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

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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

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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)

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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)

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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)

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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

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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

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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
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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.

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5'-Tetrachlorobiphenyl (PCB 44) 2.3.2-Dichloropropane 2.3'.2'.4.4.2-Dichloroethene Dichloromethane (Methylene chloride) 1.2'.4.2'4.4'.4'. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.4'-Tetrabromodiphenyl ether (BDE 66) 2.2'.4'. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4'-Tetrabromodiphenyl ether (BDE 47) 2.2'.4.1-Dichloroethene (Vinylidene chloride) cis-1.2'.3-Tetramethylbutyl] phenol) Triclosan (2.1.4’.5'-Hexabromodiphenyl ether (BDE 153) 2.5'.html.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.6'-Hexabromodiphenyl ether (BDE 154) 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .5.6'-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 2.2-Dichloroethene trans-1.4'-Tribromodiphenyl ether (BDE 28) 2. The process for selection is described at http://www.3.5. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.1.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.5'-Tetrachlorobiphenyl (PCB 49) 2.2-Dichloroethane (Ethylene dichloride) 1.4’.4.2'.4. Table 1.gov/exposurereport/chemical_selection.6-Heptabromodiphenyl ether (BDE 183) 2.5.4'.1.2'.4'-Pentabromodiphenyl ether (BDE 85) 2.2’. Paradichlorobenzene) 1.3.3.2'3.2-Dichlorobenzene (o-Dichlorobenzene) 1.6-Pentabromodiphenyl ether (BDE 100) 2.4.4.What’s New in this Report What’s New in this Report In this Fourth Report.4.2-Trichloroethane Trichloroethene (Trichloroethylene) m.5.2'.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4.4.4.4'.5’.2'.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.4-Tribromodiphenyl ether (BDE 17) 2.1-Trichloroethane (Methyl chloroform) 1.4-Dichlorobenzene (p-Dichlorobenzene.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.cdc.1-Dichloroethane 1.1.3’.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.5-Pentabromodiphenyl ether (BDE 99) 2.6.2.3-Dichlorobenzene (m-Dichlorobenzene) 1.

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

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

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

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

This improved procedure makes each repeated value unique by adding a unique negligibly small number to each repeated value. 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. we have improved the procedure for estimating percentiles to better handle this situation.Data Sources and Data Analysis Report. Therefore. Taylor JK. Fourth National Report on Human Exposure to Environmental Chemicals 7 . occasional percentile estimates may differ slightly in the current Fourth Report than in the Third Report. Appendix A gives the details of the new procedure for estimating percentiles. 1987. Lewis Publishers. Quality Assurance of Chemical Measurements.

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

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

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

1994). widely distributed in tissues.6) 90. such as potatoes and some grains. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.7 (55.1 (47.6-104) 82.7) 75th 79.2-118) 98. Recently.4-76.5-80.6 (56.2) 57.0 (69. acrylamide has produced upper airway irritation following inhalation of high levels.1-64. and from dermal contact with products that contain residual acrylamide.9 (54.0 (57. interval) 61. Elimination occurs mainly in the urine as mercapturic acid conjugates.6-108) 61.3) 86. 2004.7) 73. Animal studies indicate that acrylamide is well absorbed.2 (75.6-75. Natural substances in the food are converted to acrylamide.0-49. but are generally above the U. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U. glycidamide. People may be exposed to acrylamide from foods.6-66.0-66.8 (91. Acrylamide is not thought to accumulate in the body at environmental doses.9-61.9 (60.S. 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.8 (57.9) 57. and an average daily intake is estimated as 0.5 (74.3 (55. acrylamide is synthesized and used in the production of polyacrylamide polymer.4-60.2) 57.4-89.4 (53.2 (62.5 (44. (NTP-CERHR.0 (67. and in the synthesis or compounding of dye materials.0 (53.4 (51.3) 63.3) 70. 2005).4-60.8 (81. In 1997. 1990. smoking. see Data Analysis section) for Survey year 03-04 is 3.6) 71.1) 55..4 (54. and cosmetics (NTP-CERHR.9-105) 86. 2006). and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. and is either metabolized to the reactive epoxide.2-93. in permanent press fabrics.S.2 μg/kg/day (U.1 (52.7) 54. and in some cosmetics. soil conditioners.7 (65.7 (58.7) 58.7-64.6-61.0) 85. FDA. the main source of exposure is from the diet.1) 62.0) 57. pulp and paper production. ocular and dermal irritation from direct contact with acrylamide containing materials.S.1 (83. and binding agents. EPA.2-77.3 (53. but can covalently bind to form adducts with proteins. 2002). 2005.7-60.9) 58.3-71.4 (59. These estimated intakes are hundreds of times lower than occupational exposures. population from the National Health and Nutrition Examination Survey.5 (79. Since acrylamide has limited volatility and high water solubility. Commercially.1 (88.S.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. it was discovered that acrylamide is formed when starch-rich foods.5) 66.1) 46.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.1) 101 (95. or to glutathione conjugates (Calleman et al. FAO/WHO.6 (51.0-58.2-59. Fennell et al.S. 2005). gels.7-64. are heated at temperatures used for frying and baking. Estimated intakes in children are about twice that of adults (DiNovi and Howard.2-70.0 μg/kg for adults (FAO/ WHO.1) 53. Tareke et al.Acrylamide Acrylamide CAS No.8-57. 2005).4-83. and well below doses known to cause nerve damage or carcinogenicity in animals.9) 63. 2005).2-67. mineral processing. 2006.5) 58.4) 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 54.9 (69.4) 57.2-114) 163 (147-191) 96. In humans.1 (73.0-108) 152 (139-175) 126 (111-142) 108 (86. 2004). in some sealing grouts.6) 50.4) 57. EPA reference dose of 0.7 (63.1-64. Survey Geometric mean (95% conf.7) 96.5 (52.6) 73.6 (81.4 (54.2 (58. EPA. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. In the general population..6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.1-61.0. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.8-55.1-57.9) 75.2-91.8 (52. Polyacrylamides are useful water-compatible polymers used in water treatment. as an absorbent in disposable diapers. Fourth National Report on Human Exposure to Environmental Chemicals 11 .6-65. 217 million pounds of acrylamide were produced commercially in the U.9-52. 2005). drinking water.5-85.4) 100 (89..3-2.

U.2-68. most non-smokers had levels less than about 100 pmol/gram hemoglobin. 2005. 2005. male germinal cell injury.0-93. 2005.6 (66. 2005.. thyroid.4) 46. 2002. 1997. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.4-59.4 (57.1) 60.2 (56.9) 65. dominant lethality).1-60. Rice. 2001).2 (63.5) 71.2) 55.0 (80. Vesper 2005) and smoking (Bergmark. In addition.4) 83.3) 59.7 (87. 2008).3-78.4-98. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. 2009). NTP-CERHR.7) 61. Additional information is available from U.2) 87. Vesper et al.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71...int/ ipcs/food/jecfa/summaries/summary_report_64_final. 2004. 1997.0-62.5 (56..4 (90.4 (81.4) 53. interval) 59.7 (57.1-70.8 (44. 2006). presynaptic nerve terminal binding (LoPachin.8-49.9-77.9) 59.2-90.8-48. U. 2005. 2004).0) 94.1 (70.4 (51.3) 59.2-91. 2005.5-94.4-65.0 (75. uterine. EPA.0 (52. 2005.4-103) 79.6-62. 2008).9-62... and cancer (mammary.5-66. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.8 (51. and neuronal DNA reactivity (Doerge et al.9) 75.4 (61..7) 74.0. EPA at: http://www.5) 75th 85.9-138) 143 (130-159) 96.9-76.9-78.0 (70.2 (72. Hagmar et al. 2005).5 (59. 2005).6-90.0-103) 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. 2005.9 (58.4 (56. 2005.. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. EPA.7-62. IARC classifies acrylamide as probably carcinogenic to humans.6-64.5-64.S.pdf..7 (61. reproductive effects (reduced litter size. 2006.5) 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. scrotal. probably through its epoxide metabolite.0) 118 (103-126) 121 (112-134) 113 (94. Axonal degeneration.3) 85.3-101) 95. although different analytic methods can affect results. 2002.1 (57.. Mucci et al. Acrylamide is clastogenic and can produce dominant lethal mutations. Glycidamide has been shown to react with DNA (Doerge et al. see Data Analysis section) for Survey year 03-04 is 4.1-62. AHA levels have been shown to increase with dietary intake (Hagmar et al. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. 2005) have been demonstrated in animals.5 (83. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.7-86. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).7-64.9 (57. Puppel et al.5 (42. 12 Fourth National Report on Human Exposure to Environmental Chemicals . 2005).. altered gene expression in testicular tissues (Yang et al.8) 45. 2003.5) 87. glycidamide (NTP-CERHR.. After exposure ceases..9-64.1 (66. fetal death.S.3) 59.. and other sites) (FAO/WHO.7) 60. Survey Geometric mean (95% conf. 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.1 (82. Maniere et al.3 (56.6 (90.Acrylamide occupational exposures.who. 2005.S.8) 60. adrenal.1 (56.1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59.2) 65.epa. 2006)..9 (81.7 (84.5-92. 2005).1) 56.S..7) 90. respectively) are markers of integrated acrylamide exposure over the preceding few months.1) 62. 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.. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.9) 87. population from the National Health and Nutrition Examination Survey. 2005...1-56. Klaunig et al. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al. Puppel et al. 2006) have been demonstrated after acrylamide dosing.. Schettgen et al. Schettgen et al.8-61. 2005) and sperm DNA adducts (Xie et al.

054472. Cheong HK. Wirfalt E. Toxicol Appl Pharmacol 1993. J Agric Food Chem 2008. 2001. Osterman-Golkar S. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. References Bergmark E. [Epub ahead of print] Dybing E. July. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Summer SCJ. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Bruze M. Godard T. morphological and molecular endpoints in animal models. Nordander C. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. Illinois. 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. National Toxicology Program. Food and Drug Administration (FDA). et al. He F.fda.pdf.int/ipcs/ food/jecfa/summaries/summary_report_64_final. 2001). Alexander J. Zhang S. Fennell TR. Toxicol 2005. 2009 Jan 8. Haugen M. Bridson WE. February. Toxicol Sci. et al.. Available at URL: http://www. Maniere I. Mutat Res 2005. Rome. Adv Exp Med Biol 2005. 2/3/09 Klaunig JE.niehs. Chicago. Calleman CJ. Doerge DR. McDaniel LP.120(1):45-54. Beland FA. Paulsen JE. Twaddle NC. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Farmer PB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Guffroy M. Churchwell MI. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). DiNovi M and Howard D. Hagmar et al.126(2):361-371. 1999). Andersen M. 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. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Chem Res Toxicol 1990. Perez et al.27(4):219-226. 64th Meeting: Summary and Conclusions (FAO/WHO). CFSAN/Office of Plant and Dairy Foods. 2/3/09 Hagmar L. 2/3/09 Perez HL.580(1-2):157-165. Kamendulis LM. Acrylamide intake through diet and human cancer risk. 8-17 February 2005. In another study. Spicer R.580(1-2):131-141. Kautiainen A. Granath F. Bergmark E. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Toxicol Sci 2005. Uncertainties. Wilson KM.3:406-412. Mutat Res 2005.gov/chemicals/ acrylamide/Acrylamide_Monograph. Paulsson B. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation.561:21-37. Becher G. Rosen I. 2005. Human exposure and internal dose assessments of acrylamide in food.who. 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. Malmberg B. Chem Res Toxicol 1997 Jan. April 13-15. Magnusson AL. Joint FAO/WHO Expert Committee on Food Additives. He F. et al. NIH Publication No. Bjellaas T.43:365–410. Mechanisms of acrylamide induced rodent carcinogenesis. Mutat Res 2005. Burgess J. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers.10(1):78-84.Toxicol Appl Pharmacol 1994. Costa LG. smoking habits and gender. Doerge DR. Tornqvist M. et al. Calleman CJ.. Duale N. Wu Y. Adv Exp Med Biol 2005. 2004. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes.cfsan. Bergmark E. Mucci LA. 6013-6019. Yang JS. Scand J Work Environ Health 2001. Italy. Hagmar L. 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. Acrylamide neurotoxicity: neurological. Available at URL: http://cerhr.. 1994).561:49-62.nih. Food Chem. Metabolism and hemoglobin adduct formation of acrylamide in humans. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide.. Snyder RW.Acrylamide In occupational settings. Bergmark E.html#u1004. LoPachin RM.85:447-459.580(1-2):119-129. and Research Strategies. smokers and nonsmokers. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Fennell TR. Available at URL: http://www. Laurentie M. 1993. Axmon A.. Tian G. Aprea P. da Costa GG. 2006. Churchwell MI.56.pdf. Survey data on acrylamide in food: individual food products. Costa LG. gov/~dms/acrydata. Tornqvist M. The Updated Exposure Assessment for Acrylamide. Calleman CJ.

Han DU. Toxicol Lett 2006. Liu Y. Benetou V. Toxicological effects of acrylamide on rat testicular gene expression profile. et al. Lee SH.S. Ospina M. Drexler H. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Lee MH. Washington (DC). Han CH. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. propylene oxide. Myers GL. Licea-Perez H. U.Acrylamide glycidamide by gas chromatography-mass spectrometry. Hemoglobin adducts of ethylene oxide.epa. Schettgen T. Agudo A. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Jin Y.50(17):4998-5006. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Drexler H.htm.gov/iris/subst/0286. Chemical Summary for Acrylamide. Mutat Res 2005.txt. Eriksson S. Liu K. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Tjønneland A. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Puppel N.206(1):9-14. Anal Biochem 1999. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. J Agric Food Chem 2002. Meyers T. Meyers T. Tareke E. Tjaden Z. The carcinogenicity of acrylamide.S. Ding X. et al. Reprod Toxicol 2005. J Agric Food Chem 2008. Rice JM. Rossbach B. Available at URL: http://www. Schettgen T.20(6):959-64. Letzel S. Kutting B. Integrated Risk Information System (IRIS). Acrylamide. Angerer J. Vesper HW. Int J Hyg Environ Health 2003.gov/chemfact/s_acryla. Marko D. Weiss T. U.S. Angerer J.580(1-2):71-80. Available at URL: http://www. Karlsson P.56(15):6046-53. Adv Exp Med Biol 2005. 1994. 2/3/09. a carcinogen formed in heated foodstuffs. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Drexler H. Sun H.19(4):527-34. Rapid Commun Mass Spectrom 2006. Tornqvist M. Choi JH. Xie Q. 2/3/09 Vesper HW.274(1):59-68. Hallmans G. September. Angerer J.163(2):101-8. Fu D. Vesper HW. EPA). Chae C. Mutat Res 2005 Feb 7.S. Rydberg P. Yang HJ. EPA). Office of Pollution Prevention and Toxics. Gray JG. Toxicol Lett 2002. Ingham L. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Broding HC. Analysis of acrylamide. Environmental Protection Agency (U.epa. revised 1/3/06.561:89-96. Environmental Protection Agency (U. Smith A. Slimani N.580(1-2):3-20. Int J Hyg Environ Health 2004.134(1-3):65-70. Ospina M. Schettgen T. Fueller F.207(6):531-9.

30) 2.080-.066 (.137 (.090-.500 (. see Data Analysis section) for Survey years 99-00.87-3.180) .060-.110 (.740-1.139) * .071) .75) 1.65 (1.090-.23-2. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.087-.35 (2.48-3.200) 1.670) .076-. emphysema.505 (.94) 1.312) .580) .54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .080-.066-.950 (.350-.570 (.190-.137-.20-2.990) .234) .32-2.96) 2.060 (<LOD-.308 (.075 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.108) * . 2004).470-.95) 1.130) .43 (1. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.430-1.02) 1.44) 2.220) .99) 2.086 (. 2004).180) .059-. cardiovascular disease.12-4.09-3.220) .210 (.30) * .190-.540 (.18-3.790) .70) 2.910-1.01 (1.950-1.54 (1.63-2.5% nicotine by weight (Kozlowski et al.93) .50) 3.150) .40) .81-2.310) 90th 1.180 (.068) .53 (1.726) .14) .20) 1.920 (.084) .220-.450-.840) 3.S.85 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.070) .260) 1.047-.84-3.140 (.164 (.087) < LOD < LOD .900-1.350 (.061) < LOD .12 (2.506 (. ** In the 2001-2002 survey period.094) .060) .96-4.070) 75th .060 (<LOD-.310) .00) 1.740-1. maternal exposure during pregnancy can result in lower birth weight.S.23 (1.280 (.28-1. Cigarettes contain about 1.68) 2.080 (.20) .180 (.570-1.120 (.05.068) .34 (1.110 (.089) Age group 3-11 years 99-00 01-02** 03-04 .050 (<LOD-.68 (1.580-1. and 17% had an LOD of 0.087 (.62 (2.66 (1.19) 1.26-1.89) 1.02 (.110 (.030-.120-. stroke.820) .120 (.620 (.710 (.19-2. DHHS.42-4.28) .198) * .100-.68) .160 (.131 (.201) .160) .050) . and exacerbated asthma (U.05 ng/mL.860 (.540-..660) .630 (.154-.115-.55 (1.21 (.57) 2.620-1.70-2. ear problems.043-.48-2. respectively.96 (1.040 (.12) 1. 83% of measurements had an LOD of 0.040 (. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.350-.770) .77 (2.110 (.690 (.83-2.060 (.059-.110-.050-.20 (.533-. acute respiratory illness.080-.153-.066) .66) 1.930 (.44 (2.213) .190-.110-.625) .320) .22) 2.77 (1.144 (.187) .111-.62) 2.730 (. Fourth National Report on Human Exposure to Environmental Chemicals 15 .050) .073) < LOD .14-1.180) .76 (1.360) .050 (.077) .77 (1.15) 2. population from the National Health and Nutrition Examination Survey.050 (<LOD-.070) .110 (.00) .193) .580 (. Children exposed to ETS are at increased risk for sudden infant death syndrome.188) .88 (1.052 (<LOD-.148-.110) .09-3.04 (1.120) .54) 1.050-.50-4.16) .030-.030 (.071 (.080-.160-.17 (1.480-.124 (.50-1.050 (<LOD-.175 (. 2006).53-4. 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.44 (1.630 (.110-.062 (.600-1.120-.160) .020-. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.60-2.12 (1.160 (.150) .88 (.160 (.216 (.20 (1.047-. 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. and various other disorders (U.163) .120 (.370-.080) < LOD .300) .145) .410) . Survey Geometric mean (95% conf.140-.17) .260-1.106-. 1998).02) 1.090-. < LOD means less than the limit of detection.54 (1.17 (.50 (1.060 (.14) .015.01) 3.92) 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 .39) 3.126) .47-3.302) .990 (.120 (.110) .21-1.164 (.052 (<LOD-.167 (.39 (1.140 (.11) .130 (.058 (.66-3.428-. and 03-04 are 0.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .240 (.480-1.050 (<LOD-.32-2.104-.21-1.S.99) 2.850 (.060-. and 0. which may vary for some chemicals by year and by individual sample. DHHS.163 (.140-.053 (<LOD-.770-1.Cotinine Cotinine CAS No.180) .180) .09-2.15 (2.30) 2.230) .23 (.630 (.770) .142-.080 (.520 (.040 (.960-1.070 (<LOD-.015 ng/mL.040-. Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.030-.49) 1.310-1.510 (.42 (1.79) 3.45) 1.197) .040-.800 (.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.19) .92 (1.49) 1.060-.05) 1.997-3.063) .78) 2.38-2.057-.054 (.32) 1.310-1.088-. acute respiratory infections.621-1.33-2.077) .63 (2.070-.23 (2.230 (.55-2.400-.44) 2.080) < LOD < LOD .120 (.

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

Coordinating Center for Health Promotion. Benowitz NL. U.57(1):79115. 2004. Kozlowski LT. Benowitz NL. Jacob P III.7:369-375. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. the United Kingdom. Sosnoff CS. Available at URL: http://www. Flegal KM.gov/tcrb/monographs/10/. Cotinine as a biomarker of environmental tobacco smoke exposure.275:1233-1240. population to secondhand smoke: 1988-2002. Available at URL: http://monographs. National Center for Chronic Disease Prevention and Health Promotion. Fong I. Lewis PJ. Tobacco Smoke. U.S. 4/13/09 Perez-Stable EJ.niosh. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Available at URL: http:// cancercontrol. BMJ 1975. [online].fr/ENG/Monographs/ allmonos90. Benowitz NL. Pickett MA. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA): 2005. Am J Public Health 2004. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Centers for Disease Control and Prevention.S. Kira S. IARC Monogr Eval Carcinog Risks Hum. Turner DM. Dollery CT. Hukkanen J. Giovino G. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Tobacco related exposures. and the United States. cigarette smokers: the Third National Health and Nutrition Examination Survey.S.280:135-140. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. Available at URL: http://ntp. June. George CF. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. 1999-2002. Filter ventilation and nicotine content of tobacco in cigarettes from Canada.pdf. Pollack HA.cdc. Tobacco Smoke and Involuntary Smoking. Strauss WJ. Jacob P. JAMA 1998. 11th ed.surgeongeneral. Tob Control 2006.gov/ntp/roc/eleventh/profiles/ s176toba. Aiba M. Vogler GP. Centers for Disease Control and Prevention. Summary of Data Reported and Evaluation [online] 1986. et al. Smoking and Tobacco Control Monograph 10 [online]. Curtin LR. Racial/ethnic differences in serum cotinine levels among adult U.280:152-156.nih. Ethnic differences in N-glucuronidation of nicotine and cotinine.15:302-307. International Agency for Research on Cancer. Epidemiol Rev 1996.iarc. Schober SE. 4/13/09 Centers for Disease Control and Prevention (CDC). Metabolism and disposition kinetics of nicotine. Soliman S. Bernert JT.4:313-316. Herrera B. Vol 83. Department of Heath and Human Services. JAMA 1996. Environ Health Perspect 2006. In Report on Carcinogens. References Armitage AK. J Pharmacol Exp Ther 1999. Maurer KR.114(6):853-858. Perez-Stable EJ. available at URL: http://mtn.pdf. Herrera B. Coordinating Center for Health Promotion.fr/ENG/Monographs/allmonos90.S.gov/eid/rmca/critdocs/ criteriadoc/33. iarc. Jacob III P. Mehta NY.php.S. Tob Control 1998. Richter PA. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Pechacek TF. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Pharmacol Rev 2005. Clin Pharmacol Ther 1994. Respiratory nicotine absorption in non-smoking females during passive smoking. Etzel RA. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Brody DJ.cancer. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Bernert JT.niehs. National Toxicology Program (NTP).S. IARC Monogr Eval Carcinog Risks Hum.gov/library/ secondhandsmoke/. Warner K. 4/13/09 Iwase A. Summary of Data Reported and Evaluation [online] 2004.18:188-204. Benowitz NL. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . Absorption and metabolism of nicotine from cigarettes. Department of Heath and Human Services. Caudill SP. Schwartz SS.56:483-493. 1988-1991. Houseman TH. Jacob P III. Office on Smoking and Health [online] 2006. 4/13/09 U.S. DHHS). Benowitz NL. 1999. Pirkle JL. Exposure of the U.S Department of Health and Human Services (U. Caraballo R. Available at URL: http://monographs. Pirkle JL.291(3):1196-1203. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace.63:139-43.S Department of Health and Human Services (U. Pechacek TF.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. 1988-1991. Jarvis MJ. JAMA 1998. Centers for Disease Control. Sweeney CT. 4/13/09 International Agency for Research on Cancer.php. National Institute for Occupational Safety and Hygiene (NIOSH). 4/13/09 National Cancer Institute (NCI). Nicotine metabolism and intake in black and white smokers. Modin G. DHHS). Vol 38. Brody DJ. U. Trends in the exposure of nonsmokers in the U. Int Arch Occup Environ Health 1991. Giovino GA.94(2):314-320. et al. Mowery PD. 1991.

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

including seizures and encephalopathy. have been reported as result of self-poisoning by ingestion or excessive dermal application. Sudakin and Trevathan.250) < LOD . 2003). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .100-.150) < LOD .S.110 (.100-. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations. DEET has low acute toxicity. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.100 (<LOD-.180 (.100-. 2003). population from the National Health and Nutrition Examination Survey.N-Diethyl-meta-toluamide (DEET) N.130 (. Its use is recommended for prevention of several vector-borne diseases.220 (. 2005). (U. (Kolpin et al.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . DEET is not genotoxic.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2002).S..110-.S.110 (<LOD-.110 (.240) < LOD . EPA.130 (.S.110-.120-. 1998).130-. DEET can be applied to clothing and the skin to repel biting insects.130) < LOD . Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.130-.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 . People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.EPA. and they range in concentration from 4% to 100%.120-. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1995.140 (.100-.140) < LOD .270) 688 678 518 700 598 956 Limit of detection (LOD. One survey detected DEET in 74% of sampled streams in the U.100-..130) < LOD . After absorption.. Neurological effects in humans. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al. and it has not been rated by IARC or NTP with respect to human carcinogenicity.520) < LOD .EPA. DEET is also used in combination with dermal sun screens (U. Fourth National Report on Human Exposure to Environmental Chemicals 19 .110 (. Additional information is available from U.EPA at: http://www.110 (<LOD-. 1998). 2002).449 and 0.180 (.130-.130-.210 (.140-.100-. DEET is not registered for use on agricultural commodities.110 (.560) < LOD . There are over 225 insect repellents brands containing DEET.130 (.160) < LOD .170 (.N-Diethyl-meta-toluamide (DEET) CAS No.140) < 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 . About 3-8% of dermally applied DEET is absorbed. DEET is not a developmental or reproductive toxicant in animals (U.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 .epa.S.180 (. 134-62-3 General Information N. which may vary for some chemicals by year and by individual sample.gov/pesticides/. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.190) < LOD .140) < LOD .180) < LOD .N. Survey Geometric mean (95% conf. Urinary N. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.1.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957.170 (.

130 (<LOD-.190 (.N.640 (. 2007).250) < LOD .350) < LOD .150-.230) < LOD .410 (. Urinary N.490) < LOD .390-.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 .320 (. Survey Geometric mean (95% conf.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.240-.270) < LOD . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.190 (<LOD-. 2005).S. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.350) < LOD .280 (.230-.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.440) < LOD ..290-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .370-.200 (.270 (<LOD-.230-. population from the National Health and Nutrition Examination Survey.93) < LOD .410 (. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.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 . In this survey period. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.250-.630) < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.300 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.190-.150) < LOD .270 (.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.170-.330 (.140-.500) size 1977 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .270-.320) < LOD . 1992).410-.240) < LOD .. representative subsamples from NHANES 2001-2002.S.350-.480 (. Urinary DEET levels as high as 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .190 (.250 (.280-1. 20 Fourth National Report on Human Exposure to Environmental Chemicals .330 (.370) < LOD .500 (.

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

Disinfection By-Products (Trihalomethanes)

Disinfection By-Products (Trihalomethanes)
Bromodichloromethane CAS No. 75-27-4 Dibromochloromethane (Chlorodibromomethane) CAS No. 124-48-1 Tribromomethane (Bromoform) CAS No. 75-25-2 Trichloromethane (Chloroform) CAS No. 57-57-8 General Information Disinfection by-products (DBP) are a class of chemical by-products also referred to as trihalomethanes (THMs), formed when chlorine or bromine interacts with the natural organic materials found in water. DBPs also include other formed products, such as haloacetic acids, haloacetonitriles, haloketones, and chlorophenols. The composition and levels of specific DBPs are determined by water quality, water treatment conditions, and disinfectant type (IPCS, 2000). Primary sources of DBPs are chlorinated drinking water and recreational water bodies, such as swimming pools.

In drinking water, trichloromethane is the predominant DBP, usually found at much higher levels than bromodichloromethane; tribromomethane is the least abundant (Krasner et al., 1989). DBPs are volatile at room temperature and can be detected in ambient air during activities such as showering, bathing, dishwashing, and swimming (Backer, et al., 2000; Gordon et al., 2006). Trichloromethane has industrial applications and is used to produce refrigerants and feedstock. It may be released into the environment where chlorine-based chemicals are used for bleaching and disinfecting processes or disposed at hazardous waste sites (IPCS, 2004; LaRegina, et al. 1986). Tribromomethane has limited industrial uses, mainly in geological assaying, electronics manufacturing, and as a solvent in laboratory analyses (ATSDR, 2005). DBPs tend not to bioaccumulate in aquatic organisms or persist in open or surface waters or soils, but they can remain in water within closed pipe systems. Workplace exposure may occur during the production of trichloromethane or tribromomethane, or in workplaces where DBPs may be generated, such as pulp or paper manufacturing, swimming pools, and water treatment plants (IPCS, 2004). General population exposure to DBPs occurs primarily through ingesting chlorinated water and inhaling the water

Blood Bromodichloromethane
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 2.21 (1.65-2.97)

Selected percentiles
( 95% confidence interval)

50th 2.30 (1.56-3.21) 1.40 (1.10-1.90)

75th 4.63 (3.24-6.20) 3.40 (2.60-4.20)

90th 8.45 (5.86-12.0) 6.20 (5.30-7.00)

95th 12.0 (7.68-19.2) 9.50 (7.00-12.0)

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

1.50 (1.20-1.86)

Sample size 785 1322

01-02 03-04

2.21 (1.65-2.97) 1.50 (1.20-1.86)

2.30 (1.56-3.21) 1.40 (1.10-1.90)

4.63 (3.24-6.20) 3.40 (2.60-4.20)

8.45 (5.86-12.0) 6.20 (5.30-7.00)

12.0 (7.68-19.2) 9.50 (7.00-12.0)

785 1322

01-02 03-04 01-02 03-04

2.19 (1.60-3.00) 1.48 (1.18-1.85) 2.24 (1.66-3.01) 1.51 (1.21-1.90)

2.31 (1.63-3.21) 1.40 (.940-2.00) 2.28 (1.49-3.24) 1.50 (1.10-1.90)

4.64 (3.21-6.08) 3.40 (2.60-4.30) 4.63 (3.09-7.01) 3.30 (2.50-4.20)

7.96 (5.74-15.3) 6.60 (5.40-7.20) 8.62 (5.26-12.9) 6.10 (4.69-7.30)

13.0 (6.93-20.5) 11.0 (7.20-14.0) 11.1 (7.68-25.0) 7.80 (6.40-12.0)

382 650 403 672

01-02 03-04 01-02 03-04 01-02 03-04

3.28 (2.29-4.68) 1.65 (1.15-2.38) 2.32 (1.82-2.94) 1.56 (1.15-2.13) 2.02 (1.42-2.87) 1.42 (1.11-1.81)

3.32 (2.19-4.70) 1.60 (.820-2.80) 2.50 (1.56-3.55) 1.70 (1.10-2.20) 2.16 (1.36-3.09) 1.30 (.850-1.90)

6.81 (3.71-10.4) 3.50 (2.60-4.90) 4.57 (3.60-5.56) 2.90 (2.15-3.80) 4.34 (2.92-6.01) 3.30 (2.30-4.40)

10.8 (8.24-14.7) 7.30 (4.50-10.0) 8.69 (5.63-9.49) 5.10 (3.80-6.60) 7.33 (4.72-15.3) 6.20 (5.20-7.20)

14.7 (11.1-20.5) 10.0 (7.30-11.0) 10.0 (5.89-13.5) 6.60 (4.90-13.0) 11.1 (6.01-26.1) 9.80 (6.70-13.0)

227 244 130 290 365 684

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.233 and 0.62. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds.

22

Fourth National Report on Human Exposure to Environmental Chemicals

Disinfection By-Products (Trihalomethanes)

vapor. Dermal absorption also may occur during bathing and swimming (ATSDR, 1997, 2005; Dick, et al., 1995; Leavens et al., 2007). Each of the DBPs is rapidly absorbed and distributed widely throughout the body. In animals, these chemicals undergo hepatic metabolism to reactive chemicals, which can bind to cell macromolecules and be toxic in large amounts (IPCS, 2000). Ultimately, DBPs are metabolized to carbon dioxide, which is eliminated in exhaled air within a few hours. Only a small amount of each DBP is eliminated unchanged in urine. Elimination halflives for these chemicals are less than four hours (ATSDR, 2005; Leavens et al., 2007). Human health effects from DBPs at low environmental doses or at biomonitored levels from low environmental exposures are unclear or unknown. Humans exposed to massive levels of trichloromethane or tribromomethane develop central nervous system depression and hepatotoxicity (ATSDR, 2005, 1997). Acute animal toxicity studies of each of these chemicals have found central nervous system depression, liver and renal damage or necrosis, and occasionally, cardiac depression and arrhythmias (IPCS, 2000). In studies of rodents chronically fed high doses of either trichloromethane or bromodichloromethane, carcinomas occurred in the liver and kidney; large intestine tumors and

polyps were also noted with bromodichloromethane (NCI, 1976; NTP, 1987). Chronic feeding studies in rodents with either dibromochloromethane or tribromomethane showed inconsistent evidence of carcinogenicity across species and genders. The DBPs did not produce reproductive or developmental effects in animals unless maternal toxicity was present, but bromodichloromethane altered sperm motility (IPCS, 2000). Numerous epidemiologic studies of the relationships between chlorinated water source and various cancers, adverse reproductive outcomes, and cardiovascular disease have been inconclusive (IPCS, 2000). IARC classified trichloromethane and bromodichloromethane as possible human carcinogens, and NTP determined that these chemicals are reasonably anticipated to be human carcinogens. However, IARC found dibromochloromethane and tribromomethane to be unclassifiable regarding human carcinogenicity. The U.S. EPA has established drinking water and environmental standards for “total THMs.” OSHA and ACGIH have established workplace standards and guidelines, respectively, for trichloromethane and tribromomethane. Information about external exposure (i.e., environmental levels) and health effects is available from ATSDR at: http://www.atsdr.cdc.gov/toxpro2.html.

Blood Dibromochloromethane
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) .867 (.521-1.44)

Selected percentiles
( 95% confidence interval)

50th .780 (.340-1.90) < LOD

75th 2.61 (1.22-4.38) 1.30 (1.00-1.80)

90th 5.46 (3.53-9.71) 3.60 (2.70-4.80)

95th 8.96 (5.04-12.9) 7.20 (4.80-8.60)

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

*

Sample size 781 1333

01-02 03-04

.867 (.521-1.44) *

.780 (.340-1.90) < LOD

2.61 (1.22-4.38) 1.30 (1.00-1.80)

5.46 (3.53-9.71) 3.60 (2.70-4.80)

8.96 (5.04-12.9) 7.20 (4.80-8.60)

781 1333

01-02 03-04 01-02 03-04

.850 (.481-1.50) * .884 (.550-1.42) *

.730 (.300-2.25) < LOD .820 (.340-1.69) < LOD

2.66 (.960-4.38) 1.30 (1.00-1.90) 2.54 (1.37-4.31) 1.30 (1.00-1.80)

4.77 (3.33-9.20) 3.70 (2.70-5.70) 6.30 (3.28-10.1) 3.60 (2.50-4.80)

8.06 (4.31-14.6) 7.20 (5.20-8.60) 9.91 (5.02-13.0) 6.60 (3.80-9.20)

371 657 410 676

01-02 03-04 01-02 03-04 01-02 03-04

1.61 (.843-3.06) 1.20 (.963-1.50) 1.03 (.505-2.09) * .736 (.413-1.31) *

1.49 (.670-3.99) 1.10 (.810-1.40) .930 (.530-2.03) < LOD .640 (<LOD-1.93) < LOD

4.59 (1.93-8.89) 2.30 (1.50-4.10) 2.03 (.770-7.06) .970 (.650-1.60) 2.49 (.870-4.27) 1.30 (.950-1.80)

9.26 (5.21-12.1) 5.20 (3.80-6.90) 4.22 (2.01-10.5) 1.90 (1.20-3.20) 4.57 (3.00-7.12) 3.30 (2.50-4.60)

12.0 (9.63-16.1) 7.70 (5.20-11.0) 8.09 (2.80-16.5) 3.20 (1.80-5.20) 6.98 (4.27-11.1) 6.60 (3.70-9.20)

233 256 128 288 357 685

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.271 and 0.62. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Fourth National Report on Human Exposure to Environmental Chemicals

23

Disinfection By-Products (Trihalomethanes)

Biomonitoring Information Levels of blood DBPs reflect recent exposure. Geometric mean blood trichloromethane levels were 0.039 and 0.043 ng/mL among non-smoking and smoking adults, respectively, in a subsample of NHANES 1999-2000 participants (Lin et al., 2008), which were at least twice as high as comparable levels in NHANES 2001-2002 and 2003-2004. In a non-representative sample of NHANES III (1988-1994) participants, the geometric mean and median blood trichloromethane levels, respectively, were 0.043 and 0.023 mg/L (Churchill et al., 2001). Similar median blood trichloromethane levels were reported in smaller studies of U.S adults (Ashley et al., 2005; Backer et al., 2000; Buckley et al., 1997) and in this Report. Immediately following bathing or showering with chlorinated water, median blood levels of trichloromethane, dibromochloromethane, and bromodichloromethane can increase two to four times over baseline levels, and then return to baseline rapidly during the next one to two hours (Ashley et al., 2005; Backer et al., 2000). Finding a measurable amount of one or more of these THMs in blood does not mean that the level of THMs causes an adverse health effect. Biomonitoring studies of blood

THMs can provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of THMs than levels found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Blood Tribromomethane (Bromoform)
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 1.57 (1.07-2.31)

Selected percentiles
( 95% confidence interval)

50th 1.39 (.960-2.02) < LOD

75th 2.78 (1.76-4.63) 1.80 (<LOD-2.80)

90th 6.05 (2.92-29.2) 3.74 (2.30-7.10)

95th 15.5 (3.68-85.4) 6.40 (3.60-14.0)

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

*

Sample size 774 1310

01-02 03-04

1.57 (1.07-2.31) *

1.39 (.960-2.02) < LOD

2.78 (1.76-4.63) 1.80 (<LOD-2.80)

6.05 (2.92-29.2) 3.74 (2.30-7.10)

15.5 (3.68-85.4) 6.40 (3.60-14.0)

774 1310

01-02 03-04 01-02 03-04

1.49 (.944-2.34) * 1.67 (1.17-2.39) *

1.29 (.850-1.98) < LOD 1.46 (1.05-2.21) < LOD

2.65 (1.49-5.05) 1.90 (<LOD-2.87) 2.86 (1.89-4.57) 1.72 (<LOD-2.65)

6.12 (2.26-33.9) 4.00 (2.40-6.80) 5.69 (3.30-27.5) 3.20 (1.93-7.70)

14.9 (2.79-69.9) 6.50 (4.00-13.0) 22.2 (5.09-49.6) 6.10 (3.10-31.0)

374 645 400 665

01-02 03-04 01-02 03-04 01-02 03-04

2.34 (1.15-4.77) * 1.51 (.857-2.67) * 1.47 (.980-2.22) *

1.66 (.990-3.38) 1.60 (<LOD-3.10) 1.47 (.780-3.15) < LOD 1.29 (.840-2.06) < LOD

4.03 (1.42-36.5) 3.30 (<LOD-9.40) 2.58 (1.39-4.64) 1.60 (<LOD-2.30) 2.58 (1.51-4.91) 1.70 (<LOD-2.90)

28.3 (4.39-49.2) 7.60 (3.60-14.0) 4.34 (2.57-8.48) 2.50 (1.80-3.20) 5.69 (2.84-21.2) 3.50 (2.00-7.70)

40.8 (31.5-57.9) 11.0 (5.60-210) 6.27 (3.28-15.2) 3.20 (2.40-6.10) 11.0 (3.30-69.9) 5.90 (3.30-21.0)

234 242 121 289 362 680

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 0.596 and 1.5. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

24

Fourth National Report on Human Exposure to Environmental Chemicals

Disinfection By-Products (Trihalomethanes)

Blood Trichloromethane (Chloroform)
Geometric mean and selected percentiles of blood concentrations (in pg/mL) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey years# 01-02 03-04 Geometric mean
(95% conf. interval) 16.6 (13.0-21.1)

Selected percentiles
( 95% confidence interval)

50th 16.1 (11.9-22.2) 10.0 (8.50-13.0)

75th 31.7 (23.9-40.4) 20.0 (17.0-24.0)

90th 55.5 (44.5-68.6) 35.0 (29.0-40.0)

95th 72.1 (57.3-105) 50.0 (37.0-65.0)

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

10.2 (8.56-12.2)

Sample size 744 1222

01-02 03-04

16.6 (13.0-21.1) 10.2 (8.56-12.2)

16.1 (11.9-22.2) 10.0 (8.50-13.0)

31.7 (23.9-40.4) 20.0 (17.0-24.0)

55.5 (44.5-68.6) 35.0 (29.0-40.0)

72.1 (57.3-105) 50.0 (37.0-65.0)

744 1222

01-02 03-04 01-02 03-04

16.8 (12.0-23.5) 10.1 (8.43-12.1) 16.4 (13.4-20.1) 10.4 (8.41-12.7)

16.1 (11.0-24.8) 10.0 (7.90-14.0) 16.6 (12.0-21.5) 10.0 (8.40-13.0)

34.3 (22.4-48.7) 20.0 (17.0-25.0) 29.2 (24.0-36.5) 20.0 (16.0-23.9)

57.0 (39.9-76.4) 36.8 (29.0-49.0) 53.5 (38.4-68.9) 33.0 (26.0-40.0)

75.2 (54.5-156) 53.0 (36.8-69.0) 69.5 (53.3-104) 46.0 (35.0-65.0)

358 599 386 623

01-02 03-04 01-02 03-04 01-02 03-04

17.0 (10.5-27.6) 9.17 (7.45-11.3) 19.1 (12.9-28.1) 11.8 (9.54-14.6) 15.6 (12.0-20.2) 9.84 (8.09-12.0)

14.5 (10.0-32.7) 9.30 (7.60-11.0) 20.9 (9.28-37.4) 12.0 (8.90-15.0) 15.2 (11.2-20.5) 10.0 (8.10-13.0)

35.1 (18.6-57.6) 19.0 (15.0-24.0) 38.4 (27.7-46.0) 20.0 (15.0-30.0) 26.8 (20.4-39.5) 20.0 (16.0-23.0)

60.7 (41.5-100) 34.0 (24.0-44.4) 55.9 (45.5-69.8) 35.0 (28.0-59.0) 53.5 (35.3-72.1) 33.8 (27.0-40.0)

93.0 (49.7-243) 44.4 (30.0-59.0) 68.9 (51.9-74.0) 61.0 (34.0-100) 69.5 (53.5-105) 47.0 (35.0-67.0)

223 225 116 272 348 630

Limits of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 2.37 and 2.11. # Survey period 2001-2002 is a one-third subsample of 20-59 year olds; Survey period 2003-2004 is a one-half subsample of 20-59 year olds.

Fourth National Report on Human Exposure to Environmental Chemicals

25

Disinfection By-Products (Trihalomethanes)

References Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for chloroform update. 1997 [online]. Available at URL: http://www.atsdr.cdc.gov/toxprofiles/tp6.html. 4/26/09 Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological profile for bromoform and chlorodibromomethane. 2005 [online]. Available at URL: http://www.atsdr.cdc.gov/ toxprofiles/tp130.html. 4/26/09 Ashley DL, Blount BC, Singer PC, Depaz E, Wilkes C, Gordon S, et al. Changes in blood trihalomethanes concentrations resulting from differences in water quality and water use activities. Arch Environ Occup Health 2005;60(1):7-15. Backer LC, Ashley DL, Bonin MA, Cardinali FL, Kieszak SM, Wooten JV. Household exposures to drinking water disinfection by-products: whole blood trihalomethane levels. J Expo Anal Environ Epidemiol 2000;10(4):321-326. Buckley TJ, Liddle J, Ashley DL, Paschal DC, Burse VW, Needham LL. Environmental and biomarker measurements in nine homes in the lower Rio Grande Valley: multimedia results for pesticides, metals, PAHs and VOCs. Environ Int 1997;23(5):705732. Churchill JE, Ashley DL, Kaye WE. Recent chemical exposures and blood volatile organic compound levels in a large populationbased sample. Arch Environ Health 2001;56(2):157-166. Dick D, Ng KM, Sauder DN, Chu I. In vitro and in vivo percutaneous absorption of 14C-chloroform in humans. Hum Exp Toxicol 1995;14: 260-265. Gordon SM, Brinkman MC, Ashley DL, Blount BC, Lyu C, Masters J, Singer PC. Changes in breath trihalomethane levels resulting from household water-use activities. Environ Health Perspect 2006;114(4):514-521. International Programme on Chemical Safety (IPCS). Environmental Health Criteria 216. Disinfectants and Disinfectant By-Products. 2000 [online]. Available at URL: http://www. inchem.org/documents/ehc/ehc/ehc216.htm.4/26/09 International Programme on Chemical Safety (IPCS). Concise International Chemical Assessment Document 58. Chloroform. 2004 [online]. Available at URL: http://www.inchem.org/ documents/cicads/cicads/cicad58.htm. 4/26/09 Krasner SW, McGuire MJ, Jacaugelo JG, Patania NL, Reagan KM, Aieta EM. The occurrence of disinfection by-products in US drinking water. J Am Water Works Assoc 1989;81:41–53. LaRegina J, Bozzelli JW, Harkov R, Gianti S. Volatility organic compounds at hazardous waste sites and a sanitary landfill in New

Jersey. An up-to-date review of the present situation. Environ Prog 1986;5:18-27. Leavens TL, Blount BC, De Marini DM, Madden MC, Valentine JL, Case MW, et al. Disposition of bromodichloromethane in humans following oral and dermal exposure. Toxicol Sci 2007;99(2):432-445. Lin YS, Egeghy PP, Rappaport SM. Relationships between levels of volatile organic compounds in air and blood from the general population. J Expo Sci Environ Epidemiol 2008;18(4):421-9. National Cancer Institute (NCI). Report on the carcinogenesis bioassay of chloroform (CAS No. 67-66-3). National Cancer Institute Carcinogenesis Technical Report Series March 1, 1976. [online]. Available at URL: http://ntp.niehs.nih.gov/ntp/htdocs/ LT_rpts/trChloroform.pdf. 4/26/09 National Toxicology Program (NTP). Carcinogenesis studies of bromodichloromethane (CAS No. 75-27-4) in F344/N rats and B6C31F mice (gavage studies). Technical Report Series No. 321. 1987 [online]. Available at URL: http://ntp.niehs.nih.gov/ntp/ htdocs/LT_rpts/tr321.pdf. 4/26/09

26

Fourth National Report on Human Exposure to Environmental Chemicals

Environmental Phenols

Benzophenone-3
CAS No. 131-57-7 General Information Benzophenone-3 (2-hydroxy-4-methoxybenzophenone) occurs naturally in some flowering plants. It is commercially synthesized as a sunscreen for use in lotions, conditioners, and cosmetics. It is also used as a UV stabilizer in plastic surface coatings and polymers. Benzophenone-3 is a common ingredient in sun-blocking agents. People may be exposed through dermal application of sunscreens and cosmetic products. Small amounts of benzophenone-3 can be absorbed through human skin and excreted in the urine, mostly as a glucuronidated conjugate (Gonzalez et al., 2006; Gustavsson et al., 2002; Janjua et al., 2004; Ye et al., 2005). After dermal application of a 4% lotion over the entire body daily for 5 days, one study found that 1.2-8.7% of the applied benzophenone-3 amount was recovered in the urine (Gonzalez et al., 2006). Human health effects from benzophenone-3 at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Following dermal application, some cases of photoallergy or allergy to benzophenone-3 have been reported. Male reproductive toxicity has been inconsistently reported in chronic high dose animal studies (Daston et al., 1993; French, 1992). Benzophenone-3 has weak estrogenic activity or weak anti-androgenic activity (French, 1992; Schlecht et al., 2004; Schlumpf et al., 2001; Schreurs et al., 2005). No human hormonal changes were observed during four days of application of 10% benzophenone-3 lotion (Janjua et al., 2004). Benzophenone-3 is not considered mutagenic (Robison et al., 1994). IARC and NTP have no ratings as to human carcinogenicity of benzophenone-3. Biomonitoring Information Urinary benzophenone-3 levels include both conjugated and unconjugated forms and reflect recent exposure to the chemical. The NHANES 2003-2004 levels of urinary benzophenone-3 have been described by Calafat et al. (2008). The analysis showed that female participants had slightly higher urinary levels than males and that nonHispanic whites were more likely than non-Hispanic blacks to have levels above the 95th percentile of the overall population. In a study of 90 U.S. females aged 6-8 years, the median urinary benzophenone-3 level of 14.7 µg/L was comparable to the median level of children 6-11 years of age (17.2 µg/L) in the NHANES 2003-2004 subsample (Calafat

et al., 2008; Wolff et al., 2007). Total benzophenone-3 urinary concentrations were detectable in 90% of a small sample of adults in whom the values ranged up to 3000 μg/L (Ye et al., 2005). Following short-term application of 10% benzophenone-3 lotion, men and women had mean urinary levels of 140 and 60 μg/L, respectively (Janjua et al., 2004). Finding a measurable amount of benzophenone-3 in urine does not mean that the levels of benzophenone-3 cause an adverse health effect. Biomonitoring studies on levels of benzophenone-3 provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of benzophenone-3 than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

Fourth National Report on Human Exposure to Environmental Chemicals

27

Environmental Phenols

Urinary Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone)
Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 22.9 (18.1-28.9)

Selected percentiles
( 95% confidence interval)

Sample 95th 1040 (698-1390) size 2517

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

years 03-04

50th 18.1 (15.5-23.2)

75th 94.0 (67.5-123)

90th 370 (225-570)

03-04 03-04 03-04

21.2 (16.4-27.3) 22.9 (18.0-29.3) 23.1 (18.0-29.6)

17.2 (14.9-25.9) 20.1 (16.1-25.1) 18.1 (14.7-23.3)

66.7 (38.7-102) 67.1 (45.2-93.8) 109 (72.1-140)

158 (106-246) 170 (137-240) 450 (315-733)

246 (154-618) 407 (183-717) 1220 (769-1750)

314 715 1488

03-04 03-04

16.8 (13.2-21.3) 30.7 (23.7-39.8)

13.7 (11.4-16.8) 26.0 (20.2-34.1)

55.3 (33.2-86.6) 137 (106-172)

178 (134-324) 596 (403-769)

567 (238-1350) 1340 (776-1790)

1229 1288

03-04 03-04 03-04

16.5 (10.9-25.1) 12.8 (9.38-17.4) 27.7 (20.3-37.8)

11.9 (8.50-18.3) 10.2 (7.40-14.4) 24.4 (16.8-32.0)

45.5 (25.9-78.2) 34.3 (22.8-50.6) 121 (83.6-162)

178 (76.4-412) 127 (90.8-176) 507 (316-769)

412 (178-2180) 247 (143-499) 1340 (733-2070)

613 652 1092

Limit of detection (LOD, see Data Analysis section) for Survey year 03-04 is 0.3.

Urinary Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) (creatinine corrected)
Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval) 22.2 (17.6-28.0)

Selected percentiles
( 95% confidence interval)

Sample 95th 1080 (686-1600) size 2514

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

years 03-04

50th 16.2 (12.7-21.6)

75th 82.0 (58.7-108)

90th 415 (283-577)

03-04 03-04 03-04

25.8 (19.5-34.1) 17.2 (13.7-21.5) 22.8 (17.8-29.1)

22.4 (14.4-33.7) 12.9 (10.4-16.5) 16.2 (12.7-21.9)

84.6 (41.0-131) 43.6 (29.5-57.7) 93.2 (66.0-130)

171 (132-365) 136 (91.7-239) 491 (361-700)

427 (171-710) 350 (173-646) 1330 (880-1880)

314 713 1487

03-04 03-04

13.6 (10.8-17.1) 35.5 (27.1-46.4)

10.3 (8.36-12.9) 28.2 (20.2-37.0)

40.0 (24.9-62.5) 144 (101-224)

169 (93.3-316) 686 (491-1130)

381 (229-685) 1850 (1220-2580)

1228 1286

03-04 03-04 03-04

15.1 (9.44-24.0) 8.78 (6.49-11.9) 28.3 (20.6-38.8)

11.1 (6.95-16.0) 6.80 (5.27-9.00) 22.0 (14.6-32.7)

40.7 (18.3-85.8) 19.7 (13.5-33.4) 116 (73.5-175)

158 (87.4-362) 79.8 (46.8-139) 510 (380-760)

595 (118-1860) 185 (79.8-536) 1330 (852-2410)

612 651 1091

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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

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.jrc. Endocrinology 2008. Koulova AI.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. An evaluation of the possible carcinogenicity of bisphenol A to humans. Pyo MY. Caudill SP. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Ispra..S. Yoshinaga J. Hanaoka T.59(9):625-628. 2/4/09 Ouchi K. 2002. Howdeshell KL.69(22):2611-2625. Ikka T. Watanabe C.eu/ health/ph_risk/committees/sct/documents/out156_en.pdf. Available at URL: http://ec. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Needham LL. Cunha G. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. vom Saal FS. Pharmaceuticals.14(2):149-157. Brussels. Haighton LA. Joskow R. Available at URL: http://ecb. Nippon Eiseigaku Zasshi 2004. bisphenol A glucuronide. Bradley S. Arakawa C. Proc Natl Acad Sci USA 2005. T. Zacharewski TR. Rat two-generation reproductive toxicity study of bisphenol A. 5: 505-523. Barr JR. Research Triangle Park. et al. Meyer MT. Occup Environ Med 2002. Regul Toxicol Pharmacol 2002. Lynch BS.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. N. Barr DB. Serizawa S. Fujii S. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. 2003. Watanabe S.gov/chemicals/bisphenol/bisphenol. Sottas CM.113(4):391-395. DirectorateGeneral Health and Consumer Protection. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Exposure of the U. Environ Sci Technol 2002.pdf. Available at URL: http://cerhr.68(1):121-146.. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. National Toxicology Program. Belgium.59(4):403-408. Zaugg SD. Toxicol Sci 2002. Shin HC. J Chromatogr B Analyt Technol Biomed Life Sci 2002. 1999-2000: a national reconnaissance. Tsugane S. May 22. Han SS. Timms BG. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). K. Gray GM. Kim JC. Furukawa M. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Ye X. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. J Am Dent Assoc 2006. niehs. Biochem Biophys Res Commun 2003.S. Thomas BF. Park S. Kim CS. 4. and Hardy MP. Keimowitz AR. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Matthews JB. Calafat AM. Joint Research Centre Institute of Health and Consumer Protection. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). and other organic wastewater contaminants in U. Available at URL: http://cerhr. Imai H. 2/4/09 European Commission. Hara K. European Commission. Chung MK. Reprod Toxicol 2001. Cohen JT. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents.780(2):365-370. Rhomberg et al. Twomey K. Harazono A. Leranth. Barber LB. Kim YH.145:592-603.gov/chemicals/bisphenol/BPAFinalEPVF112607.europa.pdf .nih. hormones. Calafat AM. Hum Ecol Risk Assess 2004. Marr MC. et al. Hughes C. NC. Kroes R.. Department of Health and Human Services. Doull J.niehs. streams.116(1):39-44. Klinefelter GR. 2008. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.Environmental Phenols References Akingbemi BT.35(2 Pt 1):238-254. 2/4/09 Fujimaki K. Human Health.36(6):1202-1211.10:875-921. Reidy JA. Barton L. McConnell EE. Thurman EM. Endocrinology 2004. Bisphenol A. November 26. Szigeti-Buck. Ecotoxicity and the Environment (CSTEE). 2007. Richter CA. In vitro and in vivo interactions of bisphenol A and its metabolite. C. with estrogen receptors alpha and beta. Myers CB.nih. Furlong ET.312(2):441-448. National Institute of Environmental Health Sciences. niehs. Italy. Koh WS. Available at URL: http://ntp. and Hajszan. Ekong J. Yang M. Kawamura N.102(19):7014-7019. National Institutes of Health.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. U.S. Reidy JA. MacLusky. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats.pdf . Tyl RW. Rubin C.J. Hlywka JJ.pdf. Needham LL. Cha SW. Kolpin DW. Kuklenyik Z. August 2001. Life Sci 2001. Wong LY. Needham LL. Chem Res Toxicol 2001. et al. Environ Health Perspect 2005. Brine DR. Gender differences in the levels of bisphenol A metabolites in urine. September. Environ Health Perspect 2008.149:988-994. Calafat AM. Kiguchi M. Munro IC. Ema M.Scientific Committee on Toxicity. Han SY.nih.137(3):353-362.

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

Survey Geometric mean (95% conf.274-. the various alkylphenols have also been used as emulsifiers and modifiers in paints.80 (1..20) 2.400) 1.60) 613 652 1092 Limit of detection (LOD.50) .5% of 139 U.60-3.90) 2.20) 314 715 1488 03-04 03-04 * * .50) 1.20 (1. 1996).10-2.600) 1. and from contact with some personal care products and detergents.60-3. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.60) 1.800-1. leading to inhalation as another potential exposure route (Rudel et al. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.200-.40) * 03-04 03-04 03-04 .507) * < LOD .30-2.300 (<LOD-.600-1.900 (. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. The alkylphenol ethoxylates enter the environment through human use of products containing them.g.2.60-3.50) . and was quickly eliminated from the blood (Certa et al.80) 2.70 (1. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.400 (.500) 75th .300 (<LOD-. In 1999-2000.10) 2. 1997.500) . impaired steroidogenesis.60-3.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.300 (<LOD-. Less frequently. which may vary for some chemicals by year and by individual sample.30 (1.400 (. Laws et al.S. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.300 (<LOD-.1.299-. which are anionic surfactants used in detergents.g.500-1.... fish) and drinking water. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.10) 1..50) 1. 4-octylphenol monoethoxylate was detected in 43.80 (1. < LOD means less than the limit of detection.20-2.10 (.50) 1. 2002).. have demonstrated estrogenic effects particularly when injected at high doses in animals.900 (. and some personal care products.20-2.30 (.200-.30 (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 .500) . 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.600) .900 (.20-2. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.600-1.40) 1.30 (1. an alkylphenol.900 (. orally administered 4-tert-octylphenol was well absorbed. 2006. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and the polyethoxy chain may consist of up to 50 ethoxy units. and emulsifiers.600) .500-1. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).00 (.369 (. 2003. The alkylphenols can bioaccumulate in some fish.00 (. 2000.30) 90th 1. 2000. 2002).600-1.60-3. including 4-tert-octylphenol. In rats.600-1..20-2.40 (1.477) .10 (1. 1995.00) 1229 1288 03-04 03-04 03-04 * .Environmental Phenols 4-tert-Octylphenol CAS No. textiles.S. did not bioaccumulate.30) 1.300 (<LOD-.20-2. through sewage.. Several alkylphenols. altered neonatal sexual development. Disposition in humans has not been studied sufficiently. altered estrus cycles and reproductive outcomes. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. over 500. to shorter chain alkylphenol ethoxylates.60) .600-1.00 (1.900 (.000 tons of alkylphenol ethoxylates were produced annually worldwide. and some of their degradation products are toxic to aquatic life. is used to manufacture alkylphenol ethoxylates. In the 1990s.500 (. see Data Analysis section) for Survey year 03-04 is 0.268-.497) * .500) .600) . streams in 30 states (Kolpin et al.3.. and through manufacturing waste streams (Warhurst.20) 1. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.10 (. and to alkylphenoxycarboxylates. 2004).50-2. Blake and Boockfor.90) 2. Ying et al. testicular atrophy.70 (1. population from the National Health and Nutrition Examination Survey.300-.70 (1. Katsuda et al.389 (.300-. Saito et al..70 (1.60-3.30 (1.50-3. Indoor and to a lesser extent.357 (. 140-66-9 General Information 4-tert-Octyphenol. pesticides. During the 1980s and 1990s.700-1. industrial cleaners. and impaired spermatogenesis (e. 34 Fourth National Report on Human Exposure to Environmental Chemicals .400 (.40) 1. Urinary 4-tert-Octylphenol (4-[1. Bian et al.20-2.30) 2.80 (1.40) 2.600-1.40) 2.50 (1.

460 (.00 (.370 (<LOD-.269 (.85 (1.15) 1.18-4.470-1.25-2.43) 1. at lower or environmentally relevant doses (Blake et al.05-2.270 (. 2000.54) * 03-04 03-04 03-04 .199-.00) 2.260 (<LOD-. 2003. 2001..02-4.910 (. In a small number of adult Japanese volunteers.S. Yoshida et al.470) 75th . Fourth National Report on Human Exposure to Environmental Chemicals 35 .25) 90th 1.14) 314 713 1487 03-04 03-04 * * .890-2.59) 1.65-3.36-3.530) .320 (<LOD-.3.81 (1. 2004).740 (.11) 2.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.420) .96-4.860 (.41) .00 (.08) 1.33 (2. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect.630-1.730-1.62) . It is unclear if estrogenic or other effects occur in animals through oral dosing.71) 2.740 (.450) .03 (1.53-3.300 (<LOD-.620-1.60 (1.400) .62 (1. Nagao et al.. Urinary 4-tert-Octylphenol (4-[1.770 (.160-.17 (.270-.78) 1228 1286 03-04 03-04 03-04 * . 1999).. Kawaguchi et al. 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.76 (2. Tyl et al. 2001).22) .435 (.270 (.73) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.00) 2..450) 1.03 (1.1.276 (.20 (1.06 (2.540-1.850 (. nonylphenol.550-1.43) 1.00) 1.67-2.500-1.10-2.560) .31-2. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.349) * < LOD . 2004.40-4.25) 2.470-1.620) .29) 2. Sweeney et al. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.78) 3. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.570) .337-. 2005.59 (1.03-6.610) .170-..11-2.40 (1.384) * . Calafat et al.Environmental Phenols Myllymaki et al. 4-tert-Octylphenol is not considered directly genotoxic.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.68) 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. or their corresponding ethoxylates with respect to human carcinogenicity.33) 3.380 (<LOD-.410 (.43-3.78 (1. representative subsample of NHANES 2003-2004.00) 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 . IARC and NTP have not rated octylphenol.64 (.207-.11) 1.640-1.280-.62 (1. Survey Geometric mean (95% conf.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.68-2.50 (2. population from the National Health and Nutrition Examination Survey.31 (1.

Saito I. Nicol L. Indoor air pollution by alkylphenols in Tokyo. Taya K. J Chromatogr B Analyt Technol Biomed Life Sci 2004. nonylphenol. Yoshimura Y. Nakagomi M. Toxicol Appl Pharmacol 2000. Katsuda S. Korn LR. Camann DE. Boockfor FR. Muller AM.54(1):154-167. testis size. Roche JF. Wang X. Exposure of the U. Nagao T. An environmental assessment of alkylphenol ethoxylates and alkylphenols. streams.71(1-2):112-122. Brooks AN. Kookana R.207(1):59-68. Zaugg SD. and sertoli cell number. Wiegand HJ. Two-generation reproduction study with para-tert-octylphenol in rats. Ono H. Paranko J. Williams B. Millette CF. Regul Toxicol Pharmacol 1999. Wong LY. and testosterone. Takenaka A. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Yoshimura S.co. Brine DR. Toxicol Sci 2000. Raychoudhury SS. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Thurman EM. Katsuda S. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Taya K. et al. Inoue K. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone.18(1):43-51. prolactin. Ye X. Izumi S. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Toxicol Appl Pharmacol 2005. Seto H. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Myers CB. bisphenol A and methoxychlor in rats. Qian J. Maekawa A. Rudel RA. Calafat AM.799(1):119-125.36(6):1202-1211. Certa H. 2003. Okada F.14(5):325-332. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Watanabe G. Bodman GJ. Needham LL. Fail PA. pesticides. Estrogenic activity of octylphenol. Arch Toxicol 1996. Yoshida M. 1995. Kawaguchi M. Watanabe G. Brody JG. Maekawa A. et al. et al.pdf. Haavisto TE. and other endocrine-disrupting compounds in indoor air and dust. Blake CA. Phthalates. Karjalainen M. Warhurst AM. 2/4/09 Ying GG. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Available at URL: http:// www. hormones. Pharmaceuticals.S. Blake CA. Bolt HM. Boockfor FR. Yoshida M. 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. Environ Sci Technol 2002. Kawaguchi M. Environ Health Perspect 2008.57(2):255-266. Biol Reprod 1997. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Environ Sci Technol 2003.foe. Barber LB. Cooper RL. and other organic wastewater contaminants in U.folliclestimulating hormone. Reprod Toxicol 2001. Makino T. Furlong ET.165(3):217-226. Carey SA. Toppari J. Meyer MT.141(7):2667-2673. Fedtke N. 36 Fourth National Report on Human Exposure to Environmental Chemicals .uk/resource/reports/ethoxylates_alkylphenols. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Endocrinology 2000. Tyl RW. Ito R.116(1):39-44. alkylphenols. Song L.15(6):683-692. Environ Int 2002. Nair-Menon JU. et al.37(20):4543-53. McCoy GL. Ferrell JM.44(8):1355-1361. Toxicol Lett 2001. Chen J. Sakui N. Horie M. Anal Chim Acta 486:41-50. Usumi K. Saito Y. Indoor Air 2004. Xu L. 1999-2000: a national reconnaissance. Kolpin DW. Spengler JD. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats.S. Food Chem Toxicol 2006. Myllymaki SA. Reidy JA.Environmental Phenols References Bian Q. Onuki A. Inoue K. Sweeney T. Seely JC.28(3):215-226.30(2 Pt 1):81-95. polybrominated diphenyl ethers.121(1):21-33. Marr MC. Reprod Toxicol 2004. Laws SC. Takai N.

Moss et al. There is some concern that widespread use of triclosan and other biocides can alter antibiotic resistance in bacteria (Aiello et al. Human health effects from triclosan at low environmental doses or at biomonitored levels from low environmental exposures are unknown. It acts by inhibiting bacterial fatty acid synthesis. IARC and NTP do not have ratings with respect to human carcinogenicity. Mezcua et al. 2004). 1976. In a study of 90 U. 2000..Environmental Phenols Triclosan CAS No. it is excreted over several days in the feces and urine as primarily as unchanged triclosan (Kanetoshi et al. and medical devices.S. Fourth National Report on Human Exposure to Environmental Chemicals 37 . 2007)... toothpastes. representative subsample of NHANES 2003-2004.. and has not been considered mutagenic or carcinogenic (Bhargava and Leonard.6% of 139 U. Biomonitoring Information Urinary triclosan levels reflect recent exposure. 1996.2 µg/L was comparable to the median level (8. Triclosan can be absorbed across skin into the blood stream. 2007. Finding measurable amounts of triclosan in the urine does not mean that the levels of triclosan cause an adverse health effect. Veldhoen et al. and wound disinfection solutions. 2005. 2008 has shown higher levels during the third decade of life and among people with the highest household income.S... In a U. mouthwashes.. Triclosan has a low bioaccumulation potential in fish. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2 µg/L) of children 6-11 years of age who participated in NHANES 2003-2004 (Wolff et al.. Biomonitoring studies on levels of triclosan provide physicians and public health officials with a reference values so that they can determine whether people have been exposed to higher levels of triclosan than are found in the general population. 1969). 2000). Lyman and Furia. Some reports show endocrine effects are observed in amphibians and fish (Foran et al. 2002). 1987).. it has low acute toxicity. toys. Triclosan can remain present in the oral saliva for several hours after the use of toothpaste containing triclosan (Gilbert et al. 3380-34-5 General Information Triclosan is a phenolic diphenyl ether used for over 30 years as a preservative and antiseptic agent.. Matsumura et al.. In 1999-2000.. (Sandborgh-Englund et al.8-dichlorodibenzo-p-dioxin (Aranami et al. acne medications. streams sampled in 30 states (Kolpin et al. In animal studies. Triclosan formulations may rarely cause skin irritation. General population exposure results from dermal and oral use of products containing triclosan. 1988. In animal and human studies. Calafat et al. Triclosan enters the aquatic environment mainly through residential wastewaters.. 2007.. Calafat et al. Triclosan is not considered teratogenic at maternally toxic doses. 2007). young girls. Triclosan has been added to soaps. but not by race/ethnicity and sex. deodorants. triclosan was found in 57. In the body it is conjugated to glucuronides and sulfates (Bodey et al. and has also been impregnated into some kitchen utensils. It can be photochemically and biologically degraded. a process that can result in the formation of small amounts of 2. 2008).S. 2006). the median urinary triclosan level of 7..

5) 20.2) 12.10) 84.1) 9.92-12.82 (8.6 (12.48 (8.55 (4.4) 357 (225-456) 203 (87.1) 7.7 (28.3) 47.20-10.4 (12.4 (11.30-14.9 (50.9 (11.6) 90th 212 (172-241) 03-04 03-04 03-04 9.0) 49.6) 12.4) 317 (231-433) 144 (96.2 (13.00-8.7 (11. Survey Geometric mean (95% conf.5-86.45-10.9) 8.72-13.0-19.8) 7.10-9.1) 9.0 (8.2-46.6 (30.0-15.8-112) 30.1) 11.2 (27.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.8-60. population from the National Health and Nutrition Examination Survey.9-236) 193 (90.3) 6.0 (26.6-37.2 (37.3 (8. interval) 13.3 (9.38-18.0) 9.6 (10. population from the National Health and Nutrition Examination Survey.6-65.16 (6.4) 7.6) 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 9.3 (26.20 (7.4) 51.0-73.43-13.1 (8.1) 9.9) 7.0 (34.7 (14.2 (25.3-35.7) 292 (151-432) 132 (78.2 (10.9 (33.6 (9.70-16.2-14.11-11.4) 90th 249 (188-304) 03-04 03-04 03-04 8.1) 13.5) 66.4 (38.45-13.3.6-15.50) 10.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.94 (7.2 (11.29-12.1) 14.89-11.48-10.5 (11.5) 13.40-17.3 (11. interval) 12.74 (5.20 (7.9) 32.S.1 (15.6) 39.9) 75th 47.54 (8.32-14. see Data Analysis section) for Survey year 03-04 is 2.6) 10.5-14.2) 9.Environmental Phenols Urinary Triclosan (2.50-10.20-11.3-67.18 (5.6) 31.00 (4.0 (11.1-39.2-58.5) 11.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.2-58.86-12.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.9-61.4-19.3-31.1 (45.60 (6.21 (6.S.0 (36.45 (5.9 (8.3-15. Survey Geometric mean (95% conf.2) 13.4) 75th 43.4) 73.0) 65.6-14.1) 50.1) 9.6-14.7 (9.7) 123 (36.80 (5.4-18.1) 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 9.22-10.6-111) 33. Urinary Triclosan (2.8 (21.8) 14.4.40-11.0-213) 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 .90-10.4) 25.3) 10.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.7) 10.93 (7.8) 116 (39.60 (8.7 (39.8-85.8-63.0-15.8) 9.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4 (32.6-20.8-127) 37.4.20-13.

38(4):361370. Fernandez-Alba AR. Bodey GP.524:241-247. Williams PE.7/2. Howes D. IMS Ind Med Surg 1969. Aranami K. Gunderson MP.69(20):1861-1873. Skirrow RC. Aguera A.116(3):303-307. Lyman FL. Bennett ER. Watanabe N. Pinney SM. 4’-trichloro-2’-hydroxydiphenyl ether.50(1-5):153-156. Foran CM.80(3):217-227. 4. Wigmore H. Pharmacokinetics of triclosan following oral ingestion in humans. Pharmaceuticals. Ishibashi H. Biol Pharm Bull 2005. 1999-2000: a national reconnaissance. Environ Health Perspect 2007. Okui T. Am J Infect Control 1996.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Benson WH. Wong LY. Zaugg SD. Percutaneous penetration and dermal metabolism of triclosan (2.66:1052-1056.38(2):64-71. Ferrer I. Teitelbaum SL. Br J Clin Pharmacol 1987. Kaneshima H.S. et al. Photolytic degradation of triclosan in freshwater and seawater. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. and phenols in girls. Hirano M. Ekstrand J. Shiratsuchi H. Larson EL. Pilot study of urinary biomarkers of phytoestrogens. Thurman EM.4’-trichloro-2’hydroxydiphenyl ether).28(9):1748-1751. Anal Chim Acta 1004.45 Suppl 2:S137-S147. Barber LB.Environmental Phenols References Aiello AE.24(3):209-218. Hong HC. Gomez MJ.115:116-121. Reidy JA.4. Kanetoshi A. Sandborgh-Englund G. Aquat Toxicol 2006. Moss T. Toxicology of 2. hormones. Erratum in: Aquat Toxicol 2007. et al. Chemosphere 2007. Kolpin DW. Food Chem Toxicol 2000. Needham LL. J Toxicol Environ Health A 2006. Hernando MD. Triclosan: applications and safety. Adolfsson-Erici M. Chelimo C. Windham G.. Environ Sci Technol 2002. phthalates.S. The oral retention and antiplaque efficacy of triclosan in human volunteers. Wolff MS. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Matsumura N. Environ Health Perspect 2008. Furia T.23(5):579-583. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Furlong ET. Meyer MT. and other organic wastewater contaminants in U. Ogawa H. Calafat AM. Gilbert RJ. et al. Ebersole R. Arch Environ Contam Toxicol 1988.67(4):532-537. Levy SB. Odham G. streams. Mezcua M. Mar Environ Res 2000. Osachoff H.17(5):637-644. Bhargava HN. population: 2003-2004. Nagao Y. Veldhoen N. J Invest Dermatol 1976. Britton JA. Williams FM. Katsura E. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Urinary concentrations of triclosan in the U.83(1):84. Ye X. Readman JW. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Evidence of 2.36(6):1202-1211. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. Leonard PA. et al. Clapson DJ.

350 (. ingestion of contaminated food or water. herbicide.350) < LOD .350) < LOD .64) 1.590-1. Human exposure to PCP has become less common.350) < LOD .30) 1.350) < LOD .650 (.890 (.350-.390 (.5.350 (.37 (.10 (.350-2.860-2.51) 1.04) 1. and it is used primarily as a preservative for wood to be used outdoors (e.00) 1.350-.350-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. 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 (.91 (1.660 (.350 (.350) < LOD < LOD 75th .350 (.350-.10) 1.350-.78) 1. Since 1984.00 (.630 (.500-2.350) < LOD .350 (.350-1.75) 2.350-.350 (.60) 1.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . along with small amounts of tetrachlorohydroquinone and conjugates.350) < LOD .350-2. Effects including hyperthermia.350-1.76) 1.62 (.770 (. Survey Geometric mean (95% conf.890-1.50) 1.30) .73 (1.350) < LOD . utility poles and fence posts).76) ..990-2.980 (. and metabolic acidosis were observed in CAS No. To-Figueras et al.10 (<LOD-1.350-.350-.350 (.350-.350-. air. and animals. PCP is eliminated over a few days (Braun et al.350-.47-3.350 (.350) < LOD .650) 1.350) 90th . < LOD means less than the limit of detection. 1976.510-5.350 (.01 (<LOD-1. which may vary for some chemicals by year and by individual sample.30 (. the elimination half-life may be a week or more (Uhl et al. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and possibly of lindane (IPCS. 1986).48 (. After a single dose.30 (1. 40 Fourth National Report on Human Exposure to Environmental Chemicals .70) 2.94 (1.65 (.S.350) < LOD . General population exposure to PCP may occur by inhalation of contaminated air.350-1.54-2. PCP is absorbed rapidly and well by all exposure routes.350 (.350 (.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .00) 1.67) 1..37) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350-.30 (.390 (.350) < LOD . hypertension. 2002.350) .350-2. bactericide.32 (. plants.40 (. PCP use in the U. Workers who manufacture or apply PCP may Urinary Pentachlorophenol Also a Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.350-.90 (1.350 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Kohli et al.70) .65 (.58-2.350 (.25 and 0.42) 696 680 521 696 603 951 Limit of detection (LOD.83 (2. population from the National Health and Nutrition Examination Survey.350 (.350-. algaecide and insecticide. mollusicide.350-.350-1.850-2.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin. Acute. The parent compound and conjugates.350 (. After absorption. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.960) 1.33-2..10 (1. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene. PCP cannot be used on wood in residential or agricultural buildings.350) < LOD . are eliminated in the urine.480-2. 1997).350-. other polychlorinated benzenes.47-5.53) 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 .33) .350) < LOD .350 (.530) 1.350-. and dermal contact with PCP-treated products. PCP has been detected in soils.350 (.90) 1.45-2. water and sediments because of the large amounts that were produced and used historically.90) 2.09) .94 (1.510-3.30) 1.350-. has been restricted.58-2.23 (.350-.98 (1. In the environment. PCP is degraded by sunlight and metabolized rapidly by microorganisms..350 (.680-1.990 (<LOD-2.350) < LOD .350 (.350-.60) 1. with repeated or chronic exposure.350-2.350-2. 1979).350) < LOD .350) < LOD .48-2. PCP is distributed to most tissues and is not extensively metabolized.g.00) 2.80) .350-.08-3.350) < LOD .S. so it is relatively non-persistent.350 (.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .18 (<LOD-1.350-.10) 1..

82 (1.19) 2. OSHA has established an occupational standard.9 mg/L. Survey Geometric mean (95% conf. 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 (4.830) < LOD .00-1. Death can result from seizures and cardiovascular collapse.57 (1.13 (.95) 3.570 (.25-2.25 (1.590-1.650 (.350) < LOD .40) 1.490) < LOD .330-.360 (. 1995).epa.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . In animals.990 (.220-.510-. respectively) (Becker et al.78) 1. Among adults in the NHANES 1999-2000 subsample.290-. 2003). and the FDA has established a standard for bottled water.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 . In a small sample of U. 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.11) 2.950-1. carcinogenic.510-.25 (1.09 (<LOD-2.90) 1.920 (. Pentachlorophenol is not mutagenic or teratogenic.75 (<LOD-2.30-2. In NHANES 2001-2002 subsamples..300 (.67 (1.55) 1.300 (.0 mg/L.30 (.67-3. EPA has developed standards for PCP in drinking water and the environment.710-1.280) < LOD .35-2.35) 1.52) 1.36) .94 (1.590) < LOD ..650 (. EPA at: http://www. environmental levels) and health effects is available from the U. Urinary PCP levels at the 95th percentile in this Report are approximately half the corresponding 95th percentile values found in German adults evaluated in 1998 (Becker et al.06) 1.19) 2.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .67 (1.84-4.760 (.220-.40) 1. The U.21 (.30) 1. More information about external exposure (i.610 (.320) < LOD < LOD 75th .16 (.18 (1.gov/ toxpro2.09-1.250 (.310) < LOD .40) 1. 2004.84 (1.83 (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. 1989).67-3.320 (. chronically administered high doses of PCP were hepatotoxic.560-.48-2.270-. van Raaij et al.25-2.73 (1.850 (.67 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.52 (<LOD-1. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.69 (1.40) 1.40-2.79) 1.500 (.40) 1. children in the 1980’s.320) < LOD . 2000).gov/ pesticides/ and from ATSDR at: http://www. 1991).270-.780) < LOD . inhalation.340-.S.67 (1.82) 1.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .00) 1..420) < LOD .52 (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.250 (.300 (.10-2.440 (.430-.94-3. respectively) (Seifert et al. 1989).06 (.430) < LOD .S.html.700-2.16-1.310-.26 (1.35-2.260 (.e.34 (..6 and 14.35) 1.75) 1.780-1.800-1.470 (.500-. 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.S.950-1.26 (1. Fourth National Report on Human Exposure to Environmental Chemicals 41 .Fungicides adults and children severely exposed to PCP through ingestion.560) < LOD .360-.290) < LOD .630 (.67-2.00-1.800) < LOD 1.25) 1.900-1.320) < LOD .580-.19 (1.400 (. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.290-.560) < LOD .56) 1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.94 (1.51) 1. and adversely affected thyroid function (U..08 and 5.57 (.92) 1. or skin absorption.25-1.370 (.730) < LOD .06-3.EPA..78) 1.18) . population from the National Health and Nutrition Examination Survey..cdc.380-.84) 1.67 (1.19) 2.S..S.240-.21-2.950-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.29-3.atsdr.650) 90th 1.52 (<LOD-1.500-1.910-1. 2003).30) 1.10 (1.

et al. U.105(1):78-83. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Environmental Protection Agency (U. Barrot C. house dust. Otero R. Toxicology 1991: 67(1):107-16. Fast DM. Shealy DB. Int J Hyg Environ Health 2003. Seiwert M. Notten WR. Arch Toxicol 1986. Becker K. et al. Bailey SL. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. 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. 11/30/2004. Pharmacokinetics of pentachlorophenol in man.S. International Programme on Chemical Safety (IPCS). 4/21/09 Kohli J. The metabolism of higher chlorinated benzene isomers. Can J Biochem 1976. Braun WH. Hill RH Jr. References Becker K. Environ Res 1995. To T. 2002. 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. Cline RE. Gregg M. Schmid P. Engel R.S. Head SL.10:552-65. Needham LL. htm. PCP: Human Risk Characterization [online]. Schulz C. Sala M. Kaus S. van den Berg KJ. Uhl S. Rodamilans M. Environ Health Perspect 1997.org/documents/jmpr/jmpmono/2002pr08. Phillips DL. Schlatter C. 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.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Chenoweth MB.18:475-481. Available at URL: h t t p : / / w w w. To-Figueras J. Helm D. Schulz C. r e g u l a t i o n s . Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Needham LL.58:182-186. Santiago-Silva M. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Arch Environ Contam Toxicol 1989. Krause C.18(4):469-474. EPA). Seifert B. drinking water and indoor air. urine. Jones D. J Expo Anal Environ Epidemiol 2000. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Seifert B. Lindane. Safe A. Smith SJ. Holler JS. hair. Hill RH.54(3):203-208. 4/21/09 van Raaij JA. Hill RH Jr.71:99108. Seiwert M. Dev Toxicol Environ Sci 1979.inchem. Bragt PC. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Baker S. Arch Environ Contam Toxicol 1989. et al. 206:15-24.4:289296. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. 42 Fourth National Report on Human Exposure to Environmental Chemicals . available at URL: http://www. Blau GE. Pesticide residues in urine of adults living in the United States: reference range concentrations.

28-3. 2006).02) 1.90 (1.10) .389-.490 (<LOD-.645) * . fungicides.490 (<LOD-.570 (.860 (.621) * .10) 2.40-2.498 (.EPA.490 (<LOD-.60-3. Survey Geometric mean (95% conf.364-.40-5.450 (<LOD-.402-..640) < LOD .20) 2.570-. however.22) 2. or apply these chemicals may be more highly exposed than the general population.17 (.00 (1.580-1.34) 1.50 (1.40-5.696) * .552 (.3..50-3. In the past.61) 2. which may vary for some chemicals by year and by individual sample.520 (.570-1.07 (.20-2.30) < LOD 1. OPP is volatile. Cnubben et al.S. such as fruits and vegetables.570 (.389-.370-.S.830 (.860) * 99-00 01-02 99-00 01-02 99-00 01-02 . inhalational.40-7. Workers who manufacture.390-.770 (.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.970 (.EPA.890 (. it was used in home sanitizers for surfaces.890 (.60 (1.S.450 (<LOD-.00) < LOD .50) < LOD .40 (.90 (1.624) * .600-1.10 (1. interval) .350-1.60-2.30-2.Fungicides ortho-Phenylphenol CAS No.560-8.509 (.80-3.750-2. OPP is efficiently absorbed from the gastrointestinal tract and through the skin. whereas SOPP is not volatile and is more water soluble.00) .50) 1.90) 2. EPA.19 (.370-.770 (.760-2.80) 1. Most agricultural food applications have been revoked.50 (1. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.03) 1.638) * .710-2.00 (1. Timchalk et al. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 . OPP is considered to be moderately toxic after acute oral doses in animal studies.670) 2.740 (.30 (1.20-3.600) < LOD .466 (. Fourth National Report on Human Exposure to Environmental Chemicals 43 .28 (.890) 1. are antimicrobial agents used as bacteriostats.690-1.80) 1.20 (1. 1998.50-4. Estimated human intakes have been below recommended intake limits (U. 2002.690) < LOD .3 and 0.00) .370-.790) 2. leaving the chemical residue OPP.90) . 90-43-7 General Information Ortho-phenylphenol (OPP.80 (2. 2006). and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.27 (.33 (.497 (. < LOD means less than the limit of detection.540-2. or 2-phenylphenol) and its water-soluble salt. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.386-.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 .433-.880-2.600) < LOD 75th .836) * .60 (1. in paints.850 (.742) * . 1998).00 (1.10) .50 (1.90) 1.600) < LOD 1.50-2. 2006).50) .470 (<LOD-.30) < LOD .636) * .50) < LOD .600-1.88) 1. but OPP and SOPP are still used on pears and citrus (U.570-2.930 (.23) 695 680 520 695 603 953 Limit of detection (LOD.20 (..800-3.00 (1.950) < LOD .50) < LOD .92 (.480-1.85) 2.00-2.30) 1.349-.840-1.450 (<LOD-. Available evidence suggests that OPP does not accumulate in the body. 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.410-.60 (1.630) < LOD .600-1.610-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (1. on ornamental plants and turfs. 1989). and it has limited water solubility.490 (<LOD-. sodium ortho-phenylphenate (SOPP).30-7.10-1.493 (. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.09) 2. Both have been used in agriculture to control fungal and bacterial growth on stored crops.710) 3. population from the National Health and Nutrition Examination Survey.90) . Both chemicals degrade within hours to weeks in the environment (U.30) < LOD 90th 1. SOPP is applied topically to the crop and then rinsed off. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.567 (.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .420 (<LOD-.610 (.10) 1. and sanitizers. OPP is still used as a disinfectant fungicide for industrial applications.20 (1.590-2. formulate.508 (.10-2.600) < LOD .76) 1.820 (.490 (<LOD-.780) < LOD .20) < LOD 1. 2006).10) .22 (.10) 1.500-2.550-1. General population exposure can occur via dermal.14 (<LOD-3.496 (. and as a wood preservative.S.20) < LOD 2.

17 (.500) < LOD .00 (1.750 (.666) * . 2002).11) 4.93 (1..05-2.38) 2.. CDC.291-.91 (1.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .560) < LOD 75th .248-. U.361-. 1992. Biomonitoring Information Urinary OPP levels reflect recent exposure.473) * . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.620-1. 1993.25-6.89 (1.403-.47) .470 (<LOD-.580-1. U.514 (.550-.62) .43 (1.17) * 99-00 01-02 99-00 01-02 99-00 01-02 . Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.11 (.75 (1.epa.484) * .53) 1.940-2.343 (.453 (.S.69 (1. population from the National Health and Nutrition Examination Survey.29) 1.880-1.550) < LOD .27) < LOD .97 (2.29) 1. reproductive.02 (.86 (1. 1984.08-1.620-1.24-2.656) * .84 (1.510 (<LOD-. 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.58) 2..910 (. and it has classified OPP as not classifiable with respect to human carcinogenicity.990) < LOD .06 (1.43-2. 2000.06-5.gov/pesticides/.64 (2..590) * .91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.410 (<LOD-. In high dose animal studies. leading to production of two metabolites. Bomhard et al.780 (.17) 2.750-2. Detectable levels were seen in over half the U.420 (<LOD-. Murata et al.59) 1.440 (.570) < LOD 1.Fungicides anemia. less likely.EPA at: http:// www.93) .480-.S. Zhao et al. by possible genotoxic mechanisms (Hagiwara et al.26) 1.S. Survey Geometric mean (95% conf..43) 3.640-1. 2002. Pathak and Roy.800-1.301-.860 (. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.270-.96-4. 1999.31) < LOD .0) 1.810) < LOD . 1999. 2005). 1998.46) < LOD 1. 2005). or developmental toxicity was observed (Bomhard et al.74 (1.28 (2.32) 1.61 (.311-.360 (<LOD-.38-3. Smith et al.09-3.33) .670 (..560-2. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.455-.600-1.860 (. or. Nakagawa et al.970) 1.00 (.791) * .20) < LOD 3.04-4.EPA 2006).08-2.650-1.11 (.900-1.385 (.44 (1.750 (.S.52 (..810-1.21) 1.59) .21 (.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 .09-6.S. but no neurologic.568) * . Ito et al.07) 2.353-.980 (<LOD-1.690 (.900) < LOD . 1997.21-2.28 (<LOD-4. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.93) .780-14.17 (.550 (. 1986).75 (1.88-4.840 (.910-1.18) 2.61 (2.12-2.81) 1..96 (1. 2002.24-2.08) 1. IARC has classified SOPP as a possible human carcinogen.444 (.980 (. 44 Fourth National Report on Human Exposure to Environmental Chemicals .470) < LOD .4) 3. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.508) * .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.320 (<LOD-.43-2.11-1.910 (<LOD-1.510-.EPA 2006).770-2.420 (<LOD-.460-..410 (<LOD-. 2005.40-13.96 (1.11) < LOD 90th 1. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.580) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.38) 1.93) 1.496 (.06-4.09 (1.558) Selected percentiles ( 95% confidence interval) Sample 95th 2. Volunteers exposed to 0..670) < LOD .670 (. interval) .32) 3.12) < LOD 1. Kwok et al. 1984.13) 1.950) < LOD . Additional information is available from U.78 (2.380 (.01) 1.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 . Brusick.610) < LOD 1. OPP was not found to be mutagenic. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.33-2.61 (1.51-3.329-.96) 1.382 (.

Brendler-Schwaab SY. Timchalk C. Sangha GK. Leser KH. Environ Mol Mutagen 2005. Glas K. Mendrala AL. Crit Rev Toxicol 2002.S. Bomhard EM. Identification of SARA compounds in adipose tissue. Fourth National Report on Human Exposure to Environmental Chemicals 45 . Mutat Res 1993. National Toxicology Program (NTP). Eastmond DA. Narang A.32(6):551-625. Shirai T. Richter M. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). The carcinogenicity of the biocide ortho-phenylphenol.niehs.17(8):411-417. Bartels MJ. Sangha G. Christenson WR. Vogel JS.gov/oppsrrd1/REDs/ phenylphenol_red. Atlanta (GA). Pathak DN. Roberts AL.EPA). Bormett GA. EPA).gov/ntp/htdocs/LT_ rpts/tr301. Shibata M. Hirose M.43(7):14311437. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Turteltaub KW. Ito N. July 28. Moriya K. March 1986. Fukushima S. J Agric Food Chem 2006. St John MK. 2005. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. EPA 739 R-06004. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. food additives and natural products as promoters in rat urinary bladder carcinogenesis.45(5):460-481.28(6):579594. Drugs. Hum Exp Toxicol 1998. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Environmental Protection Agency (U. IARC Sci Publ 1984. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice.286(2):309-319. Coelhan M. Nakagawa Y. Brusick D. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Smith RA. Imaida K.(56):399-407. Available at URL: http://ntp.pdf. Arnold LL.159(1):18-24. Elliott GR.150(2):402-413. Bromig KH. Stanley JS. van de Sandt JJ. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Arch Toxicol 2000.pdf. Moore GA. U. Murata M. Kawanishi S. Hakkert BC.20(5):851-857. EPA-560/5-89-003. Ito N.S.35(2 Pt 1):198-208. Environmental Protection Agency (U. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Meuling WJ. Bartels MJ. 4/13/09 Onstot JD. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. McNett DA. Herbold BA. et al. Bartels MJ. Toxicol Appl Pharmacol 1998. U.74(2):61-71.703(12):97-104. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Fukushima S. J Chromatogr B Biomed Sci Appl 1997. Buchholz BA. Xenobiotica 1998. Comparative metabolism of orthophenylphenol in mouse. 2006. Hagiwara A. Zhao S.50(11):3351-3358. Selim S.S. 4/9/09. Brzak KA.22(10):809-814. Eadon G. Toxicol Appl Pharmacol 1999. Inoue S. Christenson WR. et al. rat and man.. Office of Toxic Substances. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Moldeus P. Food Chem Toxicol 1984. Timchalk C. Tayama S.nih. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Available at URL: http://www.epa. Freyberger A. Hagiwara A. Carcinogenesis 1999. Bartels MJ. Roy D. Kwok ES. J Agric Food Chem 2002.Fungicides References Appel KE. Regul Toxicol Pharmacol 2002. 90-43-7) in Swiss CD-1 mice (dermal studies).54(16):5731-5735. Centers for Disease Control and Prevention (CDC).S. Cnubben NH. 1989. Gierthy J. Third National Report on Human Exposure to Environmental Chemicals. Cano M. Biochem Pharmacol 1992. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers.

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

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

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

Barr DB. Heederik D. Available at URL: http://www. Kier L. Linhart SM. pages 3682-3690. 2000. 1998. Xenobiotica 1994. Environmental Protection Agency (U.pdf. Curwin BD. Linderman R. Dialkylquinonimines validated as in vivo metabolites of alachlor. Number 15. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Volume 65. Sci Total Environ 2000. March 2006. J Agri Food Chem 1989. Third National Report on Human Exposure to Environmental Chemicals. Camann DE. Quistad GB. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Environ Sci Technol 2005. U. Environ Health Perspect 2000. epa. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Lefevre PA. Feil VJ. Roberts AL.39(17):6561-6574.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100.111(5):749-756. et al. acetochlor. Environmental Protection Agency (U. Thurman EM. EPA 738-R-00-009. Centers for Disease Control and Prevention (CDC). Federal Register: January 24. Green T.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Davison KL. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Wilson AG. sulfonamide. EPA).15(6):500-508. Sanderson WT. Coleman S. Ward EM.17(6):559-566. J Expo Anal Environ Epidemiol 2005. Peter CJ.S.EPA): http://pmep. Whyatt RM. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Occurrence of sulfonylurea. Hsiao JJ. Sci Total Environ 2000. Andrews HF. Hein MJ. Alavanja MC. Kinney PL. Atlanta (GA). Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Deddens JA. Chem Res Toxicol 1998. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. Hines CJ. Comparative metabolism and elimination of acetanilide compounds by rat. Barr DB. Larsen GL. EPA). Hum Exp Toxicol 1996. Environ Health Perspect 2003.S.248(2-3):115-122. Striley CA.108(12):1151-1157.15(9):702-735.S. and other herbicides in rivers. et al. 5/30/06 U. Casida JE. reservoirs and ground water in the Midwestern United States. Reynolds SJ.html. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.24(10):1003-1012. imidazolinone.248(2-3):123-133.cornell. Available at URL(non U. 5/30/06.37(4):10881093. Jefferies PR. 2005. Barr JR. Acetochlor (Harness) Pesticide Petition Filing 1/00. Battaglin WA. Rose RL.cce. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Olsson AO. and metolachlor herbicides in rats. J Expo Sci Environ Epidemiol 2007. Kolpin DW. Hodgson E. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Feng PCC. Barr DB. et al.S. Wratten SJ. Bravo R. Tinwell H.S.11(4):353359. Furlong ET.Herbicides References Ashby J. Burkhardt MR. Hladik ML.

U. Additional information about is available from U. 2003). 2003). and uveal degeneration. 1988. 1996. 2005). about 20-25% of the U. 1998. mercapturate conjugates were predominant metabolites. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. hemosiderosis.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.. whereas 60% of applicators had detectable amounts. soybeans. USGS. ranged from 0.Herbicides Alachlor CAS No. NTP and IARC do not have ratings regarding human carcinogenicity.. In 1993-1995. 1998). EPA at: http://www. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. U.S.S. Jefferies et al. formulators.EPA. WHO. the dermal exposure route is potentially significant for applicators. Hill et al. It is absorbed by plants and inhibits plant protein synthesis. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. peanuts and other crops.. In chronic animal testing. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. but another metabolic pathway can produce 2. 1996. 1998). In a study of applicators and workers exposed to alachlor. WHO. 2000. but shows little bioaccumulation. Alachlor has a soil half-life of a few weeks.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. 1998).. but not likely at low doses. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. Hines et al. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al.S. In animal studies. 2003).EPA. 2005.S.. stomach.. Because it can be absorbed through skin.S. Estimated human intakes have been below recommended limits (U.EPA considers alachlor to be a probable human carcinogen at high doses.EPA. Alachlor and its degradates are leachable from agricultural soils and have been detected in watersheds of agricultural land including ground and surface waters (Battaglin et al. Tessier and Clark. 1998.gov/pesticides/.S.epa. 2000.1 mg/L at various collection times (Sanderson et al.EPA. 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. 1999. (2003) showed that 2. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. including corn. Alachlor has low potential for acute toxicity. Feng and Wratten.. alachlor has demonstrated hepatotoxicity. 1995). but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. 1996). Alachlor itself is not considered mutagenic. corn cropland was treated with alachlor. Since the late 1980s alachlor use has been declining. 50 Fourth National Report on Human Exposure to Environmental Chemicals . U.EPA. 1995. WHO. but has not shown developmental or reproductive toxicity in mammalian systems (U. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. 1998. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2003). 1994. 1997. 1989.1 to 1. WHO. 1999 and 2007. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. and on non-crop land for general weed control..S. IPCS.. mean values of urinary concentrations of alachlor metabolites. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. Hladik et al.. In animals. and field workers. Kolpin et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. U. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. as measured through conversion to deethylamine. the latter may account for some observed effects (Davison et al.6-diethylaniline and its reactive metabolite.

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

Hsiao JJ. Casida JE. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. 2005. Feng PCC.44(18):1325.pdf. Environ Sci Technol 2005. Whyatt RM. sulfonamide. Am Ind Hyg Assoc J 1995. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Quistad GB. March 2006. Striley CA.php. Biagini RE. Atlanta (GA).18(6):363-391. 1996. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Burkhardt MR.24(10):1003-1012. Available at URL: http://water. U. Kinney PL. Shealy DB.43(25):2087-94. Sci Total Environ 2000.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. 4/2/09 U. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Hines CJ. Gilliom RJ). Circular 1291. Hladik ML. Casida JE. Biagini R. ALACHLOR. Hull RD. Barr JR. Feil VJ. Geological Survey (USGS). Sacramento. WHO/ FAO Data Sheets on Pesticides.htm. Kier LD. Available at URL: http://www. Life Sci 1988. Roberts AL. Dialkylquinonimines validated as in vivo metabolites of alachlor. Thurman EM. Tessier DM. Davison KL. Supplemental Technical Information (available on-line only). Ann Occup Hyg 2003. Sci Total Environ 2000.gov/oppsrrd1/ REDs/0063. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Hill AB.47(6):503-517.111(5):749-756. Kolpin DW. Casida JE. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Centers for Disease Control and Prevention (CDC). J Ag Food Chem 1995. 1999. Bull Environ Contam Toxicol 1996. Available at URL: http:// www. Lau H. Erratum in: Life Sci 1989. 2003.S. Brown MA. 1999. Wratten SJ. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. who. Reregistration Eligibility Decision (RED) Alachlor. 1998. Thake DC. Kimmel EC. Geological Survey (USGS). 2/27/09 Jefferies PR. and other herbicides in rivers. EPA 738R-98-020. Quistad GB. Larsen GL. 1992-2001. Heydens WF.Herbicides References Battaglin WA. Wilson AG. 2007. Environ Health Perspect 2003. J Agri Food Chem 1989. Hill RH Jr. World Health Organization (WHO). No. and metolachlor herbicides in rats. Sanderson WT. Peter CJ. International Programme on Chemical Safety (IPCS).int/water_sanitation_health/dwq/chemicals/en/alachlor.395(2-3):159-171. Third National Report on Human Exposure to Environmental Chemicals.epa. Thelin GP. Geneva.S. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor.37(4):10881093. DNA adduct formation by alachlor metabolites. et al. Brown KK. revised February 15. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Martens MA.248(2-3):123-133. Tolos W. imidazolinone.pdf. World Health Organization. December 1998.S.S. EPA). Camann DE. California. Background document for development of WHO Guidelines for Drinking-water Quality.39(17):6561-6574. 1997. Chem Res Toxicol 1998. Comparative metabolism and elimination of acetanilide compounds by rat. 98-4245 (by Barbash JE. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. et al.org/documents/pds/pds/pest86_e. Occurrence of sulfonylurea. Furlong ET. MacKenzie B. Andrews HF.inchem. Hines CJ. Linhart SM.248(2-3):115-122. Barr DB. Driskell WJ. 2/27/09 U. 86. Clark JM. acetochlor. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. Alachlor in Drinking-water.11(4):353359. Environmental Protection Agency (U. Shoemaker DA. Xenobiotica 1994. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.56(9):883-889. Available at URL: http://www.usgs.43(9):2504-2512.56(6):853-859. Mutat Res. Deddens JA. Kolpin DW. Jefferies PR. Hum Exp Toxicol. Henningsen G. reservoirs and ground water in the Midwestern United States.

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

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

The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Saiz SG. Goldman JM. Gammon DW. Stuart AA. Collins A. Vonk A. 2007). et al. Extrom PC. Barr DB. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Bersani M. Wetzel LT. J Toxicol Environ Health 1994. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Sanderson WT. Wetzel LT. Grzywacz JG. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Brown KK. Bradway DE. Steroids 1999.. Biagini RE. Fleenor-Heyser DG. Toxicol Sci 2003. Environ Health Perspect 2001. Cooper RL. Biological monitoring of human exposure to atrazine.43(2):155-167. Eldridge JC. Simpkins JW. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . 82. Goodrow MH. Catenacci G. et al. Cottica D. Blewett C. Toxicol Sci 2000. World Health Organization. ATRAZINE. In small studies of Maryland residents in 19951996 (MacIntosh et al. Perry et al. Hayes TB. Noriega N. Heederik D. In a study of 60 farm worker children. et al.43(2):155-167. Gillis JH..58(2):366-376. Geneva. Tapia J. Shoemaker DA.cdc. Eldridge JC. Toxicol Sci 2000.org/documents/pds/pds/pest82_e. Jones AD. 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. 2005). 2000).gov/toxprofiles/tp153. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Barr DB. Agency for Toxic Substances and Disease Registry (ATSDR). Ann Occup Hyg 2003. Ferrell JM. Hermaphroditic.. Available at URL: http:// www. 2001). diamino-S-chlorotriazine and hydroxyatrazine. Seiber JN. Hein MJ. J Toxicol Environ Health 1994. 2005. 1996. Centers for Disease Control and Prevention (CDC). Stoker TE.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. J Expo Anal Environ Epidemiol 2005. A risk assessment of atrazine use in California: human health and ecological aspects. Toxicological profile for atrazine. Breckenridge CB.. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Quandt SA. Freeman NC. 3/11/09 Laws SC. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Maroni M. Lee M. et al. In the NHANES 2001-2002 subsample. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides.109(6):583-590. Barr DB. Eberly LE. Environ Health Perspect 2007.76(1):190-200. Schmid J. Carr WC Jr. References Adgate JL. 2005). 1993). 2003.. Barbieri F. The geometric mean of urinary atrazine mercapturate was 1. Curwin BD. Clayton CA.53(2):297-307.30(2):244-247. McElroy WK. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Moseman RF. Mendoza M. Cooper RL. 2001 [online]. Tyrey L.. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. atrazine was detected in only four children (Arcury et al. et al. Sanborn JR.15(6):500-508. Pfeifer KF. Atlanta (GA). Proc Natl Acad Sci USA 2002. Stevens JT.99(8):5476-5480.69(2):217-222. Deddens JA.htm. Pest Manag Sci 2005. No. 3/11/09 Arcury TA. Hines CJ. Laws SC. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. Reynolds SJ. J Agric Food Chem 1982.61(4):331-355. In a small number of field workers. International Programme on Chemical Safety (IPCS). Stoker TE. Aldous CN. levels of atrazine mercapturate were generally not detectable (CDC. Stoker TE..html.64(9):672-678. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Third National Report on Human Exposure to Environmental Chemicals. Ferrell JM.47(6):503-517. WHO/ FAO Data Sheets on Pesticides. et al.115(8):1254-1260. Lioy PJ. Ferioli A. Gillis JH. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Striley CA. Toxicol Lett 1993. Chen H. Cooper RL.inchem. Available at URL: http://www.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Lucas AD.atsdr.

Wood C. Case No.58(1):50-59.182(1):44-54. Cooper RL.S. Stoker TE. Osborne DW. Urinary biomarkers of atrazine exposure among farm pesticide applicators.10(7):479.61(1):27-40. Lansbergen GW. A review of epidemiologic studies of triazine herbicides and cancer. Breckenridge CB. Laws SC. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Kastl PE. Laws SC.epa. 3/11/09 U.pdf. Fenton SE. Environmental Fate and Effects Division. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Singzoni B. Ryan PB. Stevens JT. J Expo Anal Environ Epidemiol 1999. Environmental Protection Agency (U. EPA). Toxicol Sci 2002.epa. 2003b.usgs. J Toxicol Environ Health A 1999. Office of Prevention. revised February 15. van den Berg M. Christiani D. Hammerstrom KA. A longitudinal investigation of selected pesticide metabolites in urine. Stoker TE. Supplemental Technical Information (available on-line only). Cooper RL. Boerma J. Ann Epidemiol 2000. EPA Office of Pesticide Programs. Toxicol Appl Pharmacol 2002. Sathiakumar N. Chem Res Toxicol 1993. Toxicology 1990.67(2):198-206. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats.27(6):599612. Sanderson JT. Rayner JL. Pesticides and Toxic Substances. Pesticides in the Nation’s Streams and Ground Water.56(2):69-109. Crit Rev Toxicol 1997. Langvardt PW. Timchalk C. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals . Dagenhart D. EPA). 6/1/09 U. Tortorelli J. Needham LL. 0062.9(5):494-501. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function.6(1):107-116.Herbicides development of a biomarker of exposure. Interim Reregistration Eligibility Decision For Atrazine. 1992-2001.pdf. Toxicol Appl Pharmacol 2004. Available at URL: http://www. Wetzel L. Guidici DL.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. The Quality of Our Nation’s Waters.S.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. May 2003a. Guidici DL. Available at URL: http://www.S. Environmental Protection Agency (U. Circular 1291. March 2006. Washington (DC).php.S. A risk characterization for atrazine: oncogenicity profile. Delzell E. 2007. Available at URL: http://water.S.gov/oppsrrd1/REDs/ atrazine_ired. White paper on potential developmental effects of atrazine on amphibians.195(1):23-34. MacIntosh DL. Toxicol Sci 2000. Dryzga MD. Perry M. Geological Survey (USGS). U.

10 (<LOD-1.810-1. the chlorophenoxy herbicide 2.4-Dichlorophenoxyacetic Acid CAS No.210 (<LOD-.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.660) 1.730 (. 2004).05-2.310 (.760 (.02-1.S.22) < LOD .70) 1.. < LOD means less than the limit of detection. but at higher levels they are herbicidal.420-. Sauerhoff et al.EPA.540-.550-1.560-.Herbicides 2. 1974. dizziness.890) < LOD . although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . abdominal pain.43) 1.27 (1.30 (<LOD-2.930-1. It is poorly bound in soils.07 (.960-1. and aquatic environments.610-. 2007).400) < LOD .13) < LOD .420) < LOD .350) < LOD < LOD < LOD .910) 1.48) < LOD 1. hypotension.00-2.37) 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 .680-1.690-1. At low levels..10) < LOD 1.4-dichlorophenoxyacetic acid (2.490) < LOD < LOD < LOD .EPA. agricultural. with a half-life of several days to several weeks. It is not well absorbed through the skin.21) 1. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms. 1989. by direct contact with agricultural and residential areas after applications. Survey Geometric mean (95% conf. MCPA.952 and 0. Recent estimates of chronic intakes of 2.230 (<LOD-. Once absorbed. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.80) 1. It was first registered with U. It is rarely detected in ground waters (USGS.690 (. headache. and by consuming food or drinking water contaminated with 2. 2.4-D have been below recommended intake limits (U.930 (.S.32 (1.740 (.250 (<LOD-.560-1. it acts as a plant growth hormone.330 (. As much as 62 million pounds of 2. these herbicides can enhance plant growth. population from the National Health and Nutrition Examination Survey.310) < LOD .490 (.27 (.4-D can be applied either as an aqueous salt or as oil-soluble esters..910) < LOD .4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.27-2.16) < LOD .4-D or exposed for prolonged periods.690 (.60) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.S. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. myotonia.20 (<LOD-1. and delayed Urinary 2.EPA in 1948. Kohli et al.4-D is rapidly absorbed via oral and inhalation routes. and mecoprop).66) < LOD 1.4-D were used in the U.250 (<LOD-.03) 695 659 520 668 589 892 Limit of detection (LOD.690 (. 2005). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1977). 2. Human health effects from 2.4-D has low acute toxicity.20 (.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2.370-. General population exposure to 2. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. 4-D.320) 90th .4-D) controls broadleaf weeds in residential.410) < LOD .08) < LOD .51 (1.230-.4-D may occur during residential applications.610 (.890 (. 2.55 (1. in 2001 (U. 2.260 (<LOD-.670-1. renal and hepatic injury.210-. Fourth National Report on Human Exposure to Environmental Chemicals 57 . 94-75-7 General Information Widely used throughout the United States. nausea.10 (<LOD-1.S.S. Similar to other chlorophenoxy herbicides.40) 1.24 (.440-1.

2001.56) .780-1.08 (.EPA.410) < LOD 1. 1994). 2005). Frank et al. IPCS.4-D reflect recent exposure.S. 2004).EPA 2005). Pearce and McLean.24) 1... 2000).790) < LOD .490 (.590 (<LOD-1.410) < LOD < LOD < LOD . Survey Geometric mean (95% conf.850) < LOD .550-. 2005. 2005. Additional information is available from U. in small samples of children (Hill et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.380 (<LOD-.480 (.270-. 2005). CDC..660 (.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 .41 (1. 2005. adrenals and gonads (NTP.520-.810-1. IPCS.S.700 (.13 (. 1992).570) < LOD . eyes.980) < LOD 1.410 (<LOD-. Epidemiological studies have reported associations of several types of cancer.270 (<LOD-. thyroid.590 (<LOD-1.440 (.990-1. Hill et al. IPCS.gov/pesticides/. and of adults and children (Baker et al.380-.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1996.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. Post-application levels in farmers and home gardeners were dependent on Urinary 2. 58 Fourth National Report on Human Exposure to Environmental Chemicals .810-1.610-.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.27-1. liver.4-D production plant workers and a few forestry workers spraying 2. 1980.340-.350 (<LOD-.EPA at: http://www. Kolmodin-Hedman and Erne.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .08 (.. other exposures.4-D are eye irritants. myotonia.35) < LOD . 2003. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides.790) 1.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. U. In previous samples of the U.410) 90th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.19) .4-D levels were detectable in less than a quarter of the individuals studied.380 (<LOD-.4-D does not have significant reproductive..890-1.660) < LOD . Biomonitoring Information Urinary levels of 2.. The acid and salt forms of 2.. population (Hill et al.780) .S.epa.14 (.. 2002.3.640 (. It is unclear whether these associations are related to the chlorophenoxy herbicides.780 (. 2005.32 (<LOD-2. 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.670 (.05) . Kutz et al. 1996.580-.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert.17 (.680) < LOD . 2005).4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..330-. 1995). urinary 2.EPA.EPA.S.380) < LOD . or teratogenic effects in chronic rodent studies (Charles et al.890) < LOD 1. and evidence of histological injury to the kidneys. Acute high doses administered to laboratory animals produced ataxia.820-1.560-. Knopp et al.920) < LOD 1. IOM.13 (. 2. 2005). 2. 1985. Average post-application urinary levels of 2.73) .670 (. U.390) < LOD < LOD < LOD . IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. U. 1996. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.S.560-.08 (. developmental. U.16) 1.470) < 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.S.. 2006. or to contaminants in the herbicide formulations (specifically 2.340 (. 2002.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.930-1.Herbicides neuropathy (Bradberry et al.39) < LOD 1. 1995.670 (<LOD-1. 1989).740 (.620-.7.720 (.610-. 2.S.

Cole DC.htm.15(6):500-508. Bus JS. Gupta BN.10(6 Pt 2):789-798. Pesticide residues in urine of adults living in the United States: reference range concentrations. Developmental toxicity studies in rats and rabbits on 2. Stephenson GR.4:97-100. et al..edu/catalog.. and the use of protective clothing or equipment (Arbuckle et al. 914. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Kolmodin-Hedman B.S. Murphy RS. Biomonitoring of herbicides in Ontario farm applicators. Survival and Growth Curves from NTP Toxicity Studies. To T. 2003. Barr DB. 2005). general population. Veterans and Agent Orange: update 2002.31 Suppl 1:90-97.org/documents/jmpr/jmpmono/v96pr04. Cook BT. Hill RH Jr. J Expo Anal Environ Epidemiol 2005 Nov. Brody D. Ripley BD.51(3):152-159.31 Suppl 1:98-104. Harris SA. Selected pesticide residues and metabolites in urine from a survey of the U. Khanna RN.nap.71(2):99-108.nih. Xenobiotica 1974. Carter-Pokras OD. Scand J Work Environ Health 2005. National Toxicology Program (NTP). Vet Hum Toxicol 1989. Needham LL. Fast DM. Board on Health Promotion and Disease Prevention. et al. Garabrant DH. van Ravenzwaay B.4-D. Sirons G J. Shealy DB. 1992).4-dichlorophenoxyacetic acid in man.4-D will result in an adverse health effect. Tandon JS.60(1):121-131. Bailey SL. Biomonitoring for farm families in the farm family exposure study. Reynolds SJ.gov/index. Tables. Head SL.. Arch Environ Contam Toxicol 1985.4 dichlorophenoxyacetic acid (2. Needham LL. Campbell RA. Baker BA.4. Dhar MM. 3/17/09 Institute of Medicine (IOM).4-D) epidemiology and toxicology. Philbert MA. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . the amount of pesticide applied. Hanley TR Jr. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Beeson MD.18(4):469-474. Occup Environ Med 1994. 2005. Finding a measurable amount of 2. Environ Res 1995. 3/17/09 Knopp D.4-D and 2. Holler JS. 2005). In farm families. International Programme on Chemical Safety-INCHEM (IPCS). TOX-63: TOXICITY REPORT CURVES.4:318-321. Hill RH Jr.4-dichlorophenoxyacetic acid (2.php?record_id=10603. Kohli JD. Beasley VR. 2006.4-D). Ritter L. Atlanta (GA). Scand J Work Environ Health 2005. Mandel JS. Crit Rev Toxicol 2002. Kutz FW. geometric mean urinary levels of 2. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.31(2):121-125. J Expo Anal Environ Epidemiol 2000.niehs. Review of 2. Alexander BH. Toxicol Sci 2001. TOX-63 Peroxisone Project (2. References Arbuckle TE. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Gregg M. et al.4-.4-dichlorophenoxyacetic acid and its forms.. Baker SE. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Pesticides residues in food: 1996 evaluations Part II Toxicology. Biomonitoring studies of 2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Herbicides the time since application. Dichlorophenoxyacetic acid. Forestry workers involved in aerial application of 2.4-Dichlorophenoxyacetic Acid). Arch Environ Contam Toxicol 1989. Arnold EK. Curwin BD.4-D): exposure and urinary excretion. 2. Third National Report on Human Exposure to Environmental Chemicals. Hein MJ. Estimation of occupational exposure to phenoxy acids (2. the number of acres to which it was applied (Curwin et al.4:427-435. Chapman P.4-D were highest in the farmers who applied the 2. Centers for Disease Control and Prevention (CDC). Frank R. Assessment of exposure to 2.32(4):233-257. Washington (DC): National Academies Press. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Sircar KP. Smith SJ.4-dichlorophenoxyacetic acid (2. Erne K. 2005.27(1):23-38. 2005 Charles JM. Acquavella JF. Baker S. Absorption and excretion of 2. Sanderson WT.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study.4-D in urine does not mean that the level of the 2. J Toxicol Environ Health 1992. Heederik D. Available at URL: http:// www.inchem. Arch Toxicol Suppl 1980. Driskell WJ. Honeycutt R. Mandel et al. Barr DB. Updated March 7. Harris et al. Exposure of homeowners and bystanders to 2.4-D than levels found in the general population.37(2):277-291.5-T). Available at URL: http:// www. Available at URL: http://ntp. J Environ Sci Health B 1992.4-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. Wilson RD. Solomon KR.

2000 and 2001 market estimates.S. Environmental Protection Agency (U.S.S. 3/17/09. The fate of 2. May. Environmental Protection Agency (U.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. The Quality of Our Nation’s Waters.8:3-1U. 60 Fourth National Report on Human Exposure to Environmental Chemicals . 2. 4/2/09 U. gov/oppbead1/pestsales/01pestsales/market_estimates2001. 2004. Available at URL: http://water. Available at URL: http://www.S.EPA. Circular 1291. March 2006.epa.epa.S.php. 3/17/09 U. S. Toxicology 1977. Available at URL: http://www. Braun WH. Supplemental Technical Information (available on-line only).4-D RED Facts.EPA). 2007.4-dichlorophenoxyacetic acid (2.pdf. Gehring PJ. June 2005.4-D) following oral administration to man.Herbicides Sauerhoff MW.usgs. EPA 738 F-05-002. Pesticide industry sales and usage .gov/oppsrrd1/ REDs/factsheets/24d_fs.EPA). Washington (DC): U.htm. revised February 15. Office of Prevention Pesticides and Toxic Substances. Pesticides in the Nation’s Streams and Ground Water. Geological Survey (USGS). 1992-2001. Blau GE.

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

670 (<LOD-. 62 Fourth National Report on Human Exposure to Environmental Chemicals . Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. 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. 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 .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 size 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 580 831 1127 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .200 (<LOD-.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey.200 (<LOD-.740) 679 700 957 < 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.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .440 (<LOD-.240) 679 701 957 Limit of detection (LOD. < LOD means less than the limit of detection. 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.

S. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Thurman EM. Available at URL: http://www. EPA). Curwin BD.html. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. 2007. Ward EM. Centers for Disease Control and Prevention (CDC).ESTfeature_gilliom.php.Herbicides References Battaglin WA.gov/oppsrrd1/ REDs/0001. Geological Survey (USGS).gov/nawqa/ pnsp/pubs/wrir984245/text. R. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Linhart SM. Supplemental Technical Information (available on-line only). Hsiao JJ. April 1995. reservoirs and ground water in the Midwestern United States. Furlong ET. Sacramento. Barr DB. Larsen GL. Peter CJ.39(17):6561-6574. acetochlor.int/water_sanitation_health/dwq/chemicals/ metolachlor. Wratten SJ. et al. Hodgson E. Environ Health Perspect 2003. Biagini RE. Available at URL: http://www. Camann DE. J Agri Food Chem 1989. et al. Casida JE. sulfonamide.15(6):500-508. Sanderson WT. Dialkylquinonimines validated as in vivo metabolites of alachlor. Sci Total Environ 2000. 4/2/09 U. Xenobiotica 1994. Alavanja MC. 3/26/09 U. 2005. Brown KK.S.S.47(6):503-517. 6/1/09 Whyatt RM. Available at URL: http://water.S. Environ Sci Technol 2007. Barr JR. Roberts AL.epa. California.41:3409-3414. Jefferies PR. Comparative metabolism and elimination of acetanilide compounds by rat. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Rose RL. Ann Occup Hyg 2003. Atlanta (GA). Geological Survey (USGS). Background document for development of WHO Guidelines for Drinking-water Quality. 1992-2001. Sci Total Environ 2000.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Quistad GB. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. and other herbicides in rivers. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Reregistration Eligibility Decision (RED) Metolachlor.11(4):353359. EPA 738R-95-006. Environ Sci Technol 2005.usgs.248(2-3):115-122. imidazolinone. Kinney PL. U. Feng PCC. 1999.pdf 3/30/09 Hines CJ. Pesticides in U. Heederik D. Environmental Protection Agency (U. Hein MJ. usgs. Barr DB. Kolpin DW.who. 2003.pdf. Chem Res Toxicol 1998. Occurrence of sulfonylurea. Available at URL: http://water. Gillion.gov/nawqa/pnsp/pubs/files/051507. Davison KL.111(5):749-756. 1998. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Linderman R. Circular 1291. World Health Organization (WHO). Environ Health Perspect 2000.S.24(10):1003-1012. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. revised February 15.108(12):1151-1157. Andrews HF.pdf. Hladik ML.usgs. Gilliom RJ).248(2-3):123-133. Deddens JA. Shoemaker DA. Available at URL: http://water. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Kolpin DW. and metolachlor herbicides in rats. Coleman S.37(4):10881093. 98-4245 (by Barbash JE. Third National Report on Human Exposure to Environmental Chemicals. streams and groundwater. Metolachlor in Drinkingwater. March 2006. Feil VJ. Burkhardt MR. J Expo Anal Environ Epidemiol 2005. Striley CA. Thelin GP. Reynolds SJ.

nausea. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.4.5-Trichlorophenoxyacetic acid (2. Mohammad and St.4. but higher levels are herbicidal.5-T was once applied as either an aqueous salt or as an oil-soluble ester.5-T is eliminated mostly unchanged in the urine.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. 1989.7. Human health effects from 2. 1974). 1992.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5-T and 2.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States. The half-life of 2.4.5-T use as a herbicide in 1985. myotonia. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. 2.4. < LOD means less than the limit of detection. Agent Orange).4..4. it is not well absorbed through the skin.S.4. Survey Geometric mean (95% conf.4-D were used as defoliants in the Vietnam War (e. dizziness. hypotension. 2004). abdominal pain. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. 93-76-5 General Information 2. which may vary for some chemicals by year and by individual sample. Given the commercial unavailability of 2.5T is rapidly absorbed via oral and inhalation routes.5-T. Chlorophenoxy herbicides act as plant growth hormones.5-T degrades to 2. 2. 1986.4.3.. Nelson et al. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.4.4.1.2 and 0.4. Although 2..Herbicides 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4. At low levels. 2007). Epidemiological studies have reported associations of several types of cancer.5-T has been rarely detected in ground waters (USGS. Ester forms of 2. renal and hepatic injury.5-Trichlorophenoxyacetic Acid CAS No.4. headache. Once absorbed into the body.g. the general population is unlikely to be exposed to it. with an elimination half-life of approximately 19 hours (Arnold et al. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. these herbicides can enhance plant growth. 64 Fourth National Report on Human Exposure to Environmental Chemicals . ranging from several weeks to many months.4.. Omer. and delayed neuropathy (Bradberry et al.5-T in soil varies with conditions.5-trichlorophenol and other degradates. 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. 2.5-T (Holson et al. population from the National Health and Nutrition Examination Survey. Kohli et al.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4.. 2.. 1992).4. and concern about contamination with 2.

4. other exposures. 2005.5-T were generally below the limit of detection.5-T also were below the limit of detection (Kutz et al.4.4.3.Herbicides or contaminated herbicides.4. Mean urinary levels of 2. 2002.S. similar to results of NHANES II (19761980). Urinary 2. or to contaminants in the herbicide formulations (specifically 2. 2. 1980). U.S. in which urinary levels of 2.S.EPA.EPA at: http://www. Finding a measurable amount of 2. 2004). Pearce and McLean. Survey Geometric mean (95% conf.4. Biomonitoring Information Urinary levels of 2. 1996. It is unclear whether these associations are related to the chlorophenoxy herbicides. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.4. Biomonitoring studies on 2.. 1992). * Not calculated: proportion of results below limit of detection was too high to provide a valid result. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.5-T does not mean that the level will result in an adverse health effect.5-T reflect recent exposure. IOM.gov/pesticides/. 2003.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. urinary levels of 2.5-T than levels found in the general population.epa.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne. IPCS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.7. Additional information is available from U.5-T itself is not mutagenic.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.5-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 2.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < 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.4. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 65 .4.4. 2005).

org/documents/jmpr/jmpmono/v96pr04. Fundam Appl Toxicol 1992. 2004. Fundam Appl Toxicol 1992.5-trichlorophenoxyacetic acid (2. 3/17/09 Institute of Medicine (IOM). Dhar MM.23(2):65-73. Nelson CJ. Atlanta (GA).EPA). U. Erne K. et al.EPA. Environmental Protection Agency (U. Beasley VR.inchem. Poisoning due to chlorophenoxy herbicides. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Murphy RS.5-trichlorophenoxyacetic acid (2. Scand J Work Environ Health 2005. Nelson CJ. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Brody D.4. Available at URL: http://www. LaBorde JB. Veterans and Agent Orange: update 2002. Dichlorophenoxyacetic acid.nap. gov/oppbead1/pestsales/01pestsales/market_estimates2001.4.edu/catalog. Available at URL: http:// www.5-T in four-way outcross mice. Board on Health Promotion and Disease Prevention. general population. Vet Hum Toxicol 1989. Bradberry SM. Garabrant DH.4-D and 2.pdf. Centers for Disease Control and Prevention (CDC). 2. Developmental toxicity of 2. Washington (DC): National Academies Press.4:318-21. Philbert MA. Gupta BN. Sircar KP. et al. Carter-Pokras OD. Gaylor DW.4-D) epidemiology and toxicology. I.5-t mixture. Office of Prevention Pesticides and Toxic Substances. Wolff GL. II. Washington (DC): U.8(5):551-60. Crit Rev Toxicol 2002. 2005. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Tandon JS. McLean D. Vale JA.37(2):277-91. Third National Report on Human Exposure to Environmental Chemicals. Agricultural exposures and non-Hodgkin’s lymphoma.4-D/2.2000 and 2001 market estimates.Herbicides References Arnold EK.5-trichlorophenoxy acetic acid in man.5-T).S. Behavioral and developmental effects in rats following in utero exposure to 2. Available at URL: http:// www.S. Holson JF. Cook BT.19(2):286-297. Pearce N.4. Gaines TB.5-T). Holson JF. Gaines TB. Absorption and excretion of 2. 210:250-255. Selected pesticide residues and metabolites in urine from a survey of the U.4. Proudfoot AT.19(2):298-306. S. Pesticide industry sales and usage . The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.htm.32(4):233-257. LaBorde JB. May. Review of 2. Pesticides residues in food: 1996 evaluations Part II Toxicology.5-T).php?record_id=10603. J Toxicol Environ Health 1992. Toxicol Rev 2004. Developmental toxicity of 2.31 Suppl 1:1825. McCallum WF. Neurobehav Toxicol Teratol 1986. Mohammad FK. 914. Sheehan DM. St Omer VE. Multireplicated dose-response studies with technical and analytical grades of 2. Arch Int Pharmacodyn Ther 1974. 3/17/09 Kohli JD.S. Khanna RN.4. Arch Toxicol Suppl 1980.4. discussion 5-7.31(2):121-125.4. Kolmodin-Hedman B.epa. International Programme on Chemical Safety-INCHEM (IPCS). 2003.4-dichlorophenoxyacetic acid (2. Estimation of occupational exposure to phenoxy acids (2.4. Kutz FW.4-.

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

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

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

50 (8.1 (13.4) 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 8.80-9.110 (.1-18.2) 15.069) < LOD < LOD .2-15.120) .117) < LOD .140-.130-.130 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.112-.120-.110) .10 (<LOD-16.4 (12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.139 (.1) 10.120 (.101) .180) .1 (18.2) 12.100) .064) 90th .149) .80 (<LOD-10.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.102 (.062 (.077 (. 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 9.4) 95th 20.070 (<LOD-.3 (19.147 (. which may vary for some chemicals by year and by individual sample.0) 19.070) .109-.50) 15.5) 21.5-15.6-24.138) .130-.110) .139 (.089 (. population from the National Health and Nutrition Examination Survey.190) .177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .059 (.6) 16.1) 15.049-.3-21.090-.090-.170) .9-38.9 (13. Fourth National Report on Human Exposure to Environmental Chemicals 79 .090 (<LOD-.8.40-9.120 (.3 (13.4) 21.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.6) 9.054-.0-21.8) 15.60-10.3 (14.0 (10.4) 20.053 (<LOD-.110 (.112) 95th .182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .9 (14.9 (12.00 (8.8-25.109 (.7 (14.6 (15.7 (15.098 (.130) .202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.S. population from the National Health and Nutrition Examination Survey.080 (. which may vary for some chemicals by year and by individual sample.1) 14.160) .S.1) 13.5-17.5 (<LOD-11.084-. see Data Analysis section) for survey years 01-02 and 03-04 are 10.048 (<LOD-.108-.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 .140 (.9-23.056-.90) 90th 15.110 (.1) < LOD 9.080) .2) 14.062 (.086-.063-.1) 15.242) .083-.5 and 7.130-.0 (10.8 (11. < LOD means less than the limit of detection.80-10.073-.0 (15.100-. 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 .080-.077-.060) .150 (.190) .5) 19.138 (.0 (11.100) .9 (13.00-14.2) 11.058) < LOD .160 (.100-.6) 19.116) .109-.130) .3 (18.103 (.8-17.110-.0) < LOD 9.140) .088-.4) 539 456 484 487 980 885 Limits of detection (LOD.5 (16.30 (8.3 (18.090 (.7-22.062-.150 (.0-25.8 (9.5-17.8 (18.113 (.1) 20.124) .6 (15.30 (8.090-.4) 14.8-19.9 (12.4) < LOD < LOD 16.1-24. Survey years 01-02 03-04 Geometric mean (95% conf.054-.160 (.180) .9-22.8-24.054-.070-.70 (7.064 (.8-17.8) 14.4-17.8) < LOD 8.4 (12.40-10. Survey years 01-02 03-04 Geometric mean (95% conf.093) .1-19.100 (.6-33.130) .5) 15.7-19.1-16.100-.7 (<LOD-15. 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.0) 21.158) .6 (14.6-24.7) 15.075) < LOD .4) 19.4-18.103 (.120 (.096-.055 (.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.

Toxicol Lett 1992.64-65 Spec.14:95-102. Neurotoxicol 2005. Buckland SJ. Mann D. Vol. Frey JM. Aldrin and Dieldrin [online].109(Supp1):113-139.47:1059-1087. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Priestly BG. Serrano FO.html. 4/21/09 Bates MN. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.27:405-421. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. September 2002. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes.103(Suppl 7):113-122. Toxicological profile for aldrin/dieldrin [online]. J Toxicol Environ Health. Andersen A. Wienburg CL. 15. 2 Classes of Pesticides. Int Arch Occup Environ Health 1994.atsdr. PA. Psychopharmacology (Berl) 1987. August 2008. and epidemiology in the United States. Environ Health Perspect 2001. Facca A. Lancet 1998. Handbook of Pesticide Toxicology. United States Geological Survey (USGS).9:1357-1367. Grandjean P. J Occup Environ Med 2005. Available at URL: http://pubs. Kanthasamy A. Ginsburg KS. Finley B. et al. 80 Fourth National Report on Human Exposure to Environmental Chemicals . VT. bioaccumulation. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Kanthasamy AG. Inc. Shore RF. Anantharam V. Part A 2000. Patterson DG Jr. 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. 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. Olea N. References Agency for Toxic Substances and Disease Registry (ATSDR). either singly or in combination. New York. Stehr-Green. David VL. Available at URL: http://www. No:429-436. Food and Drug Administration (FDA). and lymphocyte sister chromatid exchange. Chlorinated Hydrocarbon Insecticides. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Jr. Song S. 6/1/09 Ward EM.usgs.352:1816-1820. Chemosphere 2004. Mumtaz MM. Environmental Health Criteria 91. 731-915.66(4):229-234. Chung KL. J Toxicol Environ Health 1989. Needham LL. Kitzazwa M. plasma dieldrin. Soto AM.fda. Narahashi T. Available at URL: http://www. Edwards JW. Garrett N. 1989. Smith AG. 2007 [online]. Chapin RE. Sanchez-Ramos J. Six high-priority organochlorine pesticides. Available at URL: http://www. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. are nonestrogenic in transfected HeLa cells. Organochlorine exposure and risk of breast cancer. Corrigan FM.gov/~dms/ pesrpts. Daniel SE. 4/21/09 Hoyer AP. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Brock JW. Exp Neurol 1998. Cox. Teta MJ. Revised Feb. Sonnenschein C. et al.26:701-719. Schulte P. 4/21/09 Jorgenson JL. Jorgensen T. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Tully DB.cdc. McIntosh LJ. Basit A. 1991. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.htm.inchem. Grajewski B.54:1431-1443. Environ Health Perspect 1995. Eds.150:263-271. Carlson JN. 1992-2001. Hartvig HB. In Hayes WJ. Patterson DG Jr.59:229-234. Jr and Laws ER. Li AA. International Programme on Chemical Safety (IPCS). Demographic and seasonal influences on human serum pesticide residue levels. Reprod Toxicol 2000. Fernandez MG. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Mink PJ.html. pp.91(1):122-126. toxicology. Pesticides in the Nation’s Stream and Ground Water. Academic Press.gov/toxprofiles/ tp1. Ellis H. Roy ML.cfsan. Turner W.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Rosellini RA.gov/ circ/2005/1291/.org/documents/ehc/ ehc/ehc91. Cancer Epidemiol Biomarkers Prev 2000.

3 (21.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12. and 03-04 are 14.0-13. As a result of the manufacturing process.0-33.1-25.7 (43.10-11.37 (8.8-31.5-41.1-50.0 (32. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.0) 20.1-65.7 (34.6) 20.6) 39.0 (20.2-26.2-49.5) 9.5.2 (28.3 (26.20 (<LOD-11.7-14.5) < LOD < LOD < LOD < LOD 13.6-12.7-39.6 (9.9) 31.3 (11.7) 19. and dairy products are the usual sources of exposure to these chemicals in the general population.9 (26. 2007).1 (16.0 (37.1-19.5) 38.1 (<LOD-12. Technical grade chlordane had contained 7% trans-nonachlor.9 (17.5-40.7-12.2 (41.4 (30.9) 37.9-42.4 (22. 2007).2) 34.8-43.0-67.3-43.8-23.5) 44.3) 10.6) 9.82-11.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2-21.2-56.5-38.1 (15.5-32.9-21.6) 48.1 (17.5) 56.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11. and 7.6-24.2 (21.8-20.2 (36.9 (15.9) 13.S.9 (31.7 (<LOD-13.8) 52.7-70.6-45.6-24.8) 53.0) 41.4 (31.8 (18.1-25.9 (29.1 (25. Since 1992. 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.5-42. Consequently.4-45.5) < LOD < LOD 9. buildings.2) 46.4 (10.7 (42. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.1 (40.9 (18. foods high in fat such as meat.5-44. 01-02. chlordane was used to kill termites and other insects on agricultural crops.1-51.9) 23. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.1 (44.6 (43.5) 10.9) 11.4-51.6) 8. see Data Analysis section) for Survey years 99-00. fish.1 (<LOD-12.5 (<LOD-12.3) 10.3 (<LOD-19.9-38. the technical grade product of each chemical contains 10%-20% of the other chemical.2 (37.6) < LOD 11.0-25. which may vary for some chemicals by year and by individual sample.7 (10.4) 39.3-24.7) 9.4-40.9 (11.63 (8.0 (<LOD-12.4 (30.4) 18.2) * 12.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11. lawns.1) * 11.8) 18. 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.3 (9.7) 31.3-45.8-33. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.8) 27. population from the National Health and Nutrition Examination Survey.5 (33.2-28. Chlordane is not currently produced or used in the U.1-15.5-47.3-49.2) 33.8 (10.89-10.8 (40.4) < LOD 11.1) 90th 34.6-18.7 (<LOD-32.6) 23.4) 12.6) 9.0) 75th 20.8-33.5.5-13.0-61.2) < LOD 11.5-65.S.9-40.9 (26.7 (32.9 (11.7 (19.2 (9.9) 11.8-32.69-10.7) 35.4) < LOD < LOD < LOD 23. 10.4-21.3) 37.1 (11. 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.1) 16.0) 27. respectively.7) 19.2) 22.1) < LOD < LOD < LOD < LOD < LOD 8.9-21.10 (8.1) * 11.6 (9.4 (35.2) 37.2) 36.9 (15.90 (8.8-42.30-11.4) 37.7-25.6) 49.20-10.8) 52.8.8 (42.3 (27.4-14.0 (26.1 (27.6 (16.1 (20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5 (8.9 (36. from the early 1950’s until the mid-1980’s.0-12. 1994.5 (41.8 (10.7-56.3) 41.9) 47.0 (16.4) 29.1) 30. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.6) 11.9) 23.2 (10. Until 1988.6) 36.8-73..9) 36.8 (17.3) 18.3 (25.6 (25.0) 37.4 (<LOD-12.5) 37.9) 17.3 (28.74 (<LOD-10.5) 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.S.0) 31. in addition to trace amounts of numerous other related compounds (ATSDR.9) 39.8) 44.0-18.3-32. heptachlor use has been limited to treatment of fire ants near power transformers. Survey Geometric mean (95% conf.Organochlorine Pesticides Chlordane CAS No.6-53. 57-74-9 Heptachlor CAS No.5 (34. 1994).0) 21.6) 48.1 (<LOD-12.7) 28. and in soil.3 (20.9 (21.8-61. Fourth National Report on Human Exposure to Environmental Chemicals 81 .5 (31.2) < LOD 11.3-45. < LOD means less than the limit of detection.7 (34.5) 21.2 (39.70 (<LOD-10.4) 22.36-11.2-49.3) 18.1) 30.5-43.1) 22.20-11.10-18.7) 42.8 (17.9) 10.7 (17.

410) .250-. 1986).310 (.320 (.350 (.370 (.083 (.130 (.430) .057-.150 (.200 (.070 (<LOD-.130-.190-.230 (.170) . Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS. Le Marchand et al.231) .090) .056 (.065-.340) .090-.148-.260-.280 (.227) < LOD .320 (.290) .290-.315 (.170-.053-.068) 75th .160 (.074-.170) .213) * .100-.240 (. neonatal mortality.320 (.120-.070) < LOD < LOD < LOD < LOD < LOD .069 (<LOD-.180) .120-. Survey Geometric mean (95% conf.110-.149 (.300) .207) .066-.082 (.133) 90th .207 (. 1991.450) .258-..400) .080) . No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.300) .070 (<LOD-.130 (.286 (. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.080 (. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.216-. dermal. and heptachlor epoxide in foods and bottled water. interval) Selected percentiles ( 95% confidence interval) Sample 95th . Smith.180-.S.280-.200-.270 (.057 (.290 (.104-.058 (.064) < LOD .208 (.150) .100 (.210 (.077) .200-.090) .140 (.055-.070) .050 (<LOD-.140) .302) . 1986). 2001.246-.230-.150-.290-.320 (. and alterations in immune function of offspring.146) < LOD < LOD . population from the National Health and Nutrition Examination Survey. Shindell and Ulrich.165-.400) .060 (<LOD-.230) .310) .130-.108-.100-.076) < LOD .. OSHA has established occupational exposure criteria.079) < LOD < LOD < LOD .220-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.070 (<LOD-.245-.290-.350) .066 (<LOD-.280-.128 (.330 (.190-.104) .280) . 1991).068) . characterized by seizures and paralysis. 2006).225 (.130-. 82 Fourth National Report on Human Exposure to Environmental Chemicals .077) .063 (.100 (<LOD-.269 (. and inhalation exposure.270 (.223) .148) .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 * * * * .180) .230-.066-.310) .350 (.053-.047 (<LOD-.204 (.112 (.115-.063-.370 (.070-.063) * .253-. FDA established allowable residues of chlordane.250 (.087-. to heptachlor.075 (.130-.286 (.560) . both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.130) .310) .440) .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .240) .057) * . IARC.258 (. which may vary for some chemicals by year and by individual sample.170) .140 (.240-. 2002. In laboratory animal studies.126) .240-.290) . Takahashi et al.S.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .146) .150 (.130-.110 (<LOD-.106-.199-.058-.340) .050-. heptachlor.S.063) .058-.092) .220 (.063 (.120-.360) .200-. 2007.168-.170) .380) . The major metabolite of heptachlor is heptachlor epoxide.048-. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.287) .080) . 1977a.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.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .210 (.260 (.140 (.150 (.115 (.271 (.083) . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.066 (. IARC considers chlordane and heptachlor as possibly carcinogenic to humans. Elimination of all these chemicals from the body occurs over months to years.070-.280 (. and breast milk is a major excretion route in lactating women.160) ..136) .220-.062) < LOD .230 (.068-.430) . The U.080) .063 (.120 (.070 (.260 (.140-.270 (. which is also persistent in the body (ATSDR.180-.189 (.310-. Chlordane and heptachlor are absorbed after oral. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.071 (. Information Serum Oxychlordane (whole weight) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.091) .320) .126 (.300) .080 (. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.210-.073 (.130 (.320) . and the U.070 (<LOD-. chronic doses of heptachlor have produced liver enlargement and injury.130) .063 (.370 (.. Acute. Rogan.070-.079) .073) < LOD < LOD < LOD < LOD .189-. 1996.450) .300-.140 (.348) .190-.260 (.203-. EPA has established environmental criteria for chlordane and heptachlor.230-.510) .067 (.160) .242-.373) .049 (<LOD-.280-. 1981).250 (.140-.077) .300) .170) .119 (.077) . 2007).300 (.061-. 1977b.Organochlorine Pesticides (Dallaire et al.160) .

. For the exposed persons drinking milk in the Arkansas episode. Biomonitoring Information Serum oxychlordane and trans-nonachlor levels in NHANES 1999-2000. 1993).htm#ref. 2002). In the Hawaii episode.html. inchem. In serum samples obtained in between 1994 and1997 from Inuit women in different Arctic countries. 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. 1988). 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.cdc. mean serum heptachlor epoxide and oxychlordane levels were about sevenfold and threefold higher..org/documents/cicads/cicads/cicad70.gov/toxpro2. than the 90th percentile values of NHANES 1999-2000 (Stehr-Green et al. respectively. environmental levels) and scientists plan and conduct research on exposure and health health effects of chlordane and heptachlor is available effects.e. trans-nonachlor. than the 90th percentile values of NHANES 1999-2000 (Baker. 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. 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.. or heptachlor epoxide in serum does not mean that the level of oxychlordane.atsdr. Biomonitoring studies on levels of oxychlordane. 2004).. Two episodes (one each in Arkansas and Hawaii) of inadvertent heptachlor contamination of dairy cattle feed occurred in the early-to-mid 1980’s. Finding a measurable amount of oxychlordane. resulting in human exposure to heptachlor epoxide that was excreted into the milk. the mean serum heptachlor epoxide and oxychlordane levels were more than twice as high. or heptachlor epoxide causes an adverse health effect. 2003).. A recent assessment of heptachlor is available at: http://www.. transnonachlor. 2001-2002.Organochlorine Pesticides about external exposure (i. 2000). respectively. transnonachlor. from ATSDR at: http://www. and 2003-2004 subsamples were comparable to levels measured in Swedish women from 1996-1997 (Glynn et al. Biomonitoring data can also help Fourth National Report on Human Exposure to Environmental Chemicals 83 .. 2006). Serum transnonachlor levels among females in the NHANES 19992001 subsample were about one half the levels obtained between 1994 and 1996 from women in New York (Wolff et al.

5) 19.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.2) 20.7 (10.1-16.7 (13.8.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0-17.8 (18.6 (<LOD-27.2) 13.8-23.0) 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 13.0-19.3 (<LOD-25.6) 14.8) 20.2 (18.0-54.2-16.4 (<LOD-19. 01-02. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.5 (18.6) 13.S.8) 21.9-16.6-21.6 (16. Survey Geometric mean (95% conf.7 (16.3) 10.6) < LOD < LOD < LOD 27.3-18.10-13.3) 22. 84 Fourth National Report on Human Exposure to Environmental Chemicals .0-17. see Data Analysis section) for Survey years 99-00.8) 13.8) 14.3) 16.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.4) 18. 10.4 (<LOD-54. which may vary for some chemicals by year and by individual sample.8-46.2) 15.9-25.4 (11.2 (<LOD-16.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.8) 15.8-24.8 (15.3) 18.2-27.5 (11.4 (15.1-38.3 (13.6-17. respectively.3) 23. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8 (13.8) 19.7-19.9-29.0 (15.6 (16.5 (10.90 (<LOD-9.3) 18.0 (11. and 03-04 are 14.2 (<LOD-62.4 (11.5 (<LOD-21.5) < LOD 14.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.1 (19.6 (13.0-16.1 (16.1) 23.8) 16.6 (12.1) 20.40) 15.1-29.1-15.9 (15.8-24.8 (18.8) 13.7-18.6 (8.8 (<LOD-23.8-24.0) 13.3) 18.9-29.2-17.7-25.6.9 (12.6 (11.9) 15.3) 27. and 7.5 (11.5 (<LOD-32.8 (13.1) 13.5.8) 19.2 (<LOD-25.50) < LOD < LOD < LOD 17.20 (<LOD-9. population from the National Health and Nutrition Examination Survey.2) 26.6) 22.2-27.4) 21.8) 14. < LOD means less than the limit of detection.6 (14.9-23.

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

2-18.6 (57.5) 77.8-79.9 (51.4-22.5 (44.8 (19.9-65.9 (36.1) 14.8) 47.6 (15.1-28.0 (13.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.3) 18.7 (30.9-20.0-37.2) 59.9) 51.8) 51.6-66.6-54.2 (25.0) < LOD < LOD 8.6 (56.2-23.9-40.4-62.0-23.5) 14.7-160) 86.1) 32.7-77.8 (28.6 (<LOD-14.8 (45.6 (12.9 (29.6) 56.5-69.1 (22.0-20.8 (16.0 (16.9 (15.7) 56.2) < LOD 10.7) 15.7-34.7-17. < LOD means less than the limit of detection.8 (28.0 (19.5) 78.2) 17.86-13.2 (14.7) 78.6) 56.8 (71.3-58.2 (64.6) 34.70 (<LOD-12.9-58.7-32.2-16.8-41.7) 78.3) 16.5) 20.8 (28.9 (66.2 (27.2-37.6) 82.2-21.1) 17.9 (<LOD-14.9) 14.7) 17.6) 54.9 (16.0-93.3 (16.7 (35.8 (15.8-16.5-20.0-123) 74.0-38.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.2 (7.9-69.5 (15.1) 17.9-22.2 (19.4-67.3) 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.0-143) 112 (68.4 (45.0 (14.3 (56.7-18.7 (16.8-19.1 (48.3) 18.5-111) 68.4) 59.9) 51.4-52.7) 14.0) 13.7-35.1-16.0 (42.3 (14. 10.1 (47.6-19.2 (26.1) 62.4 (28.8-77.9-45.4) 55.3 (45.5 (15.5.8 (13.0-93.7-22.8 (13.0 (62. see Data Analysis section) for Survey years 99-00.5-19.1) 17.6) 60.5. Survey Geometric mean (95% conf.1 (41.2 (59.1) 17.4-36.1) 78.3) 15.0-22.1) 17.2 (36.7) 28. interval) 18.2) 34.2 (60.8 (26.6) 25.8 (30.0) 49.8 (49.1) 18.5 (13. respectively.1) 30.8) 19.0-113) 68.0) 18.1-22.7 (18.9-65.1 (10.8-90.7-29.1) 17.6 (32.9-36.8-67.6-88.4) 48.0) 33.5-95.9 (28.3-30.3) 32.0-23.1) 16.5) 90th 55.2) 20.1-34.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.3-74.9-64.4-23.0) 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.S.5-17.4 (12.8-16.0-24.2) 30.6 (52.7) 52.3 (49.8-21.8 (26. which may vary for some chemicals by year and by individual sample.5 (25.5) 48.0 (42.7 (11.5 (45.1) 78.5) 36.3-32.6 (16.8-129) 74.7-38.2-17.8 (<LOD-20. 01-02.5) 26.7-113) 68.8-90.5) 30.4) 20.3-86.1 (17.3-39.4) 19.3-21.2) 39.1-51.8 (12.0 (48.5) 22.8.7 (59.9 (51.3) 32.3 (14. population from the National Health and Nutrition Examination Survey.0) 40.4 (30.9) < LOD < LOD < LOD 20.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.6-82.0 (60.8 (17.8-110) 59.9) 14.4 (16.2) 19.0 (13.1) 31.9-35.7) 35.0 (15.1-34.1) 18.4-35.1-16.2 (15.7 (28.8 (42.5) 35.5) 19.6) 13.7-23.3 (17.5-87.4 (11.9 (47.1-18.7 (59.6-20.5-36.7 (74.0) 19.4) 107 (84.7-21. and 03-04 are 14.3) 25.1-126) 67.7) 59.8) 80.0 (16.1 (65.6-22.6 (56.3) 30.6 (50.2-18.9 (19.5) 9.4-18.6) 10.4 (67.1) 17.2-88.1-20.3-57.0-68.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.9 (15.0 (15.8 (26.3) 36.8-19.0-59.2 (14.10 (<LOD-11. and 7.3-50.3) 19.0 (29.1-55.3) 30.7-20. 86 Fourth National Report on Human Exposure to Environmental Chemicals .0) 75th 31.8 (11.7) 73.5) 14.9-89.7 (13.3 (58.6) 84. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 16.

330-.470 (.081-.367) .210) .272-.240) .103 (.079-.301-.078-.211) 90th .590 (.279-.130) .068-.330-.125 (.202 (.141) .094 (.430-.082) .055 (<LOD-.116 (.360-.090) .210-.285-.127) < LOD < LOD .590) .960) .081 (.124) .800) .112 (.130) .120) .080) .470-.380 (.120) .430-.160 (.220 (.110 (.760 (.092 (.390-.327 (.232) .350-.085-.450) .400-.490) .180-.070 (.220 (.079-.310-.104-.116-.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .260) .098 (.085-.690) .047-.190-.340) .237) .340-.250) .370 (.190-.830) .286-.190-.680 (.480) .320-.098 (.090-.288 (.559) . which may vary for some chemicals by year and by individual sample.160-.580 (.410-1.090-.210) .186-.130) .097) .324 (.093-.390) .103 (.310-.390) .110) .S.098) .270-.400 (.069-.440) .093-.119) < LOD < LOD < LOD .158-.054-.330 (.510 (.350 (.310 (.565) . Survey Geometric mean (95% conf.096-.490 (.080-.130) .087 (.135 (.111 (.109 (.114) .390 (.430-.120-.420) .250) .573 (. population from the National Health and Nutrition Examination Survey.113) .470-.110 (.497-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .580 (.417 (.420 (.078 (.397-.460) .096-.520 (.690) .131) .220 (.170 (.120) .390 (.171-.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.092 (.085-.390 (.260) .130 (.288-.099-.300) .230 (.400 (.395) .112 (.210 (.091) .060) .180-.113) < LOD .240 (.108 (.090 (.190-.410-.190-.100-.071 (<LOD-.409-.161-. Fourth National Report on Human Exposure to Environmental Chemicals 87 .084-.190-.061-.173-.145-.080-.340-.095-.242) .090 (<LOD-.470 (.220 (.130) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.119) Selected percentiles ( 95% confidence interval) Sample 95th .098-.210 (.830) .470 (.640 (.930) .400-.20) .126) .104 (.120 (.651) .130) .069) .180-.106 (.041 (<LOD-.300-.500) .520) .405) .210-.110 (.120-.120 (.091-.105 (.600) .414 (.100-.110 (.210 (.520 (.390 (.630) .290-.090-.093) .460) .458 (.395-.310-.183 (.220) . interval) .090-.490 (.580 (.140) .120 (.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.360-.240-.220 (.108) .594) .122) .370 (.100-.134) .106 (.122) .080-.090-.141) .090-.096) .460-.237) .089 (.130) .062 (.550 (.191 (.177-.630) .220 (.125) .110 (.220 (.100-.440-.060-.080-.129) .186 (.310) .594) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .100 (.510-.840) .106 (.600 (.080 (.461 (.108) 75th .130 (.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .240) .590 (.371) .680) .117) .630) .128 (.540) .490-.320-.280) .234) .109 (.205 (.220 (.110 (.684) .210) .120) .099-.100 (.060 (<LOD-.120-.400) .116) .343 (.240) .110-.111-.317 (.355 (.161) .310-.150) .250) .150) .093-.

6/1/09 National Toxicology Program (NTP).41:145–148. Ayotte P.org/ documents/cicads/cicads/cicad70.nih. 2001. Sci Tot Environ 2006.pdf. Willman E. et al. Stehr-Green P. Poland. Concise International Chemical Assessment Document 70 Heptachlor [online]. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Arch Pediatr Adolesc Med 1996. et al. Arch Environ Health. In Hayes WJ. Senie R. International Agency for Research on Cancer (IARC) . 4/21/09 Dallaire F.htm. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Voorspoels S. Darnerud PO. Hansen JC. Berkowitz GS. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Takei G. et al. Keller JA. Kolonel LN. 1993. Available at URL: http://ntp. Environ Health Perspect 2003. Vol.8:1-123.gov/ntp/ htdocs/LT_rpts/tr008. 2006.org/site/foundation/ research/projects2.inchem. 88 Fourth National Report on Human Exposure to Environmental Chemicals . August 2007. 79. 1994-1997 organochlorine compounds. Atuma S. Dendle WH. Brower S. Shindell S and Ulrich S. 4/21/09 Baker DB. Smith AG. Charles MJ. Barker J. 731-915. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Environ Health Perspect 2002. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Wong L. Chlordane and heptachlor [online]. Baker DB. Chlorinated Hydrocarbon Insecticides. 2 Classes of Pesticides. Bioassay of heptachlor for possible carcinogenicity. Pollutants in breast milk. Chashchin V. Dewailly E. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). LeMarchand L. 6/1/09 Rogan WJ. Jr. May 1994. Hertz-Picciotto I. Odland JO.372:20-31. Lawrence River (Quebec. Gilman A. Available at URL: http://www. Vol. National Toxicology Program (NTP). Dewailly E. Jr and Laws ER. 1963-1967. Toxicological profile for heptachlor and heptachlor epoxide [online]. Hawaii Med J 1991.50(3):108-118. A Report to the Hawaii Heptachlor Research and Education Foundation. Organochloride pesticide residues in human milk in Hawaii. maternal serum and milk from Wielkopolska region. New York. Canada). 4/21/09 James RA.html. Laliberte C.gov/ntp/ htdocs/LT_rpts/tr009. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR).atsdr.84:151-161.heptachlor. Bioassay of chlordane for possible carcinogenicity. Van Oostdam JC. 9/25/07 International Programme in Chemical Safety (IPCS). 1986. Wohlleb JC. Jaraczewska K. Environ Res 2000.html. Organochlorine exposures and breast cancer risk in New York City women. Available at URL: http://www. Toxicological profile for chlordane [online].org/documents/iarc/ vol79/79-12. Muckle G.28:497501. Aune M. 1991 pp. Circumpolar maternal blood contaminant survey.330:55-70.niehs. Organochlorines in Swedish women: determinants of serum concentrations.gov/toxprofiles/tp31.html.9:1-109. Tartter P. Available at URL: http://www.259(3):374-377. Royce W.nih. Lulek J. Available at URL: http://ntp. Distribution of polychlorinated biphenyls. Siegel BZ.110(8):835-838.cdc. gov/toxprofiles/tp12.Summaries & Evaluations. Handbook of Pesticide Toxicology. et al. Head SL. Wolff MS.111:349355.110:617-624. Covaci A. Bleiweiss IJ. Drews K. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. J Occup Med 1986. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. International Agency for Research on Cancer (IARC). Sci Total Environ 2004. 1979-1980.niehs. Loo S.inchem.pdf. Academic Press. Bull Environ Contam Toxicol 1981:27:506-511. Inc. Saidein D. Eds.htm.150:981-990. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Available at URL: http://www. Mortality of workers employed in the manufacture of chlordane: an update.atsdr.cdc. KalubaSkotarczak A. Environ Health Perspect 2002. Granath F. Available at URL: http://www. JAMA 1988. Bjerselius R. Glynn AW. Takahashi W.

7) < LOD 18. and trace amounts of several related compounds.2-95.3 (<LOD-31. which is a mixture containing p.5) 25. including 1.7) 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. These chemicals are highly persistent in soil. which may vary for some chemicals by year and by individual sample.2-65.1-71.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.p’-DDD (4% or less).4) < LOD 17.90 (<LOD-12. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.0 (18. population.0-27. In the body.0-15. when virtually all use of it was banned.0) 20.50-11.5 (14.10-13.0) 26.1 (<LOD-39.9) < LOD < LOD 9.8-26. DDT usually refers to the technical product.6 (22.9 (21.3-16. sediments.4) < LOD < LOD < LOD 61.8-23.2) 30.0 (10.10 (<LOD-12. DDT was used at one time as a treatment for head and body lice.1-27.6 (25. p. particularly for endemic vector and malaria control. DDT can be absorbed after ingestion.p’-DDT (15%-21%).2) 155 (59. fish. and water.6 (31. Gunderson.5 (15. after World War II until 1972. although DDT and DDE intakes have decreased over time (FDA. and dairy products. 1991). DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.9 (10.3) 22.00 (<LOD-10.3) 21.6 (9.8.6-33.9-34.9 (<LOD-20. It was produced and used in the U. Survey Geometric mean (95% conf. see Data Analysis section) for Survey years 99-00.3) 21.6 (<LOD-25.3-590) 293 (104-541) 48.7-16.8-39.8) 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 8.0-155) 83. inhalation.5) 23.3 (27.0 (18. Fourth National Report on Human Exposure to Environmental Chemicals 89 .7 (15.2) < LOD < LOD 9.8) 36.70 (8. food.7 (19.S.5-36. Both Serum p.4.5 (23. DDT is converted in the environment to other more stable chemical forms.S.3) 28.1’-dichloro-(2. 17. respectively.8) 30. 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.9) 29.9) 14. depending on conditions. continues to be the primary source of DDT exposure.0 (21.0-37. DDT and DDE can cross the placenta.S. or dermal exposure.7) 12. DDT is converted to DDE and several other metabolites.0) 19.9 (10. 2008. 01-02. as well as in plant and animal tissues.0-35. < LOD means less than the limit of detection.2 (<LOD-40.9 (10. The biodegradation half-life of DDT in soil varies from 2 to 15 years.9-28.1 (33.p’-DDT (65%-80%).5-54.1 (23.5 (23. 1988).8-17. population from the National Health and Nutrition Examination Survey. and 7. and 03-04 are 20. 2002. Smith.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.3-236) 24.5) < LOD < LOD 9.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.9) 17. air. particularly meat. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. Food imported from countries that still use DDT may contain the chemical or its residues. o.4 (23.1) 31.1) 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 12.7.2 (11. Only a small proportion of DDT is metabolized and excreted (Smith. It is still used in some countries.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.0) 40.0-53.8) 15.1’-(2. 1991).3 (<LOD-21. resulting in fetal exposure.2-bis(p-chlorophenyl) ethane (DDD). In the general U.

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. 2006. Beard. 2000.180 (.400 (. resulting in exposure to nursing infants (Rogan.201 (.048 (<LOD-. In laboratory animals. Jusko et al. 2006).170-.065-.078 (.180 (.260) . Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.189-. polychlorinated biphenyls. 2004.130 (<LOD-. Survey Geometric mean (95% conf.080-. Gladen and Rogan.250 (.343) < LOD .063 (<LOD-.130 (<LOD-. other organochlorines.530) .00) .130-.068-.220) . 1998). Longnecker et al.114-.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 . Jusko et al.130 (<LOD-.. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. 90 Fourth National Report on Human Exposure to Environmental Chemicals .180) .190 (..059-. and o. accidental exposures.074-.051 (<LOD-. 2006).. Calle et al.146 (.190 (.180-.095) < LOD .105-. 2002. 2002.120 (<LOD-.26) 1.140) . overt signs of acute human toxicity include vomiting.150-.p’-DDD and p. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.62 (..00 (.g.150-.400) .530 (.313 (.150) .220) . interval) Selected percentiles ( 95% confidence interval) Sample 95th . 1996)..200 (.240) . have not been consistently demonstrated (Beard.240 (.143) < LOD < LOD . In high dose.071 (. premature delivery.054-..140-.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 . lung cancer.190-1.180) .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. 1956)..34) .071-. Hayes et al.S. Animal studies reported reduced fertility. dioxins and furans).106) < LOD < LOD .290) .146 (.078-.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 .128 (. 2001).230) . and altered behavior after neonatal exposure (Eriksson and Talts.084 (.064 (.112 (.230) . Gray et al.098-.061) < LOD < LOD < LOD . Snedeker. fertility. Studies of DDT exposure and pancreatic cancer.p’-DDE can produce anti-androgenic effects (Gray et al.Organochlorine Pesticides chemicals are excreted in breast milk. 2001).250-1.160-. 2001).108 (. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR.203) .079) < LOD < LOD .. 2002. 2006.570-4. which may vary for some chemicals by year and by individual sample.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * . and seizures.627) .069) .330-4. and leukemia have also been inconclusive (ADSDR.170 (.. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e...106-.170) .150 (<LOD-.106) .150 (<LOD-. 2006. Mariussen and Fonnum.086 (. and duration of lactation. 1997). DDT may bind to estrogen receptors (Chen et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.01) . reproductive organ abnormalities.087 (. Reproductive effects in humans affecting birth weight.420) . tremor. 2002. 2006).132-. A workplace standard for DDT has been established by Serum p.120-. 2001).075) 1. 1995. population from the National Health and Nutrition Examination Survey.142 (..

Survey Geometric mean (95% conf. 2002. environmental levels) and health effects is available from the U.3.S.gov/ pestcides/ and from ATSDR at: http://www. population declined by about fivefold to tenfold.e.. 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. for males and females in the NHANES 19992000 subsample (Pavuk et al.0-114) 269 (213-323) 285 (249-337) 233 (175-314) 185 (141-237) 213 (172-253) 167 (123-240) 608 (530-693) 695 (595-798) 557 (420-734) 339 (243-479) 319 (282-389) 341 (211-586) 1260 (1030-1550) 1480 (1310-1700) 1270 (877-1800) 528 (339-812) 456 (343-722) 522 (313-1430) 2020 (1520-2730) 2550 (1980-3080) 1990 (1500-2470) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 249 (220-283) 285 (252-323) 235 (193-288) 270 (226-322) 305 (273-341) 241 (193-301) 223 (182-262) 248 (222-285) 200 (164-262) 234 (184-302) 256 (219-297) 207 (161-281) 494 (380-578) 520 (441-627) 466 (331-653) 601 (492-711) 708 (567-844) 539 (386-735) 1010 (789-1130) 1160 (937-1360) 1000 (763-1400) 1350 (1040-1720) 1480 (1410-1710) 1250 (813-1900) 1430 (1080-2160) 1900 (1580-2490) 1610 (1210-2320) 2210 (1570-2810) 2670 (1940-3300) 2010 (1500-2450) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 674 (574-792) 652 (569-747) 444 (362-545) 295 (241-362) 324 (262-400) 262 (233-295) 217 (189-249) 253 (226-284) 208 (165-263) 624 (545-701) 561 (455-690) 373 (283-522) 251 (199-313) 248 (223-296) 216 (173-267) 194 (162-238) 225 (203-254) 177 (148-238) 1350 (1090-1660) 1400 (1050-1950) 875 (608-1170) 668 (492-874) 762 (583-999) 589 (453-747) 438 (355-507) 463 (402-558) 417 (302-564) 3090 (2040-4950) 4110 (2520-6550) 2150 (1520-2470) 1850 (1040-2220) 1620 (1180-2980) 1620 (1130-2310) 825 (647-1010) 1150 (878-1340) 907 (574-1480) 4950 (3070-9350) 7080 (3080-15600) 3290 (2380-9240) 2300 (1560-5680) 3260 (1270-6900) 2860 (1880-3440) 1160 (1010-1350) 1640 (1410-1940) 1490 (909-2300) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites Limit of detection (LOD. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person.epa. 2003. Smith.. and 7. Stehr-Green. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.. Fourth National Report on Human Exposure to Environmental Chemicals 91 . 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.Organochlorine Pesticides OSHA and a guidance established by ACGIH.. and 03-04 are 18..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. Biomonitoring Information DDE persists in the body longer than DDT.S. 8. 2002. 2004). EPA at: http://www. 2005). mean serum levels of DDT and DDE in the U. 1998. In a population-based sample of men and women from eastern Slovakia.6 (81. Declining DDE levels over time have also been observed in the German population. More information about external exposure (i. 1991). In general.6. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. 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.html.. see Data Analysis section) for Survey years 99-00..p’-DDT) as a possible human carcinogen.S. population from the National Health and Nutrition Examination Survey. compared to levels observed in this Report (Anderson et al.atsdr. respectively. Since the 1970’s. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. IARC classifies DDT (p.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97.8. 2003). 2004).cdc. Link et al. NTP considers DDT as being reasonably anticipated to be a human carcinogen. Heudorf et al. 01-02..gov/ toxpro2. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al.7-119) 113 (100-140) 93. 1989). Compared to females in the NHANES 1999-2000 subsample. respectively.

3 (9.90) 22.39 (3.81 (1.7-20.72) 1.p’-DDT (Stehr-Green.66) 1.4) 14.51-49.93 (7.85-4.57 (1.36-11.24 (1.65 (1.43-4.p’-DDT were below the limits of detection.6) 13.6) 9.96) .4) 13.91) 3.37-4.56-6.3 (8.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.04-1.2 (19.39) 1.34) 2.35) 1. Biomonitoring studies on levels of DDT and DDE provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DDT or DDE than are found in the general population. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.51-8. Survey Geometric mean (95% conf.1) 40.7 (8.5) 16.40 (3. 1971).12-1.22-1.57) 2.88-35.500-.09-1.54 (1.32) 1.46 (1.9-38..10) .02-8.385-.01-15.6) 9.75) 2.43-8.26-10.60-13.963-1.57-2.13-2.0) 2.27) 3.6) 9.18-4.32-1.12 (6.07) 1.488-.635) 1.64-2.994-2.64) 3.4 (12.21) 90th 7.00 (.Organochlorine Pesticides nearby agriculture (Botella et al. 1989).77 (1.10-1.58) 1.6 (8.26-2.24-17.53) 1.76-3.39-1.9 (15.87 (5. 2005).62-6.61 (1.00) 7.03-4.77 (1.7-48.28) 1.19) 4.69 (2.51) 3.55-9.2 (9.8-90. serum levels of o.4-19.52-6.7) 16.31-2.88 (2.71 (5.39-2.83 (1.70) 1.40-4.36) 3.19-14.534-.66) 4.30-1.44) 1.06) 1.49 (1.0 (9.38 (1.41-12.1 (9.14) 2. In a subsample of NHANES II (19761980) participants.11-1.47) 3.34-11.47 (1.8 (13.3) 16.16-1.59 (1.56-2.56) 2.45 (1.796 (.48 (6.25) 8. population from the National Health and Nutrition Examination Survey.92) 1.05) 1.04 (6.41 (1.7) 13.6) 11.75 (8.53) 7.680-1.0 (12.82) 1.51-15.646) .34) 6.561 (.22 (7.80 (2.2 (9.80) 1.36-1.590 (. 1991)..66) 1.2-32.9) 7. 2004). High mean levels of whole blood DDT (about 3.75) 1.419-.3) 10.34 (7.03-1.730) .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.65) 1.78 (4. Finding a measurable amount of p. Serum p.17 (3.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.53 (2.14) 2.70-3.66) 3.5) 5.75 (4.3) 13.68-4.11 (2.32 (1.68) 2.91-3.600) .23 (7..01-11.5) 10.00-1.32 (1.76) 1.46 (1.40-4.75) 6.611-1.32-9.85 (1.456 (.80) 1.68 (2.37-1.85-10.6 (9.59) 6.12 (.6 (17.p’-DDT.25-14.27-1.S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.59) 3.05 (3. o.63 (1.7) 9.8 (13. 2004).8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.01-11.57 (1.1 (8.01-1.50 (2.6 (7.25) 1.30 (1.46-2.9) 5.54) 8.57 (3.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.92 (3.69 (1.0) 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 .57-3. or p.965-1.32-1.81 (7.9 (26.26) 3.516 (.520 (.17-3.1) 7.99) 1.25-16.40-8.57-13.18-1.18-3.4) 9.80) 3.7-19.33-1.01) 1.8 (9.71 (6.20 (.07 (5.59 (4.2) 26.p’-DDT.37 (1.18-1.623 (.2) 19.00 (6.87-16.69) 4.13) 4.18) 1.97 (3.58) 75th 3.5) 7.37-16.79) 4.49 (1.07) 1.72) 1.71) 12.81) 11.81-5.10) 2.66-2. 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.51) 1.820-1.18 (6.01) 1.02 (2.870 (. 309 versus 268 ng/g lipid.45 (1.61-2.54-7.25 (1.71) 32.63-15.29 (1.58) 1.66-4.24) 1.84 (3.76 (2.82 (1.14-9.51 (1.8 (14.726) .49) 8.31 (1.53-15.13 (1.01-5.22) .55 (2.3-43.34-3.14 (1.31-12.38 (1.84-3.56-3.63 (6.14-1.4 (8. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.15-4.30 (1.557) 1. less than one percent had detectable serum levels of o.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.36-2.890-1.9-17.21) 3..69 (. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.06) 3.26 (1. considerably higher than levels in this Report (Smith.10-5.50-17.91-2.1) 12.97-4. interval) 1.8) 15.43-4.48-4.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .02) 1.69) 8.81-18.6) 9.96) 1. In the NHANES 1999-2000.91 (6.860 ng/L) and DDE (about 14.52 (1.63 (1.01-1.36 (3.49 (6.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.59 (1.76) 1.430-.16 (2.5) 22. 2001-2002 and 2003-2004 subsamples.6) 12.2 (6.6) 8.30-1.37-10.92 (3.66-17.52 (3.25 (.43 (5.90-8.

S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey years 99-00. 17.8.7. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.4. and 7. and 03-04 are 20. 01-02. Fourth National Report on Human Exposure to Environmental Chemicals 93 . which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.Organochlorine Pesticides Serum o. population from the National Health and Nutrition Examination Survey.p'-Dichlorodiphenyltrichloroethane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. respectively.

p'-Dichlorodiphenyltrichloroethane (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.S. population from the National Health and Nutrition Examination Survey. 94 Fourth National Report on Human Exposure to Environmental Chemicals . 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. Survey Geometric mean (95% conf.Organochlorine Pesticides Serum o. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

atsdr. et al. Needham LL.358:110-114. Swanson MK. et al. Hayes WJ. hypospadias.cdc. DDE. September 2002. Int J Hyg Environ Health 2002. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Brock JW. Kulkarni PK.97(2):178192. Beard J. April 1982 to 1984. Charles MJ. Durham WF. Olson J.96:34-40. Greenfield TA. Olson JR. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Rogan WJ. selected elements.205:297-308. Burse VW. Cerrillo I. Bates MN. Olea-Serrano MF. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Willman EJ. Klebanoff MA.111:349355. Gray LE Jr. Kashyap R. Falk C. lindane (g-HCH). Kaus S. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study.21(1-2)37-48.cfsan. DDE and shortened duration of lactation in a northern Mexican town. Profiles of ortho-polychlorinated biphenyl congeners. 4/21/09 Gladen BC. Frumkin H. Atuma S. Hanrahan L. Parks L. Moysich KB. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Environ Health Perspect 1998. J Assoc Off Anal Chem 1988. Wolf CJ.7(3):248-264. Schulz C. Barr DB.355:7889. Food and Drug Administration (FDA). Zhou H. Klebanoff MA.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Gabrio T. Buckland SJ. Maternal serum level of 1. Darnerud PO. Davis MD. Heudorf U. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Brock JW. Koepsell TD. Crespo J. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Maternal DDT exposures in relation to fetal and 5-year growth. Bloom MS.1-dichloro2. Eriksson P. Bull Environ Contam Toxicol 2004. Garrett N. Environ Health Perspect 2003. Bjerselius R.gov/~dms/ pesrpts. Piechotowski I.112(17):1761-1767. Organochlorines and breast cancer risk. DDT and human health. Baker RJ. dichlorodiphenyldichloroethylene.17(6):692-700. hexachlorobenzene. Arnold SF. Lambright C. Am J Epidemiol 2002. Hum Reprod Updat 2001. Krause C. Effects of environmental antiandrogens on reproductive development in experimental animals. Am J Public Health 1995. Jr. et al.155(4):313-322. Hurd C. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Gunderson EL. Saiyed HN. Needham LL.gov/ toxprofiles/tp35. and polythelia among male offspring. Zaidi SS. Epidemiology 2006. Gray KA. and DDD [online]. and HCB residues in human blood in Ahmedabad. et al. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Botella B. Link B.71(6):1200-1209. Patterson DG Jr. Henley SJ. 4/21/09 Anderson HA.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism.fda. Zhou H. Chemosphere 2005. Paepke O. Needham LL. Granath F. FDA total diet study. et al. Sci Tot Environ 2006. Biomonitoring of persistent organochlorine pesticides. Drexler H. August 2008. Herrman T. Olea N. Chemosphere 2004. Toxicological profile for DDT. Longnecker MP. Environ Health Perspect 2004. Angerer J. Biochem Pharmacol 1997. Bhatnagar VK. Environ Res 2004. et al.85:504508. Longnecker MP. et al.106(5):279-289. Jr. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Cueto C.html. Available at URL: http://www. Aune M. et al. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. and other chemicals. Ellis H. Seiwert M. Zoellner I.206:485-491.72:261265. Chen CW. Int J Hyg Environ Health 2003. Organochlorines in Swedish women: determinants of serum concentrations.54:1431-1443.html. Hediger ML. Ostby J. Thun MJ. Lancet 2001. Gladen BC. dietary intakes of pesticides. Levels of DDT. Environ Res 2005. Talts U. JAMA 1956.58:1185-1201. Available at URL: http://www. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Rivas A. Glynn AW.52:301-309. Exposure of women to organochlorine pesticides in Southern Spain. Katz SH. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Jusko TA. et al. Becker K. Vena JE.53(8):1161-1172. and dichloro(diphenyl)ethylene (DDE). Savitz DA. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. HCH. Vorojeikina DP. Lepom P.162:890-897. Furr J. Notides AC. The Great Lakes Consortium. Calle EE. CA Cancer J Clin 2002. India.. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Klebanoff MA. Neurotoxicol 2000.

Eds. et al.36:253-589. Fonnum F.53:455-477. Nims R. Cerhan JR. Pollutants in breast milk. New York. Arch Pediatr Adolesc Med 1996. Vol. Jones CR. Thomas PE. and dieldrin.109:35-47. Pavuk M. Stehr-Green. Reddy AB. Rogan WJ. Inc. Schecter A. children and newborn infants. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Chlorinated Hydrocarbon Insecticides. Snedeker SM. Rey AA. Jr and Laws ER. Academic Press. Petrik J.Organochlorine Pesticides Mariussen E. Crit Rev Toxicol 2006. et al. Astolfi E.20(2):186-193. Chovancova J. DDE. Deichmann WB. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Pesticides and breast cancer risk: a review of DDT. Fox S. Chemosphere 2004. 1991 pp. 731-915. 2 Classes of Pesticides. and DDD in male rat liver and cultured rat hepatocytes. Jr. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Demographic and seasonal influences on human serum pesticide residue levels. DDE. Smith AG. Environ Health Perspect 2001.27:405-421. Comparative pharmacodynamics of CYP2B induction by DDT. Handbook of Pesticide Toxicology. 96 Fourth National Report on Human Exposure to Environmental Chemicals . In Hayes WJ.54:1509-520. Lubet R. Radomski JL.150:981-990. J Toxicol Environ Health 1989. J Toxicol Environ Health Part A 1998. PA. Toxicol Appl Pharmacol 1971. Lynch CF.

50) < LOD < LOD < LOD 5. Endrin was not widely used as a termiticide. 1987). General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. and occasionally at low levels in sediment and surface waters. Depending on soil conditions.. total diet surveys (FDA. 2008). Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces.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.S.40-5.40) < LOD < LOD < LOD 1022 885 1165 940 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5.. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. 72-20-8 General Information Endrin. have been cancelled by the U. EPA.60 (5. endrin has been detected with declining frequency in U. Kavlock et al..20 (<LOD-5. 1992). 1991). manufactured.S. 1979. anti-12hydroxyendrin. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. Fourth National Report on Human Exposure to Environmental Chemicals 97 . rodenticide and avicide. Endrin does not accumulate in body tissues (IPCS.09 and 7.50) < LOD 5.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. 1996. fatty infiltration. Hepatic effects of endrin exposure have included necrosis..10 (<LOD-5. a stereoisomer of dieldrin. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. Endrin is absorbed rapidly after ingestion. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. population from the National Health and Nutrition Examination Survey. inhalation or dermal exposure routes. 1981). An epidemic of acute endrin poisoning.20 (<LOD-5. unless the dose is high and the exposure is very recent. 1992). Survey Geometric mean (95% conf.30) < LOD 5.40 (<LOD-6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. endrin usually is not detected in serum of exposed individuals. All uses of the pesticide in the U. Endrin has been detected in soils. Because it is metabolized so rapidly. In the body. is no longer manufactured in the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. unlike aldrin and dieldrin.10 (<LOD-5. IPCS.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. Endrin was used as an insecticide. and inflammation (Smith. 1992). High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. which may vary for some chemicals by year and by individual sample. endrin can persist for years. or from contact with contaminated soils and sediments in areas where endrin was applied. endrin is converted rapidly to its major metabolite.30 (<LOD-6. 1992. 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. < LOD means less than the limit of detection. or discarded.S. see Data Analysis section) for Survey years 01-02 and 03-04 are 5.8. At high doses.Organochlorine Pesticides Endrin CAS No. Over time. Smith. 1991). Ketoendrin is a major photodegradation product (IPCS.

html. EPA has established environmental standards for endrin.. IARC has determined that endrin is not classifiable with regard to human carcinogenicity.Organochlorine Pesticides The U.020-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .S.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 . with the highest value 6.020) < 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-. This finding is consistent with other general population studies (Bates et al. environmental levels) and health effects of endrin is available from ATSDR at: http://www. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2004.020 (.020 (<LOD-.020 (<LOD-. 2000).020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level. endrin was detected in 9% of serum samples. In a small study of Spanish women hospitalized for elective surgery. 2004). Information about external exposure (i.020 (<LOD-. Survey Geometric mean (95% conf. Biomonitoring studies on levels of endrin provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of endrin than are found in the general population.020) < LOD .020 (<LOD-. serum levels of endrin were below the limit of detection..gov/toxpro2.020) < 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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.24 ng/mL (about 6.S. Workplace exposure standards for endrin have been established by OSHA. Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect. Ward et al.atsdr.24 ng/g of serum) (Botella et al.020) < LOD . which may vary for some chemicals by year and by individual sample.e. and the FDA monitors foods for pesticide residues. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples.cdc.020) < LOD < LOD < LOD . Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.. 98 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey..

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

.9 (25.8 (26.7 (19.2 (24. The FDA dietary surveys have shown that over time.4-15.2-15.3-26..S.6 (21.9-17.6) < LOD < LOD 14.4) < LOD < LOD 22.0-19. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications. Although it is not manufactured as an end-product in the U.9-30. HCB has been detected in fewer foods since the 1980s (FDA. population from the National Health and Nutrition Examination Survey.5) < LOD < LOD 18.9 (14.9) < LOD < LOD 16. or game taken from areas with HCB contamination. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.4) < LOD < LOD 23.4 (22.0. air. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.9 (23.4) < LOD < LOD 19.6-TCP) (To-Figueras et al.9-20.6) < LOD < LOD 24. distributes widely throughout the body.4. Urinary metabolites include pentachlorophenol (PCP).7-16. 1988). respectively.7 (27.5-14.2 (14.6 (23.5-trichlorophenol (2.0 (25..6-26.0) < LOD < LOD 24.5-33.8) < LOD < LOD 27. water. HCB is well absorbed after oral administration. 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.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.1) * * 15.4) < LOD < LOD 14.4 (18.9 (25. 31.3 (20.6-19.1 (14. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.9) < LOD < LOD 20.7-29.7-26.2-31.5 (13.1 (13.9-15.8 (22.4 (11.5-15.1 (14. primarily as a fungicide and seed treatment until the U.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.1-20. 1997).7-30.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.4.3 (22. see Data Analysis section) for Survey years 99-00.4) < LOD < LOD 33.9-24. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28. Gunderson.0-28.7-22.9) < LOD < LOD 19. breast milk is an additional route of elimination in nursing women.6) < LOD < LOD 26.2-15.5-18.2 (17.3-20. particularly by consuming fish.0 (18.2) < LOD < LOD 13.3) 24.3) < LOD < LOD 20.3 (16.. < LOD means less than the limit of detection. The general population may be exposed to HCB through diet. 2008.3 (14.0) * * 15.5 (13.6) < LOD < LOD 25. 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.8-15.7) < LOD < LOD 24.5 (14.9-32.6-44.5-14. HCB is slowly metabolized.8 (15.3 (22.1) < LOD < LOD 15.S. and 03-04 are 118.9) < LOD < LOD 15. 2.6) < LOD < LOD 26. 1976).7 (15.6-33.4.7-16. Survey Geometric mean (95% conf.1-16. and 7.2) < LOD < LOD 29.7-15. and accumulates in fatty tissues where it persists for years.0-25. and foods with a high fat content. EPA cancelled its use in 1984.7) * * 14. 2002). 01-02.6-trichlorophenol (2. and has been detected in soil. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.4.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.9) < LOD < LOD 28.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.5-15.5-TCP) and 2.0) < LOD < LOD 15.3 (12. Therefore.Organochlorine Pesticides Hexachlorobenzene CAS No.9) < LOD < LOD 20. 2005).7-21.4) < LOD < LOD 18.8.2 (13.1 (17.S.6-32.4.3) * * 15.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0-16.3) < LOD < LOD 29.9) 19. and sediment (Barber et al.2 (14.7 (15.0 (18. wildfowl.S.3-22. 100 Fourth National Report on Human Exposure to Environmental Chemicals . these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.6 (24.4-16.4 (18. and elimination occurs by renal and fecal routes.0 (14.0) < LOD < LOD 15.

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

58:1185-1201. Lackmann GM.html. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. 2005). Peters HA. Hexachlorobenzene in the global environment: emissions.. Kemper FH. Link B. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. 2002. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Sala M.atsdr. Muckle G. Barr DB. Bertram et al.. HCB levels were directly related to age. Chemosphere 2005.cdc. Dewailly E. Bryan GT. As a result of the lower limit of detection in NHANES 2003-2004. Paepke O. Bertram HP. 2002) and among children (Link et al. Environ Health Perspect 2002. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Safe A. Aune M. more HCB levels were quantified. References Agency for Toxic Substances and Disease Registry (ATSDR). Lecha M. 1986. Schwartz JM. Environ Health Perspect 2003. dietary intakes of pesticides. Sci Tot Environ 2005. 2005). declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Becker K. Lackmann. Over the past two decades. 2005. Biomonitoring of persistent organochlorine pesticides. Santiago-Silva M.9% of participants had quantifiable levels (Stehr-Green. Jones D. van Wijk D. HCB detection in serum also was proportional to age. 2002.39(12):744-749. Available at URL: http://www. Otero R. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. In Spain. Gunderson EL. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.205:297-308. Seiwert M. Darnerud PO. Kaus S. Toxicological profile for hexachlorobenzene update [online]. Food and Drug Administration (FDA). April 1982 to 1984. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. September 2002. Reference values updated. Int J Hyg Environ Health 2002. Glynn et al. J Exp Sci Environ Epidemiol 2007. Zoellner I. 4/21/09 Barber JL. 102 Fourth National Report on Human Exposure to Environmental Chemicals . trends and processes. Canada). lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Bradman A. Gocmen A.fda. selected elements. Cripps DJ.. Link et al.gov/~dms/ pesrpts. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. Eskenazi B. Gabrio T. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. 2002).. Krause C. et al..gov/ toxprofiles/tp90. J Assoc Off Anal Chem 1988.111:349355. August 2008. 2003). 2006). Piechotowski I. et al. distribution. Biol Neonate 2002. 2002. The metabolism of higher chlorinated benzene isomers. Kohli J. Granath F. et al. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Lawrence River (Quebec. Schulz C. Dogramaci I. Bjerselius R.349:144. levels. Ozalla D. Jones KC. Herrero C. In a representative sample of the 1998 German adult population. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Arch Neurol 1982.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Herrman T..cfsan. Laliberte C. but overall.54(3):203-208. Holland NT. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. only 4.17:388–399. IARC Sci Publ 1986..html.. 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. 1989). Muller C.. Available at URL: http://www. FDA total diet study. Sweetman AJ.81(2):82-85. 4/21/09 Glynn AW. respectively. In the 1976-1980 NHANES subsample. et al. Dallaire F.44 mg/L. Lepom P. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. Organochlorines in Swedish women: determinants of serum concentrations.135(4):400404. and the geometric mean concentration of HCB in whole blood was 0. 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. Arch Dermatol 1999. Fenster L. however. Bradman et al. FDA Pesticide Program Residue Monitoring 1993-2006 [online].110(8):835-838. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Ayotte P.71(6):1200-1209. Lackman. and other chemicals. Atuma S. 1999). Can J Biochem 1976.. 2002.77:173182.

Rodamilans M.Organochlorine Pesticides Schmid R. N Engl J Med 1960. Stehr-Green. Demographic and seasonal influences on human serum pesticide residue levels. PA. To-Figueras J. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. J Toxicol Environ Health 1989. Cutaneous porphyria in Turkey.263:397-398. Sala M. Fourth National Report on Human Exposure to Environmental Chemicals 103 . Santiago-Silva M. Barrot C. Otero R.27:405-421. et al. Environ Health Perspect 1997.105(1):78-83.

4 (8.0-70.7-166) 70.3-38.3 (62.9-178) 48.7-96. See the section “What’s New” at the beginning of this Report for details.80 (6.0 (<LOD-12.8) 27.1-27.1 (18.5 (16.1) 13.2 (48.8.6) 16.1-32. exists in several isomeric forms.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 21.6-18.5) 67.2-20. environmental levels declined.0-21.1-37.8-19.0) 7.0) 8. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.2) 142 (99.S.8 (64.1) 12. and have been used either as fungicides or to synthesize other chemicals.3 (13. HCH isomers.6) 50. It is no longer produced or sold in the U. the U.7) 23.6-47.8) * * * * * * 15.9-51. population from the National Health and Nutrition Examination Survey.5 (37.5 (24. As pesticide applications of HCH were increasingly restricted or eliminated.8) 7. EPA cancelled agricultural uses of lindane (ATSDR. beta.7 (25.0 (19.3) 37.0-20.2 (34.2-67.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.2-98.5) 29.7) 32.2-42.8 (32.6) 35.9-56.46-11.8) < LOD 10.8) 12.6) 653 758 589 1240 1533 1370 20 years and older 10.2 (31.2-46.1-36.8 (23.7 (62.4 (52.70 (8.9 (62.7-69. and sediment as a result of historic production and use.1-49. 2005).4-50.0 (37. water. formerly referred to as benzene hexachloride.2-87. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.5) 14.70-19.8-68.61-12.4) < LOD 9. and 7.7 (<LOD-16. 104 Fourth National Report on Human Exposure to Environmental Chemicals . **In survey period 2001-2002. containing about 64% alpha and 10%-15% gamma isomers.8 (10.70-12.7) 27.0) 17.5) 90th 42.7-69.9-24.66-12.6) 47.4-45.1 (12.8-16.89 (<LOD-9.6-42.1 (21.3) 34.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.87 (9.0-23.5 (14.3-85. Lindane has a half-life of about two weeks in soils and water.7 (13.6-37.0) 71.6 (22.7-20.7) 73.1-32.3) 51.7 (30. HCH isomers are lipophilic.6 (10.1) 12.4) 44.6 (17.3 (42.5 (43.7) 18.0 (8.4) 27.9 (9.8) 39.6-20.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.68 (<LOD-10.90-8.1 (30.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.7) 10.4) 21.90) 7.50) 8.20-16.5) 11. soil.4-111) 84.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.7) 56.2) 9.0-70. 01-02.7 (29. and delta. In 2006.04-10.9 (30.9) 15.9 (50.8-54. gamma.5-123) 49.36. Technical grade HCH is a mixture of all four isomers.30-11.2) 62. interval) 9.2 (29.3) 25.9) 17.4) 51.76.7 (35.1 (27.1 (9.8-199) 134 (85.6 (33. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.8) 95th 68.1 (16.7-26.2-55.6-14. respectively.0 (35.3-56. The other isomers can be formed during the synthesis of lindane.8 (21. particularly alpha and gamma have been detected widely in air.2 (50.5) 40.6-62.60-13.4 (11.6) 36.2) 13.4 (50. However.9) 81.1) 31.90-8.4) 10.1) 71.9-21. so they can accumulate in fatty tissues of animals. 608-73-1 beta-Hexachlorocyclohexane CAS No. 2005).6 (40.2-17.4) 901 1067 952 992 1224 1007 Females 11.6 (16.8-87.Organochlorine Pesticides Hexachlorocyclohexane CAS No.2 (18.7 (53. < LOD means less than the limit of detection. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70 (6.3 (42. see Data Analysis section) for survey years 99-00.5) 16.5 (8.6) 18.3 (26. including alpha.56-12.0) 41.4-73.5) 22.80 (<LOD-14.9 (40.8 (33.0 (33.0-111) 70.2-22.8) 52.9) 45.1-16.0-34. commonly known as lindane. 6.4 (12.7) 97.7-96.9-81. and 03-04 are 9.1 (9. 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.0 (14.S. 319-85-7 gamma-Hexachlorocyclohexane CAS No.4) 11.1 (11.5 (11.S.5-29.8 (17.4 (16. each result has been multiplied by 1.8 (9. which may vary for some chemicals by year and by individual sample.43 (<LOD-9.4) < LOD < LOD < LOD 46.6-135) 69.9-14.9 (26.9 (11.5528.3) 14.0) 35.1-15.6-89. The gamma isomer.9 (32.2-52.2) 36. 58-89-9 General Information Hexachlorocyclohexane (HCH).7) 10.2 (9.

32) .221-.510) .077) < LOD . enlarged livers.070-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.382-.170-.814) .092 (.077) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 105 .287 (.200 (.214) .070-.310) . 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.244-.S.180-.700) .290 (.100) .067 (.480 (.170-. tremors.057 (<LOD-.146-. Rogan. and seizures.068-.160 (.372 (.065 (.360-.050 (.680) ..230-.110) . for lindane.200-.070-.056-. After dermal application of lindane 1% lotion.050) .587) 653 758 589 1240 1533 1370 20 years and older .Organochlorine Pesticides exposure to HCH is through the diet.240-.089-.410) .057-.690) .210) .110-. Workers who directly handled HCH have complained of headache.350 (.210-.057-.560 (.250 (.400) .570 (.090 (.050 (<LOD-.190) .216 (.420-.062 (.086) < LOD < LOD < LOD < LOD < LOD < LOD .290) .100) .119) . Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.260-.144 (.560) .200-.167 (..080 (.480) .01 (.050 (.089) .160-.140) .250 (.120-.150) . 1983).174) .118 (.120 (.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 .131-.190) .048 (<LOD-.390 (. each result has been multiplied by 1.270 (.190-.05) .260) .090 (. 1996.220-.191-. Saxena et al.100 (. The beta isomer accumulates in fatty tissues and is metabolized more slowly. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.124-.103) 90th .450) .280-.100 (.910 (.120) .139 (. resulting in a half-life of about seven years.5528.. HCH isomers are absorbed after inhalation. population from the National Health and Nutrition Examination Survey.210 (.290 (.250-.090-.310 (.410-.191-. probably by blocking inhibitory neurotransmitters in the central nervous system.410) .442 (.130 (.600) .37) 1. ataxia.058 (<LOD-.056-.710) .410 (.330 (.150 (.103-.098 (. and nephropathy developed (IPCS.210 (.460) .521 (. 2002).140) .120 (.080) .340) .100-.S. interval) . 2008. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.620) .110) .580 (.340-.130-..118-.310) .308-.390-.080 (.150-.072 (. the serum half-life was about 20 hours among children (Ginsburg et al.350) .160) .120 (. See the section “What’s New” at the beginning of this Report for details.110) .050-.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .250-.450 (.290 (.080-.051-.090 (.140 (.222 (. respectively. Distribution is mainly to fatty tissues. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.050-.220-.234 (.060) .470) . or dermal exposure.661) 901 1067 952 992 1224 1007 Females .320 (. When animals were chronically fed lindane at high doses. from 6% of samples in 1982-1984 to 2% in 1994 (FDA.140) .281 (. and FDA has established a bottled water standard and food residue tolerances for lindane. which may vary for some chemicals by year and by individual sample.173-.840) .280-.220) .470 (.080-.294-.096) .480 (.120-.305) . EPA has established a drinking water standard.069) .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. 1981).040-.080-.064 (.083) . OSHA and ACGIH have established workplace standards and guidelines.360) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.404) .064) .078 (.150) .051 (<LOD-. U.073-. 1986).319) .120-. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane. 1977).070 (.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .370-.360 (.254) 95th .250 (.070 (. ingestion.120) .580-1.620-1.400) .083 (.331 (.250) .220 (.S.050 (<LOD-.050-.175 (. hepatic enzyme induction.330-. **In survey period 2001-2002.065 (.240 (. The U. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways. Gunderson 1988).070) .130) .080) * * * * * * .100-.062 (.125) < LOD < LOD < LOD .081-. paresthesias. 1971.091) .290) ..100-.059-.297-.260) . and memory loss (Nigam et al.050-.460 (.300-.067) .380 (.047-.190-1.103 (. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.412 (.501) .450-.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .

Sturgeon et al. 106 Fourth National Report on Human Exposure to Environmental Chemicals .. respectively. and 2003-2004. Biomonitoring Information Because of its longer half-life. 1971.. population from the National Health and Nutrition Examination Survey..Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. 2004. 1998). 2004) and India (Bhatnagar et al..atsdr. 2002.. serum levels of lindane were generally below the limits of detection.. were similar to the 95th percentiles in this Report. 1989. and 7. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. Stehr-Green. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR.8.. 10. Additional factors associated with higher beta-HCH levels include rural residence. EPA 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. Stehr-Green. 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. Link et al. 1991.. 2005. In NHANES 1999-2000. and a diet that includes meat (Becker et al. environmental levels) and health effects is available from the U. 1998. 2005. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. which may vary for some chemicals by year and by individual sample. male sex.5. 2004). In populationbased studies of New Zealand adults and German adults and children. Kutz et al. older age. Bates et al.S... see Data Analysis section) for Survey years 99-00.5.e.S.gov/toxpro2. 01-02. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. 1989). the maximum and 95th percentile beta-HCH values.. Survey Geometric mean (95% conf. Kutz et al. and 03-04 are 14. In recent years. aged 9-11 years. 2001-2002..html. More information about external exposure (i. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. Becker et al. < 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. In an earlier (1996-1997) sample of German children.gov/pesticides/ and from ATSDR at: http:// www.cdc. 2002). 1991. Radomski et al. respectively.epa.

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

Environ Health Perspect 1998.cdc. Toxicol Appl Pharmacol 1971. Glynn AW. Cerrillo I. Absorption of lindane (g benzene hexachloride) in infants and children. Gabrio T. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Becker K.52(1):59-67.cfsan.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Deichmann WB. Exposure of women to organochlorine pesticides in Southern Spain. 4/21/09 Ginsburg CM. Rivas A. Bhargava AK.71(6):1200-1209. Environ Res 2004.150:981-990. HCH. Lindane. J Assoc Off Anal Chem 1988. 2002. Herrman T. Needham LL. Granath F. Placental transfer of pesticides in humans. et al. Chemosphere 2004. Majumder SK. Hanrahan L. Ellis H. International Programme on Chemical Safety (IPCS). and other chemicals. PA. Int Arch Occup Environ Health 1986. Buckland SJ. Karnik AB. Astolfi E.58:1185-1201. Paepke O. Burse VW. Krause C. 4/21/09 Anderson HA. Cancer Causes and Control 1998. Bjerselius R.54:1431-1443. Int J Hyg Environ Health 2002. Lowry W. Maass R. Darnerud PO.html.inchem. Toxicological profile for hexachlorocyclohexanes update [online].gov/~dms/pesrpts. Occupational exposure to hexachlorocyclohexane. Bull Environ Contam Toxicol 2004. August 2005. Wood PH. children and newborn infants. Reisch JS. Available at URL: http://www. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. org/documents/jmpr/jmpmono/2002pr08. Environ Health Perspect 2003. Atuma S. Falk C. Levels of DDT.91:998-1000. available at URL: http://www. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Stehr-Green. Rothman N. Needham LL. Raju GS. FDA total diet study. Olea N.120:1-82. dietary intakes of pesticides.72:261265. Kutty D.fda. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Siddiqui MKJ. Olea-Serrano MF.9(4):417-424. Rey AA. J Pediatr 1977. Bates MN. Available at URL: http://www. Potischman N.48:127-134. The Great Lakes Consortium. et al. Radomski JL. Brock JW. India.111:349355. et al. Nigam SK. Crespo J. 4/21/09 Kutz FW. Needham LL. Saxena MC. Bottimore DP.205:297-308.htm. Arch Toxicol 1981. Piechotowski I. Visweswariah K. Kaus S. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Pollutants in breast milk. Zoellner I. Metabolism of gammahexachlorocyclohexane in man. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.html. Aune M.atsdr. Patterson DG Jr.27:405-421. Angerer J. Bai KM. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Link B. Bhatnagar VK. August 2008. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Gunderson EL. Demographic and seasonal influences on human serum pesticide residue levels. Arch Pediatr Adolesc Med 1996. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Lepom P. Krishna Murti CR. Rogan WJ.20(2):186-193. Seiwert M. Brinton LA. Olson J. et al. et al. April 1982 to 1984. Saiyed HN. Schulz C. J Toxicol Environ Health 1989.106(5):279-289. et al. Heinrich R. selected elements.57(4):315-320.96:34-4Food and Drug Administration (FDA). Garrett N. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Botella B. and HCB residues in human blood in Ahmedabad. Rev Environ Contam Toxicol 1991. et al. Zaidi SS. gov/toxprofiles/tp43. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Biomonitoring of persistent organochlorine pesticides. Organochlorines in Swedish women: determinants of serum concentrations. Sturgeon SR. Chemosphere 2005. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Int Arch Occup Environ Health 1983. Kashyap R. Kulkarni PK. VI.

7 (<LOD-47. Mirex is not metabolized in the body.S.6.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15. where it was applied directly to soil and by aerial spraying.40 (<LOD-13. population from the National Health and Nutrition Examination Survey.4 (8.0 (14. 10.3-225) 15.4-230) 18.90-29.6-305) 15.70-24.4) < LOD 63.3 (15. resulting in exposure to newborns and nursing infants. < LOD means less than the limit of detection. aquatic organisms.5 (<LOD-115) 153 (30.S.6 (<LOD-23.4) < LOD 15. Formerly.5-82. especially those from persons living in the southeastern U.1) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 16. water.10-37.5 (<LOD-42.3 (15. disposal.1 (8. Mirex has been detected in air. 1991). sediments. Mirex can cross the placenta and be excreted in breast milk.6) 9. after which it is widely distributed in the body and stored in fat. Occupational exposure is limited to workers at sites where mirex contamination is present. Mirex binds strongly to soil.2-230) 13.0 (<LOD-108) < LOD < LOD 50.3) 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 13.7 (12. where it has a half-life of 12 years.0-374) 11. Mirex is absorbed through the skin and from the gastrointestinal tract.5.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. In studies conducted in the 1970’s and 1980’s.S.S. it is a highly persistent chemical in the environment.0 (12.S.70 (<LOD-15.7) 8. see Data Analysis section) for Survey years 99-00. since 1977.2 (7. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.6 (<LOD-108) 9.10 (<LOD-15. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. mirex was detected in human adipose samples. and 7. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.2) 51.Organochlorine Pesticides Mirex CAS No.1 (13. which may vary for some chemicals by year and by individual sample. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.5 (9.8) < LOD 15.6 (<LOD-31.70-40. respectively.7) < LOD 66.8 (12. 2385-85-5 General Information Mirex has not been produced or used in the U. 1995). Fourth National Report on Human Exposure to Environmental Chemicals 109 . (Kutz et al. and foods.1 (<LOD-65. and 03-04 are 14. soil.8 (<LOD-73..6) < LOD < LOD < LOD < LOD 71. or pesticide application. 01-02. 1985.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. animals.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Some states and the U.5-291) 11.0) * * * 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. Survey Geometric mean (95% conf..5-425) 40. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.8.

090-1.170) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .268) < LOD .37) .112 (. and 4.430 (.090 (<LOD-.170-3. serum mirex levels were generally below the limits of detection (Stehr-Green.79) . 1989). 2004). 7.02) .cdc.html.106 (.S. 1991). EPA has established environmental standards for mirex. reproductive toxicity included decreased fertility and testicular damage.S.510) < LOD < LOD .080-1. 110 Fourth National Report on Human Exposure to Environmental Chemicals . as well as in a subsample of NHANES II (1976-1980) participants.470) .070-1.470) . The U.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .079 (<LOD-.054 (<LOD-.064 (<LOD-. which may vary for some chemicals by year and by individual sample.100 (<LOD-.080-1.110 (<LOD-.090-1.100 (<LOD-.062-.450) 1.92) .610) < LOD < LOD < LOD < LOD .106) < LOD . and NTP classifies mirex as reasonably anticipated to be a human carcinogen.8.059 (<LOD-.Organochlorine Pesticides exposures are unknown.370 (. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.450 (. Survey Geometric mean (95% conf.470 (..090 (<LOD-.089-.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .690) . 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.220) .170) < LOD . The geometric mean mirex levels of the Inuit mothers were 8. 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. IARC classifies mirex as possibly carcinogenic to humans.73) .256 (. 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.41) .gov/toxpro2.077 (<LOD-.084) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . More information about external exposure (i..055-.410 (. 2001-2002. In addition.79) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD . Biomonitoring Information In the NHANES 1999-2000.220 (<LOD-.052-. Laboratory animals fed high doses developed liver enlargement and liver tumors.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 .053-.e.090 (<LOD-..140 (<LOD-. environmental levels) and health effects is available from the ATSDR at: http://www. In samples obtained between 1994 and 1997.102) < LOD < LOD < LOD < LOD . 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. Smith.108 (. 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. 1995. 2005).090-1.635) < LOD .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.310 (.08 (. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.093 (.atsdr. and 2003-2004 subsamples.7 ng/g of lipid.

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

6-Trichlorophenol CAS No.60 (4.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.00-8.0 (3. public drinking water systems did not detect 2.40) < LOD 4.940-3.980-3.40) < LOD 6. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. soils.80-41. may occur by inhalation or dermal routes.50 (.4.80 (2.5-trichlorophenol (2.920-3.10-3.60) < LOD 8. surface water.6-trichlorophenol (2. 1999). and sediments.4.50-16.80 (1.60 (2.27) 696 661 521 696 603 939 Limit of detection (LOD.20) < LOD 1. 1999).4.0) < LOD 11.7.30-44.4.0 (4.30 (. Trichlorophenols are no longer manufactured commercially.30-27.950 (<LOD-1.0 (4.00 (2.0) 2.40-18.4.S.20) < LOD 90th 5.0 (5.4.27) size 1994 2497 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th 1. which may vary for some chemicals by year and by individual sample.S.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2. Both chemicals have been detected in air.30) < LOD < LOD < LOD < LOD < LOD 1.900-2.40 (2.19 (<LOD-6. 2. 2006). 1976).0) 14.40) < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4.0) < LOD 5.40 (1.0) < LOD 21. 2.90-33.30-11.4. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.57 (<LOD-15.60-8.20 (4.4.40 (2.40 (2.9 and 0.40 (2.9 (<LOD-121) 9. Exposure to trichlorophenols also may result from metabolism of lindane.4.40-11.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30-3. < LOD means less than the limit of detection. other organochlorines.6-TCP). 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.50) < LOD 1.42 (<LOD-12.0) < LOD 5.3. recent sampling of U.00 (3. population from the National Health and Nutrition Examination Survey.72) < LOD 1. Such workers would probably Urinary 2.40 (. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.60 (.0) 2.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR. Occupational exposures. are metabolites of several organochlorine chemicals. including hexachlorobenzene and hexachlorocyclohexanes.42 (<LOD-8.5TCP and 2.50 (2.980-3. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.50 (1.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .7) 24.71 (<LOD-8.6-TCP in any of the samples (U.0) 5.03) 9.4.20-71. usually at herbicide production or waste incineration facilities.40 (1.5-Trichlorophenol CAS No.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Survey Geometric mean (95% conf.0) < LOD 11. Formation of 2. 112 Fourth National Report on Human Exposure to Environmental Chemicals .8) 21. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.0 (8. hexachlorobenzene. and polychlorinated benzenes (Kohil et al.60-18.50-63.71 (<LOD-8.4.0) < LOD 5.40 (.0) 2. Historically.Organochlorine Pesticides 2..30-27.0 (4. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.5-TCP) and 2. however.5-trichlorophenol.0) 2. EPA.30) < LOD 4. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.0) 2.50-25.S.20) < LOD 5.20-36.6-TCP were used as intermediates in the production of certain pesticides.00-3.30-27.0) 2. 2.80) < LOD 1.9.0 (3.63) 18.31 (<LOD-9.00-3.30-40. 95-95-4 2.

36 (1.4.16) < LOD 90th 5. The 95th percentiles for 2.6-TCP as reasonably anticipated to be a human carcinogen.0 mg/L. 7.S..920-2.24) < LOD 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.53-3. IARC classifies combined exposures to polychlorophenols.74) 11. as being possibly carcinogenic to humans.9 (5. More information about external exposure (i.82 (<LOD-32.4. population from the National Health and Nutrition Examination Survey.4.93-11. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.62-20. leukemias. Radon et al.31) < LOD 2. animals showed hepatocellular abnormalities.2 (2.73 (<LOD-8..3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . the 95th percentile urinary 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11. Urinary 2.4.6) 4.29 (1.43) < LOD 12.02-3. Laboratory animals chronically fed high doses of 2..5-TCP nor 2.47-8.5) 11.86 (3.0) 7.3 mg/L reported in German adults aged 18-69 years (Becker et al.820-2. Survey Geometric mean (95% conf.19-4..75 (3.68-4.60-3.9) 12.67 (1.81 (<LOD-9.4.atsdr.95 (3.90 (4.33) < LOD < LOD < LOD < LOD < LOD 2.e.6-TCP levels at the 95th percentile were up to eight times higher than 3. 2003). but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al. the 95th percentile urinary 2.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.5-TCP.64 (4.6-TCP. 2003..3 mg/L in a nonrandom subsample from NHANES III (Hill et al.78) < LOD 1.69-18. Fourth National Report on Human Exposure to Environmental Chemicals 113 .4.50) < LOD 2.00-19..5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999).17) 9.13-13. 2004).46 (1.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.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.6-TCP had increased rates of hepatic tumors.02) < LOD 7.44 (1..43 (2.8) < LOD 9. However. In the same 2-6 year old children.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.57 (<LOD-7.53-3.00) < LOD 4.20-6. and other chlorinated compounds.gov/toxpro2. NTP classifies 2.27-17.80 (1.1 (<LOD-58.4.4.44 (.83-12. 1995) were similar.78 (3.6) 4.Organochlorine Pesticides be exposed to mixtures of chlorophenols.8) 4.980 (<LOD-1. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.00-29. Among 6-11 year old children in NHANES 1999-2000.32) < LOD 4.11) 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 2.05-8.2) < LOD 5.28-25.4) < LOD 3.24) < LOD 1.37-11. urinary 2.1) 2.67 (1.4.4. Human health effects from 2..15) < LOD 2.cdc.16 (.4. which includes trichlorophenols.5-TCP and limited for 2.05-17.24) < LOD 6..57 (3.49 (1. furans. 1989). IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. and lymphomas. At lower doses.19-12.88-16.4) < LOD 3. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.2) 2.7 (4.4 (6. 1995) and up to 19 times higher than the 95th percentile value of 1.html. 1989).24 (3. 2003).4.55 (4.79-4.69 (2.5-TCP or 2.57 (<LOD-7.68 (<LOD-8. Neither 2.4.37) 16.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.24-11.75 (<LOD-6.4) 5.8 (5.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.6) 4.5) < LOD 12.78-19. environmental levels) and health effects is available from ATSDR at: http://www.3 (5. in addition to dioxins.

99) 6.53) 4.31) * 2.0 (7..2-0. the median urinary 2.10) 6.20-23.45) < LOD 11.85) * 3.S.6TCP values.89 (3.46-3.0) 6.0 (20.7 (13.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.0) 13.4.4.06) * 2.0) 17.54) 6.0 (8.6-TCP exposure and health effects.40 (2. Urinary 2.0) 9.0) 10.3 (11. was about six times lower than the median urinary levels for males in this Report (Radon et al.91-4.74-3.70 (2.0) 17..04) 2.0 (16.32) 3.98-11.90 (3.10 (5.00-21.00 (4.08 (2.6TCP causes an adverse health effect.66 (8.0) 13.28) 24.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.8) 18.5-TCP and 2.85 (2.45 (2. 1998).60-3.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.47 (3.80-6.63) 90th 15.8-13.0) 19.44) 75th 4.0 (6.0) 9.70-3.00-4.92 (2.2) 25.4.0 (13.51-12.75 (8.9 (13.87-14.4.0) 7.67-12.4 (8.80 (3.60-37.0-41.28) * 2. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.30-33.5-TCP (0.7 mg/L.30) 4.7 (9.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.53) 2.90) 2.12) 2.57 (<LOD-2.80 (2.0 (14.4.20-3.0) 13.69 (3.23) 3.0 (12.73-9.55-3.6-TCP level.6-19.89-6.6-17. respectively.95-6.5-TCP or 2.20-6.8 (9.1 (8.30-11.6-TCP than are found in the general population.6) 26.45-9.4 (9.4.30-2.33-4.0) 13.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.78 (2.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.4.80-25.60 (3.0) 19.98-7.79 (5.24 (2.4. Biomonitoring studies on levels of 2.5-TCP level of 0.4 (10. 1991). Mean values of 2.0 (15.0-54.0) 12.4.35-3.26 (2.18-3.40) 2..0) 7.09) 15.7-16.4..70) 1.4.00 (1.52-3.6-TCP (0.7-3.9) 694 677 519 696 602 931 Limit of detection (LOD.40) 2.95) 3.40-14.8-15.40-2.3 (11.6 mg/g creatinine) and 2.36-5.72-10. < LOD means less than the limit of detection.90 (4.5-TCP or 2.80-7.0-38.14 (2. 0.2 (14.6 (12.59-6.3) 20.78 (2.60) 6.60-21. which may vary for some chemicals by year and by individual sample.4. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.23) 2.07 (<LOD-3.0) 14.70-6. population from the National Health and Nutrition Examination Survey.0-38.5-TCP or 2.10-2.65 (5.76) 3.65) 15.4.40-32.6-TCP in urine does not mean that the level of 2.1-25. Survey Geometric mean (95% conf.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.80 (2.60 (3.1) 16.30-2. 114 Fourth National Report on Human Exposure to Environmental Chemicals .74 (2.6 (11. 2003).7) 21.02) 2.25-11.5-46.0) 11.3) 23.80) 1.0) 11.9 (11.8-24.2) 12. Finding a measurable amount of 2.40 (2.36 mg/g creatinine.4.40-4.6-22.0 (11.58-3.0 (8. Biomonitoring data will also help scientists plan and conduct research about 2.68 (<LOD-2.0-18.4.3) 37.5-TCP and 2.48-26.50-5.7) 33.0) 15.70) 5.70) 5.4.5-TCP or 2.60) < LOD 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) 4. 2004).59) 4.9) 13.3-26.84) 2.40-2.49 (6.10-3.4.10-3.4-17.95 (4.67) 4.45 (5.0) 14. Urinary 2.1 (10.52 (2.9) size 1989 2503 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.3.09-7.10) 2. similar to the limit of detection for this Report (Anderson et al.90-8.0 (9.5 mg/g creatinine) were similar to the limit of detection for 2.0 and 1.4 (17.6) 21.32) * 3.0 (20.70 (2. interval) 2.20 (3.31 (3.0 (6.0 (6.0-44.8) 32.40) 4.40-7.58 (1.3-17.40) 3.4. for males in NHANES 19992002 (Agramunt et al.80-20.0) 10.23-2.4.20 (3.70) 3.32-4.0-43.0 (14.0 (15.0 (4.0-68.56 (3. In harbor workers exposed to chlorophenol-contaminated river silt.01-6.00 (2.70-6.36 (1.50 (2.0-37.4.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0-50.6-TCP levels that were as much as 450 times higher than the median level among adults in the NHANES 1999-2000 subsample (Pekari et al.0 (14.60 (2.5-TCP and to the median 2.

Survey Geometric mean (95% conf.7) 6.76) 2.5-28.68) 2.42 (2.6) 12.40 (7.14-2.6 (10.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.83-6.72) 32.05 (3.38 (4.0) 10.41 (3.89-2.88) 5.83 (3.S.79-17.48-2.6 (6.26 (6.0) 8.18-2.66-4.05 (6.59 (2.81-9.53 (3.1) 14.13-6.6 (9.56 (7.8) 11.5) 12.22-2.5) 8.8 (8.50-8.47-5.2 (13.91 (7.51 (2.63-15.19-5.9) 19.75) 75th 4.25-2.5 (8.2) 19.65) 18.63-13.30-2.20-2.87-6.2 (8.72-16.53-11.90 (1.94-13.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.6 (5.22 (1.Organochlorine Pesticides Urinary 2.4) 9.50 (2.27-9.06-2.65) 2.40 (2.82-2.22-9.0 (9.53) * 2.9) 7.9) 8.88-7.04-2.52 (3.23) 4.77) 2.88 (2.78) 90th 12.23 (1.6-31.68) 2.88) 4.6) 8.15 (6. interval) 2.1-21.71 (3.63 (<LOD-2.73) 5.87) 2.43 (<LOD-2.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.4 (12.1) 11.1 (8.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.8) 12.4) 4.51-21.28-4.1 (13.82 (8.98 (1.29 (6.65-21.33) * 2.6) 13.10-9.91-2.25-17.76) 1.8) 21.33 (1.5) 9.3-37.63) * 4.67-17.00 (2.60 (4.17) 13.63 (2.3-23.9-32.92) 4.99-2.16-10.24 (1.73-22.43-7.51) 18.13 (1.46-14.02) 3.09-3.10 (6.9-64.78) 2.32 (2.0 (11.5 (7.70-9.91 (3.87-7.8 (7.60-2.21-11.6 (12.6 (9.29-4.81) 2.26-13.0 (6.33-2.7 (14.9 (9.2 (12.83-5.08-2.25 (3.52 (5.15 (1.49-3.35 (3.82 (3.1-32.53) 4.55-2.78 (2.32-19.38) 22.22 (3.9 (9. population from the National Health and Nutrition Examination Survey.98) 10.25 (3.22 (<LOD-2.88) * 2.42) 2.58 (4.5) 11.56) < LOD 11.62-15.49) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (22.04-16.8) 19.89) 10.3 (9.06) 4.6) 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 2.00) 4.54 (2.9-29.18-4.65-2.95-2.17) 2.00) 4.87) * 2.77-4.4 (11. Fourth National Report on Human Exposure to Environmental Chemicals 115 .5) 11.63) 4.11) 10.4.2 (7.82) 2.3) 8.87 (3.9-34.56-5.96) < LOD 4.52) 2.06) 11.38-5.88) 1.52) 2.41-6.5 (10.38 (2.90) 2.76) 4.44 (3.76-8.4) 8.01 (3.29-4.10) 4.02 (1.17-4.00 (3.43 (2.14-13.7-36.25-15.88) 4.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.83-6.33 (7.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.7) 25.9) 8.

Needham LL. Jones D. Lindroos L. Urinary excretion of chlorinated phenols in saw-mill workers. Can J Biochem 1976. Heinrich-Ramm R. U. July 1999. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Gregg M. et al. Kohli J. Bailey SL. Toxicol Lett 2003. S. To T.63:57-62. Toxicological profile for chlorophenols [online]. Hill RH Jr.106(5):279-289.18(4):469-474. Kaus S.146:83-91. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Safe A. Arch Environ Contam Toxicol 1989. Aitio A. Jarvisalo J. The metabolism of higher chlorinated benzene isomers. Hill RH Jr. Pekari K. 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]. Environ Health Perspect 1998. Burse VW.54(3):203-208. Fast DM. Environ Res 1995. Radon K.epa. Hanrahan L.cdc. Schulz C. Domingo A. Am J Ind Med 2004. Seiwert M. Head SL.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Int J Hyg Environ Health 2003. Olson J. Falk C. Luotamo M. Smith SJ. The Great Lakes Consortium.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Environmental Protection Agency (U. 4/21/09 Agramunt MC. Anderson HA. Corbella J. Seifert B. December 2006 Draft. Becker K. Poschadel B. Shealy DB. et al.EPA). Baker S. Pesticide residues in urine of adults living in the United States: reference range concentrations. et al. Baur X. Domingo JL. Available at URL: http://www.71:99108. Holler JS. Int Arch Occup Environ Health 1991. html. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals .atsdr. Available at URL: http://www.45:440-445.gov/toxprofiles/tp107. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. Szadkowski D.pdf.S. Wegner R. Needham LL. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. 206:15-24.

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

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

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

290 (<LOD-.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 1.670-1.67) 3.12-19.58 (3.490-2. population from the National Health and Nutrition Examination Survey.90) 2.8 (14.56 (4.20 (. 120 Fourth National Report on Human Exposure to Environmental Chemicals .2 (9.05-7.32) 1.0 (7.8) 11.50 (4.0-28.52-11.0) 15.00-27.20 (.20-30.10 (2.22 (. and 03-04 are 0.42-3.4 (9.52) 6.0) 11.830 (<LOD-3.0) 5.80) 4.10 (.23-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) 3.80-24.0) 10.51) 2.860-2.970-2.0 (5.3) 16.40-11.1 (9.780) < LOD 3.2 (7.12) 4. 0.15-12.17-3.1-23.86 (1.80) 2.16) 4.28) 1.2.0) 20.0) 6.740-2.2 (14.01) * * 1.1) 10.2 (7.70-14.15) 14.72) 5.03 (.981 (.79 (5.599-1.80) .81) 1.890 (<LOD-2.00) 3.71 (2.0 (8.96-3.7) 11.50 (.1) 95th 13.70-23.94) * * .8) 19.1) 13.30-6.600 (<LOD-1.0 (6.61) 4.20-7.0) 11.94) 3.3) 14.60-18.63) 1.79-7.55-6.0) 5.579-1.623-1.0 (9.70-19.2 (9.00 (5.32 (.0) 9.27-3.60-25.0) 10.3-15.81) 11.0 (7.20-4.76 (2.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.66) * * 1.4) 18.0) 6.85 (3.21) 9.58 (2.3) 17.60 (5.00-12.07-10.39 (8.0 (7.44-3.0) 10.56 (1. which may vary for some chemicals by year and by individual sample.30 (4.0) 11.97) 8.530 (<LOD-2.40-1.42) .8 (12.80) .40-19.7 (14.8-32.0) 11.00-12.74 (8.1.9 (8.10 (2.70) < LOD < LOD 75th 3.80) 2.13 (2.2 (11.2) 14.0) 6.02) 4.58 (5.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.10-7.0 (6.2) 16.82-12.34-3.0 (4.90-4.86-15.8) 7.35-12.2-20.33 (5.54 (3.61 (3.40-14.80) 2.08-15.80-4.02-5.35-16.40-16.9) 8.10) < LOD < LOD 4.4 (9.20 (.9-18.757-2.73) * * .97) 90th 7.36-4.46) 10. see Data Analysis section) for Survey years 99-00. and 0.8 (9.90 (1.30-4.2) 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 1.04) < LOD 1.56 (6.48-7.717-1.2.26-8.83 (5.2 (7.13 (2.21 (.68-7.10) < LOD .98-5.82) 10.70) .80) 11.38-5.98-12.16 (2.44 (2.2) 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 (12.20 (.10 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.33-18.5) 15.4) 20.19) 9.00-19.4) 17.4 (7.750-1.4 (7.7 (12.0 (8.52) * * 1.70 (2.89) 9.00 (1.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.34-7.5-16.26 (5.44-38.8) 7.0) 10.8 (8.74 (8.35-11.99 (5.2 (14.5 (11.955 (.70-11.57-7.0) 7.30 (2.91) 4.00-7. respectively.08-2.60-11.1 (10.0) 12.13-2.47) 5.70 (4.60) < LOD < LOD 4.95) 5.290 (<LOD-1.93 (4.5) 20.93-24.620-1.43-12.39 (3.90) 3.55-8.6) 18.40-5. < LOD means less than the limit of detection.700-1.S.11 (.27-15.2) 16.00 (4.840-1.50-5.30 (2.0 (8.45 (2. 01-02.1-17.40 (. interval) 1.0-27.0) 10.71-9.0) 5.5 (8.80) 3.53) 4.9) 14.37 (3.758-1.81) 11.90-5.20 (2.810-1.50) 2.00-27.6) 7.08 (<LOD-2.56-13.60) .47) * * 1.50-36.954 (.0 (9.50 (2.70) < LOD < LOD 1.5-17.60 (1.80-22.26-6.0 (7.80 (2.29) * * 1.80 (4.14) * * .

82-26.2 (6.60) 2.56) 4.540-1.7 (9.6 (9.25) 6.2) 8.5-20.21-23.533-1.2) 5.28-9.03 (2.47 (3.87 (3.29 (2.75 (7.1 (10.6) 9.52) 4.5) 8.4) 4. population from the National Health and Nutrition Examination Survey.23) 4.56) 7.98) .870-2.9 (5.66-34.76-4.90-5.30) 2.60-9.88-10.6) 13.855 (.95 (3.8) 6.47) 2.28 (2.40-14.00) 8.19 (4.710 (<LOD-1.01-2.95) 2.75) 14.40 (3.82-14.55-20.31-14.830-1.68-4.7 (8.2 (10.3) 12.98) .4 (9.2) 9.03) 2.77 (6.62) .29) * * .93) 9.47) * * .9) 11.6) 11.62-5.07 (.9 (9.S.2) 95th 12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2) 7.28) 10.932 (.3) 16.02 (7.40) 4.2) 5.14 (3.68) < LOD < LOD 3.94 (2.69) 4.64-5.25) < LOD .98-5.5) 11.633-1.6) 8.53 (6.79-9.3) 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 1.71-2.58) * * 1.510-1.88-15.40) < LOD < LOD 75th 2.780 (<LOD-1.98-22.50) 7.73 (1.45-5.5) 7.7 (10.34 (6.750 (<LOD-1.06-2. Fourth National Report on Human Exposure to Environmental Chemicals 121 .549-1.32-12.960 (.40-5.1) 4.72) 11.1 (6.0) 7.46) 2.5-13.37 (4.900 (.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.57) 4.38) .34 (6.66 (5.1 (7.79-3.54-4.53) 9.00-19.960 (<LOD-2.8) 7.88) 2.53-11.44 (2.10 (3.57 (6.820 (. interval) .40-3.574-1.09 (.94-10.45-5.13) 4.94-22.35 (1.608-1.92-5.80 (7.82-14.93-9.85 (6.03 (7.560-1.83 (7.42) 12.3) 15.8) 8.93-5.27) < LOD 2.860 (.54) .03-6.5 (4.5) 12.23 (4.66 (2.36) * * 1.11-6.54-15.18 (.0 (8.02 (2.773-1.02-2.566-1.75-7.87-5.42 (3.66-15.60) * * .57 (4.57-10.40-28.75 (3.69 (4.76) < LOD .00-13.7) 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 .51-5.8) 16.94-23.90-8.9-28.1) 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 1.37-3.5-16.66 (1.35) < LOD < LOD 3.1 (8.0) 6.80) 9.47 (1.4) 13.04 (1.26) * * .05 (1.28 (4.5-32.500-1.81 (1.69) 2.82-6.61 (1.54-11.41-12.7) 12.5) 7.28 (5.05) .4 (4.78 (2.1) 4.47 (3.54-2.67) 4.40-12.20-8.89-3.46-5.37 (5.570-1.7) 18.94 (4.85) 2.9 (9.05 (.996 (.1 (9.818 (.10-13.41) Selected percentiles ( 95% confidence interval) Total * * 50th .4) 4.15-10.9) 12.00-17.03) 2.02-14.56) .2) 13.88 (5.883 (.43 (3.39 (2.81-5.650-1.34) < LOD < LOD .56-13.430-1.61-29.440 (<LOD-2.7) 5.8) 12.7) 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.00 (4.8 (10.890 (<LOD-1.1-15.24-3.00 (4.890 (<LOD-1.92-2.1 (11.37-5.920 (.61-13.45-11.98 (3.67) 1.04-6.61 (1.09) 2.69-10.41) .37) 9.84 (5.790 (.84) 7.2 (8.30 (1.9) 16.31 (3.34) * * .94-9.74) 4.89) * * 1.43 (.67-19.75) 2.3) 5.80 (2.98) 9.620-1.71) 10.924 (.80 (6.74) 90th 7.87 (1.38 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.83) 8.09-11.43) 2.6 (10.

5.8 (12.22 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 122 Fourth National Report on Human Exposure to Environmental Chemicals .0) 12.60) < LOD < LOD 2.75 (3.96) 3.80-4.47-6.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.63-14.34-5.18 (3.20) .0-19.24 (2.52 (6.90 (6.60 (5.3) 22.80-21.2) 14.0) 14.29-4.77-14.35 (6.42 (1.80 (2.92) 9.8-20.04 (3.8) 8.39 (5.61-32.10-10.29) < LOD < LOD < LOD < LOD 3.2 (7.6) 18.670 (<LOD-1.66-13.0) 13.0-24.0) 13.90-31.78) 5.60 (2.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.7 (11.0) 9.3 (6.70 (8.90-15.8) 9.62-17.89) 2.3 (11.35-3.16-1.90 (2.77-3.80-8.70) 2.0) 12.0) 6.7) 15. and 03-04 are 0.740 (<LOD-1.50) 3.74) * * * * * 1.46-28.30) 3.27 (7.00-4.95-9.10 (<LOD-1.3) 20.7) 14.650-1.50-4.00-18.06 (2.92-17.7 (10.31) 1.90 (2.9) 95th 14.27 (3.3) 10.50) .5) 471 576 310 664 822 717 814 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .0) 7.00) 3. which may vary for some chemicals by year and by individual sample.40 (2.3 (12.90-9.22 (6.88) 10.50-5.0 (10.9) 10.98-9.96) 90th 7.30) 3.40 (2.4 (10.28 (7.80 (2.8-21.41-5.80) .27) 4.81-6. respectively.15-6.1) 11.18) * * * * * * * * 1.0 (10.3) 14.6-19.00-18.0) 14.27) 9.86-10.1-23.5 (8.3 (7.580-2.20-18.0 (14.90-15.66) 4.39-13.20) 3.80 (5. and 0.0 (5.22-12.31-12.70-9.0) 18.3 (9.0) 11.1 (10.34 (6.6 (10. population from the National Health and Nutrition Examination Survey.0) 9.80-12.8) 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. see Data Analysis section) for Survey years 99-00.95 (5.50) 5.58 (1.0 (9.9) 16.790 (<LOD-1.70 (1.90) 8.670 (<LOD-1.4 (14.95 (2.10-15.30) 8.6) 11.60 (6.15-2.14 (6.22) 8.70-9.6) 14. 01-02.90 (1.2 (9.99 (3.64) 10.17 (7.7) 22.00-16.3) 8.59-3.00-4.40) < LOD < LOD 75th 2.10-4.67-10.6 (10.82) 8.20 (<LOD-2.80-3.34-3.8-17.61 (3.0) 12.73) 7.0-33.0 (13.0 (15.41) 3.7) 10.S.27) .5.80) .00 (.97-4.89 (2.80) 5.90 (6.6-41.5-26.910 (<LOD-2.3 (9.30) < LOD < LOD .90) 4.6) 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 * * * 1.0-29.4-17.9-15.70-5.31-7.25 (2.80-6.7) 16.37 (3.0) 19.11-6.4 (10. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .45 (3.9 (12.7-21.46-4.0) 23.00) 7.4) 11.9 (7.00) 3. < LOD means less than the limit of detection.90 (6.5) 21.72) 2.0 (9.4) 7.51) < LOD 1.00) 8.80-14.0 (7.53 (3.1 (10.67) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.12 (4.90 (2.01 (2.00) < LOD .970 (<LOD-2.680 (<LOD-1.75 (2.8-20.0) 11.9) 9.6) 14.34-10.49-4.90 (6.33-11.37) 2.24-5.8 (12.67) 3.670 (<LOD-1.58.5 (9.9-14.0-24.5 (8.88) 3.0 (8.670 (<LOD-1.10 (.7-19.20-4.30) < LOD < LOD 4.20-8. 0.10) 6.90 (5.70-8.35) 4.84-4.9-17.00-9.20) 3.

8) 11.4-16.63 (2.04) 9.77 (2.99) 2.910 (<LOD-1.27) 5.89-10.79-6.12) < LOD < LOD 4.760 (<LOD-1.74-19.27) 1.3) 9.38 (.88 (1.95) 90th 8.30-5.99 (4.32) 2.51-7.89-3.78-10.68-4.38 (1.2) 10.29) 3.530-1.690 (.4-15.75-3.6) 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 * * * * * * .83 (6.70-35.6 (12.3-17.51-10.4-18.50-17.3) 12.4-16.67 (1.7 (8.38) 1.03) 3. population from the National Health and Nutrition Examination Survey.15) < LOD < LOD 75th 2.36 (2.82-8.3-34.4) 7.S.0-21.92 (5.00) 2.7) 14.30) 7.6) 13.6-19.77 (2.42) 7.07) 2.09-11.4) 16.41 (7.38-13.8) 14.89-13.1 (19.6) 7.64-11.00 (5.28-12.27-13.50 (6.30) 2.0-19.89 (2.58 (4.93 (2.07-3.72-4.6 (13.6 (11.620 (<LOD-.93-10.5 (15.00 (3.71 (1.6) 6.3) 6.82-11.91-9.81 (7.06 (<LOD-1.45) 6.74-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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.89) 5.7 (10.43 (2.780-1.95 (2.33-10.3) 8.01-5.3-17.7-23.55) .55) 16.1) 13.52-3.1 (8.7 (10.0 (11.11-3.6) 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 * * * .03 (6.2) 12.2) 12.34-18.00 (<LOD-1.78 (4.3-15.5 (10.7) 12.32-8.75-3.42) 8.53-8.4 (11.7) 14.5) 13.9 (9.4) 7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.92) 3.25-9.38 (2.7) 9.94-14.2) 19.63 (6.78) 4.77) 3.3-21.0 (8.9) 16.86 (3.7-19.23-3.6) 12. Fourth National Report on Human Exposure to Environmental Chemicals 123 .55 (2.78 (6.28) 6.44-6.9) 19.54 (7.8 (8.4) 15.920 (<LOD-1.8) 16.12 (7.97) < LOD .06) .37) 3.61 (2.88-7.00 (7.00 (<LOD-1.34) < LOD < LOD < LOD < LOD 3.71) < LOD < LOD 2.07 (5.70-2.87 (3.890-2.96-10.5 (9.5) 8.19) 3.7) 15.37-5.16-14.97-4.9-17.6 (11.86) 9.850 (<LOD-1.2) 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.09-11.8 (10.68-10.4) 6.0 (10.25 (4.2) 8.94 (5.1 (13.1) 20.30) 8.39-17.2) 15.940) < LOD < LOD 1.27) < LOD .2-30.3 (7.00 (2.85-17.85-8.950) .95) 3.2) 12.9 (9.18) 2.6 (13.72) 4.4) 9.2-15.05-3.7 (11.2 (9.11 (5.68-19.6) 14.20-3.6) 95th 16.96-11.973 (.33) 3.86-3.2 (9.00) 8.27) * * * * * * * * 1.14 (2.0 (13.59-3. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .29 (2.03 (2.6 (10.6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.54-5.47-9.810 (<LOD-1.21) * * * * * 1.68) .1) 10.0) 14.28 (1.91) 3.5 (8.48 (2.5 (11.93 (<LOD-2.79-9.02-4.69-11.89-3.93 (6.45) 3.5-17.2) 16.5) 22.67 (7.21-21.9 (9.590 (<LOD-.80) 3.4) 7.54) 9.5) 10.83 (7.07) 2.89 (3.16 (3.29 (5.15 (1.29-2.9-25.73 (5.42-19.

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 * .459 (.740-.510 (.336-.83 (2.400) .40 (1.730) .80) 2.76-6.47) 2.59-2.09.80 (2.17) 1.60 (2.61 (1.460-.57 (1.240 (<LOD-.17-4.490 (<LOD-.18 (. and 03-04 are 0.16) 2.30) 2.30 (1.680-1.380-.23-3.570) * .15) 2.10) 3.20) 1.70-7.260 (<LOD-.550 (.880 (.388-.79) .30-1.14 (1.690) .820 (.75 (2. interval) Selected percentiles ( 95% confidence interval) Total * .70 (1.657) * * .22-8.830 (.20) 2.960) .960-1. < LOD means less than the limit of detection.960) .00-2.90 (1.1.2.89-6.950) 90th 1.20 (1.96-3.83) .949) .50-2.22-3.76 (1.54) .930 (.89) .13) .970) 1.620-1.960) 1.32) 3.570 (.94 (3.41 (2.930-1.570 (.20) 3.910-1.32-1.45 (1.00 (1.10) 1.98 (2.05-2.970) .55 (3.17) 1.32 (1.00-4.46 (1.303-.33-2. see Data Analysis section) for Survey years 99-00.97 (2.880) < LOD .750-1.86) 3.34) 2.940) < LOD .790 (.31-3.09 (.74-5.592) * .780 (.540 (.30) 4.584) .690-.39) 2.95 (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 * .670) .45-4.710 (.580-.20) 3.50 (1.57 (2. which may vary for some chemicals by year and by individual sample.80) 3.19-1.95) 2.29-2.04) 1.340-.10-1. 01-02.00) 2.455 (.700) .680-1.343 (.14-1.10-1.05-3.380) .592) * 50th .70 (1.800 (.03) 1.98-3.78) Sample size 1949 2519 1905 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .382-.90-4.880) < LOD 75th .840 (.88) 1.587) * * .69-4.80) 2.585) * * .78) .10) 1.650-.41-5.30-3.22-3.600 (<LOD-.35) 1.08 (2. and 0.780) .00) 1.30) 4.740-1.26) .60) 2.86 (1.467 (.350-.30-3.780 (.37-2.22-2.720-1.79) .20-2.449 (.77 (1.65 (2.46 (2.390-.90) 2.91) 2.80 (1.690-1.980) 1.80) 5.590-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. respectively.87-3.510 (<LOD-.600-1.560-.04) .720 (.505 (.20) 1.31-3.398-.810) .30) 1.98) .40 (1.20 (1.20-1.70-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.18 (1.740 (.11-3.S.580-1.910 (.440-.75-2.94) .48 (2.60-4.49) .20-2.83) 2.50 (1.710) .89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.13) 2.95-5.570-1.26 (2.31) 95th 2.457 (.16-3.550 (.450 (<LOD-.549 (.30 (.15) 2.21) 3.20 (1.47 (1.80) 3.31) 2.90) 2.29) 1.618) * .16) 1.425 (.50 (1.90) 3. population from the National Health and Nutrition Examination Survey.01-3.01-1.77-2.749 (.73 (2.710 (.36-4.50-2.720-1.759) * .30 (.850) < LOD .38) 1.68-5.453 (.390-.930) < LOD .01) .45 (2.600-.54-2.359-.910) 1.27 (2.80) 3.08 (2.280-.89) 1.700) .750) 1.11-3.592-.22 (1.25-1.380-.500 (<LOD-.690 (.73 (1.201-.50 (1.63 (1.210 (<LOD-.740 (.64 (1.46-3.30 (.20) 2.96-5.46) 1. 124 Fourth National Report on Human Exposure to Environmental Chemicals .59-6.45 (1.960 (.760 (.54 (2. 0.350-.50 (1.70 (1.27 (3.34) 2.60) 3.42-2.50) 1.58 (1.930) 1.10) 1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (2.820 (.20-3.83) 1.597) * .570 (<LOD-.94 (2.990-1.83 (2.74) 3.73-5.353-.49) 2.160 (<LOD-.570 (<LOD-.48 (1.860) < LOD < LOD .

population from the National Health and Nutrition Examination Survey.310-.440-1.285-.20) 1.460) .16) 1.04-1.740) < LOD 1.20-7.790) . Fourth National Report on Human Exposure to Environmental Chemicals 125 .69 (1.05) 1.710 (.350) .590 (.515) * * .11 (.485) * * .305 (.41 (.31-1.530 (.270-.32-1.480-1.60 (2.38 (2.04) 95th 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.81) 2.330 (<LOD-.24) 4.84 (2.50 (1.61-3.820) 1.18-2.71) .470) .250 (<LOD-.39 (1.25-3.700 (.79) 1.510-.38 (1.23) 2.75 (2.368) * .22 (2.720-1.08 (.330-.310 (<LOD-.393 (.79 (1.47-4.250 (<LOD-.680 (.43) 1.700 (.720 (.05-4.32) 1.950-2.742) * * .73-3.02-6.69 (3.61 (3.552 (.00 (3.403) .800) < LOD .42 (.830) 90th 1.30) 3.67 (1.61-3.730) .535 (.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 * .300 (<LOD-.760) < LOD 75th .06-2.42) .310 (<LOD-.57 (3.390) .57 (1.77-3.940-1.07 (.630) * .22) .460 (.470 (<LOD-.640 (.05-2.870 (.253-.47 (1.97 (1.348-.19 (1.77-4.67-3.04-5.640 (.07) 5.75 (1.710 (.57-4.80) 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 * .78) 3.910) < LOD .97) 2.55 (1.400) .740) .89-3.380-.47 (1.380) .560 (.509 (.09) .11) 1.00-3.66 (2.44-2.07-2.02-3.07) 1.17-2.670 (.840) .92 (1.300-.08) 2.70 (2.10) 2. interval) Selected percentiles ( 95% confidence interval) Total * .90) 2.790 (.471-.377-.22-3.920) .43) 2.500-.230 (<LOD-.580-.180 (<LOD-.990-1.08-3.688) * .42-6.88) .930-1.05) < LOD .23) 1.45 (2.57-2.66) .87 (2.84-6.97) 1.560-.55-3.72) 1.99) 1.820) .453 (.52) 3.52 (1.580) .13 (1.67 (1.320-.02-3.270 (<LOD-.43 (1.234 (.63 (1.62 (1.318-.58 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.07) 1.17) 2.71) 2.23 (.29-4.840) 1.72) Sample size 1949 2518 1903 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .335-.08-3.67) .94) .540-.99) 2.07-3.590) * 50th .71 (1.61) 2.520 (.136-.92) 3.645) .739) * .97 (1.33) .510 (.11-2.760) .64 (2.32 (.98) 1.800-1.97) 672 678 478 509 694 552 595 948 744 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.32) 5.460-1.44) 2.91 (1.08-2.640 (.65) 2.480) .510 (.444-.880) 1.45 (1.60 (1.03-2.520-.07) 1.00-1.690) < LOD < LOD .34 (1.53) .14 (2.08 (2.412-.840) 1.447 (.73 (2.750 (.870) .89 (1.490 (.03-1.50) 1.580 (.16-2.550-1.08-3.08-2.43) 2.560-.23) 3.32) 2.39) 2.390-1.372 (.77 (3.448 (.550-.400-1.750 (.49 (1.980-1.17) 2.590-1.830 (.67) 1.38-3.75) 6.82 (2.92-8.88 (1.30-2.22-2.S.36) 3.60) 1.22-3.49-4.70 (3.850) 1.20-2.900) 1.62 (2.597) * .72 (1.33 (1.06) 4.08-2.08) 1.270-.710 (.60) .72 (2.58-6.550) .76) 1.80) 2.58) 3.72-4.28 (1.591 (.95) 1.08-3.370-.660-.75-3.280 (<LOD-.22) 4.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.320-.05 (1.700 (.380-1.23) 2.64 (2.42-8.82) 2.22) 1.16-1.550-.

7-22.8) 952 1187 946 996 1331 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.0) 42.0) 28.92) * 2.0) 3.10 (1.06 (1.0-49.7) 47.44) 3.0) 20.0) 471 575 310 664 822 717 813 1121 938 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.5) 69.8 (12.10) 39.33 (5.0) 19.0-41.41) 5.0-31.09 (4.0) 4.0 (19.46 (.0 (6.00 (.53) 40. population from the National Health and Nutrition Examination Survey.43-7.59 (1.0-29. see Data Analysis section) for Survey years 99-00.0) 17.2-47.30) 11.70) 1.85 (1.57-2.1-47.30) 4.0) 28.1 (26.87-7.1 (25.830-3.61-2. and 0.1-46.3) 26.98) * 2.1) 140 (46.48-2.76 (2.23-2.44) 2.50 (2.10 (1.41-4.80-2.88) 3.1-40.1 (11.5.0) 20.0 (20.1 (22.0-41.0) 13.6 (9.0) 18.0-92.4) 38.0) 30.0-260) 34.0 (8.2) 16.57-2.8) 39.94 (1.27-6.8-21.0 (21.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6 (11.6-27.60) < LOD 1.0 (8.78) 9.4 (19.78 (1.7 (12.00-24.10 (1.5-40.0) 3.470 (<LOD-1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.31-6.8) 62.9 (23.46-6.69) 2.0-53.13 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-58.76 (2.18) 20.0) 3.98 (1.0-41.21 (3.0-39. 01-02.80-18.0-110) 42.50-2.0-50.2-33.26 (.52 (4.16) * 1.06) * 2.44) Selected percentiles ( 95% confidence interval) Total * 2.71 (4.50-5.70 (1.80) 90th 38.25-3.79 (2.8) 41.71-2.0 (24.7 (12.02 (2.07-5.0 (13.18.8-24.12 (3.05-3.46-2.0-110) 34.0-62.0-69.9) 48.7) 20.83-2.70 (1.48) 5.660-2.79 (1.2-80.0) 5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7 (28.0-62.75-14.0 (33.0) 16.0) 33.0) 15.0-230) 35.1) 95th 48.90 (1.5-20.82 (1.0 (38.81-2.85) * 2.9) 17.86 (1.8 (26.0-58.86-3. which may vary for some chemicals by year and by individual sample.41) 1.4-22.70) 1.1 (10.0) 8.48-2.53) 1.41) 1.14) 5.690-3.81-3.97) 6.6 (26.0-52.49-2. 126 Fourth National Report on Human Exposure to Environmental Chemicals .05) * 2.19-2.1-19.0 (40.90-8.11) 2.0 (17.0 (20.3) 38.83 (3.2-27.9) 18.21 (1.17-2.S.3 (23.7-41.5-27.36-2.3 (12.16) 2. and 03-04 are 0.23) 9.13 (1.0 (38.10-13.2) 31.18) 6.64-8.40-4.45) 2.18) 14.74-2.5-74.65 (4.3 (12.9 (10.3 (10.71) 5.63-6.5 (24.40) 50th 2.4 (10.0) 4.30-14.77 (1.10) .0-39.40) < LOD 2.79-2.6-22.8) 32.60 (2.530-4.4) 19.40) < LOD 1.90 (1.5-45.23-2.32 (2.83 (1.42) 1.04) 3.29-4.6 (15.04-8.00 (.0 (25.0) 31.1) 38.0-47.9 (19.29) 2.0) 6.53 (1.2 (19.1 (25.83-2.35-6.0 (38.610 (<LOD-1.29-9.0 (26.6-45.99 (2.26) 75th 11.830-4.45) 2.1-25.58) 16.50-17.6) 52.2-39.54 (1.70 (.0) 17.0) 45.4-76.50-7.80) .70 (7.72 (1.2-27.0-43. < LOD means less than the limit of detection.96) 5.20) 1.3 (24.9 (19.3) 33.64-3.8 (22.95 (5.0) 32.0 (7.9-21.58-2.54 (3.0 (8.2-62.600-2.1) 18.0-53.04 (<LOD-2.90) 11.40-16. 0.2 (12.66-5.0) 16. respectively.44-7.53) * 2.3 (14.80) 1.5) 30.10-4.0 (32.19) 2.20 (2.0 (11.21 (4.80) < LOD 1.9-51.11 (4.2-26.13) 12.0) 15.61 (1.70-6.3) 31.12) 1.4.93-3.3) 28.0) 3.9) 38.20-4.0) 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 2.8 (12.0 (38.50-20.6-54.41 (1.9 (27.59 (1.0 (38.05) 1.0 (38.91 (4.70) 5.67 (1.30 (.92-5.10 (1. interval) 1.0) 4.1) 38.70-17.1-20.0 (38.10 (7.88) 1.0 (37.4 (15.77) 38.

6) 23.20) Selected percentiles ( 95% confidence interval) Total * 1.2) 36.41 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.670-1.43-2.11-2.28) 1.0 (17.8 (7.4 (9.0 (25.18-1.9 (10.2-38.22-3.01 (.23) 37.27-3.12) 3.6) 7.19) 5.07-2.46-6.06-1.46-5.9 (26.22-2.54-15.1 (34.27 (6.2) 33.84-13.06) 1.75) * 1.0-71.3-19.59-15.680-4.890-4.5-36.00) 1.3) 13.0 (6.14-8.88 (1.30) 28.2) 13.68) 47.46) 1.8) 23.51) .0) 30.5) 27.79 (2.57 (6.1) 13.67 (1.02 (.69-5.71 (1.0 (23.61-22.08 (1.26-2.0) 48.60 (.67-16.5-190) 30.19) 5.59-2.39 (1.61 (1.80 (1.930 (<LOD-1.69-18.22 (2.7) 30.17) 2.48 (4.16-2.6 (24.60) 4.5 (17.53) 1.2-70.26-4.0 (39.1) 36.91 (6.3 (10.3 (10.1 (33.7-109) 22.86) * 3.2 (15.1) 27.0) 3.2-28.03) 1.6-38.6-32.1) 27.52 (1.16 (1.15 (.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 2.2) 41.36-13.4-39.1) 13.94-20.90 (.2 (16.03-2.2) 671 678 497 509 694 578 595 947 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.6 (11.20-5.7 (11.4-34.5 (6.3 (9.86) * 2.S.7 (24.6) 3.1-60.47 (3.44) 9.1) 17.82) 1.36) 10.8) 15.48) 1.7 (18.33-5.1) 25. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (7.40 (2.16 (1.9) 24.6) 19.4 (25.8-43.96) 2.8) 3.3-27.33) 1.14 (.4) 14.35 (2.99-4.4-71.40-4.71) 8.21 (4.1-63.22 (.31) 2.5 (8.06) 75th 9.9) 54.56 (2.19 (1.4) 12.8-45.00-16.1 (25.70 (1.09 (5.19-14.7-38.9-52.4-67.3 (20.2-47.0) 13.7 (18.83 (.1-22.51) < LOD 1.17-3.12 (1.0-118) 29.9-95.33) < LOD 1.0) 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 1.5-97.9-18.8) 31.2-34.32-3.899-2.43) * 2.82 (2.80-8.67 (1.11) < LOD 1.57) 4.4 (11.96-16.2 (22.7-20.27) 50th 2.02) * 1.66 (1.27) 10.95) 90th 32.38-5.7) 61.4 (21.5 (13.28 (1.870-3.94) 1.24 (1.79-17.75-6.7) 95th 51.93) 5.9 (39.97 (1.40-7.40 (5.9-37.750 (<LOD-1.95 (2.58-2.38 (3.870-3.6) 11.32 (3.1 (39.55 (2.66 (1.888-1.0-40.07-2.59-2.56) 1.33) 2.29-5.71-2.5) 70.5-43.8-34.7) 23.9) 3.4 (12.0 (19.23-1.18) 3.1) 52.08) 1.2) 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 1.88 (4.8) 32.5 (34.1) 15.25-3.66) 8.63-5.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.62 (2.7) 26.6) 112 (40.88 (1.3-22.3 (8. population from the National Health and Nutrition Examination Survey.0 (23.870-3.2 (8.9 (19.34) * 1.36 (4.16 (1.46-22.9) 24.4-21.7-19.95-16.38) 5.68 (1.64 (1.6) 3.0-70.67-3.47-17.7) 66.75 (1.50 (2.50-5.72) 2.1 (50.1 (12.4) 3.06) 1.62) 4.02) 1.8) 11.5 (15.2) 4.37 (1.860 (<LOD-1.75 (1.0) 25.8-37.9 (13.5 (41.2) 13.37-2.88 (4.4 (19.91-2.3) 28.1) 25.0) 10.8-26.9-36.6 (27.76-2.6-51.9) 12.7-47.5 (15. Fourth National Report on Human Exposure to Environmental Chemicals 127 .38-1.43-12.7 (10.94) 19.47 (1.45 (1.07) 9.58-17.7-37.4 (5.7) 15. interval) 1.9) 3.61-2.2 (9.00) 6.83) .9-41.3-42.35) .95-16.0 (32.4 (25.4) 12.18) * 2.6-49.23) < LOD 2.9 (7.52-4.7) 34.70-4.0) 47.2 (21.00 (4.35) 1.7-43.45-1.19-6.0 (14.54-2.

630 (.870 (.410) < LOD < LOD < LOD < LOD .36) .180) .860) .860-1.120-.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.290) < LOD < LOD < LOD < LOD 90th .630 (.320-.570) .120-.460-. population from the National Health and Nutrition Examination Survey.10) .162) * * * * * .210 (.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 .190 (.730) .220 (<LOD-.1.090 (<LOD-.760) < LOD .090 (<LOD-.230-.450 (.640 (.120 (<LOD-.870 (.140) .160) .620 (.740) < LOD .410-.680-1.680 (.10 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .190 (.700-1. < LOD means less than the limit of detection.610 (.130) .690-1.380-.140-.360-.400-.10) .940 (.600 (. and 03-04 are 0.640-1.290 (<LOD-.42) .140-.320 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.820 (.130-.650-1.117 (.05.150) .830 (.170-.310 (.830) < LOD .130-.460 (.080 (<LOD-.990) .650) .850 (.090 (<LOD-.410-1.720-1.650) . see Data Analysis section) for Survey years 99-00.820 (.530-.1.100 (.310) < LOD < LOD < LOD < LOD .160) .540) .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 * * * * * * .03) .900 (.540) .130-.42) .420-.090 (<LOD-.410-.440-1.360-.370-.310-.370-.290) < LOD < LOD < LOD < LOD .990) .090 (<LOD-.770) < LOD 95th .540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .084-.470 (.730-.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 * * * * * * * * * .680-1.60) 1.090 (<LOD-.470-1.700-1.830) .32) .610-1.S. and 0.200) < LOD < LOD .130) .140-.560 (.640) .310) < LOD < LOD < LOD < LOD .850) < LOD .720) .12 (.510-1.610 (.280) < LOD < LOD < LOD < LOD .550) .450 (.490 (.080 (<LOD-. 0.210 (.110-.610-.240 (<LOD-.660 (.390 (.300-1. 01-02.330-.850 (.930 (.300-.310 (. respectively.40) .430-.260 (.130 (. 128 Fourth National Report on Human Exposure to Environmental Chemicals .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.700-1.450 (.15) .10) .350) .270 (.30) . which may vary for some chemicals by year and by individual sample.150 (<LOD-.700-1.13) .870 (.20) .840) .560 (.160-.390) < LOD < LOD .30) .720 (.380-.870 (.171) * * . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.680) .350) < LOD < LOD < LOD < LOD .430 (.00) .870) < LOD .230) .650 (.830 (.190 (.380-.050-.640) .220 (.30) .099-.870 (.650-1.770 (.540 (<LOD-.990 (.840) .58) .780) < LOD 1.

400 (<LOD-.360-.20) 1.330-.19 (.540) .380-.670 (.490-1.500 (<LOD-.60) .360) < LOD < LOD < LOD < LOD .660-1.730) .38) 1.700 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.62) 1.320 (<LOD-.410 (.090 (<LOD-.03 (.01 (.670 (.710-1.180-.200 (.410) < LOD < LOD .760) .380 (.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.290) < LOD < LOD < LOD < LOD 90th .570 (.860 (.03 (.260) .450) .060-.260-.440 (.080 (.410) .540 (. population from the National Health and Nutrition Examination Survey.740 (.161) * * .110) .550 (.050 (<LOD-.200 (.580-1.190-.070 (<LOD-.S.500-1.670-1.580 (.550 (.370 (<LOD-.240-.300 (.740) < LOD 1.120) .111) * * * * * .86) .850 (.12) < LOD .03 (.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 * * * * * * * * * .880 (.500) .190 (.110) .700-1.340-.140-.080) .310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.410-.86) .116 (.120) .170 (.360 (.720 (.450 (.230-.570-1.02-1.170) < LOD < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 129 .170 (.140-.330-.380-.810 (.140) .310) < LOD < LOD < LOD < LOD .070 (<LOD-.070 (<LOD-.78) .720 (.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 .610-1.67) .220) < LOD < LOD < LOD < LOD .14) 1.700) .140-.410 (.780 (.03) .220 (.870) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.080 (<LOD-.070 (<LOD-.190 (.570-.730) .300-.400) .29 (.650) < LOD .090 (.940) .084-.380-.390-.270 (.970) .250-.730 (.330-.58) 1.800-1.360-.990) .057-.940) .210 (.580) .100 (<LOD-.880-1.230 (<LOD-.140-.43) .540 (.00) < LOD .600) .300-.860-2.470 (<LOD-.520-.110-.330 (.560 (.09) .24) .510-.110) .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 * * * * * * .36 (1.440-1.410-.730) .990) .520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .860 (.780) < LOD 1.750) < LOD 95th .650-1.580 (.230) < LOD < LOD < LOD < LOD .24 (.280) < LOD < LOD < LOD < LOD .640-1.100-.270) < LOD < LOD < LOD < LOD .600-1.390-.02) .66) 1.890 (.960) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .580) < LOD .700 (.380-1.330 (.460 (.150-.140-.110) .

36-3.400-1.0-38.32 (1.370-.67 (1.87) 5.10 (3.190-1.50) .0 (17.590 (.110 (<LOD-. which may vary for some chemicals by year and by individual sample.46 (1.60) .610) < LOD < LOD < LOD < LOD < LOD 2.10-3.6) 5.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.0) 7.67) .0 (13.88-3.0 (6.960 (.12-1.30) .750-2.90-9.0) 4.0) 5. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.0) 2.86) 4.20-4.90) .40) 2.13 (3.07 (3. 130 Fourth National Report on Human Exposure to Environmental Chemicals .0 (7.30-7. < LOD means less than the limit of detection.96 (1.770) 2.53 (2.07 (1.360-1.70) 2.49) 17.40 (1.23-6.03 (.35) 5.70-30.20-17.10-9.55-4.82-4.35) 11.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.49 (1.74 (3.07 (3.830 (.900 (.580 (.740 (.90-20.47 (3.720) 2.260-.90) .70-17.65) 1.210-1.67 (2.99 (1.960 (<LOD-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.850) 16.05 (2.53-7.90 (1.83) 2.24-7.55-8.10-3.640 (.51-8.0 (17.05 (3.14) 2.31-10.170-1.18) 1.0) 2.425-1.36-3.0) 2.840-3.0) 2.62) 471 575 306 664 821 699 814 1122 925 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .50) 2.0 (17. respectively.0) 4. see Data Analysis section) for Survey years 99-00.0 (17.11 (1.07-3.480-.59-5. and 0.99) 11.33 (4.42) .750-1.30 (1.99) 19.0 (3.00) 1.0-39.53) 20.90-37.39 (2.80 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40 (1.66) 4.21-3.90-28.12) * * * * * * * * .0 (5.00-17.S.870) < LOD < LOD .1.0) 5.0-44.0 (5.0) 4.510-.0 (5.0-40.40) 1.21) 3.30 (2.730 (.380-.0-38.97) 20.30-3.0) 2.00 (1. and 03-04 are 0.0) 3.52 (1.840 (<LOD-1.28-9.00-17.0 (5.76 (1.640 (.31) .32-9.00 (.0-38.68) 2.30 (1.00) .11) .26 (2.52 (1.38-3.691 (.0 (17.08.0) 2.48) 13.1.0) 5.01) 5.30-6.10 (.85-3.0-40.45 (2. population from the National Health and Nutrition Examination Survey.330 (<LOD-1.0 (4.800-4.94-8.350-.83-3.20-4.250 (<LOD-.83-3.620-1.40-8.0) 5.14-5.20 (1.94 (1.97) 20.840 (.52) 5.30 (1.880) 5.10 (3. 0.07-3.90 (2.350-.05-3.62-8.28) .61 (1.63 (3.49 (1.610 (.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 * * * * * * * * * .51 (2.60) 1.15) 14.07) 1.74) 5.910) 2.70-50.43-4.37) .30) 95th 19.0) 4.0) 2.42) 2.800) 17.0 (5.800) 90th 13.39) .70-3.28) 1.48 (2.70-7.29-10.94-3.11) 13.080-1.690 (. 01-02.90) .890 (.0 (4.40-4.16) 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 .30 (.00) .35-10.87) 12.40-7.0 (16.20) < LOD < LOD < LOD < LOD < LOD 1.14) .15) 19.63) 32.40-20.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.20 (1.770 (<LOD-1.600 (.

2 (8.96) 2.580 (.800-2.560 (.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 * * * * * * .18) 1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.88 (.8) 4.50 (4.44) .62 (1.8) 7.50 (2.7) 5.11) .17) 5.14 (1.0 (4.790) 11.57) 8.37) 4.7) 4.630-1.850-3.4-34.48-42.0) 4.39) 20.56 (1.45 (1.96-25.8 (20.36 (.S.25-38.44-11.73 (4.12-4.1 (7.67) 2.07 (2.09-3.5) 2.04 (1.7) 6.91) 2.89 (2.79 (.48 (4.56) 2.8) 2.69) 2.01 (1.00-19. population from the National Health and Nutrition Examination Survey.330-1.660) < LOD < LOD .80) 3.69-7.700) < LOD < LOD < LOD < LOD < LOD 1.470 (.1) 672 678 497 509 694 551 595 947 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.31) .29 (4.9) 6.03) 2.4 (4.150 (<LOD-.62-17.500 (.33 (3.22) 2.40 (.91-4.1) 2.31-18.51-44.29-4.590) 2.840-3.48-7.47) 5.370) < LOD < LOD < LOD < LOD < LOD 1.190-1.10) 2.60 (1.740-1.820) .9) 5.4) 2.780-4.5) 2.25-9.02 (.00) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50) 11.67) 1.830 (.21-3.710 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.650 (.270 (<LOD-.0 (9.18) 95th 21.55 (3.53) .260-.65 (2.430 (<LOD-.580) 16.06 (.860-2.700) 6.08) .790 (.540 (.5-40.320-1.96-8.05) .57) 1.41 (4.340 (.540-1.47-10.14-6.580-1.80 (.8-33.71 (.75) 5.340-.77 (.8) 2.890 (.59 (1.50) .930) .32-6.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.8) 7.74 (2.82-11.450 (.84) 9.41) 18.25 (1.55) 21.02-4.86) .49-2.02) .33-4.32) 9.820 (.11-5.67 (2.940-4.430) 1.360 (.1 (5.33-3.83-11.5 (9.10-3.40-2.5 (11.33-5.07-21.748 (.85-3.3) 3.830-3.35 (.56) .02 (1.18) * * * * * * * * .66-47.51-4.33 (1.390-.47-10.71 (2.22-27.240-.57-40.690-5.3) 2.81-17.670 (.55) 21.730-3.24) 3.620-3.13 (2.88) 17.98 (4.12 (4.40) 1.7 (12.67-6.04-16.85 (1.28-6.90-6.5 (8.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.960 (.43) .03) 16.6) 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 * * * * * * * * * .370 (.250 (<LOD-.2-38.580) 1.15) 9.970-3.17 (1.86 (3.474-1.770) .47) .23-7.40-12. Fourth National Report on Human Exposure to Environmental Chemicals 131 .370-1.340-.31-7.8) 1.27 (2.340-.600 (<LOD-1.57 (.64) 30.38 (2.88-3.83 (4.650) 90th 10.10 (2.64-4.88 (2.97) .5) 7.270-.7 (6.31) .9 (11.52 (.53) 27.260-.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 .92 (2.30 (4.7) 3.310-.

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National Research Council (NRC). EPA). Dinoff TM. Scand J Work Environ Health 1998. discrimination. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Heaton RK. Seiber J. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Lambert WE. Lancet. vibration sense and tremor among South African farm workers. Robson MG. Smit LA. Environ Health Perspect 2005. low-level organophosphate exposure on delayed recall.44(4):352-357.12(2):134-141. van der Hoek W.2000 and 2001 market estimates. Berry H. Effects of chronic. Neurotoxicology 2005. Jamal GA. Samuels S. Rothlein J. Phillips J. Bull Environ Contam Toxicol 1994. Rothlein J.113(4):504-508. Neurotoxicol Teratol 1998. 1993 [online]. Barr DB. Buccafusco JJ. 1/12/09 Peiris-John RJ. J Toxicol Environ Health A 2005.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI.php?record_id=2126&page=1.38(4):546-563. Lancet 1995. Neurotoxicity among pesticide applicators exposed to organophosphates. Bravo R.30(2):98-103. Daniell WE. Savage EP. Lasarev M.edu/ openbook. Terry AV Jr. Scherer J. Pilkington A. Keefe TJ. Chronic neurological sequelae to organophosphate pesticide poisoning. 4/7/09 Young JG.68(3):209-227 Maizlish N. Santana J. Buchanan D. Frasca G. et al. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. O’Malley M. Eskenazi B. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Muniz J. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Int J Occup Environ Health 2006. U. A behavioral evaluation of pest control workers with short-term. Masala G. Pedersen L. Ruberu DK.pdf. 2004. Myers JE. Ames RG. Office of Prevention Pesticides and Toxic Substances. McConnell R.24(1):18-29. Saieva C. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides.nap. The Pesticide Health Effects Study Group. et al. Rohlman D. Stark A. Occup Environ Med 1995. and cholinesterase status of date dusters and harvesters in California. Available at URL: http://www. Prendergast MA. Pesticide industry sales and usage . Fourth National Report on Human Exposure to Environmental Chemicals 133 . Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. May. et al. 1991. Aprea C. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Arch Environ Contam Toxicol 2000. Hore P. Mounce LM. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. metabolite clearance.52(2):190-195. Am J Public Health 1994. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Malathion deposition. Kidd M. Beach J. Lu C.20(2):115-22.52(10):648-653. Gladstone EA. Tumino R. Bradman A.43(1):38-45. Burcar PJ. Steenland K.332(1-3):71-80. Marshall E. Rosenstock L. Environ Health Perspect 2006. Levy LS. London L. Effects of long-term organophosphate exposures on neurological symptoms.338(8761):223-227. Calvert IA. Available at URL: http://books. 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. Arch Environ Health 1988.58(11):702710. Russo J. Vitayavirasak B. Weerasekera G. Caltabiano LM. Washington (DC): U. S. Occup Environ Med 2001. and spatial learning in monkeys and rats. Visuthismajarn P. Chrislip D. Muniz J. Irish RM.S. Wickremasinghe AR. J Occup Environ Med 2002. Salvini S.epa. Chronic neurological sequelae of acute organophosphate pesticide poisoning. McCauley L. Spurgeon A. Rodnitzky RL. Jenkins B. Lasarev M. et al.114(5):691-696. Sci Total Environ 2004. Takamiya K. Environmental Protection Agency (U. low-level exposure to the organophosphate diazinon.26(2):199-209. Johnson C. Hansen S. Am J Ind Med 1987. EPA. Stokes L. Pesticides in the Diets of Infants and Children. Nell V. Keifer M. Schenker M. Washington (DC).S. et al. National Academy of Sciences. Weisskopf C. Narang A.84(5):731-736. Lewis JA.12(2):153-172. Petchuay C. Arch Environ Health 1975. Claypoole K.345(8958):11351139. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Gillham R. Thompson ML. Stephens R.

These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides. malathion is metabolized to malathion dicarboxylic acid. For general information about the organophosphorus class of insecticides. parathion and methyl parathion are metabolized to para-nitrophenol. the level may reflect exposure to the environmental degradation products of these pesticides.” 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.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.6-Trichloro-2-pyridinol (6515-38-4) 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol 2-Isopropyl-4-methyl-6-hydroxypyrimidine (2814-20-2) Malathion dicarboxylic acid (1190-28-9) para-Nitrophenol (100-02-7) 2-(Diethylamino)-6-methylpyrimidin-4-ol/one 134 Fourth National Report on Human Exposure to Environmental Chemicals . For example. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report. In addition to reflecting exposure to the parent insecticide.

47-9.83) 1.30-5. For instance.60) 5.45 (1.90 (3.00-24.05-5.0) 8.EPA. dermal.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.3 (10.40) 2.47-11.59) 2.00) 2. USGS.80 (1.4 (9.40 (5.0) 12.40-2.63 (2.20) 2.97) 7.2 (10.20 (2.70-17.0 (10.40 (5.80) 2.5 (8.19-3.35) 2.25) 1.4-15.46-2.4 (10.34) 1.72-4.10-17.97-7.90-2.0) 11.13 (1.66-15.51-2.5.8-15.66-4. 1999.77-15.80) 4.9 (10. Fourth National Report on Human Exposure to Environmental Chemicals 135 .80 (7.28) 2. staying bound to soil particles.89-2.80) 12.10 (4. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.90 (1.84) 1.60-3.5-24.90 (6.60 (5. air. Survey Geometric mean (95% conf.44-2.61-7. 2002).00-8. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.70-5.90-7.26) 7.21) 3. 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.30-9. Estimated intakes from diet and water have not exceeded recommended intake limits.71 (6.000 pounds are used per year.20 (4.20-11.63 (8.0 (7.9-18.70 (1.39-2.50 (2. and is infrequently detected in ground water (IPCS.28-3.40-10.10) 2.74 (1.50-2.94 (4.60 (4.40 (6.30 (2.77-6. interval) 1.4 and 0.92 (1. in 142 urban homes and preschools in North Carolina. and on plants for days to several weeks.19 (1.90) 7.77) 1. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.20-4.51) 1.29) 90th 7. Exposure can also result from contact with contaminated surfaces.74-9.3) 8.0) 7.89 (2.47 (4.61) 75th 3.00) 3.62-2.60-2.25) 3.96) 3.61 (1.50-8.4.0) 12.72) 2.20-2.10 (3.10 (5.70-15.30-11. and dust.70-11.30-12.59-2.0) 10.02 (7.30) 4.1) 5.44 (3.31-2.71 (1.50-2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.13-3.3 (11.1-16. but can be detected in streams receiving runoff from application sites.EPA.30-2.0) 8. 2007).7-23. applied to structures to kill termites.50-4. population from the National Health and Nutrition Examination Survey.0) 14.24-1.76 (1.95 (4.S.20-3.04-10.80-8.39) 4. It also has been applied directly on animals to kill mites.43-2.0) 6.67 (2.40) 9.52-2.90-4.20) 2.17 (1.29-1.97) 4.70-16.10) 6.80-10.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.79-2.35) 1. Chlorpyrifos is Urinary 3.0 (7.55-5.87-6. pre.50 (2.30-1.0 (7.90) 3.30) 4.36 (4.04-10.22) 2.37 (1.64) 3.5.0) 10.0) 12.31-2.0) 12.44-5.0 (7.90 (2.88 (1.97) 2.27 (7.9 (7.00) 1.32) 2. chlorpyrifos was no longer registered for indoor residential uses in the United States.20-16.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.38 (3.8) 9. The general population may be exposed to chlorpyrifos via oral.6) 7. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.57 (2.52-12.14) Selected percentiles ( 95% confidence interval) Sample 95th 10. 5598-13-0 General Information The chemical 3.97) 2.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.91 (1. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.50 (2.50-5. It has low leachability.68 (7.50-4. Approximately 21-24 million pounds per year were used domestically from 1987-1998.0 (13.15 (1. Approximately 80.70 (1.20) 4.03) 1. and inhalation routes.50 (1. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.91) 16.7) 9.32-1.02) 1.37 (4.95) 7.40-26.3) 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 1.47) 1. 2005).22 (1.S.30 (2.0) 9.67 (1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.20) 10.68-2.0-28.0) 10.90-8.02 (1.5) 7. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.24-3.50-14.70) 1.60 (2.8) 10.60-3.81-2.0 (7.63 (1.0) 12.9 (9.78 (7.09 (3. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.0) 15.0 (9.S.40-13.30) 5. After 2001.30 (4.90 (1.3 (8.and post-construction structural applications for termite control were to be phased out by 2005 (U.9) 11.9) 697 660 521 701 602 947 Limit of detection (LOD.50 (1.67 (2.05) 1.43-2.09 (2. 2921-88-2 Chlorpyrifos-methyl CAS No.53 (1.51 (1. and sprayed to kill mosquitoes.98-15.37) 5.47-13.16) 2.76 (1.7) 8.20-14. 2002).60-4.86) 4.71 (2..77 (1.99-4.4 (8.01) 1.80) 1.10 (1.7) 13.0) 18.

16) 6.6) 10.44 (6.62) 90th 5.63 (5. and seizures.92 (1.12-3. 2000). Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis. vomiting.21-6.12-1.58 (1.41 (1. Roy et al. 2002). Howard et al..97) 3.24-1.47 (1.47 (5.15 (4.1-38.99) 1. Slotkin et al.83-2.58-5. 2006a.62) 1.22 (6.05-8.60-3. 2005.3 (7.39 (2.88-10.83-11.24) 5.94-12. and producing acute symptoms such as nausea..81 (3.94-14.00 (7. 2005.20 (2.75 (1.85) 4.91) 2. Ricceri et al.52 (5.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.5) 5.92-2.7) 7. 2006.34-1.78 (1.98 (7.86 (3.48 (1.05-3.06-4.75) 6.91 (3.53 (2.19-2.11 (2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).81) 2.56) 5.76 (3.93 (2.66 (1.35-1.44 (1.59-2.46 (1.6) 9.56 (4.91) 1.80-4.33 (5.57) 9.70-4.97 (3.71) 3.09 (1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.19) 3..93) 2.68) 1.97) 3. weakness.00-8. and other metabolites.47 (1.68) 6.0) 12.89) 4.11) 7.57-2.24-5.55) 1.64-7.91) 10.44-6.91 (4.2 (7.83) 1.77) 1.54 (2.4) 4.66-11.48 (2.73 (1.8) 9.80-6. 2006b).82 (2.09-3.07) 1.940-1.65-11.82 (3.35) 2.38) 3.69 (1.91) 1.85-4.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.16 (4.27-1.60 (1.01) 3.02) 7.17-4. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.71 (1.90-9. TCPy is more persistent in the environment than chlorpyrifos itself (U.27-7.42 (5.80-11.44 (5..57-2.6-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.24-4..EPA.28) 2. 2006.05-4.88-8.24 (1.42-2.30-4.85 (3.72) 2.54) 5..1-21.96) 3.09-1..45 (1.56 (1. 2005.36) 1.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.S.17-4. cholinergic effects. TCPy can also occur in the environment from the breakdown of the parent compounds.39-1.24-24.97 (2. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.56) 2.00-13.43 (4.43-10.95 (3.28) 2.12) 1.55 (1.93 (4. Survey Geometric mean (95% conf.88-9. Thus.09-2.9 (12.47-2.22 (4.31-1.30-1.82-4.0) 6.1 (7.06 (1.84-6.44 (1. Based on animal data and human cholinesterase monitoring during occupational exposure.11-9.23-1.44 (5.57) 2.3) 8. Metabolic hydrolysis leads to the formation of TCPy.87-3.01) 1.25-11. 1984).63-2.42 (6.00) 1.92) 3. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.86 (1.23) 14.19) 6.46 (2.37 (1.39 (4.64-2.2) 6. Betancourt et al.53-5.63 (4.82) 8.49-2. In pesticide applicators.08) 6.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1..05-1.33) 2. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.01) 3.91-4.14-8.02 (5. population from the National Health and Nutrition Examination Survey.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.45-1.93) 5.66) 1.72-2.33 (.5.07) 5.33 (1.65-15.79-13.86 (1.49-2.5 (6. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.25-12.85) 1.80) 3.3) 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. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates. 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.29 (3.S.21-1.97-3.05) 3.22-6.49-2.88 (1.26-14. resulting in excess acetylcholine at nerve terminals. Once absorbed.58 (1.64 (1.72) 1.58 (4.0) 10. paralysis.32) 1.31-4.40) 1.50 (4.24) 75th 2.1 (10.56-2. neurotransmission.39) 6.88) 6. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.31) 1.22) 1.91-13.14) 1. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals . These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.93 (1.19-1.20-1.88-8. interval) 1.99-8.3) 8.25-1.0) 16.06 (5..33-7.55 (4.88 (1.62-7.98 (6.58) 1.11 (2.76 (2.58) 5.74) 1.85 (2.59) 3.35) 1. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.3) 9.95 (1.51 (1.49 (1. Urinary 3.03) 1.

Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. EPA at: http://www.Reference values of urinary 3. 2005). 2005).S. Carr RL.. In Minnesota and South Carolina farmers who used chlorpyrifos. 2005). the geometric mean urinary TCPy levels were similar in parents and children. 2004). Garabrant D. Replacing conventional diets with organic diets in 23 children led to about a fourfold decrease in urinary levels of chlorpyrifos. 2002). 2004). CDC. Finding a measurable amount of TCPy in urine does not mean that the level will result in an adverse health effect...atsdr. et al. the weighted population mean of TCPy measurements was approximately three times higher (Adgate.S. 2003. Aldridge JE. 76% had detectable levels of TCPy and levels were similar to those reported for NHANES 1999-2000 (Eskenazi et al.. Barr DB. Barisano A. 1995) and were similar to levels reported in studies of healthy adults in Germany (Koch et al. 2000). 2005).82(2):305-312. Environ Health Perspect 2001.. Fourth National Report on Human Exposure to Environmental Chemicals 137 . MacIntosh et al. Additional information about external exposure (i. Toxicol Sci 2006. Following crack-and-crevice application of chlorpyrifos in their homes. 2006) and episodically many times higher for pesticide applicators than median levels from NHANES 1999-2000 (CDC.cdc.. Clayton CA. median urinary levels on the conventional diet were several fold higher than those in the NHANES 1999-2000 subsample (Lu et al. Aprea C. Betancourt AM. Chlorpyrifos exposure and biological monitoring among manufacturing workers. References Adgate JL.. Freeman NC.. 2007). Levels of TCPy in the U. Some reproductive and teratogenic effects in animal testing were only observed at high doses of chlorpyrifos that caused overt maternal toxicity. 2005) appear roughly similar to values reported for a nonrandom subsample of NHANES III (1988-1994) participants (Hill et al. Measurements of urinary TCPy in single spot urine collections show variability over time in environmentally exposed individuals and are poorly correlated between collections. Urinary levels of TCPy have been found to be hundredsfold higher for chlorpyrifos manufacturing workers (Burns et al. urinary TCPy levels in children were reported not to have increased (Hore et al. 1992. 2006). Of 482 pregnant women living in an agricultural community. Meyer A. 2005.. Burgess SC. Koch et al. representative subsample of NHANES 19992000 (CDC. 2005. 1999).html and from U. Albers JW. Environ Health Perspect 2005. but not chlorpyrifos.Organophosphorus Insecticides: Specific Metabolites 2004. population (CDC. (1999) reported mean urinary TCPy levels in a sample of Maryland adults that were about three times higher than adults in the U. In a probability-based sample of 102 Minnesota children aged 3-13 years. 2005). Chlorpyrifos is not considered to be mutagenic or carcinogenic (NTP. Slotkin TA. Magnaghi S. urinary TCPy levels averaged about sixfold higher than those in the NHANES 1999-2000 subsample (Mandel et al. Whyatt et al. Chlorpyrifos levels in house dust and hand rinses did not correlate with levels of TCPy in urine (Lioy et al.epa. Occup Environ Med 2006. subsamples of NHANES 1999-2000 and 2001-2002 (CDC. 2005).92(2):500-506. Eberly LE.. Berent S. Alterations in central nervous system serotonergic and dopaminergic synaptic activity in adulthood after prenatal or neonatal chlorpyrifos exposure. Seidler FJ. Betta A. 2001).113(8):1027-1031. In Iowa farm families using several different pesticides. suggesting changing low-level exposure and variance in collection timing with respect to exposure (Meeker et al.gov/pesticides/. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Burns CJ. 2001) and Italy (Aprea et al..EPA. Catenacci G.S. Lotti A.109(6):583-590. et al. Haidar S.6-trichloro-2-pyridinol in the Italian population—validation of analytical method and preliminary results (multicentric study). Estimation of dose or intake based on the urinary excretion of TCPy indicates that environmental doses are generally below recommended limits (Hore et al. Perera et al. Curwin et al. 2001) than the corresponding values reported for the group aged 6-11 years from the NHANES 1999-2000 subsample (CDC.e. Giordani B.. Other small studies of environmentally-exposed persons have shown a high frequency of detecting low levels of TCPy. et al..S. but levels were roughly four to six times higher than the geometric means in the U. Effect of developmental exposure to chlorpyrifos on the expression of neurotrophin growth factors and cell-specific markers in neonatal rat brain. U. J AOAC Int 1999.63(3):218220.... Lioy PJ.S. 2005. Biomonitoring studies of TCPy provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of chlorpyrifos or chlorpyrifos-methyl than are found in the general population.5. environmental levels) and health effects is available from ATSDR at: http://www. Biomonitoring Information Urinary TCPy levels reflect recent exposure.gov/toxpro2.

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Neurologic function among termiticide applicators exposed to chlorpyrifos. Environ Health Perspect 2004.niehs. Ricceri L. February 5. Acquavella JF. Bradman A. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Environ Health Perspect 2000. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats.15(4):297-309. Meeker JD. Barr D. Howell RJ. J Expo Anal Environ Epidemiol 1999. 1999. Hines CJ. Yang D. International Programme on Chemical Safety-INCHEM (IPCS). Barr DB. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Chlorpyrifos. Chapman P. Irish R. Bucelli R. Available at URL: http://ntp. Steenland K.93(1):105-113. et al. Pesticide residues in urine of adults living in the United States: reference range concentrations.114(5):746-751.5. Environ Health Perspect 2006b. Environmental Health Criteria 198. Harley K. Barr DB. Robson M.htm. Bruun D. Tate CA. Ryde IT. Bennett DH.6-trichloro 2-pyridinol in their everyday environments. Slotkin TA. Baker BA. Int J Hyg Environ Health 2001. Zhang J. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites.5. Jones PA.org/documents/jmpr/jmpmono/ v99pr03. et al. Croghan CW. Levin ED.71:99108. Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition. Environ Health Perspect 2005. J Expo Anal Environ Epidemiol 2005. Ryan L. Sanderson WT. Interim registration eligibility decision for chlorpyrifos.207(2):112-124. Kromhout H. Environ Health Perspect 2006a. Shealy DB. Barr DB. Gurunathan S. Freeman N.113(2):211-219. gov/ntpweb/index. Urinary pesticide concentrations among children. et al. Kinney P. Freshour NL. Seidler FJ. Head SL. Baker S. Environ Res 1995.114(10):1542-1546. Brain Res Dev Brain Res 2005. Weltzien E. Slotkin TA. Tsai WY. Alexander BH. Temporal variability of urinary levels of nonpersistent insecticides in adult men.15(3):271-281. Fenske RA. et al. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3. Morgan MK. Adgate JL.S.6-trichloro-2-pyridinol. Levin ED. Nolan RJ.204(2-3):175-180. Bravo R. Striley C. Robertson GL. Howard AS. Chlorpyrifos: pharmacokinetics in human volunteers. Jewell NP. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Chrislip DW. Ozkaynak H. Ann Occup Hyg 2007. Hill RH Jr. 2005.114(2):260-263. Slotkin TA. chlorpyrifos.51(1):53-65. Atlanta (GA).108(4):293-300. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Hardt J. Toxicol Sci 2006. Exposures of preschool children to chlorpyrifos and its degradation product 3.

Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns.Organophosphorus Insecticides: Specific Metabolites 01-007. Kinney PL. et al. Camann DE.gov/circ/2005/1291/. Fourth National Report on Human Exposure to Environmental Chemicals 139 . revised February 15. March 2006.pdf. Available at URL: http://pubs. Environ Health Perspect 2003.111(5):749-56.usgs. 1992-2001. 6/1/09 Whyatt RM. Available at URL: http://www. Pesticides in the Nation’s Streams and Ground Water. Barr DB. 1/14/09 U. The Quality of Our Nation’s Waters. Barr JR.gov/ oppsrrd1/REDs/chlorpyrifos_ired. February 2002. Geological Survey (USGS). 2007 [online].epa. Andrews HF.S.

In a nonrandom study of 140 adults and children in the United States. or for residential use.g. Coumaphos is not considered mutagenic and rated by the U.Organophosphorus Insecticides: Specific Metabolites Coumaphos CAS No.EPA. 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. weakness. It is not registered for uses on food crops. In the NHANES 2001-2002 subsample. 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. cholinergic effects. and certain other farm animals. EPA at: http://www. 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. Farm and animal workers may have higher exposures as a result of absorption through dermal and inhalational routes. and arthropod pests on beef cattle. Additional information about pesticides is available from U. Once absorbed. Also.epa.EPA. Coumaphos may enter the environment from spillage of animal dipping and spraying solutions (U. and alkyl phosphates. Biomonitoring Information Urinary levels of 3-chloro-7-hydroxy-4-methyl-2Hchromen-2-one/ol reflect recent exposure. At high doses. Olsson et al. Coumaphos is considered to be an organophosphorus insecticide of moderate-to-high acute toxicity in animal studies. paralysis. coumaphos is an organophosphorus insecticide that is used to control ticks.S. coumaphos and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. swine.S. and seizures. Toxic effects below doses that cause inhibition of acetylcholinesterase are unknown. Coumaphos is highly toxic to birds and aquatic invertebrates and moderately toxic to fish.. lice.EPA as not likely to be carcinogenic in humans (U. General population exposure to coumaphos is unlikely.gov/pesticides/. most of the measurements of 3-chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol in urine were below the limit of detection. and producing acute symptoms such as nausea. 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 140 Fourth National Report on Human Exposure to Environmental Chemicals . 2000). Animal studies indicate elimination in the urine over a period of a week.S.. First registered in 1958.200 μg/L for the non-Hispanic black subsample (CDC. though the 95th percentile was 0. 1998).S. resulting in excess acetylcholine at nerve terminals. e. Metabolic hydrolysis leads to the formation of 3-chloro-7-hydroxy-4-methyl2H-chromen-2-one/ol. 6-hydroxyl3-methylbenzofuran. reproductive effects such as decrease litter size are unlikely at doses that do not inhibit acetylcholinesterase (Astroff et al. vomiting. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). Human health effects from coumaphos at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Estimated intakes from diet and water have not exceeded recommended intake limits (U. it has limited use in controlling mites in honeybee hives. 56-72-4 General Information The chemical 3-chloro-7-hydroxy-4-methyl-2H-chromen2-one/ol is a metabolite of coumaphos. 2000). 2000). It degrades to chlorferon. mites.EPA. and other metabolites. phosphorothioates such as coumaphos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide. ornamentals. Coumaphos is generally immobile in soils and can persist for up to a year in some types of soils. though exposure through dietary meat and milk intake is possible.

670 (<LOD-1.S. see Data Analysis section) for Survey year 01-02 is 0. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2. Fourth National Report on Human Exposure to Environmental Chemicals 141 .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 . Survey Geometric mean (95% conf. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (<LOD-.380 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . < 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. 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 .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 . Survey Geometric mean (95% conf.270) < LOD 659 701 920 Limit of detection (LOD.200 (<LOD-.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.

Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos.376(6):808-815. Sadowski MA. Anal Bioanal Chem 2003.S.gov/oppsrrd1/ REDs/0018tred. 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. Environmental Protection Agency (U. Freshwater KJ. Nguyen JV. Atlanta (GA).S. Available at URL: http://www. Centers for Disease Control and Prevention (CDC). Reprod Toxicol 1998.12(6):619-645. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . EPA 738-R-00-010. 2005. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. EPA). U.pdf. Eigenberg DA. Barr DB. Olsson AO.epa. September 2000. Third National Report on Human Exposure to Environmental Chemicals.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. Before these restrictions. Survey Geometric mean (95% conf. seed and foliar applications are planned to be phased out (U. diazinon produced wild bird kills before use restrictions were in place. USGS.EPA.49 (<LOD-2. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. 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. Inhalational and dermal routes of exposure can be significant for pesticide applicators. but these uses have been phased out. Most granular formulations. vegetable. It is toxic to birds. since 2004. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. Once absorbed. aerial. and forage crops. 2004). in some pest strips. and other metabolites. Fourth National Report on Human Exposure to Environmental Chemicals 143 . dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). and particularly when it was ingested in granular form. diazinon was widely used in residential and garden application. < LOD means less than the limit of detection. 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.2 and 0. 1998.11) < 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.S. population from the National Health and Nutrition Examination Survey. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. It is also used for cattle ear tag applications to control flies and ticks and. 2004). about 13 million pounds of diazinon were used annually on agricultural sites in the United States. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. which may vary for some chemicals by year and by individual sample.S. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. in the past. 2007).7.45 (<LOD-3. Estimated intakes from diet and water do not exceed recommended intake limits (U.EPA. 1998). diazinon cannot be sold for residential use. an organophosphorus insecticide that is used to control insects on nuts. Prior to 2000. but is rapidly absorbed orally (IPCS. Diazinon is not well-absorbed through the skin. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks.S. 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. fruits.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD.

subsamples of NHANES 1999-2000 and 20012002. Thus. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.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. respectively.. 2003). Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown.. animal carcinogen. environmental levels) and health effects is available from ATSDR at: http://www. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate.gov/pesticides/. and producing acute symptoms such as nausea. 1998). In animals. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 144 Fourth National Report on Human Exposure to Environmental Chemicals . 2002).epa. The U. respectively (Baker et al. Survey Geometric mean (95% conf. In addition to being a human metabolite of diazinon.S. weakness.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.. or reproductive toxicant (IPCS.S. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants. 1986 Rajendra et al.S. cholinergic effects. vomiting. paralysis.72 (<LOD-4. Diazinon is not considered to be a mutagen. 1998). diazinon does not accumulate in tissues (IPCS. population from the National Health and Nutrition Examination Survey.S. and seizures. resulting in excess acetylcholine at nerve terminals. Seifert and Pewnim.Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1.45 and 1. 2000. In the U.76 (<LOD-3. 1992). Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. EPA at: http://www.html and from U. Diazinon has moderate acute toxicity in animal studies. in the 2001-2002 subsample (CDC. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al.e.EPA considers diazinon unlikely to be carcinogenic in humans. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1842 2534 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 1986. Olsson et al.49 μg/L. 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.. agricultural. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. In two nonrandom samples of United States adults and children.gov/toxpro2. and indoor applications have been documented.. At high doses.cdc. Intoxications in humans from intentional overdose. teratogen. Additional information about external exposure (i. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound.atsdr..

Diazinon. Cocker J. 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. Dumas P.10(6 Pt 2):789-798. Oloffs PC. Drobnis EZ. International Programme on Chemical Safety-INCHEM (IPCS). 4/7/09 Lu C. Available at URL: http://www. Toxicol Lett 2002. Kruse RL. Barr DB. Bravo R. Barr DB. Environmental Health Criteria 198.S. EPA). Biochem Pharmacol 1992. 1/14/09 U. 2006). In a small number of men visiting fertility clinics in Missouri and Minnesota.S. Redmon JB. Olsson AO. 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.epa. Environmental Protection Agency (U. Beeson MD. Sadowski MA. Third National Report on Human Exposure to Environmental Chemicals. revised February 15. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Garfitt SJ. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. 1998. Centers for Disease Control and Prevention (CDC).. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.9(2):117-131. J Expo Anal Environ Epidemiol 2000. In 54 Canadian greenhouse workers.376(6):808-815. Study for Future Families Research Group. Interim reregistration eligibility decision (IRED. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Pewnim T. May 2004. The Quality of Our Nation’s Waters. Effect of sublethal levels of diazinon: histopathology of liver. References Anthony J. Mason HJ. Nguyen JV. Banister EW.org/documents/ehc/ehc/ehc198. Swan et al. Seifert J. Toepel K. U. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. 2005. Diazinon. Available at URL: http://www. Oloffs PC.S. Environ Health Perspect 2003. Semen quality in relation to biomarkers of pesticide exposure. Pesticides in the Nation’s Streams and Ground Water. Ann Occup Hyg 2006. Irish R. Rajendra W. Environ Health Perspect 2006. Liu F. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al.Organophosphorus Insecticides: Specific Metabolites 2005). Noisel N.usgs. Geological Survey (USGS). Baker SE. Available at URL: http://pubs. et al. Swan SH.37(4):501-507.gov/circ/2005/1291/. 2007 [online]. Driskell WJ.gov/ oppsrrd1/REDs/diazinon_ired. Brunet RC. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. Drug Chem Toxicol 1986. Needham LL. Bouchard M. Anal Bioanal Chem 2003. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al.htm. Banister E. Jones K. In 23 children.134(1-3):105-113. 2006). March 2006. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids.44(11):2243-2250. Bull Environ Contam Toxicol 1986.50(5):505-515. Carrier G.114(2):260-263. EPA 738-R-04-006.pdf.111(12):1478-1484.. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Atlanta (GA). 1992-2001. Barr DB. Barr DB. Fenske RA. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon.inchem.

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

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

Erratum in: Toxicol Sci 2003 Aug. Prasad SB. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. MacIntosh DL. Trzeciak A. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues.112(10):1116-1124.77:1009-1010.15(2):164-171. metabolite clearance.org/documents/jmpr/jmpmono/v2003pr06. Mutat Res 2002. Toxicol Sci 2003 May. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. 6/1/09 U. Dinoff TM. J Expo Anal Environ Epidemiol 1999. Griffith W. Bradman A. International Programme on Chemical Safety-INCHEM (IPCS). 2005. Goldhaber M. Barr DB. J Expo Anal Environ Epidemiol 2005. Giri S. Gosselin NH. Weltzien E.usgs. Flessel P. Jewell NP. Eskenazi B. Reproductive outcome in women exposed to malathion. Quintana PJ. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Grether JK.pdf. EPA 738-R06-030. Hooper K. Third National Report on Human Exposure to Environmental Chemicals. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Lu C. Giri A.epa. The Quality of Our Nation’s Waters. EPA).Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Albertini RJ. Environ Health Perspect 2006.S. Available at URL: http://www. July 2006. et al. Petitti D. A longitudinal investigation of selected pesticide metabolites in urine. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. et al. Samuel O.S. Available at URL: http://www. Am J Epidemiol 1990. March 2006. Clayton CA. and cholinesterase status of date dusters and harvesters in California. Cancer Res 1996. Rappaport E. Geological Survey (USGS). Harley K. Freeman NC.74(2):following table of contents. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . Bouchard M. Irish R. Swan SH. Curl CL.38(4):546-553. Neutra R. Barr DB.109(6):583-590.S. Reregistration eligibility decision (RED) Malathion.73(1):182-94. Eberly LE. Environ Health Perspect 2004. Pluth JM. et al. Harris JA. O’Neill JP. Dumoulin MJ. Toepel K. Lu C. Arch Environ Contam Toxicol 2000. Available at URL: http://pubs. Atlanta (GA). Bravo R. Environ Health Perspect 2001. Pesticides in the Nation’s Streams and Ground Water. Malathion deposition. 4/7/09 Kissel JC.inchem. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.gov/oppsrrd1/REDs/ malathion_red. Blasiak J. U.gov/circ/2005/1291/. Lioy PJ. Am J Public Health 1987. Jaloszynski P. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.9(5):494-501. Sharma GD.56(10):2393-2399. Szyfter K. Centers for Disease Control and Prevention (CDC). revised February 15. 2007 [online]. Kedan G.514(1-2):223231. Brunet RC. Needham LL. 1992-2001. Mutat Res 1999. htm. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.114(2):260-263. Hammerstrom KA. Thomas D. Environ Mol Mutagen 1993. Environmental Protection Agency (U.22(1):7-17. Barr DB. Krieger RI. Carrier G. Ryan PB. Genetic toxicity of malathion: a review. Nicklas JA. Hertz-Picciotto I. Fenske RA.132(4):794-795. Barr DB.445(2):275-283. Malathion (addendum).

05) 4.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .32-3.850) < LOD .60-19.92-2.33 (1.50-9. Methyl parathion is not registered for residential use in the United States..700 (<LOD-. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. 2002.72 (3.10-1.910) < LOD < LOD < LOD 1.50 (1.13-1. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.21-1.S.40-4. all registered uses were voluntarily cancelled (U.70-3. and to a lesser extent.0) 3.45 (1.62 (1.70-6.70 (2.70-6.71 (2.EPA. It had been applied to cotton.300-.37) 2.61) < LOD 1.16) < LOD 1.44) 2.70 (<LOD-3.40-4.70-6.67) < LOD 1.02-6.90-11.48) 90th 2.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .50) 3.27) 2.0) 3. and of the chemical nitrobenzene.S.09-1.58) 3.50 (1.50 (1.22-3.60-5.66 (2.80 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.41-4.30-16.90 (1.60 (4. 2006).10) 4. Methyl parathion has low water solubility.12) < LOD < LOD 1. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.28-4.21 (2. binds tightly to soils resulting in low leachability. fish.50) 3.92) 5. and eliminated rapidly from the body after absorption (Kramer et al.40) 2.70 (2.74) 5.50) 1.46 (3.67 (1.32 (1.49 (1.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.37-4.70 (3.70) 2.910) < LOD < LOD . population from the National Health and Nutrition Examination Survey.34 (3. Given its limited use.01) 4.730 (<LOD-.860 (<LOD-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.28 (1.30-3.80) 2.EPA.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 1.69) 4.70) 2.89 (2.57) 1.19 (.10 (3.32-1. pulmonary.61) < LOD 1.47) 2. In the 1990s.33) 2.01-4.00) 3.1. with limited applications in agriculture.70 (2.790 (<LOD-.37-2.70-3. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.10 (<LOD-6.32-1.990-1. peak domestic use was as high as 5-6 million pounds per year. Methyl parathion use is highly restricted.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .15-3. which may vary for some chemicals by year and by individual sample.36-1.11) 2.0) 4.45) 5. In animal studies. Fourth National Report on Human Exposure to Environmental Chemicals 149 .60-24.298-00-0 Ethyl Parathion CAS No. 2000).0) 3.50) 2.20 (2. and aquatic invertebrates.40) 4.79) 4.00 (2.60) 1.30 (2.0) 3. Estimated intakes from diet and drinking water have been below recommended limits. Both are toxic to birds.50-14. ethyl parathion. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.20-5. 1977). and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. first registered in 1948. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.60-36. more slowly absorbed through the skin..91-3. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.40 (1.00 (2.11-4.940 (<LOD-2.910) < LOD .69 (2. 2007). and oral routes can occur in pesticide and agricultural workers (Muttray et al. Once absorbed. methyl parathion was rapidly absorbed after ingestion.10) 22. Ethyl parathion. Increased risk of exposure via dermal. 2003).0) 2.40-3.18-3.85 (2..20 (<LOD-2.10 (3. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30-5. Morgan et al. Many previous registered agricultural uses of methyl parathion have been cancelled (U.20) 5.57-4.01) 695 660 518 679 603 941 Limit of detection (LOD. and has a short half-life in soils and on plants.770 (.80 (2.80 (2.10-11.S. Methyl Parathion.28 (1.70) 2. but by 2003.50 (2. was once a restricted-use insecticide with limited applications on certain agricultural crops.50 (1.8 and 0. on cereal grains.40) 1.50 (2.26 (1.71 (3.37-4.0) 3.30 (1.90-9.0 (3.

730-1.7) 3.78) 2.3) 2.30-1. At high animal doses of methyl parathion.33-6..60 (1.13-12. methyl parathion.970 (.800-1. ethyl parathion.970 (.97 (2.95) 1. U.29) 1.840 (.33-3..61) 4.44-3. EPA at: http://www.88) 1. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.EPA considers methyl parathion unlikely to be carcinogenic to humans.55 (<LOD-3.55) 2. and other metabolites. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.07 (1.96 (1.4 (3.92 (2.440 (<LOD-.78-2. 1995).S. Methyl Parathion.500) < LOD < LOD . Orsorio et al.23) 1.35-3.11-4.310-.83 (1.01 (2. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.31-3.43) 4.9) 1.cdc.90 (1.20) .96 (1.09) 2.29) 2.15-10.21-21.17-4. 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.930 (.39) 1. 2004).76-14. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.87 (1. Parathion and methyl parathion have high acute toxicity in animal testing.16-4.26) 17.720-1.930 (.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .59 (1.94-47. 1991). Slotkin et al.950) < LOD .640) < LOD < LOD 1.20 (3.20) 3.530) < LOD < LOD < LOD .30) 3.25 (2.84) 3.26 (1. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.720 (<LOD-.05) 4.07) 2.93 (2. accidental exposure.88 (1.38-3.1) 2.79) 1.98-7. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.60-2.80 (1.29 (2.21) 1.940 (<LOD-1. cholinergic effects.790-.04 (2.Organophosphorus Insecticides: Specific Metabolites Metabolites”).82 (2.. 1978. 2005.78 (2.56-2. population from the National Health and Nutrition Examination Survey. 2004).2) 2.23) size 1989 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th . environmental levels) and health effects is available from ATSDR at: http://www.e.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.10 (1. Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion. and unintentional acute or chronic high-level occupational exposure (Hill et al.71 (1. gov/toxpro2. Additional information about external exposure (i.690-1.67-2. 2006.11) 1.91 (1.680 (<LOD-1. In addition to being a metabolite of methyl and ethyl parathion. and seizures.html and from U.00 (1.86 (2.57) 6.82) < LOD .80 (1.00 (1.08 (1.89 (2. teratogenic..97 (<LOD-4.01-3.14-3. weakness. Jaga and Dharmani.73 (1. and producing acute symptoms such as nausea.72-2.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. resulting in excess acetylcholine at nerve terminals.S.2) 2.epa.44-3..870) < LOD .57-7.77-7.850-1. Survey Geometric mean (95% conf.. Zurich et al.70) 3.31) < LOD .67 (3.atsdr.94-4.39 (1.10) 90th 2.48-4.33-3.71) 1.04) 1.35-3. The metabolite.400 (<LOD-. does not inhibit acetylcholinesterase enzymes. WHO.25) 1..57-2. paranitrophenol.880 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.S.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Thus. but lists ethyl parathion as a possible human carcinogen. 150 Fourth National Report on Human Exposure to Environmental Chemicals . 2006.08-3.78-2. In large doses. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.17) .980 (.79 (1.. Karanth and Pope et al. 1990.830-1. 1995.08) < LOD . Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.60) 2.13) 4.91) 1.97-10. Methyl parathion is not considered genotoxic.37-1. vomiting.370 (<LOD-.790-1. paralysis.430 (.89 (2. 2003. Lores et al.41-2.01 (.15) 3. gov/pesticides/.00) 2.540) < LOD .

Pesticide residues in urine of adults living in the United States: reference range concentrations.. Kissel JC. and levels were similar or slightly lower that those in a small convenience sample of the U. 1995..Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure.. Pesticide workers may have much higher levels following pesticide applications.14(4):213-216. McCann et al. Centers for Disease Control and Prevention (CDC). 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. Head SL. 2005). Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Third National Report on Human Exposure to Environmental Chemicals. Bradway DE. Kramer RE. 1995).htm. Rubin et al. Baker SE. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. 2005..15(2):164-171. Neurotoxicol Teratol 2003. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. International Programme on Chemical Safety-INCHEM (IPCS). population (Olsson et al. Environ Health Perspect 2002. Morgan DP. Pharmacokinetics of methyl parathion: a comparison following single intravenous. Slach EF. Leng G. Rockhold RW. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lin LI. Karanth S. Methyl parathion: an organophosphate insecticide not quite forgotten. Pope C. 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. Occup Environ Med 1999. Griffith W. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Moseman RF. J Anal Toxicol 1990. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Barr DB. 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. 2004). J Expo Anal Environ Epidemiol 2005. oral or dermal administration. et al. Curl CL. 1999). Head SL. Lores EM. Environ Res 1995. CDC.. 2002). Arch Environ Contam Toxicol 1977. Jewell NP. 2005). Bailey SL. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. et al. Bradman A. Dharmani C. Role of individual susceptibility in risk assessment of pesticides. Gregg M. Pathak S. Lewalter J. Shealy DB. et al. Turner WE. 2005. Environ Health Perspect 2002. Alley CC. Toxicology 2005.110 Suppl 6:1085-1091.. Lu C.9:311-320.215(3):182-190. Hryhorczuk DO. Ashley DL. Runkle KD. Barr DB. In a study of workers who handle parathion. 2002. Moomey CM. Costa LG. Eskenazi B. Needham LL. Chicago area methyl parathion response. McCann KG. 2005. References Barr DB. Barr DB. DiPietro E.. McClure PC. Harley K.inchem. Fourth National Report on Human Exposure to Environmental Chemicals 151 .5 mg (500 µg)/g creatinine for workers at the end of shift. Hill RH Jr. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation.110 Suppl 6:1075-1078. ACGIH recommends a BEI of 0. Baker S. Barr JR.56(7):449553.112(10):1116-1124.71:99108. Arch Environ Health 1978. et al. Wellman SE. Clark JM. et al.org/documents/jmpr/jmpmono/v95pr14. general population (CDC. Kedan G.S. Rev Environ Health 2006. 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. Parathion-Methyl (addendum). Atlanta (GA). Environ Health Perspect 2004. Hetzler HL.S. J Biomed Sci 2002. Cline RE. and many residents were symptomatic (Barr et al. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Hill et al. Laboratory investigation of a poisoning epidemic in Sierra Leone. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Baker RC. 2002.25(5):599-606. Available at URL: http:// www.21(1):5767.6(2-3):159-173. Giordano G. Weltzien E. 4/7/09 Jaga K. Hill RH Jr. Guizzetti M. a range of values several hundred times higher than levels found in the U.33(5):270-276.

gov/circ/2005/1291/. Interim reregistration eligibility decision (IRED) for Methyl Parathion. 5/19/09 Zurich MG.Organophosphorus Insecticides: Specific Metabolites Muttray A.S. 0153. Ryde IT. Hill RH Jr. gov/oppsrrd1/REDs/methylparathion_ired. Available at URL: http://pubs. Barr DB.int/water_sanitation_health/dwq/chemicals/ methylparathion. Toxicol Lett 2006. Nguyen JV. EPA).110 Suppl 6:1047-1051.S. Jung D.376(6):808-815. Available at URL: http://www. 1992-2001.162(2-3):219-224. Geological Survey (USGS). Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Available at URL: http://www. Dunlop B.usgs. 2007 [online]. Facts. Yacovac R. Honegger P.D.who. Kieszak S. Rosenberg J. Schilter B. Case No. Backer G. Letzel S.epa. 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. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. May 2003. R. External and internal exposure of wine growers spraying methyl parathion. Mengle DC.pdf. Osorio AM. The Quality of Our Nation’s Waters. Tate CA. Toxicol Appl Pharmacol 2004. U. Hill G. Seidler FJ. Monnet-Tschudi F. WHO/SDE/WSH/03. Olsson AO. Environ Health Perspect 2006.pdf. March 2006. Rubin C. Levin ED. Esteban E. Costa LG. revised February 15.S. 1/12/07 U.04/106. Anal Bioanal Chem 2003. EPA). Ethyl parathion.201(2):97-104. EPA-738-FOO-009. Sadowski MA. Environ Health Perspect 2002. pdf. Environmental Protection Agency (U. Slotkin TA.E. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. 1/14/09 U.114(10):1542-1546. 1995-1996. Methyl parathion in drinking water. et al. Ames RG.S. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Environmental Protection Agency (U.gov/oppsrrd1/REDs/factsheets/0155fct. 2004. September 2000. Available at URL: http://www.epa. Am J Ind Med 1991. Pesticides in the Nation’s Streams and Ground Water. Ohio.20(4):533-546.S. 6/1/09 World Health Organization (WHO). Investigation of a fatality among parathion applicators in California.

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

Survey Geometric mean (95% conf.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.21) < LOD .780 (<LOD-1.300-1.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .250 (<LOD-.00) 669 687 929 < 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th .55) .27) . which may vary for some chemicals by year and by individual sample.850 (.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.470 (.S.430 (<LOD-.780 (.610 (<LOD-1.840 (.15) < LOD . see Data Analysis section) for Survey year 01-02 is 0.950) < LOD < LOD 1.700-.840) 669 687 929 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th .200-.64) .780 (.780 (<LOD-1.94) .210 (<LOD-.210-1.740 (.500 (.670 (<LOD-1.S.17 (.2.770) 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 .820) < LOD < LOD .760 (<LOD-.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .580-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 154 Fourth National Report on Human Exposure to Environmental Chemicals .460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .740-1.210-.700-1. population from the National Health and Nutrition Examination Survey. 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.680 (<LOD-.31) .07) .410 (<LOD-1.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.

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

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

Ose K. Abell AD. motor activity. Caudle WM.html. Okuno Y. Moniz AC. 2006. Wolff MS. Leng G. et al. Kim HS. J Environ Monit 2006. J Reprod Dev 2004.cdc. 2004.. Shin JH. Toxicological profile for pyrethrins and pyrethroids. Varoli FM. Ranft U. 2001. Cruz-Casallas PE.gov/pesticides/ and from ATSDR at: http://www. Hu JY. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Bernardi MM. Garey J. Song L. Neurosci Lett 2001. Pauluhn J. Wang SL.205(6):459-472. Kunimatsu T..atsdr. Pogo BG. Ray et al. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. 2005). and striatal dopamine levels in male and female rats. Shaw IC. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Leng G. 2003.. EPA at: http://www. epa.62:101-108. 2002). 2006. 2006). Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.. Leng G. Estrogenicity of pyrethroid insecticide metabolites. cdc. 2003. Moniz et al. Shukla Y. et al. 1999. In developing rodents. Regul Toxicol Pharmacol 2002. Wieseler B. bioallethrin and deltamethrin.108(1):78-85.27(4):609-614. Berger-Preiss E. Leng A. Effects of prenatal exposure to deltamethrin on forced swimming behavior.. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Garey and Wolff. Int J Hyg Environ Health 2002. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Sunami O. Neurotoxic effects of two different pyrethroids. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Guillot TS. 2000.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects.23(6):665-673. choreoathetosis. 2003.107(3):173-177. Idel H.S. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. WHO. Kamita Y. Elwan 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. Kunimatsu et al. Seth PK. Pyrethroid pesticide-induced alterations in dopamine transporter function.. Kim et al.251(3):855-859. McCarthy et al.300(3):161-165.8(1):197-202. Additional information about pesticides is available from U. Toxicol Appl Pharmacol 1991. Hu et al. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. 2002). [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. 2001. Idel H. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO.. Eriksson P. September 2003. Kim IY. Neurotoxicol Teratol 2005.. Toxicol Appl Pharmacol 2006. dopaminergic. 2003.gov/toxprofiles/ tp155. References Agency for Toxic Substances and Disease Registry (ATSDR).html. Zhao RC. Salzgeber SA. Fredriksson A. Miller GW. and seizures (ATSDR. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. et al. Elwan MA. 1998. Agrawal AK. Yamada T. Go et al. 2005). Soderlund et al. 1991. Biochem Biophys Res Commun 1998. Yang J. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid.atsdr. Florio JC. Thomson BM. Shafer. Xenobiotica 1997.. 2002. Generally. tremor. Adhami VM.50(2):245-255. Available from URL: http://www..1/15/09 Aziz MH. Kuhn K. Sugiri D. hypersensitivity. 2005). Wolff MS. Garey J. fenvalerate. 2005). Eriksson and Fredriksson. Lazarini et al. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Kuhn KH. Richardson JR. Lee SJ. Spinosa HS. salivation. Levsen K. neurochemical changes in cholinergic. Chen JH. Neurotoxicol Teratol 2001. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Kim TS. Environ Health Perspect 1999. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al.35(2 Pt 1):227-237.gov/toxpro2..27(12):1273-1283.. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Go V.8(1):18-21. Lewalter J. and permethrin) in the Hershberger and uterotrophic assays. Lazarini CA. Bernardi MM.. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Lemonica IP. Bull Environ Contam Toxicol 1999. Kang IH.211(3):188-197. Fourth National Report on Human Exposure to Environmental Chemicals 157 . et al. Indoor pyrethroid exposure in homes with woollen textile floor coverings. McCarthy AR. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. In California.

19962002. sumithrin synthetic pyrethroids for mosquito control. Pyrethroid illnesses in California.171:3-59. and therapy.S. Soderlund DM.S.gov/oppsrrd1/REDs/ factsheets/permethrin_fs. Pesticide and Evaluation Scheme. Sargent D. Available at URL: http://www. March 2006. O’Malley M. pdf. Available at URL: http://www. Pyrethroid insecticides: poisoning syndromes.htm. Piccirillo VJ. Permethrin. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .gov/oppsrrd1/REDs/cypermethrin_red.who. Pesticides in the Nation’s Streams and Ground Water.pdf. synergies. Meyer DA.S.38:95-101.S. April 2002. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.10. Lesser JE. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs.gov/ circ/2005/1291/.S.epa. resmethrin. Safety of pyrethroids for public health use. 5/26/09 Woollen BH.epa. Toxicology 2002.usgs. Available at URL: http://pubs. Marsh JR. J Toxicol Clin Toxicol 2000. Crofton KM. Laird WJ. Environmental Protection Agency (U. Sheets LP. World Health Organization (WHO). U.htm. June 2006a.epa.S. et al. 2007.113(2):123-136. Mullin LS. 5/26/09 U. 1992–2001. 2005. Available at URL: http://www. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). EPA). Forshaw PJ. June 2006b. Geological Survey (USGS). 5/26/09 U.S. 5/26/09 U. Xenobiotica 1992. Reregistration Eligibility Decision for Cypermethrin. Environmental Protection Agency (U. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration.22(8):983-991. Revised February 25. Shafer TJ. Clark JM. Available at URL: http://whqlibdoc.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Spencer J. Rev Environ Contam Toxicol 2006. Environmental Protection Agency (U. EPA). Environ Health Perspect 2005.Pyrethroid Pesticides Ray DE. EPA).186:57-72.

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

Survey Geometric mean (95% conf.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. 160 Fourth National Report on Human Exposure to Environmental Chemicals .S. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. population from the National Health and Nutrition Examination Survey. 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.2.2 and 0. < LOD means less than the limit of detection. 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.

Fourth National Report on Human Exposure to Environmental Chemicals 161 .S. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 830 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 700 594 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid (creatinine corrected) Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Rev Environ Contam Toxicol 2006. 19962002.109(3):213-217.Pyrethroid Pesticides References Baker SE.77(1):67-72.186:57-72. Williams RL. J Expo Anal Environ Epidemiol 2003.13(2):112-119. Angerer J. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Becker K. Centers for Disease Control and Prevention (CDC). Barr DB. O’Malley M. Environ Health Perspect 2001. Spencer J. Heudorf U. Kolossa-Gehring M. Sugiri D. Drexler H. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Atlanta (GA).209(3):221-233. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Seiwert M. Third National Report on Human Exposure to Environmental Chemicals. Schulz C. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Idel H. 2005. Angerer J. Butte W. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Heudorf U. Hoppe HW. Int Arch Occup Environ Health 2004.206(2):85-92. Angerer J. Krieger RI. Ranft U.46(3):281-288. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Pyrethroid illnesses in California. Ball M. et al. Leng G. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Angerer J. Arch Environ Contam Toxicol 2004. Int J Hyg Environ Health 2006. Bernard CE.209(3):293-299. Int J Hyg Environ Health 2006. Olsson AO. Hadnagy W. Berger-Preiss E. Int J Hyg Environ Health 2003. Heudorf U.

570 (.140 (<LOD-.380-.260 (.680 (. 1999).77 (.380) .580) 1.220-.690) .960 (. The presence of cis-3-(2.210) 90th .120-.740) 1.920) 1.410) .330) .890 (.850 (.170 (. the presence of trans-3-(2.370-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1999).2-Dichlorovinyl)-2.510 (.110-.210-.1.530 (.68 (.490-1.160 (.710) .or trans-3-(2.200) < LOD < LOD < LOD .44 (. 1985.80) . which may vary for some chemicals by year and by individual sample.and trans-isomers. cis-permethrin.890 (.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.490-.230) .202 (.670-1.200-.1 and 0.600) .490-1.740 (.900 (. Kuhn et al. Generally.670-2.670 (.340) .300 (.120-.870) 1.600-1.790 (.110-.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.15) .820 (.240) .155-.13 (.510 (.500 (.07 (. and ciscyfluthrin.460-.120-.490-.240) .680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .730 (.510 (.640 (.2-dichlorovinyl)- CAS No.700) .220-. In the body.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.200 (.68) .400-.11) . but it can also reflect exposure to cis-3-(2.420-.180 (.110 (<LOD-.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides. population from the National Health and Nutrition Examination Survey.380-.580-1. Similarly.24) 1.2-dichlorovinyl)2.650-1. but can also reflect exposure to trans-3(2.270 (. more of the trans-metabolite than Urinary cis-3-(2.520) .21) .28) 671 680 518 701 591 957 Limit of detection (LOD.12 (. trans-permethrin.770-1.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.410) .200) .28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .270 (.160 (<LOD-.250-.43) .880 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.550) .50) .280 (.250 (.200-.270-.380 (. 52315-07-8 CAS No.08) .300-.2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.440 (.910-5.35) .790-1.460 (.2-dichlorovinyl)-2.630) .790-1.180) . Survey Geometric mean (95% conf.310) .47 (.470-1.68359-37-5 Cypermethrin Permethrin CAS No.340-.140 (.680-3. Cyfluthrin.53) .730 (.740-2.630-. transcypermethrin and trans-cyfluthrin. The chemical trans-3(2.300 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.2dichlorovinyl)-2.120-.300-.270 (.200) .150 (.262) * * * < LOD < LOD .790) .280-.500 (.710-1.220) . Kuhn et al.220-.770) .740-1.380-.780) .08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * . The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.430-.630) .350) . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. Biomonitoring Information Urinary levels of cis.200-.220-. cis-3-(2.32) . < LOD means less than the limit of detection.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 .110-.610) .210) .600 (. Fourth National Report on Human Exposure to Environmental Chemicals 163 .570-.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.35) 1.S.330 (. 1985.. ciscypermethrin and cis-cyfluthrin.460-1. trans-cypermethrin.730 (. and trans-cyfluthrin.950-2.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.2-dichlorovinyl)-2.68) .54) ..340) .670-1.630 (. cis-cypermethrin.2dichlorovinyl)-2.370 (.470 (.610) .160 (.

though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.840 (.250-. 2006) and 1177 urban adults and children (Heudorf et al.340) .430-1.2dichlorovinyl)-2.450-.37) .440 (.150-. 2002). interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300 (.390-.11) .220) .150-. 2005) In a small group of indoor pest-control operators.390-.880) .170 (.400-1.380) .560) 1.370-.240 (<LOD-.29 (.250) .550) .190) .200) .2-dimethylcyclopropane carboxylic acid did not increase.580) .250) 90th . These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.680-1.540) . post- Urinary cis-3-(2.420 (.370-.270) .440 (.700-2.200-.640-1.780) 1.190) .250 (<LOD-.200-.290) .340) .2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC..190 (.560) ..920 (.300) . In a study of volunteers.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC. In a study of urban residents in Germany (Berger-Preiss et al.220 (.350 (.12 (.540 (.810 (.890) ..260) .200 (.830) .440-. 2005).380-.360-1.750 (. median urinary levels of trans-3-(2. Studies in Germany of 396 children and adolescents (Becker et al.300 (.640 (.12-2. Lu et al.and trans-3-(2. 2006.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . representative NHANES 2001-2002 subsample (CDC. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.380 (.570) .11) .450-1. 2006.430-.03) 1.280 (.2dichlorovinyl)-2.370-.320-..210-.11 (.2-dichlorovinyl)-2.800 (. the median and 95th percentile of urinary levels of cis-3-(2.550 (.138 (.250) .2-dichlorovinyl)-2.160 (<LOD-. 2005).. 2002).59) .350) . 2001) showed urinary levels of cis..80) .170 (.24) .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 .680-1.680 (.640) 1.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .580-1.530 (.340-. Schettgen et al.230-..11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .2-Dichlorovinyl)-2.500 (.59 (1.440-. Survey Geometric mean (95% conf. 2006).710 (.11) 1. 164 Fourth National Report on Human Exposure to Environmental Chemicals . 2006).Pyrethroid Pesticides 2.640-.33 (. Cyfluthrin.600 (..890 (. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al. In the same residents.230-.550) .180 (.220 (. 2003).67 (.700) .300) .2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates. urinary levels of cis-3-(2.700) ..250-. In these volunteers.430 (.300-.540 (.182) * * * < LOD < LOD .59) .170) < LOD < LOD < LOD .840 (.750-1.104-.S.250-.780 (.590) .140-.33) . 2001.150-. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.270-. 2004).and trans-3(2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin. population from the National Health and Nutrition Examination Survey.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.260 (.390 (.21) .080-.510-1.290 (.180-.S. Other studies have provided evidence that urinary levels of cis.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.260 (.120 (.320) .260 (.710-3.230 (.270) . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.590 (. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC. urinary trans-3-(2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.270 (.410) .2-dichlorovinyl)-2.280-.67) .400 (. 2003).640-1..49) .470-1.550-1. 2005).550-1. 2005).2-dichlorovinyl)-2.290-.450 (.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.31) .900 (.690-1.290) .130-. 2004.530 (.230-.260-..

490-1.10) 2.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .or trans-3-(2.77 (1. Finding a measurable amount of cis.66) .560 (.25-3.69 (1.01 (1.64-4.570) 90th 1.470 (.500 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.750) .490 (<LOD-.20 (.920-1.2-Dichlorovinyl)-2.01) 4.09 (. Urinary trans-3-(2.and trans-3-(2.68) 1.940 (.670) .470 (<LOD-.43) 2.17 (. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.39 (1.63) 1.850-1.77) 1.95) 2.85) 4.37 (1.23) 2. trans-Cypermethrin.2dichlorovinyl)-2.42) 1.90) 1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.62 (1.620) < LOD 2.14-6.55-3.910-1.14) 1.560 (.54 (1.2-dichlorovinyl)-2. Survey Geometric mean (95% conf.28 (2.580 (.700) .500-.35) 1.77) 2.08-4.91 (1.400-.500) .520) .54) 4.49-3.68) 2.760) .2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.48) 4.56) 2.710 (.55-5.26 (.49-3.2-dichlorovinyl)-2.530) .11-2. population from the National Health and Nutrition Examination Survey.56 (1.08) 1.97-11.S.410 (<LOD-.68-2.410-.23 (.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .460-.700-1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.19 (2.420 (<LOD-.55-4.63) 1.60) 1.670) .830-1. 2005).14-2.840-1.680-1. The maximum post-application urinary levels.13) .49-5.20 (.94 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.520-.780 (.39-5. < LOD means less than the limit of detection.84 (1.76-4.440 (<LOD-.410-. 2005).7) 2.22 (1.76-3.60-4.17-1.60) .27 (1.25 (1.03-1.03-1.11-1. which may vary for some chemicals by year and by individual sample.17 (. Biomonitoring studies on urinary levels of cisor trans-3-(2.70) 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 .20 (.400 (<LOD-.480-.4 and 0. however.59 (1.970 (.12-6.460-.41-14.19 (3.68-3.19) 1.81) 2.410 (<LOD-.910-1.07-3.69) 1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.89 (2.810-1.40 (1.5) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.Pyrethroid Pesticides application median urinary levels of summed cis.860) .730) .08-6.95) 3.56) 2.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .50 (1.2-dimethylcyclopropane carboxylic acid provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pyrethroid pesticides than are found in the general population.68) 1.550 (.660) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.87 (1.16) 1.610) 1.07 (1.800-1.66) 691 680 518 690 595 954 Limit of detection (LOD.28 (1.4.560 (.56 (1.42 (2. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.820) .41 (1. Fourth National Report on Human Exposure to Environmental Chemicals 165 .

166 Fourth National Report on Human Exposure to Environmental Chemicals .11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .750) .520 (<LOD-.28) 2.48 (1.29) 1.880 (<LOD-1.770) < LOD 2.89) 2.08 (.70 (.880 (.60) 2.15) 2.86 (2.65 (2.500-.800-1.3) 2.34-3.57) 3.67 (2.570 (.15-3.22-2.780) 90th 1.00) 5.970 (.720-1. trans-Cypermethrin.08 (.730) .36 (1.760 (.91 (1.64 (1.07-1.87 (1.15) 3.540) .580 (.27-2. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.00 (1.440-.570-.91-11.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.850) .30-6.22) 1.74) 2.39) 1.930-1.900 (<LOD-1.720-1.820-2.410-.00) 1.55 (2.610-.470 (.19 (1.12 (.15 (1.02-1.Pyrethroid Pesticides Urinary trans-3-(2.37 (1.07-2.31 (2.60 (1.91) 1.16 (1.570 (<LOD-.80) 1.11) .74) .00-5.850) 1.34-4.56-2.07-3.00) 1.780) .13) 1.S.36) 2.87-8. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.780 (<LOD-.30-3.26 (1.720 (<LOD-.40-2.33-1.13) .45-2.65) 1.19) .480-.800-1.20 (1.39 (1.15-3.530 (<LOD-.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .15-3.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.87) 1.27-2.41) 1.87-3.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2-Dichlorovinyl)-2.47-2.670) .42) 1.530 (.12-1.700 (.31) 1.850-3.22-1.35 (1.87) 1.47-2.10) size 1976 2524 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th . and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.07) 2.75 (1.47 (1.560 (.48-2.60) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.68) 3.44) 2.580) .700 (.45 (1.470-.98 (1.35) 1.56-5.33 (1.57 (1.07) 2.55 (2.61) 1.31 (.55 (2.700-.640) .42 (.20-2.880-1.33-2.660) .740) .81 (2.56 (1.

Heudorf U. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Leng G. Ranft U. Idel H. Heudorf U. Ball M.77(1):67-72. Third National Report on Human Exposure to Environmental Chemicals. Int J Hyg Environ Health 2002. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Angerer J. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Idel H. et al. Atlanta (GA). A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Bull Environ Contam Toxicol 1999. Int J Hyg Environ Health 2006. Kolossa-Gehring M. Int J Hyg Environ Health 2006. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.134(1-3):141-145. Leng G. Sugiri D. Centers for Disease Control and Prevention (CDC).205(6):459-472.Pyrethroid Pesticides References Becker K. Schettgen T. Angerer J. Permethrin and its two metabolite residues in seven agricultural crops.209(3):293-299.68(6):1160-1163. Int J Hyg Environ Health 2003. Drexler H.109(3):213-217.114(9):14191423. Bravo R. Angerer J. J AOAC 1985. 2005. Berger-Preiss E. Angerer J. Seiwert M. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Environ Health Perspect 2001. Berger-Preiss E. Lu C. Levsen K. Leng G. Barr DB. Int Arch Occup Environ Health 2004.62:101-108. Kuhn K. Hadnagy W. Wieseler B. Heudorf U.206(2):85-92. Ranft U. Int Arch Occup Environ Health 2003. Bartell S. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Schulz C. Hardt J. Environ Health Perspect 2006. Biological monitoring of workers after the application of insecticidal pyrethroids. Hoppe HW. Sugiri D. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Angerer J. Angerer J. Drexler H. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.76(7):492-498. George DA. Heudorf U. Butte W. Pearson M. Idel H. Indoor pyrethroid exposure in homes with woollen textile floor coverings.209(3):221-233.

2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS. 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. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2-dibromovinyl)-2.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid of 0..2-dibromovinyl)-2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 168 Fourth National Report on Human Exposure to Environmental Chemicals . 2005). 2005). 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample. Urinary levels for adults and children in these studies were similar (Heudorf et al. 2001. 2001) showed that urinary levels of cis-3-(2. Outside the U. 52918-63-5 General Information Cis-3-(2. Baker et al. Deltamethrin can degrade to cis-3(2.2-dibromovinyl)2. Studies in Germany of 396 children and adolescents (Becker et al. Following residential spraying with deltamethrin for malaria protection in Mexico. deltamethrin has been used against mosquitoes that carry malaria.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.. (2004) reported a geometric mean concentration of cis-3(2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect. Finding a measurable amount of cis-3-(2. in some situations replacing the use of DDT.2-dibromovinyl)-2. urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.2-dibromovinyl)-2. 2005)... Thus.2-dibromovinyl)-2. 1990). In the NHANES 2001-2002 subsample.5 μg/L) than the detection limit (0.S.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. Biomonitoring Information Urinary levels of cis-3-(2.39 µg/L. in detection of cis-3-(2.1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dibromovinyl)-2.. 2006) and 1177 urban adults and children (Heudorf et al.2-dibromovinyl)-2. mean peak urinary levels of cis-3-(2.2dimethylcyclopropane carboxylic acid formed in the environment.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.3-0.. 2004).Pyrethroid Pesticides Deltamethrin CAS No.

Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD. < LOD means less than the limit of detection.2-Dibromovinyl)-2. population from the National Health and Nutrition Examination Survey.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1 and 0. Fourth National Report on Human Exposure to Environmental Chemicals 169 .1.S. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.Pyrethroid Pesticides Urinary cis-3-(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 1698 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 830 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 700 527 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.2-Dibromovinyl)-2.Pyrethroid Pesticides Urinary cis-3-(2. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. 170 Fourth National Report on Human Exposure to Environmental Chemicals .

et al. Heudorf U. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Fourth National Report on Human Exposure to Environmental Chemicals 171 . and genotoxicity in exposed children. 5/26/09 Ortiz-Perez MD. Environ Health Perspect 2001. Deltamethrin. Environmental Health Criteria 97. Available at URL: http://www. Third National Report on Human Exposure to Environmental Chemicals. Angerer J.inchem. Schulz C. [online] 1990.209(3):293-299. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.htm. Centers for Disease Control and Prevention (CDC). et al. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Seiwert M. Hoppe HW. Heudorf U. Int J Hyg Environ Health 2006. Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Drexler H. 2005. Torres-Dosal A. Angerer J. Angerer J. Batres LE. Atlanta (GA). Int J Hyg Environ Health 2006.109(3):213-217. International Programme On Chemical Safety (IPCS). Ball M.77(1):67-72. Environ Health Perspect 2005. Int Arch Occup Environ Health 2004. Butte W. Heudorf U. Grimaldo M. Carranza C.113(6):782-786. Lopez-Guzman OD. Kolossa-Gehring M. toxicokinetics.209(3):221-233.Pyrethroid Pesticides References Becker K.org/documents/ehc/ehc/ ehc97. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.

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

23 (2.387) .830-2.69 (1.210-.560-1.369) .374) 99-00 01-02 99-00 01-02 99-00 01-02 .62) 5.830) 90th 1.321 (.620-1.260 (.750) .33 (1.320) .50 (2.550-.267 (.53) 1.62-6.590-.71 (1.160-.43) 3.55 (1.83-11.92-3. interval) .250 (.35 (1.28) 1.710 (.02-6.53-3.320) .73) 1.428-.48-2.270) .230 (.81 (1.240 (.36) 1.292 (. Deltamethrin.21 (2.93 (1.25 (2.820) .8) 3.63-3.277-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.60) .190-.39) 2.32 (1.586) .27-2.45-5.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .360) .390) .560-.434) .353 (.48-2.230 (.530-.780) 4.78) 1.314) .600 (.79) 3.940) 1.230-.470-.51-6.450 (.355) .S.370) .04-5.63 (3.04) .990) .276-.13) .750) .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 .42-2.1) 3.440) .27-11.630) .76 (1.26) 2.230-.406) .570-1.430-.710 (.65-2.49-2.46) .190-.340) 75th .27-2.325 (.78 (1.300 (.1 and 0.247-.45 (2.870 (.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.25-4.266-. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.260 (.41-2.25-1.680 (.34 (2.330) .32 (2.69) 3.41) 3.49 (1.314 (.65 (1.35) 2.800 (.86 (1.850) .820) .30) 3.270 (.320) .75 (1.41 (1.246-.840-1.35 (2.64) 697 680 524 701 603 957 Limit of detection (LOD.510-.33) .210-.260 (. Survey Geometric mean (95% conf.35) 1.373) .300 (.44) 5.288 (.530-.340) 1.200-.427) .200-.454 (.740 (.30 (.52-4.288-.300 (.490-.350-.90) 1.49 (1.320) .78) 1.29-1.190-.35) 2.230-.328 (.01 (1.730 (.14-6.420) .298 (.364) .384) .595) .56-5.290 (.640 (.1) 3.25-7.273 (.590 (.336 (.38 (2.280 (.507 (.41-3.34-6.271-.26-2.227-.650 (.700 (.760 (.226-.16-1.810) 1.38 (2.570-.03 (3.740 (.72 (1.260-.233-.250 (.180-.800) 1.1.200-.610) .32-21.311 (.700-1.1) 3.18 (2.960 (.417 (.34) 8.78) 6.52-5.330) .33 (2.190-.510-.560-.240 (.250-.490) .18 (1.49-2.601) .51-3.250 (.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .292-.315 (.295) .297 (.160-.352-.12) 4.16) 1.05) 1.30 (1.300) .340) .750-1.253-.430-.238-. Fourth National Report on Human Exposure to Environmental Chemicals 173 .12 (.13 (. population from the National Health and Nutrition Examination Survey.850) .220-.670 (.26) 2.62-8.520 (.05) .265-.46) 2.12) .25 (2.89-71.54) 1.362) .320 (.

280 (.07) 2.390-.61-2.750-1.270 (.13 (.67) 1.230) .03 (.62) 1.238-.19-6.63-3.53 (1.580 (.240 (.88-5.49) 3.810) 1.210 (.280-.91) .240 (.270 (.09-2.250 (.490 (.250 (.67 (1.246 (.41-4.43 (2.48 (1.510 (.534) .640 (.75-8.25) 2.410-.S.227 (.840-1.860-1.13-1.335-.670) 3.312 (.17-1.760) .270-.590) .230-.330) 75th .43 (1.44 (1.225-.350) .530-.240 (.250) .275 (.36-6.11 (.550 (.330) .96 (1.610 (.300-.220-.960-1.290) .37) 1.240-.400-.423 (.370-.91 (2.550 (.272 (.54 (1.329) . interval) .510 (.400) .677) .530-.43) 1.06-3.280 (.272) .330 (.540 (.300-.90) 3.280) .35 (1.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .190-.35) .410) .67 (1.330) .270) .94 (1.730-1.440-.95) 1.202-.25-5.03-1.200-.590-1.480-.274-.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .450 (.07-5.190-.00) 1.02 (2.372) .52 (1.480 (.72 (1.590) .21-4.62) .11 (.323 (.41) 1.420-.64-5.91) 9.27) 1.37 (1.460-.200-.380 (.380-.590) .09-2.35) 1.290-.216-.280 (.83) 1.261-.329) .13-1.365) 99-00 01-02 99-00 01-02 99-00 01-02 .91-4.362 (.320) .04 (3.650) .190 (.240 (.40 (1.220 (.49-2.328) .60) 1.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.280) .39) 1.224-.580) .261 (.271-.10 (2.387) .200-.730) .60-4.560 (.22 (1.160-.210 (.83 (1.21 (1.309 (.670) .720) 90th 1.35-3.178-.510 (.210-.32 (2.350 (.240-.80) 4.84 (1.321-.16-4.229-.270) .17 (.437) .370 (.860-1.15-2.570) . Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.09 (.274 (.240-.490-.02-1.73-4.05-3.63) 1.25-2.00) 5.19) 2.730) .550 (.740) .09) 3.40) 2.44) 2.52) 2.36 (1.49 (1.234 (.290) .400-.357) .278) .720 (.173-.264 (.230-.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .630) .226-.04 (.860 (. Deltamethrin.43-64.310) .490 (.378 (.150-.330) 1.55 (1.500) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.401) .446) .930) 1.640 (.440-.51-7.73) 1.49) 1.299-.19 (2.460-.81 (1.55) 3.440-.316 (.309) .0) 3.240-.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 . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.253) .200-.00) 1.700-1.86 (1.311 (.930) .74) 3.

Deych E. Centers for Disease Control and Prevention (CDC). Hoppe HW. Leng G. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. et al.206(2):85-92. 2005. Biological monitoring of workers after the application of insecticidal pyrethroids. Leng G. Bartell S. Carranza C. Angerer J. Environ Health Perspect 2003. Berger-Preiss E. Third National Report on Human Exposure to Environmental Chemicals. Bravo R. urban cohort.114(9):14191423. Barr DB. Hadnagy W. Torres-Dosal A. et al.76(7):492-498.205(6):459-472.46(3):281-288. Indoor pyrethroid exposure in homes with woollen textile floor coverings.209(3):221-233. Environ Health Perspect 2006. Ranft U. et al. Grimaldo M. Int J Hyg Environ Health 2006.113(6):782-786. Lapinski R. Barr DB. Godbold J. Angerer J. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Int Arch Occup Environ Health 2003. Olsson AO. Lu C. Arch Environ Contam Toxicol 2004. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Becker K. Exposure to indoor pesticides during pregnancy in a multiethnic. Environ Health Perspect 2005. Obel J. Int J Hyg Environ Health 2002. Sugiri D. Batres LE. Ortiz-Perez MD. Idel H. Berkowitz GS. Sugiri D. Liu Z. Ranft U. Atlanta (GA). Int J Hyg Environ Health 2003. Kolossa-Gehring M. Seiwert M. Hardt J. Levsen K. Lopez-Guzman OD. and genotoxicity in exposed children.Pyrethroid Pesticides References Baker SE.111(1):79-84. Idel H. Ball M. Pearson M. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. toxicokinetics. Berger-Preiss E.

320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.180 (.280-.390) .190) .120-.100 (.109-.070-.190) .400-.120 (.150-.320 (.110) .197) .103) .300 (.400) .200 (.157) .370-.240 (.120-.410) .200) .310 (.260-.120) .140 (.200 (.136) * . distribution.200 (.190 (.125 (. and as a fire-retardant in textiles and plastics.240 (.180 (.140) .184) .250) .710) .330) .190-.260 (. fireworks.330-.170) .490) . and pewter.220) .280-.070 (<LOD-.130 (.130) .100) . interval) .090) 75th .095-.123 (.390) .108 (.130-.130-.120-.140) .400 (.180-.140 (.130-.122 (.340 (.190-.141-.240) .080) .164-.110-.490 (.230 (.135) * .330) .145) Selected percentiles ( 95% confidence interval) 50th .140) .140) .320-.400) . sheet and pipe metal.270 (.330 (.300-.150 (.280) .160) .300) .220) 95th .120-.190 (.210 (.320) Total .200) .130) .210) .340 (.150-.130) < LOD .410) .160-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.470 (.300 (.310 (.120-.250 (. solder.158 (.160-.S.130) .134-.190-.220-.600) .300) . and 03-04 are 0.260) .126 (.250-.120 (.360 (. It is used in metal alloys.170-.137) .110-.170-.110-.460 (. coal-fired plants.156-.250 (.160) .330 (.176 (.087-. to a lesser extent.130 (.131-.136-.108-.180 (.250-.140-. castings.180-.143 (.160-.290-.250-.100 (.320-. Antimony enters the environment from natural sources and from its use in industry.320-.133) * .350-.310) .210) .570) .350 (.190) .230-.230) .144) .200-.440) .220 (.120 (.160) .080 (<LOD-.090 (<LOD-. 01-02.150) .170 (.150-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120 (.280 (. ceramics.110-.260 (.150 (.210) .190) .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 .175 (.430 (. and excretion of antimony vary depending on its oxidation state.280) .180 (.360-.290 (.220 (.150) 90th . Antimony can exist in one of four valences in its various chemical and physical forms: -3.150) .160) .130 (.200 (.220) .150) . Urinary excretion appears to be greater for pentavalent antimony Urinary Antimony Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.230 (. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite. Dermal contact with soil.410-.079-.120 (. 0.440 (.099 (.350-.170-.120) .Metals Antimony CAS No.114) .370) . metal bearings. storage batteries. population from the National Health and Nutrition Examination Survey.190 (.120) .400 (.220) .340) .230-.270 (.117-.207) .210) .088-.230) .130 (.154) .320) . and refuse incinerators that process or release antimony.440) .170 (.250-.220-.350) .230-.160 (. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.150-.350 (.210-.180 (.320-.430 (.128 (.100-.390-.330) .140 (.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 .260-.310-.154) .190-.270-.105 (.240 (.115) .200-. ammunition.093 (.350) .220-.170-. which may vary for some chemicals by year and by individual sample. or other substances containing antimony is another means of exposure.300-.470) .310 (.260 (.390) . < LOD means less than the limit of detection.280-.119-.220-. and +5.169 (.120-. water.220-.270) .200) .280-.310 (.160 (.180) .130 (.270) .350-.160) .120) .500) .430 (.280-.126-.148-.500) .130 (.260) . 176 Fourth National Report on Human Exposure to Environmental Chemicals .190 (.161) .200-. respectively.350) .240-.180-.210-.090 (.134 (.119) .270 (.270 (.200-.100-.140) .160) . +3. see Data Analysis section) for Survey years 99-00.250 (.360) .390-.120-.132 (.130 (. and 0.260) .150-.390 (.145 (. 7440-36-0 General Information Antimony is found in ores or other minerals.130-.180) .230-.350 (.350 (. 0.170-.560) .240-.280) .390-.530) .200) .090-. Workplace exposures can occur at smelters.310-.160-.350 (.154-.070 (<LOD-.230) .220-. from air and drinking water.310) .150 (.130-.350) .420) .115-.190) .140 (.240 (.300) .230 (.240 (.360) .090-.04.330-.110 (.400 (.460 (.160 (.280) .117-.300-.460) .230-.140) .460 (.137) .180-.330 (.142 (. The absorption.470) .130 (.132 (.190 (.210 (.07.146 (.200 (.180 (. enamels.080-. and glass.080) .095 (.330) .400) .098-.128 (.320 (.04.360 (.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 .180-.290-. Stibine is a metal hydride form of antimony used in the semiconductor industry.510) .280 (. It is also used in paints.112-.210) .200 (.130-.120-.130-.120-. People are exposed to antimony primarily through food and.178) .190-.390) .

and kidney have been demonstrated in high dose animal studies depending on the dose.114 (.333-.185-.255-.321) .286 (.256 (.241-.265-.224 (.075 (.111 (.233-. liver.147-.233 (.310 (.194-.192) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.343 (.167 (.294) Total .086 (.205-.109 (.727) .113-.124) .080 (<LOD-.069-.116 (.280-.121 (.135) .092) .183) .333-1.338 (.156-.185 (.267) .086) 75th .092-.107-.167 (.310) .263-.115-.163 (.278) .245) .S.119-.188-. population from the National Health and Nutrition Examination Survey.229-.352) . 1944).195-.159-.095-.199-.281-.175 (.126 (.102-.250-. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.124-.108-.485) .114 (.146-.238) .133) .235-.126-.138-.085) .096-. 1995).076-.357) .203) .317) .295 (.225 (.250) .Metals than for trivalent compounds (Elinder and Friberg.204-.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 .261) .181) .068 (.239-.333 (.099-.097-.130 (.257) . Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.139 (.209-.124-.195-.146-.112 (.146-. diarrhea.115) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.134) .160 (.200-.200) .300 (.098-.117-.238 (.220) .315) .208 (.217 (.128-.119 (.271-.080 (. skin.076-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.222 (. Acute antimony poisoning may cause a metallic taste.127) .173 (.425) . and ulcers (Werrin.333) 787 682 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.211) .132) . Fourth National Report on Human Exposure to Environmental Chemicals 177 .124 (.417) .138 (.250-.30) .113-.250-.265 (.280 (.131) .171) .122 (.320-.145) . 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.288 (.444) .164 (.255) ..230) 95th .112 (.317) .298 (.143) 90th .149) .100 (.159-.226 (.276 (.108-.263 (.153 (.143 (.146) .071-.153-.111-.414) .127 (.135) . 1986). 1958) and occupational exposures (Briegner et al.061-.129 (.429 (.318-.117-.163 (.278 (.214) .187) .131-.173-.122 (.105-.129) .250 (.364 (.371 (.191 (.250-. 1954).173 (.200-.200-.338 (.095-.143) .115 (.130) .. and route of exposure (Elinder and Friberg.272) . species.186) . 1962).364 (.238) .137 (.417) .181) .129) * .103-.098-.138-.185 (.104-.164) .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 .130) .104-.120 (.248) .135 (.193 (.150-.333 (. abdominal pain.228 (.253 (.172-.123) . and gastrointestinal symptoms such as vomiting.108-.102-.140) < LOD .267-.380 (.300) .078 (.178-.189 (.068-.120 (.082) .373) . Ming-Hsin et al.126) .250 (.193) .320-.391) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.209) .269 (.151) .385 (.313-. 1973).167 (.333-. Histopathologic inflammatory and degenerative changes in the lung. 1988.208-.244-.081) ..266 (.161) .181) .178 (.338) .173) .308-.192-.333-.357-. Inorganic antimony salts irritate the mucous membranes.405) .198) .120 (.156 (.207) .121 (. interval) .161) .317) .074 (..176-.444) .143) .248-.131 (.170 (.125 (.277 (.121) .139 (.114 (.268) .069-.106-.115 (.195 (.447 (.113) . The toxicity of stibine after acute inhalational exposure is similar to that of arsine.192 (.107-.148-.182 (.480) .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 .148) * . myocardium.320) .118 (.159-.138) * .333 (.162-.123 (.129 (.421) .075 (.149-.082 (<LOD-.438) .. and eyes.127) .089) .152) .320 (.471 (.108 (.118 (.109-.164-.103-.116-.247) .087) .209) .127) .228 (.115 (.084) .209 (.213 (.352 (.147) .117-.107-.148-.259 (. 1986).130) .179-.391) .203) .310) .188) .242-.127) .167-.300) .144-.500) .471) .150-.741 (. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown. resulting in hemolysis with abdominal and back pain (Dernehl et al.308) .227-.106-.152) .081 (<LOD-.333) .109 (.196 (.233) .253-.082) .430) .320 (.132 (.112-.135) .241-.429) .143) Selected percentiles ( 95% confidence interval) 50th .236 (.176 (.077) .400 (.079 (<LOD-.741) .098) .318-. 1953).225) .120 (.125-.230-.119-.206-.115-.154-.176 (.267 (.136) .099-.135 (.228-.140) .

Costeloe K. Third National Report on Human Exposure to Environmental Chemicals. Leinemann M.. Dezateux C. eds. References Berman JD. Fuchs A. Ju-Sun P. Mayne P. Yang C-Y. 2004. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. clinical efficacy. 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. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Br J Ind Med 1991. Semisch CW. Environ Health Perspect 1998. Cordasco EM. Arsine.13:361-362. Nau CA. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Luedersdorf R. and 2003-2004. Antimony trioxide is rated by IARC as a possible human carcinogen. Petrucci F. pp. Industrial antimony poisoning. Handbook on the toxicology of metals. Mahieu P. 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. 26-42. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. EPA.76:432436. Suchenwirth R.46:931-936. Chia-Yu H. et al. Iavicoli I.. and future strategies. Information about external exposure (i. Review of elements in blood.. Weltle D.48:93-97. Liao Y-H. Rev Infect Dis 1988. O’Regan M. Gebel TW. Friberg L.51:238-240. Lenert G. Atlanta (GA). Arch Dis Child 1997. Kiberd B. 1987). Schaller KH. gov/toxpro2. Delves HT. 1991. Biomonitoring of a worker population exposed to low antimony trioxide levels. which may be due to methodologic. Apostoli P. Bailly R. population. Antimony in blood and urine of infants. J Trace Elem Med Biol 2002. 1997). Dezateux et al. 1998) or compiled reference ranges (Hamilton et al. even when exposure levels were below workplace air standards (Bailly et al. Int Arch Occup Environ Health 1995. HH.)1954. VI.10(3):560-586. In: Friberg L. Industrial Medicine and Surgery (Dec. environmental levels) and health effects is available from ATSDR at: http://www. Wu M-T. et al. et al. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000.59:469-474..S. Sabbioni E. Chemotherapy for leishmaniasis: Biochemical mechanisms. Shao-Chi C. Van der Venne MT. 2002. Kuo-Juie Y. Briegner H. Bolten C.76(2):103-115.158:165-190. Cullen A. Centers for Disease Control and Prevention (CDC). Minoia C. Wade A. Piatnek DA. Chin Med J 1958. arsenic.. 1998..106:33-39. New York: Elsevier. Antimony.. Ludersdorf et al. 1986. Roland H. Skulsukai G. Chest 1973. 1995. Buchet JP.16: 33-39. Ming-Hsin H. Cheng-Wei L. Nordberg GF. Yu H-S. Caroli S. or exposure differences. Industrial Medicine 1944. Biological monitoring of exposures to aluminum. Kentner M... Delves HT. 2nd ed. indium. J Clin Pathol 1998. 1994) have reported values slightly higher than those in this Report. Konings J. Carelli G. Pozzoli L.e. Gallorini M. Stocks J. Kentner et al. Earlier measurements in general populations (Minoia et al. Paschal et al. Pilgrim L.Metals to antimony have been established by OSHA and ACGIH. J Occup Environ Med 2004. Mayer P. Stone FD. Stasney J. 1990. 1998). Lauwerys R. Sci Total Environ 1994. Trace element reference values in tissues from inhabitants of the European community I. Iavicoli et al. Urinary antimony in infancy. Dunkelberg. and hydrogen sulfide. Liao Y-H et al.64(2):182-185. External and internal antimony exposure in starter battery production.. gallium. 2005. Ho C-K. Alimonti A..cdc.521-523. Biological assessment of exposure to antimony and lead in the glass-producing industry. respectively.. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Element reference values in tissues from inhabitants of the European community.atsdr. Stead FM. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Dernehl CU.html. Sabbioni E. and antimony in optoelectronic industry workers. and a drinking water standard has been established by the U. Pietra R. Elinder CG.67:119-123. stibine. Schacke G. Matthews T. Hamilton EI. 20012002. Chen J-R. Pulmonary edema of environmental origin. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . Int Arch Occup Environ Health 1987. Vouk VB.

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

interval) 8.55 (7.5-178) 46. and other metals.3-19.Metals Arsenic CAS No. pesticides.90-11.2) 46. particularly arsenic trioxide. and in lead-acid storage battery grids. 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 forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.27) 9. Arsenic trioxide (As2O3.19-9.8) 29.12-10.2 (51.2 (13.70) 8.10 (6.3) 10.5 (40.5) 41.90) 75th 16.0 (22.90-7. copper arsenates. alloys.4) 13. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.5 (36.9-62.6-141) 53. and produce.97) 8. lead. Although it is still widely used in the United States. arsenic compounds. mental disorders.84) 8.0 (11.8 (48.8) 34.90 (5.1-18.00-9.66-8.8-77. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.57) Selected percentiles ( 95% confidence interval) 50th 7.90 (7.4) 60.6) 618 722 1074 Limit of detection (LOD.8) 33.3) 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 7.20 (8. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. The United States no longer produces arsenic from mining but imports about 22.6 (13.2-61.7-95. meats.6-43. and arsenosugars.5 (23. arsenocholine. Before the 20th century. sodium arsenite. grain.5-52. ocean and fresh waters.8-61. and gray forms).2 (41.5-19.77) 6. trimethylarsine oxide.0-60.6-35.8) 30. Gallium. Arsine (AsH3) is a reactive.50 (8. In the last century.4 (31.34-10.9-46. and as homicidal poisons. or rarely as elemental metalloids (yellow.4 (24. Since the 1940s.5-41. arsenites.41 (7.1) 7.7) 90th 37. and foods. Survey years 03-04 Geometric mean (95% conf.2-17.40) 7.80 (5. and indium arsenides are used in the semiconductor industry.2 (12.80) 6.0 (43. though in some locations arsenite may be prevalent (WHO. Also.5) 66. population from the National Health and Nutrition Examination Survey.0 (14.70 (6.9-34. the smelting of copper.80-9. arsenic as elemental metalloids may be used in some ammunition.8) 17.02-8.10) 10.5) 43. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine. Water sources contain mostly inorganic arsenate.00 (6.3-111) 78.1) 1281 1276 03-04 03-04 03-04 9.70-9. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.6) 11. and as a cosmetic to lighten complexion. General population exposure to inorganic arsenic can occur through consumption of drinking water and.74.29 (8.90-14.000 metric tons annually.90-8.1-40.5) 95th 65. Arsenic and its compounds have had many uses in the past and present as medicines. referred to as inorganic arsenic compounds.30) 17.7 (11.5 (14.30 (6. and play sets.6 (32.90) 16. aluminum. retaining walls.9 (17. 2005). Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.6 (9. semiconductors. In nature. solders. Arsenic is measurable in most soils.50-14. from coal burning.10-10. cacodylic acid. 180 Fourth National Report on Human Exposure to Environmental Chemicals .9) 21.5 (34.1) 15.4 (48.7) 24.08 (5.8) 7.7) 65.25-9.S.13-8.4-65.1 (32.12 (6. +3 and +5). lead hydrogen arsenate. gaseous hydride manufactured in small quantities for use in the semiconductor industry. and.84) 8. mostly for use in wood preservation (ATSDR.4) 40.2-20. and arsenates (oxidation states of -3.30 (7. black. to a lesser extent.90 (7. Various arsenic compounds were used in paint pigments and for tanning animal hides. Arsenic trioxide is approved to treat acute promyelocytic leukemia.0 (15.0-19.2) 15. as alloy in metal bearings.1) 290 725 1542 03-04 03-04 9.4 (7. were used as treatments for syphilis.9) 68.34-9.1 (38.3-15. psoriasis. 2001). to a lesser extent.2-93.10-7.7-83.90-8. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.8) 7.9 (8. such as arsenopyrite (FeAsS) and realgar (As4S4). it is found in over 200 crystalline or mineral forms. cancers.6 (15. see Data Analysis section) for Survey year 03-04 is 0. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.4 (26.

but is poorly absorbed dermally (WHO. Tseng. Arsenate is reduced in the body to arsenite (oxidation state +3).5 (9.4 (24.1) 8.23-7.4-64.9) 53.93-8.66 (7.0 (17.. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.1 (14. Survey years 03-04 Geometric mean (95% conf. so exposure to the general population is extremely limited.20-9.28-7.4 (26.7) 28.8 (20. arsenic does not show biomagnification in the food chain (WHO. population from the National Health and Nutrition Examination Survey.3 (27.1-36.33 (6.88) 7.4 (42. 2001).0) 1281 1276 03-04 03-04 03-04 8.8) 27.6 (10.11 (5.0) 12.0) 42. 2001). 2006.4 (40.06 (4.2) 90th 30. selenium. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. age.47 (6.58-10.61 (7.25 (6.4) 32.6) 45. though some reduction may occur in the gut prior to absorption.10-8.35) 7.8 (11.66-8.45) 5.18 (5. trimethylarsine oxide (TMAO).8-75. 2006.96) 12. Though modest bioconcentration occurs in some aquatic life.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.g.2-46. arsenocholine. After absorption. 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.50 (6. Inorganic forms of arsenic demonstrate high acute toxicity.6 (17.59) Selected percentiles ( 95% confidence interval) 50th 7.3-53.5) 17. 2007.0-26.7-17.7-35. organic arsenic can be converted back to methylated and inorganic arsenic.04) 7. U.7-188) 27.75) 13.1) 24.4 (11..1) 6.3 (24.9) 13.76 (6.7 (25. EPA’s maximum contaminant level (Hughes. WHO.66-8.4 (12. In aquatic organisms.1) 7. as observed in Bangladesh where millions of people have been exposed.0-69. 2001).3) 6.04 (5.3-41..2) 15. kelp. have caused clinical arsenic poisoning.0-38.00 (6. inorganic arsenic is widely distributed within the body.8-62. 2007.2-15. dose level. and folate status (Chen et al.0) 26.5) 290 725 1542 03-04 03-04 8.7-34. In aquatic sediments. Direct exposure to DMA and MMA may result from use of the two pesticides.. Gamble et al.75 (5. WHO.. 2001).47-6.6-17.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.9 (45.3) 9.33-10.4) 54.S. cacodylic acid and monosodium methyl arsenate.99-9. gallium arsenide and indium arsenide. shellfish.9-56.2 (12. dust.2) 40. 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.S. 2001).25-9.07-9.8 (21. 2001).40) 8.93-9.64 (7.13) 8. and contact with CCA-preserved wood structures.8-32. Smoking tobacco is also a source of inorganic arsenic.0 (31. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.44-11. 2001. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. 2007.0-18.3-64. 2001). with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.1 (11. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.7 (11.41) 6.31 (6.8 (12.10-16.81-9. NRC. 2001). Extremely high groundwater arsenic levels.32 (5. 2001. Children may have additional exposures from ingestion of contaminated soils (e.5-17. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.86-17.0) 33. and some other seafood can contain organic forms of arsenic including arsenobetaine. 1988).9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .88 (5.S..47 (7.8) 22. interval) 8. and arsenosugars. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.51) 75th 14.01) 7.1) 58.38-10.7 (9.0) 14.30-9. The semiconductor dopants.44) 6. EPA.3-62.8 (27.7-18.5-120) 40. are used in enclosed ultraclean operations within the semiconductor industry. Fish. mine tailings). Chowdhury et al.12-10. Steinmaus et al.7) 95th 50.24 (7.01) 11. 2003. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.6 (35.

Chile). 2001). can cause peripheral sensorimotor neuropathies. 2001).10 (<LOD-1. Acutely. including inhibition of numerous enzymes. 2001. WHO.10 (<LOD-1. population from the National Health and Nutrition Examination Survey. renal failure. WHO.20 (<LOD-1.. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose.. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e.10 (<LOD-1.S. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. Laboratory studies using inorganic arsenic have shown chromosomal aberrations.g. and it also will inhibit succinate dehydrogenase. WHO. and by uncoupling oxidative phosphorylation (NRC. food residue.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. Cardiac arrhythmias. which may vary for some chemicals by year and by individual sample.10 (<LOD-1.60) 1. < LOD means less than the limit of detection. lung. U. and environmental standards for arsenic and arsenic Urinary Arsenic (V) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. hepatotoxicity.. 2001). Bredfeldt et al. 2006) or when exposure occurs in smokers (Chen et al. 1998. but additional or confirmatory research is needed (Kapaj et al.. NRC. 2007..30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.. arsenic trioxide) includes hemorrhagic gastritis with nausea. hematocytopenias. Although arsenate is reduced in the body to arsenite. substitution in phosphate metabolism. hypertension. apoptosis. Bangladesh. some of these effects may take years to develop. 2007).. peripheral vascular disease. Raml et al.30) 1. fatty acid oxidation.S.. increased oxidative stress. respectively. Such actions may lead to decreased energy production. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. 182 Fourth National Report on Human Exposure to Environmental Chemicals . leading to a decrease in adenosine triphosphate energy production. 2001. which can lead to dehydration and shock.60) 1. Chronic arsenic exposure in humans is considered to be a cause of skin. hyperkeratosis. see Data Analysis section) for Survey year 03-04 is 1. and childhood neurodevelopmental effects in observational human studies. 2001). and hyperpigmentation of the skin (NRC. interference in signal transduction pathways. Arsenic has many actions demonstrated in cellular studies. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. noncirrhotic portal hypertension. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide.. gluconeogenesis. 2001).EPA. Taiwan. 2004).50) 621 725 1078 Limit of detection (LOD.. 2001).50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. Chronic elevated arsenic intakes have been associated with diabetes. With chronic exposure.. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 1.20 (<LOD-1.50) 1. NRC. and altered gene expression.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al.. 2000. 2006. Cellular glucose uptake. and production of glutathione may be affected as well. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. 2007.20 (<LOD-1. 2004). drinking water have not been associated with increased cancer rates (Schoen et al. and endothelial injury (Kumagai and Sumi. and bladder cancer (IARC.10 (<LOD-1. 2004.S.0. vomiting. The U. including drinking water sources with elevated arsenic levels (e.g.S. Chronic human intake of arsenic at less than acutely toxic doses.20 (<LOD-1. 2006. cell transformations. and diarrhea. The organic forms of arsenic occurring in seafood have little known toxicity. cytotoxicity. WHO. Cohen et al.EPA has established drinking water. 2006.80) 1. Survey years 03-04 Geometric mean (95% conf. Studies of arsenic at levels typical of U. and DNA repair inhibition (Cohen et al.

18) 3. 2001).. Additional information about external exposure (i...S. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 2006).. 2008)..75 (<LOD-2. urinary arsenic levels have been accepted as a good biomarker of dose (WHO.41) 3. 2008). Caldwell et al. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2004. In a Nevada town where groundwater levels were naturally elevated. 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.S. but generally only at maternally toxic doses (WHO.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. Pellizzari and Clayton. had decreased since the prior 1990– 1992 survey.61 (<LOD-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 1992. 2007.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.80 (<LOD-4. 2003. Levels of total urinary arsenic in the U.18 (<LOD-3.. population (Rubin et al. WHO.. gov/toxpro2.50) 1.. 2006). 2006. 2000. Meza et al. Survey years 03-04 Geometric mean (95% conf. 2000). Consequently. Josyula et al. 2001). Compared with this Report. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.. 1999). 2007. environmental levels) and health effects is available from ATSDR at: http://www. 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. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. Shalat et al. In the German Environmental Survey III of 1998. 1998.. 2001). 1999. 2006). Valenzuela et al. population in NHANES 2003–2004 (Schulz et al. Offergelt et al.75 (<LOD-2.. 1986).. DMA produced bladder cancer in some chronic rat studies (Cohen et al. 2006). 2006.Metals compounds.S.. 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.19) 3. median urinary total arsenic levels in 4052 adults varied with seafood intake. population from the National Health and Nutrition Examination Survey. and the FDA has established a bottled drinking water standard.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 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.S. Vahter et al. 2008. Pellizzari and Clayton. 2006.69 (<LOD-3.33 (<LOD-3. Calderon et al.. Pellizzari and Clayton 2006). Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. In animal studies.atsdr... 2004. 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.. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. arsenic has been fetotoxic and teratogenic. 1999.33 (<LOD-3. 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. and were about two-fold lower than those for the U. although urinary arsenic levels were not associated with CCA contact (Shalat et al.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2..00) 1. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.cdc.04 (<LOD-3..html. Caldwell et al... Shalat et al. Though CCA-treated wood contains several thousand times more arsenic than untreated wood..e.

70-21.90-29. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9 (6.S.7 (13. 2008).05) < LOD . arsenocholine.6.1-94. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. arsenocholine. In most human studies.2 (6. Survey years 03-04 Geometric mean (95% conf.00 (.62) 2. DMA and MMA.20 (..871-1. MMA.83) Selected percentiles ( 95% confidence interval) 50th 1. 2008.S.00-12. In the residents of a Chilean town who consumed water with high levels of arsenic. Arsenate.20) 3.6 (13. In the late 1980s..8.9) 13.20 (4.7) 13..900-1. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.40-7.800) 1.40-6.3% of a representative sample of the U.. 2000. 2005.50) 90th 16.3) 1284 1284 03-04 03-04 03-04 1. dermal keratosis.60-3.70) 6.19 (.00) 3.6.0) 4.3) 95th 35. 2007) with higher levels of arsenic in the drinking water.70 (5..5) 292 728 1548 03-04 03-04 1. 1996..1) 18.. see Data Analysis section) for Survey year 03-04 is 0..3) 35. population (Sun et al.800-4.60) 1.3-39. arsenobetaine. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine. 2008.7) 15. 1. Measurable organic arsenic species in this Report are three biologically generated environmental forms.28) 1. Pellizzari and Clayton. geometric mean levels were about 70-fold higher than for the U..S.70-21. 2008).. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.4-35.66 (1. which may vary for some chemicals by year and by individual sample. 2008).S. in NHEXAS 1995–1996.80) 1.17-1. 2005.1-25.9 (7.45 (1.. Chowdhury et al. population showed a higher contribution of arsenobetaine (Caldwell et al.55 (1.. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.11-1.5 (26. Caldwell et al..6 (11.2-35.29 (1. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.4) 31.. These associations are stronger at higher urinary levels. and two methylated metabolic products. Some noncancer effects of arsenic (e. WHO. 1990..50) . vasospasm.e. China..31-1.80 (.5) 621 725 1078 Limit of detection (LOD.800 (.00 (1.6-44. 2000.20 (1.8 (17.4.Metals other areas of the world (Ahsan et al.5 (14. 2008). methylation capacity.90-7. 184 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey. population (Ahsan et al. 1985. Valenzuela et al.600 (.30 (1.6 (25.g. 2006). After recent seafood ingestion. Caldwell et al.10) 4.0 (26.400-. Individually measurable species resulting from inorganic arsenic exposure are arsenate..20-25.5) 32. 4.00-1.40) 75th 5. 2000. population in the NHANES 2003–2004 subsample.900 (.10) 8.80 (4. Sun et al. 2003).10 (4. and duration of exposure are also considered important.80 (3.50-6. 2007).30 (2. Caceres et al.7 (21.30) 2.8-40. For residents of Inner Mongolia. 2005.. respectively.700-1.93) 1.0) 29. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. < LOD means less than the limit of detection. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.20-3. and other factors such as nutrition. and 0.20) 7. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.70 (3.30) 10.500-1.68) .7-22. Blom et al.8) 35. Caldwell et al.2-38. with DMA.80-5. Aposhian et al.9-23.37 (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 * * 1.0 (27. When seafood intake is avoided.1-51. 2001).3 (9.00-4.48-2. arsenite. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.800-1.800 (. 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. Tseng et al. when seafood organic arsenic is subtracted).0-23. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and TMAO.8 (12. Also..40) 5.00-6..S. and TMAO were detected in only 7. The higher percentiles of total urinary arsenic levels in the U.20-190) 31.74 (1. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.8-50.50) .1) 45.700-1. interval) 1.4) 23.20 (2. arsenite.5) 29.20) 18. 2001.4 (16.3 (21.43-1. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.

2008)..0-36.16 (.21) 5.68 (1. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.78-5.73-6.18-1.10 (..82) 4.9) 32.30-1. In recent years.2 (12. 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..54 (1.3 (10.11 (.Metals as with DMA.13-39.938-1.28) 1.00 (1.638) 1.67) 4.64-29. 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.05 (.9 (13.30) 1.877 (.58 (3.65 (1.3) 95th 29.3-24.25-7.3) 1284 1284 03-04 03-04 03-04 1.7) 9.5) 17.82) Selected percentiles ( 95% confidence interval) 50th 1.55) 1.43) 75th 5.7) 17. 2008). interval) 1.2 (12.51-2. 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..78 (3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.0 (9.39-3. 2007).1 (26.67) 1. which is below the ACGIH BEI (Caldwell et al. WHO. population for the sum of inorganic related species was 18.19-2. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al. not to imply a safety level for general population exposure.47 (1.53 (. 1998.62-6.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Vahter et al. Caldwell et al. 2003..37-2.61-6. population from the National Health and Nutrition Examination Survey.51) 5.1-36.786-1.6) 19.36) 2.6-29.9) 14.6-32.76-27.40 (1.50-7.44 (1.1-18.47 (2.5-20.959-1. Survey years 03-04 Geometric mean (95% conf.2 (13.4-82.91 (4.91) 90th 16. 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.612-1. The 95th percentile of the U.00 (3.4) 292 728 1548 03-04 03-04 1.4 (24..833-1.70) 5.43) 14.S.9-18. Fourth National Report on Human Exposure to Environmental Chemicals 185 .81 (4.4-28.5 (18.6-46.93 (1.8) 29..7) 30.4) 32. Information about the biological exposure indices is provided here for comparison.4) 13.400-.S.3 (10.79 (1. 2001).72) 12.1) 26.88 (5.4 (11.9 μg/L..83) 8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.15-1.2 (4.14 (1. 2001). 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.531 (. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.15-4. 1992.6 (6.9 (25.80) .901-2.15-1.6 (9.05) 1.909-1.4) 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 * * 1.83) 2. 1986.80-153) 17.45) 1.29-14.50-15. 2006.5 (18. Sun et al.25 (.88) 2.5) 26.12) < LOD .4-21. Offergelt et al.40) 1.32-7.29 (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 < 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. 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. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.S.S.6. * 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. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 621 725 1078 Limit of detection (LOD. 186 Fourth National Report on Human Exposure to Environmental Chemicals . Survey years 03-04 Geometric mean (95% conf. 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.

< LOD means less than the limit of detection.80) < LOD 621 725 1078 Limit of detection (LOD. 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 1.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Fourth National Report on Human Exposure to Environmental Chemicals 187 .Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.20 (<LOD-1.00 (<LOD-3. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.S. population from the National Health and Nutrition Examination Survey.44) 2.40 (<LOD-1. Survey years 03-04 Geometric mean (95% conf. Survey years 03-04 Geometric mean (95% conf.00 (<LOD-2.08 (<LOD-4. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00) 1.2.70) < 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 2.95 (<LOD-2.

13-4.0 (14.44 (2.0) 13.00-4.10) 3.39-3.00) 5.00-9.0) 17.0) 12.0 (10.37 (3.0) 11.62) 4.0 (13.00-22.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.95 (4.61-11.70 (3.00) 7.00-10.05) 10.59 (6.95-6.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.32 (8.5) 95th 13.34-4.24-4.0-17.9) 12.32-10.00-7.0) 10.00 (3.38 (3.69-6.00-7.16-11.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .S.0 (12.90) 2.17-4.90) 5.1-18.14) 3.30) 3.0 (10.00 (5.0 (13. Survey years 03-04 Geometric mean (95% conf.9 (7.1-22.27 (2.85 (3.16 (4.00-4.0-16.14) Selected percentiles ( 95% confidence interval) 50th 3.8) 7.86-7.03 (3.1-15.0 (10.20-4.09 (7.31-4.0 (9.44) 5.1 (8.60-6.S.00 (5.0 (8.0) 14.57 (3.5 (11.95-4.00-11.32 (4.0 (9.0) 95th 16.00 (3.00 (4.0-16.12 (3.0-18.27-2.0 (10.73 (3.00-7. Survey years 03-04 Geometric mean (95% conf.67) 9.0) 621 725 1078 Limit of detection (LOD.71) 3.82-9.9) 11.0) 9.80) 2.80-5.82) 3.7. population from the National Health and Nutrition Examination Survey.2) 10.46 (4.79 (3.31) 4.82-5.69-3.0) 16.20-12.00) 3.61-16.55 (2.60-3.00) 12. population from the National Health and Nutrition Examination Survey.50 (4.00) 6.00 (3.48 (3.22) 4.94) 3.00 (3.30 (7.00-4.05) 3.74 (2.52) 3.17-6.00-12.84-8.70-3.19) Selected percentiles ( 95% confidence interval) 50th 3.00 (5.00-4.0 (11.15) 4.70) 5.00-3.65-6.49-4.00-15.71 (4.42) 3.00-15.00-3.92) 3.81 (5.34-4.7) 1284 1284 03-04 03-04 03-04 4.37 (2.7-16.6 (9.05) 5.00 (3.78) 4.00) 3. interval) 3.60-4.00 (3.20) 11.92-12.0) 13.00) 6.7 (10.00 (6.77 (3.11 (3.5) 12. interval) 3.00 (7.18 (6.00-13.00-11.10) 6.8) 7.80 (4.00 (7.70-4.00) 6.50-15.00-7.08 (2.27 (3.86 (2.00) 6.3 (8.80-3.00) 90th 11.16 (2.6) 292 728 1548 03-04 03-04 3.00) 4.90 (3.00) 4.78 (4.0-17.69 (3.49) 10.9 (11.69 (3.00 (5.00 (6.4 (7.84-18.45) 8.34) 3.00) 75th 6.29-4.0) 16.12-4.34 (3.73) 6. see Data Analysis section) for Survey year 03-04 is 1.0) 9.71 (3.72 (4.9) 13.48 (2.45 (8.03-6.80-6.86-21.0-25. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.70-12.6) 1284 1284 03-04 03-04 03-04 4.67) 8.00-11.0 (8.91) 75th 5.0) 292 728 1548 03-04 03-04 4.88 (4.34 (3.0) 11.57-5.60-7.65-8.7) 13.98) 4.74) 90th 9.25 (4.00-4.27-5.0-19.0) 9.33) 3.71-4.00 (5.95-3.8) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 3.11) 4.00-12.00) 9.00 (6.89 (3.00-4.33-4.28) 2.0) 17.00-15.94-3.00-8.24) 3.80) 7.00-5.0 (12.50-5.3 (8.0 (9.9) 5.06) 5.97-3.45) 3.0-12.6-18.7) 12.17 (2.3 (7.

20 (1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.37 (1.40) 1.40) 2.10-1.40-3.70) 2.10 (<LOD-1.86 (2.40-3.80) 1.10-3.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.96-2.00) 2. Fourth National Report on Human Exposure to Environmental Chemicals 189 .61) 2.00 (1.36 (1.00 (2.80 (1.80-2.33 (1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.80) 1.816 (<LOD-.00 (<LOD-1.23) 1.52 (2.61-3.33 (1.50) 621 725 1077 Limit of detection (LOD.70-2.60 (1.00) 1.50 (<LOD-1.46 (1.88 (1.9.50-2.70-2.70-2.00 (2.84-3.88-2.90) 2.20 (1.00-4.05-1. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.900-1.80 (1.985) 1.82-2.85) 1.88 (1.86) 3. population from the National Health and Nutrition Examination Survey.90) 1.30 (1.10 (1.20) 2.10-1.36) 1.10 (1.82-2.40 (1.15-1. which may vary for some chemicals by year and by individual sample.60) 2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.85) 2.18-1.90) 2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.50 (1.58) 2.17) 2.10) 95th 2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.86 (2.28 (1.00-2.20-1.00-1.57) 95th 2.60) 2.07) 2.40-2.22) 3.07-3. 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.853-1.50) 1.30) 90th 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.30 (1.50 (2.20 (1.53-2.10 (.18-1.30 (2.60 (2.63 (<LOD-1.46-2.10) 2.14-1.30-2.00) 1.30) 1.77) 1.40) 1.00-2.28 (1.20 (1.60) 1.20 (1.93) .53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1. population from the National Health and Nutrition Examination Survey.86) 2.70-2.54) 90th 2. < LOD means less than the limit of detection.S.80 (2.35-3.00) 1.30-1.45) 3.20 (1.22 (1.80 (1.79) 2.16 (2.90 (1.40 (2.30) 1.31-3.81) 1.43-3.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.20-3.71-2.00 (<LOD-1.00-1.53 (1.10 (.30) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.11-1.30 (1.40-2.50 (1.07 (1.73-2.60-2.S. Survey years 03-04 Geometric mean (95% conf.00) 2.70-3.34) 2.80-2. Survey years 03-04 Geometric mean (95% conf.80 (1.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.90 (2.30-1.62) 2.31 (1.

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

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Fourth National Report on Human Exposure to Environmental Chemicals 193 .93-2.70-2.51) 1.87) 7.50 (1.78) 1.91) 6.65-8.61 (2.12) 6.95-6..46) 1.21 (1.20-1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract. such as brazil nuts.70) 1. water.50 (4.87-14.40-13.82-6.36-1. see Data Analysis section) for Survey years 99-00.30 (3.76-7.00) 1.00-8.12 (2. fireworks.60 (1.30 (5.26-1.54-8.21-2.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.49) 8.50) 2.87-9.69 (1.61 (5.66 (4.18 (6.20-8.80 (2.90-9.25-11.85 (2.63) 1.S.88) 1.15 (6.30-1.31-2.70-8.61 (1. are high in barium (Genter.82) 1.51) 2.63 (5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40 (5.15-1.49-1.37 (4.64-3.90 (1.12.30) 4.19-1.15 (2.54) 1.14-1.40) 3.42 (1.44-2.30 (2.50 (1.55-7.33 (1.60-10.71) 95th 6.49) 2.30 (5.37-1.64) 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 2.63 (8.51 (1. In single dose animal studies.65) 1.39) 1.12) 7.88) 4.04-2.39 (1.50 (6.80 (1.00 (1.73-5.70 (5. Barium compounds are used by the oil and gas industries to make drilling muds.77 (3.20-8.09 (2.10-5.43 (1.20 (4.29-1.28) 90th 5.50-1.47) 4.43) 6.74) 3. In nature.70-5.36) 5.76) 1.25 (1.63) 1.15 (1.74-3.73 (5.37-8. glass. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.65 (5.11 (2.53) 1.51) 7.56) 1.40 (5.86 (4. 2001).40 (4.20-6.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.06-1.22-1.19) 2. Some barium salts are freely soluble in water.80-5.70) 5.81-3.49-9.62) 1.27) 2.90 (6.70 (1.48 (6.50-6.40 (1. Certain foods.41-1.70) 3.81-2.00-3. Barium compounds are also used commercially in paint.48-4.25-1.11-1.30-2.63) Total 1.17-1.18-1.34 (1.35 (1.27 (1.50-1.02 (7.71-9.70) 4. it combines with other chemicals such as sulfur or carbon and oxygen.35 (2.66) Selected percentiles ( 95% confidence interval) 50th 1.54) 2.86 (4. respectively. 7440-39-3 Medically. Barium salts have also been available as rodenticides. and 03-04 are 0.47-1.62 (1.41-3.30) 5.57) 3. and food.61-8.18) 3.30-1.10) 3.00 (2.20-5.87-3.38) 8.88) 7.15) 5.8 (6.50 (4.32-7. interval) 1.90) 4.46) 1.8) 9.67) 6. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey. soluble forms of barium.20-8.41) 1.40 (1.30-2.38) 2.22-1.20 (3.10 (4.05-2.50) 4.53-5.40) 7.22) 6.86-5.29) 5.52 (1.54 (6.8) 5.35) 5.32-1.49 (1.59-11.30) 2.40 (1.90 (4.50 (4.20-1.16 (1.54) 1.96-2.15-1.38 (1.12.70-6.08-8.06-2.70-2.46-1.20) 2.53) 2.49) 4.80 (1.50) 2.56) 4.91) 2.75-3.65-1.60-2.g.63 (1.50-6.07 (2.91 (2.4) 6.16) 5.93 (4.56 (6.50 (1.85) 1.88 (5.56 (1.43 (1.10) 5.35-4.97 (1.54-1.44-5.4) 9.20-1.71) 2.65) 3.60-3.48-4.81-2.65-5.73) 1.87 (5.28-1.63 (2.10-4.92) 2.64 (1.4) 7.10) 1083 1335 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.12 (2.2) 6.57 (5.90-2.34) 2.50 (2.11 (3.05% of the earth’s crust.37) 1. and ceramics.90-13. barium sulfate and barium carbonate).01 (4.80-2.24 (4.29-5.62 (1.80 (2.80) 7.45) 7.61 (3.35-1.30-3. whereas others are practically insoluble (e.54-1.75) 2. 0.34 (2.86) 6.50 (5.73 (6.60-6.26) 5.03 (1.39-1.34 (1.43 (5.37) 5.09 (1. Small amounts of barium can be released into the air during mining and other industrial processes.77-3.40 (5.55-3.14-6.20 (1.26) 2.40) 7.70-3.10 (2.71) 1.78) 1.80 (5.32) 8.56 (2.27 (1.78-3.31.76 (3.68 (1.84) 5.87-7. The general population can be exposed to low amounts of barium in air.62) 1.30) 3.15-11.45 (1.50 (3.77) 1.43) 2.76-2.98) 1.95 (4.60 (2.94-6.44 (1.93-8.21-8.86-4.60-6.71 (2.59) 3.00) 4.14 (6.82) 2.49) 11.52 (4.10 (3. and 0. bricks. rubber. depilatories.99-5.90) 2.30-5.80) 1.60) 1.61 (1.35-1.26-7.36 (4.30) 5.65) 1.30 (1.85) 1.99 (4.24-1.00-76. tiles.48) 1.9) 5.Metals Barium CAS No. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).36 (1.87 (6.72) 1.47-1.50 (1.39) 4.39 (1.12-1.56 (1.80-3.1) 9.36-1.60) 1.50) 1.08 (6.73) 3.30) 8.04-6.76-3.11 (3.31 (2.60) 4.78-2.72) 75th 3.21 (1.80) 6. such as barium chloride.80-7.80 (1.30) 5. 01-02.70) 7.60) 3.35 (3.01-7.20-1.90) 1.54 (2.90) 2.38 (1.57-7. Workers employed by industries that make or use barium compounds can be exposed to barium dust.00) 6.48) 1.72) 4.50 (1.70) 1.00) 1.24-1.74-2.

84 (3.38) 1.51) 4. Perry et al.46) 2..62 (4.09) 6.57-7. 2001). hypertension.91 (3.45) 95th 6.57-5.24 (3.14-2.56) Selected percentiles ( 95% confidence interval) 50th 1.67-6.45-8.24-3.42) 1.68 (3.55 (1. Barium is not rated for human carcinogenicity.89) 90th 4.68 (2.34-5.24 (5.26-1.44-2.25) 4.39 (3.48) 2.64) 7. population from the National Health and Nutrition Examination Survey. Following intravenous injection in animals.11-2.55 (1.11) .81-7.59 (1.36 (5.72) 4.65 (2.76-3.64 (1.47) 10.99 (2.35-3.60) Sample size 2180 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.23-1.08-1.06) . interval) 1.32) 2.58 (4.37) 2.34) 1.06) 2.64 (1.27-3.96 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10) 6.38-1.36-2. 1989).28) 5.38 (1.45) 1.91) 2.42) 1.26-4.53-21. paralysis.56) 4.76 (2.20-8.51-3.74) 1. in urine.02-5.25-11.5) 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 1.10) 3.55 (4.31-1.80) 4.29) 1. 1990).38 (4.24-6.41 (1.39-1.70) 4. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.99 (4.80-6.86) 5.40 (1.20 (1.22-1.90-2.92 (4.35-1.29 (1.0) 5.54 (1.68-3.55-5.72 (2.45-6.49-1. vomiting.48-5. 1994.55 (5.73-2. NTP.47) 1.77) 1..30) 2.68) 1.20-2.81-6.33-1.72) 6.915 (.47) 1.54 (2.60 (1.89 (2.29-3.60 (2.48 (1.33 (5.62 (1.97) 1.47 (5. 1985.70) 1.00) 6.36 (3.97 (5.75) 2.01 (4.36 (1.28-7.38 (4.61 (4.75) 1.39-5.31-1.2) 5.46) 3.710-1.50) 1.60 (2.66 (1.03) 1.30 (1.43) 1.47) 4.49 (1.88 (6.97 (4. Chronic exposures to natural low levels of barium in drinking water have not produced general health effects or evidence of cardiovascular risk (Brenniman and Levy.84) 2.47 (2.91 (3.2 (3.20-1.53 (2.3 (6.96) 7.26) 4.68 (3.52) 7. such as those used in medical radiographic procedures.28-6.59) 1.69 (5..19-1.96) 4.70) 10.Metals was eliminated primarily in feces and to a lesser extent.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 .39 (2.34 (1.61) 2. and route of exposure. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.02 (3.50) 1.36 (1. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.02) .24-1.75) 1.48-3.11) .58 (2.73) 2. Symptoms following acute high dose include perioral paresthesias.38) 1.41) 4.56 (1.81-6. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. are not absorbed when administered.19-1.31 (4. Toxicity from soluble barium salts is rare.00-1.91-2.38 (1.10-1.96 (4.S.16-1.40 (1.97-3.51) 4.58) 75th 2.46 (2.19-2.33 (1.76 (3.0) 7.44-2.31 (1.24-1.00) 4.52 (3.24-6.55-6. Insoluble barium salts.00) 4.50) 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 1.84-5.18 (1.18 (1.29-4.52) 2.26-1.84-2.04) 5.86-7.38-5.63-4.49 (1.49-1.50) 2.8) 4.68) 3.86 (2.13-3.2) 6.19-1.46) 1. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.01 (5.05-1.32) 2.16 (1.76) 2.52) 1.881 (.85-5.03) 2.0) 6.96) 4.29 (3.77) Total 1.60 (5.00-7.45 (1.51 (1.99) 1.45-1.39-10.01) 1.37-2.13-2.77-5.82) 1.25 (1. water solubility.29-1.10-2.87) 1.36 (3.76) 1.04 (2.78 (2.33 (1.32 (1.703-1.82) 1.54) 2.04) 1. a benign condition that may occur among barite ore miners.33) 6.22-1.28 (1.96-6.75-22.26-1.16) 11.36-1.57) 2.75) 2.46-22.39-1.62) 2.59-7.34-1.31) 5.32 (1.22-2.63) 1.74 (5.20) 4.39 (2.905 (.4) 5.59 (1.08-2.51) 6.58) 4.71 (5.40-1.48-1.57-10.24-11.51 (3.64 (1.27) 7. and cardiac dysrhythmias.45 (3.41 (1.52-10. weakness.39) 4.23-2.64) 7.65 (5.37 (1.88 (2.68-3.60 (1. diarrhea.98 (2.54) 1.73-4.42 (4.48 (1.03-1.27 (2.39 (2.77) 1.00 (2.56-3.31-1.62 (2.00) 1.29-4.83) 2.22-4.921 (.33) 1.51 (1.40 (1.33-4.03) 3.79) 1.76 (4.21 (1.77) 1.832-1.34-3.12) 2.36-1.41 (2.74) 1.4 (5.38-7.57 (6. 1986).69-9.75-3.35-1.50 (4.64 (1.02) 4.41) 5.76) 2.47-8.15-4.43-6.10 (6.49-1.28-11.03-1. Chronic high doses in animals resulted in kidney damage (McCauley et al.27-1.58) 1.26-1.44 (1.55) .45-1. 1984.59) 1.963 (.00 (3.29-7.30 (1.32 (2.83) 3.77) 5.891 (.52-4.00 (3.79-5.3) 6.37 (1.97-4.00 (5.38) 4.56 (1.92) 2.24) 3.48 (1.23-5.28-1. Wones et al. The health effects of exposure to barium compounds depend on the dose.58-6.754-1.96) 4. chemical form.880-1.53) .59) 2.777-1.37-1. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.80) 3.

Pozzoli L. 221-252 Komaromy-Hiller G. et al. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. Calabrese EJ.niehs. Ash KO. and a drinking water standard has been established by U. 1986. 1990. Schaller KH. Paschal et al. Weltle D.e. Clin Chim Acta 2000. 1994. Barium. patient population and literature reference intervals for urinary trace elements.pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. Reeves AL. 1989.gov/ntp/htdocs/LT_rpts/tr432. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report. NTP. Frohman. Minoia C. ed. Vol 2: Specific Metals. Information about external exposure (i. 2000) to levels in NHANES 1999-2000 and 2001-2002. Comparison of representative ranges based on U. and 2003-2004 (CDC. Cohressen B.atsdr. EPA. et al. Princeton (NJ): Princeton Scientific Publications. et al. In: Inorganics in drinking water and cardiovascular disease. Sabbioni E. Pietra R. Laurie RD. Fourth National Report on Human Exposure to Environmental Chemicals 195 .cdc. Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000. Jackson RJ..niehs. Apostoli P.296(1-2):71-90. 231-249. National Toxicology Program (NTP). Jr. New York: John Wiley & Sons. Biomonitoring Information Levels of urinary barium reflect recent exposure.28(3):373-388. Atlanta (GA).Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. Gallorini M. Inc. 2001. 1992). [online]. Environ Health Perspect 1990. Douglas BH. 2005.95:89-105. Levy. and radium In: Bingham A. J Toxicol Environ Health... Pirkle JL. et al.. and serum of Italian subjects.. McCauley PT. Stadler BL. 4/8/09 Paschal DC.197210. Int Arch Occup Environ Health 1992. Investigations into the effect of drinking water barium on rats.S. A study of 46 elements in urine. Advances in modern toxicology. Environ Res 1998. Morrow JC. 1998). Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. Kopp SJ. In Friberg L. Perry HM. Available at URL: http://ntp. Zschiesche W.S. References Brenniman GR. strontium. environmental levels) and health effects is available from ATSDR at: http://www.nih. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no.64(1):13-23. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. PS.html. calcium. p. 1984. Minoia et al. In: Calabrese EJ.76(1):53-59. Exposure to soluble barium compounds: an interventional study in arc welders.. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies).85:355-359. 2001-2002. 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. ed. Centers for Disease Control and Prevention (CDC). Vouk VB. pp. Lack of effect of drinking water barium on cardiovascular risk factor. Trace element reference values in tissues from inhabitants of the European community I. Howerton K. Nordberg GF... Third National Report on Human Exposure to Environmental Chemicals. Ting BG. Costa R. Magnesium. the welders had no obvious adverse clinical effects (Zschiesche et al. Handbook on the Toxicology of Metals. New York: Elsevier. p.html?charset=iso-88591&url=http%3A//ntp. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Trace metals in urine of United States residents: reference range concentrations. Wones RG. Sampson EJ. Perry EF. eds.. 84-94. LA. Genter MB. 1985.gov/toxpro2.nih.gov:8080/cs. Princeton NJ: Princeton Scientific Publications. 5th ed. eds. 2nd Ed. Patty’s toxicology. Sci Total Environ 1990. Epidemiological study of barium in Illinois drinking water supplies. blood. p. 2005. Powell C. barium.

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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and machine-parts industries. and dental bridges. In studies of laboratory animals. 196 Fourth National Report on Human Exposure to Environmental Chemicals . Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 0. and from breathing tobacco smoke.13.13. 01-02.S. bertrandite and beryl. and 03-04 are 0.13. < LOD means less than the limit of detection. the lightest of all metals.130 (<LOD-. coal. near some hazardous waste sites. 7440-41-7 General Information Pure beryllium is a hard gray metal. respectively.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. x-ray machines. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes. Low-level beryllium exposure in the general population can occur through breathing air. beryllium is used in instruments. In medicine. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. Two types of minerals. or drinking water containing the metal.140 (<LOD-. aircraft. and refined beryllium is used in mirrors and special metal alloys for the automobile. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air.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 . Exposure to beryllium occurs mostly in the workplace. soil.Metals Beryllium CAS No. and 0. Beryllium compounds are commercially mined.130 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 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 . A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. see Data Analysis section) for Survey years 99-00. eating food. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. and can be found in mineral rocks. computer. and volcanic dust. nuclear. are mined for commercial recovery of beryllium. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. electrical.

respectively. 2003. NTP considers beryllium to be a known human carcinogen. including contact dermatitis and subcutaneous nodules.391) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 1990).281 (<LOD-. Maier.. Skin exposure can result in delayed hypersensitivity reactions. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al.Metals days has been calculated for beryllium elimination from the human skeleton (IPCS. EPA. based upon excess lung and central nervous system cancers in studies of workers. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. Fourth National Report on Human Exposure to Environmental Chemicals 197 . and drinking water and environmental standards have been established by U. 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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa. 2002). S.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 . Chronic beryllium disease.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 .346 (<LOD-. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. or berylliosis. which produces pneumonitis. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. IARC has classified beryllium as a human carcinogen. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. population from the National Health and Nutrition Examination Survey.S.231 (<LOD-. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 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 .

1 μg/L). 2001).gov/toxpro2.13 μg/L.. In other studies. blood. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Paschal DC. environmental levels) and health effects is available from ATSDR at: http://www.cdc. Centers for Disease Control and Prevention (CDC).158:165-190. Sci Total Environ 1990. Weston A. which approximate this Report’s limit of detection. et al. Paschal et al. population are lower than levels in workers. Given these results. et al. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure.e. Pozzoli L.atsdr.org/documents/ehc/ehc/ ehc106. Maier L. Schaller KH. References Apostoli P. Morrow JC. less than 0. Clin Chest Med 2002. 0. and the 95th percentile for males in NHANES 2001-2002. Atlanta (GA) 2005. Jackson RJ. Kriess K. Element reference values in tissues from inhabitants of the European community. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Am J Epidemiol 2003. Levels of beryllium in urine for the U. Ash KO.S. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Gallorini M. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. Ting BG. Comparison of representative ranges based on U. Review of elements in blood.html.157:388-398. Clin Chim Acta 2000. patient population and literature reference intervals for urinary trace elements.S.. Sci Total Environ 1994. A study of 46 elements in urine. Minoia C. Costa R.. 20012002.12 to 0.76(1):53-59.e.Metals (i. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al.. International Programme on Chemical Safety (IPCS).296(1-2):71-90.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. and the fact that most NHANES participant levels were undetectable. Third National Report on Human Exposure to Environmental Chemicals. Pietra R.23:827-839. HLA-DPB1 and chronic beryllium disease: a HuGE review. Hamilton et al. plasma and urine and a critical evaluation of reference values for the United Kingdom population. 2000. Minoia et al. VI. Van der Venne MT. Apostoli P.. 1990. 106. 3/27/08 Komaromy-Hiller G. McCanlies EC. Genetic and exposure risks for chronic beryllium disease. Trace metals in urine of United States residents: reference range concentrations. Sabbioni E. Beryllium [online]. Andrew M.S.74:162-166. population were generally undetectable in NHANES 1999-2000. Hamilton EI. 1990. Environ Res 1998. They reported urinary beryllium levels ranging from 0.htm. Available at URL: http://www. it is likely that urinary beryllium levels in the U.95:89-105. Pirkle JL. Howerton K. Sabbioni E. Environmental Health Criteria. and serum of Italian subjects. Trace element reference values in tissues from inhabitants of the European community I. and 2003-2004. 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. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure.inchem. 1998). Sampson EJ. Int Arch Occup Environ Health 2001.

80) 1.90) 1.300) .300 (.200-.600) .50 (1.400 (.20) 1.60 (1.700) .600 (. Other uses include pigment production.50 (1.600) .500-.00 (.500-.468 (.00-1.200-.00-1.400) .331) .300) 75th .20) 1.00-1.200-.70) 1.600-.40 (1.300 (.00-1.400-.600 (.400 (.00 (.700 (.400) < LOD < LOD < LOD .600) .S.600) .300-.900-1.275-.300) .usgs.700) 1.400) .30 (1.900 (.500 (.289-.600) .60 (1.300-.10 (. or copper smelters (U.300 (.900-1.50-1.700-1.300-.449) Selected percentiles ( 95% confidence interval) 50th .800) .300) .403 (.20) 1.300) .300-.500) .300 (.500 (.400) .300-.60-1.900 (.376-.600) 1.300) 1. population from the National Health and Nutrition Examination Survey.300) .300-.600 (.00 (.500 (. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.60) Total * .300 (. Fourth National Report on Human Exposure to Environmental Chemicals 199 .460) .400-.00-1.300 (.10 (1.70) 3913 4339 4131 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .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 * * * * * * .266-.403) .421 (.50) 1.296-.14.400) .200) .400-.300-.400) .300) .300) .200-.900-1. cadmium use has declined in response to environmental concerns (http:// minerals.300 (.600-.420 (.40) 1. respectively.500 (.300) .367-.20) 1.200) .500-.500) .500 (.600 (.50-1.00 (.500-.600 (.304 (.200 (<LOD-.400) .30) . and 0.400 (. as zinc sulfide) and to a lesser extent.344) .337) .00 (.333 (.400) < LOD .700) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700-1.300) .40-1.500-.300 (.300 (<LOD-. malleable.400 (.313 (.400-.500-.400 (.283 (.309-.304-.600) .600 (.216-.400) < LOD .600 (.500 (.600 (.10) 1.70) 1.20-1.00 (1.400 (.20) .20-1.600 (.20 (.400 (.30-1.10) 1.200 (<LOD-.30-1.50) 1.800) 1. Since 2001.400 (.300-.400) .255) .400 (.00 (.40 (1.900-1.00 (1.368-.500-.300-.700) .20-1.500-.50 (1.10) 1.800 (.600-.500-.513) .20) 95th 1.500-.00) .300-.20-1.70) 1.500 (.398) < LOD < LOD < LOD < LOD < LOD < LOD .50 (1.500-. 0.60) 1.425 (.20) 1.300 (.00-1.500 (.500-.300-.500) .200 (.10 (1.300-.00-1.900-1.300-.700-1.30-1.600 (. 01-02.700) .300 (<LOD-.600-1.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.600) .400) < LOD . coatings and plating.10) 1.900-1.300) .00-1.60 (1. lead.600) .400-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.300-.3.60) 1.gov/minerals/pubs/commodity/cadmium).361-.400) . U.500-.20-1.700) .400-. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.30) 1. Cadmium also may be emitted into the air from zinc.900-1.10) 1. and nonferrous alloys.30-1.500-.470) * .300-.S.10 (1.300) .500) .300 (. 7440-43-9 General Information Cadmium is a soft. and 03-04 are 0.40 (1.441) * .400-. and incineration of municipal waste materials.393 (.400) .600 (.50-1.30) 1.00) .800-1.378 (.378-.30-1.400 (.20-1.300 (.304 (.200 (.400 (.50-1.700) .300-.40 (1.400-. during refining of lead and copper from sulfide ore.20) 1.500-.600) 90th 1.40-1.300) .500 (.300 (.412 (.300 (.300-.400) .10 (1.30) 1.300-.300 (<LOD-. plastic stabilizers.400) .20 (1.50) 1.400 (.424) * .00-1.600 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.300-.20) .300) .427) * .300-.700) .00 (.20) 1.382 (.395 (.700) .426-.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .300 (.600 (.Metals Cadmium CAS No.900-1.70) 1.10) 1.400 (.400 (.3.80) 1. which may vary for some chemicals by year and by individual sample.500-. interval) .300 (<LOD-.60) 1.452) .500) .600) .10 (1.386-.600 (.900-1.10) 1.00 (.40) 1.800 (.40 (1. see Data Analysis section) for Survey years 99-00.80 (1.500) .400 (.900-1.326 (.400-.10 (1.800) . EPA.235 (.10) 1. < LOD means less than the limit of detection.500-.60 (1.40 (1.400) .40 (1.359-.400) .200 (.10 (1.366) * * .00 (.400 (.60 (1.362-.400-.500) .20-1.00 (. The predominant commercial use of cadmium is in battery manufacturing.400 (.20) 1.400) .300-.200-.S.300-.800-1.500-.400-.

281 (.390-.078 (.230 (.229-.101) .077 (.170-.231) . and various seeds.189-.261-.209 (.272-.170 (.476-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.249-.330-.806) .210 (.199 (.080 (.170-.310 (.260-.243-. Cadmium absorption may be increased with iron deficiency (Berglund et al.279 (.51 (1.870) .475 (.200-.184-.498-. With chronic exposure.38) 1.520-.800 (.150) .157) .262) .860) 1.960) 1.192-.875) .299) .20-1.717-.17) .206) .109 (.479) .36) 1. 1999.06.220 (.229) .892 (.551 (.061 (<LOD-. Cadmium is absorbed via inhalation and ingestion.559 (.545 (. Diamond et al. 2001).858 (.748-1.989-1. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.223 (.800-.339) .34) 1.180 (.190-.387) . respectively.836-1.918-1.226) .83) 1.232 (.818 (.510-.366-.211-.19) 1.763-.190-.596) .38) .261-.519) .240-.148-.820 (.110-.686-.980 (.01-1.700-.500) .01 (. 0.26) 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.455 (.480) .766 (.458 (.229) .13-1.481) .230) 75th .290-.285-. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.24) 1. 01-02.490) 1.200 (.160) .206 (.960 (.400-.232) . 200 Fourth National Report on Human Exposure to Environmental Chemicals .17 (.191-.412) .201 (.20 (1.265) .237-.519) .700-.077 (.246) .470-. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.316 (.623) .551) .210 (.141 (.04 (.151-.990) .202-. 2004a.440 (.300) .210) .171-.112-. 2003).092 (.109-.980) .530 (.136) . ingestion through food is the largest source of exposure.394-.284) .270 (.790 (.440 (.28) 1.843-1.963-1.28 (1.388-.100-..160) .160-.257-.175 (.060-.238-.366) .507) .589 (.120 (.436-.175 (.430) .466 (.452 (.253-.12-1.169-.28-1.220-.** Survey Geometric mean (95% conf.810-1.173) .886-1.875 (.134) .067-.03) .430-.114-.790 (.210 (.204 (.17 (.892-1.257) .092) .239 (. and 0.189-.219 (.183-.633-1.Metals 2000).57) 1.450 (.148) .482) .362) .310) .447 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .067-.38) .09-1.221) .390-.165-.880) .26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .393-.640) .741-1.208-..13 (.203 (.260 (.580) .233) .22 (1. calcium.222) .381-. however.247) .74) 1. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.179-.445 (.372) .01) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.255) . rice.227 (.980-1.839 (. see Data Analysis section) for Survey years 99-00.283 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.260-.539) .128 (.733) .607) .02-1.38) 1.194-.207-.06-1.886) .12 (.313) . About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.233) . 2003).234 (.251) .82) 1.220-. wheat.492 (.360) .354) .426 (.308) .17 (.32 (1.115-.700-.187 (.47) 1.306 (.06.22 (.510) .157-.177-.198) . Cadmium in soil is absorbed by plants.219 (.351-. drinking water is a source for cadmium intake.160 (.326) .820) 1. The kidney is a critical target and shows the earliest sign of cadmium toxicity. Horiguchi et al.135-.065-.200 (.255) .327 (.210 (.20 (1.817 (.195-.210 (. including many food crops such as cereal grains. Kikuchi et al.25 (1.433-.30-1.302 (.733-.193-.52 (1.462 (.680 (.440-.193 (.135 (.493-.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.820-1.196-.200-.210) . population from the National Health and Nutrition Examination Survey.610) .329 (. an inducible metal binding protein.S.249) .240) . For nonsmokers who are not exposed to cadmium in the workplace.980-1. Renal tubular and glomerular damage.090) .540) .06. potatoes.855-1.890 (.977) .41 (.713) .366-.235) .07-1.15 (.241) .980) .289-.214-.090) . Inhalation of cigarette smoke is a predominant source of exposure in smokers.255) .153-. 2003.43) 1. whose body burdens of cadmium can be approximately twice that of nonsmokers. zinc.530) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.121 (.972 (.087-.423-.203) .705-.06-1..230) .300 (.20) 1. interval) .220) .219 (. and 03-04 are 0..72) 1.940-1.081) .273 (.730-. copper) and protein.191 (.714-1.336) ..320) . 2003).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 .061-.400-.221 (.25) 1.753-.280 (.890-1.270 (.211 (..277 (.15) .190-.919) .20 (1.130 (. 1994).167-.150-.126) .06) .192-.813 (.265 (.107-.181 (.140 (.216 (.191-.390 (. To a lesser extent.817 (.456-.633 (.445 (.350 (.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 .500) 90th .202 (.04 (.490) .322 (.282 (.263) .550 (.238) .13) .450 (.189) .295) .178-.10 (1.48 (1.848 (.15) 1.

826-1.839) ..441-.813-.200 (.917) .769 (. However.147-.531 (.136-.308 (.222-.940-1.516-.630-. Noonan et al.05) 1.131-. At lower environmental exposures.111-.206-.185 (.090 (.225) .423-.364) .100 (.830-1.224 (.219 (.190 (.647-. population from the National Health and Nutrition Examination Survey.147-.156) .288) .236-.268 (.826-1.227-.449) .281) .181 (. 2002.270 (.02 (.412 (.198) .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 .296 (.267 (.827) .184-.757 (.288-.472) . Fourth National Report on Human Exposure to Environmental Chemicals 201 .985 (.283 (.693 (.289) .281) .086 (.094) .666-.560-.261 (..292) .147 (.250) .137-.215 (.813-1.404) .979 (. 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. Jarup et al.168-.784) .256-.183) .473 (.414 (.07 (.431) ..818) .13) .175 (.415) .297) .700 (.07) .123-.156-.687 (.191-.789 (.856 (.194-.727-. most often a result of occupational exposure (Roels et al.387 (.245 (. During the 1950’s and 1960’s.700) .S.181) .234 (.444-.208-.228-.650-. 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.184-.096) .321) .210 (.690-.551) .219 (.247-.175 (.202 (.157-.173-.097) .04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .267 (. 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.500-.518) .161-.166 (.199 (..266-.833-1.653) .266) .240) . 1999).08) .414-.170 (.238) .174-.078 (.398-.631) . 1996.927-1.818) .207) .226) 75th . 2003. 1999).280 (.591 (.491-.470) .240) ..229) .479 (.104) .303) .10) 1.421 (.197-.136-.873 (.184) .418) .140-.783) .779 (.690 (.432 (.157-.232) .538) .274) 1.325 (.783 (.253 (.340) . Horiguchi et al.137 (.071 (..077-.708-1.481 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.719 (.617 (.440) .143-.338 (.940 (. 2004).091 (.113-.391-. 1999).261-. 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.255-.063-.686 (.130-.757) .687-.718 (.235) .487 (.098) .168-.288 (.189-.382-.** Survey Geometric mean (95% conf.536 (.148 (.438-.712 (.067-. Staessen et al.336-.38) .173 (.729 (.144-.211 (.377-.426-.239-.12) 1. 2002.261) .208 (.433-.112) .716) .212 (.223) . 2002.688-.304-.177) .171-. Olsson et al.126 (.106) .182) .311) .470) .559-.182) .725-1.143) .263-.210) .795) 1.247-.438) 90th .754) .830) .09 (.802 (.247-. can result from high dose chronic exposure.440) .150-.941 (.696-..241) .233 (.740 (.263 (.182) .806-1.388-.998) .178) .238-.084 (.146-.159 (.501 (.404 (.537-.293-.170-.158-.316 (.234) .331 (.382) .176 (.163 (.352) .674-1.085-.107) .085 (.154 (.209) Selected percentiles ( 95% confidence interval) Sample 95th .221 (.716-.00 (.242) .278) .490 (.196 (.191) .533) .350) ..691-.091 (.16) ..00 (.181 (.876-1.143-.218) .159 (.078-.232) .929) .767) .101) .850) .122 (..191 (.104) .209) . 2000.917 (.207-. interval) .316) .909-1.162 (.175-.919 (.093 (.446) .722-.225) .252 (.183 (.962) .199-.792 (.343-.476) .289) .220 (.135) .663 (.123-.084-.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .418-.884) .667) .140-.253) .075-.387-.607) .545) .507-.906) .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.828) . two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.273 (.181-.185) .051-.690-.17) .865 (.381-.190 (.622 (. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.668-.678-.210 (.614) .318 (.221-.950) .484 (.204-.091) .423 (. 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.767 (.06 (.645-.168 (.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 .074-.856) .163) .678 (.931 (.304) .16) 1.176 (.156 (.308) . 2004b).192) .187) .075 (<LOD-.234-.874-1.282 (.300-.850) .201-.562-.541) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.216-.434 (.335 (.187-.329 (.178-.154-.083-.205 (.

2002. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect.e. Noonan et al. Zhang et al. Wennberg et al. not to imply a safety level for general population exposure.. Olsson et al. Ezaki et al. Friedman et al. 2004. However. CDC.. Both IARC and NTP consider cadmium a human carcinogen.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al... Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures... 2003). Several studies of populations residing in areas with higher cadmium soil concentrations or with frank cadmium pollution have reported mean blood and urine cadmium levels considerably higher (as much as 10 times higher) than control groups or representative U. 2005. 2006. respectively. 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).46 mg/gram of creatinine) (Ezaki et al. 2002).... In the typical environmental exposure. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity... 1999. Creatinine-corrected urine cadmium values in U. Becker et al. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. Becker et al. 1999). In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies.. 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. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1.. 2004. 2003. Salpietro et al.. Olsson et al. Information about external exposure (i.. Staessen et al.. and drinking water and environmental standards have been established by U..1 mg/L (Alfven et al.S. Jarup et al... 2003. 2005). Staessen et al.. 2000. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al.. 2002). 2006. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. as may occur from welding cadmium-alloyed metals.26 and 3.S. 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. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals .. 2002. 2000. respectively. Women had higher blood and urine cadmium levels compared to men of similar ages. 2004). Occupational standards are provided here for comparison only..... 2006). Animal studies have demonstrated reproductive and teratogenic effects. EPA. Wennberg et al.gov/ toxpro2. 2004b).. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. 2000). data (CDC. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al.. 2005. Wilhelm et al.cdc. 2005. In adults aged 60 years and older. Horiguchi et al. Moriguchi et al.. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. 2003.. Olsson et al. 2006). maternal blood or maternal urine and birth weight (Nishijo et al. For NHANES 19992000. 2004. Acute and heavy exposure to airborne dusts and fumes. In postmenopausal women. Cadmium can produce lung. 2002. 2004b. 2003. 2003. 2002. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH......html.. potentially fatal pneumonitis (Fernandez et al. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. approached these values associated with subclinical changes in renal function and bone mineral density. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney. 2005. intermediate in former smokers and lower in never-smokers (Becker et al.atsdr. Staessen et al. Blood and urine cadmium levels are typically higher 202 in cigarette smokers.. 2000. 1996. Horiguchi et al. Subtle increases in markers of renal tubular effects have been associated with urine cadmium levels as low as approximately 1 mg/gram of creatinine (Akesson et al. 2004. 1988). environmental levels) and health effects is available from ATSDR at: http://www. 2002. 2002) and length at birth (Nishijo et al.. Ezaki et al.. Komaromy-Hiller et al.. Jarup et al.. has resulted in severe.S. Suwazono et al. with peak values observed in the fifth to sixth decades (CDC. 1996). Becker et al. 2002). 2002). Mannino et al. Further research is needed to address the public health consequences of such exposure in the United States. Jin et al. 2002. 2002).. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. 2003. 1999).

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Nakagawa H.epa.209:301305. EPA). Relationship between newborn size and mother’s blood cadmium levels.gov/ttn/atw/ hlthef/cadmium. Honda R. Cadmium carcinogenesis. eds. Nakagawa H. Hazard Summary. Environ Res 2006. lead. lead. Int J Hyg Environ Health 2006.59(1):22-25. Lundh T. Zhu HD. Suwazono Y. Tawara K. Nordberg GF.S. 2004. Merlino MV. Toyama.100:330-338. United States Environmental Protection Agency (U. Environ Res 2000. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Kathman SJ. Cadmium compounds. iron status. Environmental exposure to cadmium.Metals Nishijo M. Effects of exposure to low levels of environmental cadmium on renal biomarkers. Zhao YC. dietary intake. Lancet 1999. cadmium. Nogawa K. Lijnen P. et al. or cadmium in controlling occupational and environmental risks of nephrotoxicity. 2001. Thijs L. Revised and new reference values for arsenic. Kobayashi E. Bergdahl IA.84 (Section A):4455. 4/8/09 Waalkes MP. et al. 2000. Campagna D. Sarasua SM. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. Bensryd I. Revised 2000 [online]. Sager PR. Jansson J-H. Lundh T. Honda R. Stegmayr B. Wilhelm M.21(3-4):251-262. Gallmans G.59:394-397. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. Buchet JP. Liu QF. Bruiglia S. Ren Fail 1999. Staessen JA. Noonan CW. Nordberg M. J Perinat Med 2002.533(12):107-120. Schultz C. Friberg L. Occup Environ Med 2002. Environ Health Perspect 2002. J Environ Sci Health B 2004. Ginucchio G. Ottosson H. pp. Kido T. Salpietro CD. Roels HA. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. Usefulness of biomarkers of exposure to inorganic mercury. Gangemi S. Environ Health Perspect 2002. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. Tanebe K. Biological monitoring of cadmium. created 1992. Schwenk M. lead. age. Nakagawa H. Hoet P. Cadmium in blood and urine – impact of sex. Nordberg GF. Stelitano A.39:2507-2515. Lybarger JA. Oskarsson A. Roels H. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk. and mercury in the population of northern Sweden. 151-168. and risk of fractures: prospective population study. Available at URL: www. Roels HA. Staessen J.3:26-41. Nishijo M.html. Biological monitoring of toxic metals. Saito S. Fan YG. and former smoking – association of renal effects. In: Clarkson TW. Mutat Res 2003.353:1140-1144. Japan. Mueller PW. Vangronsveld J. et al. Wennberg M. Okubo Y. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan. Minciullo PL. Zhang YL. et al. J Cardiovasc Risk 1996. Emelianov D. Olsson IM. et al.30(5):395-399. Lauwerys R. Arch Environ Health. Skerfving S.110:151-155. New York: Plenum Press. Time trends in burdens of cadmium. Wang JX. et al.110:1185-1190. Tanebe K. Lison D. Kuznetsova T. forearm bone density.

03 (4.6 (11.50) 5.37) 7. However. although cesium was generally of low toxicity when given to animals.20-4.14.08-5. the body half-life is estimated to be 70-109 days based on 137Cs exposures.80-11. Radioactive 137Cs has been used medically to treat cancer. 01-02.64-10.50 (4.14 (4.20) 8.0 (10.17) 4.80 (4.80-6.20 (4.44 (8.50 (6.10-8.81-14.93 (4.05-5.96 (6.0) 12. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.56) 5.81) 4.4) 10.60-7.Metals Cesium CAS No.89) 5.9 (10.30 (6.70 (8.04 (4.2-14.00) 6. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.53-11.60-12.60-7.00-9.0) 9.87 (4.15-8.97) 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 4.37) 5.60) 5.02 (4.40) 7.7 (9.4) 9.00-8.7 (11.3 (8.77 (4.82) 5.25-5.87 (4.76-6.00-4.80 (8.2 (9.97 (7. and as polymerization catalysts.00) 7.3 (8.70 (4.59) 7.59-5.0) 10.5 (8.10-7.23) 9.45-8.1) 11.68) 9.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.29) 4.74) Selected percentiles ( 95% confidence interval) 50th 4.8) 9.20) 4.80-10.2) 12.57-5.70 (9.13 (5.81) 4.74 (4.59 (5. diarrhea.62) 4. 0.90-12.10-5.2.1) 10.34) 9.30-10.99-11.8 (10.23-4.7 (9.86-11.70) 5.05) 5.8) 12.62 (5.60 (8.20-7.55 (7.00 (7.32 (3.09) 5.60-5.9 (11.38) 5.3) 10.12-11.1-12. and clay. semiconductors.87 (4.2-13.34 (4.8) 9.30) 5.84) 5.33 (5.46) 7.5-14.72) 4.S.25) 4.90) 5.80-10.10 (8.1-12.13 (8.36 (3.7 (8.13 (7.1 (10.4) 10.5-13.39-4.84-9.52) 7.1 (9.99) 9.03-4.35-5.90-10.77-8.50) 9.40 (4.95-4.13-8. see Data Analysis section) for Survey years 99-00.1) 9.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.12 (4.90) 4.69-6. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.4) 12. and 0.12) 5. Fourth National Report on Human Exposure to Environmental Chemicals 205 .86-12.8) 11.14.00-10.63-4.50-7.5-16.60) 7.01-6.30 (6.49) 75th 7. and 03-04 are 0.6 (9.26) 4.8-13.21) 90th 9.7 (10.56 (4.01) 7.0) 12.4) 12.47-4.00) 4.40-5.42) 7.2-13.49 (4.0) 11.26 (3.80-13.03 (4.64) 5.90) 7.42-7.9) 11.27 (7.20) 5.95) 5.4) 95th 11.3) 10.10 (6.05-5.61) 7.55-11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.91-8.3) 10.0 (9.74-5.16-6.90) 5.72-7.9 (10.26) 7.53 (6. For absorbed cesium salts.99-6.70) 7.50 (7.20-8.61-6.33-5.71-5.71 (4.0-15.9 (11.70-5.97) 4.8) 12.8) 11. photographic emulsions.80-10.12-5.60) 7.90 (6.90-10.6 (9.71) 4.67 (4.68 (7.94 (4.70 (6.97-7.9) 340 368 290 718 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 4.59-5.6 (11.90) 9.40-7.5) 9.82-4.08-5.5) 12.91 (7.52-9.83-4.08 (7.08) 7.92-13.35 (4.27-5.6 (9.70) 5.63) 6.90-12.20) 7.7) 10.4-13.45-5.64) 4.55 (4.8 (11.27) 4.04) 7.50 (4.30) 7.1) 11.64 (4.84 (4.3) 9.99-11.70 (5. soil. population from the National Health and Nutrition Examination Survey. cesium hydroxide is corrosive and irritating at high concentrations.66 (7.20-5.39) 7.64-5.36 (6.77 (9.7) 11.16-6.0) 12.49) 4.35 (4. infrared lamps.7 (9.90-8.63 (4.50 (4.5) 10.70-8.87) 5.1) 9.7) 11.40-5.40-5.40-11.80 (8. Little is known about the health effects of this metal. respectively.6 (9.98 (7.7) 10.40-11. and high-power gas-ion devices.73-5.2-12.40) 5.81) 9.17-6.60-6. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4 (9.32) 4.36) 3.40-5.56-11.7 (10.94) 4.10 (8. Whether cesium compounds are carcinogenic is unknown.8) 12.87-7.4 (9.86 (7.00-8.3) 12.1 (11.07) 4.9 (11.5-14.4) 11.71-9.40) 5.60-6.9) 8.24) 4.6) 11.3-13.2-13.22-4.42) 6.32-5.90-10.6) 10.88 (8.60 (7.80) 7. scintillation counters.29 (4.95 (3.31-8.80 (8.30-5.70 (6. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.05) 5.90 (4.71 (8. nausea.2 (9.99) 7.79 (4.0) 11.7 (10.47-8.9) Total 4.89) 4.10 (6.71-8.56 (4. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.26-11.43-8.98 (7.07-11.84-5.84) 8.9) 12.94 (4.81 (4.21 (4.43 (5. and cardiac arrhythmia (ATSDR.17 (6.77 (9.7-14.9 (11.73-11.5 (10.80 (4.0-13.94-4.10-9.3-15.54) 4.62 (5.08 (6.2) 11.4 (10.20 (6.22 (4.70 (8. 2004).80 (4. Most human exposure to cesium occurs through the diet.1-13.64) 5.49 (5.33 (6. interval) 4.3-13.01-8.3) 10.8 (10.09-5.25 (3.54-11.83) 6.89-5.59-5.

90 (7.74-11.72-5.29) 5.03-5.74) 75th 5.20) 5.31 (4.47) 7.43 (8.3 (10.79) 6.3) 9.42 (4.99) 4.53 (6.91 (5.07-4.24 (3.58-5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.08 (3.36-10..04) 6.57) 3.66 (6.71) 6.23 (7.81 (4.19-3.28 (5.95) 8.56 (4.14 (6.75 (6.9) 10.3 (8.10) 7. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.08-3..90-8.18 (7.47 (4.84-7.12) 3.51 (3.50) 4.63) 6.96) 4.08 (6.5) 9. Minoia et al.96) 4.91-9.2) 11.00-8.1) 11.75 (7.S.08-7.37-3.41 (8.35-11.03-6.48) 7. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.41 (5.43 (4.04-5.85) 5.97) 8.77 (6.07) 8. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.18-7.29) 4.63 (6.22 (3.90-3.34 (5.00-5.40-5.65 (6.74 (5.28) 7.8) 10.87) 5.60-10.68) 6.4) 10.11 (5.50 (7.43) 8.89-4.50 (5.16-5.29-3.02-4.25) Selected percentiles ( 95% confidence interval) 50th 4.03) 5.98 (6.52-5.91) 5.00-5.38-7.73 (3.95-6.80) 6.S.3) 11.27) 4. 2005.16-8.33 (5.6) 6.35 (3.9 (9.09) 8.09 (4.16) 5.64-6.60 (3.44-9.29) 4.28 (4.05-4.06) 5.62-8.86 (4.63 (7.97-5.03) 6.38 (3.16-8.00-9.68 (4.8 (9.41) 9.53) 3.37) 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 5.27-6.39) 5.43-11.33-3.41-4.50 (6.44) 3.26 (3.58 (6.71 (7.31 (4.39) 8. population.99 (3.60) 3.04) 5.65-4. Two small studies of European populations reported urinary cesium levels similar to U.51 (4.09) 4.02 (5.20-8.58) 3.15-11.04-11.41) 4.97-4.51) 4.68) 3.3-15.38-12.74 (4.48) 90th 7.82-4.30-4.13-9.85-4.64) 9.20-4.11 (5.42-4.40) 6.13) 7.83-7.82) 7.67 (5.98) 5.68) 4.91) 5.50) 8.05 (4.55-5.43 (4.61-3.05) 3.33 (5.27-4. Komaromy-Hiller et al.98) 5.43-6.95 (5.91) 4.13 (3.64 (4.51 (3.26 (4.38) 10.72 (4.50) 4.21-3.94) 7.95 (3. 2004).50) 4.62) 5.56-10.08) 3.84-9.92) 3.8) 5.98 (7.27 (6.28) 8.99-4.24-4.2 (8.36-3.63 (4.77 (7.96-4.20-4.5) 7.14-6.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.54 (4.45 (4.06) 4.8) 6.10 (3.91 (5.29-3.61 (7.42-4.79) 9.93-9.47) 4.73-4.78) 4. 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.46-8.59-8.2) 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 3.10 (3.99-9.18) 8.66 (5.78 (3.35-7.07 (5.07) 8.18-6.78 (3.91-6.67) 5.40) 7.05-3.60-20. population results shown in this Report (Alimonti et al.00) 6. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.17-4.26-6.3 (9.19-6.22) 6.7) 10.38 (3.96-4.47) 6.06 (3.30-4.76-6.53 (4.51 (4.06 (5.27 (6.35) 3.30 (3.15-4.14) 4.48-6.5 (9.83) 8.54 (5.63-6.84-7.77 (4.81 (4.41-7.43 (3.14) 4.64 (8.58) 8.53) 6.00-4.24-10.9 (10.55) 4.0) Total 4.08 (5..79-5.00-10.68-11.27 (8.56) 4.46 (8.30 (7.51 (7. and were also roughly similar to those in this Report.30 (4.42-6.17 (6.79) 4.21-5.15 (7.63-6.44-5.01-8.21-4.50-5.14-7.83-6.17) 4.44 (4.6 (9.77-5.72) 4.49) 3.70) 7.96 (4.47) 6.00 (8.14-4.3) 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 3.45-6.76-9.17) 9.25) 4.88-10.7-12.0 (7.13-9.08) 4.65-3.10-4.90-8.67 (6.99-9.59) 4.30) 10.60 (5.36-6.54 (3.46) 6.58 (4.47 (7.31-6.44 (8.92 (5.54 (4.95) 10.87 (5.93-7. population from the National Health and Nutrition Examination Survey.64) 4.5) 9.91-7.66-6.46 (7.85) 4.08) 4.21 (2.66 (5.84-11.94 (5.79 (5.2 (8.70 (7.35 (4.87-4.55 (3.74) 3.39 (5.56) 4.12 (3.31-4.22-11.33-8.7) 10.95-12.42 (5.S.64) 5.30) 10.20-4.41 (4. Using clinically submitted specimens. 1990).95) 4.84-9.10 (5. (2000) found urinary cesium levels that were slightly lower than those reported for the U.56) 3.46-4.0) 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 .0) 7.75-11.70) 6.6 (9.15) 95th 8.88-4.05-3.12-6.77) 4. interval) 4.05) 6.78) 4.

Assessment of urinary metals following exposure to a large vegetative fire. Voorhees RE.S. J Expo Anal Environ Epidemiol 2004. A study of 46 elements in urine.gov/toxprofiles/tp157. et al. Pozzoli L. antimony and tungsten. Paschal D.cdc. Mincione G.14:120-128.2004 [online]. Centers for Disease Control and Prevention (CDC). Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. Mott JA. 4/8/09 Alimonti A.atsdr.95:89-105. Sci Total Environ 1990. Third National Report on Human Exposure to Environmental Chemicals. Fourth National Report on Human Exposure to Environmental Chemicals 207 . Wolfe MI. Costa R. 2000. patient population and literature reference intervals for urinary trace elements. et al. Forte G. Rapid Commun Mass Spectrom 2005. cesium. Trace element reference values in tissues from inhabitants of the European community I. Toxicological profile for cesium. Available at URL: http://www.296(1-2):71-90. blood. Spezia S. Howerton K. Comparison of representative ranges based on U. Sabbioni E. Sewell CM. New Mexico.html. Komaromy-Hiller G.19:3131-3138. and serum of Italian subjects. Gallorini M. Ronchi P. Clin Chim Acta 2000. Gatti A. et al. Apostoli P. Atlanta (GA) 2005. Ash KO. Pietra R. Minoia C. Wood CM.Metals References Agency for Toxic Substances and Disease Registry (ATSDR).

750 (.380 (.430-.390-.32-2.410 (.01 (.418 (.53) 1.04-1.370) .620-.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 .02-1. Cobalt compounds are also used in manufacturing battery electrodes.700) .460) .370-.33-1.320 (.370-.487) .12) 1.14) 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 .09 (.470 (.07.650-.520-.56) 1.890-1.06 (.S.410 (.360-.46 (1.900-1.334) .570 (.900) .800-. hard metal (alloys of cobalt and tungsten carbide).48) 1.12) 1.499 (.290-.583) .17 (1.730) 1. and soil.520-.92) 1.570) .550 (.32 (1.670-.350-.47) 1.348-.300-.22 (1.50 (1.73) 1.330 (.379 (.42) 1.410 (. respectively.01 (.950 (.259-.07-1.340) .550-.379 (.630 (.16 (1.660) .04) 1.610) .06 (.280-.05 (.390 (.424) .24 (1.430 (. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.08) .490-.S. Cobalt occurs naturally in airborne dust.16) 1.860 (.940-1.520 (.07 (.460 (.340-.950-1.26) Total .640) .03 (.375 (.660-.434 (.530) .59 (1.430) .465) .530 (.452 (.435 (. and in synthesizing polyester and other materials.428-.410-.760) .400-.540-.620-. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.359 (.820 (.28 (1.690-.52 (1.367 (.680 (.450-.750-.99) 1.16 (1.47) 1.670 (.330-.16-1.19) .710 (.09) .790 (.610) .50) 1.294 (.920) 1.22-1.800) .417) .690 (.270-.47 (1.600 (.810-.460-. 0.620-.377-.930) .870 (.44) 1.540-.03) 1.319) .564) .420 (.380-.01-1.67) 1.410 (.416) .340-.950-1.37-1.540-.450-.291-. Cobalt is used as a drying agent in paints.05) 1.600-.68 (1.430 (.03 (.680 (.23) .610-.502) .950) .890-1.410-. large appliances.28 (1.460 (.17 (1.07-1.24 (.360-.454 (.590) .740 (. hard metal or in combination with other elements.03) 1. shiny. interval) .520-.890-1.348-.310 (.650 (.380 (.336-.510) 1. 01-02.523) .620) .13) 1.450) .480 (.980-1.01-2.370-.17 (.900) .22) 1.590 (.07.430) .450) .570) .520) .920-1.820 (.461 (.900) .660) .369 (.386) . population from the National Health and Nutrition Examination Survey.32 (1.330) .800-.26-1.26-2.316 (.940-1.352 (.340) . 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.880 (.26) 1.760 (.630 (.17-1.313) .398 (.350-.81) 1.520 (.640) .710) 1.410) .410-. It is emitted into the environment from burning coal and oil and car and truck exhaust.540-.08-1. 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.850) 1.670 (.496) .380 (.590-.680) .270-.840) .16 (.650 (.350-.580 (.870-1.308-. and inks.431) .394) .47 (1.380-.640) .370 (.404) .543) .580 (.305-.850-1.48) 1.930 (.371 (.790) .515 (.410) .340 (.285 (.570-.890) .14-1. and kitchenware.75 (1.520 (.364-.29 (1.33 (1. Usual human exposure is from food sources.500) .390) .14) .81) 1.630-.373-.427-.270-. automobile airbags.350 (.600) .450) .21) 1.750 (.399) .339 (.331-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.419) Selected percentiles ( 95% confidence interval) 50th .25-1.520-.16) 1.790-.420) .670-. steel-belted radial tires.519 (.520) .770) .343 (.327-.570-.04 (.60 (1.960-1.470) . blue-colored pigments. The cobalt used in U.405-.460) .410 (.480 (.740-.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 .16-1.333-.414) .710) .64) 1.301 (.700) .463-.469-.08.430 (.28-2.450) .750 (.810) .350) 75th .32) 1.32) 1.360-.581) . industry is imported or obtained by recycling scrap metal that contains cobalt.900-1.880-1.690-.980) .333-.390 (.910-1.810) .388-.316-.06-1. seawater.490-.00) .45 (1.398) .440-. diamond-polishing wheels.940 (.05 (.670 (. and 03-04 are 0.23-2.310-.Metals Cobalt CAS No.560 (.520 (.550) 90th . varnishes.338-.03-1.374 (. and fertilizers.500 (. Cobalt compounds are used as catalysts in producing oil and gas.20 (1.930-1.580 (.610 (.420) . 208 Fourth National Report on Human Exposure to Environmental Chemicals .590-.850) .15 (1.372) .890) 95th 1.15-1.950 (.03) . and magnetic recording media.740-.540) 1. see Data Analysis section) for Survey years 99-00.680) .870 (. and 0.355-.820 (.373) . It is also a component of porcelain enamel applied to steel bathroom fixtures.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.65) 1.830-1.09 (.39) 1.393-.530-.850-1.04-1.36) 1.300 (.28 (1.460) .390 (.480-.04-1.431) .

327 (.376 (.380-.469-. in the feces.547 (.955) .329-.700 (.310) .362 (.522) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf..660-.638-1.. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.323) . Once absorbed and distributed in the body.S.302-.303-.314 (.581) .313-.319-.15) 1.06 (. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.272-.949) .290 (.554 (. an essential human nutrient.792 (.435-.630-.368) .49) 1.396) .513 (.57) 1.533 (.462) .29 (1.599) .830 (.785) .301) .234 (.632-.00-1.353-.03 (.259 (.777-. 1994.861-1.750) .990-1.842) .727 (.563-.16) .393 (.585) .963) .280-.313-.11-1.595) .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 .281) .419) .534 (.313-.740-1.328 (.786-.361 (.937 (.591 (.960 (.552 (.616-.393-.382-.471 (. population from the National Health and Nutrition Examination Survey.781-1.333-.508-.60) 1.50) 1.900-1.44 (.409) .691 (.324-.391) Selected percentiles ( 95% confidence interval) 50th .00 (.983-1.515 (.331-.562) .23 (1.679-.634-.503-.388 (.523 (.29 (1.562) .342-.964 (.744) 1.804) 1.938-1.279 (.316 (.328) .396) .344-.635 (.337) .488) .381) .707) .337 (.290 (. Exposure in the workplace may come from electroplating.29) .256-.363) .847) .738 (.594) .378-.358 (.09) 1. respectively.475 (.378-.500-.975 (.457-.560-.16 (.27) 1.335 (.644 (.737 (.00) .703-.408 (.03-1. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.300) .404-.542 (.733-1.750-.476-.294-.27) 1.297) .523 (. or using diamond-polishing wheels that contain cobalt metal.626-.550-.29 (1.343-. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.29) 1.313 (.600-.289) .362) . 1972).851 (.00 (.449-..273 (.25 (.704-.938) .829) .479-.417) .582-.60) 1.932-1.00 (.513-.606 (.247 (.343 (.35) .673-.471-.756 (.328 (.435 (.388 (.50) 1. A portion of cobalt retained for long periods is concentrated in the liver. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.407 (.442-.700 (.251-.334) .257 (..278-.10-1. cobalt is excreted predominantly in the urine.352 (.990) .434-.857-1..04-1.313-.500 (. and to a lesser extent.495 (.898 (.861 (. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.872 (.457 (.461) .297-.455 (.392 (.728) .368) .36) 1.963-1.608 (.372) .16 (. 1972).529 (.00) .50 (1.309) .361-.333-.352) .237-.333 (.983) .296) .615) .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 .500-.290 (.387) .317 (.365) .304-.421) .282 (.428-. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.895-1.534-.349) .662) .275-.513) .723 (.760-1.757-1.611) .963) .753-.433) .277-.457) . Smith et al.438) .346 (.952 (.463-.215-. refining or processing alloys.593) .355) .429) 1.850-1.738 (.439) .911-1.386 (.257-.33) .905) . Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).15 (.268 (. 1994).844 (.640) .278 (.826-1.774 (.561) .04 (.353 (.425) .369 (.352 (.329 (.838 (.598 (.833-1.378-.487-.792-1.313-.248-.781) 95th 1.243-. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.471-.12 (.55) .895-1.301-.963-1.481) 90th .30 (1.33) 1.425-. Cobalt is absorbed by oral and pulmonary routes.14 (.574-. 2003).821 (.917) .259-.. 1979).279) .293 (.361-.609) .291 (.850 (.360) .449) .426 (.306 (.630-.667-1.28) 1.694) .444 (.35) 1.537 (.362-.296-.271 (.19) .689 (.286) .324) .400 (.683-.976 (.647) .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 .365-.543) .468) .274-.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 .848 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.753) 1.36) 1.250) .326-.394) . interval) .304) .339-.548 (.Metals fabricated from cobalt alloys (Lhotka et al.10) .275-.368 (.16 (1.333-.467-. using hard metal cutting tools.83) 1.239-.728 (.17) .407) .11-1.452-.821-3.327-.955) .25 (.505) .391 (.73) 1.248-.554 (.298 (.24) .361 (.10 (.669) .479) .306) 75th .708) .929) .10) Total .54) 1.348) .259) .736-.384) .02 (.824 (.611) .12-1.282-.00 (.879-1.402 (.829-1.378 (.417 (.667-1.487-.

html.. 1997). 1994). Atlanta (GA).. Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. 2001. Linnainmaa and Kiilunen. Iavicoli et al. Morgan WKC. Sci Total Environ 1994. 2001). The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al. Information about the BEI is provided here for comparison. 2001. Sills RC.. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . White and Sabbioni. Haseman JK. Shirakawa et al. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. 1988).. Available at URL: http://www.. 1993). Alexandersson R. Dunstan et al.gov/ exposurereport/. 1997... Arch Environ Health 1988. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans. 1993). an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis.53:395417. 2003. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al.atsdr. 2005. Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. 1989).. usually in combination with tungsten carbide (Cugell et al.. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al.. Hailey JR. “Hard metal” disease. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L... Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al.. population (CDC. A clinical and pathological study of twenty-eight cases.. Third National Report on Human Exposure to Environmental Chemicals. Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al.. Swennen et al. not to imply that the BEI is a safe level for general population exposure. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. Cobalt-beer cardiomyopathy. 1999). 1990). and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al. A 1982-1992 surveillance programme on Danish pottery painters.cdc... Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Lisi. 2006. Lison et al. Thomassen et al.gov/toxpro2.43(4):299-303. 2005 [online]. 1955). 2005.. Poulsen OM. 1985. Krause et al.. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. Toxicol Sci 1999. Centers for Disease Control and Prevention (CDC). Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al. 1994. For workers exposed to cobalt in the air. MacDonald et al. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. has been associated with exposure to dusts that contain cobalt. 2001. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. Lauwerys and Hoet. although substantial occupational exposures have produced elevated urinary levels for many weeks... 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. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. 4/3/08 Christensen JM.e.. 1992). Information about external exposure (i.49:56-67.cdc. Cobalt was once added as a foaming agent to beer. 1998). population results in this Report (Kristiansen et al. Rubin A. Perkins DG. environmental levels) and health effects is available from ATSDR at: http://www... Bucher JR. 1994. with mean levels that were about 15-20 times higher than in the general U. Daniel et al.Metals Toxic effects of cobalt have been encountered in workplace settings. Blood and urinary concentrations as estimators of cobalt exposure. Urinary measurements mainly reflect recent exposure. 1998). Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al. 210 2006. Roycroft JR. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. References Alexander CS. 1972).50(13):95-104. Am J Med 1972.S. et al..S. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect. Cugell DW. 1988). Grumbein SL. 2003). 2003.

et al. Vitali MT.51(7):447450.55(4):269-276. Buchet JP. Respiratory health of cobalt production workers. 3rd ed. et al. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Schramel P. Zhuber K. Chest 1989.204:147-160. Hoet P. Zobelein P. Wild P. Sci Total Environ 1994. The release of metals from metal-onmetal surface arthroplasty of the hip. Molders J. Kraus T.150(1-3):167-171. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Szekeres T. Kirsch-Volders M. J Bone Joint Surg Br 2006. Leghissa P. Unwin P. Alessandrelli M. Epidemiological survey of workers exposed to cobalt oxides. cobalt salts. Int Arch Occup Environ Health. Absorption and retention of cobalt in man by whole-body counting. White MA. oxides. Laippala P.69(3):193-200. Dunstan E.21(2):189-195. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group.150:177-183. Bourne RB. Co-sensitivity between cobalt and other transition metals. Outcome of occupational asthma due to cobalt hypersensitivity.34:620-626. Schaller KH. Health Phys 1979. Sci Total Environ 1994. Angerer J.(1-3):133-139. Bacis M. MacDonald SJ. Occupationallyinduced “isolated cobalt sensitization. and cobalt metals. Meyer zum Buschenfelde K-H. Goto S. Goldberg MA. Cobalt and antimony: genotoxicity and carcinogenicity. Meier R. Cleland D. Dickel H.45:246-247.50(9):835-842. Salvatori S. Trace element reference values in tissues from inhabitants of the European Union. Cannon SR.28(5):1121-1128. Contact Dermatitis 2003. Steffan I. Swennen B. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. et al. Science 1988.150. Goto S. Mosconi G. Zedda S. Barnaby CF. Thakker DM. Health Phys 1972. Buchet JP. Falcone G. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Palmroos P. Linnainmaa M. J Occup Med 1992.58(10):631-634. Lauwerys R. a study of 13 elements in blood and urine of a United Kingdom population.148:241-248. Romazini S. Lison D. Sabbioni E. Br J Ind Med 1993.” Contact Dermatitis 2001. Oksa P. Lhotka C. Thabe H.157:117121. Stanescu D. Chess DG. X. Am J Ind Med 2003. Carnes WH.22:359367. Sabbioni E. Peltier A. A report of two cases from mineral assay laboratories and a review of the literature. Kato M. Pisati G. Hammon E. J Bone Joint Surg Br 2005. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Kusaka Y. Christensen JM. Gross RT. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Lasfargues G. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Lung cancer risk in hard-metal workers. Edmonds CJ. 1985. Ziaee H.242:1412-1415. Kriss JP. McCalden RW. Iavicoli I. Lisi P. et al. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Daniel J. Jarvis JQ.48:172-173. Int Arch Occup Environ Health 1997. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Sanghrajka AP. Iversen BS. Arch Intern Med 1990. Robinson C. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust.20(1):25-31. Schank M.87(5):628-631. Heki S.533:135-152. salt. Ghat IS. Diepgen TL.88(4):443448. Hoher T. Linna A. et al. DeSantis V. Sci Total Environ 1998. Moulin JJ. Roto P. Bunn HF. Cresti R. Cobalt cardiomyopathy. Salama A. Long-term clearance of inhaled 60Co. Shirakawa T.406:282-296. and hard metal dust.36:732-734. Kristiansen J. Kiilunen M. et al. Smith T. Swennen B.216:253-270.95:29-37. Kuska Y. Clin Orthop Relat Res 2003. Lison D. Lauwerys RB. McMinn DJ. Am J Epidemiol 1998. Lison D. De Boeck M. Weyher I. Occup Environ Med 1994. Lauwerys R. 2001. Zweymuller K. Sci Total Environ 1997. Ichikawa Y. Thomassen H. Biological monitoring of workers exposed to cobalt metal. Bozec C.44:124-132. Dunning SP. Fujimura N. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Blunn G. J Rheumatol 2001. Occup Environ Med 2001. Boca Raton (FL): Lewis Publishers. Weber A. Tilley S. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Hedge AG.Metals effects of cobalt. Mutat Res 2003. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. HoffmannB. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. J Orthop Res 2003. Rorabeck CH. Uitti J. J Trace Elem Med Biol 2006. Pradhan C. Radulescu M. Sabbioni E.

interval) 1.00) .40) Total 1.80 (3.60 (4.90) 1.50-5.20-3.50 (1.20) 90th 3.20 (3.43-1.50-5.90-4.20 (3.66 (1.90) 3.09) 1.00 (4.80 (1.10) 3.75 (1.00) 2.70-1.10 (1.00) 1.70) 3.10 (2.90-4.80-3.986) .48) 1.00-4.68-1.10) 3.40 (1.30) 2.40-1.55 (1.90 (3.Metals Lead CAS No.60 (3.70-1.90 (2.90 (3.10-2.80) 1.60-2.80 (1.32-1.96-2.70-2. malleable.00-2.40 (2.50) 1. dense.40-6.70) 3.50 (2.40-4.23 (1.60 (2.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.12-1.30-6.60 (3.45 (1.10-2.80) 3.10) 1.10-4.80 (2.50 (4.30 (2.60) 1.50 (2.53) 1. population was aerosolized lead emitted from combustion engines that used leaded gasoline.40-2.60) 3.60 (1.60) 5.50 (3. Lead has a variety of uses in manufacturing: storage batteries. Lead is most often mined from ores or recycled from scrap metal or batteries.90-3.65 (1.50-3.32-1.60 (1.49-1.10-6.40-3.40-1.69) 1.70 (2.00 (2.900-1.50-1.40) 2.00-5.60 (1.80-3.20) 4.60 (1.40-2.80 (1.60) 1.20 (2.30-1.40 (3.62-1.30-1.60-1.10-4.75-1.800-1.50-1.83 (1.02) 1.20) 4.70 (2.10-3.g.91) 1.20) 3.40) 2.70) 1.39-1.10-1.00-4.70 (1.20 (3.40-3.60) 3.900 (.87 (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.80-5.10) 2.50) 1.00) 1.10-1.60) 4.75-2.50 (4.60 (1.14-1.20) 5.80) 2.20 (3.40-5.10-6.66) 1.56 (1.80-4.30) 5.25 (1.70) 1.10-2.10) 3.51 (1.60) 1.20 (1.80 (1.95) 1. 7439-92-1 General Information Elemental lead is a soft.00 (3.25) 1.36-1.14-1.20-1.30 (1.20-1.50-3.50) 1.00) 3.31) 1.60-2.70) 4.60 (1.20 (3.70-2.00 (5.60) 2.40 (1.34-1.00-6. In the past.60 (1.10) 2.30 (2.80) 1. 01-02.14-1.80) 2.40) 1.60-4.80 (1.80-2.60 (3.80-3.60-1.50-6.00-4.00-1. Before the 1980’s.40-1.36) 1.90) 2.80) 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 1.52 (1.00) 2.S.50-2.40 (4.30-2.90-2.80 (5.60-4.72) Selected percentiles ( 95% confidence interval) 50th 1.28.10 (3. see Data Analysis section) for Survey years 99-00. leaded glass.10-2.10-3. ammunition.51) 1.90 (1.00 (6.40) 2.60-1.90-2.30-4.60) 2.50) 5.20 (3.60) 3.30 (2.60) 3.80) 2.55-1.90) 2.30-5. and 0.80 (2.70) 4.30) 95th 5.50) 2.86) 1.40 (5.70 (3.50 (1.70 (1.80 (1.10) 1.10 (1.00) 5.50 (2. respectively.20) .40) 2.22 (1.60) 4.30 (4.10) 5.90 (3.40) 1.60-6.10) 1.50 (1.50-1. and 03-04 are 0.20-6.10-8.3.90) 5.70 (5.60) 5.70) 2. ceramic glazes.50) 1.20-3.80 (4.50) 75th 2.946 (.30-1.80 (2.90) 2. Lead was used in plumbing for centuries and may still be present. 212 Fourth National Report on Human Exposure to Environmental Chemicals .30 (1.00) 3. metal alloys (e.30) 1.30-2.50) 3.30 (1.50 (2. solders.00 (1.40-1.50 (3.00) 1.80-3.40-3.60) 4.37-1.55-1.39) 1. bronze).10 (2.50) 4.78 (1.71-1. antique-molded or cast ornaments.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 2.90 (1.87) 1.10 (4.00) 6.70 (2.70-4.40 (1.40-1.3. and for radiation shielding.20-4.50-2. the main source of lead exposure for the general U.60 (2.20 (1.70) 4.40-6.50) 4.89) 1.70-1.899-.40) 1.30-2.30) 2.20 (2.30 (1.00) 2.43) 1.80) 1.30 (3.01 (1.90 (4.52-1.50-4.70) 1.00) 4.50) 7.62) 1.43 (1.30-1.00) 1.60 (2.45-1.70 (1.20) 3.90) 1.50 (2.30-1.90) 3.30-1.77 (1.36-1.942 (.70) 1.10 (2.90-6.70-3.93-2.52-1.S.40-1.60) 2.60 (2.70) 3.00 (4.69 (1.50-2.62 (1.20 (1.00) 2.50 (1.20) 3.10-3.25 (1.69) 1.878-1.20-3.50-2.40 (1.04-1.90 (2.37 (1.900 (.10-2. lead was added to gasoline and residential paints and used in soldering the seams of food cans. blue-gray metal that occurs naturally in soils and rocks.80 (4.40 (2.60) 2.60) 4. 0.30) 2.70) 4.90-2.17) .70-6.20-3.20-2.40) 3.60) 2. such as lead phosphate and tetraethyl lead.20) 3.50-4.20 (1.10-3. brass.90-4.90) 1.50) 5.80) 2.90) 2.30 (2.90-4.70 (1.30-2.70-2.43) 1.00-1.20 (1.20 (3.60 (2.50-1.37 (1.00 (1.10) 4. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.90 (3.00) 4.90) 2.40) 5.43 (1.40) 4.90-2.60 (3.20) 1.20 (4.80) 1.30 (2.10-1.50-1. Since lead has been eliminated from gasoline.60-3.30 (2. Elemental lead can be combined with other elements to form inorganic and organic compounds.19 (1.30 (4.00) 1.10 (1.20-2.69 (1.20) 2.60 (2.46 (1.30 (2. population from the National Health and Nutrition Examination Survey.90 (3.60-1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.50) 2.30 (4.75) 1.80) 1.40-2.70 (3.10-2.70) 1.60) 1.80-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. plastics.70-5.80-4.60) 1.81) 1.80 (5.

04-2.30) 1.10 (1.g. population from the National Health and Nutrition Examination Survey.59-2.60-1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.540-.82 (1.757-.90-3.Metals occupational (e.986) .600-.600) .86 (1.40 (1.40-2.40-1.30) 2.86) 95th 2.30-1.10 (1. CDC.700 (.900) .857) .90 (2.10 (.480-.11 (1.700 (.50 (2.30-1.572-.848 (.50 (1.89) 2. Fourth National Report on Human Exposure to Environmental Chemicals 213 .10) 1.80) 2.49) 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 .23-4.50) 1.40) 1.600 (.535-.00) .900) .04 (.600-.00-1.30) .40) 1.500-. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.13) .70 (1.637-.24-1.97) 4.30) 1. 0.80-2.900-1.800 (. pewter utensils and drinking vessels.33 (2.800) .00-1.18-1.70) 3. 01-02.20 (1.00 (1.40-5.90 (1.50) 1.33.50) 3.90 (1.745-.710-1.10-1.900) .30) 1.80 (2.20 (2. interval) .10 (1.30 (1. However.00) 2.07-1.650) 1.700 (.833 (.900 (.10-5.44-2..75) 3.1.620 (.02) 1.729-.935) 1.900-1.32 (1.659 (. Approximately half of the absorbed lead may be incorporated into bone.506-.80) 2.60 (2.564 (.40) 1.40 (2.60 (1.35 (.800) .50-2.540 (.00-2.700-.00 (.30) 1.21 (2.920 (.700) .60-2.674) 1.40) 1.91) 2.40-1.70) 1.S.20 (1.800 (.80) 3.66 (2.600-.90-2.613) .22) 1.833-1.960-1.920 (.33-2.14 (1.04) 2.70 (2.86) 1.09) 1.708-.14-1.27) 1.701) .40) 2.800 (.941) .78-2.10) . battery and radiator manufacturing) and recreational sources.00 (1.30) 2.900 (.640 (.590 (.60-3.40) 2.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.862) .636 (.680-. bullet fragments retained in human tissue.900) .700 (.40 (2.651) .00) 1.60-2.80) 1.570-.828) Selected percentiles ( 95% confidence interval) 50th . 2000).75) 4.80-3.610 (.616) .07 (.20) .80) 2.800-1.800-.04 (.20 (1.20) .90-3.64) 2.695 (. lead-based painted surfaces undergoing renovation or demolition.753 (.800-.31-3.850 (.00) .70) 3.10-1..20) 1.27 (1.40 (1.70-2.80 (1.90-2.820-1.20) 1.731 (.808 (.90-2.04) .20-2.10) 2.600-.749) .80-2.700-1.900) .30-3.700-.30) 2. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.00) . 1991).72) 1.730 (.52-1.680-. and 0.23) .810-1.620) 1.70) 1.90) 2.661-.700-.19 (1.40) 1.960 (.752 (.700) 1.70 (2.30 (2.10 (1.20 (2.31 (1.30-1.20 (1.30-2.50-2.955-1.20 (1.90 (2. 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.03-2.589-.80 (1. In the blood.558 (.30 (3.00 (1.90) 2.29 (2.660) . dust. see Data Analysis section) for Survey years 99-00.90 (1.90-4.800 (.40-1.20-1.40 (2.80) 1.640-.600-.10-3.10-1.78-2.923 (.718) .10 (.671-.50-1.17 (1.60) 2.20 (2.630 (.690) 75th 1. lead-containing folk remedies and cosmetics.30-5.29) 2.30-1.40) 2.49 (1.785) .800) .02 (.970-1.40 (2.90) 2.10-3.800) .70-3.990) 2.60 (1.40-1.14 (1.579-.605) .00) .10-1.70) 2.80) 2.40) 3.20) .20 (3.60-3.10 (.50-3.70 (2.641-.50) 2.773) .815 (.30) 1. respectively.20) .900) .800) . or after soluble lead compounds are ingested.00) 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 1.73 (1.560-.700-.03 (1.50) 1.52-1.52 (1.12) 90th 2.78-2.579-.50 (1. stained glass framing.940 (.580-.526-.20-2.00-1.40) 2.677 (.60 (1.595-.700 (.766 (. older plumbing systems with leaded pipes or lead soldered connections.50-2.82 (2.66 (2.931) .628) 1.738) .625-.10-3.62-4.13-3.10) .553-.680) .20-1.40 (1.50 (2. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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 1.90-2.06) .80) 1.00 (2.600 (.800-1.591 (.910-.573 (.60 (1.10-1.62) Total . Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.960-1.700 (.990) 1. or water contaminated by mining or smelting operations.900 (.10) 2.688 (.818) .11) 2. imported children’s trinkets and toys.90 (2. 2007.80) 2.20-1.840 (.59) 1. lead-contaminated dust in indoor firing ranges.700-. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.691-.790 (.41) 2.40-3.00 (1.642 (.00-2.70 (2.600) .70) 1.604 (.900-1.625 (.710-. and contact with soil.1.50 (2.900-1. and 03-04 are 0.90) 1.20) 1.40 (1.822-1.50) 2.20 (1.795 (.00-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.86-2.556-.40 (1.80) 3.915-1.

97-18.601-.608 (.72-2.670) 1. interval) .722 (.997-1.793-1.77) 2.810 (.85 (1.693 (.851) .45 (1.61) 3.508) .39-1.65-2.622 (.71 (1.679) 1.633 (. and nails (Leggett.18) 1.400) .655) 75th 1.988 (.707 (. zinc.46 (2.89-5.03) 2.27 (1.72) .755 (.06 (.19-5.918-1.53-1.667) .61) 1.11 (1. through the inhibition of certain enzymes.02) 1.00 (1.83 (2. based on prospective population studies.541-. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.917-1.639 (.22-2.731-.40-1.63) 4.33) 2.648 (. BLLs and associated toxic effects differ in children and adults.35) 2.623 (. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.914 (.404-.461) .11-1.41-1.26) Total .88) 1.992-1. with a half-life of years to decades.603 (.20) .644 (.00 (1.79 (1.594-.88 (1.962 (.61) 1.718) 1.914-1.22-1.73-2.625 (.893) .957-1.971 (.10 (1.07 (.59-3. 1991.00) .701 (.96 (1.94-2.638 (.09-1.0) 3. 2007)..882-1.436) .25-1.03 (.S.66) 2. O’Flaherty.05-1.383-.654) .62-1.708 (.37-1.730) 1.662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1. Approximately 70% of lead excretion occurs via the urine.89-2.559-.725) .914 (.88-2.853-1.677-. For instance.649 (.29 (1.50-2.88) 2.43) 2.605-.14 (1.01 (.05 (1.64) 2.988-1.64) 95th 2. CDC.18) .561-.33) 1.36-2.18) 1.790) .603-.667-.97) 1.88) 2.659-.920-1.900 (.469 (.946-1.615 (.64-2.632 (. 2004.977) 1.603-.342-.14) 1.658 (.01) .510-.92) 2.62) 2.06) .682) .408-.702-.938-1.28) .639 (.838) .529-. scant amounts are lost through sweat.688) .588-. hair.841-1.87) 1.828-1.608-.68 (1.618 (.41 (1.668-.677 (.720 (.72-2.43 (2.43) 1.03) 1.03 (.31 (2. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.535) .11) .898) .38 (2. 1996).44 (1.58) 1.08-2.592-.55 (1.56-3.696 (.62-2.876-1.746) . 1993).15) 1.33 (1.50-2.44 (1.17-1.94 (1.11 (.11) 1. In 1991.06 (1. Nash et al.51) 1.05-1.31) 1.742) Selected percentiles ( 95% confidence interval) 50th .677) .702) . Schwartz.56) 3.712 (.03 (1.460-.53) 1.09-1.20) 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 ..579-.926 (.38 (2. 1993.55 (1.10) 1.75 (2.43 (1.00 (1.887 (.98 (1.763) .975-1.657) 1.639) .46 (1.617-.26) 2.79) 2.635 (.571-.645-.50) 1.19) 1.52) 1.37-1.698) .50 (1.04) 2.12-1.721 (.938 (.586-.03 (.64 (1.56-2.38 (2.23 (1.812-1.15-3.61) 1.52 (1.621 (.51 (1. 2003.725) .765) .933) .828) .604-.11 (1.22) .85-2.918 (.870 (.22) 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.56 (1.655-.11 (.612-.609 (.03) 1.862-.753) .98) 2.667-. with lesser amounts eliminated via the feces. population from the National Health and Nutrition Examination Survey.718) .990 (.43-1.66 (1.686) .652 (.09-1.758) .698) .63) 1.10 (.03) .404 (. and paralysis. encephalopathy. and iron.83) 1.31) 1.606-.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 .25-1.50-1.20-3.82) 1. Large amounts of lead in the body can cause anemia.432 (.00 (.73) 2. seizures.74 (1.71-2.31 (1.47) 1.98-2.10) 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 .06) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.623 (.681-.992-1.673) .676) .739) .588-.62-3. abdominal pain.61) 1.963-1.02-1.645-.774 (..28) 2.615 (.18) 2.31 (1.97 (1.710) .33-1. 1995).679-.44) 1.03) 90th 1.703) .75-2.47 (1.404 (.07-1.583-.607-.48 (1.702) .97) 1.85-2.47 (2.644) .15) 1.03) .08) . Staessen et al.639 (.800-. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.683-.70 (1.681-.67-4.17 (.979 (.569 (. 1995.15-2. Lead can cross the placenta and enter the developing fetal brain.380-.20) .641 (.50-2. The toxic effects of lead result from its interference with the physiologic actions of calcium.700-.593 (.09) 1.28-1.03-2.940 (.08) .41) . kidney injury.551-.18 (1.78-4.594-.781-1. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.720 (.496 (.742) .428) .796-1.34-1.03) 2.655) .66 (1.24 (1.701) .492-.981-1.05 (. The skeleton acts as a storage depot.15-2.86 (1.49 (1.Metals 90% of the body lead burden in most adults.78 (2.79) 1.671 (.69 (1.65 (1.22) 1.722 (.709 (.375 (.07) .734) . and through binding to ion channels and regulatory proteins.04-3.85) 1.571-.587-.933-1.

both the geometric mean (1. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U.5 per 100.cdc. 2007)..gov/toxpro2..html.0 µg/dL in females (Soldin et al. Pirkle et al.21% of approximately 3. including minority race or ethnicity. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects.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. seizures. particularly in the skeleton. 1999). premature delivery. 2002a). 2006). the prevalence rate has declined annually since 1994 (CDC.. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al.. Fourth National Report on Human Exposure to Environmental Chemicals 215 . BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors. lead in women may be associated with hypertension during pregnancy. Muntner et al.. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. 2003. 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. reduce sperm count. 1994).07 µg/dL (Becker et al.g. Jones et al. EPA. 2002). 2003. 2000). Information about external exposure (i. Both drinking water and ambient air standards for lead have been established by the U. Korrick et al. 2003). 1991. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH.S.. Schwartz et al.S. Telisman et al... 2005b. Bellinger 2005. 2000). For example. and low family income (CDC. 1995.. Borja-Aburto et al. though there is greater individual variation in urine lead than in blood and greater potential for contamination. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. and decrease fertility (Alexander et al. 2003. CDC..3 million children tested had BLLs of 10 mg/dL or higher (http://www.S. respectively. Schwartz. However. Urine levels may reflect recently absorbed lead. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC.e.000 adults.. when the geometric mean BLL was 2. adults in the 1999-2000 NHANES sample. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. with overt encephalopathy. 1999). the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.6%) were lower than those from NHANES 1991-1994. More recently.... 2002. Data submitted through state public health programs from 2006 showed that 1. The U..4% in NHANES 1999-2004.S. may alter sperm morphology. 1996. almost double the geometric mean of 1. 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. and spontaneous abortion (Baghurst et al. 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.6% in NHANES 1988-1991 to 1..Metals µg/dL or higher as the level of concern in children. residing in housing built before the 1950’s. 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.. 1987. approximately 11.75 µg/dL in U. High dose occupational lead exposure. urban residence.. BLLs reflect both recent intake and equilibration with stored lead in other tissues. Surveillance data reported by U. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. 1984..2 µg/dL in males and 3. and organic lead compounds not classifiable with respect to human carcinogenicity. Overall. In NHANES 1999-2002 in children 1-5 years old. 1996. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. 2009).7 µg/dL and 4. Staessen et al.S.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1. which is an 84% decline. 2001). 2006). Payton et al. adult residents.. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.xls).gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006.cdc. and peripheral neuropathy generally occurring at much higher levels (e. higher than 100-200 µg/dL).4% of children had BLLs of 10µg/dL or higher (CDC. 2005a). Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. 2005b). usually with BLLs greater than 40 mg/dL.. At low environmental exposures. the geometric mean BLL was 3. adults in the 19992000 NHANES sample (Apostoli et al. IARC considers inorganic lead compounds probable human carcinogens..S.. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al.atsdr. 1996. In occupationally exposed adults. 1998). Lanphear et al. environmental levels) and health effects is available from ATSDR at: http://www.

Speizer FE. Lead and hypertension in a sample of middle-aged women.htm. Available from URL: http://www. Seiwert M.101(7):598-616. Atlanta (GA).205:297-308. Jacobson SW. Dietrich K. Available at URL: http://www. 1999-2002. Blanco J. Leggett RW. Chiodo LM. Sparrow D.gov/toxprofiles/tp13.348:15171526. Atlanta (GA). Pirkle JL.10:43-50. Roberts RR. Lanphear BP. Third National Report on Human Exposure to Environmental Chemicals. Jones RL. IARC Monogr Eval Carcinog Risks Hum 2006.cdc. Managing Elevated Blood Lead Levels Among Young Children. Rotnitzky A. Ga. Brody DJ. Blood lead levels measured prospectively and risk of spontaneous abortion.89:330-335. Rios C. Int J Hyg Environ Health 2002. 4/14/09 Centers for Disease Control and Prevention (CDC). Kaufman JD. Neurodevelopmental effects of postnatal lead exposure at very low levels. 1991 [online]. Lanphear BP. Korrick S.gov/nceh/lead/ CaseManagement/caseManage_main. Birth Defects Research (Part A). Ronchi L. Bavazzano P. Kim R. van Netten C.atsdr.275(15):1171-1176. et al. Henderson CR. Blood lead levels—United States. Baghurst PA. Hertz-Picciotto I. Centers for Disease Control and Prevention (CDC). Wager C. Hu H.cdc. Cory-Slechta DA. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. 4/14/09 Alexander BH. Teratogen update: lead and pregnancy. Lead. Rotnitzky A. Apostoli P. Toxicological profile for lead. Neri A. 2003-2004. 2005. Pediatrics 2004.gov/nceh/lead/publications/ books/plpyc/contents.55(32):876-879. Krause C. CDC. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Available at URL: http://www. Hu H. Hänninen H. Hu H. Adult blood lead epidemiology and surveillance—United States. Checkoway H. 1988-2004. Cox C.htm. Occup Environ Med 1996. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development.53:411-416. Inorganic and Organic Lead Compounds. Am J Public Health 1999. Rojas LM. Manton WI.82:60-80. 4/14/09 Centers for Disease Control and Prevention (CDC). JAMA 1996.87:1-471. Am J Epidemiol 1999. Blood lead reference values: the results of an Italian polycentric study.113(4):1016-1022. et al.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. Muller CH.26:359-371. Scand J Work Environ Health 1984. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. References Agency for Toxic Substances and Disease Registry (ATSDR). Kuehnemann TJ. Batuman V.73:409-420. Atlanta. Canfield RL. Ganzi A. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Acquisition and retention of lead by young children. Bellinger D. et al.115:521-529. McMichael AJ. 2005b. Luukkonen R.gov/mmwr/preview/mmwrhtml/ mm5532a2. Caldwell KL. Aro A. Aug 2007 [online]. Cox C. Hernberg S. Environ Health Perspect 1993. Jacobson JL. Semen quality of men employed at a lead smelter. Vimpani FB.8(3):395-401. Weiss ST. Wigg NR. Robertson EF. Ewers TG. Lepom P.54(20):513-516.275:1177-1181. Sci Total Environ 2002. Angle CR. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas.html. Available at URL: http://www. doi:10. Homa DM. Mantere P.cdc. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Bellinger D. 2002 [online]. Pediatrics 2009. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Age-specific kinetic model of lead metal in humans. Korrick SA. Vupputyuri S. Kaus S. et al. et al. The relationship of bone and blood lead to hypertension.htm. Becker K. Payton M.1542/peds:2007-3608. Meyer PA. MMWR Morb Mortal Wkly Rep 2006. Neurotoxicol 1987.cdc. 4/14/09 Centers for Disease Control and Prevention (CDC). Hunter DJ.123:e376-e385. Environ Res 2000. Public Health Rep 2000. Coresh J. Sparrow D.150(6):590-597. Auinger P.htm.cdc. N Engl J Med 2003. Reese YR. Neurotoxicol Teratol 2004. Stanek KL. Available at URL: http://www. Muntner P. Farias P. Schulz C. 4/14/09 Centers for Disease Control and Prevention (CDC). gov/mmwr/preview/mmwrhtml/mm5420a5. Preventing Lead Poisoning in Young Children. MMWR Morb Mortal Wkly Rep 2005a. JAMA 1996. Borja-Aburto VH.287:1-11. Baj A. Jusko TA. Weiss ST.

Kinetics of lead disposition in humans. Flegal AR. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Schwartz J.63:1044-1050. 50:31-37.S. Amery A. Staessen JA. and tibia lead with neurobehavioral test scores in South Korean lead workers. Lee GS. Lustberg M. Environ Health Perspect 1998.289(12):1523-1531. Sparrow D.106:745-750. Soldin OP.9:303-327. cadmium.140:821-829.118:16-29. Exposure of the U. et al. Blood lead.153(5):453464. Schulz D. Osterloh JD. population to lead: 1991-1994. Roels H. Hickman T.108(1):45-53. Payton M. et al. JAMA 2003. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Rubin R. Schwenk M. Pirkle JL. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Pizent A. Hwang KY. Physiologically based models for bone-seeking elements. Brody DJ. dimercaptosuccinic acidchelatable lead. Toxicol Appl Pharmacol 1993. Int J Hyg Environ Health 2006. Low-level lead exposure and renal function in the Normative Aging Study. Smith DR. Gavella M. Lee BK.209:301305. Magder L. IV. blood pressure. Cvitkovic P. Revised and new reference values for arsenic. and copper in men. Soldin SJ. Kidney Int 2003. Stewar WF. Telisman S. Lead. Hu H. Nash D. Lauwerys RR. Weiss ST. stable lead isotopes to determine release of lead from the skeleton. cadmium. blood pressure and cardiovascular disease in men. Blood lead concentrations in children: new ranges. Am J Epidemiol 2001. Clin Chim Acta 2003. Schwartz BS. Rocic B. lead. zinc.104(1):60-66. O’Flaherty EJ. Lee SS. and hypertension in perimenopausal and postmenopausal women. Environ Health Perspect 2000.Metals results from NHANES III. Kaufmann RB. Low-level lead exposure and blood pressure. Environ Health Perspect 1996. Paschal DC. Am J Epidemiol 1994. J Hum Hypertens 1995. Arch Environ Health 1995. Sherwin R. Wilhelm M. Association of blood lead. Gunter EW. Jurasovic J. Use of endogenous. Hanak B. Kaufmann R.327:109-113.

Also.877 (. Atmospheric elemental mercury can be deposited on land and water.60 (2.600 (.700-. with the highest concentrations occurring in the kidneys (Barregard et al. thimerosal.30) 5.00) 1.30 (2. and dental amalgam. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges. 2002).927) .903) Selected percentiles ( 95% confidence interval) 50th .800-1.979 (.400-.20 (2.400 (.20-4.g. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.900) .655-.400-.60-5.563 (.00 (.672) . merbromin).30) 1.80) 1.919) .600) 1.30-2.700) .90 (1. see Data Analysis section) for Survey year 03-04 is 0.00 (2.703-.40) 3.30-4.02) .20-4.800-1. have often required public health intervention (Zeitz et al.60-6.419 (. which can bioaccumulate in aquatic and terrestrial food chains.40-2.50) 5.90 (1.689-. Hursh et al.800 (.800 (. which create an episodic potential for volatization and inhalation of mercury vapor.60 (1.90) 3. Kingman et al. solid-waste incineration.. 1994. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.12) . 1998. Elemental mercury is a shiny.60-6..700-.60) 1.30) 3.00 (1.50) 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 .326 (..S.80) 3.40-1.900) 1. population from the National Health and Nutrition Examination Survey. 1999 . The kinetics of the different forms of mercury vary considerably. and organic forms.70) 911 856 2081 4525 03-04 03-04 .70-2.700) . may contain inorganic mercury.50-2. 1993).90) 95th 4. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic).776 (.10) . inorganic. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.50-1. predominantly from fish and other seafood.90-3.80 (3.50) 4.714-.10-3.. Survey years 03-04 Geometric mean (95% conf.60-2.50) 1.40-3.. Apart from methyl mercury.40-2.40 (3.285-.30) 1.00-5. Other major uses include electrical equipment (e.g. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).900 (.. synthetic organomercury compounds were once used in pharmaceutical applications. phenylmercuric acetate) or topical antiseptics (e.40) 1.70 (1.00) 4.800-1. In addition. electrical lamps.500 (.00 (.800 (. and mining and smelting.574) .40-1.00 (2. an organic form of mercury.30) 3.500-.500) . and is distributed to most tissues.50-3.800-1.30-5. interval) .00 (.900) 1. constitutes the main source of dietary mercury exposure in the general population.70 (1. and mercury compounds are still used as preservatives (e.860-1.70 (4.900) 75th 1.800 (.40 (4.20) 2.60-3. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications.300 (.00) 1.30) 4132 4241 03-04 03-04 03-04 .g.g.700 (. or oxygen.. 2007).00 (. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Accidental spills of elemental mercury.50) 2.00-1. such as chlorine (e.700-.60) 1.500 (. sulfur.753-1.372) .90) 90th 3.781 (.60 (1. elemental mercury is absorbed mainly by inhaling volatilized vapor.40 (4. After elemental mercury is absorbed.00 (2.00) 3.80 (1.20-3.70 (3. Some cosmetic skin creams from countries other than the U..800-1.418-.30 (1.500-. 218 Fourth National Report on Human Exposure to Environmental Chemicals . thermometers. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.60) 2085 2293 3478 Limit of detection (LOD. thermostats and switches).300-.80 (1.700-.814 (.90 (4.S.00) . elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.30-6.886) .490 (.472-.40 (3. sphygmomanometers and barometers.Metals Mercury CAS No.80 (1.300) .700-.80) 4.900) 1.797 (. to form inorganic mercury compounds or salts. Woods et al. 1980.484) . IARC.363-.2. Poorly absorbed from the gastrointestinal tract. mercuric chloride). The ingestion of methyl mercury.

10) .500-.90 (3.60 (1.700-.40-2.. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations. 1996). 2005). 1999).299-. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.00-2.00 (2.30 (1. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . a measure of accumulated dose (Cernichiari et al.318 (.70 (1..738-.800-1.300) .35 (1. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.307 (. 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.00) 7.700) 2.300) .70-3..200-.80-3. McDowell et al. Geometric mean Survey years (95% conf.60 (1.500 (.90 (4.10 (1.20-2.200-. 2004.00 (2. 1975.00-2.40 (1. 1994.600) .300) . and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.700-1.60) 2.10 (.30 (1. 1993).377 (.200 (.300) ..30 (1.. Smith et al.200-..70 (1.900-1...3) 4.800) 1.10 (5.200-.50) 2.40 (1..01) .300) .20) . 1998).369) 1.541-.70) 4..500-. 2003).500-.00 (3.30 (.700 (.500 (. 1990).800) .10 (1.800 (.29) .60 (1. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.343 (.00-3.60 (3..664-1. interval) Selected percentiles (95% confidence interval) 50th .20) 1.200 (.50) 95th 2.300 (.900 (.70-5.475) .800) ..20-3.80 (3. Methyl mercury is incorporated into growing hair.329 (.90) 90th 1. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury. and a useful marker of exposure in epidemiologic studies (Grandjean et al..10 (. 1999-2002.10) 1.820 (.700-1.265-.300 (.50-12.50) 1.80 (1. Miettinen et al.300 (..Metals the tissues to mercurous and mercuric inorganic forms.825-1.10) .00-6.50) 1.377) . After exposure to elemental mercury.395) .726-1.200-.0) 4. Methyl mercury enters the brain and other tissues (Vahter et al.. 1973). urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.70-3. with most elimination occurring through in the feces (Sherlock et al.800) 1.200-.374) .500-1.30) 1.23) .800-1..14 and 0. Excretion occurs by renal and fecal routes.800 (.30-3. 1996.70-5.30-4.700-.00) .317 (.60) 3. thereafter.70) 1.90) 2.40) 2.00-1..27) .60 (3.20) .60) 1. Suzuki et al.06 (. 1971).256-.00 (1.30-4.30-5...00) 1.300 (.50-3. Sandborgh-Englund et al.871-1.500-.90 (4. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.50-2.00 (2.400-.40) 5.30-6.70) 4.50 (1. 1995.30-6. 1992). The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.50) 3.944 (.00) 2.20 (.60) 1. Jonsson et al.73) 1.700 (.90 (1.900 (. Smith and Farris.600) . 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. 1992 and 1999. Vahter et al.667 (.297-.00) 6.300) ..00) 1.10 (3.90 (1. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.10 (1. National Health and Nutrition Examination Survey. Myers et al. Vimy et al.600 (.40) 1.10-1.20 (2.60 (2.10-3. 1991. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.40-1.02 (.407) .S.90) 3. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.269-.900-1..700 (.7) 4.700 (.30) 1.30) 3.697-. 1969. Fourth National Report on Human Exposure to Environmental Chemicals 219 . 1994) and then undergoes slow dealkylation to inorganic mercury.940) Race/ethnicity (females.14.80) 579 527 370 436 588 806 Limit of detection (LOD. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days. 1994).70 (1.500-.20-11. 2003).06-1.90) 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 .00-2.20-3..40-2. 1993).50 (2. 1992. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.70-6.20-3.268-.900 (.90) 2.800 (.30-2.80) 1.90) 5.833 (.800) 75th . for both acute and chronic exposures.824) 1. 1998). 1984.00) 4. population.30-6.30-11.800-1.919) .

500-. In recent epidemiologic studies. dysarthria. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. 2002.600) . Inorganic mercury exposure usually occurs by ingestion. Salonen et al. Rice.700-. and neurocognitive and behavioral disturbances. < LOD means less than the limit of detection. altered physical growth. 1963).600 (. Acute.42. 2005.. irritability. and pinkish discoloration of the hands and feet (Tunnessen et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2004.. 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. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH...600-. short-term memory loss.700 (. 1993). 2006. Smith et al. particularly irritability..800) . 220 Fourth National Report on Human Exposure to Environmental Chemicals .500-. Vupputuri et al. 2006. 1996). 2004). 2000. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. 1995.600) . Once absorbed. sensory impairments. Drexler and Schaller.500-.700 (. fatigue. Stern 2005.500-... 2004).700 (.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . ataxia. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. 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. Survey Geometric mean (95% conf. At levels below those that cause acute lung injury.S. which may vary for some chemicals by year and by individual sample. DeRouen et al.600) . the existence of a causal relation is unresolved (Chan and Egeland.600 (...Metals may be more efficient for inorganic mercury (Grandjean et al.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . 1998.600) .500-.700 (.600) ..500-.600 (.500-. cerebellar ataxia. pain in the extremities.600) .600-. depression.600-. Bellinger et al. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation.500 (.700) 2007 2240 3406 Limit of detection (LOD. Sakamoto et al. Rissanen et al. population from the National Health and Nutrition Examination Survey. The constellation of findings may include anorexia..600-.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .600) . hypertension.700-... anorexia. Sakamoto et al. 1970. 1987). and progressive constriction of the visual fields. typically after a latent period of weeks to months. insomnia.600) . maculopapular rash. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.500 (<LOD-.700) . causing parasthesias. Smith et al.500-.700-. 2005).600) . limb deformities. see Data Analysis section) for Survey year 03-04 is 0. 2000. Oskarsson et al.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 . Factor-Litvak et al. hearing impairment. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. overt signs and symptoms of chronic inhalation may include tremor. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. 1983). 1951.600 (.600 (.600 (. 2003).500-. and cerebral palsy (NRC. and sleep disturbance (Bidstrup et al..800) .600 (.700 (.500 (. 2000). 2004. high-dose exposure to elemental mercury vapor may cause severe pneumonitis.500 (<LOD-...700 (. 1995. dysarthria. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al.. Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.500) ..600 (. Overt poisoning from methyl mercury primarily affects the central nervous system. gingivitis.

405-. Sanzo et al. Mahaffey et al..88) 287 722 1529 03-04 03-04 .Metals standard for inorganic mercury has been established by U. Among the three racial/ethnic groups.63-2.55 µg/L.16 (.433 (.00 (.30) 3. the median concentration of blood mercury was 0.78 µg/L for adults and 0.cdc. 2002).gov/toxprofiles.34-3.19 (2. In Germany the geometric mean for blood mercury was 0. 2009).68 (2.410-. interval) .54 (2.14-2.31) 2.280-. particularly methyl mercury.382-.31) 1266 1272 03-04 03-04 03-04 .00) 1.420 (. et al.549) . and increased slightly in non-Hispanic white children (Caldwell.460) .930-1. aged 18 to 69 years.509) .870-1.870-1. 2000).60) 619 713 1066 Limit of detection (LOD. average age 33 years..440 (.447 (. 1998).304) .770-1.416 (.9 years). and the age-related changes differed across the groups (Caldwell et al.530) . Schober et al.14) 90th 2.23) 2.58 µg/L for 4645 adults.76-3.atsdr.250) .890 (.. total blood mercury geometric mean levels in females aged 16-49 years did not change. In NHANES 19992002.99-6.840) 1.463) ..610-1.330 (.555) .76-4. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.200 (.05) 3.530-. Information about external exposure (i. These distinctions can help interpret mercury blood levels in people.442-..67-2.S. Fourth National Report on Human Exposure to Environmental Chemicals 221 . the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.S. slightly higher total blood mercury levels were found in U. EPA.52) 2.700 (. During the same survey periods.441 (. population from the National Health and Nutrition Examination Survey. range 40 years to 78 years) had an average total blood mercury concentration of 2. Biomonitoring Information In the general population.840-1.60-2. Kingman et al..28) 1.840-1.05) 1.358 (. average age 9. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females.S. 2006).330-.360-.88 (1.330-.480) 75th 1.476 (.88-3..430) . 2004. the total blood mercury concentration is due mostly to the dietary intake of organic forms..epa.03-4.940 (.400 (. 2003).430 (. EPA at: http://www. Grandjean et al.406-.76-3.408) .96 (1. environmental levels) and health effects is available from the U.16 (1.67-3.07 (. Over the NHANES 1999-2006 survey periods.78-2. 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.97) 2.24) 1.S.19 (1.413-.09 (2.93 (1.66) 3.313-.213-..290-. 1998). Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.370) .14.26 (1..89) 3.580) .61) 1. see Data Analysis section) for Survey year 03-04 is 0. 1995. Total blood mercury levels increase with greater fish consumption (Dewailly et al.08 (1. 2001. 2003). From 1996 through 1998. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.24 (2.520) .340-.460 (.42) 95th 3.360 (. Survey years 03-04 Geometric mean (95% conf. adult women in several ethnic subgroups (Hightower et al.160-.530) .960 (.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 .08 (1. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.495 (. However...01 (.420 (. military veterans (mean age 52.77-2.492) Selected percentiles ( 95% confidence interval) 50th .700-1.39-3. Benes et al. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2009).90) 2.350-.gov/mercury and from ATSDR at: http:// www.480 (. total blood mercury increased with age. A cohort of 1127 U.20 (1.509) .534) . 1997..46 µg/L for children. 758 children.S. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.254 (.60 (1. 2001. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al..23) .12 (.29) 1.360-.96 (1.65) 1.13-2.85-2.330-.430 (.33 (2.8 years.e. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.18) 2.570) . who participated in a 1998 representative population survey (Becker et al.396-.46) 3.

463 (. 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..616) .78-4.714-1..09) 1..87 (1.508 (.969-1.11-2.289) .566) .301-.630) .275) .79 (1.28 (. An expert-panel report recently prepared for the U.447-.S.362 (.04-3.768 (. mean urinary mercury was 3. Urinary mercury levels in recent German (Becker et al.18-1. women of childbearing age have generally been much lower than these levels (CDC.522-. reversible increase in urinary N-acetyl-glucosaminidase.347) . DeRouen et al.51-2. and Italian (Apostoli et al.537) .63) 1.54 (2.391) .13-2.32 (1.. population from the National Health and Nutrition Examination Survey.333-.88-2.784) 1.455) . 2003).472-. a biomarker of perturbation in renal tubular function..16) 1.307-.208-. Czech (Benes et al.40-1.61) 1..486) Selected percentiles ( 95% confidence interval) 50th .64-2.46-2.384 (.225-.32-2.12-3.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals . 1988.56) 1266 1271 03-04 03-04 03-04 .455-.785-1.00) 90th 1.35 (1.365 (.365 (.217 (. Levels in U.06 (.11) 1. 1998).67 (1. Survey years 03-04 Geometric mean (95% conf.309-.455-. 2009). Information about the biological exposure indices is provided here for comparison.30) 1.297 (. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.Metals 2000).620-. Langworth et al.368) .255 (.964-1.909 (.800-1.358) . Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.400) . 2002) adult population surveys were similar to those in a U. the urine mercury increased by approximately 0.875-1.385-. military veterans with dental amalgams.404-.196-.687) .619-.40 (1. interval) .417) .06 (.23-2.88 (1.31 (1.485 (. 2009). 1992).480) .545 (. 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.447 (.535) 1.276 (. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.S.25 (.44) 1.652) .79) 1.400-.990) . and on average.343 (.30) 2. In the study of U.265-.13 (1. 2006).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 .11) 2. not to imply a safety level for general population exposure.65 (1.667-1.07) 1. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.01) 2.443 (.391-. et al.77 (2.67 (1.498) 75th .599) .464 (.525 (.21) 1.1 µg/L.88-2.587 (..00 (.280-. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.87) 2.86) 95th 2.696 (. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.. et al.S. 2002).39) 1.246-.00) 286 722 1529 03-04 03-04 . 2006.306 (. Department of Health and Human Services noted that several studies have observed a modest.03) 2.970 (. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.76 (1. 2005)..392-.476 (.. Urine mercury and the number of dental amalgams were correlated.1 µg/L for each surface with a dental amalgam (Kingman et al.376-.41-2.532 (.S.62 (1. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.588) .

557-.98 (5.450-.07-2.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.475-.809) .719 (.650 (.32 (1. 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.62 (3.43-1.69 (1.710 (.00) 2.65-4.516 (.41 (1.706 (.23-1.501-.22-3.21 (1.48 (2.03 (.615 (.14) 3. Geometric mean Survey years (95% conf.00 (2.560 (.95 (2.31-1.35) .616-.38) 4.61-6.37 (1.655 (.21-3.28 (1.824) .32) 2.47) 1.27-1.83-3.45-3.53-3.46-4.76 (1.87-4.41 (1. National Health and Nutrition Examination Survey.17) 95th 5.632 (.520-.03) 1.79) 1.606 (.57-4.540-.656-.99 (3.636-.850-1.540 (.637) .37) 1.46) 3.04-1.06 (.699) 1.44) 3.665) .45-2.553-.631-.426-.42) 2.85) 4.68) 3.32-3.47) 1.07-5.910) .810) .07) 1.387-.09-1.742-1.685 (.77) 2.10-2.799) .99-2.710) 1.97) 2.870) .81 (3.84 (2.84 (2.89 (2.582-.09-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.54) 595 531 381 442 594 826 Limit of detection (LOD.410-.740 (.21 (2.03 (. 16-49 years) 99-00 01-02 .25) 2.91 (2.526-.966) .600 (.30 (1.724 (. interval) Selected percentiles (95% confidence interval) 50th .806) .569-.18 (3.16-5. 1999-2002.578-.41 (2.Metals Urinary Mercury−Females Aged 16-49 Years Old.50 (2.670) 75th 1.99 (2.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 . Geometric mean (95% conf.56 (1.00 (3.686) .59-5.85-3.56) 3.97 (1.97) 2.92) 2.831) .592 (. interval) Selected percentiles (95% confidence interval) Survey years 50th .522 (.579-.50 (1.658 (.13-4.520-.81-6.97) 2.30 (2.68 (3.45 (1.51) .13 (2.500-.930) .15 (2.639 (.35 (1. National Health and Nutrition Examination Survey.70 (2. 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.42-3.691) .52) 3.55-3.624-.55) 90th 3.580 (.709) .05 (2.420-.14 and 0.846) . Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .69-3.30-2.76) 2.657 (.39-3.560-.15-1.30 (2.508-.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .94) 1.565 (.710 (.51 (3.18) 3.41-6.833) .24-1.45) 2.16) 5.790) .772 (.45) 95th 3.723 (.709) 75th 1.580-.605-.622-. population.10-4.45) 2.596 (.92) 4.50-4.774) .99) 1.31 (1.502-.892) . 16-49 years) 99-00 01-02 .24) 6.03-2.42) 90th 2.77) 1.650) 1.27 (2.04-10.S.56) 4.76-5.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.92) 3.62 (1.68-3.832-1.760 (.909-1.46 (1.62 (4.79) 3.61) 1.3) 5.831) .610-.721 (. population.91-7.05 (3.650 (.23-1. 1999-2002.22 (.72) 1.27 (1.14-1.S.664) .65) 1.14-2.744) 1.14.620 (.

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Takahashi Y. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings.258(4 Pt 2):R939-945.79:786789. Environ Res 2005. Hongo T. Daniels JL. Aguinagalde FX. Vupputuri S. Turner MD. Smith JC. The hair-organ relationship in mercury concentration in contemporary Japanese. Zeitz P.128(2):25125-25126. Sherlock J. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Guo S. Yoshinaga J. Kaye WE. Blood mercury levels in US children and women of childbearing age.4(5):981-988.110:129-132.97(2):195-200. Newton G. Effects of occupational exposure to elemental mercury on short term memory. Nakazawa M. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Jones RL. Environ Res 2005. 1999-2000. Hum Toxicol 1984. Bolger PM. Hislop D. JAMA 2003. Toxicol Appl Pharmacol 1994. Vahter M. The kinetics of intravenously administered methyl mercury in man. Public Health Nutr 2001.37:245-252. Arch Environ Health 1993. Methyl mercury pharmacokinetics in man: a reevaluation. Orr MF. Acrodynia: exposure to mercury from fluorescent light bulbs. et al. Stern AH.98(1):133-142. Toxicol Appl Pharmacol 1994. Lind B.289(13):1667-1674. Mottet NK. et al. DeRouen TA. Allen PV. McMahon KJ.31:687-700. Patil LS. Matsuo N. Langolf GD. Amurrio A. Osterloh J. Sandler DP.2:117-131. Friberg L. Whittle K. Azpiri MA. Environ Health Perspect 2002. Hall LL. Toxicol Appl Pharmacol 1996.40:413-419. Leroux BG. Shen DD. Lorscheider FL. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Imai H.48(4):221229. Farris FF.124:221-229. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Dorronsoro M.111(12):1465-1470. Fisher HL. McDowell M. Sinks TH. Amiano P. Am Ind Hyg Assoc J 1970. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Martin MD. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Longnecker MP. Pediatrics 1987. Goldberg J. Effects of exposure to mercury in the manufacture of chlorine. Bernardo MF. Smith RG. Br J Ind Med 1983. Burbacher T.115(10):1527-1531. Vimy MJ. Leitao JG. 1993-1998. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect 2003. Baser M. Tunnessen WW. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment.Metals Sanzo JM. Mooney TF. et al. Woods JS. Schober SE. Most B. Am J Physiol 1990. Suzuki T. Smith JC. Stern AH. Environ Health Perspect 2007. The contribution of dental amalgam to urinary mercury excretion in children. Smith PJ. Vorwald AJ. Smith AE. Topping G.

2) 79.7-122) 93. interval) 45.0) 84. More recently.9 (34.0) 97.Metals Molybdenum or ore deposits.9 (78.9-109) 97.4 (48.7-92.9-83.1-88.5-41.0-100) 63. 1996).4) 52.4 (80.7) 86.5) 80.7 (37.9 (40.8-108) 87.0) 62.4) 49.2) 41.3 (71.4) 45.1-52.6 (73.2 (55.1-59. At a daily oral molybdenum dose of 24 µg. 7439-98-7 General Information Elemental molybdenum is a silver-white. and 03-04 are 0.8 (67.8) 40.2 (38.0-101) 82. and xanthine oxidase (Kisker et al.7-96.9-85.1-44.0-110) 90. respectively. Fourth National Report on Human Exposure to Environmental Chemicals 227 .8-94.2-79. 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.5-52.4) 76. 0.7 (44.1) 60.2-37.4-61.0-62.3 (46.9) 67.8) 75.5-91.6) 53.3-75.1) 35. and in pigments for ceramics.2) 48. 2001).. urinary excretion over six days CAS No.5 (37.7) 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 78.6) 71. chemical reagents in hospital laboratories.1) 46.4 (72.4-82.8.8-49.0 (46.2 (49.9-82.3-44.0-77. semiconductor and battery industries have begun to use molybdenum.7-68.2) 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 (98.2) 52. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4-75.0) 45.0-38.9 (44. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.6-58.8 (85. lubricants.1-63.9 (32.2 (40.0 (43.7-47.3-108) 215 (161-278) 169 (145-194) 148 (136-163) 154 (132-180) 158 (130-177) 127 (114-139) 1121 1335 1281 1136 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 47.6 (52.6 (55.6-46.0 (41.5-68.5-66.6 (43.5-65.3 (73.0) 60.0 (42.6-111) 267 (159-840) 197 (161-291) 181 (138-235) 188 (146-216) 179 (155-227) 143 (130-156) 168 (143-206) 150 (130-166) 133 (119-144) 310 368 290 648 762 725 1299 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 52.2 (61.3 (55. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.1) 82.4) 56.7-91. 2001.1 (91.0 (81.5 (41.2-59.9 (73.0 (42.6) 51.5) 47.1-52. aldehyde dehydrogenase.6-72.4) 42.2 (49. population from the National Health and Nutrition Examination survey.0-65. and paints.3 (79.3) 83.8 (82.3) 65.3) 54.6 (55.5) 44.5 (81.7-41.0 (48.7) 57. 1997).5-52. hydrogenation catalysts.7 (71.7) 78.8-90.2-70. and 1.0) 39.3 (38.1) 59.6 (40.1 (38.7 (58.9 (37.6-62.8) 44.7-60.2 (69.4 (34. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.7 (36.2-53.7) 77.6 (40.7 (50.9 (33.8-46.0-71. WHO.4 (79.7-84. 01-02.6) 71.7-39.7) 51.4 (48.2) 37.8 (42.7-105) 69.8) 48.7 (45.8) 46.7-73.7 (51.3 (55.S.6-42.4-52.9) 62.5) 60.2 (63.6) Selected percentiles ( 95% confidence interval) 50th 50.3) 37.0) 55.9 (52.6) 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. Excretion occurs predominantly via the kidneys.3-91.3) 47.7) 75th 84.2 (56.8-106) 88.8.9-55.3 (84.7) 45.1 (71.1) 126 (106-147) 109 (94. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.5 (74.2 (83.6) 93.3 (47. inks.0-85. which exert homeostatic regulation over molybdenum balance. In humans.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.5-46.3 (53. see Data Analysis section) for survey years 99-00.0-53.5) 85.0 (76.0) 54.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.3-47.5) 80.7-50.5.6-96.8) 39.3 (64.9) 34.6-55.2-59.4) 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.1) 57.5-124) 108 (92.5 (48.2) 40.7-51.6-82.5 (43.2) 53.9-55.0-56.3) 85. Compounds of molybdenum are also used as corrosion inhibitors.2-91.1-48.3 (37.7 (73.7) 78.1-55.7) 46.5 (41.1 (34.2-42.5 (67.1-51.9-56. hard metal widely used to add strength and hardness and retard corrosion in metal alloys. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.3) 41.5 (49.

8) 79.3-44.4) 58.2-46. and urinary levels reflect intake from all sources.2 (33.2 (43.5 (39.4 (44.0-46.2) 39.0) 88.1-43.9-41.7 (66.1 (30.9) 92..4) 47..1-43.1) 37.3 (36.0) 39.6-41.9 (39.5-119) 90.3 (36.9 (64.0 (35.0) 53.1 (82.3) 64.0 (74.5-50.3) 43.2) 42.2) 42.6-63.1) 56.2 (37.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.3 (51.5 (41.8 (75.1-112) 78.9) 40.5) 73.8-67.8-84.3) 61.5 (80.1-41.1 (38.6) 39. Based on studies finding adverse reproductive effects in rats and mice.6 (42. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3) 57.0-120) 85.3) 44.2 (69.7) 42.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.2 (36. interval) 43.4-107) 85.4 (55.3 (71.9 (39.5 (36.0) 72.1) 43.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.8 (36.3) 40.9-96.0-133) 119 (88.3-43. In industry.4) 89.5-92.9-117) 57.4) 61.9 (49.4) 44.3-68. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.9-61.6) 39.4) 122 (107-133) 109 (99.0) 39.4-118) 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 .8-118) 81.9) 31.9 (79.5 (50.2) 58. but available epidemiologic data are scant.7) 45.2-80.3-45.0-56.6-63.0-46. 1961.7) 112 (95.8 (57.5-70.6-76.9-87.5-35.4-66.5 (35. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP. 1997).2-65.6) 36.S.4) 48.2-103) 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. respectively.8-65.8) 38.5-99.4-42.7-137) 129 (109-155) 112 (97.0-38.3) Sample size 2257 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 85.7-120) 87.7-100) 77. EPA.2) 39.7) 53.1 (33.8) 61. Biomonitoring Information Molybdenum is an essential element for health.9 (64.6 (57.3) 37.7) 75th 63.S.9-71.3 (37.4) 116 (101-126) 104 (88.8-66.1-67.5 (39.0-103) 103 (90.8-42.6) Selected percentiles ( 95% confidence interval) 50th 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 40.1-38.6) 48.0) 38.4) 60.9) 79. 1993).5-46.2 (57.2-96.2-41. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.7-43.2 (40.5 (40.5 (54.4) 77.1 (40.4 (37.7) 62.2 (73.8 (56. of the ingested dose (Turnlund et al.7-62.6-61.9-45.1-127) 90.5 (37.4-39.3) 56. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1) 40.5-62.4-76.8-52.7-38.1 (44.7) 115 (93.5-44.3 (37.5 (79.5 (78.2-47.2) 37.2-96.3) 41. population from the National Health and Nutrition Examination survey.9 (73. 1995).5-45.4-185) 106 (94.5 (83.5-97.1-39.6-88.5) 71.3 (58.3 (55. urinary excretion over six days rose to 50% and 67%.5 (65.1-45.2-40.3-52.Metals was 18% of the ingested dose.9-45.9 (40..9 (36. 1999).9 mg/kg/day and established a tolerable upper intake level of 0.4 (78.7) 41.6-45.7-93.5) 60.5) 72.9-42.5) 63.0) 44.8) 45.8) 62.3 (83.5-48.4 (59.5 (41.7) 57.6 (71.5 (35.9-40.2) 43. U.9 (35.3-115) 98.5) 90th 108 (97.1) 101 (83.8) 71.6) 43.5 (38.8) 39.3-59.1-100) 86.2 (52.4 (67.0-41.6-78.1 (49.7-52.8) 38.5 (34.0) 36.4-41.0) 33.5 (37.4-106) 85.1 (54.5 (40.3-141) 109 (81.03 mg/kg/day in humans (IOM. and clinical or epidemiologic evidence of adverse effects is limited.3-46.8-47. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.2-121) 107 (92.2 (40.1 (38.0 (80.9-68.2-49.7-40.1-81. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.1 (39. 2001).3 (71.3 (53.7 (75.6 (59.2 (40.8-46.6 (38.5 (65.8-47.2) 37.8 (37.1 (42.1-34.1-39.9) 44.1) 65.7-44.7 (30.2) 38.1 (37.1-40.8 (90.2 (50. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.3-56.0 (58.4 (40.9-118) 91. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.1) 37.5-60.6-61.7 (77.5 (59.6 (36.6 (36.2) 55. at daily oral doses of 95 µg and 428 µg.4) 40.4-120) 101 (84. Molybdenum is generally considered to be of low human toxicity.4 (56.1-109) 89.5-69.9) 41.1-79.4 (53.8) 37.0) 62.

Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al. 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. Ronchi A. Environmental Protection Agency (U. U. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Washington. iron. Minoia et al. Occupational risk factors of lung cancer: a hospital based case-control study. 420-441. TR-462. vanadium. Turnlund JR. Molybdenum. World Health Organization (WHO).123(1):81-85. Sabbioni E.php?record_id=10026&page=420. Molybdenum absorption. 144-154. Sciarra G. (DC): National Academy Press.62(4):790-796.S. vitamin K.nih. White MA. J Trace Elem Med Biol 2001. Sabbioni E. silicon. Vermeire PA.gov/index. Schleyerbach U. In: Trace elements in human nutrition and health.gov/iris/ subst/0425. van Sprundel MP.S. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Weyler JJ. Geneva: WHO. copper. Shmavonyan DM. et al. Available at URL: http://books. Molybdenum 1993 [online]. arsenic. Rapid Comm Mass Spectrom 2002. and zinc: a report of the Panel on Micronutrients. Third National Report on Human Exposure to Environmental Chemicals. Turci R. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Christensen JM. X. 4/14/09 White MA. Schaub J. Occup Environ Med 1999. pp.nap. Available at URL: http://www. 2005. Rees DC.Metals in urine for the U. nickel. pp. Analyst 1998. Fourth National Report on Human Exposure to Environmental Chemicals 229 . Am J Clin Nutr 1995. Minoia C. excretion. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Trace element reference values in tissues from inhabitants of the European Union. Yarovaya GA. Institute of Medicine (IOM). 4/14/09 Iversen BS. 2005). 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Available at URL: http://ntp. 1998). 4/14/09 Sievers E. White and Sabbioni. EPA). Ann Rev Biochem 1997. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces.. 16:1313-1319. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Kisker C.66:233-267.15(2-3):149-154. Van Meerbeeck JP. Peiffer GL. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. 1998. edu/openbook. Keyes WR. Droste JHJ. Food and Nutrition Board. A study of 13 elements in blood and urine of a United Kingdom population. National Toxicology Program (NTP). 2001).epa. Sci Total Environ 1998. Kristiansen J.S. 2002. molybdenum. iodine. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Schindelin H. Atlanta (GA). Zhurnal Obshchey Biologii 1961. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al.22(3):179-191. Koval’skiy GA. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC.. chromium. 2001.niehs. boron. 56:322-327. Menne C. Dietary reference intakes for vitamin A. Aprea C.216:253-270. manganese. Gatti A. 1996.htm.. References Centers for Disease Control and Prevention (CDC). Molybdenum in infancy: methodical investigation of urinary excretion.

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

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

Ruff F: Platinum and platinosis. Schierl et al. 2004. Saindelle A. Available at URL: http://www. et al. Wilhelm et al. Influences on human internal exposure to environmental platinum. Int Arch Occup Environ Health 1997. Hauff K.. Patty’s Toxicology. Environ Health Perspect 1975b. Several studies have shown that background concentrations in general populations were usually less than 0. 206:15-24.Metals the International Programme on Chemical Safety at http:// www. Urinary platinum levels associated with dental gold alloys. Angerer J.. Arch Environ Health 2001. Bocca B. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Gieler U. Biomonitoring Information Urinary platinum levels reflect recent exposure.19:685-691.4(1):27-36.207(1):69-73. Petrucci F. 2000.61(7):636-9. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Wilhelm M. Stilianakis NI. Hysell D. Hall L. et al. Pethran A. Schulz C. and gold excretion of patients after insertion of noble-metal dental alloys. Uptake of antineoplastic agents in pharmacy and hospital personnel. Kuster W. Part 1: monitoring of urinary concentrations. Kulka U. Occup Environ Med 2004. Schulz C. Turfeld M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Czerczak S. Schierl R. Int Arch Occup Environ Health 2003. Platinum concentrations in urban road dust and soil. 289-380. Hysell D. and in blood and urine in the United Kingdom. 1991 [online].01 µg/L (Becker et al. Herr CE. ruthenium. New York: John Wiley & Sons. 3/31/08 Moore W Jr. Int J Hyg Environ Health 2004. which elevate urinary platinum by five to twelve-fold (Begerow et al. Ruff F: Histamine release by sodium cholorplatinate. Schierl R. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. and platinum. rhodium. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Ensslin AS. palladium. Raab W. 1998). Gromiec JP. Analyst 1998. 2003). Crocker W. Begerow J. Farago ME. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Iavicoli I. International Programme on Chemical Safety (IPCS). Biomonitoring of traffic police officers exposed to airborne platinum. 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.56(3):283-286. Seiwert M.. Alimonti A. van de Weyer C. Levels of platinum in urine for the U..13(1):24-30. palladium.10:63-71. 2004). Carelli G. Biomarkers 1999. Campbell K. Cohrssen B. Kazantzis G.005 µg/L (Iavicoli et al.. Kavanagh P. Grimm CH.htm. Thornton I. Senofonte O. Environ Res 1975a. Herr et al. 1997. Urinary excretion of platinum from platinum-industry workers.org/documents/ehc/ehc/ ehc125. 1998).. Huber R.. 2003. Occup Environ Med 1998.. eds. 2004) or less than 0.35:313-321. Seifert B. Neuendorf J. 5th ed. Fries HG. Br J Pharmacol 1969. Schierl R. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Parrot JL. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al.70(3):205-208.04 µg/L) in this Report. Schierl.htm. Jankofsky M. Kaus S.123(3):451-454.S. Pethran et al. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Duneman L:Long-term urinary platinum.. Blanks R. Nowak D. International Journal of Hygiene and Environmental Health 2003. In: Bingham E. Nickel. population were below the limit of detection (0. Fruhmann G. Saindelle A.inchem.. 1999. Platinum. 2003. pp. Herr et al. osmium.inchem.org/documents/ehc/ehc/ehc125. Kelly J. Schierl R. Biomonitoring studies on levels of platinum provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of platinum than are found in the general population. Allergy and histamine release due to some platinum salts.55(2):138-140. Rommelt H. et al. J Expo Anal Environ Epidemiol 2003. 2003.. Boos KS.76(1):5-10. Powell CH. et al. Moore W Jr. Arch Environ Health:1969. 2001). Environmental Health Criteria 125. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Ewers U. Pethran A. Hebert R.9:152-158. References Becker K.

200 (.430-.420) . It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.400 (.310 (.173-.185 (.370 (.220 (.150-.170-.148-.310 (.370 (.440 (.280) .196) .200) .220 (.400-.370 (.144 (.184 (.330-. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.400-.154-.520) .180-.250-. see Data Analysis section) for Survey years 99-00.170) .172 (.190 (.200 (.167-.310) .490) Total .420 (.191 (.260-.260-.470 (.410-.400-.173) .330-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 01-02.250-.390-.217 (.240-.400-.173) .410 (.460) .188) . From these and other sources.500) .180) 75th .190 (.300-.440 (.170 (.185-.330) .150-.360 (.470) .192) Selected percentiles ( 95% confidence interval) 50th .180 (.400) .450 (.180 (.145-.500 (.410-.300 (. respectively. Thallium disappears from the blood with a half-life of several days.410 (.260 (. and 03-04 are 0.230-.430-.440) .510 (.390) .330-.146 (.S.170-.220) .550 (.380) . Human health effects from thallium at low environmental CAS No.270) .206) .147-.145 (.260-. In the past.440 (.157-.430 (.420-.520 (.220-.340-.250-.210) .480) .370 (. In addition.170-.250-.200 (.153-.160 (.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 .170 (.200 (.270 (.180) .150-.350) .280 (.290) .350-.02.165) Sample size 2413 2653 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .210-.190 (.220) .330-.183) .147-.440 (.200-.230 (.420) .170 (.320) . representing distribution into other tissues..490) .330-.280-.180-.201 (.200-.240-.400) 95th .290) .160 (.360-.500) .420) .167 (.159 (.320) .197-.250-.181-.220) .220) .450 (.420-.Metals Thallium depilatory cosmetics.370-.230) .160-.400 (.400) .450 (.350-.410) .420-.360-. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.170-.218) .290) 90th .480) .210 (.175) .220) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.470) .300 (.220 (.640) .149 (.380-.137-.320-.420) .217) .420) .135-.410-.290 (.250-.280-.430 (.215) .280) .370-.159 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals. however.340-.202) .163) .172) .200-. the latter being the current major industrial consumer of thallium in this country.430 (.280 (.200) .260-.360-.230) .360) .380 (.300 (.180-.220 (.340-.390-.197 (.410 (.171 (.176 (.520) .180 (.370 (.350-. and 0.350) .170-.239) .150-.290-.172 (.400) .155 (.160-.430-.202 (.200) .350-.410 (.230) .460 (.280 (.630) .300) .133-.250-. 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.590) .450 (.170-.560) .450 (.156) .400) .260 (.162-.240) .290 (.196) .500) .165 (.190 (.02. In the United States.280) .410-.200 (.210 (.240-.350-.147-.300) .370 (.330-.250 (.490 (.300) .250) .360-.440-.270 (.360 (.350 (.430) .480) .200) .390) .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.160-.290-.183) .201 (.180-.158) .450) . 0.330) .440) .240) .350 (.450 (.270 (.150-.230-.520) .340) .270 (.340-.310 (.440) . it has not been specifically mined or refined in the United States since 1984. interval) .200) .410-. 2005).260 (.200 (.430 (.178) .370) .240) .160 (.330) .200-.230) .450 (.330) .145-.420-.340) .380 (.390 (.370-.270 (.190-.156) .160 (. population from the National Health and Nutrition Examination Survey.390) .243) .320 (.220) .410 (. thallium was obtained as a by-product of smelting other metals.390-.370) .470 (.390) .420) .370-.187-.156-.170) .160-. thallium readily crosses the placenta and also distributes into breast milk.290 (.410 (.360 (.190 (.167-.170) .170-.320) .218) .390-.330-.340 (.690) .360 (.380-.250-.134-.225) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .270-.510) .290 (.260) .177) .160-.290 (.200) .450 (.430) .390 (.160 (.159 (.179-.410-.360-.290) .182-.220 (.290 (.270-.300) .370 (.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 .250 (.450 (.590) .400 (.290) .150-.190 (.140-.350-.270) .02.470) .260-.420) .490) .480) .490) .310-.230-.400 (.400-.270-.400 (.480) .460-.202 (.

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

Paschal DC. 1980. 1985). 1981. Sampson EJ. Martin J-C. Pirkle JL. Wiegand H. Schaller et al. Int Arch Occup Environ Health 1981. Available at URL: http://www. Challeton-de Vathaire C. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. 1992 [online]. Trace element reference values in tissues from inhabitants of the European Union. A study of 46 elements in urine. Ewers U. (1981) studied 1. population) are thought to correspond to workplace exposures at the threshold limit value of 0.. Third National Report on Human Exposure to Environmental Chemicals. Buhlmeyer G. Fourth National Report on Human Exposure to Environmental Chemicals 235 . X. Sabbioni E. 1998.47(3):223-231. Sabbioni E. Raithel HJ.gov/toxprofiles/tp54. Valentin H. Pozzoli L. Jackson RJ. White and Sabbioni. Morrow JC. Marcus RL.S. A study of 13 elements in blood and urine of a United Kingdom population. et al. Centers for Disease Control and Prevention. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Manke G. Investigation of a working population exposed to thallium. blood. Minoia et al. Pietra R. Int Arch Occup Environ Health 1980. Sci Total Environ 1998.48(4):375-389.76(1):53-59. Dolger R. References Agency for Toxic Substances and Disease Registry (ATSDR). There was no increase in the prevalence of symptoms at levels less than 20 μg/L and only a slight increase in nonspecific symptoms greater than 20 μg/L. Schmidt M.265 people living near a thallium-emitting cement plant in Germany. Celier D. et al.cdc. Soddemann H.1 mg/m3 (Marcus. 2005) and are shown with results from NHANES 2003-2004 in this Report. Brockhaus A. et al.113(1):47-53. 1990. Kramer U. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect.atsdr. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. White MA. Investigations of thallium-exposed workers in cement factories. with concentrations ranging up to 76.35(1):4-9. 2005. 7/15/09 Blanchardon E.. Environ Res 1998. 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. Schaller KH. Paschal et al. Gallorini M. Apostoli P. Minoia C. 1998). Ting BG. Boisson P.. Atlanta (GA).5 μg/L. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging.216:253-270.95:89-105. Toxicological profile for thallium. Trace element reference values in tissues from inhabitants of the European community I. and serum of Italian subjects. J Soc Occup Med 1985. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al.Metals (CDC. Brockhaus et al.. Cassot G.html. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Sci Total Environ 1990. 2005. Trace metals in urine of United States residents: reference range concentrations. Radiat Prot Dosim.

500) .210) .310) .400-.151) .210 (.350) .120) . 236 Fourth National Report on Human Exposure to Environmental Chemicals .160-.310 (.120 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.460 (.200 (.620 (.113 (.069) .060 (.230-.105) .350 (.113 (.320-.092 (.200-.520) .130) .120) .230) .250) .260 (. and as catalysts in the petroleum industry.390 (.250) .180-.120) .070 (.100) .100 (.190 (.060 (.074-.180 (.092) .180) . 01-02.076 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.090-.270-.S. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.300 (.132) .130) .04.120) .400 (.150) .100-.530 (.420-.400 (.086 (.330) .065 (.380-.170) .340-.400 (.100-.460 (.400) .220) .070 (.160 (.080 (.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 .370-.300 (.04.550) .360) .440) .350) . Little information is available on the toxicity of tungsten.270 (.370) .120-.280-.460) .087-.170) .370 (.060 (.250) .420-.096 (.300) .430 (.140 (. bronzes in pigments.140 (.160-.070) .090) .380-.060-.370 (.470 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.120) .060-.130-.290) .150-.088) .690) .110-.110 (.330-.190 (.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 .160) .500 (.490 (.190-.280 (.110-.250) .620) .380-.066-.300 (.290) .260-.065-.071-.158 (.800) .101-.240-.460 (.110 (.380-.640 (.080-.Metals Tungsten CAS No.140 (.170 (. mainly as scheelite (CaWO4).110 (.380 (.430-.060 (.100 (.830) .062 (.113 (.090-.091) .260 (.800) .073) .210 (.400 (.080) .084) .410 (.069-. 0.058-.160-.090-.220 (.220-.340-.360-.090 (.105 (.130) . filaments for incandescent lamps.630) .120-.210 (.360 (.056-.810) .160-.260-.100-.620) .204) .180-.190-.210 (.097-.460) .080 (.050-.070 (.100) .590) .160) .050-. and 0.230-.071 (.123-.100) Selected percentiles ( 95% confidence interval) 50th .050-.100) .060 (.550 (.093 (.080) . and for producing ferrotungsten.350-1.190-.140 (. Tungsten compounds are used as lubricating agents.310-.110 (.560 (.080) . Occupational exposure is from dusts released during grinding or drilling of hard metals.170 (.360-.560) .082 (.240 (.070) .470 (.340) .116) .250-.160 (.070) .096-.350) .110) .430) .062 (. interval) .130 (.110) .320) .080 (.080-.073-.560) .090-.150 (.950) .270 (.260) .430 (.510-1.095-.077-.360 (.080) 75th .510 (.270-.220) .070-.290-.100) .430 (.550) .180) .093) .073 (.470-.570 (.130) .360 (. population from the National Health and Nutrition Examination Survey.060 (.650) . which are used in rock drills and metal-cutting tools.180-.580) .320-.084 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.340-.080-. see Data Analysis section) for Survey years 99-00.520) .070-.160 (.470) .250-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.330-.135) .380 (.070-.790) .480) Total .450 (.120-.160 (.056-.122) .120-. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.310-.090 (.00) .109) .180) .084-.100) .190-.073-.210 (.250) .770 (.130-.126) .140) 90th .090) . Evidence is lacking for the carcinogenicity of tungsten.170) .093-.090-.370 (.170-.300) 95th .250) .280 (.082-.120-. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).180) .110-.090) . and 03-04 are 0.107 (.550) .560) .200) .230) .310-.060-.110 (.210-.380) .260-.070) .270-.090) . Tungsten is used mainly for producing hard metals.140-.140-.070-.520) .070-.100 (.230-.370-.530 (.330 (.088 (.095-.064-.290-.050-.530 (. which is used in the steel industry.290-.082 (.111-.130-.060-.270-.090-.068) .130 (.390) .230-.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.310-.53) .080 (.150 (.180 (.04.101 (.300-.170) .180-.310-.330) .270 (.320 (.510-.560) .130-.120) .060-.450-.670) .082) .080 (.090-.081 (.104) .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 .470) .113 (.190) .230 (.160 (.490) .137 (.410-.133) .090 (.320 (.500 (.078-.130) .076 (.100 (.430-.220) . respectively.090-.150 (.087) .092 (.290 (.570 (.120-.060-.

063-.059 (.145 (.108-.093) .085-.081) .083-.090-.131-.094-.081-.161) .300) .077-.084 (.074 (.308) .122-.094) .070 (.184 (. (1987) found possibly due to methodologic.453) .098-. Nicolaou et al.301) .258-.253) 95th .057-. interval) .231 (.079) .426) .139-. 2003.250 (.081 (.049-.180-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.082) .074-.061-. population.071 (.055-.068-.385 (.216 (.261-.091) .326) .117) .459) .080-.208-.167-.075-.098) .119-.287) .080 (.121 (.823) .197) .064-.074) .108) .329-.075 (.078 (.130 (.091 (.S.148 (.075) .(Kraus et al.083 (.199 (.077) .188-.133) .431) .359 (.080-.187) .090-.144 (.061-.215 (.136-.125 (.143 (.331-.073 (.198-.333 (.426) .153) .154) .065) .126-.150 (.S.058-. 2001).124 (.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 .218 (.284) .462) .081 (.084) .279 (.293 (.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.222) .358) .267) .074) 75th .201) .071) .203-.088) .301) .138) .308) .375) .072-.094) .072 (.347 (.152-.392) .158 (.300-.138 (.158) .168 (. 1998).216 (.283) .176-.157) .065-.146) .165) .067 (.169) .069-.452-.103-. 1997).333) .167-. Patients with medically-inserted tungsten found at increased levels in drinking water.211 (.073 (.436-1. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.056-.339 (.059-.136-.272-.253 (.354) . 2001-2002.085 (. similar to those in this Report (Schramel et al.109-..089) .270 (.431) .091) .075) .099-.333-.079) .154) .074-.344-.250-.148) .065 (.071-.151 (.070 (.084) .117 (.071 (.201 (.100) .105 (.087) .214) .078) .179-.484) .069 (.410-.053-.360 (.133) 90th .383 (.317) .085) .333-.174 (.066 (. population from the National Health and Nutrition Examination Survey.197 (.214-.130-.275 (.078-.068 (.186 (.302-.098-.278-.439 (.412 (.164 (.067-.317 (.255-.062 (.339 (.095-.091) . 2005).100) .237) .122 (.341 (.265 (.086) .667 (.465) .237-.250 (.079) .067 (.078) .083) .063-.079 (.116) .206-.066 (.205-.414) .465) .089 (.880) .060-.302-.431) .098-.063-.300-.482 (.063-.167) .294 (.258 (.176-.237) .439 (.267-.060-.197-.082) . population (CDC.071) .181 (.381) .073 (.439) Total .125) .S.078 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.179-.083) .285) .077-.359 (.197) .075 (.286-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.069 (..116-.107-.072-.098 (.071 (.096) .111 (.065-.079 (.667) .124-.122-.095) Selected percentiles ( 95% confidence interval) 50th .727) .315-.353 (.538) .317-.300 (.28) .075-. Using neutron activation analysis to 2000.086) . or exposure that a control group of non-metal workers had mean levels differences.797) .136-.436) .200-..092) .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 .167) .071) .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 .084 (.087 (.139) .065 (.190) .133) .054-.073 (.555 (.240-.077) .063 (.120) .170-.353 (.174) .100 (.059-.150-.224) .059-.158) .121-.064-.231-.216-.279 (.079) .605) .056-.253-.217-.333 (.354-.083 (.500) .364 (.329 (.169 (.222-.088) . measure urinary tungsten.139 (.306) . A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.086) .146 (.091 (.061-.739) .146 (.279 (.255 (.379 (.063 (.082 (.054-.144-.106 (.120) .255 (.153-.119 (.150-.109 (.634 (.233-.080 (.060 (.105 (.333 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.093-.554) .215) .155-.116 (.216-.484 (.301) .199 (. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.136-.138 (.065-.104-.086-.198) .386) .216-.340 (.091) .209-.299 (.200-.582) .245-.057-.333 (.136 (.497 (.143-.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 . 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.217-.333) . and 2003-2004 (Paschal et al.158) .

Trace metals in urine of United States residents: reference range concentrations. bismuth. 2005. Paetzel C. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. Angerer J. Pietra R.(2):73-77. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Centers for Disease Control and Prevention. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. 4/15/09 Centers for Disease Control and Prevention. lead. Schramel P. Catheter Cardiovasc Interv 2004. Cancer Clusters. The determination of metals (antimony. Mosconi G. tellurium.Metals blood. Jackson RJ. Feuerbach S. [online] 2003. Available at URL: http://www. Sabioni E. Schramel P.62:380-384.cdc. Wendler I. palladium. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. National Center for Environmental Health. thallium. Paschal DC. platinum. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Pirkle JL.htm. Zobelein P. and hair (Bachthaler et al.69(3):219-223. References Bachthaler M. Weber A. Int Arch Occup Environ Health 1997. Link J. Lenhart M. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Environ Res 1998. Nevada Exposure Asssessment. 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.. cadmium. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Morrow JC. Kraus T. Sampson EJ.58(10):631-634. Cassina G. Angerer J. Atlanta (GA). Churchill County (Fallon). Seghizzi P. Schaller KH. mercury. Ting BG. Occup Environ Med 2001. 238 Fourth National Report on Human Exposure to Environmental Chemicals . J Trace Elem Electrolytes Health Dis 1987.76(1):53-59. 2004).gov/nceh/clusters/Fallon/study. urine. Manke C. Nicolaou G. Third National Report on Human Exposure to Environmental Chemicals.

010) * .033) .041 (.017) .008 (.088) .008 (.037 (.013 (.009) .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 .020-.013) .008 (.016) .011) .052 (.036) .012 (.029 (.034) .038 (.023 (.012) .009) Selected percentiles ( 95% confidence interval) 50th .018) .008 (.023) .060 (.009-.011 (.008 (.007) .009) .010-.009 (.010) .031 (.004.012-.020-.046) .007-.015 (.045) .015) .008 (.008) .008 (.017) . and 0.010-.007 (.009-.049) .054) .016) .009 (.009-.016) .033 (.009-.016) .023-.007 (.022-.020 (.008) .028 (.010 (.031 (.019 (.012) . Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).008 (.021 (.017 (.007-.027) .055 (.009) .044 (.006-.073) .026) .031-.021 (.158) .040 (.032 (.026 (.024 (.010) .006-.036-.009 (.013-.008-.010 (.039-.036-.007 (. Thus.005.012-.008) .022-. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.009) .019-.046-.008 (.069) .027-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.005-.016 (.030 (.015 (.011-. 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.007-.007 (.062) .030 (.008 (.020-.038) .005-.013 (.017-.017-.012) .012 (.009) .048) .009-.019-.018-.006-.019-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.017-.012-.007-.013 (.007-.009) .007-.023) .012 (.016-.036) . 01-02.037) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.008) .021) .004.021) .008) .028-.035-.009) * .012-.026) 95th .039) .011-. and as an aid in electron microscopy and photography. human exposure occurs primarily by inhaling dust and other small particles. and 234U.006-.012) .017-.007 (.008) Sample size 2464 2690 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .008 (.022) .009 (.010) .026-.008-.030-.026 (.114 (.014 (.011) . including nuclear weapons.007 (.013-.015-.041 (.007-.016) .009 (.008-.047 (.005-.028 (.006-.013 (.279) .027-.017) .008 (.034-.009 (.018) . 0.031 (.009-. or processing.067) .050) .031 (.017 (.048 (.013 (.027) . and 03-04 are 0.011) .012 (.053) .014 (.011) .066) .009) .005-.020-.010-. see Data Analysis section) for Survey years 99-00.009-.011-.015 (.018 (.127) .017-.018 (.017) .037) .010) .063) .009) . interval) .011-.056) .008-.008-.007 (. Since the 1990’s.043) .017) .010) .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 .026-.013-.013 (.035) .053 (.007) .037) .021-.023) .036 (.006 (.021) .007-.006-.010) * .006-.011 (.015) .026) .014 (.006 (.050) .011-.006 (.007) .007-.014 (.027 (.065) .036 (. respectively.006-.008-.S.011) .029-. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.028 (.010-.022 (.040 (.007 (.040) .012 (.009-. In workplaces that involve uranium mining.007 (.007-.010) .021-.006-.024-.008-.054) .042 (.72%).012 (. population from the National Health and Nutrition Examination Survey.007-.022-.012-. 235U (about 0.023-. Fourth National Report on Human Exposure to Environmental Chemicals 239 .007) .009 (.046 (.005-.019-.054-.010) .064 (.034-.013) 90th .009) .010 (.040-.009 (.008 (.006-.023 (.016-.016) .Metals Uranium CAS No.011) .056) .007 (.010-. nuclear fuel.015 (.011-.009 (.011-.009-.027 (.037) Total .007-.007-.023 (.007-.026 (.010 (.020-.021 (.007 (.033 (.030) .007) . Variable concentrations of uranium occur naturally in drinking water sources.006-.008 (.009) .042) .036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.067) . in some ceramics.045) .020) .009-.024-.008 (.008-.007-.065) . 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.024-.027-.040) .010) .012-.046 (.007-.051) .006 (.008 (.029-.009 (.006-.025-.027 (.039) .049) .027) . Uranium has many commercial uses.007-.018) .009) .027) .030 (.011) . the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.018) .046 (.033-.020) .013 (.006-.010-.043 (. milling.017-.007) 75th .023-.008 (.040-.072) .016-.014 (.031 (.023-.010 (.007-.027 (.028-.035) .009) .037-.046 (.009) .014 (.

014) .033 (.018-.007 (.007 (.067) .016) .017 (.005-. Inhaled uranium-containing particles are retained in the lungs.027-.011) .007 (.015 (.016-.010) .017) .015-.029 (.019-.006 (.020 (.018-.008-.020) .024) .010-.007 (.009) * .054) .012 (.029 (.012 (.023-. the initial half-life of uranium is about 15 days (Bhattacharyya et al.009) .024) .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.014) 90th .009 (.039) .027 (.030 (.011-.007-. 2005).007 (.051 (.022 (.027-.011-.017-.020-.015 (.006-.032) .009-.006-.034 (.007 (.006) .007 (.011 (.033 (.009 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.050) .045 (.006 (.008-. 1992).041) .Metals impact.021 (.027-.011-.039) Total .017) .015 (.011-.011-.007 (.010-. liver.006-.022-.006-.146) .011) ..006 (.007 (.007 (.015-.012 (.013 (.007) .034) .026 (.006-. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.018-.007-.011-. interval) .056) .009 (.035 (.016-.027) .077) .042-.029) .008-.037 (.010) .010-.011) .030 (.016) .006-. Health effects from uranium exposure result from chemical toxicity to the kidney.010) .034-.009 (.030) .017 (.006-. with much slower elimination from bone.008 (.006) .027) .015-.010-.030-.019 (.006-.016-.008 (. Depending upon the specific compound and solubility.008 (.050) .019 (.018-.008 (.007 (.011-.006-.006) .006-.028 (.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 .025-.007) . 0.009) .010-.051) .010-.008) .030) .012 (.019) .020-.058) .010) .009-.012 (.012-.047) .013 (.028-.015-.020-.020 (.009) .005-.009 (.013 (.022-.025 (.013-.010 (.014 (.025) 95th .007 (.006-.024-.039) .015 (.016) .019-.009-.019-.009-.024 (.005-. After exposure to soluble uranium salts.030-.007) .048) .026 (.008) .007-.029) .033 (.005-.019-.013 (.010 (.025 (.009) .009) .013) .029) .034 (.011) * .006-.016) .008) .006-.012) .050 (.053) .010-.028) .019-.063) .039) .032) .005-.080) .024-.018-.010-..008) .005 (.018 (.007 (.009-. low level exposure.014-.009) .007-.010 (.026) .008) .010-.011 (.005 (.031-.042) .011-.015) .029) .013) .022) .017-.053) . Radiation risks from exposure to natural uranium are very low.021) .016) .007 (.015) . which can occur occasionally from high occupational exposure.010 (.028) .008-.006-.007-.015) .013 (.006-.009) .006 (.022-. kidneys. 2003).031 (.012 (. Uranium is eliminated in feces and urine.017-.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 .025-.024) .013) .006-.006-.017) .014) .013 (.008 (.013 (.007-.019) .028) .008 (.027 (.008) .008) .006 (.014 (.009) Selected percentiles ( 95% confidence interval) 50th .015) . After long term or repeated exposure.024) .010) .006-.006-.007 (.013 (.021-.012) .020 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.048) .027 (. 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.030 (.016-.013 (.035 (.007 (.006-.007 (.014) . 240 Fourth National Report on Human Exposure to Environmental Chemicals .027-.006-. where limited absorption occurs (less than 5%).024) .1%-6% of an ingested dose may be absorbed.009) .. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.006) .028 (.074) .006-.059 (.270) .016) .007-.012) .058) . After inhalation.033) .010) .016 (.004-.007-.022 (.008) .100 (.040 (.007 (.006 (.009) .026 (. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.025-.061) . which represents distribution and excretion.042) .007-.026-.010) * .008) .021 (.009) .010-.014-. In cases of retained DU shrapnel.005 (.011-.014-.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 .012-.021 (. population from the National Health and Nutrition Examination Survey.029 (.019 (. the shrapnel acts as a source of chronic.018) .034 (.016) .007 (.016) .008 (.007 (.028) .006-.004-.008) .022 (.008) .015-.005 (.009) .025-.006-.008 (.051) .007 (.033 (.051) .034 (.008-.008-.S.034 (.013 (.010 (.005-.008 (.024 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.034-.008) 75th .005-.010-.008 (.024-.020-.007-.006) .044) .021 (.017-.043 (.012 (.024 (.009-.

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. the median urinary uranium concentration was 2. Thomas RG.gov/ toxpro2.. ingestion. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.078 μg/L (ranging up to 5. Fourth National Report on Human Exposure to Environmental Chemicals 241 . et al. and no consistent effects on multiple endpoints of kidney function were found.S.html. 41 (1). 1978). urinary levels of uranium were as high as 9. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Breitenstein BD. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al.S. 2006. but in whom no shrapnel was embedded. (Kurttio et al. Dang HS. 2005. and 2003-2004 (Dang et al. Drinking water and other environmental standards have been established by U. 2001-2002. In 17 U. 2003. 2000). Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH. 2002. 1991. eds. Mil Med 2003.162 μg/L) (Orloff et al. 1994. Boyd P. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. In the same study. A cohort of 46 U. Benedik L. In a study of 105 persons exposed to natural uranium in well water. Galletti. 2006). Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. had a mean urinary uranium concentration of 0.011 μg/L (McDiarmid et al. McDiarmid M..Metals injury associated with elevated urinary uranium levels (Kurttio et al. in that the levels were below their respective detection limits (Byrne et al.. Zimmerman I...65 μg/L). Atlanta (GA). pp. EPA.. 28 soldiers who may have been exposed to DU by inhalation.62:562-566. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. soldiers evaluated before..066 μg/g creatinine (Gwiazda et al.S.. Pullat VR. 2004).. Uranium content of blood. Metivier H. although slightly increased during and after deployment. In: Gerber GB.. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU.. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. the geometric mean urinary uranium concentration was 0. Pillai KC. Sci Total Environ 1991. Hamilton MM.S. with emphasis on quality control. Information about external exposure (i. Kent (England): Nuclear Technology Publishing.e. 2004). 2004). 1-49. 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. References Bhattacharyya MH. Byrne AR. Stradling GN. 2006).. environmental levels) and health effects is available from ATSDR at: http://www. 2000). Volf V. 2006).. Horan P. McDiarmid et al. respectively..107:143-157. Karpas et al. during. 1992.78:143-146.. (May et al. the median urinary concentration was 0.. Six workers in a depleted uranium program showed concentrations of 0.1996.55 μg/L (median 0.cdc. The U. Hamilton et al.atsdr. Carmichael AJ. Health Phys 2000. Squibb K. Durakovic A. Komaromy-Hiller et al. 2002). population. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al.. Tolmachev et al. Guidebook for the treatment of accidental internal radionuclide contamination of workers.1992.. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. 2006). NRC. 2004). Determining the normal concentration of uranium in urine and application of the data to its biokinetics. Ejnik JW. Health Phys 1992. IARC and NTP have no ratings for uranium human carcinogenicity.168(8):600-605. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. Dietz LA. and after deployment had geometric mean urinary uranium concentrations that were less than the NHANES 1999-2000 and 2001-2002 geometric means at all three time periods. Third National Report on Human Exposure to Environmental Chemicals. Muggenburg BA. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. Radiation protection dosimetry.61 μg/g creatinine.S. Vol.110 to 45 μg/L (Ejnik et al. 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. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. Centers for Disease Control and Prevention (CDC). or wound contamination.

Roth P. et al. Scott K. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Health Phys 2002. Element reference values in tissues from inhabitants of the European community. Ash KO.86:12-18. Saha H. Biologic monitoring for urinary uranium in Gulf War I veterans.85:228-235.158:165-190. Gucer P. Karpas Z. NRC). Sampson EJ. Health Phys 1996.Metals Galletti M. 242 Fourth National Report on Human Exposure to Environmental Chemicals .S. Saha H. J Toxicol Environ Health A 2004. Costa R. Kidney toxicity of ingested uranium from drinking water. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Squibb K. Oberbroekling KJ. concentration and daily excretion of uranium in urine of Japanese.91(2):144-153. Kane R. Kurttio P. Oeh U. Charp P. Kalinsky V. Andrews WS. Marino R. Mistry K. Marko R. Bennett LG. Shelly T. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Makelainen I. Kuwabara J. Cremisini C.22–Bioassay at uranium mills. Metcalf S. Li WB. Ting BG. Pirkle JL. et al. Biokinetic modeling of uranium in man after injection and ingestion. Salonen L. Health Phys 2006. Lorber A. Comparison of representative ranges based on U. VI.94:319-326. Tolmachev S.44:29-40. Van der Venne MT. Salonen L. Noguchi H. Pinto V. Halicz L.67(8-10):697-714. rapid. Ough EA. Smith D.82(4): 527-532. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Squibb K. Nuclear Regulatory Commission (NRC) Guide 8. Wahl W. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Uranium daily intake and urinary excretion: a preliminary study in Italy. Environ Res 2004. U.87:51-56. Lewis BM. Engelhardt SM. et al. Ejnik J. Hamilton EI. Jarrett JM. May LM. Kurttio P. Int Arch Occup Environ Health 2006. Paschal DC. Health Phys 2004. Heller J. Renal effects of uranium in drinking water. Komulainen H. Pekkanen J.296(1-2):71-90. Uranium and thorium in urine of United States residents: reference range concentrations. Auvinen A. Englehardt SA.47(6):972-982. Katorza E. Environ Health Perspect 2002. Human exposure to uranium in groundwater.110(4):337-342. Nuclear Regulatory Commission (U. Harmionen A. Karpas Z. Health Phys 2003. Howerton K. et al. Environ Res 1999. Auvinen A.S. Radiat Environ Biophys 2005. et al. D’Annibale L. Hancock RG. McDiarmid M. Health Phys 2004.S.71(6):879-85. Review of elements in blood. Gwiazda RH. patient population and literature reference intervals for urinary trace elements. Roiz J. Jackson RJ. Sabbioni E.81:45-51. Orloff KG. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Paretzke HG. Hollriegl V. Wilson PD. Inductively coupled plasma mass spectrometry as a simple. Cordero S. et al.79(1):11-21. Oliver M. McDiarmid MA. Washington (DC): NRC.S. Sci Total Environ 1994. McDiarmid MA. Komaromy-Hiller G. July 1978. U. Clin Chim Acta 2000. Am J Kidney Dis 2006.

35 (3. 2007).75-3. matches.30) 6.50-7.10 (7.12) 3.0) 10.20) 7.70-11.60-7.60) 3.62 (3.40) 90th 10. and certain plants with high water content (e.0-18.EPA.50-4.5 hours and has a small estimated volume of distribution (Crump and Gibbs.40) 3.70-6.40-6.29-3.90 (3.74-3.20 (4.40-4.30-7. Drinking water. Perchlorate was added to the U.40 (4.00) 3. leather tanning.76 (3.22 (2.50) 5.00-5. or ammonium salt.0) 11.80-12.0) 13.90-11.47-4.0) 95th 14.70-3.0) 9.10-11.0-15.0 (11.60 (7.70-7.18-3.0-17.90 (2.0 (11.10-7. 2005).0 (11.81-16.40) 4.0 (11.05.93-4.45-4.80-4.0) 13.20 (2.90-9.80-15.0 (11. It is normally found and produced as the anion of a sodium.0-29.60 (4.39-4.0) 14.0 (8.0) 9.68) 4.50-3.0) 9. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.0) 13.00) 4. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.40 (8.Perchlorate Perchlorate (Urbansky.87-3.0) 13. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.00-6. but has strong oxidant properties in the presence of concentrated acids.67-5.20-4.20 (7.05 (2.20) 3. In addition.0 (9.96 (3.80-4.00) 5.90-10.0) 16.89-3.90-6.50) 3. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .20-4.40) 6.40 (5.44-4.49-3.54 (3.26 (2.80) 75th 6.90) 6.50-4.40-11.03) 3.80-6.0-15.0-19.0-17.50 (5.0 (8.19-4.02 (3.60 (4.0-18.80 (6.10) 5. and electroplating.g.0) 13.80 (3.16) 3.10) 3.20 (2.0) 9.60) 8.90 (5.05 and 0. laboratory analysis.0 (11.0) 9.76) 4.0-20. fabric dyeing.40) 3.0) 8.0) 14.0 (8.0 (9.40 (4.40 (5.50) 6.0 (12.40) 3.70 (3..93-3.20-11. interval) 3.00) 7.80-8.0) 10.70-12.0 (11.0 (9.10 (2.20 (4.90-9. certain catalytic metals.30 (2.30-6.0-18.0 (12.30 (5.0) 15.0) 12.0 (12.70-5.90-12.30) 6.90) 5. milk.21 (2.40-7.08-3. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.0-14.01 (2.50-11.20-3.0) 10.51 (3.40-4.38) 5.00-6.30-19.09) 3..90-3.32 (3.00) 3.0 (8. potassium. and reducing agents.90 (5.0-17.0 (11.50 (8.80 (7.20) 4.0-17.60) 5.0) 15. Other manufactured uses include fireworks.10) 12.0-17.07-4.10) 5.90 (4. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.81) Selected percentiles ( 95% confidence interval) 50th 3.20 (5.40 (5.0 (13.0) 11.11) 3.79 (2. 2005).0 (11.90-11.30-7.0) 708 617 681 652 1228 1092 Limit of detection (LOD.10 (5.40-13.40-5. 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.0) 19.93 (4.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.70-9.80) 12. 1998). 2006) and accumulate in nitrate-rich mineral deposits mined for use in fertilizers Urinary Perchlorate Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.90-3. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.0-23.0) 9.30 (2.0) 13. Survey years 01-02 03-04 Geometric mean (95% conf.10) 3.40) 2.10-11.11) 4.10-4.46) 3.0) 14.0 (8.0) 13.70 (3.S.31) 2.0) 8. Perchlorate is stable under most environmental and physiological conditions.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 3.10-12.0 (9.0 (10.70) 3.20 (8.40 (3.0 (9.30-17.70 (3. and limited applications in pharmaceutics.0-17. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.80) 7.0) 11.10 (6.22-5.90 (5.50 (3. 2002).0 (12.56) 3.20-12. lettuce) can be the main sources of intake for humans (FDA.50) 11.50) 5.66) 3.0 (9.51 (3.80) 3.60-6. population from the National Health and Nutrition Examination Survey. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.65) 3.80 (3.84) 14.30 (5. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.S.0 (11.20 (6.0 (9.19 (3.40 (3.70-3.75 (3.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.88) 3.S.0) 13.10 (6.

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.50) 5. 2000). 2005).60-5.97-5.20-10.15-12.64-3.40) 3.80-3.80 (4.60-8.99-3.61 (5.37 (4.1) 8.58) 2.08 (3.0-14. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.0) 14. 2002.67) 5.70 (2.02) 3.61-10.10 (2.33 (7.40 (3.80 (7.34-3.29-6. gender. 2005).09 (7.20 (4.6) 12.60) 8.76-3. NAS.70-3.90) 5.20-4.. 2007).70-15. interval) 3. 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.19-6.21 (2. However.20 (7.0-14.24 (4. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.00-11.07 (2.91) 4.g.00 (6. nitrate..29) 2.50-3.70 (4..20 (3. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.22-4.36 (8.70-5.18-3..0) 11. U.40) 5.22-4.10) 6.37-13. 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) 6.93-8.10 (4.S.0) 12.80 (7.5 (13.96) 2.93-7.60) 10.41-9.39-4. 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.35 (2.0) 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 .4 (10. levels.0) 12.43) 6. 2001. 2002).2) 8. Steinmaus et al.16-3.0) 9.60) 3.45) 3.60-6.0 (9.10 (6.10-7.0 (9.1 (8.20 (6.0) 7.20-9.30) 5.00 (2. menopausal status.40 (4.46-4.S.24-2.8 (11.EPA.50-9.90-2.30-5.5) 8.47) 2. 1999.56-3.54 (3.93-5.22-6.39) 2.89-3.4) 8..50) 95th 12.1 (11.95 (2.70 (2.87) 2.42 (3.0) 9.60-8.0) 13.S.4) 13. 2005.60 (3.12 (6. and the presence of other substances known to affect thyroid function (e. although iodine intake was higher than U.60-11.10) 3.1-14.0) 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. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.04-3.60-3.53 (2.4 (11. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.30 (6.90-3.51-4.56 (3.30-5.60-15.75) 3.0) 6.40 (3.S. in a representative sample of U. Also.4 (11. thiocyanate.90-11. Li et al. Lamm and Doemland.0 (11.90-20.52 (8.0-19.84) 2.70) 2.90-9.30) 3.26) 4.3 (10.10 (4. Survey years 01-02 03-04 Geometric mean (95% conf.05 (4.25) 5. Many factors may be important in consideration of perchlorate action on the thyroid: dose.19-10.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.2) 8.80) Selected percentiles ( 95% confidence interval) 50th 3.00-2.10-3.72 (3.87 (7.0 (8.30) 90th 9. 2005.32) 5.44-6.46-13.73) 3.30 (3.20-3.1-16.25) 5.98) 3.12-2.87-3.4 (8.10) 4. levels and sufficient in most participants (Tellez et al..35) 3..50) 2..93) 3. 2005). Lawrence et al.30 (5.25 (3.4-16.90 (2.90 (7.0-44.0) 12. 2006.7 (11.0) 12.87 (5.20) 3.52-9.0) 13.. age.10 (1.51 (3.64) 5.45-2.09) 3.S.S.93-5.50) 9.26 (3. perchlorate is negative in most genotoxic assays (U.59) 3.00 (4.70) 10. In the U.00) 9.50 (3.20) 8.. women with urinary levels of iodine less than 100 micrograms per day.3) 12.86) 4.61-5.3) 11.60-11. During gestation and infancy.74) 7.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3. In these small short-term experimental studies on males and studies of male perchlorate workers with doses or estimated exposures thousands-fold higher than known environmental exposures.54 (2.20 (2.71 (5.25) 5.70-4.03 (2.39 (3.60-5. chronicity of exposure.50 (6. medications).90 (4.77 (3.02-4.08) 3.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3. population from the National Health and Nutrition Examination Survey.00) 4.40) 17.30-10.90-15.80-3.66) 3.90 (2.82 (5.40 (7. 2002.89 (2.0 (9.0-17.20-3.44) 3.35 (4.04-3. dietary iodine intake.1-22. 2003.76 (3. Greer et al.22 (2.14 (2.Perchlorate inhibition (RUI).0 (11.6) 20.0) 10.50) 2.00-3.0 (11.87) 7.3) 8.6-17.99 (5.EPA.0) 4.0 (10.46 (3.33-12.83 (5.S.10) 13. up to 68% RUI has been demonstrated.30) 75th 5.50-5. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.40-10.0 (8.81-3.1-13.33-6.3-14.00) 3.

. Jackson WA. 2005). Perchlorate Exposure of the US Population. References Blount BC. Environ Health Perspect 2002. Erratum in: Environ Health Perspect 2005.S.atsdr. Dasgupta PK. Chacon PM. 2007). National Research Council of the National Academies. Lamm SH. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey.45(10):1116-1127. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Pleus RC. 2005).S. Additional information about exposure and health effects is available from the U. Perchlorate in the United States. Neonatal thyroxine level and perchlorate in drinking water.gov/toxpro2. Erratum in: J Occup Environ Med 2004. 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.html. Greer SE.fda.90(2):700-706. 2005.41(5):409-411. Valentin-Blasini L.17(4):400-407. most of the population is considered to be below the U. Environ Health Perspect 2005. Skeels MR. J Expo Sci Environ Epidemiol 2007. National Academy of Sciences (NAS). Blount BC. The effect of perchlorate. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Landingham CB. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Buffler PA. J Occup Environ Med 2000. Barnard JC.html and from ATSDR at: http://www. J Clin Endocrinol Metab 2005. Also. Washington (DC): National Academy Press.11(3):295. Lau EC. Environ Health Perspect 2007. Rutherford GW. (2007) analyzed a subsample of NHANES 2001-2002 which demonstrated detectable perchlorate in all urinary samples and showed slightly higher levels in children as compared to adults. et al. Crump KS. Kirk AB. Lamm S. Environ Health Perspect 2006. Valentin-Blasini L. Richman K. Deyhle GM. Available at URL: http://www. et al. CFSAN/Office of Plant & Dairy Foods. Kelsh MA. Osterloh JD. and environmental perchlorate exposure among residents of a Southern California community.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Lamm SH. and nitrate on thyroid function in workers exposed to perchlorate long-term. Food and Drug Administration (FDA).115(9):1333-1338. Doemland M. J Occup Environ Med 2003. Li FX.46(5):509. Abarca CR. Lawrence JE. 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. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. epa. Thyroid 2001. 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.EPA at: http://www. et al.S. Analysis of relative source contributions to the food chain. Pirkle JL. Health Implications of Perchlorate Ingestion. EPA reference dose (Blount et al. Pino S. Environ Sci Technol 2006. Li Z. Low dose perchlorate (3 mg daily) and thyroid function. Lamm SH. Benchmark calculations for perchlorate from three human cohorts. The effect of short-term low-dose perchlorate on various aspects of thyroid function. thiocyanate. Howd R. Cross M. Pino S. Page Last Updated: 05/28/2009. newborn thyroid function.113(11):A732. Thyroid 2000. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Magnani B. Steinmaus C.gov/safewater/ccl/perchlorate/perchlorate. Osterloh JD. Braverman LE. Crump KS.cdc.40(21):6608-6614.42(2):200-205. Lawrence J. Primary congenital hypothyroidism. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Braverman LE. Gibbs JP.110(9):927-937. Goodman G. Sesser DE.. Blount BC. Pirkle JL.htm.114(12):1865-1871. Mauldin JP. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002.10(8):659-663. population.. Daaboul JJ. Braverman LE.113(8):10011008. Miller MD. He X. et al. Blount et al. Caldwell KL. Tellez RT. Byrd D. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. 6/2/09 Greer MA. May 2007.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Dyke JV. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. 2001-2002.

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

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

8 years (Olsen et al.. C6. peroxisomal proliferation.. pancreas.. 2006. Olsen et al. hepatotoxicity. The liver toxicity of several PFCs is evident by vacuolization and lipid accumulation in both rodent and monkey livers (Seacat et al.. Vanden Heuvel et al. 2004). PFOA preparations used in many studies may also contain a small percentage of other chain length perfluoroalkyl acids (i. 2005).. 1990). 2004. Keller et al. Unlike many organohalogen contaminant chemicals.. Guruge et al. C5. endocrine and immune effects. In some cases... in a wide variety of marine and land animals (Kannan et al. Human health effects from PFCs at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5 years and for PFOS.e. which may vary for some chemicals by year and by individual sample. Some of the effects in animals may be mediated through peroxisomal proliferation. see Data Analysis section) for Survey year 03-04 is 0. heptadecafluoro-1-decanol. and β-oxidation of lipids (Kudo et al. 2003. Lau et al..... growth retardation and delayed sexual maturation (Kennedy et al. 2004. Survey Geometric mean (95% conf. PFOA (and probably other perfluoroalkyl acids) exist in the anionic state at physiologic and environmental pHs and their distribution in the body is determined.Perfluorochemicals PFOS greater than 2000-fold over aquatic levels). Bookstaff et al.S. but the relevance of peroxisomal pathways in humans is unclear (Kennedy et al. Taniyasu et al. The ammonium salt of PFOA has been tested at high doses in mammalian animal studies and produced altered weights of the liver. EPA. PFOA has been reported to cause liver. Excepting PFOS and PFOA. C7). 2002. but probably include dietary sources (Kannan et al. 2007). by high protein binding in plasma and other proteins. All sources of human exposure are uncertain. thymus and spleen. 2003).. Kannan et al.. 1995. 2000. including immunologic effects and tumor induction...4. 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.. 2007a). but limited observations in humans suggest that only one-fifth of the total body clearance is renal (Harada et al. Tittlemier et al. 248 Fourth National Report on Human Exposure to Environmental Chemicals . The elimination half-life of PFOA in humans is roughly estimated to be 3. It is unclear if environmentally degraded telomer products are a major source of other PFCs. < LOD means less than the limit of detection. 2003a and 2004a). 2005). U. 2004... 2003). 1993). 2005. 2004. 2006a. The PFCs often measured in human serum are listed in the table. and in offspring. the 8-2 telomer... 2005. * 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. there is limited information on the sources. but still can have long residence times in the body. or effects of other PFCs. PFCs have been identified in surface coastal and ocean waters (Yamashita et al.. human toxicokinetics. the perfluoroalkyl acids (PFOA and PFOS) do not tend to accumulate in fat tissue. in part. approximately 4. For instance.. 2004) and may be attributable to the ability of PFCs to affect intracellular lipid binding proteins..S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD. Both PFOA and perfluorodecanoic acid have been shown to reduce androgen levels in laboratory animal studies (Biegel et al. 2005). 2004). kidney.. environmental fate. PFOA is mostly excreted in the urine in animal studies. 2005. Serum Perfluorobutane sulfonic acid (PFBuS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Lau et al. and in human blood and semen (Calafat et al. PFOS and PFOA levels in archived bird eggs from Sweden have increased thirtyfold from 1968 to 2003 (Holmstrom et al. may metabolize or degrade to PFOA (Dinglasan et al. Prevedouros et al.

In such studies.S.500-1.. 2003). Olsen et al.400 (<LOD-..400-1.80) 640 1454 03-04 03-04 * * < LOD < LOD . 2007b. 1999.800 (.. Olsen et al. 2007. At doses causing maternal toxicity.. possibly related to lung immaturity (Lau et al. which may vary for some chemicals by year and by individual sample.10 (. thyroidal).500) . Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. However.. Cook et al.40) .900 (.400-1.400) .800) 1. Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. interval) Selected percentiles ( 95% confidence interval) Sample 95th .500-3. monkeys..400-1. 2004a. hepatotoxicity. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. Fourth National Report on Human Exposure to Environmental Chemicals 249 ..00) . 2003a.400-.10) * 03-04 03-04 * * < LOD < LOD < LOD .80) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th . EPA. 2003a.600 (.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.300 (<LOD-.600 (. 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. Animal studies of PFOS have demonstrated weight loss.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. 2007a. see Data Analysis section) for Survey year 03-04 is 0. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.500) . the potential to estimate risks to humans from animal doses is uncertain.300 (<LOD-.400 (<LOD-.700 (.500) . EPA.500-1. and changes in thyroid hormone concentrations (Grasty et al.500) 90th . the median PFCs values tend to be roughly similar in these age categories (Olsen et al.3. 2003).00) .400-1. Fei et al. 2005).80) 485 538 962 Limit of detection (LOD. 2003a.108 times higher than background serum levels in humans (Butenoff et al. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al.600-2.500) .800 (.500-1. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.S. 2004.300 (<LOD-.. Harada et al.500 (<LOD-1.. PFOA.. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. 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. and there was no clear evidence of excess all-cause or diseasespecific mortality..10) . 2007b). 2001. 2003).800 (. U. 1992.00) . Olsen et al. and perfluorononanoic acid (PFNA) are detectable in a high percentage of the participants and PFOS levels are generally 3-10 times higher than PFOA levels (Calafat et al..S. Thibodeaux et al. developmental and teratogenic effects were demonstrated in offspring. At high but non-toxic maternal doses of PFOS.500 (. elderly and children.. U.700) .. PFOA. 2005). and humans.800) 1.00 (. 2007a.. 2003a). and no substantial age trends were seen within adults ages 20-69 (Olsen et al. 2004.800 (.400 (<LOD-. PFOS. In comparing three separate reports on adults..600 (. < LOD means less than the limit of detection. 2003a). 2003. population.S. population from the National Health and Nutrition Examination Survey. 2007).. 2004). 2004b).900 (. 2003. 2004). or increased cancer rates (Alexander et al.500-. development in offspring was stunted and hypothyroxinemia was observed.400-1..400-..500-1. Kennedy et al.500 (...900 (. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.50) . PFOS.300-1.20) . reproductive. 2003.10) . Lau et al. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. perfluorohexanesulfonate (PFHxS).

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

400 (<LOD-.500) 485 538 962 Limit of detection (LOD.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .500 (<LOD-.600 (. Fourth National Report on Human Exposure to Environmental Chemicals 251 .400) .500-. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th .600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600) < 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. < LOD means less than the limit of detection. population from the National Health and Nutrition Examination Survey.900) < LOD .400 (.0.300 (<LOD-.S.400 (<LOD-.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (<LOD-.300-. population from the National Health and Nutrition Examination Survey.S. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 03-04 is 1. see Data Analysis section) for Survey year 03-04 is 0. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.3.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.

80-3.08) 2.800-1.966 (.40) 2.00 (5.90) 1.826-1.00-6.30 (3.3.80) 5.50-6.67-2.10 (.00 (.10) 6.30 (1. see Data Analysis section) for Survey year 03-04 is 0.800 (.30 (2.91) 2.00) 1.80-4.809) 1.60) 3.30 (1.3 (9.14 (.10 (1.20-1.90) 90th 5.40) .60 (1.30 (1.54) .20-1.10 (.816-1.12) .40-1.50 (2.900-1.00-1.900) 1.30) 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 1.01 (1.00 (.70) 13.90 (1.50) 2.20) 2.40 (1.10) 1053 1041 03-04 03-04 03-04 .50 (6.20) 03-04 03-04 2.40) 4.51) 1.20) 485 538 962 Limit of detection (LOD.70-2.900-1.56-1.16) .40) 1. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.586-.80-12.05-2.30 (7.60-7.0) 8.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.70 (1. Survey Geometric mean (95% conf.00-8.10 (4.80-8.90 (1.20 (6. population from the National Health and Nutrition Examination Survey.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 1.60-2.00) 2.30-9.73-2.20 (6.6) 7.60-2.27) 1.30-12.20-3.20-1.20 (1.70) 1.834-1.90 (1.10) 1.60) 9.42 (1.26) 2.5) 5.00 (1.70) 2.40-3.60-4.5) 8.900-1.90) 8.90) 1.30 (2.689 (.10) 75th 3.80-8.80-7.80) 90th 2.852 (.20 (1.00 (2.17 (1.900-1.984 (.90 (4.70 (2.700-1.60-8.50 (1.70-5.S.10) 5.50 (1.10 (4.90 (2.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.60) 1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.30-6.50-3.900 (.00-1.20) 1.70-7.87-2.900 (.963 (.10) 8.04) .10) 75th 1.30) 3.10) 1.09 (.77-2.30 (6.00) 1. interval) .10 (. interval) 1.835-1.20 (1.20) .70) 2.70-10.50) 2.600-.80 (4.80-7.40 (1.700 (.10-9. population from the National Health and Nutrition Examination Survey.90 (4.90-10.00 (1.93 (1.20-1.60 (6.1) 485 538 962 Limit of detection (LOD.92 (1.1.697-1.40) 640 1454 03-04 03-04 2.80-6.44 (2.50 (6.900-1.03) 1.72 (1.50 (4.0) 1053 1041 03-04 03-04 03-04 1.72) 1.40) 640 1454 03-04 03-04 1.30) 3.10-5.20 (1.60-2.50-10.86 (1.10) 6.30-2.17-1.70-2.900-1.30) 03-04 03-04 .912-1.861 (. Survey Geometric mean (95% conf.60 (1.40 (1.S.60-3.90-2.80 (1. see Data Analysis section) for Survey year 03-04 is 0.80-4.20) 1.80) 3.60) 2.50 (4.90-19. 252 Fourth National Report on Human Exposure to Environmental Chemicals .70) 1.80-2.80 (1.90 (1.40) 1.40-1.50 (1.30) .60 (1.30 (1.20-2.60-4.00 (1.80) 4.10) 4.80-4.00-7.50) 6.00 (1.50-6.70) 3.50 (1.40 (1.10) 4.90) 3.60-3.00) 3.721-1.62-2.70-6.10-9.40 (2.90) 1.80) 1.80-3.

30-11. interval) 20.9) 22.0 (20.7-49.1-36.35) 3.6) 62.70 (5.8-22.20) 10.60 (6.6) 9.2-22.40 (6.2 (27.30-5.90 (7.3) 41.8) 27.80 (6.8-78.1-24.70-10.3-22.10-3.40-17.89 (3.27) 4.79) 4.7 (35.4) 20.80-12.20) 5.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.5) 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 21.9) 22.5-33.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.60-9.5) 32.9 (22.90-12.47-4.00) 3.70) 4.60) 03-04 03-04 3.3) 28.S.7 (13.50) 4.10 (6.0) 43.3) 485 538 962 Limit of detection (LOD. see Data Analysis section) for Survey year 03-04 is 0.4) 75th 30.9) 27.4 (23.70-9.00 (3.7-53.40) 5.5) 57.1-35.3 (28.2) 640 1454 03-04 03-04 4.30) 7.5) 1053 1041 03-04 03-04 03-04 14.40 (4.9-38.60 (3.0) 21.8-35.47 (4.40-10.4-17.3 (35.30-8.2 (16.30 (5.4 (17.0) 90th 41.5 (28.2) 45. Fourth National Report on Human Exposure to Environmental Chemicals 253 .4 (19.20) 4.0-20.5) 18.20-9.6) 7.70) 3.20) 7. population from the National Health and Nutrition Examination Survey.80 (7.53) 3.80) 8.5) 9.4-25.80 (5.80-9.95 (3. Survey Geometric mean (95% conf.70 (3.6-24.8-81.60 (6.5) 8.90 (7.1-25.2 (18.2) 30.65-4.67-4.S.6-45.9 (13.30 (3.3-61.7) 39.11 (2.2-57.5 (28.9) 9.4-42.60) 8.20 (4.00 (5.1 (24.70-7.1) 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 4.90-4.3 (44.3 (17.21-3.50 (3. see Data Analysis section) for Survey year 03-04 is 0.10) 5.6 (19.7 (43.60-6.6) 35.0-16.8-22.8 (34.1 (23.4 (19.60 (4.4.3) 42.30-6.99-3.50-4.6 (35.40-6.96 (3.90) 6.1-33.90 (7.20) 7.60-13.1-52.6) 42.60 (7.4) 640 1454 03-04 03-04 23.8) 32.4 (28.8 (37.70 (5.30 (3.9 (17. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.7-69.7-33.70-7.0) 36.1.6) 1053 1041 03-04 03-04 03-04 3.2) 30.8-30.90-4.10 (3.7 (35.10 (3.18 (3.0) 485 538 962 Limit of detection (LOD.2 (28.40) 75th 5.7 (7.60-14.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.91) 3.85-4.6 (42.50) 7. Survey Geometric mean (95% conf.7 (43.40) 3.7 (19.1 (19.8 (45.82) 4.5-21.6-50.20) 5.80 (6. interval) 3.1) 15.0-66.9-23.1) 57.50-6.90 (5.5-23.9-19.20-5.5) 19.50-13.6 (44.80-4.2 (21.07-4. population from the National Health and Nutrition Examination Survey.4) 56.0-70.0) 03-04 03-04 19.0) 23.3 (35.6) 21.2 (19.20 (4.4) 21.8) 46.20-4.7-23.84-3.37 (2.30-3.30) 6.8-22.50 (4.40-14.60 (5.7-30.9 (19.5) 7.40-6.5-62.00 (5.70-5.0) 21.40) 90th 7.70) 6.6) 18.0 (27.

300 (.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .S.200-.300) . which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf.500) < LOD 485 538 962 Limit of detection (LOD. Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500) .300) .2. population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .200-.300-.300 (.300 (. Survey Geometric mean (95% conf.200-.300 (.300) .200 (<LOD-.300 (.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.300 (.300-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .300 (. see Data Analysis section) for Survey year 03-04 is 0.300 (.300 (.300 (.200-.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .500) .300-.400 (<LOD-.200-. < LOD means less than the limit of detection. see Data Analysis section) for Survey year 03-04 is 0.300) . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300 (. which may vary for some chemicals by year and by individual sample.200-.4.300-.200-.500) .200-.200-.200-.500) 485 538 962 Limit of detection (LOD.S.300 (. 254 Fourth National Report on Human Exposure to Environmental Chemicals . population from the National Health and Nutrition Examination Survey.300) . < LOD means less than the limit of detection.

see Data Analysis section) for Survey year 03-04 is 0.600 (<LOD-1.10 (.30 (1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .90) .700 (<LOD-.500 (<LOD-.3.00) < LOD .600 (<LOD-.00-1. population from the National Health and Nutrition Examination Survey.900) 485 538 962 Limit of detection (LOD. see Data Analysis section) for Survey year 03-04 is 0.40) 1.30) 1.50 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10 (.700 (<LOD-.300 (<LOD-.10) .10-1.400 (<LOD-.600) . Survey Geometric mean (95% conf.800 (<LOD-. Survey Geometric mean (95% conf.900 (<LOD-1.900-1.700) 90th 1.700 (<LOD-2.30) . Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.700 (<LOD-.10) .10-1.00 (.80) 1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .900-1.700) 1.30 (1.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.S.10-1.900) .60) 485 538 962 Limit of detection (LOD.900) 1.700 (<LOD-.400 (<LOD-1.S.800) .00 (.900 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .800) .900-1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .700) . which may vary for some chemicals by year and by individual sample.600 (<LOD-1.60) 640 1454 03-04 03-04 * * < LOD < LOD .00 (.600 (<LOD-1.900-1.70) 1.700 (<LOD-.20 (1.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th .700) 1.10) 1.6. which may vary for some chemicals by year and by individual sample.300 (<LOD-1.10-1.900-1.30) 1.10) 1.30 (1.20) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection.900-1.700 (<LOD-. population from the National Health and Nutrition Examination Survey.00 (.10) * 03-04 03-04 * * < LOD < LOD .900-1.40) < LOD < LOD .10 (1.10 (.80) 1.50 (1.10-1.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .20-1.300-2.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.

Environ Sci Technol 2005. Yamashita N. Aguilar-Villalobos M. Reidy JA. et al. Seacat AM. Calafat AM.63:490496. et al. Mohotti KM. Harada K. Saito N. Day RD. Sasaki S. Yoshinaga T. Environ Sci Technol 2007a. Grey BE. Saito N. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Environ Health Perspect. Laane RW. Herbstman JB. Reidy JA. Moore JA. Taniyasu S. Chlorinated. Kuklenyik Z. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Inoue K. in vivo.60(10):722729. Birth Defects Res B Dev Reprod Toxicol 2003. Needham LL. Toxicol Appl Pharmacol 1990. Cook JC. Perfluorinated chemicals in selected residents of the American continent. Loganathan BG. Bandai N. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Inoue K. Hurtt ME. Kawashima Y. Olsen J. et al.and perfluorinated acids. Cook JC. Perkins RG. Reidy JA. Tully JS. Kannan K. Environ Sci Technol 2005. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Environ Sci Technol 2004. J Environ Monit 2005. Witter FR. Hurtt ME. et al.134(1):18-25. Falandysz J. Calafat AM.179:99-121. Kudo N. O’Connor JC. Occup Environ Med 2003. Kuklenyik Z.39(23):9057-9063.124(2):119-132. Needham LL. McLaughlin JK. Kumar KS. Frame SR. et al.113(2):209-217.Perfluorochemicals References Alexander BH. Needham LL. Bignert A.41:2237-2242. Environ Health Perspect 2007. Ingall GB. The influence of time. Rev Environ Contam Toxicol 2003. Kannan K. Bookstaff RC. Murray SM. Fluorotelomer alcohol biodegradation yields poly. Cook JC. Frame SR. Mandel JS. Yoshinaga T. Lau CS. Taniyasu S. Edwards EA.38(17):4489-4495. Arendt MD. Environ Sci Technol 2005. Evans TJ. Calafat AM. Moore RW. Calafat AM. Peterson RE. Grasty RC. Jarnberg U. Toxicol Appl Pharmacol 1992. Holmstrom KE. Yamashita N. Keller JM. Environ Health Perspect 2007. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Hekster FM. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Olsen GW. Hurtt ME. Kuklenyik Z. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth.40:21282134. Characterization of risk for general population exposure to perfluorooctanoate.S. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Kannan K. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Kuklenyik Z. Harada K. et al. Seneviratne HR. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Olsen GW.99(2):253-261. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Dinglasan MJ. Katakura M.115(11):1596-1602. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000.60(1):44-55.38(10):2857-2864.Koizumi A. Wijeratna S. Biegel LB. Fei C. Corsolini S. Tarone RE. Toxicol Sci 2001. Caudill SP. Polyfluoroalkyl chemicals in the U. Environ Sci Technol 2004.115(11):1670-1676. Biegel LB. Rodricks J. Tully JS. de Voogt P. and perfluorinated contaminants in livers of polar bears from Alaska. brominated. Guruge KS. Kamiyama S.115(11):1677-1682. Mandel JH. et al. Chemosphere 2006b. Halden RU.68(6):465-471. Environmental and toxicity effects of perfluoroalkylated substances. The toxicology of perfluorooctanoate. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. and ex vivo studies.S. Environ Res 2005. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Chem Biol Interact 2000.104(2):322-333. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Suzuki E. O’Connor JC. Burris JM. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Rogers JM. Wong LY. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro.39(3):363-380. Toxicol Appl Pharmacol 1995. Regul Toxicol Pharmacol 2004. Watanabe T. Olsen GW. Calafat AM.46(2):141-147. Liu RC. Butenhoff JL. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Mabury SA. Kennedy GL Jr.7(4):371-377. Fillmann G.34(4):351-384. Gaylor DW. Morikawa A.39(1):80-84. Mandel JH. Reidy JA. Yun SH. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Koizumi A. Needham LL. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats.39(23):9101-9108.1968--2003. Environ Sci Technol 2006a. J Occup Health 2004. 2007b. Caudill SP. Butenhoff JL. Ye Y. Apelberg BJ. Crit Rev Toxicol 2004.

Hanson RG. Lundberg JK. fish. Taniyasu S. Mandel JH. Miller JP. Peterson RE. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Petrick G.gov/opptintr/pfoa/pfoara.74(2):382-392. Kannan K. Seacat AM. The developmental toxicity of perfluoroalkyl acids and their derivatives.115(9):1298-1305. Olsen GW. Hansen KJ..S. Zobel LR. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. fast foods. van Belle G. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. EPA). et al. Buck RC. Biochim Biophys Acta 1993. birds. 2003a.82(1):359. Huang HY. Olsen GW. Church TR.40(1):32-44. Lundberg JK.S. Available from URL: http://www. and food items prepared in their packaging. 2003. 1/15/06 Vanden Heuvel JP. Hansen KJ. htm.113(5):539-545. Yamashita N. Half-life of serum elimination of perfluoroo ctanesulfonate. Church TR. Taniyasu S.111(16):1900) Olsen GW. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Nesbit DJ. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. J Children’s Health 2004b. Seacat AM. Helzlsouer KJ. Burlew MM. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Kannan K. Burris JM. Hansen KJ. Toxicol Sci 2003. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Burris JM. Ehresman DJ. Mandel JH. Biol Pharm Bull 2003. Froehlich JW. Burris JM. Environ Health Perspect 2005. Mair DC. II: postnatal evaluation.54(11):1599-1611. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. and humans from Japan. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors.epa. Hansen KJ. Pepper K. Environ Sci Technol 2003. 2007a. Sterchele PF. (Erratum in: Toxicol Sci 2004. J Occup Environ Med 2003b. Rogers JM. Mandel JH. et al. et al. Grey BE. Stanton ME. Moisey J. Grey BE.111(16):1892-1901. Environmental Protection Agency (U. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water.55:3203-3210. Cao XL et al. Ehresman DJ. Olsen GW. Butenhoff JL. Reagen WK. Kawashima Y. Butenhoff JL. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Sources.45(3):260-270. Butenhoff JL. Toxicol Sci 2002.37(12):2634-2639. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. I: maternal and prenatal evaluations. Lau C.68:105–111. Burris JM. and perfluorooctanoate in retired fluorochemical production workers. Butenhoff JL.26(1):47-51. Washington. Olsen GW. Gamo T. U. Bronson R. Prevedouros K. perfluorooctanoate andother fluorochemicals in human blood. Toxicol Sci 2003. Mar Pollut Bull 2005. Church TR. Coordinate induction of acyl-CoA binding protein. Butenhoff JL. Olsen GW.41(9):799-806. Butenhoff JL. Chemosphere 2004a.) Tittlemier SA. fate and transport of perfluorocarboxylates.198(2):231-241. Olsen GW. Historical comparison of perfluorooctanesulfonate.Perfluorochemicals Kudo N. Olsen GW.2(1):53-76. Ellefson ME. Yamashita N. Thibodeaux JR. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Cousins IT. et al.1177(2):183-190. Horii Y. Lau C. fish. J Ag Food Chem 2007. Horii Y. Toxicol Appl Pharmacol 2004. Seymour C.51(8-12):658-668.74(2):369-381. Environ Health Perspect. Rogers JM. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Olsen GW. Hanari N. Chemosphere 2007b. (Erratum in: Environ Health Perspect. et al. Korzeniowski SH. Thibodeaux JR. et al. J Occup Environ Med 1999. Larson EB. Environ Health Perspect 2003a. Barbee BD.68(1):249-264. Rogers JM. Thomford PJ. Case MT.perfluorohexanesulfonate. Mandel JH. Hanson RG. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Burris JM. A global survey of perfluorinated acids in oceans. Environ Sci Technol 2006. Hansen KJ. Richards JH.

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

. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. Slakman AR. Assessment of critical exposure pathways. McDonnell DP.805:49-56. Evaluation of a recombinant yeast cell estrogen screening assay. Lovekamp-Swan and Davis.. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. McKee et al. Herbert AR. at higher doses.. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. testicular atrophy.gov/ toxprofiles/tp9. In animals. Kessler et al. 1985. phthalates have been shown to induce peroxisomal proliferation in rodents. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester.atsdr. 2004. 2003. 4/20/09 Albro PW. 2006). Coldham NG. Dave M... The Handbook of Environmental Chemistry. Needham LL. and extent of metabolite conjugation to glucuronide (Albro et al. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). reducing estrogen production. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. dibutyl phthalate (DBP). Food Addit Contam 2001.cdc. J Chromatogr B 2004. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al.html.cdc.gov/toxpro2. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . but there are known species-related differences in the hydrolysis of diester phthalates. High doses of di2-ethylhexyl phthalate (DEHP). which may be a pathway to the development of liver toxicity and cancers in these animals. Massey RC. Drug Metab Rev 1989.gov/toxprofiles/ tp135. In Staples CA (ed).html).e.. Pharmacokinetics.gov/ reports/index. These differences may contribute to species-specific differences in toxicity (ATSDR. 227-262. Clark K. Population estimates of concentrations of specific phthalate metabolites may differ by age. gender.. Dirven HA. interactions with macromolecules and species differences in metabolism of DEHP. 2005). Calafat AM. 2002. Environ Health Perspect 1982.html.html. Also. 2000c.21:13-34.Phthalates and metabolites have been tested. van der Broek PH. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. Available at URL: http://www.. 2000a. Silvapathasundaram S. at very high levels. Rhodes et al. Metabolism of di(2-ethylhexyl) phthalate. Sauer MJ. Hoppin et al. References Agency for Toxic Substances and Disease Registry (ATSDR)..niehs.atsdr. 105:734-742. 2004.. 1982. Springer. 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. Vol. 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. Anderson WA. Connor C. 2003.45:19-25. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2007). pp. Schroeder JL. Part Q: Phthalate Esters. 2002). environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. 2000b. 2001). However. Hauser et al. Mackay D. Environ Health Perspect 1997.18(12):10681074. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. variation also occurs in the same person during repetitive monitoring (Fromme et al. phthalates produced anti-androgenic effects by reducing testosterone production and. Matthews HB. NTP-CERHR. 2006). 2001.New York. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. Springall C. 2007. Silva MJ. 1982). 1986). Information about external exposure (i. 2001..cdc. and race/ethnicity (Silva et al. atsdr.nih. Scotter MJ. and Sertoli cell abnormalities in the male animals and. Castle L..3. 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.. Peck and Albro. 2004).. ovarian abnormalities in the female animals (Jarfelt et al... Cousins IT. 2004. 2002). Jordan S. Jongeneelen FJ. efficiency of intestinal absorption. Albro PW and Lavenhar SR. Hauser et al. Toxicological profile for di-n-butyl phthalate update [online]. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. Available at URL: http://www. 2004. Corbett JT. 2005.

Hauser R.25(2):293-302. Gans G. J Androl 2004. Lovekamp-Swan T. Davis BJ. Filser J. McKee RH. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Hoppin JA. et al. consumer milk. 2006 [online]. The estrogenic activity of phthalate esters in vitro. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Csanády G. 2000b [online].18(1):122. 2000c [online]. 6/2/09 NTP-CERHR.22(3):688-695. Silva MJ.112(17):1734-1740. Kalita JC. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Grote K. Yokoyama Y. Yoshimura M. Park S. Albro PW. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Sumpter JP. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Environ Health Perspect 1997. 2000a [online]. Tsukino H.195:142-153. Mechanisms of phthalate ester toxicity in the female reproductive system. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Nielsen J.103:582-587. Zhang S. Andersson A-M.gov/chemicals/ phthalates/dbp/dbp-eval. Calafat AM. Borch J. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.112(17):1740]. Jacobsen H. Wang P. Hass U. Hanaoka T.niehs.11(5):381-387. Brock JW. Environ Health Perspect 2003. Kano K. Chen Z. Research Triangle Park (NC). Available at URL: http://cerhr.16(4):487-493. Giwercman A. Hauser R. Environ Health Perspect 2004.html. Biol Pharm Bull 2003. Sumpter JP. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Skakkebaek NE. Jarfelt K. Silva MJ. Parker MG.nih. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. 6/2/09 NTP-CERHR. Richthoff J. Davis BJ. Akesson B. Milligan SR. Duty SM. Jonsson BAG.46(11):643-647. Suzuki T. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Am Ind Hyg Assoc J 1985. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP).gov/chemicals/dehp/dehp-eval. et al. White R. Research Triangle Park (NC). Epidemiol 2005. Toxicol Appl Pharmacol 2004.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. 6/2/09 Okubo T. Angerer J. Environ Health Perspect 1998. Koch HM. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004.niehs.111(2):139-145. Research Triangle Park (NC). gov/chemicals/dehp/dehp-eval.html. Ladefoged O. Available at URL: http://cerhr. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Meeker JD. Hagmar L. Duty S. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Liss GM.210:21-33. Scand J Work Environ Health 1985. Numtip W. Fromme H.105:802-811. and infant formula by tandem mass spectrometry (LC-MS-MS). Reprod Toxicol 2004. Bolte G. Int J Hyg Environ Health 2007.64(8):555-560. Anal Bioanal Chem 2005. Jobling S. Drexler H.niehs. Environ Health Perspect 2002.Phthalates in human urine samples. Calafat AM. 6/2/09 NTP-CERHR. et al.nih.19(4):505-515. Skerfving S. Research Triangle Park (NC). David RM.382:10841092.niehs. Balasubramanian AV. Int Arch Occup Environ Health 1993. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.110(5):515-518. Available at URL: http://cerhr.106(1):23-26. Ryan L. NTP-CERHR. Pan G. Meeker JD. Chahoud I. Harris CA.html. Brock JW. Silva MJ. Boehmer S. Hartle RW.nih. Rylander L. Stringer WT. Leffers H. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Henttu P.nih. Kessler W. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Reynolds T. Reprod Toxicol 2005. Park MG. Hum Reprod 2007. Main KM. Mortensen GK. et al. Reproducibility of urinary phthalate metabolites in first morning urine samples. Baird DD. Environ Health Perspect 1995. Determination of phthalate monoesters in human milk. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).26(8):1219-24. 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et al. Toxicol Sci 2000. Peters JM. Meek MD. Fourth National Report on Human Exposure to Environmental Chemicals 261 .36:459-479.58:339349. Silva MJ. Bratt H. Rusyn I. Jackson SJ. Toxicol Sci 1998. Rhodes C. Matthews JB. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Environ Health Perspect 2006. Malek NA. Batten PL. Cunningham ML. Abbott BD. Clemons JH. 112(5):A270].Phthalates phthalate (DEHP): a cross-sectional study in China.45:11-17. et al. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Crit Rev Toxicol 2006. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Wu ZF. Barr DB. Zacharewski TR.114(11):1643-1648. Environ Health Perspect 2004. Pratt IA. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Albro PW.112(3):331-338. Caudill SP. Peck CC.S. Fielden MR. Lambright CR. Reidy JA. et al.65:299-308. Klinefelter GR. Hodge CC.46:282-293. Parks LG. Urinary levels of seven phthalate metabolites in the U. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Ostby JS. Orton TC. Environ Health Perspect 1986. Barlow NJ. Environ Health Perspect 1982.

0-85.2-20.4-120) 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. 2004.8 (80.8-35. see Data Analysis section) for Survey years 99-00.9) 12.2-16.3 (22.6) 14.6-79.9) 13.1 (14.2) 14.4 (13.6) 25.8-98.1 (14.7-16.8 (28.7 (82.0-106) 58.2-116) 122 (102-143) 101 (84.4-25. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. IARC considers BzBP not classifiable with respect to human carcinogenicity.8) 14.9 (16.2 (11.6-43.8 (71.0) 16.7 (12.1 (20.0 (55.5-36.0) 33.3 (30.7-58.6-18.1) 68.3-18.0 (12.1) 12. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.2) 15.5) 27. and 0.1 (13.4 (29.2 (47.3.3) 13.1) 31.1-61. particularly male animals (McKee et al. population from the National Health and Nutrition Examination Survey.5 (13.4 (53.6) 63.5) 82.3) 15.5) 16.8-14.5) 65.S.4-16.4-15.5) 23.0 (15.2-16.2) 14.9-49.7 (51.0-130) 101 (86.9-14.8 (53.0-26.7) 38.5-94.8 (71.3-27.4 (32.6-17.3-82.1 (19.4) 49.5-36.9-16.9) 18.7 (15.1-16.0) 90th 67.8) 24.2 (14.3 (12.8-18.0) 23.3) 54.8 (10.6) 16.4) 38.2-31.9) 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 39.0 (30.2-155) 91.7 (53.2-39.8 (38.4) 75th 35.3-88.5-33.4 (10.3) 63.5 (66.3) 37.8-17.3-161) 99.9 (11.6-116) 122 (102-142) 101 (85.5) 15.2) 12.6 (12.7-13.6) 35.7) 40.7-35.2) 17.1) 76. High dose BzBP and its monoester metabolites.9) 15.9-47.3 (29.5-14.5 (27.6 (41.5-84.9-27.4) 12.1 (10.3-130) 122 (88.8-13.6-38.1-39.3-12.1) 29.4) 80.2-183) 101 (78.1-15. NTPCERHR.5-41.7-82.3 (33.8-14.8 (14.1 (58.5 (55.1) 13.5) 30.7-15.7 (80.0) 32. and 03-04 are 0.4) 33.4 (59.8-121) 79.1-43.4-62.5 (67. sealants.1-120) 52.7-170) 169 (134-198) 152 (99.8 (50.8-17.6) 24.4) 81.9 (12. respectively.4) 98.2) 33.4 (10. 2000).6 (13.3 (12.1-116) 122 (93.3) 13.3-75.9 (70.9) 43.3-91.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.4) 71.6-92.6-132) 103 (84.6) 14.7-16.2 (19.4 (53. interval) 15.5 (26.0 (15.6) 67.0 (33.2-115) 113 (91.4-127) 80.5 (76.8-48. and to a lesser extent.1-15.2 (43.5-25.7 (70.8-133) 89.6-29.6) 13.4) 65.8 (86.5) 55.9 (12.1-214) 166 (116-191) 145 (110-213) 88.5-62.9 (22.1 (13.6) 35.4 (32. can produce developmental and reproductive toxicity in rodents.2) 78.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3-43.3-21.8-76.4 (63.5-145) 138 (106-241) 143 (127-179) 120 (99.1 (32. and 2003-2004 were generally similar those reported in U.0) 20.2) 32.Phthalates Benzylbutyl Phthalate CAS No.6-72.2-38. 2000).2) 66.1) 67.1-16.1-35.4 (27.2-19.6) 15.9 (13. 2001-2002.6-39.4 (48.6 (66.9-190) 86.8-64.0-55.2 (10. it can be released into the ambient air during use or disposal of the products.6 (13.1) 14.9-62.5-35.4-92.1-90.3-125) Total 15. 0.8) 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 16.0 (11.4 (31.9-30.6) 50.4) 14. 262 Fourth National Report on Human Exposure to Environmental Chemicals .1.0 (34.2-17.8 (30.9 (21. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.4) 51.1) 32.6 (13.1-18. 01-02. and diet is the major source for general population exposure.0 (23.2-40.1) Selected percentiles ( 95% confidence interval) 50th 17.4) 35. Food crops take up BzBP.4) 108 (96.9 (28.6) 37.3 (29. vinyl tile.0) 34.3-18.7-16..7-25.2 (19.4 (68.S.8-41.5 (61.3) 94.8-16.8) 28.6) 13.8-16.6 (53.6-92.7-14.9) 14.0) 24.0 (14.8-72.6 (13.9) 11.7) 23.7 (13. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.9-28.4) 129 (98.8 (12.5-97.2) 13.0 (43.6) 29. including MBzP.3 (13.5 (57.2) 22. car care products..8) 63.7-119) 99.0 (30.3-74.3 (12.8) 33. BzBP can be released into the environment during its production and.0 (20.0 (26.9) 49.7-17.5) 15.0) 70. 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 (21.8.9-87.2-33.6 (21.0 (27.2) 69.3-34. because it is not bound to products in which it is incorporated.3) 23.9) 14.5 (47.6-150) 94. some personal care products.9 (39.2 (25.3 (44.1-38.6 (32. residents (Blount et al.5-18.6) 95th 103 (94.7 (11.1 (55.5-40.7-172) 103 (74.4-24.3 (54.4) 35.

7-69.2-49.0) Selected percentiles ( 95% confidence interval) 50th 13.8 (30.7-15.5 (10.8 (49.7-123) 77.3) 89.7 (11.4) 21.4 (74.6 (11.8) 56.1 (25.5) 78.. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al. Hoppin et al.7 (55.1 (18.4) 60.5 (12.1 (23.4 (11.7 (18.1 (21.0 (41.5) 46.4) 13.9 (10.7-19.6 (22.0 (67.1-12.1-120) 77.8) 16.2) 11.8-15.4-42.3) 37.7 (59.7) 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 40.8) 68.7) 56.6 (34. 2007).2 (56.5) 41. In an annual sample of German university students. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4 (34.8) 26.5) 17.8-14.S.0) 24.1 (15.9-83.3 (24. 2005).8) 13.8 (13.3) 13..2-57.4) 28.0) 49.5-42.2-117) 95.5 (9.6 (19.2-78.5-29.0 (12.0 (49.73-12.7 (38.5 (10.5-99.8) 53.5 (11..9 (9.6-47.1-27.2-15.2) 67.5) 95th 77.3-11. adolescents compared with adults. 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.3 (12.9 (29.4-27.2) 15.7) 25.8 (64.4-60.6) 38.5-79.6-116) 74. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7 (13.8-48. 2002).3 (38.1 (53.2 (27.9) 42.4) 12.9-62.7) 19.0 (11.6 (51.4 (60.4-14.3) 29.4) 14.4) 17.5-23.3) 13. population from the National Health and Nutrition Examination Survey.1) 17.5-61.9) 12.3-73.5) 14.6-99.9 (10.5) 23.4 (63.1 (9.1-14.1 (34.4 (12.0) 24.9-104) 62.2) 26.7) 38.8-80. 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.69-11.5 (35.8 (11.7-19.6 (24.4) 44.5-213) 49.2-13.6-40.4-102) 70.3-64.4 (21.1) 142 (99.4 (10.0 (10.9-40.1-58.6) 12.7-15.2-13.6-13.4) 50.6 (15.9-13.3) 18.1 (41.3-16. In NHANES 1999-2000. in young Swedish men (Jonsson et al.8-16.9-23. 2003).9-115) 57. 2004).8-60.1) 39.7-12.9 (15.6) 75th 25.3 (23.7-56.1 (21. 2004.9 (15.1 (43.0-109) 65.0-51.6 (14.2-12.9-14..7-20.9 (51.5-31.8) 15.4) 13.6-26.3 (35.6) 53.7 (14.5) 10.1 (21. 2007). Weuve et al.8 (50.4-23.3) 21.1) 80.4 (13.3) 14.2-26.7-14.6 (11.4 (11.4-90. interval) 14.5-16. 2006).2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.2 (41.4) 15.0) 13.9-28.7-397) 70.8) 11.8) 71.7 (23.9 (54.8 (57.8) 53. Biomonitoring studies on levels of urinary MBzP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BzBP than are found in the general population.4) 90th 50.0 (38.1 (21. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.8 (69.0 (41.8-27.4-14.3) 67.9-16.1) 12.6-81.1-35. and in a small sample of German residents (Koch et al.5-26.4-99.8 (12. 2002.8-14.1) 24.1) 24.6-20.8) 80. 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.7-14.3) 73..3) 55. Hauser et al.8-85.9) 24.9 (24.8-42.9 (43.9 (12.4 (33.7 (12.2-51.7-61.8) 33.9) 12.8-39.5) 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 .95-14.2-17.0) 11.8) 46.3 (13.5) 16.5 (48.4) 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) 11.8) 33.7-31.9) 100 (80.7 (54.2 (40.0-27.5-58. 2003).3 (15.6 (30.3 (60.5-76..1-29.5-26.8) 108 (75.7-29.4-18.4-17. 2005.9-69.8) 54.8) 24.1-125) 86.0-90.9 (12.9 (22.1-12.1 (11.8 (10.7 (11.7-90.2) 11. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.1-79.9) 11.1 (14.9-13.3) 90.4-15.0) 60.5) 20.6-12.0-26. A small study of African-American women in Washington.4-79.1 (46.4) 104 (89.2) 11.6) 30.6) 58.9 (39.5-13.3) 14.5) 13.3-38.8) 34.8-13.4) 51.7-20.6 (11.6-86.1 (13.0-15.8 (46.5 (49.3) 13.0) 15.8-13.6) 25.Phthalates York City (Adibi et al. and females compared to males (Silva et al.7 (11.9) 64.3) 16.4 (26.7 (21.8-64.1) 27..8-13.7 (19.3) 12.5-58.9 (55.4 (11..6) 13.4) 25.7) 46.4-93.1) 23.9) 52.8-15.3) 36.4 (25.0) 12.1 (19.4 (69.9) Total 14.6) 12.0 (12.2-15. in men attending a Boston infertility clinic (Duty et al.1) 35.8-69.0-48.2 (69.1 (13.0 (13.5 (56.9 (24.4-19.0-53.2-21.9) 12.6 (36.6) 73.2) 32.8-34.4-116) 73..4-142) 134 (116-176) 136 (85.6-15.9) 11.3 (39.5-57.6 (57.6 (30..4 (46.0 (33.5 (42.0 (62.7 (13.2) 12.3-34.8-173) 195 (121-305) 229 (99.5-38.

Caudill SP. Perera FP. J Androl 2004. Meeker JD. 2000 [online]. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Environ Health Perspect 2004. Rylander L. et al. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Wittassek M.68:309-314. Urinary phthalate metabolites and biomarkers of reproductive function in young men.niehs. Barr DB.18(1):122. Richthoff J. Available at URL: http://cerhr. Needham LL. Helm D. Poland. Calafat AM. et al. Environ Health Perspect 2006. Barr D. Hauser R.html.110(5):515-518. Baird DD. Singh NP. Blount BC. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Int J Hyg Environ Health 2007. Phthalate monoesters levels in the urine of young children. Silva MJ.22(3):688-695. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Jacek R. Prenatal exposures to phthalates among women in New York City and Krakow. Butala JH. Needham LL. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP).111(14):1719-1722. Gans G. McKee RH. Camann DE. 2005. Davis BJ.25(2):293-302. et al.210(3-4):319-333. Hilborn ED. Hagmar L. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.nih. Calafat AM. Centers for Disease Control and Prevention (CDC). Silva MJ. Environ Health Perspect 2000.Phthalates References Adibi JJ. et al. Reprod Toxicol 2004. Environ Health Perspect 2003. 264 Fourth National Report on Human Exposure to Environmental Chemicals .114(9):1424-1431. 112(5):A270]. Duty S.S. Environ Health Perspect 2002. Chen Z. Brock JW. Sampson EJ. Brock JW. Weuve J. Rossbach B. et al. Hum Reprod 2007. Environ Res 2003. Reidy JA. Epidemiol 2005. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. David RM. Ryan L. Silva MJ. Green RA. Sanchez GN. Koch HM. 4/20/09 Silva MJ.16(4):487-493. Urinary levels of seven phthalate metabolites in the U. Jedrychowski W. Schettler T. Angerer J. Duty SM. Malek NA. Pirkle JL.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Research Triangle Park (NC). Drexler H.112(3):331-338. Hodge CC. Wiesmuller GA. Atlanta (GA). Giwercman A. Caudill SP. Brock JW. Bull Environ Contam Toxicol 2002.108(10):979-982. Levels of seven urinary phthalate metabolites in a human reference population. Hu H. Hoppin JA. Ryan L.93:177-185. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Reproducibility of urinary phthalate metabolites in first morning urine samples. Jonsson BAG. Third National Report on Human Exposure to Environmental Chemicals. Dobler L. Caudill SP. NTP-CERHR. Koch HM. Eckard R. et al. et al. Silva MJ.

5-24.00) 4.10 (3.40-3.6) 17.3 (19.. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.50) 5.97) 2.20-2. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.28-5.20) 7. 2005).0-18. 2000).50) 2.00) 10. NTP-CERHR.40 (2. In addition.6) 17.30) 10.5-29.11-3.55) 2. about 65% to 80% of a dose is eliminated in urine within 24 hours.3-24. 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. population from the National Health and Nutrition Examination Survey.1-17. residents (Blount et al.3-19. pharmaceutical coatings.70-4.00-4.0) 9.6-26.33 (2.40-3..3 (13.3-18.22) 3. When total DBP metabolites have been measured.1 (13.20-12.7-31.50-2. 2003).40-9.70-4.20) 4.6 (13.0 (19..40-4.2 (8.2-14.30-2.46 (3.50) 8.84) 4.00 (7.30) 2.46-5.40 (7.56) 3.1-20.90-2..60-6.30-6.90-4..5) 22.5) 23.4-27.63) 3.6 (10.4) 22.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.4-12. 2005).7) 18. 2005).7-31.90) 12.00 (5. OSHA has established a workplace air standard for external exposure to DBP.3 (13.10) 11. 2003).0-14.5 (20.00-6.20-12. they have been referred to as monobutyl phthalate (MBP).10 (4.6 (29.90 (6.22 (3.5 (27.2) 5. CDC.30 (4.30-3.5) 18.5) 14.10) 9.00-6.Phthalates Di-n-butyl Phthalate CAS No.50-10.50-4.2 (12.68 (2. Fourth National Report on Human Exposure to Environmental Chemicals 265 .97) 4. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.3-20.10-9. 2004.80 (2.9) 15.30-6. interval) 2.9 (16.7 (17.1) 25.30) 5.6-20.10-9.2-22.0) 24.37) 6.5) 18.26 (2.6) 12.3) 3.7-18.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.43) 6.8) 40.6 (13.81 (3.9) 10.3 (16. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.7 (18.9-23.73-5. DBP can produce reproductive toxicity in male rodents (McKee et al.40 (2. in men attending a Boston infertility clinic (Duty et al.56 (3.60 (4.80 (5.91) 4.3.50 (3.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.82-3.40-17. and insecticides.20 (3.30 (3.1-25. Hauser et al. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.5) 19.3 (16. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.1) 16.55 (3.6) 26.0 and 0.17 (2. and in a small sample of Japanese adults (Itoh et al.60 (5.70) 5.7) 14.71 (2.5 (11.8) 21.00) 4.02) 4.80) 75th 5.1-12.50) 18.0 (13.49-2..80 (3.2 (11.7) 4. 2007).5 (10.50 (6.90 (4.10-2.5-16.07 (3.20 (7.85-6.4 (20.9-14.6-14.6) 16.3-30.46 (2.90-7.6 (10.56 (5.97-7.7 (17.00) 7.0-25.30) 6. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.7 (16. Following oral administration of DBP to humans.7 (9.20-9.0-38.30-11.24-8.60 (2.20 (6.30) 10. 2005. 2000.40) 5.70) 3.8) 677 652 703 699 1216 1088 Limit of detection (LOD.00) 6.80 (2.4) 12.5-16.4) 5.6-34.6) 10.73 (2.0) 12.3) 33.67 (5..0 (13. Koch et al.10) 2.3-48.96) 3.6) 16.72-3.4 (14.1 (8.80-5.10) 3.S. in a small sample of pregnant women in New York City (Adibi et al. and also in some printing inks. Survey Geometric mean (95% conf.44-2.6 (11.40-4. 84-74-2 Di-isobutyl Phthalate CAS No.17) 4.80 (5.5 (17.66) 2.7 (7.6 (14.00-11. Biomonitoring Information Median concentrations reported in the NHANES 19992000.3 (11.7) 15.80-5.19-3.40 (3.3 (18.8 (9.6 (9.9 (16.7) 7.50) 7. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.59) 3. Studies of children found age-related differences in urine MBP levels.5) 25.50) 90th 12.50-6.S.40-12.40-5. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates..0 (11.56-4. 2001).46) 2. mostly as MnBP (Anderson et al.2-33.3-43.40 (6.48 (2.7-20..70 (2. 2004.5) 12.10 (4.6-18. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.00-9.10) 8.60) 3.0) 13.30-13.6 (14.3) 18. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.60 (8.90-4.70-8.90 (3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.30 (1.0) 20.0) 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 2.20-6.1) 22.70 (5.30-7.

25) 5.6 (15.39-3.52) 3.69-7.1-24.95) 2. while MnBP declined (Wittassek et al.69) 4.2-13.64-7.1-15.75 (4.38 (6.97-2.65 (4.82) 4.85 (2. Weuve et al.46-11.57 (3.62 (6.10-5.93-6.57-4.37) 3. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al.3) 18.1) 15.66) 10.81 (3.04-5.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.18-4.21) 10.0-18.07 (2.31 (2.18) 3.07-5.81) 9.11 (5.17 (2.31) 2. Survey Geometric mean (95% conf.26-2.66) 4.11) 5. 2007).19 (2.02 (7.04) 3.38-10.52-3.0 (12. Between 1998 and 2003.9) 12.6) 11.36-2.S.67-5.and gender.6-19.79-6. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.7) 10.68) 5.18-10. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.00-3.6-19.3) 16.20-3.30) 2.7 (11.4 (12.8-36.1 (11.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.20 (2. Over this time.6 (12. 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.81) 4. up to four and 13 fold.56) 5.28 (4.55-6.53-3.6 (9. respectively.09-2. 2005).14 (4.91-6..84 (4.29-8.66 (8.96 (3.79-8.1) 7. to about two to fourfold higher (Fromme et al. In an analysis of NHANES 1999-2000.9-40.68 (2.5 (9.3) 28.7 (21.43) 3.13 (2.47-12.00-7.78) 9.92 (7.34 (3.46 (2.58-3.57 (3.69) 6.54 (2.7-28.78) 8.46) 3.33) 3.2) 8.99) 7.7) 11.52 (2.72) 5.9 (15.76 (3.73 (5.32 (7.7) 19.82 (4. interval) 2.0) 15.31 (7.72-7.2) 24. population from the National Health and Nutrition Examination Survey. 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.9 (9.27-12.8-18.4-16.29-3.79 (4.80) 7.8 (8.6) 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 2.0 (8.13-6.6 (8.53-5.7) 3.30 (6.33-9.39) 5.11-2.75 (6.1 (10.66) 2.5) 15..59 (4.56) 2.26 (2.03-11.0) 7.95) 10.68) 3.61-3.65-11. 2002.3 (13. 2004).99-4.43) 3.1) 10. 2007).78-8.9 (11. 2004).20-2.41 (2.20 (7.8-13.20 (2.42) 2. than adults in NHANES subsamples during the same time period..51) 5.84 (8.17) 90th 8.0 (10.89) 6.51) 15.47 (3.54) 2.4) 15.1-25.47-5.18 (1.9-26.15) 3.2) 9.24) 3.58-4.21 (5. 2005).86-4.17-12..74 (4.5) 13.5 (11.94-12.0) 11.44 (3.56-4.9-16.89-5.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.8-18.6 (8.00-3.7 (13.1) 11.43) 3.3 (17.1-12.15-4.18) 4.98 (2.8 (9.03 (5. the students’ median values for MiBP levels remained relatively unchanged.2-15. samples from German university students had consistently higher median urine levels of MnBP and MiBP.32) 7.76-15.33 (3.52-20.0) 3.51) 2.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.62-12.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.05) 2.22 (2.76-3.32 (3.02-10.76-3.64-7. An analysis of NHANES 2001-2002 showed similar age.3) 13.86) 6. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.20-4.95-3.81 (6.18 (4.4) 7.88 (2.56-15.83 (2.6 (10.64-10.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .04) 7.2 (10.31) 2.08-2. 2006).74-3.65-4.45) 3.01-2.2 (11.80-3.4) 23.89 (3.6) 13. 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.69 (2.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.54 (4..3) 13.80 (3.08) 75th 4.1) 13.94) 6.28-13.03-7.53-4. ranging from more than one-tenth the NHANES median (Itoh et al.1) 4.8 (10.33 (2.8) 10.00 (3.7 (9.36-7.5-19...35) 3.94 (5.

1 (28.5) 17.5-47.3 (42.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.7-34.4) 59.6-29.3-67.3 (51.8) 43. Survey Geometric mean (95% conf.3) 26.4) 64.4-20.5) 65.0) 20.1-82.5) 21.6 (44.0) 120 (98.9-92.1 (19.1-75.1 (19.1 (54.8 (57.3) 36.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.6 (26.5) 47.4 (84.1) 31. see Data Analysis section) for survey years 99-00.5-60.7-127) 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 22.4-42.4 (36.0 (45.5) 95.3 (23.0) 30.7-92.1 (51.1) 17.1) 47.5 (30.0-73.5) 37.7-42.9) 21.9 (17. population from the National Health and Nutrition Examination Survey.3) 23.3-136) 137 (107-162) 119 (90.3 (37.1 (26.6) 21.6-31.1) 23.6 (61.6 (22.5) 40.9-87.7) 124 (98.1.8-111) 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 23.7 (22.5 (74.7) 52.6 (32.2-56.4 (38.6) 80.3-21.9-22.7 (51.1) 23.2) 62.6-36.2-23.1 (21. respectively.8-29.7-53.1) 36.9 (79.5) 36.0-32.5) 36.6 (90.2-87.5-42.1 (18.3-60.4 (25.4) 22.7-34.2-63.0 (78.9) 71.2) 38.1 (41.9-42.1-51.6) 35.7 (18.4-44.0) 38.7 (16.1-92.3-96.5 (59.0 (30.0 (18.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.6) 46.9 (20.7 (43.0) 21.1-20.0-58.3-40.5 (29.3) 40.0 (20.0 (31.2) 68.0) 117 (104-131) 112 (84.4-60. 01-02.0-26.6) 38.9-33. *In the 1999-2000 survey period.2-33.8-25.1) 19.7 (64.7-26.2 (17.0) 84.7 (33.7-106) 69.9) 36.9) 26.9-28.2-32.1 (58.5) 24.2 (59.4 (19.2 (75.7-117) 118 (108-143) 93.5-53.7 (70.2 (58.1 (31.5 (59.4) 52.0-19.6-20.1) 20. Fourth National Report on Human Exposure to Environmental Chemicals 267 .5-27.3) 24.7 (18.3 (36.7-111) 64.7 (28.7 (24.9.1) 46.0) 27.6) 39.1-24.4-18.1 (62.3) 19.9-79.6-37.7) 92.6-69.7) 74.6 (55.3 (30.2) 42.3 (23.2 (79.3) 21.6-33.6 (48.5) 78.2 (74.2-114) 73.7-24.2-159) 92.5) 85.8-22.4 (71. and 03-04 are 0.S.5) 19.9-101) 77.4 (72.3-145) 85.0 (15.4 (35. referred to as monobutyl phthalate (MBP).9) 18.1) 25.5-43.1 (19.8) 62.8-119) 90.2 (20.0 (23. 1.2 (21.7) 28.0 (17.2 (19.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.7-121) 97.4 (35.4 (21.6 (65.0-51.3-85.0 (36.8) 58.8) 75th 51.2 (18.5-121) 106 (94. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value. and 0. interval) 24.8-132) 95.7-42.4-26.6-40.1 (17.1 (34.9 (17.8) 19.1-29.3 (17.1 (36.7 (19.7 (38.8) 23.2) 26.0 (72.3-76.3 (60.1) 23.4) 20.1 (16.4 (35.9-114) 116 (97.6-24.4 (35.8 (19.6-143) 127 (99.6 (19.5-117) 95.3-79.8-42.5) 26.6-44.2-49.0-24.2) 32.6) 71.3 (30.0-21.9-53.4 (23.6 (16.1-27.9-22.4-25.9) 29.3-24.6-49.3) 18.2 (25.5-44.7-91.2 (21.7-20.0 (25.4-159) 107 (84.1) 30.2 (78.5 (28.1 (19.2-93.2) 20.9 (79.6) 20.0-24.5) 31.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.1-22.2-24.4.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9) 75.5) 34.3 (56.8-123) 101 (90.2-22.8) 48.1-80.2-21.6) 17.7-116) 95.5) 20.0-19.5-47.6-48.6-29.4-31.6-113) 108 (90.2) 90th 98.9) 46.0) 31.7) 42.

0-38.7-37.5) 17.5 (64.4) 51.7-80.0-60.9-84.7) 20.2-48.8 (18.8) 35.8-24.2-106) 64.6-27.8 (17.6-50.0 (50.9-38.8 (65.1) 61.2-18.3 (17.3-20.5-64.4-164) 96.3-23.0 (19.1 (29.3 (60.6) 34.3-21. interval) 22.9) 39.1-99.2-28.9-56.9 (64.9-26.7) 42.3 (69.2-86.6-74.3) 52.3-71.0 (16.0-92.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.6 (27.0) 81.6-24.6) 83.7 (60.8) 23.9) 14.0 (34.7-51.0-75.2 (19.4) 15.2 (83.7 (43.8-235) 137 (108-198) 88.8 (16.2) 74.3 (52.5-142) 81.4 (13.6 (25.S.6 (61.7-26.2) 31.6) 31.7 (73.1) 37.0-17.5) 84.8) 17.9-100) 86.1-83.4 (53.5-70.4 (19.9 (30.7-19.9-68.6) 18.3-18.8) 20.5-76.9) 49.4) 62.7 (19.3 (28.6-28.3 (16.0 (43.9-49.2-16.6) 24.8) 17.8) 34.0 (15.4-135) 71.2) 159 (102-263) 147 (93.7) 36.0) 53. Survey Geometric mean (95% conf.1) 20.2-108) 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.4-24.8) 13.3-21.4) 15.8) 75th 38.5-142) 89.6) 65.4 (17.0) 28.0) 108 (71.5 (15.3) 17.0-113) 104 (83.3 (24.4) 53.1-99.4-131) 81.6) 24.8) 17.4) 19.0-41.3-32.7 (27.2 (19.1) 50.6-128) 96.0-47.7-78.8-23.8 (22.3 (17.5) 134 (93.2 (16.3) 33.9-36.8) 19.5) 82.5-18.0 (52.4 (45.4 (47.7 (81.8) 20.5 (18.3 (76.7) 19.4 (20.0) 29.1-62.7 (12.6-24.7-28. 268 Fourth National Report on Human Exposure to Environmental Chemicals .0) 19.0) 55.6-23.0) 70.4 (17.5-23.9 (37.5-22.6 (31.0) 25.3 (19.1) 17.5-37.6-44.4 (16.2 (35.3 (48.9 (56.8-24.0 (70.7 (60.6-26.2-73.5 (18.2-21.3 (46.6-44.8) 22.0 (69.8-32.5-41.7 (28.3-26.0-90.9) 62.2) 16.0 (18.0-19.1-128) 97.2-27.6-119) 63.5 (81.2-22.6-19.6 (29.1 (21.4-61.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.9 (35.6-22.3 (71.6) 23.3 (55.1 (15.4 (50.0) 26.4 (68.5-30.0) 75.7-19.4) 16.3-49.1 (32.9) 52.5-21.4-47.2) 59.8 (18.6 (25.7 (57.4 (56.5) 21.4) 20.0 (61.8 (50.9 (58.9-70.9) 19.7 (54.6) 39.3-81.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.3-40.4 (37.7 (14.6 (41.9 (19.9 (30.5) 39.2-179) 84.7 (16.3-39.0 (27.6-43.6 (74.6-32.1) 44.8) 30.6) 14.5) 91.6 (19.5-16.4 (23.4-76.3) 59.3) 67.3) 35.6) 25.2 (38.4 (31.1 (56.8 (13.1) 20.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.9) 30.1) 42.9) 24.1 (46.0) 59.6-23.9-14.9 (16.0) 35.2-61.6) 37.6) 38.8) 63.6 (57.0 (20.1-21.7-23.9 (20.3) 18.1 (34.3) 20.1-23.1) 35.6) 64.8) 34.3-114) 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 17.2) 21.0 (26.1-32.7-20. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.8) 28.2-85.4-72.6 (17.8 (18.4-65.3) 21.9 (73.0) 94.9) 28.1-18. population from the National Health and Nutrition Examination Survey.4-103) 117 (83.7 (20.3-78.8) 40.2-22.6-53.1) 53.1 (61.5) 60.0 (71.9 (39.3 (21.9-105) 85.7-21.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.3) 33.3 (42.3-17.7-39.1) 21.3-38.5 (14.4 (16.9 (30.9-68.9) 91.4 (50.9 (35.4 (31.5-15.3 (17.3-106) 74.4 (33.8 (25.4-34.0 (18.6-92.2-22.4 (31.5 (30.6-155) 91.3) 19.0) 41.5) 90th 68.9 (21.6-16.6 (72.9-34.7-42.4 (18.4) 21.3) 19.3 (52.8 (33.2) 65.9) 20.1) 22.8-43.6-42.

Poland. NTP-CERHR. Food Addit Contam 2001. Research Triangle Park (NC). Wiesmuller GA.210(3-4):319-33. Koch HM. Castle L.html. Drexler H. Urinary phthalate metabolites and biomarkers of reproductive function in young men. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review].Phthalates References Adibi JJ.210:21-33. et al. Jacek R. Drexler H. Silva MJ. Jedrychowski W. Giwercman A. Calafat AM. Int J Hyg Environ Health 2005. Atlanta (GA). Chen Z. 2005. Hauser R. Ryan L. Duty S. Bull Environ Contam Toxicol 2002.25(2):293-302. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Reidy JA. Camann DE.68:309-314. Singh NP. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Needham LL.nih.18(12):10681074. Blount BC. Caudill SP. Epidemiol 2005. Urinary levels of seven phthalate metabolites in the U. Barr D. Perera FP. J Androl 2004. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Dobler L. Silva MJ. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Ryan L. et al. Centers for Disease Control and Prevention (CDC).111(14):1719-1722. Environ Health Perspect 2000. Malek NA. Anderson WA. Barr DB. Caudill SP. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Angerer J.108(10)979-982. Hilborn ED. Silva MJ. Int J Hyg Environ Health 2007. Springall C. Levels of seven urinary phthalate metabolites in a human reference population. Hagmar L. Int J Hyg Environ Health 2007. Prenatal exposures to phthalates among women in New York City and Krakow.gov/chemicals/ phthalates/dbp/dbp-eval. Helm D. Schettler T. Caudill SP. Yoshida K. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Hu H. et al. Available at URL: http://cerhr. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Hum Reprod 2007. Wittassek M. David RM. et al. Koch HM. Duty SM. Meeker JD. Boehmer S. Phthalate monoesters levels in the urine of young children.114(9):1424-1431. Environ Health Perspect 2004. Butala JH. 2000 [online]. Fromme H. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. 112(5):A270]. Environ Health Perspect 2003.18(1):122. Rossbach B. Green RA. Bolte G.niehs. Third National Report on Human Exposure to Environmental Chemicals. Brock JW.208:237-245. McKee RH. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Needham LL. Itoh H. 4/20/09 Silva MJ. Gans G. Hodge CC. Scotter MJ. et al. Sanchez GN. Angerer J.93:177-185. Environ Health Perspect 2006. et al. Sampson EJ. Eckard R. Jonsson BAG.S. Rylander L. et al. Reprod Toxicol 2004. Weuve J. Koch HM. Pirkle JL.16(4):487-493. Environ Res 2003. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Calafat AM. Massey RC. Brock JW.112(3):331-338. Richthoff J. Masunaga S. Silva MJ.22(3):688-695. et al. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites.

00 (<LOD-1.400 (<LOD-.300 (.300-.200-.300-.00) .500 (.300-. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine. 01-02.500 (. see Data Analysis section) for Survey years 99-00.00-2. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.500 (.400-. 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-. 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.400-.50) .400 (.70 (1.2.70 (1.400-.300 (.700) . including nitrocellulose.500) .500) < LOD < LOD .600) .500 (. < LOD means less than the limit of detection. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.20) .3. population from the National Health and Nutrition Examination Survey. 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.200-.10 (<LOD-2. respectively.400) 1.500) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (.300-.200-.70) .400-. only levels at or above the 90th percentile could be characterized.300 (.500) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.300-.300) < LOD . which may vary for some chemicals by year and by individual sample. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.9.00 (<LOD-1.400-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300 (.500 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. polyvinyl acetate.700) .900-1.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .200-.200-.500) 1.300) < LOD .300-.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.70) .300-.500) .10 (<LOD-1.500 (.500) < LOD 1.00 (<LOD-1.300 (.700) . 270 Fourth National Report on Human Exposure to Environmental Chemicals .400 (<LOD-.Phthalates Dicyclohexyl Phthalate CAS No.10) .500) .300 (.500) < LOD < LOD . 0.600) .300 (<LOD-.300-.10 (<LOD-1.400 (.500) 1.600 (.300 (.200-.200 (<LOD-.400) < LOD < LOD . and 03-04 are 0.400) 1.90) . Survey Geometric mean (95% conf. and polymers.500-.400 (.500 (.00-3.400 (.600) .500 (. and 0.S.400-.400-. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.300-.600) .500 (.10 (.50) .500) .400 (.300) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400 (<LOD-. resins. In this Report. and polyvinyl chloride.600) < LOD .80) .400 (<LOD-.400 (.500) 1.400) < LOD 1.600) .

44) .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 1.350-.14 (<LOD-3.360-.560) 1.690) < LOD 2.54-6.670 (<LOD-.590 (<LOD-.450 (.05) .240-.500-.950 (.530-1.74) .10) . Fourth National Report on Human Exposure to Environmental Chemicals 271 .17) .22 (<LOD-1.490) .12-1.470 (.16) .770-1.170-.54) .610 (.00 (<LOD-3.06) .910 (.660) < LOD < LOD .770-1.260-.880 (.670-1.43 (1.82 (1.18) .S.82) .940 (.16 (<LOD-3.620) < LOD .250 (.450 (.690 (.220 (<LOD-.910 (.530) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.53) .590 (.530-.910 (.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.740) .690) < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.630 (<LOD-.770 (.800-1.500 (.630 (<LOD-.33) .36-1.400-.830) 1.690-1.510 (.770) < LOD 2.380-.410 (.530) 1.380 (.420-.370 (<LOD-.770-1.470) 3.33 (<LOD-3.480 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.420-.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400-.500) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .910 (.310) < LOD . Survey Geometric mean (95% conf.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .420-.390 (.710) . population from the National Health and Nutrition Examination Survey.06) .500) 3.510-.67 (1.00) .740) < LOD < LOD .790-1.270) < LOD .53) .530 (.54 (<LOD-2.34) .660) .310-.330 (.11) .330 (.290-.

84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.1-93.. interval) 179 (156-204) Selected percentiles ( 95% confidence interval) 50th 164 (136-201) 169 (141-194) 174 (151-208) 75th 454 (370-538) 465 (415-527) 502 (457-555) 90th 1260 (1010-1480) 1230 (1040-1440) 1380 (1170-1750) Total 178 (159-199) 193 (169-220) Sample size 2840 (2150-3770) 2536 2500 (1860-3220) 2782 2700 (2160-3310) 2605 95th Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 91. and 2003-2004 subsamples were similar to median or geometric mean levels in small samples of pregnant women in New York City (Adibi et al. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. 2003) and African-American women in Washington.3 (82.3 (74..4. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.2-102) 95.9.S. and 03-04 are 1. soaps. 0. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. and hand lotions.4 (62. DC (Hoppin et al.8-111) 85. respectively. In contrast.3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. population from the National Health and Nutrition Examination Survey.2. particularly those containing fragrances. see Data Analysis section) for Survey years 99-00. 2002).5) 81. A small study of children less than 2 years old reported mean urine MEP levels that were about twice as high as levels in children (aged 6-11 years) in NHANES 2001- Urinary Mono-ethyl phthalate (MEP) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2001-2002.1 (71. 272 Fourth National Report on Human Exposure to Environmental Chemicals .. deodorants. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7 (70. colognes. Products that may contain DEP include perfumes.7) 71. shampoos.3-103) 193 (141-256) 184 (148-227) 221 (165-294) 180 (140-221) 181 (152-212) 188 (158-219) 197 (129-249) 183 (142-217) 196 (170-241) 564 (419-818) 479 (387-651) 557 (432-695) 482 (390-590) 498 (441-567) 533 (471-629) 378 (290-730) 451 (315-636) 521 (295-571) 1510 (1050-2150) 1260 (983-1480) 1250 (973-1560) 1340 (1010-1660) 1350 (1060-1660) 1590 (1220-2070) 756 (379-1070) 808 (572-1090) 827 (542-1440) 3260 (1550-4420) 2070 (1470-3050) 2310 (1360-3310) 3480 (2230-4640) 2720 (2160-3670) 2980 (2250-3800) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 179 (149-215) 182 (157-211) 197 (173-224) 178 (154-206) 174 (153-198) 189 (160-225) 154 (119-197) 171 (139-199) 171 (148-201) 174 (138-210) 167 (139-194) 182 (138-219) 523 (372-650) 502 (419-603) 536 (449-654) 425 (350-508) 427 (387-498) 478 (392-564) 1440 (1020-2280) 1450 (1060-2110) 1520 (1210-2070) 988 (880-1230) 1050 (879-1310) 1260 (969-1640) 3500 (2130-4560) 3100 (2110-4390) 2910 (2210-3480) 2230 (1370-3880) 1860 (1490-2500) 2590 (1800-3420) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 181 (157-209) 226 (195-262) 267 (239-298) 322 (275-377) 352 (324-384) 357 (310-412) 152 (133-175) 158 (141-178) 167 (145-193) 174 (146-210) 220 (190-264) 249 (212-307) 306 (256-350) 357 (290-407) 306 (253-414) 134 (108-157) 147 (119-177) 148 (125-175) 441 (390-541) 530 (444-660) 597 (523-688) 789 (635-949) 853 (709-1090) 948 (769-1150) 367 (287-482) 413 (366-451) 418 (366-477) 1280 (851-1510) 1490 (1050-2110) 1640 (1320-2180) 1890 (1410-2270) 2160 (1620-2470) 2500 (1840-2980) 986 (798-1340) 1020 (905-1230) 1210 (954-1480) 1720 (1460-2130) 2630 (1540-4460) 3050 (2230-4300) 3610 (2130-4640) 3540 (2810-5070) 4370 (2780-5910) 2470 (1590-3880) 2320 (1560-2720) 2250 (1590-3290) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and also in men attending a Boston infertility clinic (Hauser et al. 01-02. Biomonitoring Information MEP levels in the NHANES 1999-2000.9 (61.9-92. and 0.Phthalates Diethyl Phthalate CAS No. 2007).

the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups.2 (66. population from the National Health and Nutrition Examination Survey.9 (82.Phthalates 2002 (Brock et al.7-110) 81. Other population estimates also differed by sex and race ethnicity (Silva et al. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2004). 2005). Finding a measurable amount of MEP in urine does not mean that the levels of MEP or the parent compound cause an adverse health effect.. Urinary Mono-ethyl phthalate (MEP) (creatinine corrected) Metabolite of Diethyl phthalate (DEP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Median MEP levels found in a small sample of German residents (Koch et al. 2003) were slightly lower than levels found in NHANES 2001-2002.6 (65. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.5-114) 101 (87. Biomonitoring studies on levels of MEP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEP than are found in the general population...0-156) 140 (111-180) 150 (123-184) 154 (136-177) 160 (146-182) 177 (147-202) 165 (127-208) 177 (135-224) 180 (145-203) 364 (275-495) 330 (249-409) 363 (292-485) 390 (336-452) 419 (363-486) 512 (423-632) 341 (219-554) 512 (290-802) 470 (310-596) 879 (676-1260) 808 (590-1100) 791 (589-1080) 1010 (803-1460) 1060 (884-1320) 1230 (989-1610) 625 (400-784) 843 (512-1320) 719 (470-1330) 1760 (1000-2000) 1330 (868-1840) 1470 (987-2220) 2170 (1790-3350) 2120 (1520-2790) 2290 (1770-3200) 328 393 342 752 742 729 1456 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 141 (124-159) 148 (130-168) 154 (139-171) 187 (165-211) 187 (166-210) 211 (180-248) 120 (107-134) 126 (110-147) 127 (108-150) 158 (142-179) 171 (148-188) 181 (148-217) 324 (249-415) 352 (282-425) 390 (341-465) 377 (307-495) 407 (355-473) 508 (379-634) 1000 (693-1480) 1100 (839-1480) 1070 (852-1360) 822 (697-1170) 860 (712-1100) 1120 (889-1400) 1950 (1460-2900) 2120 (1490-3030) 2000 (1610-2410) 1930 (1170-3410) 1430 (1190-2010) 2250 (1440-3330) 1214 1371 1250 1322 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 164 (142-190) 213 (182-249) 241 (213-271) 208 (183-236) 247 (226-271) 254 (225-287) 149 (135-165) 157 (142-173) 165 (144-189) 154 (136-174) 199 (164-242) 233 (202-270) 196 (166-228) 227 (185-270) 212 (188-246) 128 (111-142) 136 (124-150) 135 (120-158) 382 (314-472) 461 (396-572) 533 (417-665) 443 (390-505) 557 (478-618) 619 (476-791) 313 (239-387) 338 (288-402) 386 (338-485) 814 (673-974) 1080 (860-1650) 1230 (956-1610) 1030 (762-1700) 1240 (961-1480) 1530 (1200-1970) 856 (655-1390) 919 (712-1160) 989 (831-1330) 1330 (974-1920) 1940 (1410-2630) 2270 (1810-3140) 1920 (1230-2590) 2090 (1550-2800) 2590 (2160-3500) 1950 (1480-2740) 1590 (1320-2170) 1920 (1400-2780) 813 677 652 603 703 699 908 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 273 .6 (77.0 (66.S. 2002).0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. with adjusted geometric mean levels of urinary MEP that incre