007-.029-.013-.020 (.009) .027) . 0.060 (.127) .033 (.021) .069) .034-.010-.007 (.012 (.016) .006 (.010) .011 (.007-.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 .007) .020-.046-.053 (.010 (.008-.023-.012) .009 (.013 (.008-.006-.023-.029 (.020-. Uranium has many commercial uses.048) .052 (.046 (.033 (. and as an aid in electron microscopy and photography.023) .027) .027) .008 (. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).017 (.012) .008 (.019-.040) .043 (.017-.014 (.028 (.017) .021 (.006-.006-.011-.018 (.011 (.013 (. 01-02.008 (. including nuclear weapons.009-.013) 90th .007-.062) .009) .008) .018-.049) .020-.007-. nuclear fuel.009) .046 (.006-.007 (.012 (. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.009 (.036) .011-.054) .008) .054) .006-.004.027 (.046) .034-.033-.013 (.009) .006-.011-.011) .009-.054-.015) .016) .028 (.009) .020-.011-.040) .017) .028-.009-.038) .040-.008 (.72%).023-.036-.009) .012-.009 (.011) .011) .072) .010 (.005-.010) .006-.026 (.016) .037) .029-.009) .027 (.013) .007-.031 (.023 (.009-.017 (.012-.010) . human exposure occurs primarily by inhaling dust and other small particles.024-.013 (.048 (.009-.017-.016-.041 (.050) .017) . Exposure to DU may occur in military personnel from retention internal shrapnel that contains DU or exposure to dust generated from ammunition Urinary Uranium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.012-.010) * .012-.020) .023 (.016-.012 (.016 (.015-.045) . Variable concentrations of uranium occur naturally in drinking water sources.043) .065) .005-.010) .279) .039-.008-.007 (.004.007 (.026-.007-.026) .008 (.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 .019-.030 (.027-.037) Total .010 (.010-.005-.

014) .007) .005-.030-.009) .021 (.006) .006) .022 (.007 (.007-.007) .059 (.039) .008 (.008-.011 (.012 (.042) .010 (.009-.008) .006) .007 (.053) .034 (.009-.007 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.006 (.007-.025-.015 (.015-.050) .051) .008-.017 (.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.009) .017 (.027 (.026 (.010 (.011-.014) .011-.007 (.012 (.Metals impact.007 (. where limited absorption occurs (less than 5%).031 (.077) .013-.004-.006-.006-.021 (.016-.014 (.010-.029 (.008-.024) .006-.010) .009) .010 (.018) .006-.027) .006-.010-.029) .007 (.009-.007 (.006-.028) .020-. 1992).005 (.010) .019 (.014) .013 (.034 (.010) .012-.032) . Uranium is eliminated in feces and urine. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.035 (.009) .016 (.1%-6% of an ingested dose may be absorbed.028) .015 (.051) .006 (.010-.019-.033) .022-.005-.028-.100 (.007 (.007 (.012 (.009-.005-.011) * .012 (.008) 75th .011-.008) .019-.022 (.007 (.009) .009) .006-.030) ..025 (.013 (.009 (.146) .012) .015-.016) .015) . 0.019-.014-. which can occur occasionally from high occupational exposure. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.009-.015-.009 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.023-..007-.021 (.005-.007-.012 (.014) 90th .024-.009) .017) .022-.015) .010-.024 (.006) .027) .006-.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 .S.058) .039) Total .030 (.030 (.006-.006-.007-.009-.026) .007 (.007 (.013) . kidneys.042-.013 (.027 (.008 (.030 (.034-.029) .010-.034 (.013) .008-. Radiation risks from exposure to natural uranium are very low.007 (.050) .026 (.028 (. with much slower elimination from bone.009) .013 (.007-.026-.016-.019) .008 (.018-.018-.006-.008) .008 (.008 (.017-.004-.005 (.011-.008 (.006-.013 (.034 (.006 (.015) .027 (.074) .039) .010-.010-.063) .009 (.006-.017) .019 (.005-.030-. After long term or repeated exposure.054) .011-.013) .044) .008) .039) .025-.011-.047) . the shrapnel acts as a source of chronic.016) .029 (.034-.006 (.010) .008) .035 (.005-.024) .007 (.020-.016-.010-.008-.018-.006-.024 (. Depending upon the specific compound and solubility.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 .013 (.011) .028) .008-.017-.007) .006-.019) .021) .011-.025-.016) .027-.010) .027-. liver. which represents distribution and excretion.006) .010-. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.008) .019-.037 (.010 (.016) .034 (.051 (.020 (.007 (.015-.033 (.007 (.010-. the initial half-life of uranium is about 15 days (Bhattacharyya et al.013 (.014-. Inhaled uranium-containing particles are retained in the lungs.024 (. After inhalation.006-.270) .024-.025 (.058) .031-.016) .020 (.016) .008 (.017) .032) .008 (.061) .017-.010 (.024) .009) * .029 (.006 (.009) .034) .012) .027-.013 (.022) .053) .025) 95th .007 (.012 (.056) . low level exposure.033 (.006-. interval) .028) .021-.015) .012 (.005 (.014 (. 2005).015 (.033 (.007-.013 (.045 (.011) .008) .024-.025-. 2003).006-. After exposure to soluble uranium salts.010-.030) .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 .008) .009) .019-.048) .020-.011-.020 (..016-.007-.005-.006-.033 (.006-.014-.022 (.013 (.024) . population from the National Health and Nutrition Examination Survey.011-.022-.006-.010) .016) .009) Selected percentiles ( 95% confidence interval) 50th .051) .048) .008) .029) .026 (.011 (.007-.009) .020) .008 (.041) .009 (.015 (.019 (. Health effects from uranium exposure result from chemical toxicity to the kidney.016) .007 (.018-.008) .007 (.040 (.027-.012) .007 (.018 (.018-.028 (.043 (.029) .005 (.015-.006-.067) .011) .008 (.017-.050 (. In cases of retained DU shrapnel.007 (.024) .021 (. 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.009 (.007-.010) * .012-. 240 Fourth National Report on Human Exposure to Environmental Chemicals .006 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.008) .080) .006-.042) .006-.020-.

cdc. soldiers evaluated before.066 μg/g creatinine (Gwiazda et al. 2006).65 μg/L).S. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000.e.. had a mean urinary uranium concentration of 0. Hamilton MM.. Muggenburg BA. 2005. (Kurttio 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.011 μg/L (McDiarmid et al.atsdr. 2002). urinary levels of uranium were as high as 9. Boyd P. with emphasis on quality control. Centers for Disease Control and Prevention (CDC). Mil Med 2003. Thomas RG. 2001-2002. In: Gerber GB. Stradling GN...1992. 1978).55 μg/L (median 0. 2000). Hamilton et al. 2006). eds..gov/ toxpro2. 2006. Squibb K.. 2004). 2003. In a study of 105 persons exposed to natural uranium in well water. IARC and NTP have no ratings for uranium human carcinogenicity. Volf V.S. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. Ejnik JW.78:143-146. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. Sci Total Environ 1991.S.1996.. et al. but in whom no shrapnel was embedded. Pullat VR.Metals injury associated with elevated urinary uranium levels (Kurttio et al. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. Benedik L. Uranium content of blood. 2004). EPA. Six workers in a depleted uranium program showed concentrations of 0. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al.html. 2004). Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. Galletti. Radiation protection dosimetry. Byrne AR. Dietz LA. References Bhattacharyya MH. population. Komaromy-Hiller et al. 28 soldiers who may have been exposed to DU by inhalation. Breitenstein BD. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Information about external exposure (i. ingestion. Drinking water and other environmental standards have been established by U. In 17 U.62:562-566... 2006). Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. 2004). In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU.S. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. the geometric mean urinary uranium concentration was 0. or wound contamination. NRC. 1992. in that the levels were below their respective detection limits (Byrne et al. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. the median urinary uranium concentration was 2. 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. 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. Vol. 41 (1). the median urinary concentration was 0.. McDiarmid et al.168(8):600-605. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. respectively... Dang HS. In the same study. 2000). Fourth National Report on Human Exposure to Environmental Chemicals 241 . Health Phys 1992. 1994. environmental levels) and health effects is available from ATSDR at: http://www. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. Zimmerman I.. 1991. 2006). Karpas et al. pp. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. 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. and 2003-2004 (Dang et al.107:143-157. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U.S.. Horan P. The U. and no consistent effects on multiple endpoints of kidney function were found.. Durakovic A.. Third National Report on Human Exposure to Environmental Chemicals. although slightly increased during and after deployment. 1-49. Atlanta (GA). Pillai KC. A cohort of 46 U. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. (May et al.078 μg/L (ranging up to 5. McDiarmid M. Metivier H. 2002.110 to 45 μg/L (Ejnik et al. Carmichael AJ.S. during. Health Phys 2000.61 μg/g creatinine. 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.162 μg/L) (Orloff et al.. Kent (England): Nuclear Technology Publishing. Tolmachev et al.

patient population and literature reference intervals for urinary trace elements. Health Phys 2003. Oliver M. Salonen L.85:228-235. Auvinen A. Gwiazda RH. J Toxicol Environ Health A 2004. Inductively coupled plasma mass spectrometry as a simple.S. Kane R. Roiz J. Kidney toxicity of ingested uranium from drinking water. Lorber A. et al. D’Annibale L. Jarrett JM. Harmionen A. Andrews WS. Biologic monitoring for urinary uranium in Gulf War I veterans. Uranium daily intake and urinary excretion: a preliminary study in Italy. Heller J. Cordero S. Am J Kidney Dis 2006. Saha H.91(2):144-153.67(8-10):697-714. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Wahl W. Paschal DC. Environ Res 2004.158:165-190. U. Int Arch Occup Environ Health 2006. et al. Oberbroekling KJ.296(1-2):71-90. Auvinen A. Renal effects of uranium in drinking water. Cremisini C. U.79(1):11-21. Roth P.110(4):337-342. Costa R. Komaromy-Hiller G. Clin Chim Acta 2000. Pinto V. Ting BG. Pirkle JL. Environ Health Perspect 2002. Engelhardt SM. et al. Karpas Z. McDiarmid MA. Tolmachev S. concentration and daily excretion of uranium in urine of Japanese. Salonen L.Metals Galletti M. et al. Squibb K. Englehardt SA. Kurttio P. Nuclear Regulatory Commission (U. Scott K. Radiat Environ Biophys 2005. Oeh U. NRC). Wilson PD. Health Phys 2004.47(6):972-982. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Makelainen I. July 1978.81:45-51. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Mistry K. Ash KO. Ejnik J. Marko R.71(6):879-85. Nuclear Regulatory Commission (NRC) Guide 8.86:12-18. Smith D. Squibb K. May LM. McDiarmid M. rapid.82(4): 527-532. Metcalf S. Health Phys 2002. Howerton K. Gucer P.S. Orloff KG. Charp P. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Uranium and thorium in urine of United States residents: reference range concentrations. Kurttio P.S. Sabbioni E. Sampson EJ. Komulainen H.22–Bioassay at uranium mills. Hancock RG. Sci Total Environ 1994. McDiarmid MA. Jackson RJ. Hamilton EI.44:29-40. Health Phys 2004. Review of elements in blood. Pekkanen J.94:319-326. Comparison of representative ranges based on U. Shelly T. Environ Res 1999. Katorza E. Van der Venne MT. Noguchi H. Lewis BM. Halicz L. Bennett LG. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Kalinsky V. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Human exposure to uranium in groundwater. Marino R. et al. Biokinetic modeling of uranium in man after injection and ingestion.S. Ough EA.87:51-56. Health Phys 1996. Washington (DC): NRC. Li WB. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Kuwabara J. Health Phys 2006. Element reference values in tissues from inhabitants of the European community. Hollriegl V. VI. Saha H. Paretzke HG. Karpas Z. et al.

50) 5.40) 90th 10.65) 3.0-29.90-3.0) 13.47-4.0 (8.10 (6. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.90) 5.62 (3.00) 7. and certain plants with high water content (e.0 (11.67-5.90 (2.80-8.0-17.g.30 (5.80-4.0 (11.70-5.80 (6.20-11.50) 5.20 (2.29-3. Other manufactured uses include fireworks.70) 3.80 (3.50-4.90 (3..00-6.00) 3.Perchlorate Perchlorate (Urbansky.49-3.0-17.50 (8.10 (7.30 (2. interval) 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 3.0-19.10 (6.0-14.81-16.90-6.50-11.50 (3.90-9.20 (6.0) 13.20-3.60) 5.10) 3.0-23.0) 14.0 (11.20 (8. and electroplating.40-5.90-11.40-7.74-3.60 (4.0 (11.0 (8.40 (8. see Data Analysis section) for Survey years 01-02 and 03-04 are 0. lettuce) can be the main sources of intake for humans (FDA. milk. and limited applications in pharmaceutics.0 (12.30) 6.0) 13.30-7.10) 12. 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.45-4. certain catalytic metals.0 (12.0) 16.0) 19.70-12.0) 11.70-7.S.70 (3.50-3.5 hours and has a small estimated volume of distribution (Crump and Gibbs.70 (3.70-11.0-18.80) 12.10) 3.70-9.10-7.10 (5.76) 4.0-17.40) 3.26 (2.0 (9.02 (3.11) 3.0 (9. leather tanning.0 (9. potassium.50) 6.84) 14. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism. Perchlorate was added to the U. 2005). 2005).01 (2.00-5.70 (3.0) 11. and reducing agents.40 (3.32 (3. 2007). population from the National Health and Nutrition Examination Survey.00) 5.30 (2.40) 2.79 (2.80 (3. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.10) 5.90-3.0) 14.0) 9.40 (3.0 (9.50-4.12) 3.46) 3. Drinking water.40 (4.0 (12.07-4.80-4.60 (7.81) Selected percentiles ( 95% confidence interval) 50th 3. laboratory analysis.50 (5.08-3.0-15.50-7.22-5.20 (4. It is normally found and produced as the anion of a sodium.76 (3.0) 9.80) 3.20-4.0) 9.80-6.56) 3.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.0-15.80-12.70-6.S.70-3.30-19.75 (3. 1998).20 (7.05 (2.16) 3.38) 5.90-12. fabric dyeing.60-6.0) 13.90 (4.0-18.0 (12.80 (7.80-15.0-17.51 (3.0) 708 617 681 652 1228 1092 Limit of detection (LOD.11) 4.20-12.0 (9.40 (4.21 (2.93-3. 2002). In addition.0 (13.20 (2.30-17.00) 4.40 (5.EPA.50) 3.0 (11.00) 3. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant. matches.10-11.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0 (11.50) 11.10-12.40-4.0) 8.93-4.31) 2.40) 3.0 (8.0) 13.0) 14.0) 9.87-3.60 (4. Survey years 01-02 03-04 Geometric mean (95% conf.80) 7.66) 3.30-6.89-3.40-4.75-3.0) 95th 14.20) 3.20 (5.0 (11.70-3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .60) 3.60-7.40) 3.0) 10.40 (5.93 (4.54 (3.0 (11.0-17.90-10.0) 13.0) 9.05 and 0.90 (5.0) 13.90-11.10-11.0) 9.30-7. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.0) 8. 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.00-6.80) 75th 6.40-6.19 (3.0) 10.18-3.68) 4.0 (8.90-9.40-13.10-4. Perchlorate is stable under most environmental and physiological conditions.10 (2.30 (5.0) 15.0 (11.0) 12.0 (10.0 (8. Inhibition of iodine uptake by competition for the sodium/iodide symporter in the thyroid can be estimated in humans by measuring radioiodine uptake CAS No.44-4.35 (3.20) 4.19-4.0-18.0-17.0) 15.60) 8.0) 11.20 (4.0) 10.51 (3.0 (9.10) 5.39-4.88) 3.0 (9.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.S.0-20.30) 6.40-11.40) 6. but has strong oxidant properties in the presence of concentrated acids.0) 13. 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.20-4.90 (5.20) 7.90 (5.03) 3.22 (2.05.0 (11. or ammonium salt.40 (5.96 (3.09) 3.90) 6.40) 4.

Lamm and Doemland.95 (2.20-10. nitrate.5) 8.56 (3.46 (3.40) 5.90 (7.35 (2.45) 3.04-3.0 (11.70 (2. 2002.4 (11. although iodine intake was higher than U.0) 12. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.60) 10.00-3.82 (5.50 (6.16-3.1 (11.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.10-7. Survey years 01-02 03-04 Geometric mean (95% conf.4-16.0-19.90 (4.0 (8.20 (4..10 (6.S. 2002).50-9..36 (8.84) 2.4 (11.24 (4.40 (3.10 (2.52 (8.22-4. 2005. U.33 (7.0 (8.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.29) 2.00 (4.40 (3.20) 8. menopausal status.76 (3.0) 12. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.22 (2.1-16.70-15. Ecologic studies from screening programs with elevated perchlorate in the regional drinking water have indicated no increased prevalence of abnormal neonatal screening tests for this disorder in these regions (Kelsh et al.3-14.87-3..0) 10.1) 8. 2001.50) 2.0) 9.80 (7.34-3.0) 13.30-5. thiocyanate.30) 3. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.46-13.0-14. 2005).00-2.09) 3. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.S.50) 2.39 (3.26 (3.0 (11.70 (2.10) 4.40-10.61-5.0) 11.70) 2.S.37-13.50 (3.25) 5.20) 3.10) 13.0 (9.30) 75th 5.30) 90th 9.60-5.87) 2.40 (7.56-3.20 (7..80) Selected percentiles ( 95% confidence interval) 50th 3. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.80 (4.25) 5.86) 4.30-5.89 (2.3) 11.S. 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.93-5.4) 8.54 (3.20-9.24-2.90 (2.00 (2.91) 4.77 (3. Many factors may be important in consideration of perchlorate action on the thyroid: dose.87 (7. In the U.70-3.20-4.52-9.00 (6. in a representative sample of U.32) 5. 2005).00) 4. 2002.0) 4.87) 7.14 (2.89-3.80 (7.40) 17.60-15.64-3.53 (2.90-20. interval) 3.39) 2.90) 5. up to 68% RUI has been demonstrated.0-14.21 (2.35 (4.60-6.10 (4.. 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.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5. age.09 (7.10-3.64) 5.60-11.30 (3.8 (11. Li et al. Lawrence et al.12-2.20 (6.47) 2.08) 3.30 (5.05 (4.0 (10.29-6.2) 8.00) 9.60-8. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.50) 5. gender.22-6.1 (8.3) 12.40 (4.EPA.10 (4. Follicular cell thyroid tumors would Urinary Perchlorate (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.99-3.19-10.5 (13. population from the National Health and Nutrition Examination Survey.4 (10.97-5.18-3.0 (11. 2005).0) 12.39-4.20-3.50-5.70) 10.60-11.51-4.07 (2.0) 9.0 (9.70 (4.70-4.15-12..81-3.44) 3.72 (3..73) 3.EPA.60) 3.0) 13.30-10. levels.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.0) 14. 2006.33-12. 2007).30) 5.g.S.90-15. chronicity of exposure.93-8.45-2. NAS.41-9.1-22.50-3. women with urinary levels of iodine less than 100 micrograms per day.46-4.22-4.76-3. dietary iodine intake.60-5.20 (3.93-5.61 (5.98) 3.61-10.93-7.50) 6.3) 8.90-2.93) 3.80-3.60) 8.43) 6.60-8.08 (3.10 (1.7 (11.04-3. perchlorate is negative in most genotoxic assays (U.74) 7.3 (10.33-6. medications). 2005.75) 3.00-11.20-3.40) 3.50) 95th 12.71 (5.50) 9.83 (5.1-14.54 (2. Also.58) 2. 2003.10) 3.99 (5.67) 5.0) 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 .6) 20.90-3.03 (2.Perchlorate inhibition (RUI).00) 3.19-6.87 (5.4) 13..44-6.42 (3.37 (4. and the presence of other substances known to affect thyroid function (e.0) 6. Steinmaus et al.60 (3.S. 1999.6-17.25) 5.S..6) 12.20 (2.35) 3.66) 3.26) 4.96) 2.59) 3.90-11.0) 7. 2000). However. Greer et al.60-3.51 (3.90 (2.2) 8.80-3.10) 6.02-4.25 (3. levels and sufficient in most participants (Tellez et al.0 (9.02) 3.1-13.70-5.4 (8.0-17.30 (6.0) 12. During gestation and infancy.12 (6.90-9.0-44..

Kelsh MA. Greer SE. et al. Li FX.htm. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Pino S. Barnard JC. Perchlorate in the United States. Skeels MR..113(11):A732. 2007).45(10):1116-1127. Health Implications of Perchlorate Ingestion. Primary congenital hypothyroidism. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Pino S. Jackson WA.S.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Howd R.atsdr. Environ Health Perspect 2007. Erratum in: J Occup Environ Med 2004. Environ Sci Technol 2006. Byrd D. Also. Pleus RC. newborn thyroid function.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Tellez RT. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Erratum in: Environ Health Perspect 2005. Lawrence J. Washington (DC): National Academy Press. Rutherford GW. Valentin-Blasini L.html and from ATSDR at: http://www. J Clin Endocrinol Metab 2005. thiocyanate. Low dose perchlorate (3 mg daily) and thyroid function.114(12):1865-1871. Sesser DE. Deyhle GM. Thyroid 2000. Pirkle JL. Magnani B. 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.110(9):927-937. Lawrence JE.46(5):509. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Landingham CB. Braverman LE. J Expo Sci Environ Epidemiol 2007. et al. Lamm SH.42(2):200-205. Blount BC.. Richman K. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Benchmark calculations for perchlorate from three human cohorts. He X. 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. Additional information about exposure and health effects is available from the U. The effect of perchlorate. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. J Occup Environ Med 2003.gov/toxpro2. Blount BC. Crump KS. and nitrate on thyroid function in workers exposed to perchlorate long-term. Thyroid 2001. National Research Council of the National Academies.41(5):409-411. Blount et al. Valentin-Blasini L. Steinmaus C. Daaboul JJ. Mauldin JP. References Blount BC.. Page Last Updated: 05/28/2009.10(8):659-663.113(8):10011008. Crump KS. National Academy of Sciences (NAS).gov/safewater/ccl/perchlorate/perchlorate.EPA at: http://www. Pirkle JL. Braverman LE. Osterloh JD. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Goodman G.cdc. 6/2/09 Greer MA. EPA reference dose (Blount et al. Kirk AB. Cross M. Perchlorate Exposure of the US Population. and environmental perchlorate exposure among residents of a Southern California community.40(21):6608-6614. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Caldwell KL. Osterloh JD. 2005). Analysis of relative source contributions to the food chain. 2005.90(2):700-706. Li Z. Gibbs JP. Available at URL: http://www. Miller MD. Buffler PA. Lau EC. Dyke JV. Food and Drug Administration (FDA). et al. J Occup Environ Med 2000. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lamm S. population. CFSAN/Office of Plant & Dairy Foods. epa. Lamm SH. 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.html. Neonatal thyroxine level and perchlorate in drinking water. 2001-2002. Lamm SH. et al. Environ Health Perspect 2006. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.11(3):295.S. Doemland M. Dasgupta PK. May 2007. Environ Health Perspect 2005. Braverman LE. most of the population is considered to be below the U.S. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Abarca CR. Chacon PM.115(9):1333-1338.17(4):400-407. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. 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. Environ Health Perspect 2002.fda.

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

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

4. and in human blood and semen (Calafat et al. Kannan et al. 2003). 2004.. Taniyasu et al. Unlike many organohalogen contaminant chemicals.. hepatotoxicity. but still can have long residence times in the body. pancreas. 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. Keller et al.. Lau et al.. approximately 4. Prevedouros et al. All sources of human exposure are uncertain. population from the National Health and Nutrition Examination Survey.S. Survey Geometric mean (95% conf. For instance. PFCs have been identified in surface coastal and ocean waters (Yamashita et al. in part. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. 2005). but probably include dietary sources (Kannan et al. including immunologic effects and tumor induction. the 8-2 telomer. see Data Analysis section) for Survey year 03-04 is 0. PFOA has been reported to cause liver. 2007a). 248 Fourth National Report on Human Exposure to Environmental Chemicals . Guruge et al. Olsen et al. or effects of other PFCs...S. human toxicokinetics. 2004). 2003.5 years and for PFOS. may metabolize or degrade to PFOA (Dinglasan et al. C5.. It is unclear if environmentally degraded telomer products are a major source of other PFCs. The PFCs often measured in human serum are listed in the table. C6. in a wide variety of marine and land animals (Kannan et al. endocrine and immune effects. kidney. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. and in offspring. In some cases. 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. C7). PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined. environmental breakdown products of the telomers used to make fluoropolymers or the metabolic products of fluorochemicals in the body can produce PFCs that are measured human blood. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. 2005).. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. 2004). Lau et al... environmental fate. 2005... by high protein binding in plasma and other proteins. Excepting PFOS and PFOA. 2004.... * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2006a. 2004. heptadecafluoro-1-decanol. 2000. thymus and spleen. 2002. Vanden Heuvel et al. Some of the effects in animals may be mediated through peroxisomal proliferation.... Bookstaff et al. 2005. 2006. which may vary for some chemicals by year and by individual sample. 2005).. PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. PFOA is mostly excreted in the urine in animal studies. peroxisomal proliferation. 1995. growth retardation and delayed sexual maturation (Kennedy et al. 2007).. Tittlemier et al. U. and β-oxidation of lipids (Kudo et al. 2005.e..8 years (Olsen et al.. 1990).. The elimination half-life of PFOA in humans is roughly estimated to be 3. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2003a and 2004a). 2004. 2003). < LOD means less than the limit of detection. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins. 1993).Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al.. EPA..

00) .600 (. 2003a.108 times higher than background serum levels in humans (Butenoff et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.700) .700 (. 2004).400-1.600-2.400 (<LOD-. 2003a). developmental and teratogenic effects were demonstrated in offspring.80) 485 538 962 Limit of detection (LOD.S.S. 2003).500) .400-1.400) . < LOD means less than the limit of detection.. 2004..400-1. PFOA. 2007b). Lau et al. 2003). the potential to estimate risks to humans from animal doses is uncertain. reproductive.600 (. 2004).300-1.. EPA.. development in offspring was stunted and hypothyroxinemia was observed. However. Harada et al. 2001.500) 90th .400-.500-.900 (.. 2007a.500-3. Cook et al.10 (.500-1. perfluorohexanesulfonate (PFHxS). 2003. Fei et al. or increased cancer rates (Alexander et al.800 (. At high but non-toxic maternal doses of PFOS. Olsen et al.. 2007b. 2003).300 (<LOD-. 2007a.400 (<LOD-. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.500) . Fourth National Report on Human Exposure to Environmental Chemicals 249 . EPA..500 (. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al...00 (. 2004a.. and there was no clear evidence of excess all-cause or diseasespecific mortality.800 (.3.. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U..10) * 03-04 03-04 * * < LOD < LOD < LOD .. 2004. population from the National Health and Nutrition Examination Survey. Animal studies of PFOS have demonstrated weight loss.S. which may vary for some chemicals by year and by individual sample.. 2007. monkeys. PFOA. 2003a). A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th . thyroidal).900 (.400 (<LOD-. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. 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..300 (<LOD-. PFOS.. hepatotoxicity. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. Kennedy et al. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.600 (. U.. At doses causing maternal toxicity.300 (<LOD-.80) 640 1454 03-04 03-04 * * < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th . see Data Analysis section) for Survey year 03-04 is 0.500-1.00) .500 (<LOD-1.. possibly related to lung immaturity (Lau et al. 1992. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. 1999. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. 2003. 2005). 2003. 2003a. and changes in thyroid hormone concentrations (Grasty et al. 2005). In such studies. population. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.00) ..500) .20) . Thibodeaux et al. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP.400-. In comparing three separate reports on adults.40) .800) 1. 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.900 (. and humans. 2003a.500) .800 (.10) .S.10) . elderly and children. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. Olsen et al.400-1.800 (.500 (.500-1. U.400-1. 2007). Olsen et al. 2004b).800) 1.. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.. 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.500-1.50) .20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . PFOS.

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

300 (<LOD-.600) < LOD .3. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.300 (<LOD-.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.500) 485 538 962 Limit of detection (LOD.0.400 (<LOD-. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 1. Fourth National Report on Human Exposure to Environmental Chemicals 251 . < LOD means less than the limit of detection.400 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD.300-.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.500-.S.400) .500 (<LOD-. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.S. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .900) < LOD .400 (. * 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th . see Data Analysis section) for Survey year 03-04 is 0.600 (.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.

90 (2.S.963 (.30) 3.60-2.12) .861 (.10-9.900 (.40 (1.80 (1.00 (.60-4.10 (. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (1.50-10.826-1.834-1.40 (2.20) 1.0) 1053 1041 03-04 03-04 03-04 1.721-1.50 (2.00) 1. Survey Geometric mean (95% conf.90-10.70) 1.00 (1.900-1.30 (7.10) 1.80) 5.72 (1.00-1.40) 640 1454 03-04 03-04 1.62-2.20 (6.1) 485 538 962 Limit of detection (LOD.00) 2.50 (1.90) 1.689 (.40-1.800 (.00-7.30 (1.80-4.80 (4.54) .60-2. 252 Fourth National Report on Human Exposure to Environmental Chemicals .30) 3.3 (9.17 (1.05-2.50-6.30 (2.60 (1.50 (6.20-3.60) 9.40-3.40) 4.04) .70-6.60-4.900-1.42 (1.60) 1.10) 75th 1.80-2.10-5.90 (1.80 (1.87-2.10) 8.30) 3.80-4.20) 1.00 (1.50-3.50 (6.90) 90th 5.70) 13.20-1.70-2.50 (4.10) 1.10) 6. Survey Geometric mean (95% conf.984 (.900-1.40 (1.10) 6.00-8.27) 1.10 (.20 (1.40) .80) 90th 2.90-19.60-3.20) 2.60) 2.80-8.03) 1.90) 1.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.30 (2.30-12.30-9.60 (6.30-2.50 (1.6) 7.816-1. population from the National Health and Nutrition Examination Survey.00) 3.800-1.70 (1.09 (.S.3.40) 1.90-2.17-1.70-5.60-7.86 (1.50-6.60-3.20 (1. population from the National Health and Nutrition Examination Survey.80-3.10) 5.900-1.10 (.73-2. interval) .70-7.30) 03-04 03-04 .80-7.08) 2.80) 1.697-1.00) 1.20-1.50) 6.20 (1. see Data Analysis section) for Survey year 03-04 is 0.80-3. see Data Analysis section) for Survey year 03-04 is 0.90 (4.20 (1.90 (1.20 (6.30-6.80) 4.0) 8.93 (1.700-1.90 (4.809) 1.80) 3.00 (2.80-7.10 (4.5) 8.40) 1.900 (.00-6.900-1.56-1.50 (1.51) 1.30 (6.912-1.90) 3.966 (.40) 2.30 (3.50 (4.26) 2.10 (1.80-12.67-2.700 (.20) 03-04 03-04 2.77-2.40 (1.30 (1.90 (1.14 (.50) 2.40 (1.10) 75th 3.00 (5.20) 485 538 962 Limit of detection (LOD.20-2.90) 8.92 (1.30 (1.900-1.00 (.00 (1.91) 2.70) 2.90 (1.20) .5) 5.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80-8.30 (1.900) 1.90) 1.600-.60 (1.80-4.00-1.70-2.10) 1053 1041 03-04 03-04 03-04 .10) 4.60) 3.44 (2.70) 2.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.70) 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. interval) 1.30) .40-1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.01 (1.1.70) 3.10 (4.50) 2.70) 1.20-1.586-.16) .80-6.60 (1.60-2.852 (.60-8.10-9.40) 640 1454 03-04 03-04 2.70 (2.72) 1.10) 4.50 (1.835-1.20-1.70-10.

5-62.20-9.8) 32.1) 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 (35.4 (19.3-22.5 (28.1-35.40-6.60 (3.7 (13.9 (17.30-5.5) 57.20) 10. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.18 (3.8-22.4 (23.65-4.3) 485 538 962 Limit of detection (LOD.0-16.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.60 (7.4.95 (3.0-20.3-61.1 (24. population from the National Health and Nutrition Examination Survey.30-11.40) 75th 5.90 (7.20-5.7 (43.10 (6.00 (5.3 (28.80-12.50 (4.6) 42.1 (19.80) 8.2) 640 1454 03-04 03-04 4.70-9.6) 35.27) 4.35) 3.30-6. population from the National Health and Nutrition Examination Survey.4 (28.8 (34.8-22.8-22.9-38.7-53.40-17.50-6.70) 6.90-4.7-30.S.90 (7.9) 22.5-21.9) 22.40-6.6-45.6) 18.60) 8.0 (27.5) 32.5) 7.9 (22.1-24. interval) 3.99-3.8) 27.5) 19.30-3.70 (5.6) 62.3) 41.70-7.50 (3.8 (37. Survey Geometric mean (95% conf.70 (3.3 (35.60 (6.3 (17.7) 39.0 (20.00 (5.60) 03-04 03-04 3.9) 27.60 (4.0) 21.3) 28.5) 8.40) 5.96 (3.30 (3.5) 1053 1041 03-04 03-04 03-04 14.40) 3.8-35.47-4.2 (27.30) 6.20) 7.7 (35.40 (4.5) 18.10 (3.7-33.8 (45.84-3.S.2 (16.10-3.9-23.80-9.91) 3.47 (4.8) 46.1.60 (6.89 (3.40) 90th 7.4-25.0) 36.0) 23.30 (5.00) 3.07-4.6) 7.7 (19.10) 5.6 (42.50) 7.50-13.20) 5.2 (19.6 (44.85-4.6-24.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.50-4.11 (2.9 (19.20) 4.70-10.6) 9.21-3.80 (7. see Data Analysis section) for Survey year 03-04 is 0. interval) 20.6 (19.60-13.3) 42.20) 7.2-57.0) 43.4-42.90 (5.1) 15.60-14.6-50.90-4.70-5.8-81.7 (43.2) 30.30 (3.1-25.8-30.2 (18.3 (35.70) 3.2-22.37 (2.5) 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. Fourth National Report on Human Exposure to Environmental Chemicals 253 .30-8.0-66.20-4.20 (4.4 (17.0-70.1 (23.40-14.3 (44.2) 45.5-23.6) 1053 1041 03-04 03-04 03-04 3.53) 3. see Data Analysis section) for Survey year 03-04 is 0.60-9.1-36.20) 5.9) 9.70-7.00 (3.4) 640 1454 03-04 03-04 23.60 (5.4-17. Survey Geometric mean (95% conf.50) 4.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.0) 485 538 962 Limit of detection (LOD.5-33.8-78.4) 21.6) 21.2 (21.1-52.2 (28.10 (3.40-10.5 (28.7 (7.80 (5.0) 03-04 03-04 19.7-49.4) 56.90-12.40 (6.67-4.90 (7.82) 4.70 (5.4) 20.4 (19.20 (4.9-19.30) 7.80 (6.60-6.79) 4.5) 9.1-33.90) 6.0) 21.80 (6.7 (35.4) 75th 30.0) 90th 41.7-69.80-4.70) 4.9 (13.1) 57.2) 30.7-23.

300 (.300 (.300 (.300) . Survey Geometric mean (95% conf.300) .500) < LOD 485 538 962 Limit of detection (LOD.300-.300-.400 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .500) . see Data Analysis section) for Survey year 03-04 is 0.300 (.300-.200-.500) 485 538 962 Limit of detection (LOD.200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .300 (.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .200-.200-.500) .200-. 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.4.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection. 254 Fourth National Report on Human Exposure to Environmental Chemicals . which may vary for some chemicals by year and by individual sample.S.300 (.200 (<LOD-. see Data Analysis section) for Survey year 03-04 is 0.200-. Survey Geometric mean (95% conf.300 (. population from the National Health and Nutrition Examination Survey.300) .300) .300 (.300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .200-. population from the National Health and Nutrition Examination Survey.300 (.300 (.200-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .300) .300 (.2.200-.300 (.500) .200-.300) .Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. < LOD means less than the limit of detection.S.300 (.300-. 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.

which may vary for some chemicals by year and by individual sample.80) 1.700 (<LOD-.10) .70) 1.50 (1.900) .10-1.30) 1.20 (1.30) 1.900) 485 538 962 Limit of detection (LOD.20-1.300 (<LOD-.800) .700 (<LOD-2. see Data Analysis section) for Survey year 03-04 is 0. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900 (<LOD-1. Survey Geometric mean (95% conf.10-1.600 (<LOD-1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < 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.00 (. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey year 03-04 is 0. < LOD means less than the limit of detection.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .S.600 (<LOD-1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .10) .900-1.400 (<LOD-1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .60) 640 1454 03-04 03-04 * * < LOD < LOD .900-1.900-1.10) 1.900-1.50 (1.700) 90th 1.10-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .10) 1.800 (<LOD-.600) .30 (1.700 (<LOD-.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .40) < LOD < LOD .00 (.10-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .10 (.10 (.00) < LOD .700) 1.30 (1.300-2. Survey Geometric mean (95% conf.800) .60) 485 538 962 Limit of detection (LOD.900-1.20) 1.10-1.00 (. < LOD means less than the limit of detection.80) 1.700) .S.10 (1.700) 1.700 (<LOD-.700 (<LOD-.90) .00-1.10 (. which may vary for some chemicals by year and by individual sample.40) 1.900 (.900-1.900) 1.30) . population from the National Health and Nutrition Examination Survey.30 (1.900-1.600 (<LOD-.400 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) * 03-04 03-04 * * < LOD < LOD .300 (<LOD-1.600 (<LOD-1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (.6.500 (<LOD-.700 (<LOD-.3.700 (<LOD-.

Needham LL. Bandai N.63:490496. Reidy JA. brominated.134(1):18-25. Kudo N. Chlorinated.7(4):371-377.S. Witter FR. Biegel LB. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Toxicol Appl Pharmacol 1992. Kawashima Y. Aguilar-Villalobos M. Environ Sci Technol 2004. Reidy JA. Calafat AM. Biegel LB. Wong LY. J Occup Health 2004.104(2):322-333.39(1):80-84. Halden RU. Keller JM.40:21282134. Yamashita N. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002.115(11):1670-1676.46(2):141-147. Sasaki S. Rogers JM. Butenhoff JL. Ingall GB. Fluorotelomer alcohol biodegradation yields poly. Environ Health Perspect 2007.and perfluorinated acids. Hekster FM. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Frame SR. Yoshinaga T. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Bignert A. Dinglasan MJ. Mabury SA. Kannan K. Kannan K.Perfluorochemicals References Alexander BH. Caudill SP. Burris JM. Calafat AM. Toxicol Sci 2001. Rev Environ Contam Toxicol 2003. Tarone RE. Environ Sci Technol 2005. Holmstrom KE. Lau CS. Harada K. Cook JC. Fei C. Seacat AM. Saito N. Day RD. Cook JC. Murray SM. Falandysz J. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years.38(10):2857-2864. Frame SR. Hurtt ME. Gaylor DW.Koizumi A. Ye Y. Yoshinaga T. Liu RC. Kumar KS. Watanabe T. Toxicol Appl Pharmacol 1990.68(6):465-471. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Loganathan BG. Guruge KS. J Environ Monit 2005. Cook JC. McLaughlin JK. Fillmann G.39(23):9057-9063. O’Connor JC.39(23):9101-9108. Olsen GW. Environ Sci Technol 2007a. Olsen GW. Environmental and toxicity effects of perfluoroalkylated substances. Grey BE. Herbstman JB. et al. Perfluorinated chemicals in selected residents of the American continent. Environ Sci Technol 2006a. The influence of time. Tully JS. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Kuklenyik Z. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka.60(10):722729. Calafat AM. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro.60(1):44-55. Regul Toxicol Pharmacol 2004. Wijeratna S. et al. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries.115(11):1596-1602. Crit Rev Toxicol 2004. Taniyasu S. Rodricks J.S. Peterson RE. et al. Apelberg BJ. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Environ Sci Technol 2005.99(2):253-261. Suzuki E. Hurtt ME. Hurtt ME. Seneviratne HR. Inoue K. in vivo. Edwards EA. Chemosphere 2006b. Environ Health Perspect 2007. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Kuklenyik Z. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Characterization of risk for general population exposure to perfluorooctanoate. Saito N. Olsen J. Koizumi A. Laane RW. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Kuklenyik Z. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Toxicol Appl Pharmacol 1995. Harada K.41:2237-2242. Mandel JH.39(3):363-380. Yun SH. et al. Kamiyama S. Reidy JA. Mandel JS. Birth Defects Res B Dev Reprod Toxicol 2003. Mohotti KM. Environ Res 2005. Environ Health Perspect. Kuklenyik Z. et al. et al. and ex vivo studies. Moore JA. et al.34(4):351-384. Reidy JA. Grasty RC. Environ Sci Technol 2004. Moore RW. Katakura M. Perkins RG. Butenhoff JL. Olsen GW. Jarnberg U. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. 2007b. Kannan K.1968--2003. Corsolini S. The toxicology of perfluorooctanoate.113(2):209-217. Caudill SP. Yamashita N. Chem Biol Interact 2000. Environ Sci Technol 2005. Inoue K. Kennedy GL Jr. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats.124(2):119-132.179:99-121. Tully JS. Mandel JH. Needham LL. de Voogt P. O’Connor JC. Needham LL. Calafat AM. and perfluorinated contaminants in livers of polar bears from Alaska.115(11):1677-1682. Taniyasu S. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. Evans TJ.38(17):4489-4495. Arendt MD. Needham LL. Bookstaff RC. Morikawa A. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Polyfluoroalkyl chemicals in the U. Occup Environ Med 2003. Calafat AM.

J Children’s Health 2004b.2(1):53-76. Burris JM. The developmental toxicity of perfluoroalkyl acids and their derivatives. Butenhoff JL. fish. Burris JM. Petrick G. (Erratum in: Environ Health Perspect. Yamashita N. I: maternal and prenatal evaluations. Rogers JM. Olsen GW. Toxicol Sci 2003. Mandel JH. perfluorooctanoate andother fluorochemicals in human blood. Washington.68(1):249-264. Available from URL: http://www.74(2):369-381. EPA). Buck RC. Seacat AM.40(1):32-44. Korzeniowski SH. Environ Sci Technol 2006. Olsen GW. Lau C. Church TR. Richards JH.113(5):539-545.111(16):1892-1901. Mandel JH.115(9):1298-1305. Thibodeaux JR. Seymour C. Butenhoff JL. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Moisey J. Thomford PJ. Cao XL et al. Chemosphere 2007b. Olsen GW. birds. Yamashita N. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. II: postnatal evaluation. Historical comparison of perfluorooctanesulfonate. and perfluorooctanoate in retired fluorochemical production workers. Biol Pharm Bull 2003. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Froehlich JW. Burris JM. Hanari N. Butenhoff JL. Bronson R. Cousins IT. (Erratum in: Toxicol Sci 2004. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Miller JP. Environmental Protection Agency (U. Case MT. Pepper K. J Occup Environ Med 1999. Rogers JM. Chemosphere 2004a. 2003a. Toxicol Sci 2003.41(9):799-806. Hansen KJ. Ehresman DJ. Zobel LR. Lau C. Sources. J Occup Environ Med 2003b. Mandel JH.S. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. and food items prepared in their packaging. Hanson RG.S. Ehresman DJ.1177(2):183-190.111(16):1900) Olsen GW. Grey BE. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. and humans from Japan. Olsen GW. Huang HY. Butenhoff JL. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Helzlsouer KJ. Burris JM.45(3):260-270.perfluorohexanesulfonate. Environ Health Perspect 2003a.51(8-12):658-668. Burlew MM. Prevedouros K. Larson EB.epa. Olsen GW.gov/opptintr/pfoa/pfoara.82(1):359. Toxicol Appl Pharmacol 2004. Coordinate induction of acyl-CoA binding protein. 2007a. Hansen KJ. Olsen GW. Biochim Biophys Acta 1993. Hansen KJ.Perfluorochemicals Kudo N. Thibodeaux JR. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Hanson RG. et al. 2003. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Nesbit DJ.68:105–111. Environ Health Perspect. Seacat AM. Lundberg JK. Taniyasu S. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Sterchele PF. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. J Ag Food Chem 2007. Kannan K. Grey BE. Taniyasu S. U. et al. Peterson RE.) Tittlemier SA. fate and transport of perfluorocarboxylates.. Rogers JM. Kannan K. et al. Barbee BD. Horii Y. Reagen WK. Horii Y. Hansen KJ. Hansen KJ. Ellefson ME. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse.26(1):47-51.37(12):2634-2639. A global survey of perfluorinated acids in oceans. et al. Burris JM. Environ Sci Technol 2003.198(2):231-241. Environ Health Perspect 2005. htm. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse.55:3203-3210. Olsen GW. Stanton ME. Mair DC. van Belle G. 1/15/06 Vanden Heuvel JP. Mandel JH. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Butenhoff JL. Kawashima Y. et al. Olsen GW. Half-life of serum elimination of perfluoroo ctanesulfonate. Toxicol Sci 2002. fast foods.74(2):382-392. Mar Pollut Bull 2005. et al. Gamo T. Church TR.54(11):1599-1611. Butenhoff JL. fish. Church TR. Lundberg JK.

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

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

Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Henttu P. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Grote K. Hoppin JA. Numtip W. Yoshimura M. Silva MJ. Pan G. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Albro PW.html. Stringer WT. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). 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 . Drexler H.112(17):1740]. Rylander L.195:142-153. Reprod Toxicol 2004. 2006 [online]. Int J Hyg Environ Health 2007. Silva MJ. J Androl 2004. et al.105:802-811. Tsukino H. Environ Health Perspect 2004. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Toxicol Appl Pharmacol 2004. Reynolds T. et al.niehs. Park MG. Koch HM. Brock JW. Filser J. Hartle RW. Ryan L. Liss GM. Park S. Fromme H. 6/2/09 NTP-CERHR. Ladefoged O. White R. Jobling S. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Research Triangle Park (NC). Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. Angerer J. Biol Pharm Bull 2003. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay.nih.html. Calafat AM. Determination of phthalate monoesters in human milk. and infant formula by tandem mass spectrometry (LC-MS-MS).html. Research Triangle Park (NC). Jonsson BAG. Skakkebaek NE. Jacobsen H. Silva MJ. Giwercman A. Kessler W. Balasubramanian AV. Kano K. Boehmer S.niehs. gov/chemicals/dehp/dehp-eval.210:21-33. et al. Environ Health Perspect 1998. Brock JW. 6/2/09 NTP-CERHR. Leffers H. Chahoud I.gov/chemicals/dehp/dehp-eval. Urinary phthalate metabolites and biomarkers of reproductive function in young men.25(2):293-302. Bolte G. Yokoyama Y. Hauser R. McKee RH. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Research Triangle Park (NC). Kalita JC. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Borch J.106(1):23-26. Research Triangle Park (NC). Richthoff J. Am Ind Hyg Assoc J 1985. Duty S. Parker MG. Reprod Toxicol 2005. Butala JH.gov/chemicals/ phthalates/dbp/dbp-eval. Sumpter JP. Lovekamp-Swan T. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic.niehs. consumer milk. Ryan L.niehs. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Akesson B. 2000a [online]. Wang P. Hum Reprod 2007.110(5):515-518. Chen Z. Hagmar L. Environ Health Perspect 1995. Available at URL: http://cerhr. 2000b [online]. Available at URL: http://cerhr. Anal Bioanal Chem 2005.19(4):505-515. Main KM. Harris CA. Meeker JD. Suzuki T.112(17):1734-1740. Hass U. Hauser R. Jarfelt K. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets.18(1):122. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. Gans G. Csanády G. Available at URL: http://cerhr. Environ Health Perspect 2003.64(8):555-560. NTP-CERHR. Int Arch Occup Environ Health 1993. Epidemiol 2005. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. David RM. Davis BJ. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).22(3):688-695.46(11):643-647. Reproducibility of urinary phthalate metabolites in first morning urine samples.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Environ Health Perspect 1997. Nielsen J. Kano I. Environ Health Perspect 2002. et al. 6/2/09 NTP-CERHR. Scand J Work Environ Health 1985.nih.11(5):381-387. Dalgaard M. Duty SM. Hanaoka T. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP).16(4):487-493.nih. Mortensen GK.382:10841092. Sumpter JP.Phthalates in human urine samples. The estrogenic activity of phthalate esters in vitro.html. Davis BJ.26(8):1219-24. 6/2/09 Okubo T. Baird DD. Calafat AM. Mechanisms of phthalate ester toxicity in the female reproductive system. 2000c [online]. Available at URL: http://cerhr. Singh NP.111(2):139-145.nih. Meeker JD. Andersson A-M. Milligan SR.103:582-587. Skerfving S. Zhang S.

Barlow NJ.46:282-293. Crit Rev Toxicol 2006. Toxicol Sci 1998.58:339349. Meek MD. Rhodes C. Jackson SJ. Abbott BD. 112(5):A270]. Cunningham ML. Ostby JS. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Fielden MR. Environ Health Perspect 2004. Environ Health Perspect 1982.36:459-479.112(3):331-338.65:299-308. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Barr DB. Bratt H. Urinary levels of seven phthalate metabolites in the U. Wu ZF. et al. Lambright CR. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. et al. Batten PL.S. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. et al. Silva MJ. Malek NA. Pratt IA. Environ Health Perspect 1986. Orton TC. Peck CC. Peters JM. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Zacharewski TR. Environ Health Perspect 2006. Rusyn I. Albro PW. Hodge CC. Klinefelter GR. Reidy JA.45:11-17. Toxicol Sci 2000. Caudill SP. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Clemons JH. Parks LG.114(11):1643-1648.Phthalates phthalate (DEHP): a cross-sectional study in China. Matthews JB.

0 (34.8-16.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2 (10. and diet is the major source for general population exposure.4 (53. and 0.8-48.6) 29.3) 13. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2-155) 91.3-161) 99.1 (19.0) 33.9 (16.8 (71.6 (13.4 (68.4) 71.8 (21. 0.2) 12.2-116) 122 (102-143) 101 (84.6 (53.1) 29.2-39.9 (12.8) 63.0) 16.1 (14. 01-02.1 (55.4 (59.4 (32.9-27.9 (22.7 (13.8-18.4) 108 (96.6-92.3 (13.1-214) 166 (116-191) 145 (110-213) 88.3 (22.5 (55.5 (47.1) 14.1-16.5-41.2) 15.6) 15.8 (71. 262 Fourth National Report on Human Exposure to Environmental Chemicals .9-16.5) 15.6 (21.3-12.3-34.5) 82.9) 18.6) 35.8) 28.8-76.2-16.7-35.9 (13.5-145) 138 (106-241) 143 (127-179) 120 (99.7 (82.3) 23..8-35. because it is not bound to products in which it is incorporated.7-16.2-40.7 (51.1-35.4 (27.7-119) 99.5 (67.8-98.8) 24.5-36.0) 20.9) 14.4) 33.1-90.S.7 (11. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives. and to a lesser extent.0 (30.8 (14.8-133) 89. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.5-97.0 (33.5 (57.6-29.4) 98.2-183) 101 (78.5-36.6-132) 103 (84. in a small sample of pregnant women in New Urinary Mono-benzyl phthalate (MBzP) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8 (80.4 (31.4 (13.7-170) 169 (134-198) 152 (99.2) 32.9) 43.1-18.5-84.2) 13.5-33.1-38.6) 95th 103 (94.8-17.6) 35.0 (55.4-16.3 (33.2) 14.4 (29.7) 38.7-16.0) 90th 67.2 (19.7-82.6 (32.4 (10.7 (15.5 (76.3-88.8) 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) 35.9-47.9) 12.6-92.0-130) 101 (86.1) 13.6) 50.3 (12.6-38.0 (14.1-120) 52.6) 67.S.4) 80. BzBP can be released into the environment during its production and.5-35.6 (13.2-115) 113 (91.3) 94.1) Selected percentiles ( 95% confidence interval) 50th 17.5) 55.6 (12.3-18.7-172) 103 (74.1) 68.7 (53.3) 63.0-106) 58.4) 35.8-64.9 (11.1-39.0-85.0 (15. including MBzP.3 (30.2-38.1) 12. 2000).1 (13.6) 14.3-27.5 (61. Food crops take up BzBP.1 (32.8-41. particularly male animals (McKee et al.4-15.8-14.0) 70.0 (30.2 (43.6) 13.3.3 (29.6-18.8 (12.3) 13.4) 38. residents (Blount et al.8 (38.2) 33.8-17.3 (44.0 (20.6) 14. vinyl tile.5-18. IARC considers BzBP not classifiable with respect to human carcinogenicity.6-116) 122 (102-142) 101 (85.3-75.4 (48.4) 65.3-74.5) 30.1) 32.6-39.0) 23.3-18.9) 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 39.4 (10.2) 17.0-55.1 (13.8-121) 79.9 (21.1 (20.3-82.3-130) 122 (88.2) 22. and 03-04 are 0. sealants.0 (27.3 (12.5 (26.2-20. 2001-2002.3) 15.5 (66.9) 11.6 (13.8) 33.4 (53.9) 13.5-25.1 (10.4) 51. can produce developmental and reproductive toxicity in rodents.8-16.7) 23.6) 13.8.4) 129 (98.7-15.9-30.2-19.6 (41.9-28. interval) 15.7-25.1-15.2) 78.9) 14.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.8 (86.3) 54.4) 14.7-14.5) 27.6) 24.8 (28.3 (54.6) 63. NTPCERHR.4) 12.6-17.6-43.1-43.4-24.Phthalates Benzylbutyl Phthalate CAS No.3 (12.1-15.4) 49.6) 37.6) 16.1-116) 122 (93.4-120) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 13.8 (53.6 (13.9) 49. 2000).7-58.8 (10.8-13.9 (28.9 (12.2-33.5 (13.2 (47.5-14.3-43. it can be released into the ambient air during use or disposal of the products.6-150) 94.2-31.9 (39.6-72.2-17.2 (25.5) 15.1 (58.0 (23.5) 23.0-26.3 (29.4) 75th 35.7 (12.5 (27.0) 24.3) 37.2) 69. and 2003-2004 were generally similar those reported in U.7) 40.5-40.2 (19.8-72. respectively.9-14.5) 65.1 (14.4 (63.5-94.1) 31.2) 66. 2004.6 (66.0 (26.5-62.2-16.0 (12.9 (70.2) 14.5) 16.7-17.3-91.4-127) 80.4-62.8 (50.1) 76.2 (11. High dose BzBP and its monoester metabolites. population from the National Health and Nutrition Examination Survey.9-62.0) 34.7-16.1.2 (14.4 (32.1-16.4) 81.6-79.7-13.7 (70.4-92.6) 25.9-87.9-49.4-25.1) 67.0 (15. see Data Analysis section) for Survey years 99-00. car care products.9-190) 86.3-21.9) 15.1-61. some personal care products.8) 14..3-125) Total 15. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.7 (80.0 (11.0 (43.8-14.0) 32.8 (30.

1) 24.5 (42.3) 13.7 (54. A small study of African-American women in Washington.9-69.3) 13.4 (74.5 (48.7 (11.1 (21.4) 17.6 (11.9 (22.7-20.2-15.7-61..4) 50. 2004).1 (15..9-83.6) 38.2) 11.8 (11.8 (64.0) 60. and females compared to males (Silva et al. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.9) 12.1 (9.1 (13.1-27.1 (14.6) 13.2) 11.4-19.3) 67.6 (51.9 (9.2 (69.9-28. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.7-19.7-15.0 (49. Hoppin et al.4-15.0) 24.8) 68.7) 11.9-115) 57.9-16.7) 56.1) 80.6 (24.3) 55.8) 13.5-99.0 (41.7-90.7) 19.8 (12.6 (11. In an annual sample of German university students.9 (10.6-40. 2002.2 (56. and in a small sample of German residents (Koch et al.5 (12.5-13.1-125) 86.4 (11.5 (56.8-13.3) 89.0) 12.1-120) 77.5-26.1 (11.0-48.0-27.9 (10.0) 24.0 (38..1-79.3-64.2) 32.8) 54.1 (13.5-26.4 (12.8-13.7-397) 70.8 (49.2-57.5) 78.6-13.7-12.4) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 12.7 (12.4-18.4) 60.9 (43.1 (25.1 (19.1) 35.5) 13.1-29.7-20.8-85.3) 37.6 (57.5) 16. Weuve et al.4 (13.6 (34.3 (38.2-13. 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.5-57.5-58.3-38.4-99.4 (21.0) Selected percentiles ( 95% confidence interval) 50th 13. adolescents compared with adults.4) 15.4-60.7 (59.9) 52.1) 23.2-21.9 (51.7-31.2 (40.8) 80.4 (11.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .5-16.1-35.6) 75th 25.8-42.9) 24.5) 23.S. interval) 14.7) 46.7) 25.4) 28.6) 12.8-15.1 (34.2-49..4-116) 73.4) 44. 2003).8-173) 195 (121-305) 229 (99.3) 16.4-142) 134 (116-176) 136 (85.1 (53.3) 13. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.4 (69.2-12.5-42.2) 11.9-13.8 (50.5 (49.7 (18.4 (33.1) 24.8) 108 (75.2-78.0 (62.1-58.7 (38.7-29.0 (10.1 (21.5-61.8-13.4 (26.2) 12.0) 11.5 (35.8-16.3 (35.9) 12.6-47.4) 25.9) 64.3 (13.0-53.9) 100 (80. 2005).0-15.1) 27.1) 142 (99.8-15.6) 12.6 (30.6-86.6 (11.4) 21.5-38.4-14.9-104) 62.9 (24. 2004. 2007).8-48.4-102) 70.8) 11.4 (25.9) 42.2-13.5 (11.Phthalates York City (Adibi et al.7-56.4) 12.9 (54.6 (15. 2007).3) 36.9-40. Urinary Mono-benzyl phthalate (MBzP) (creatinine corrected) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.8 (30.7 (14.6) 58.2 (41.9 (15.4) 13.3) 73.9 (24.6-12.0-109) 65.9) 11.1 (18.7 (13.8 (10.1-12.6) 25.9-23.3-34.5-23. in men attending a Boston infertility clinic (Duty et al.4 (10.0 (33. in young Swedish men (Jonsson et al.9) 12.0) 13.2-117) 95.0 (13.5) 10. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.3) 21.1-14.4-27..7-14.0 (12.8-14.5-29.6-99.4 (63.7-69.0 (67. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.8) 46.6 (14.5 (10.4-79.5) 14.9 (15.7-19.1) 12.7 (11.5-79. In NHANES 1999-2000.6-20.9) Total 14.8-34. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3 (60.4-23.9 (55.8 (69.8) 33.0-90.6 (30. Hauser et al.69-11. 2002)..8) 53.9 (39.5) 95th 77.6-81.4-93.6 (36.6) 53.4) 90th 50.9) 11.7 (21.1) 39.5) 20.2 (27.5) 46.8) 33.8) 16.0-51.3) 12.1 (43.5) 41.8-14.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.2-26..8) 71.8) 24.2-51.4) 14.95-14. 2006).9-13.8-69.9 (12. 2005.7-15.1 (41.6) 73.7 (23.3 (15.7 (13.4 (46..3-11.3 (23. 2003).4-90.1 (21.1 (21.6-116) 74..8-39.4-42. 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.2) 15.1) 17.4) 51.3-73.2) 26.6-26.7 (19.8 (13.3) 29.9 (29.4) 104 (89.2) 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 12.0) 49.5-213) 49.4-14.1-12.8) 56.5-31.3) 14.3-16.7 (11.6) 30.9 (12.8) 26.8-64.6 (19.7-14.4) 13.8-27.7 (55.9-14.1 (46.0-26.6-15.0 (12.8 (46.7) 38.8) 15.0 (11.5 (9.5-58.0 (41.5) 17.8) 34.3 (39.1 (23.8-80.2-15.7-123) 77.4 (60.4 (11.2) 67.5 (10.6 (22.3) 90.0) 15.3 (24.5-76. population from the National Health and Nutrition Examination Survey.9-62.4-17.2-17.8 (57.8) 53..3) 18.4 (34.3 (12.3) 14.73-12.8-60.

Environ Health Perspect 2000. Eckard R.16(4):487-493. Sanchez GN. Hu H. Caudill SP.Phthalates References Adibi JJ. Environ Health Perspect 2002. Centers for Disease Control and Prevention (CDC). Research Triangle Park (NC). Angerer J. Jonsson BAG. et al. David RM. Giwercman A. Poland. Calafat AM. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Epidemiol 2005. Bull Environ Contam Toxicol 2002. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.html. Chen Z. Brock JW.22(3):688-695. Jacek R. Jedrychowski W. Calafat AM. Ryan L. Hauser R. Wittassek M. Richthoff J. Duty S. Urinary phthalate metabolites and biomarkers of reproductive function in young men.93:177-185.108(10):979-982. Weuve J. Caudill SP. Silva MJ. Hoppin JA.18(1):122.114(9):1424-1431. Hodge CC. Rylander L. Third National Report on Human Exposure to Environmental Chemicals. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Dobler L. Gans G. Atlanta (GA). et al. Needham LL. Silva MJ. Urinary levels of seven phthalate metabolites in the U. Ryan L. Environ Health Perspect 2006.S. Hilborn ED. et al. Phthalate monoesters levels in the urine of young children. 2000 [online]. Meeker JD. Barr DB. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). 112(5):A270]. Available at URL: http://cerhr. Koch HM. Duty SM. 2005. Needham LL. et al. Reidy JA. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Rossbach B. Silva MJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Levels of seven urinary phthalate metabolites in a human reference population. Brock JW. 264 Fourth National Report on Human Exposure to Environmental Chemicals .210(3-4):319-333. Hum Reprod 2007. Environ Health Perspect 2003. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Davis BJ. Perera FP.nih. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. 4/20/09 Silva MJ.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. McKee RH. et al.112(3):331-338. Environ Health Perspect 2004. J Androl 2004. Singh NP. Brock JW. et al. Silva MJ. Malek NA. Barr D.25(2):293-302.niehs. et al. Butala JH. Hagmar L. Schettler T. NTP-CERHR.68:309-314. Sampson EJ. Caudill SP. Wiesmuller GA. Pirkle JL.111(14):1719-1722. Reproducibility of urinary phthalate metabolites in first morning urine samples.110(5):515-518. Baird DD. Camann DE. Prenatal exposures to phthalates among women in New York City and Krakow. Environ Res 2003. Reprod Toxicol 2004. Int J Hyg Environ Health 2007. Helm D. Drexler H. Blount BC. Koch HM. Green RA.

0-14.4 (14.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.1-20.0) 9.44-2. pharmaceutical coatings.3 (16.0 (11.00 (7.6 (9.91) 4.81 (3.7-31.2-22.4-12.40 (2.6-14.9-14.73-5.30-11.90-7.70) 3. OSHA has established a workplace air standard for external exposure to DBP.40-3.80 (5. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.0) 24.1-12.10) 8.10-9.50-10..8) 40.30 (4.60 (8.11-3.50 (6.97) 2.00) 4.07 (3.1-25.46 (2.3) 33.30-6.40 (7.70-4..46 (3.7) 15.30-3.55) 2.4 (20.40-17.6) 16.26 (2.96) 3. 2005.. 2003).5) 18.71 (2. 2005).40-5.90-4.50) 8.9-23.02) 4.90-2.70) 5.6 (14. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.3 (13.3 (16. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.2 (8.5-16. Hauser et al.50-4. When total DBP metabolites have been measured.4-27.0 (19.4) 12.7-20.0) 20.40-3.6-34. see Data Analysis section) for Survey years 01-02 and 03-04 are 1. 2003).3 (11.00) 4.3) 18.33 (2.19-3.0) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2.30 (3.7) 18.2 (12.7) 14..20-2.2 (11.40-4.80-5.50-6. residents (Blount et al.6) 10.60 (2.3-48. mostly as MnBP (Anderson et al.3-24.6-20.56 (5.22 (3.7-31.9 (16.6) 12.7) 7.67 (5.6 (29. 2007).1) 25.5 (11.9) 10.00-11.5 (27.9) 15. 2004.6 (10.3 (18. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine. about 65% to 80% of a dose is eliminated in urine within 24 hours.2-14.56 (3. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.50) 90th 12.5) 23.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.6) 16.60 (4.5) 12.6 (10.1-17.5-24.1 (8.70 (2.68 (2. 2005). Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.70 (5.5 (10.0-25.50) 7.00-4.5-16.00) 10.84) 4.00) 6.10 (4. interval) 2.80 (5.22) 3.7) 4..6 (13.40 (2.40-4.6 (14.63) 3. NTP-CERHR.30-13.46) 2.00-6. Survey Geometric mean (95% conf.97) 4.6) 17.30) 10.40 (3.2-33.30-7.80 (3. 2000..50 (3. Biomonitoring Information Median concentrations reported in the NHANES 19992000.10) 3.7 (17.80-5. Following oral administration of DBP to humans.0 (13. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.40-12.6) 26.50) 18. CDC.20 (7.28-5.6) 17.73 (2. 2001).46-5. Fourth National Report on Human Exposure to Environmental Chemicals 265 .60) 3.80 (2.20-9.40-9.90 (4.20-12.17) 4.10-2.10) 9.1) 22.2) 5.00-6..90-4.1) 16.3.5 (17.5) 18.17 (2.55 (3.1 (13. population from the National Health and Nutrition Examination Survey.5) 25.85-6.20-12. and insecticides.60-6.8) 21.30) 5. 2005). DBP can produce reproductive toxicity in male rodents (McKee et al.Phthalates Di-n-butyl Phthalate CAS No.3-19.80) 75th 5.60 (5.3-20.72-3.82-3.7 (7.4) 22.10) 2.50-2.3 (13.5) 19.50) 5. and in a small sample of Japanese adults (Itoh et al.0 and 0.0-38.24-8.30-2.7 (17. In addition. 2000).5) 22.8) 677 652 703 699 1216 1088 Limit of detection (LOD.80 (2.97-7.30) 10.10) 11. in men attending a Boston infertility clinic (Duty et al.7 (9.30-6.S.49-2. 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.90 (4.20 (6.0) 13.70-4.20-6.90 (6.S. they have been referred to as monobutyl phthalate (MBP). 84-74-2 Di-isobutyl Phthalate CAS No.94) Selected percentiles ( 95% confidence interval) Sample 95th 17..10-9.5) 14.48 (2.20 (3.6 (11.90 (3.56) 3.43) 6.00 (5.5-29.7 (18.66) 2.37) 6.40) 5.00) 7.3) 3.3 (19.10 (3.7 (16.40 (6. 2004.59) 3..0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.9 (16. Koch et al.3-30.20) 4.0) 12.30) 2.5 (20.4) 5.6-18.7-18. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate. Studies of children found age-related differences in urine MBP levels.50) 2.6 (13. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.6-26.20) 7. in a small sample of pregnant women in New York City (Adibi et al.70-8. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.30 (1.0 (13.3-18.56-4.90) 12.30) 6.8 (9. and also in some printing inks.00-9.3-43.10 (4.0-18.

20 (2.. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al.56-4.61-3.7) 11.72) 5.94-12.73 (5.9 (11..64-7.46-11.6 (8.11 (5. 2004).15-4.66) 2. the students’ median values for MiBP levels remained relatively unchanged.43) 3.15) 3.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.19 (2.1-25.76-3. samples from German university students had consistently higher median urine levels of MnBP and MiBP.00-3.33) 3.69) 6.4) 23.5) 13.80-3.0) 15.18) 4.00-7.6 (9.54 (4.21) 10.81 (6..73) Selected percentiles ( 95% confidence interval) Sample 95th 12. respectively.05) 2.3) 28. to about two to fourfold higher (Fromme et al.02 (7. 2005).1 (10.81) 4.13 (2.08-2.21 (5.96 (3.57-4.38-10.59 (4.0 (10.30 (6.89 (3. interval) 2. ranging from more than one-tenth the NHANES median (Itoh et al.58-4.3) 13.13-6.5) 15.39) 5.80) 7.5 (11.02-10.1 (11.6 (10.8-13.56) 2.35) 3.00-3.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.04-5.64-7.36-2.95) 10.4) 7.0-18.34 (3.75 (4.1) 11.46 (2.78) 9.36-7.18-4.86-4.1) 15.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.66) 4.20 (7.68) 3.74 (4.6) 11.66 (8.32) 7.54 (2. 2004).04) 7.1) 10.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .37) 3.95) 2.56) 5.17 (2.07 (2. Between 1998 and 2003. population from the National Health and Nutrition Examination Survey..65 (4.18) 3.53-3.6 (15.17) 90th 8.7) 19.7 (11.10-5.51) 15. In an analysis of NHANES 1999-2000.6 (12.82) 4.32 (7.89) 6.3) 13.53-5.4 (12.30) 2.07-5.82 (4.45) 3.20 (2. 2007).46) 3.33-9.18 (1.9-40.5-19.9 (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.01-2.76 (3.03 (5.94 (5.9-16.6 (8.33 (3.8 (8.5 (9.4) 15.54) 2.6-19. 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.52-3. 2006).53-4.27-12.03-7.11) 5.8 (9.7 (21.8-36.91-6.3) 16.78) 8.57 (3.78-8.14 (4.47 (3.75 (6.2 (11. 2005).00 (3.18 (4.66) 10.20-4.25) 5.8-18.6) 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 2.6-19.81 (3.3 (13..56-15.68 (2.2 (10.0 (12. up to four and 13 fold.18-10.2) 8.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.1) 4.S.17-12.26 (2.69) 4.92 (7.0) 3.93-6.84 (8.43) 3.2) 24.2) 9.79-8.55-6.89-5.09-2.57 (3.98 (2.3) 18.1) 7.08) 75th 4.28-13.72-7.31) 2.3 (17.58-3.8 (10.0) 7. Survey Geometric mean (95% conf.74-3.69 (2. 2002.7 (9.95-3.31) 2.62-12.8-18.7) 3.83 (2.62 (6. while MnBP declined (Wittassek et al.9 (9.52-20.42) 2.29-8.22 (2.94) 6. 2007).4-16..03-11. Over this time.86) 6.32 (3.39-3.04) 3. An analysis of NHANES 2001-2002 showed similar age.65-11.7 (13.47-5. Weuve et al.11-2.84 (4.99) 7.65-4.2-15.and gender.51) 5.47-12. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.26-2.88 (2.20-3.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.0) 11.52 (2.29-3.28 (4.67-5.0 (8. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.52) 3.76-15.31 (2. than adults in NHANES subsamples during the same time period.97-2.38 (6.20-2.85 (2.6) 13. Differences in urinary MBP population estimates by gender have also been shown (Silva et al. 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.9) 12.1-15.79-6..8) 10.24) 3.68) 5.43) 3.9-26.76-3.81) 9.44 (3.31 (7.64-10.33 (2.1-24.99-4.7) 10.41 (2.69-7.1-12.2-13.7-28.79 (4.1) 13.51) 2.80 (3.

0) 84.6) 35.9) 46.3-76.4-31.6) 17. referred to as monobutyl phthalate (MBP).0) 31.1) 17.2 (21.1 (31.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.7 (22.2) 32.9) 18.2 (25.7 (19.6 (19.3) 24.6 (32.6-44.6) 80.3-79.2 (58.7-26.8) 62.5 (59.5) 24.0) 20.3 (51.9-22.9-33.1 (19.4-60.4 (35.2-63.9-53.6-29.0 (45.9 (17.5) 19.7 (18.6-40.1-22.7-42. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value. population from the National Health and Nutrition Examination Survey.7-111) 64.1) 30.2) 38.7) 42.2 (79. 1.7) 92.3-60.4) 20.1 (26.5-47.6-113) 108 (90.3-67.2-56.0) 117 (104-131) 112 (84.5 (29.9 (20.1 (19.6) 38.8 (57.7-116) 95.0 (18.4) 52.6-49.0 (72.3-85.0 (30.7 (28.8) 23.5) 47.6 (61.5 (74.6-143) 127 (99.7) 52. interval) 24.7 (24. Fourth National Report on Human Exposure to Environmental Chemicals 267 .7-20.0) 38.9-92.7 (18.9-42.2-23.3) 23.5-27.8) 48.0-26.9-101) 77.1 (41.5) 17. and 03-04 are 0.6 (26.8) 75th 51.1-75.6 (65.1) 47.0) 120 (98.5) 78.5) 26.1 (19.8-132) 95.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.0-24.3 (42.5) 21.S.6-20.6 (22.3-24. *In the 1999-2000 survey period. see Data Analysis section) for survey years 99-00.0-58.3-21.2 (17.0 (20.3 (56.1-92.8-123) 101 (90.2 (75.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.1) 23.8) 19.3 (17.9) 71.0 (78.7 (51.4 (36.2) 26.4 (19.5) 85.6) 46.1 (34.5-53.1-51.0-73.2) 62. 01-02.6) 39.3-145) 85.5-60.0-51.8-119) 90.7-92.0) 27.4 (21.4-26.7-42.1 (18.8-29.3 (37.3 (30.9.1) 36.3) 40.4-25.9-87.1) 19.4 (23.6-24.7-53.1 (17.4-44.1 (62.9) 36.9-22.5 (30.5-44.9) 21.7-91.2 (19.5) 31.4 (35.4 (35. respectively.0 (15.9-79.1) 46.0 (23.0) 30.4-18.2-32.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.1-80.5 (28.0 (25.4) 64.9) 75.3 (23.4) 22.7-34.3) 21.2-24.6 (16.3-136) 137 (107-162) 119 (90.2 (78.2-21. Survey Geometric mean (95% conf.2 (21.3-40.9) 26.6-33.2 (18.0-21.7 (70.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.3 (30.5) 40.0 (17.9) 29.6 (48.4.8-42.4-20.0-32.5) 36.1 (54.7-127) 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 (79.7 (38.6) 21.3) 36.1 (19.9-114) 116 (97.7 (43.1-24.1) 25.3 (23.0-19.8) 43.1) 23.5-42.7) 74.1-82.4 (71.1 (58.8) 58.7-106) 69.5) 37.9 (17.5 (59.2-87.3 (60.4 (25.3) 18.2 (20.6-69.6-37.2 (74.6-48.7) 28.9 (79.2-49.1 (16.8 (19.2-159) 92.1) 20.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.5-47.7-24.1 (21.7) 124 (98.2) 90th 98.1) 31.9-28. and 0.3-96.5-117) 95.2) 68.8-25.2) 42.1-20.2-22.7-121) 97.2 (59.2-114) 73.4 (72.1-29.4 (38.3 (36.3) 19.7 (64.1-27.0) 21.7-124) 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.0 (31.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.6 (55.6-29.0-24.6 (44.7 (16.2) 20.5) 65.7 (33.2-33.5-43.4 (35.6 (90.4-42.1 (36.4-159) 107 (84.5) 20.8-22.6-31.0-19.2-93.6-36.5) 34.0 (36.4) 59.7-34.7-117) 118 (108-143) 93.5) 36.5-121) 106 (94.3) 26.1 (51.1.4 (84.5) 95.1 (28.6) 71.6) 20.1) 23.

5-142) 89.2) 59.7-19.6) 23.3) 33.3 (17.1) 20.9 (35.7 (28.9) 20.6-43.3) 18.1-18.0 (19.8-23.9-68.1) 20.7 (19.4) 53.4 (31.9-56.9 (64.5 (64.6-23.2-86.6 (19.4) 15.S.4 (47.8-235) 137 (108-198) 88.9) 62.8) 17.7 (16.6) 64.8 (16.6) 37.0-47.3 (52.8) 17.6-119) 63.1) 42.8 (33.2) 21.6-32.1) 44.6-74.5-142) 81.1) 35.1) 37.4 (16.3 (46.2 (35.2-108) 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.8 (50.1) 61.2-22.6-42.5-30.2-18.1 (15.2-48.0) 59.8) 35.4 (31.4) 15.2 (16.0 (43.3) 20.3-106) 74.4-131) 81.7) 20.3-40.9-36.0) 29.4-72.6-26.7 (57.1-128) 97.2) 74.5 (14.6) 24.9) 39.3-38.6 (41.9-68.8-24.8) 30.0 (52.3) 67.3-18.4 (37.1 (46.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.0 (26.4 (50.7 (12.3 (16.2 (38.1) 50.2-179) 84.9) 52.8-24.3) 52.9-49. population from the National Health and Nutrition Examination Survey.3 (55.2) 159 (102-263) 147 (93.5-37.1) 22.6 (31.4) 51.9 (21.8) 75th 38.3) 19.0) 26.8 (25.9 (30.3 (48.3-49.5-15.4-61.7-19.4 (20.8 (17.5 (15.9) 30.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.2 (83.7 (43.2 (19.6-22.5-23.4-103) 117 (83.6-53.9) 91.9-84.6-23.0 (18.9 (73.9) 24.3-71.0-41.7-80.2) 31.0 (71.2-16.8 (22. Survey Geometric mean (95% conf.2-22.7 (60.9 (37.2-106) 64.0) 70.5) 60.6-128) 96.3-26.7) 19.9-100) 86.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.2-28.5) 82.5-64.4) 16.4 (31.6) 24.5 (18.7) 36.7 (81.9 (16.3) 33.0 (20.3-78.8) 20.7-26.0) 81.4-76.9-26.3 (42.9 (35.9 (39.6 (25.6 (25.8-32.5 (30.0) 94.5) 134 (93.1 (56.1 (21. 268 Fourth National Report on Human Exposure to Environmental Chemicals .6-92.0-19.8) 20.3 (52.7-28.1-32.6 (27.5-18.8) 13.4-135) 71.7 (60.3 (71.1-21.7-51.4-24.9-70.6 (74.0 (34.4 (18.4) 20.5) 39.5) 84.5 (18.0-38.5-70.6) 25.0) 28. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.1 (32.2-61.0) 41.0-90.1) 17.6) 18.3) 17.3-21.7 (14.1) 53.1-83.3 (76.7 (20.1 (61.6-28.1 (34.8) 63.Phthalates Urinary Mono-n-butyl phthalate (MnBP) (creatinine corrected) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3 (69.6) 34.3-21.4 (33.4 (17.5-22.2-27.3 (24.6-44.8) 34.8) 23.6 (29.7-37.9 (58.3) 59.4) 19.5) 91.7-39.2-22.7-20.0 (69.8 (18.3-23.1) 21.1 (29.6-24.5-16.8) 22.4-164) 96.6 (61.9-14.9 (30.4) 62.4 (56.3) 21.0 (16.2-73.5-41.8-43.1-99.5) 17.3 (19.3-32.6-19.0 (50.6-24.3-20.3-17.0 (27.4 (68.4 (16.0) 25.6-27.7 (27.3) 19.7-21.6) 31.6) 83.7-23.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.6) 39.9 (20.8 (13.7) 42.5) 21.6) 14.9) 49.9) 28.0 (61.0-113) 104 (83.4 (19.1-23.6-50.0 (15.7 (73.4 (13.0-60.5-76.7 (54.0-75. interval) 22.6) 38.9-105) 85.2) 16.4 (17.4 (50.4-65.2 (19.4) 21.3 (17.3) 35.8 (18.0-92.9-34.0) 75.9 (30.8 (18.3 (21.2-21.4-47.2-85.0) 35.8) 40.7-42.0) 55.9) 19.8) 17.8 (65.5) 90th 68.5-21.1-62.0 (70.6) 65.8) 34.8) 19.3 (17.0-17.1-99.8) 28.4 (53.6-155) 91.3-81.9-38.6-16.3-114) 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 (28.6 (17.0) 108 (71.9 (19.0) 19.0 (18.3 (60.6 (72.2) 65.6 (57.6-44.9) 14.5 (81.4 (45.4-34.4 (23.3-39.7-78.0) 53.9 (56.

et al.gov/chemicals/ phthalates/dbp/dbp-eval. Available at URL: http://cerhr. 112(5):A270]. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Epidemiol 2005.210(3-4):319-33. Int J Hyg Environ Health 2007. Bolte G. Butala JH. Weuve J. Brock JW. Drexler H. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].nih. Centers for Disease Control and Prevention (CDC). Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Caudill SP. Bull Environ Contam Toxicol 2002.210:21-33. Hilborn ED. Jedrychowski W. Calafat AM. Environ Health Perspect 2004. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Malek NA. Wittassek M. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Drexler H. Research Triangle Park (NC). Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Environ Res 2003. Perera FP. Sanchez GN. Boehmer S. Silva MJ. Angerer J. Eckard R. Silva MJ.114(9):1424-1431. Urinary levels of seven phthalate metabolites in the U. Dobler L.93:177-185. Caudill SP. Singh NP. Int J Hyg Environ Health 2007. J Androl 2004.S.18(12):10681074. Rossbach B. Food Addit Contam 2001. Environ Health Perspect 2003. et al. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.25(2):293-302. et al. 2000 [online]. Levels of seven urinary phthalate metabolites in a human reference population.16(4):487-493. Barr D. Pirkle JL. Camann DE. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Koch HM.18(1):122. Poland. Hu H. Blount BC.niehs.68:309-314. Giwercman A. Hagmar L. Gans G. Reidy JA. Masunaga S. McKee RH. Phthalate monoesters levels in the urine of young children. Ryan L. Brock JW. Duty S.112(3):331-338.html. Hum Reprod 2007. Schettler T. Angerer J. 4/20/09 Silva MJ. Fourth National Report on Human Exposure to Environmental Chemicals 269 . NTP-CERHR. Needham LL. Richthoff J. Hauser R. et al. Duty SM. Green RA. Int J Hyg Environ Health 2005. Helm D. Springall C. Chen Z. Reprod Toxicol 2004. Needham LL. Rylander L. Meeker JD. Fromme H. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Calafat AM. Jonsson BAG. 2005. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Sampson EJ. Yoshida K. Koch HM.111(14):1719-1722. Massey RC. Castle L. Wiesmuller GA. Hodge CC. Scotter MJ. Itoh H. et al. et al. Ryan L. Environ Health Perspect 2006.208:237-245. Jacek R. Barr DB. Koch HM. Caudill SP. Anderson WA. Environ Health Perspect 2000. David RM. Third National Report on Human Exposure to Environmental Chemicals.Phthalates References Adibi JJ. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Atlanta (GA). et al. Silva MJ. et al.22(3):688-695. Prenatal exposures to phthalates among women in New York City and Krakow. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.108(10)979-982. Silva MJ.

400-.500) < LOD 1.500) 1.300-.300 (<LOD-.90) .200 (<LOD-. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection. 01-02.600) .400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .300 (.200-.700) .500) < LOD < LOD . respectively.300) < LOD .500 (.70) .500 (.500) 1. Finding a measurable amount of MCHP in urine does not mean that the levels of MCHP or the parent compound cause an adverse health effect.300-.400-.600) < LOD .500) < LOD < LOD .400-.700) .300 (.400 (.300 (.500) .00-2.400-.400) 1.200-.500 (.10) .900-1.300 (.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70 (1.300 (.500 (.10 (<LOD-1.400-.300) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300-.20) .700) . Survey Geometric mean (95% conf. only levels at or above the 90th percentile could be characterized.400-. and 03-04 are 0. population from the National Health and Nutrition Examination Survey.500) .500-.70) .400 (.400) 1.400 (<LOD-.00 (<LOD-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.00 (<LOD-1.400 (<LOD-. 0.600 (.500 (.10 (.400 (<LOD-. In this Report.50) .70 (1. polyvinyl acetate.500 (.50) . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.400-.3.400 (.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 . Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.300-.300-. 270 Fourth National Report on Human Exposure to Environmental Chemicals .400) < LOD 1.200-.300 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300-.600) . see Data Analysis section) for Survey years 99-00.400 (<LOD-.500) 1.300-.500 (.400 (.500) . 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.400) < LOD < LOD .500 (.200-.9.400 (.300 (. resins. and polymers.600) .600) .300-. and polyvinyl chloride.300) < LOD . < LOD means less than the limit of detection.300-.500) .400 (.300-.10 (<LOD-1.S.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 1.2.200-. and 0.200-.00-3.80) .00 (<LOD-1.00) . People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine. including nitrocellulose. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.500 (.400 (.10 (<LOD-2.Phthalates Dicyclohexyl Phthalate CAS No.600) . 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.

530 (.380 (.06) .06) .05) .590 (<LOD-.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 1.530-.560) 1.240-.82) .500-.660) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10) .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.800-1.740) < LOD < LOD .670 (<LOD-.630 (<LOD-.500 (.54) .14 (<LOD-3.940 (.250 (.450 (.370 (<LOD-.740) .11) . Fourth National Report on Human Exp