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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2'4.2'.gov/exposurereport/chemical_selection.3’.6.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .2-Dichloroethane (Ethylene dichloride) 1.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.2.5.3.2-Dichloroethene Dichloromethane (Methylene chloride) 1.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.4.4.6-Heptabromodiphenyl ether (BDE 183) 2.5'-Tetrachlorobiphenyl (PCB 49) 2.html.4. Table 1.4.5’.4'.cdc.5.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.1.4’.3-Tetramethylbutyl] phenol) Triclosan (2.3.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.3-Dichlorobenzene (m-Dichlorobenzene) 1. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.2'.2-Dichlorobenzene (o-Dichlorobenzene) 1.3'.2'.4'-Tribromodiphenyl ether (BDE 28) 2.What’s New in this Report What’s New in this Report In this Fourth Report.1-Dichloroethene (Vinylidene chloride) cis-1.4.5'-Hexabromodiphenyl ether (BDE 153) 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic. Paradichlorobenzene) 1.2'.4.4.2'.3.2-Trichloroethane Trichloroethene (Trichloroethylene) m.4'.4-Tribromodiphenyl ether (BDE 17) 2.4'-Pentabromodiphenyl ether (BDE 85) 2.3.1.4'-Tetrabromodiphenyl ether (BDE 66) 2.1.1-Trichloroethane (Methyl chloroform) 1.2'.6-Pentabromodiphenyl ether (BDE 100) 2.1-Dichloroethane 1.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.2’.4'.4’.4'.2'.4.5-Pentabromodiphenyl ether (BDE 99) 2.5.4-Dichlorobenzene (p-Dichlorobenzene.2-Dichloropropane 2.2'.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.5'.5'-Tetrachlorobiphenyl (PCB 44) 2.1.2'.2'3. 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. The process for selection is described at http://www.5.2-Dichloroethene trans-1.4.4.4'-Tetrabromodiphenyl ether (BDE 47) 2.6'-Hexabromodiphenyl ether (BDE 154) 2.4'.4.

and these data will be included in the next release of the Report. Details of this procedure are provided in Appendix A. Only slight differences should be noted when one compares the recomputations to previous releases of the Report. urinary 2. Data for other pesticides are included only for 1999-2000 and 2001-2002. Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e.g.. Fourth National Report on Human Exposure to Environmental Chemicals 3 .. 2003-2004) have been re-computed by use of this improved procedure.4-dichlorophenol and 2. Explanations for each change are provided in Appendix B. 2001-2002. the presence of an interference) that produced results of inadequate quality.1).What’s Different in this Report What’s Different in this Report The Fourth Report uses a new procedure to estimate percentiles when the percentile estimate falls on a value that is repeated multiple times (e. and polycyclic aromatic hydrocarbons (PAHs) for one or more of the 1999-2002 survey periods. Affected analytes were serum beta-hexachlorocyclohexane for the 2001-2002 survey period. Percentiles for all three NHANES survey periods (1999-2000. five results that all have the value 90.g. 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report.5-dichlorophenol for the 1999-2002 survey periods. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available.

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

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

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

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

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

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

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

7) 58.2-59. it was discovered that acrylamide is formed when starch-rich foods.S.0) 85. are heated at temperatures used for frying and baking. EPA reference dose of 0.6-66.3) 86.4) 57. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state.S.2-77..2 (62.. acrylamide has produced upper airway irritation following inhalation of high levels. and in the synthesis or compounding of dye materials.1-57.1) 55.6) 71.S. In the general population.8-57.0) 57.9-105) 86.9) 63. Polyacrylamides are useful water-compatible polymers used in water treatment.0 (67.0-108) 152 (139-175) 126 (111-142) 108 (86.2) 57. in some sealing grouts. 2005. 217 million pounds of acrylamide were produced commercially in the U.4 (54. 2004).5 (74.1 (52.4 (54.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.2-114) 163 (147-191) 96.9 (69. in permanent press fabrics. EPA. EPA. Commercially.2 (58. People may be exposed to acrylamide from foods. pulp and paper production.2 μg/kg/day (U.0 (53.8 (81.1 (73.0-104) 132 (115-151) 223 (194-243) 141 (120-152) 220 (189-237) 164 (147-191) 350 769 1889 2570 1523 3509 3592 03-04 03-04 03-04 61.1) 53.4) 57.2-67.7 (63. 2005).4-89.5-80. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.9) 57.4 (59.6-104) 82.1 (47. 2006.3-2. and from dermal contact with products that contain residual acrylamide.6-61.6) 50.6 (51.Acrylamide Acrylamide CAS No. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.S.0-49. Acrylamide is not thought to accumulate in the body at environmental doses.1) 101 (95.1 (83. and binding agents. 2005). gels. 2006). population from the National Health and Nutrition Examination Survey.6-75.4-60.5 (79.9-52.3 (53.6) 73. ocular and dermal irritation from direct contact with acrylamide containing materials. Fennell et al. Estimated intakes in children are about twice that of adults (DiNovi and Howard.6) 90.9 (60.6-108) 61.7) 54.4-83.9) 75.8 (91. 1990. FDA.7 (65.4) 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. Elimination occurs mainly in the urine as mercapturic acid conjugates.2-118) 98. 1994).7-60.6 (81.1-61.3-71.2-93.1-64.1-64. 2005).7 (55.9) 58. FAO/WHO..4) 100 (89. 2004. acrylamide is synthesized and used in the production of polyacrylamide polymer.5 (52. In 1997. smoking.3) 70.4 (53. glycidamide.S. Since acrylamide has limited volatility and high water solubility.4-76. widely distributed in tissues. but can covalently bind to form adducts with proteins.2 (75.2) 57.5) 58. Natural substances in the food are converted to acrylamide.7-64. but are generally above the U.1) 62. interval) 61. or to glutathione conjugates (Calleman et al. and an average daily intake is estimated as 0. 2005). the main source of exposure is from the diet.8-55. 2005).0-66. 2002). Survey Geometric mean (95% conf.3 (55. and is either metabolized to the reactive epoxide.7) 75th 79. These estimated intakes are hundreds of times lower than occupational exposures.7 (58. and cosmetics (NTP-CERHR.0 μg/kg for adults (FAO/ WHO.1) 46.5) 66. and well below doses known to cause nerve damage or carcinogenicity in animals.3) 63.7) 96. 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. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U. soil conditioners. see Data Analysis section) for Survey year 03-04 is 3.9-61. Fourth National Report on Human Exposure to Environmental Chemicals 11 . mineral processing. (NTP-CERHR. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. Animal studies indicate that acrylamide is well absorbed.4-60. and in some cosmetics. In humans.0-58.6-65.4 (51.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. as an absorbent in disposable diapers.8 (52.5-85.1 (88. such as potatoes and some grains.9 (54.7-64.7) 73. Tareke et al.0 (69.8 (57.2-70.0 (57.2-91. drinking water. Recently.0.5 (44.6 (56.

4 (51.3) 59. 12 Fourth National Report on Human Exposure to Environmental Chemicals .0) 118 (103-126) 121 (112-134) 113 (94.Acrylamide occupational exposures. reproductive effects (reduced litter size. 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.0 (70. respectively) are markers of integrated acrylamide exposure over the preceding few months. Acrylamide is clastogenic and can produce dominant lethal mutations. 2004.9-62.9) 87.4 (90. Vesper et al. 2006) have been demonstrated after acrylamide dosing. and neuronal DNA reactivity (Doerge et al. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).4-103) 79. 2005.2-68.1 (82.5) 71. 2005. Klaunig et al.0 (80.. 2005.4 (57. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al.4-59. 2005) have been demonstrated in animals...5 (56.2-90..epa.9-138) 143 (130-159) 96.5 (59. Axonal degeneration. most non-smokers had levels less than about 100 pmol/gram hemoglobin. 2004). presynaptic nerve terminal binding (LoPachin. Survey Geometric mean (95% conf. altered gene expression in testicular tissues (Yang et al.1-56.2) 65. 2005). 2005.5) 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.8 (51.8-61.1) 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. EPA at: http://www. 2001).7 (84.5) 87.5 (83.0-93. 2003.7) 74. 2005. 2005.5-92.5 (42.1 (70.1 (57. 2009). 2005) and sperm DNA adducts (Xie et al.1 (66. Puppel et al.4 (81.9 (58.3-78..3 (56..0) 94. U..S.1 (56. 2006). male germinal cell injury.3) 59.2 (63. 1997. 2006).8-48.7 (57. 2005. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.2-91. Hagmar et al. 2002.9-76.1) 56.2) 55. In addition..0 (75.1) 62..9-77. 2008). NTP-CERHR.0 (52.7) 60.9) 65. EPA. Schettgen et al.pdf. probably through its epoxide metabolite.6-90.4) 83.0-62.2) 87.7-62.5-66...7) 61.9-78.3) 85. 2005). fetal death. uterine.7-64. adrenal...6 (66. interval) 59. see Data Analysis section) for Survey year 03-04 is 4..7-86..8-49.9-64.1-70.0-103) 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. Additional information is available from U. Mucci et al.0. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U. 2005).4-65.4 (56. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. 2005.6-62. scrotal.S. 2006.8) 60. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.7) 90. Rice.S..7 (61. Puppel et al.4 (61.9) 75. Schettgen et al.2 (72. dominant lethality). gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. 1997. IARC classifies acrylamide as probably carcinogenic to humans.. 2005.1) 60. and other sites) (FAO/WHO.. and cancer (mammary.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.4) 46. EPA. After exposure ceases.6 (90.9 (57.5-94.9 (81.4-98. glycidamide (NTP-CERHR.8) 45.S.7 (87.3-101) 95. 2005.8 (44.9) 59. 2005.3) 59. population from the National Health and Nutrition Examination Survey. U. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.5) 75th 85.1-62.5-64. Vesper 2005) and smoking (Bergmark. AHA levels have been shown to increase with dietary intake (Hagmar et al.who.1-60.. 2008). although different analytic methods can affect results..2 (56. 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. Maniere et al. 2005). thyroid.6-64. 2002.int/ ipcs/food/jecfa/summaries/summary_report_64_final. Glycidamide has been shown to react with DNA (Doerge 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.4) 53.

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. Aprea P. smoking habits and gender. Calleman CJ. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. In another study. DiNovi M and Howard D. Available at URL: http://www. 2001).niehs. Acrylamide intake through diet and human cancer risk. 2/3/09 Hagmar L. morphological and molecular endpoints in animal models. Paulsen JE. Godard T. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. 6013-6019. NIH Publication No. Toxicol Sci. Osterman-Golkar S. Bergmark E.85:447-459. et al. References Bergmark E. Bergmark E. 2006. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. smokers and nonsmokers. Adv Exp Med Biol 2005. Mutat Res 2005. 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. Yang JS. CFSAN/Office of Plant and Dairy Foods.fda. National Toxicology Program.43:365–410.. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Bergmark E. 2/3/09 Perez HL. Axmon A. Mucci LA. McDaniel LP. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Zhang S.Acrylamide In occupational settings. Malmberg B. and Research Strategies. Survey data on acrylamide in food: individual food products. Toxicol Sci 2005.56. He F.126(2):361-371. Nordander C.nih. Maniere I.Toxicol Appl Pharmacol 1994.. Granath F. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Metabolism and hemoglobin adduct formation of acrylamide in humans. July. Andersen M. J Agric Food Chem 2008. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. 64th Meeting: Summary and Conclusions (FAO/WHO).. Bjellaas T. Illinois. 2001. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake. Twaddle NC.561:49-62. [Epub ahead of print] Dybing E. April 13-15. Calleman CJ. Mutat Res 2005. Costa LG. Tornqvist M. da Costa GG. 054472. Paulsson B. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Hagmar et al. Doerge DR. Doerge DR.10(1):78-84. et al. Rosen I.int/ipcs/ food/jecfa/summaries/summary_report_64_final. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Kautiainen A. LoPachin RM. Wu Y. Toxicol 2005. 2005. Beland FA. 1993. Cheong HK. et al. Snyder RW. Kamendulis LM. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Available at URL: http://cerhr.pdf.cfsan. Adv Exp Med Biol 2005. Mutat Res 2005. Wilson KM. 2009 Jan 8.580(1-2):131-141. Toxicol Appl Pharmacol 1993. Mechanisms of acrylamide induced rodent carcinogenesis. Scand J Work Environ Health 2001. Guffroy M.580(1-2):119-129.561:21-37. Bridson WE.27(4):219-226. Perez et al. 8-17 February 2005. 2004.html#u1004. Tian G. 1999). Acrylamide neurotoxicity: neurological. Tornqvist M.. Chem Res Toxicol 1997 Jan. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. He F. Spicer R. Bruze M. 1994).. Farmer PB. Summer SCJ. gov/~dms/acrydata. Haugen M.580(1-2):157-165. Hagmar L. Human exposure and internal dose assessments of acrylamide in food. Wirfalt E. Chem Res Toxicol 1990. Food and Drug Administration (FDA). Alexander J. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation.gov/chemicals/ acrylamide/Acrylamide_Monograph. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Uncertainties. February. Fennell TR. Calleman CJ. The Updated Exposure Assessment for Acrylamide. Italy. et al. Chicago. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Churchwell MI. Fennell TR.who.3:406-412. Costa LG. Joint FAO/WHO Expert Committee on Food Additives. Burgess J. Churchwell MI.120(1):45-54. Food Chem. 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. Available at URL: http://www. Rome. Becher G. Duale N.pdf. Magnusson AL. 2/3/09 Klaunig JE. Laurentie M. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. et al.

Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Gray JG. a carcinogen formed in heated foodstuffs. J Agric Food Chem 2008.gov/chemfact/s_acryla. Angerer J. 1994.163(2):101-8. Office of Pollution Prevention and Toxics.561:89-96. September. Ospina M. Anal Biochem 1999. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. Yang HJ.19(4):527-34. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. EPA). Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Angerer J.epa.50(17):4998-5006. Ospina M. Kutting B. Puppel N. Marko D. Toxicological effects of acrylamide on rat testicular gene expression profile. Liu K. Tjaden Z.206(1):9-14. revised 1/3/06. Hallmans G. Broding HC. Reprod Toxicol 2005.207(6):531-9. Mutat Res 2005.gov/iris/subst/0286. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells. Int J Hyg Environ Health 2004. Chemical Summary for Acrylamide. Analysis of acrylamide. Agudo A. U.S. Vesper HW. Fueller F. 2/3/09 Vesper HW. Lee MH. Rossbach B. Chae C. Rapid Commun Mass Spectrom 2006. Karlsson P. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Tareke E. Hemoglobin adducts of ethylene oxide. Han CH. Meyers T.580(1-2):3-20.274(1):59-68.580(1-2):71-80.S. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Lee SH. Integrated Risk Information System (IRIS).56(15):6046-53. Ingham L. J Agric Food Chem 2002. Rice JM. Drexler H. Toxicol Lett 2002.epa. propylene oxide. Schettgen T.htm.S. Angerer J.20(6):959-64.txt. Ding X. Fu D.134(1-3):65-70. Choi JH. Environmental Protection Agency (U. Han DU. Meyers T. Toxicol Lett 2006. Eriksson S. Slimani N. Mutat Res 2005 Feb 7. Washington (DC). Xie Q. Available at URL: http://www. Available at URL: http://www.S. Schettgen T. Drexler H. Acrylamide. Tornqvist M. 2/3/09. Int J Hyg Environ Health 2003. Rydberg P. Adv Exp Med Biol 2005. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Benetou V. Liu Y. Drexler H. et al. Licea-Perez H. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Smith A. Jin Y. et al. Tjønneland A. U. EPA). Letzel S. Sun H. The carcinogenicity of acrylamide. Vesper HW. Environmental Protection Agency (U. Schettgen T.Acrylamide glycidamide by gas chromatography-mass spectrometry. Myers GL. Weiss T.

maternal exposure during pregnancy can result in lower birth weight.21-1.790) .180) .213) .66-3.18-3.96-4.20-2.23 (2. DHHS.075 (.580-1.70) 2.030-.053 (<LOD-. 1998).052 (<LOD-.96 (1.11) .01 (1.087 (.570-1.480-.400-.111-.350-.030-.450-.62) 2.09-2.086 (.150) .167 (.144 (.740-1.63 (2.65 (1.310) . stroke.44) 2.32) 1.066-.630 (.02 (.78) 2.S.505 (.54) 1.09-3.16) .076-. emphysema.22) 2.23-2.85 (1.33-2.20) . 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.180) .428-.960-1.094) .084) .70-2.126) .140 (.180 (. and 03-04 are 0.110 (.110 (.090-.34 (1.308 (.480-1.49) 1.88 (1. Survey Geometric mean (95% conf.197) .187) .621-1.45) 1.100-.139) * . 83% of measurements had an LOD of 0.120 (.190-.140-.080 (.059-.660) .920 (.130 (. cardiovascular disease.310-1.50-4.57) 2.260-1.17 (.071 (.02) 1.047-.66) 1.730 (.28) .110-.188) .12-4.630 (.77 (1.030 (.54 (1.600-1.50-1.060-. acute respiratory illness.94) 1.087-.066 (.30) 2.110-.320) .17) .164 (.66 (1. acute respiratory infections.312) .060) .193) .068) .310) 90th 1.058 (.53-4. and 17% had an LOD of 0.05) 1.83-2.080-.087) < LOD < LOD .130) .090-.96) 2.110 (.020-.19-2.12 (2.87-3.180) .050 (<LOD-.23 (.38-2.110-.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.040-.180 (.164 (. 2006).220) .066) .48-2.840) 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 .533-.95) 1.990) .080-.44) 2.860 (.160 (. 2004). ear problems. 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.080-.997-3.30) * .42-4.510 (.115-. population from the National Health and Nutrition Examination Survey.163) .160-.05. DHHS.061) < LOD .124 (.950 (.190-.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .142-.32-2.050-.15) 2.770) .015.21-1.210 (.68) 2.080) < LOD < LOD .063) .302) .198) * .047-.77 (1.63-2.690 (.68 (1.350-.710 (.410) .153-.540-. see Data Analysis section) for Survey years 99-00.070) .131 (.53 (1.060 (<LOD-.726) . Children exposed to ETS are at increased risk for sudden infant death syndrome.15 (2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.S.625) .110 (.180) .620 (.068) .240 (.050-.070) 75th .77 (2.39) 3.071) .99) 2.059-. and 0.070-.670) .060-.48-3.120) .360) .00) 1.043-.09-3. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.770-1.26-1.040 (.50 (1.76 (1. which may vary for some chemicals by year and by individual sample.220) .040 (.220-.20) 1.20 (.990 (.145) .110) .54 (1.015 ng/mL.180) .052 (<LOD-.520 (.580 (.910-1.080 (..49) 1. 2004).050) .230) .820) .506 (.234) .14) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.080-.12 (1.110) . Cigarettes contain about 1.154-. respectively. and exacerbated asthma (U.60-2.163 (.137-.070 (<LOD-.19) 1.740-1.39 (1.540 (.770) .280 (.148-.44 (2.92 (1.057-.160 (.62 (2.190-.070) .140 (.800 (.160) .050) .01) 3.79) 3.580) .50) 3.19) .430-1.35 (2.040-.02) 1.S. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.900-1.175 (.089) Age group 3-11 years 99-00 01-02** 03-04 .20 (1. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.04 (1.470-.090-.120 (.370-.630 (.42 (1.050 (.160) .44 (1.47-3.14) .40) .260) 1.088-.23 (1.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .060 (.073) < LOD .110 (.05 ng/mL.310-1.106-.32-2.89) 1.5% nicotine by weight (Kozlowski et al.21 (.570 (.12) 1.077) .230 (.84-3.216 (.120 (.050 (<LOD-.054 (.080) < LOD .137 (.050 (<LOD-.950-1.120-.55 (1.850 (.620-1.120 (.930 (.160 (.200) 1.Cotinine Cotinine CAS No. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.99) 2.75) 1.077) .201) .300) .150) . Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.14-1.060 (<LOD-.060 (. Fourth National Report on Human Exposure to Environmental Chemicals 15 .062 (. and various other disorders (U.55-2.104-.060-.500 (.00) .350 (. ** In the 2001-2002 survey period.28-1.81-2.120 (. < LOD means less than the limit of detection.88 (.68) .93) .050 (<LOD-.040 (.17 (1.30) 2.120-.108) * .140-.43 (1.030-.

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

Benowitz NL. Jarvis MJ. the United Kingdom.niehs.gov/eid/rmca/critdocs/ criteriadoc/33. Centers for Disease Control and Prevention. Schwartz SS.S. Fong I. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace.S. 4/13/09 Perez-Stable EJ. U. U. U. Cotinine as a biomarker of environmental tobacco smoke exposure.S. et al. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Bernert JT. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Etzel RA. 1991. Racial/ethnic differences in serum cotinine levels among adult U. Herrera B. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey.pdf.fr/ENG/Monographs/ allmonos90. Curtin LR. JAMA 1998. 1988-1991.15:302-307. Pechacek TF. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.gov/library/ secondhandsmoke/. 2004. Soliman S.S Department of Health and Human Services (U.cdc. IARC Monogr Eval Carcinog Risks Hum. Summary of Data Reported and Evaluation [online] 2004. Mowery PD. iarc. et al. Lewis PJ. Modin G.S Department of Health and Human Services (U.4:313-316. Bernert JT.280:135-140. Pharmacol Rev 2005. Tobacco Smoke and Involuntary Smoking.php. Sweeney CT. Flegal KM. Trends in the exposure of nonsmokers in the U. Benowitz NL. Benowitz NL. Benowitz NL. Available at URL: http://monographs.iarc. cigarette smokers: the Third National Health and Nutrition Examination Survey. Vol 38. DHHS). George CF. 1999-2002. International Agency for Research on Cancer. 4/13/09 International Agency for Research on Cancer. Caudill SP. Pirkle JL. Kozlowski LT. J Pharmacol Exp Ther 1999. 4/13/09 U. Office on Smoking and Health [online] 2006. Centers for Disease Control. 4/13/09 Iwase A. Tob Control 2006.280:152-156. Jacob P III. Department of Heath and Human Services.gov/ntp/roc/eleventh/profiles/ s176toba.63:139-43. Pechacek TF. Smoking and Tobacco Control Monograph 10 [online]. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Tobacco related exposures. Int Arch Occup Environ Health 1991. National Institute for Occupational Safety and Hygiene (NIOSH). Warner K. Giovino G.gov/tcrb/monographs/10/.S. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children. National Center for Chronic Disease Prevention and Health Promotion. Caraballo R. Richter PA. Herrera B. Available at URL: http://monographs. Jacob III P. Department of Heath and Human Services. 1999. Absorption and metabolism of nicotine from cigarettes.57(1):79115.114(6):853-858. References Armitage AK. Pickett MA. June.php. Pollack HA. Coordinating Center for Health Promotion. Benowitz NL. Aiba M. Turner DM. Mehta NY. Summary of Data Reported and Evaluation [online] 1986.S. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Epidemiol Rev 1996. [online]. Houseman TH.56:483-493. population to secondhand smoke: 1988-2002.pdf. and the United States. 11th ed. Jacob P III. Vogler GP. Kira S. Available at URL: http://www. Available at URL: http:// cancercontrol. Jacob P.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Perez-Stable EJ. 4/13/09 Centers for Disease Control and Prevention (CDC). Pirkle JL.18:188-204. Coordinating Center for Health Promotion. DHHS). Sosnoff CS. Available at URL: http://ntp. Hukkanen J. Tobacco Smoke. Clin Pharmacol Ther 1994. Tob Control 1998. Dollery CT. JAMA 1998. Exposure of the U. Ethnic differences in N-glucuronidation of nicotine and cotinine. Centers for Disease Control and Prevention. National Toxicology Program (NTP). Brody DJ. Metabolism and disposition kinetics of nicotine. IARC Monogr Eval Carcinog Risks Hum. BMJ 1975.fr/ENG/Monographs/allmonos90. JAMA 1996. 1988-1991. Third National Report on Human Exposure to Environmental Chemicals.94(2):314-320.S. Nicotine metabolism and intake in black and white smokers.275:1233-1240.7:369-375. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary.surgeongeneral.cancer. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects.291(3):1196-1203. Respiratory nicotine absorption in non-smoking females during passive smoking.niosh. Vol 83. Am J Public Health 2004.nih. 4/13/09 National Cancer Institute (NCI). Schober SE. available at URL: http://mtn. Environ Health Perspect 2006. Maurer KR.S. Brody DJ. Atlanta (GA): 2005. Strauss WJ. In Report on Carcinogens. Giovino GA.

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

2002). General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.100 (<LOD-.180) < LOD . 1998).S.140 (.449 and 0. Survey Geometric mean (95% conf.110 (<LOD-.140) < LOD . and it has not been rated by IARC or NTP with respect to human carcinogenicity.130-. and they range in concentration from 4% to 100%.100-.140) < LOD .210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .210) 964 1191 1013 1344 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .180 (.220 (..100-.140-. which may vary for some chemicals by year and by individual sample. Urinary N.N-Diethyl-meta-toluamide (DEET) N.N-Diethyl-meta-toluamide (DEET) CAS No.270) 688 678 518 700 598 956 Limit of detection (LOD.150) < LOD .170 (.100-.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. 134-62-3 General Information N. (Kolpin et al.110-.180 (. (U. population from the National Health and Nutrition Examination Survey. DEET is not genotoxic.. 2003). Additional information is available from U.S.S. After absorption.130 (. One survey detected DEET in 74% of sampled streams in the U. Sudakin and Trevathan. < LOD means less than the limit of detection.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 . 1998). Its use is recommended for prevention of several vector-borne diseases. Fourth National Report on Human Exposure to Environmental Chemicals 19 .110 (. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. There are over 225 insect repellents brands containing DEET.. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.110-.130) < LOD .210 (. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan. DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.100-. About 3-8% of dermally applied DEET is absorbed.130-.180 (.130-.520) < LOD . EPA.240) < LOD .S. DEET has low acute toxicity.110 (. 1995.250) < LOD .110 (.560) < LOD .100-.EPA at: http://www. including seizures and encephalopathy. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130-.EPA.120-.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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 . 2003).gov/pesticides/. DEET is not registered for use on agricultural commodities. Neurological effects in humans.160) < LOD . DEET is also used in combination with dermal sun screens (U. 2002).140) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.120-. have been reported as result of self-poisoning by ingestion or excessive dermal application.130 (. DEET can be applied to clothing and the skin to repel biting insects. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.190) < LOD .N.170 (. DEET is not a developmental or reproductive toxicant in animals (U.100-. 2005).EPA.130) < LOD .S.110 (.130 (.S.110 (<LOD-.epa.

270-. Survey Geometric mean (95% conf.240-.350) < LOD . Biomonitoring studies on levels of DEET provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEET than are found in the general population.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 .240) < LOD .S.150-. Urinary N.280 (.330 (.190-.350) < LOD .93) < LOD .140-..550) 688 678 518 699 598 956 < 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.280-1.270) < LOD .230-.330 (. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.200 (.440) < LOD .300 (.250 (.410-. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.270 (. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.630) < LOD .S. 2007). Urinary DEET levels as high as 5.320 (.170-.290-.190 (.370-. representative subsamples from NHANES 2001-2002.500) 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 .640 (.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130 (<LOD-.300) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .250-.490) < LOD . 20 Fourth National Report on Human Exposure to Environmental Chemicals .500 (.150) < LOD ..480 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.250) < LOD .230) < LOD .N.390-.190 (<LOD-.230-.350-. 1992).270 (<LOD-.N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.320) < LOD .410 (. 2005).690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.370) < LOD .190 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .410 (. In this survey period. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

S. Schoenig GP.N-Diethyl-meta-toluamide (DEET) References Arcury TA. J Toxicol Clin Toxicol 2003. Atlanta (GA).gov/oppsrrd1/REDs/0002red. Centers for Disease Control and Prevention (CDC).pdf. Osimitz TG. Smallwood AW. Sudakin DL. Chemical Summary.EPA. 2005. Reregistration Eligibility Decision (RED): DEET. Thurman EM.epa. metabolism.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography.epa.S. U.25:95-100. Zaugg SD. et al.EPA). 2005 Kolpin DW. Grzywacz JG. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Washington (DC): U. Trevathan WR. and excretion of N. Int J Toxicol 2002. Available at URL: http://www. Gabriel KL. DEET: a review and update of safety and risk in the general population. Page BC. Meyer MT.S. Available at URL: http://www.16(1):10-13. Environ Health Perspect 2007. 4/9/09 U. DeBord KE.36(6):1202-1211. and other organic wastewater contaminants in U. 1999-2000: a national reconnaissance. Bell JW. Toxicity and Exposure Assessment in Children’s Health. Diethyltoluamide (DEET). U. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.2:341352.115(8):1254-1260. EPA 738-R98-010. 1-118. N. Barber LB. EPA. Hartnagel RE Jr. Fundam Appl Toxicol 1995. streams. Environ Sci Technol 2002. September 1998. pp. Lowry LK. J Anal Toxicol 1992. Third National Report on Human Exposure to Environmental Chemicals. Tapia J. Barr DB. Environmental Protection Agency (U.N-diethyl-mtoluamide following dermal application to human volunteers.gov/teach/chem_summ/ DEET_summary.41(6):831-839.N. Quandt SA.S.EPA). Selim S. Furlong ET.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers.S. Pharmaceuticals. 1993-1997. Chen H. Human exposures to N. pdf. hormones.S. Absorption.S. Veltri JC. Environmental Protection Agency (U.

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

Calafat AM. Occup Environ Med 2002. Kawamura N. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. 2/4/09 Ouchi K. Cohen JT. National Institute of Environmental Health Sciences. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. Hanaoka T. In vitro and in vivo interactions of bisphenol A and its metabolite. National Institutes of Health. Bisphenol A. Zaugg SD. Kuklenyik Z.pdf. Biochem Biophys Res Commun 2003.S. Furlong ET. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. J Am Dent Assoc 2006. Rat two-generation reproductive toxicity study of bisphenol A. Yoshinaga J. Park S. Bradley S. Barr DB. 2003. Klinefelter GR. September. Ikka T. Available at URL: http://cerhr. Munro IC.312(2):441-448. Available at URL: http://cerhr.35(2 Pt 1):238-254. Marr MC. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. Research Triangle Park. Environ Health Perspect 2005. Szigeti-Buck. Watanabe S. N. Reprod Toxicol 2001. Haighton LA. Wong LY. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Kim YH.S. Brine DR. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection.69(22):2611-2625. Italy. Available at URL: http://ec. Hlywka JJ. Sottas CM. Kroes R. Barton L. Imai H. Nippon Eiseigaku Zasshi 2004. Shin HC. 5: 505-523. Koh WS.pdf . Available at URL: http://ntp. 2/4/09 Fujimaki K. Endocrinology 2008. Barr JR. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Matthews JB. Calafat AM.10:875-921. Watanabe C. Kolpin DW. Gender differences in the levels of bisphenol A metabolites in urine. 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. Barber LB. 2002. Pharmaceuticals. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Calafat AM. Han SY. Rubin C.137(3):353-362. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Tsugane S.116(1):39-44. NC. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Human Health.gov/chemicals/bisphenol/bisphenol. Timms BG. niehs. et al.113(4):391-395. Exposure of the U. 1999-2000: a national reconnaissance. Harazono A. C. Ispra. Serizawa S. Proc Natl Acad Sci USA 2005. Toxicol Sci 2002. Hum Ecol Risk Assess 2004. Ekong J. Thomas BF. Hughes C.nih. Kim CS. Reidy JA.eu/ health/ph_risk/committees/sct/documents/out156_en. November 26. Keimowitz AR. Ecotoxicity and the Environment (CSTEE). Chung MK.pdf. Meyer MT. Joint Research Centre Institute of Health and Consumer Protection. Lynch BS. An evaluation of the possible carcinogenicity of bisphenol A to humans. Yang M. Koulova AI.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt.niehs.pdf . Caudill SP. Doull J. Reidy JA. Needham LL. Twomey K.59(9):625-628. Myers CB. Chem Res Toxicol 2001. Ema M. MacLusky.nih. and other organic wastewater contaminants in U. DirectorateGeneral Health and Consumer Protection. Howdeshell KL.14(2):149-157.jrc. European Commission. Fujii S. Leranth. 2008.. Zacharewski TR.pdf. Department of Health and Human Services.59(4):403-408. Tyl RW. May 22. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Ye X.Scientific Committee on Toxicity. Furukawa M.J. K.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Rhomberg et al. Kiguchi M. Richter CA. Environ Health Perspect 2008. Cha SW. Endocrinology 2004.. Environ Sci Technol 2002.780(2):365-370.102(19):7014-7019. McConnell EE. Joskow R. Brussels.. August 2001. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). U. Cunha G. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Hara K.Environmental Phenols References Akingbemi BT.nih. Gray GM. 2/4/09 European Commission. Available at URL: http://ecb. Belgium. Thurman EM. National Toxicology Program.S. vom Saal FS. Regul Toxicol Pharmacol 2002. with estrogen receptors alpha and beta. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. et al. Kim JC. 2007.36(6):1202-1211. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. T. 4.149:988-994. Life Sci 2001. et al. hormones. niehs.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. bisphenol A glucuronide. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population.145:592-603. Arakawa C.gov/chemicals/bisphenol/BPAFinalEPVF112607.68(1):121-146. Needham LL. and Hajszan. Needham LL. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.europa. Han SS. streams. and Hardy MP. Pyo MY.

Morgan MK. Chem Res Toxicol 2002. Environ Res 2007. Yang M. Biological monitoring of bisphenol a in a Korean population. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. Witorsch RJ. Arch Environ Contam Toxicol 2003. Chang SS. Kim SY. vom Saal FS.103(1):9-20. Large effects from small exposures. Environ Health Perspect 2005.44(4):546-51. and nonylphenol at home and daycare.Environmental Phenols Volkel W. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Fourth National Report on Human Exposure to Environmental Chemicals 33 . et al.15:12811287. bisphenol-A. Dekant W.40(7):905-12. III. Csanady GA. Nagel SC. Hughes C. Sheldon LS. Filser JG. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Chuang JC. Endocrinology 2006. Vom Saal FS. Colnot T. Food Chem Toxicol 2002. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Jang JY. An observational study of the potential exposures of preschool children to pentachlorophenol. Kawamoto T. Lee SM. Lordo RA.147(6 Suppl):S56-69. Wilson NK. Welshons WV.113(8):926-33.

fish) and drinking water.30 (..60-3.300 (<LOD-.20) 314 715 1488 03-04 03-04 * * . outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates.50) .500) 75th .60-3.200-..1..497) * .700-1.10) 2.40) * 03-04 03-04 03-04 . < LOD means less than the limit of detection. Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e. and emulsifiers.60-3. population from the National Health and Nutrition Examination Survey. The alkylphenols can bioaccumulate in some fish.500-1. 4-octylphenol monoethoxylate was detected in 43. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. 140-66-9 General Information 4-tert-Octyphenol. Bian et al. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. The alkylphenol ethoxylates enter the environment through human use of products containing them.30 (1.60-3.600) . have demonstrated estrogenic effects particularly when injected at high doses in animals. and to alkylphenoxycarboxylates.900 (. which may vary for some chemicals by year and by individual sample. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.600) .500-1.30 (1.60) 613 652 1092 Limit of detection (LOD. through sewage.g. and some personal care products. impaired steroidogenesis. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.300 (<LOD-.00 (.80) 2. and from contact with some personal care products and detergents.600-1.3. leading to inhalation as another potential exposure route (Rudel et al.900 (.90) 2. an alkylphenol.90) 2.300 (<LOD-.. Katsuda et al. the various alkylphenols have also been used as emulsifiers and modifiers in paints. 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. Indoor and to a lesser extent.357 (.80 (1.20-2.40) 1.30 (1.. 1997. In 1999-2000.400) 1.600-1.50) 1.70 (1. Several alkylphenols.00 (..20-2. During the 1980s and 1990s.300-. 34 Fourth National Report on Human Exposure to Environmental Chemicals . 2000.500) .20) 1. industrial cleaners.S. 2000.30 (1.S.10 (.600) .30) 2.30) 90th 1. and impaired spermatogenesis (e. 2004). testicular atrophy.20-2.10 (.50) .600-1.800-1. 2003. altered estrus cycles and reproductive outcomes.300 (<LOD-.g.60) .900 (. Less frequently. Laws et al.600) 1. pesticides.20 (1. and was quickly eliminated from the blood (Certa et al.20) 2.20) 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 . In rats.2. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (.600-1.200-.10-2.400 (.600-1.600-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.300 (<LOD-.60-3.30) 1.274-. 1995.00) 1229 1288 03-04 03-04 03-04 * .80 (1.40) 2. see Data Analysis section) for Survey year 03-04 is 0. Disposition in humans has not been studied sufficiently. and through manufacturing waste streams (Warhurst.40) 2.299-.000 tons of alkylphenol ethoxylates were produced annually worldwide.500) .70 (1. Survey Geometric mean (95% conf. Blake and Boockfor. including 4-tert-octylphenol. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.80 (1.477) .60) 1.50-2.900 (. is used to manufacture alkylphenol ethoxylates.900 (. Saito et al. did not bioaccumulate. In the 1990s. 2006.389 (.369 (.507) * < LOD .5% of 139 U. Ying et al. orally administered 4-tert-octylphenol was well absorbed.70 (1.10 (1.. which are anionic surfactants used in detergents.10) 1.00 (1.268-. and some of their degradation products are toxic to aquatic life..60-3. textiles. streams in 30 states (Kolpin et al.400 (. over 500.70 (1.500) . to shorter chain alkylphenol ethoxylates. 2002). 2002).Environmental Phenols 4-tert-Octylphenol CAS No..20-2.400 (.20-2.50-3. Urinary 4-tert-Octylphenol (4-[1.40 (1. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.50 (1..50) 1. altered neonatal sexual development.30-2.300-.50) 1.20-2.40) 1. and the polyethoxy chain may consist of up to 50 ethoxy units. 1996).

435 (.65-3.78 (1.270 (.560) .269 (.33) 3.1. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.68-2.00) 1.76 (2.450) .81 (1.207-.280-.17 (.730-1.06 (2. 2001). Nagao et al.31 (1.53-3.740 (.470) 75th .540-1.02-4.05-2.276 (.380 (<LOD-.260 (<LOD-. Calafat et al.. Kawaguchi et al. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.62) .78) 3.68) 2.740 (. 1999).31-2.Environmental Phenols Myllymaki et al.03 (1. Survey Geometric mean (95% conf.550-1.199-.770 (.59 (1. representative subsample of NHANES 2003-2004.25) 90th 1. population from the National Health and Nutrition Examination Survey.54) * 03-04 03-04 03-04 . Yoshida et al.10-2.640-1.78) 1228 1286 03-04 03-04 03-04 * . Sweeney et al. 4-tert-Octylphenol is not considered directly genotoxic.370 (<LOD-.00 (.630-1.71) 2.60 (1.570) .25) 2.470-1.300 (<LOD-.450) 1.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.11-2. 2004).43) 1.610) .170-..40-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.460 (. 2001.160-.410 (.420) .22) . 2005.890-2. or their corresponding ethoxylates with respect to human carcinogenicity.470-1. It is unclear if estrogenic or other effects occur in animals through oral dosing.73) 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. 2000.3.03-6.40 (1.400) .20 (1.337-.270 (.43-3.59) 1.320 (<LOD-. nonylphenol. at lower or environmentally relevant doses (Blake et al. Tyl et al.29) 2.00 (.43) 1.00) 2.67-2.S.15) 1.64 (.860 (.03 (1. Fourth National Report on Human Exposure to Environmental Chemicals 35 .14) 314 713 1487 03-04 03-04 * * .. 2004.620) ..33 (2.00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .11) 2.384) * .530) .620-1.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.500-1.25-2. 2003.50 (2. IARC and NTP have not rated octylphenol.18-4.41) .. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U. In a small number of adult Japanese volunteers.62 (1. Urinary 4-tert-Octylphenol (4-[1.96-4. 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.910 (.36-3.270-.349) * < LOD .11) 1.62 (1.08) 1.85 (1.850 (.00) 2..

et al. nonylphenol.uk/resource/reports/ethoxylates_alkylphenols. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. Boockfor FR. Kookana R. Bolt HM.207(1):59-68. Wong LY. Endocrinology 2000. Environ Health Perspect 2008.37(20):4543-53. Saito I. Sakui N.foe.165(3):217-226. Myllymaki SA. Saito Y. Seely JC. Brody JG. Warhurst AM. Kolpin DW. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Fail PA. Cooper RL.18(1):43-51. and testosterone. Nakagomi M.pdf. Taya K. Indoor Air 2004. Estrogenic activity of octylphenol.S. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Rudel RA. Muller AM. Usumi K. Brine DR. Kawaguchi M. Toxicokinetics of p-tert-octylphenol in male Wistar rats. 36 Fourth National Report on Human Exposure to Environmental Chemicals . J Chromatogr B Analyt Technol Biomed Life Sci 2004. An environmental assessment of alkylphenol ethoxylates and alkylphenols. et al. Reidy JA. Environ Int 2002. Qian J. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Takenaka A. Barber LB. Yoshida M. Ono H.Environmental Phenols References Bian Q. Anal Chim Acta 486:41-50. Onuki A. Furlong ET. Song L. Chen J. Raychoudhury SS. Yoshimura Y. Two-generation reproduction study with para-tert-octylphenol in rats.36(6):1202-1211. Makino T. Haavisto TE. Fedtke N. Thurman EM. Needham LL. 2003. Arch Toxicol 1996. Camann DE. Nagao T. Taya K. Yoshida M. Inoue K. et al. Tyl RW. polybrominated diphenyl ethers. Bodman GJ. Available at URL: http:// www. Ferrell JM. Spengler JD. Certa H. Indoor air pollution by alkylphenols in Tokyo.15(6):683-692. Environ Sci Technol 2003. Regul Toxicol Pharmacol 1999. Blake CA. Zaugg SD. Okada F.116(1):39-44. Myers CB. Nicol L. Ye X. Pharmaceuticals. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone. Maekawa A. Reprod Toxicol 2001. Horie M. Food Chem Toxicol 2006. 1995. 2/4/09 Ying GG. Millette CF.57(2):255-266.folliclestimulating hormone. Inoue K. pesticides.30(2 Pt 1):81-95. Meyer MT. bisphenol A and methoxychlor in rats. and sertoli cell number.71(1-2):112-122. Williams B. Biol Reprod 1997. Wiegand HJ. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. Brooks AN. prolactin. Carey SA. Maekawa A. Yoshimura S.44(8):1355-1361. Watanabe G.28(3):215-226. hormones. Watanabe G. Blake CA. Sweeney T. streams. Toppari J. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. testis size.799(1):119-125. Izumi S.S.co.141(7):2667-2673. Toxicol Sci 2000. Calafat AM. Seto H. Nair-Menon JU. and other endocrine-disrupting compounds in indoor air and dust. Toxicol Lett 2001. Ito R. Exposure of the U. Karjalainen M. Toxicol Appl Pharmacol 2005. alkylphenols. 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. Wang X. McCoy GL. Korn LR. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. et al. 1999-2000: a national reconnaissance. Takai N. Paranko J.14(5):325-332. Katsuda S. Kawaguchi M. Laws SC. and other organic wastewater contaminants in U. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Xu L. Environ Sci Technol 2002. Katsuda S. Phthalates. Reprod Toxicol 2004. Boockfor FR. Marr MC. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Roche JF. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004.121(1):21-33.54(1):154-167. Toxicol Appl Pharmacol 2000.

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

4) 51. Survey Geometric mean (95% conf.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 9.3-15.2-58. interval) 12.6-15.6-65. Survey Geometric mean (95% conf.93 (7.1) 13.8-63.9) 7.0 (36.5) 66.11-11.1 (8. Urinary Triclosan (2.45 (5.20-13.6) 31.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.6-111) 33.82 (8.7 (9.8) 7.2 (37.5) 20.10) 84.72-13.32-14.29-12.0-19.2-46.40-11.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.4 (11.7) 123 (36.4.7 (14.20 (7.50-10.2) 12.0) 65.8-85.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.55 (4.8) 14.S.6 (12.1) 11.38-18.3 (8.9) 32.5-86.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.6 (9.6) 10. see Data Analysis section) for Survey year 03-04 is 2.5 (11.9 (33.7) 292 (151-432) 132 (78.8) 116 (39.4) 73.2 (25.30-14.9) 75th 47.20-11.0 (8.1 (15.4) 357 (225-456) 203 (87.3-67.20-10.70-16.4 (12.0 (34.48-10.3) 10.9-61.3-35.89-11.6) 39.2 (13.8-127) 37.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.3 (26.0 (11.3 (9.9 (8.1-39.7 (28.18 (5. population from the National Health and Nutrition Examination Survey.00 (4.94 (7.8-60.80 (5.5-14.1) 50.1) 14.4-19.6) 12.3-31.4 (32.3) 6.40-17.4) 317 (231-433) 144 (96.1) 9.6-14.5) 13.1) 9.45-10.5) 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 .4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.8 (21.0 (26.10-9.2 (11.92-12.1) 9. population from the National Health and Nutrition Examination Survey.7) 10.4) 90th 249 (188-304) 03-04 03-04 03-04 8.54 (8.6 (10.7 (11.4) 25.45-13.4-18.48 (8.1) 9.9-236) 193 (90.0) 9.0-73.2-14.00-8.4.8-112) 30.20 (7.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6-14.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.3 (11.0) 49.8) 9.6) 90th 212 (172-241) 03-04 03-04 03-04 9.7 (39.6-37.S.Environmental Phenols Urinary Triclosan (2.3.1) 7.60 (8.2 (27.21 (6.6 (30.2) 13.22-10.4) 75th 43.9 (11.16 (6.9 (50.1 (45.9) 8.50) 10.6-20.90-10.2-58.43-13.2 (10.4) 7.4 (38.86-12.0-15.60 (6. interval) 13.74 (5.3) 47.2) 9.0-15.

Needham LL. Bhargava HN. Evidence of 2. 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. Photolytic degradation of triclosan in freshwater and seawater. Barber LB. Arch Environ Contam Toxicol 1988. et al. Okui T. Ekstrand J. Kolpin DW. Shiratsuchi H.36(6):1202-1211. population: 2003-2004. Gomez MJ. Pilot study of urinary biomarkers of phytoestrogens. Furia T. Sandborgh-Englund G. Mezcua M. Odham G. Adolfsson-Erici M. Gunderson MP. Toxicology of 2. Readman JW. Katsura E. IMS Ind Med Surg 1969. 1999-2000: a national reconnaissance. Teitelbaum SL. Ebersole R. Anal Chim Acta 1004. Percutaneous penetration and dermal metabolism of triclosan (2. Kaneshima H. Britton JA. Levy SB. Williams FM.28(9):1748-1751.67(4):532-537.7/2.524:241-247. Wong LY. Osachoff H. phthalates. Moss T.23(5):579-583. 4’-trichloro-2’-hydroxydiphenyl ether. Zaugg SD. Bennett ER. Environ Sci Technol 2002. Fourth National Report on Human Exposure to Environmental Chemicals 39 . streams. Ogawa H. Hong HC. Wigmore H. Lyman FL. Erratum in: Aquat Toxicol 2007. Chelimo C. Environ Health Perspect 2008. hormones. Furlong ET. Biol Pharm Bull 2005. Aquat Toxicol 2006. Nagao Y. Pharmaceuticals. Ferrer I. and other organic wastewater contaminants in U. Pinney SM. Hirano M. Williams PE. Mar Environ Res 2000. Br J Clin Pharmacol 1987. et al. Environ Health Perspect 2007. Gilbert RJ.38(2):64-71. Windham G. Clapson DJ. Kanetoshi A. and phenols in girls. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Foran CM. Meyer MT.66:1052-1056.24(3):209-218.4’-trichloro-2’hydroxydiphenyl ether). Calafat AM.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Triclosan: applications and safety.80(3):217-227. Ishibashi H. Matsumura N.17(5):637-644. Thurman EM..116(3):303-307. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Fernandez-Alba AR.83(1):84. Bodey GP.38(4):361370.Environmental Phenols References Aiello AE. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development.S. J Toxicol Environ Health A 2006.4. Aguera A.69(20):1861-1873. Wolff MS. Benson WH. et al. Pharmacokinetics of triclosan following oral ingestion in humans. Leonard PA. J Invest Dermatol 1976. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Am J Infect Control 1996. Food Chem Toxicol 2000. Chemosphere 2007. Ye X. Aranami K. Skirrow RC.50(1-5):153-156. Veldhoen N. Howes D. Watanabe N. Larson EL. Reidy JA.115:116-121. Hernando MD. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. 4.S.45 Suppl 2:S137-S147. et al. The oral retention and antiplaque efficacy of triclosan in human volunteers.

350) < LOD . are eliminated in the urine.350) < LOD .960) 1.350 (.390 (. water and sediments because of the large amounts that were produced and used historically.350) < LOD .65 (. PCP is distributed to most tissues and is not extensively metabolized.350) < LOD .350 (.350-.350-.25 and 0.98 (1. PCP is eliminated over a few days (Braun et al.350-.32 (.350-.890 (. mollusicide. and possibly of lindane (IPCS.00 (.350 (. utility poles and fence posts).70) .47-5.350-1.990-2.62 (.350-. < LOD means less than the limit of detection.350-1.350 (.350-.30) . along with small amounts of tetrachlorohydroquinone and conjugates.350) < LOD .Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.76) .37) .30) 1.350-2.10) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..350-.350 (. 1979).890-1. 2002. Since 1984. algaecide and insecticide.83 (2.350 (.90) 2. and animals. the elimination half-life may be a week or more (Uhl et al.70) 2. plants. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.00) 1.67) 1.. ingestion of contaminated food or water.65 (. PCP cannot be used on wood in residential or agricultural buildings.350) < LOD . with repeated or chronic exposure.80) .91 (1.47-3. After a single dose.350-1.33-2.350-1.350-2.630 (.350-.90) 1.350) < LOD .350) < LOD .53) size 1994 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .350-.350) < LOD .350) .g.350) < LOD < LOD 75th .. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.30 (1.350-.58-2.860-2. and dermal contact with PCP-treated products. Kohli et al.350) < LOD .40 (.350) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.350-.94 (1.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.350 (. After absorption.350-.76) 1.350 (. hypertension.30 (.01 (<LOD-1.660 (..350) < LOD .30 (. PCP use in the U.350) 90th .5.60) 1.390 (.350 (. which may vary for some chemicals by year and by individual sample. Human exposure to PCP has become less common.350-.350 (.350) < LOD . Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.350-. Acute.680-1. population from the National Health and Nutrition Examination Survey. Effects including hyperthermia.90 (1. 1997).590-1. To-Figueras et al.350-. and metabolic acidosis were observed in CAS No.350-2.500-2.350-.10 (. In the environment.350-. 1986).350 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .23 (. The parent compound and conjugates. PCP has been detected in soils.990 (<LOD-2.350) < LOD .94 (1.78) 1.10) 1. herbicide.08-3.350) < LOD .350-2. General population exposure to PCP may occur by inhalation of contaminated air. bactericide.350 (.350-2.510-5. 40 Fourth National Report on Human Exposure to Environmental Chemicals . so it is relatively non-persistent.350 (.980 (.42) 696 680 521 696 603 951 Limit of detection (LOD.350 (.530) 1. PCP is degraded by sunlight and metabolized rapidly by microorganisms. 1976.510-3.350 (.48 (.350-.350 (.350-.73 (1.650 (.S.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .S.350 (.00) 2.64) 1.10 (1.75) 2. has been restricted.54-2.350-.650) 1.09) .00) 1.45-2.350 (.350-.10 (<LOD-1.33) .850-2. Survey Geometric mean (95% conf.350-.58-2.48-2. 87-86-5 Also a Metabolite of Several Organochlorine Insecticides General Information Pentachlorophenol (PCP) and its sodium salt were once widely used as a fungicide.04) 1.50) 1. other polychlorinated benzenes.51) 1. and it is used primarily as a preservative for wood to be used outdoors (e.37 (. 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 (. air.18 (<LOD-1.350 (.350 (.770 (.60) 1.. PCP is absorbed rapidly and well by all exposure routes.480-2.30) 1.350) < LOD .

900-1.250 (.780) < LOD .310) < LOD .500-1.0 mg/L.320) < LOD .. respectively) (Becker et al. population from the National Health and Nutrition Examination Survey.500-.92) 1.06 (.S.270-.html.330-.300 (.00) 1.e.570 (.360 (.78) 1.800-1.S..590-1.40) 1.25 (1.350) < LOD .79) 1.910-1.52 (<LOD-1.34 (. and the FDA has established a standard for bottled water.56) 1.gov/ toxpro2.18 (1.25-1.25-2.560) < LOD .220-. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.82) 1. chronically administered high doses of PCP were hepatotoxic.35) 1.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .94 (1.26 (1.650) 90th 1. In animals.580-.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.84-4.310-.380-. and adversely affected thyroid function (U.35-2. 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.. environmental levels) and health effects is available from the U.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * . carcinogenic.280) < LOD . respectively) (Seifert et al. Pentachlorophenol is not mutagenic or teratogenic.290-.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 .57 (1.06-3.19) 2.370 (.67 (1.21 (. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.920 (.67-3. van Raaij et al. or skin absorption.09 (<LOD-2.290) < LOD .430-.69 (1.84) 1.340-.EPA.300 (.260 (. 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. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.320) < LOD . Among adults in the NHANES 1999-2000 subsample.09-1. 1995). 2004.9 mg/L.830) < LOD .00-1.36) .240-.490) < LOD .16-1.67 (1.440 (. inhalation..10-2.atsdr.78) 1.52 (1..430) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.S.510-.25) 1.06) 1.18) . 2003).35) 1.90) 1.710-1. Fourth National Report on Human Exposure to Environmental Chemicals 41 . 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.760 (.420) < LOD .gov/ pesticides/ and from ATSDR at: http://www.470 (. In a small sample of U.67-3.990 (. 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.75 (<LOD-2.630 (.52 (<LOD-1.10 (1.800) < LOD 1.320) < LOD < LOD 75th . EPA at: http://www.270-.560-.52) 1. In NHANES 2001-2002 subsamples.S.11) 2.51) 1.30) 1.220-. 1991).250 (.35-2.Fungicides adults and children severely exposed to PCP through ingestion.S.30-2.95) 3.780-1..26 (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.19 (1.40) 1.40) 1.82 (1.16 (.290-.300 (.510-.48-2.25 (1.40-2. EPA has developed standards for PCP in drinking water and the environment.40) 1. children in the 1980’s.29-3. 1989).94-3. 2003).700-2.84 (1.13 (.30) 1.57 (.55) 1.650 (. OSHA has established an occupational standard. 2000). More information about external exposure (i.73 (1.00-1.83 (1.epa.950-1.590) < LOD .19) 2.67 (1.950-1. Death can result from seizures and cardiovascular collapse.67-2.30 (.cdc.400 (.6 and 14.21-2.610 (.650 (.67 (1. The U.40) 1.320 (.950-1.850 (.360-.67 (1.730) < LOD .08 and 5.25-2. 1989).19) 2.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .500 (.. 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.560) < LOD ..94 (1.75) 1.

54(3):203-208. U. htm. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Dev Toxicol Environ Sci 1979.10:552-65. et al. Safe A. Phillips DL. Bailey SL. et al. Can J Biochem 1976.org/documents/jmpr/jmpmono/2002pr08. Bragt PC. Sala M. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. Needham LL. Hill RH. Seifert B. 4/21/09 van Raaij JA. et al.S. The metabolism of higher chlorinated benzene isomers. PCP: Human Risk Characterization [online]. 4/21/09 Kohli J. Barrot C. Environmental Protection Agency (U. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Schlatter C. Arch Toxicol 1986. Holler JS. Otero R. Fast DM. 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. Chenoweth MB.4:289296. To-Figueras J. Seiwert M. Needham LL.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. 2002. Krause C. drinking water and indoor air. Gregg M. Arch Environ Contam Toxicol 1989. 11/30/2004. Head SL.58:182-186. available at URL: http://www. To T. Environ Res 1995. Cline RE.18:475-481. Arch Environ Contam Toxicol 1989.18(4):469-474. References Becker K. J Expo Anal Environ Epidemiol 2000. Braun WH. Lindane. Toxicology 1991: 67(1):107-16. EPA). Shealy DB. Santiago-Silva M. 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. Pesticide residues in urine of adults living in the United States: reference range concentrations. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Seifert B. Jones D. Schulz C. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Engel R. Uhl S. Schmid P. Schulz C. Kaus S. Rodamilans M. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. r e g u l a t i o n s . Notten WR. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population.71:99108. hair. Pharmacokinetics of pentachlorophenol in man. van den Berg KJ.inchem.105(1):78-83. Int J Hyg Environ Health 2003. Becker K. Smith SJ. Hill RH Jr. International Programme on Chemical Safety (IPCS). urine. Environ Health Perspect 1997. Helm D.S. Available at URL: h t t p : / / w w w. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Blau GE. Hill RH Jr. 206:15-24. Seiwert M. Baker S. house dust.

50 (1.40 (. Most agricultural food applications have been revoked.570 (.07 (.10) 2.34) 1.S.389-. 90-43-7 General Information Ortho-phenylphenol (OPP.490 (<LOD-.480-1.30-2.590-2. or 2-phenylphenol) and its water-soluble salt.92 (.40-7. Cnubben et al.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .740 (.433-.600) < LOD .90) . OPP is efficiently absorbed from the gastrointestinal tract and through the skin.600-1. 2006).552 (.10) 1.560-8.02) 1.636) * . such as fruits and vegetables. and as a wood preservative.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 . OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.600-1.690-1. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al.Fungicides ortho-Phenylphenol CAS No.00) .410-.20 (1.27 (.22 (.50) < LOD .349-.470 (<LOD-. < LOD means less than the limit of detection.508 (. Estimated human intakes have been below recommended intake limits (U. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Both chemicals degrade within hours to weeks in the environment (U.50) < LOD .490 (<LOD-.498 (. on ornamental plants and turfs.00-2.S. 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.490 (<LOD-. and sanitizers.20) < LOD 2.600) < LOD 75th .20 (1. are antimicrobial agents used as bacteriostats.EPA. which may vary for some chemicals by year and by individual sample.420 (<LOD-. 1998).10) .09) 2.EPA.830 (.50-3.690) < LOD .496 (.610-1. population from the National Health and Nutrition Examination Survey.890 (. 1989). or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.840-1.836) * . Fourth National Report on Human Exposure to Environmental Chemicals 43 .80) 1.76) 1.880-2.930 (. EPA.750-2.20 (. In the past. inhalational.645) * .00 (1.85) 2.710) 3.624) * . Available evidence suggests that OPP does not accumulate in the body.890 (. however.696) * .402-.60 (1.90) 1.370-.30-7.50 (1.742) * .450 (<LOD-.50) 1.770 (.28 (.61) 2.20) < LOD 1.389-.493 (. 2006).10 (1.370-.17 (. OPP is still used as a disinfectant fungicide for industrial applications. and it has limited water solubility. General population exposure can occur via dermal.790) 2. OPP is considered to be moderately toxic after acute oral doses in animal studies.497 (.850 (.19 (. fungicides. interval) .00 (1.50) .40-5.60-3.10) .600) < LOD .621) * .466 (. in paints.60-2. 2002.890) 1.710-2.630) < LOD . 2006). Both have been used in agriculture to control fungal and bacterial growth on stored crops.33 (.90) .40-5.80) 1.90) 2.638) * .509 (.550-1.30) 1.50-2. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.570-. Workers who manufacture.490 (<LOD-.780) < LOD .860 (.364-.20-2.00) < LOD . OPP is volatile.490 (<LOD-. leaving the chemical residue OPP.950) < LOD .80-3.30 (1.60 (1..50-4.20-3.50) < LOD .970 (.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .80 (2. SOPP is applied topically to the crop and then rinsed off.640) < LOD .350-1.570-2.00) . 1998.770 (.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.390-.580-1.60 (1. but OPP and SOPP are still used on pears and citrus (U.370-.386-.500-2.820 (.10) . 2006).450 (<LOD-.760-2..610 (. sodium ortho-phenylphenate (SOPP).90 (1.570 (. or apply these chemicals may be more highly exposed than the general population. whereas SOPP is not volatile and is more water soluble.10 (1.670) 2.S.03) 1. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.23) 695 680 520 695 603 953 Limit of detection (LOD.600-1.567 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50 (1.00 (1.3 and 0..20) 2.600) < LOD 1.3.88) 1.14 (<LOD-3. Survey Geometric mean (95% conf. it was used in home sanitizers for surfaces.450 (<LOD-.S.90 (1.00 (1.10) 1.10-2.22) 2.30) < LOD 90th 1.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .800-3.30) < LOD .40-2.520 (.540-2.30) < LOD 1.570-1. Timchalk et al. formulate.10-1.28-3.

420 (<LOD-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..44 (1.900) < LOD .620-1.21 (.470 (<LOD-..311-. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel. 2002. 2000. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.33) . reproductive.600-1.96 (1. or developmental toxicity was observed (Bomhard et al.514 (.248-.950) < LOD .. Smith et al.24-2.17 (.470) < LOD . 1997.620-1.06 (1.656) * .64 (2.09 (1.810-1.06-4. 2005). Additional information is available from U.640-1.11 (.88-4. less likely.496 (.11 (.05-2.480-.13) 1..11) < LOD 90th 1.910 (<LOD-1.25-6.343 (.75 (1. 1999. but no neurologic.00 (1.780-14.17) 2.750-2.453 (.Fungicides anemia.S.12) < LOD 1.444 (..01) 1.550) < LOD .96 (1.403-.291-.29) 1. 44 Fourth National Report on Human Exposure to Environmental Chemicals . 1984.17 (.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 .38) 2.980 (<LOD-1. CDC. 1999.670 (.666) * ..329-.17) * 99-00 01-02 99-00 01-02 99-00 01-02 . 2002).06-5. 1998.29) 1.26) 1.770-2.4) 3. Murata et al.900-1.860 (. 2005). Ito et al. Biomonitoring Information Urinary OPP levels reflect recent exposure.568) * .S.24-2.27) < LOD .670 (. leading to production of two metabolites.382 (.08-1.62) .30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .980 (.47) .93) 1.750 (.43 (1.28 (<LOD-4..38-3.560-2.93) . OPP was not found to be mutagenic.910 (.610) < LOD 1.43-2.353-.78 (2. 1993.32) 3.11-1.301-. Nakagawa et al.508) * .750 (.61 (2.28 (2. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.484) * .410 (<LOD-.800-1.460-.860 (.84 (1.550-.97 (2.590) * .96) 1.940-2. Brusick.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.780 (.08-2. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.473) * .61 (.558) Selected percentiles ( 95% confidence interval) Sample 95th 2. Zhao et al.32) 1.91 (1. by possible genotoxic mechanisms (Hagiwara et al.380 (.gov/pesticides/.. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.580) < LOD .840 (..690 (.270-. Detectable levels were seen in over half the U.0) 1.04-4.75 (1.61 (1.S.11) 4.361-.500) < LOD . 1984.410 (<LOD-.89 (1.21) 1.86 (1.07) 2. 1992. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect. 1986).31) < LOD .EPA at: http:// www.670) < LOD .650-1.00 (.. ortho-phenylhydroquinone and ortho-phenylbenzoquinone.990) < LOD .93) . Pathak and Roy.02 (.20) < LOD 3.440 (.43) 3.910-1.epa.53) 1. 2005.69 (1.40-13.58) 2.09-3.880-1. and it has classified OPP as not classifiable with respect to human carcinogenicity.08) 1.580-1.510 (<LOD-. In high dose animal studies. Bomhard et al.510-.EPA 2006).59) 1.59) .21-2.360 (<LOD-.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 . or.970) 1.420 (<LOD-.810) < LOD .560) < LOD 75th .385 (. Survey Geometric mean (95% conf.51-3. U.52 (. IARC has classified SOPP as a possible human carcinogen.570) < LOD 1.74 (1.38) 1.18) 2.455-.09-6. 2002. 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.EPA 2006). Kwok et al.320 (<LOD-.93 (1.46) < LOD 1.12-2.S.96-4.791) * . U.550 (. interval) . Volunteers exposed to 0.4 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.33-2.81) 1. Biomonitoring studies on levels of OPP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of OPP than are found in the general population.43-2.S.

150(2):402-413. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Bartels MJ. Regul Toxicol Pharmacol 2002. IARC Sci Publ 1984. Environ Mol Mutagen 2005.S. J Agric Food Chem 2002. Buchholz BA. Bormett GA. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. et al. Gierthy J.pdf. Mendrala AL.159(1):18-24.gov/oppsrrd1/REDs/ phenylphenol_red. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Vogel JS. EPA-560/5-89-003. Environmental Protection Agency (U. Brendler-Schwaab SY. Hirose M. Bartels MJ. Elliott GR.niehs. Zhao S. 90-43-7) in Swiss CD-1 mice (dermal studies). Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Ito N.20(5):851-857. Available at URL: http://www. Glas K. Ito N.28(6):579594. Arnold LL.50(11):3351-3358. Atlanta (GA). Available at URL: http://ntp.. Bartels MJ. Drugs. Moore GA. Sangha GK.nih. Meuling WJ. 1989. J Agric Food Chem 2006.(56):399-407. Hakkert BC. U. Bomhard EM. Biochem Pharmacol 1992. Roberts AL. et al. Shirai T. Mutat Res 1993. Arch Toxicol 2000. Cano M. Coelhan M. Selim S. Kwok ES. National Toxicology Program (NTP). Fourth National Report on Human Exposure to Environmental Chemicals 45 .22(10):809-814.S. Hagiwara A. McNett DA. Moldeus P.35(2 Pt 1):198-208. Tayama S.S. Fukushima S. Eastmond DA. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol.Fungicides References Appel KE. van de Sandt JJ. Bromig KH.17(8):411-417. Kawanishi S.gov/ntp/htdocs/LT_ rpts/tr301.epa. Bartels MJ. Xenobiotica 1998. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Timchalk C. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. J Chromatogr B Biomed Sci Appl 1997. Toxicol Appl Pharmacol 1998. Third National Report on Human Exposure to Environmental Chemicals. 4/9/09. Environmental Protection Agency (U. Murata M. Brusick D. Christenson WR. Hagiwara A. Hum Exp Toxicol 1998.pdf. Fukushima S. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Christenson WR. Inoue S. St John MK. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Timchalk C. March 1986. Eadon G. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Smith RA.S. EPA).74(2):61-71. Narang A. Food Chem Toxicol 1984. Centers for Disease Control and Prevention (CDC).54(16):5731-5735. EPA 739 R-06004. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Identification of SARA compounds in adipose tissue. 2005. Brzak KA.45(5):460-481. U. July 28. Cnubben NH. Shibata M. Imaida K. The carcinogenicity of the biocide ortho-phenylphenol.32(6):551-625. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). 4/13/09 Onstot JD. Freyberger A.703(12):97-104. Leser KH.43(7):14311437. 2006. rat and man. Crit Rev Toxicol 2002.EPA). Stanley JS. Comparative metabolism of orthophenylphenol in mouse. Richter M. Roy D. Nakagawa Y. Moriya K. Herbold BA. Turteltaub KW. Office of Toxic Substances. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Carcinogenesis 1999.286(2):309-319. Pathak DN. Sangha G. Toxicol Appl Pharmacol 1999.

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

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

1. population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. 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 . 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.Herbicides Urinary Acetochlor mercapturate Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. which may vary for some chemicals by year and by individual sample. Urinary Acetochlor mercapturate (creatinine corrected) Metabolite of Acetochlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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.S.S.

Kier L. Kinney PL. Davison KL.17(6):559-566. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Rose RL. Dialkylquinonimines validated as in vivo metabolites of alachlor. Quistad GB. J Expo Anal Environ Epidemiol 2005. Wratten SJ. EPA). Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Sci Total Environ 2000. Thurman EM.EPA): http://pmep. Hladik ML.cce. et al. Battaglin WA. Heederik D. Barr JR.15(6):500-508. 1998. Chem Res Toxicol 1998. and metolachlor herbicides in rats. Barr DB.108(12):1151-1157. Occurrence of sulfonylurea. Xenobiotica 1994. J Expo Sci Environ Epidemiol 2007. Barr DB. imidazolinone. epa. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.pdf.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Green T. EPA 738-R-00-009. Wilson AG. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Reynolds SJ.S. sulfonamide. Deddens JA. Camann DE. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Number 15. Environ Sci Technol 2005. Linhart SM. 2000. Roberts AL. March 2006. pages 3682-3690. Burkhardt MR.S. EPA). Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Hum Exp Toxicol 1996.24(10):1003-1012. Environmental Protection Agency (U. Feng PCC. Furlong ET. Peter CJ. Acetochlor (Harness) Pesticide Petition Filing 1/00. Hines CJ. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Hein MJ. Linderman R. Ward EM. Jefferies PR.39(17):6561-6574. acetochlor. Hsiao JJ. Tinwell H. Sanderson WT. Whyatt RM. Bravo R. Larsen GL.37(4):10881093. Environ Health Perspect 2000.cornell. 2005. et al.15(9):702-735. Third National Report on Human Exposure to Environmental Chemicals. 5/30/06 U. Available at URL(non U. U. Centers for Disease Control and Prevention (CDC). Volume 65. Striley CA. J Agri Food Chem 1989. Feil VJ. Environ Health Perspect 2003. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. reservoirs and ground water in the Midwestern United States. Barr DB.gov/oppsrrd1/reregistration/REDs/acetochlor_tred.S. Coleman S. Casida JE. Atlanta (GA).html. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry.248(2-3):115-122. Olsson AO. Kolpin DW.111(5):749-756.11(4):353359.S. Sci Total Environ 2000. Alavanja MC.Herbicides References Ashby J. Available at URL: http://www. et al.248(2-3):123-133. Federal Register: January 24. Curwin BD. Andrews HF. 5/30/06.S. Environmental Protection Agency (U. Comparative metabolism and elimination of acetanilide compounds by rat. Hodgson E. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. and other herbicides in rivers. Lefevre PA.

1995. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC. Since the late 1980s alachlor use has been declining. Additional information about is available from U. Feng and Wratten. In a study of applicators and workers exposed to alachlor. 1994.2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown...EPA. including corn. and on non-crop land for general weed control. (2003) showed that 2. Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates.S.6-diethylaniline and its reactive metabolite. but another metabolic pathway can produce 2. 1998).gov/pesticides/. 50 Fourth National Report on Human Exposure to Environmental Chemicals . formulators. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS..epa. 2000. 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 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. the dermal exposure route is potentially significant for applicators. 2003). stomach.EPA. 1996. EPA at: http://www. the latter may account for some observed effects (Davison et al. 1999.. 2003). Jefferies et al. but has not shown developmental or reproductive toxicity in mammalian systems (U.. 2003). 1995).... mercapturate conjugates were predominant metabolites.S. WHO. WHO. WHO. Kolpin et al. It is absorbed by plants and inhibits plant protein synthesis. 2005). 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. NTP and IARC do not have ratings regarding human carcinogenicity. 1989.EPA. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect.. and uveal degeneration. peanuts and other crops. Alachlor has a soil half-life of a few weeks. WHO. 1997. U. about 20-25% of the U. Biomonitoring studies on levels of alachlor mercapturate provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of alachlor than are found in the general population.S. and field workers.S. soybeans. U. U. alachlor has demonstrated hepatotoxicity. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. Hill et al. whereas 60% of applicators had detectable amounts. In chronic animal testing.EPA considers alachlor to be a probable human carcinogen at high doses.1 to 1. 1998. General population exposure to alachlor may occur through consumption of contaminated food or drinking water.Herbicides Alachlor CAS No. as measured through conversion to deethylamine. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. USGS. Alachlor itself is not considered mutagenic. hemosiderosis. but not likely at low doses. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. Because it can be absorbed through skin. Hladik et al. 1998). 1998). U. 1998. corn cropland was treated with alachlor. 1998. In 1993-1995. mean values of urinary concentrations of alachlor metabolites. In animals. 2005. 1999 and 2007. Alachlor has low potential for acute toxicity. 1996..EPA.S.EPA. 2003).S. but shows little bioaccumulation. 1988. Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. In animal studies.1 mg/L at various collection times (Sanderson et al. Estimated human intakes have been below recommended limits (U. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al.S. ranged from 0. 2000.S. Tessier and Clark. Hines et al. IPCS.

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. see Data Analysis section) for Survey year 99-00 is 1. * 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. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.S. < LOD means less than the limit of detection. Urinary Alachlor mercapturate (creatinine corrected) Metabolite of Alachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 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.18. 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.S. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 51 . Survey Geometric mean (95% conf.

Sci Total Environ 2000. Lau H. Feil VJ. Brown KK. 1999. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Feng PCC. Quistad GB. DNA adduct formation by alachlor metabolites.pdf. Hill AB. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Environmental Protection Agency (U. Kolpin DW. 1998. EPA 738R-98-020. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Casida JE. Supplemental Technical Information (available on-line only). Martens MA. Background document for development of WHO Guidelines for Drinking-water Quality.usgs. Thelin GP. 2/27/09 U. Roberts AL. 2003.24(10):1003-1012. Andrews HF.18(6):363-391. Burkhardt MR.11(4):353359. Dialkylquinonimines validated as in vivo metabolites of alachlor. imidazolinone. Wratten SJ. Jefferies PR. Barr DB. Hill RH Jr. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.39(17):6561-6574. 4/2/09 U. World Health Organization (WHO).org/documents/pds/pds/pest86_e. Reregistration Eligibility Decision (RED) Alachlor. Bull Environ Contam Toxicol 1996. Hsiao JJ. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Hladik ML. acetochlor. An evaluation of the carcinogenic potential of the herbicide alachlor to man. Furlong ET. Circular 1291. revised February 15.248(2-3):115-122. Clark JM. and metolachlor herbicides in rats. International Programme on Chemical Safety (IPCS).inchem.248(2-3):123-133. Comparative metabolism and elimination of acetanilide compounds by rat. et al. J Ag Food Chem 1995. Geneva. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. 2/27/09 Jefferies PR. Driskell WJ. Whyatt RM.epa. 2005. Available at URL: http://www.56(9):883-889. Available at URL: http:// www. Mutat Res. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Heydens WF.37(4):10881093. Ann Occup Hyg 2003. Tessier DM. J Agri Food Chem 1989. Shoemaker DA. Thurman EM. 86. December 1998. No.S. Kimmel EC. Thake DC. Environ Sci Technol 2005. Hum Exp Toxicol. Occurrence of sulfonylurea. California. EPA). Sci Total Environ 2000. Brown MA. Alachlor in Drinking-water.44(18):1325. Shealy DB. Available at URL: http://www. Centers for Disease Control and Prevention (CDC). reservoirs and ground water in the Midwestern United States. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Hines CJ. Deddens JA. Quistad GB. Larsen GL. sulfonamide. U.S. Biagini R. et al. Tolos W. WHO/ FAO Data Sheets on Pesticides. World Health Organization. 1996. Sacramento. and other herbicides in rivers. Chem Res Toxicol 1998. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Sanderson WT.395(2-3):159-171. Kier LD. Third National Report on Human Exposure to Environmental Chemicals. Environ Health Perspect 2003. Striley CA.S. ALACHLOR.int/water_sanitation_health/dwq/chemicals/en/alachlor. Am Ind Hyg Assoc J 1995. Life Sci 1988. Geological Survey (USGS). Camann DE. who. Hull RD.htm.56(6):853-859.47(6):503-517. March 2006. 2007.php. Casida JE.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Peter CJ. MacKenzie B. Wilson AG.S.pdf. 1992-2001.43(9):2504-2512. Davison KL. 98-4245 (by Barbash JE. 1997. Available at URL: http://water. Kolpin DW.111(5):749-756. Hines CJ. Erratum in: Life Sci 1989.Herbicides References Battaglin WA. Atlanta (GA). Henningsen G. 1999. Casida JE. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.gov/oppsrrd1/ REDs/0063. Gilliom RJ).43(25):2087-94. Xenobiotica 1994. Biagini RE. Barr JR. Linhart SM. Geological Survey (USGS). Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Kinney PL.

Atrazine has limited water solubility and is not tightly bound to soil.and post-emergence to agricultural land for crops such as corn and sorghum. 1996. U. U. 2002. glutathione conjugation appeared to be the major route of biotransformation. Atrazine is well absorbed orally. 1982.EPA. Atrazine is applied pre. Fourth National Report on Human Exposure to Environmental Chemicals 53 . Urinary Atrazine mercapturate Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2005. Atrazine mercapturate products accounted for a major proportion of human urinary metabolites (Lucas et al. It has little toxicity in birds and moderate toxicity in some fish and aquatic invertebrates. More than 70 million pounds have been applied annually in recent years.S. atrazine use has progressively been restricted in an effort to reduce surface and ground water contamination.. all of which act by inhibiting plant photosynthesis.. Hayes et al.EPA. 1912-24-9 General Information Atrazine is a widely used chlorotriazine herbicide that acts against broadleaf and grassy weeds. which may vary for some chemicals by year and by individual sample. and then eliminated in the urine over a few days (Bradway et al. Catenacci et al.S. 1990). propazine. It is also used as a non-selective herbicide.. The dealkylated chloroatrazine metabolites. Applicators of atrazine may be exposed dermally and by inhalation. metabolized. drinking water is an infrequent source of atrazine exposure. population from the National Health and Nutrition Examination Survey. For the general population. In animals and humans.. atrazine is slowly degraded to dealkylated products.S.Herbicides Atrazine CAS No. and cyanazine. 2003b). with about 75% of corn cropland receiving treatment. In regions where atrazine is used.791 and 0. resulting in atrazine mercapturate and N-dealkylation products (IPCS. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.S. Bacteria and plants can metabolize atrazine to hydroxyatrazine. Survey Geometric mean (95% conf. In soils. 2003b). Atrazine does not bioaccumulate.. 1993. As a result. but it is leachable into ground and surface waters. 2007).3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Atrazine may alter the sexual development of frogs at environmental levels (Gammon et al. < LOD means less than the limit of detection. 1993).EPA. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1878 2477 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 449 568 639 809 790 1100 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 919 1162 959 1315 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 676 498 684 550 918 Limit of detection (LOD.. which have half-lives of several months. Timchalk et al. Atrazine was first registered as an herbicide in 1958. but estimates of seasonal intakes from drinking water in a small number of communities have exceeded the recommended limits (U. it is one of the more commonly detected pesticides in surface and ground waters (USGS. 2003a). Related chlorotriazine herbicides include simazine.

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

Reynolds SJ. Bradway DE. Wetzel LT.99(8):5476-5480.inchem. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. Gammon DW. Goldman JM. Cottica D. Pest Manag Sci 2005. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Available at URL: http://www. Vonk A. Curwin BD. Toxicol Sci 2000. Environ Health Perspect 2001. References Adgate JL. 2005). urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Tyrey L. et al. Toxicol Sci 2000.. Ann Occup Hyg 2003. et al. Toxicol Sci 2003. Lucas AD.43(2):155-167. Aldous CN. Agency for Toxic Substances and Disease Registry (ATSDR). Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. Schmid J.. J Agric Food Chem 1982. Gillis JH.org/documents/pds/pds/pest82_e. Heederik D. 2007).15(6):500-508.html. 2001 [online]. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. J Toxicol Environ Health 1994. International Programme on Chemical Safety (IPCS). Goodrow MH. Stoker TE. Proc Natl Acad Sci USA 2002. Jones AD. 2003. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. 2005. Freeman NC. 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. Available at URL: http:// www. ATRAZINE. Wetzel LT. Atlanta (GA). et al. J Expo Anal Environ Epidemiol 2005. Hayes TB. Pfeifer KF.. Noriega N. et al. A risk assessment of atrazine use in California: human health and ecological aspects. In the NHANES 2001-2002 subsample. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses.. Eberly LE.76(1):190-200. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al.61(4):331-355. Ferrell JM.30(2):244-247. WHO/ FAO Data Sheets on Pesticides. Stevens JT. Hermaphroditic. Deddens JA. Breckenridge CB. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Environ Health Perspect 2007. Grzywacz JG.gov/toxprofiles/tp153. Blewett C. 2001).cdc. Gillis JH. Eldridge JC. 82. Third National Report on Human Exposure to Environmental Chemicals.. Lee M. Steroids 1999. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Cooper RL.htm. J Toxicol Environ Health 1994. Ferrell JM.43(2):155-167. Collins A.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure.64(9):672-678. Centers for Disease Control and Prevention (CDC). 2005). Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Seiber JN. Clayton CA.69(2):217-222. 3/11/09 Arcury TA. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. No. et al. Barr DB. Biological monitoring of human exposure to atrazine. et al. Stoker TE. Stuart AA. Hines CJ. diamino-S-chlorotriazine and hydroxyatrazine. Toxicol Lett 1993. Extrom PC. Hein MJ. Ferioli A. levels of atrazine mercapturate were generally not detectable (CDC. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L.115(8):1254-1260. World Health Organization. Sanderson WT. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.58(2):366-376. Barr DB. Eldridge JC. 1993).109(6):583-590. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. Catenacci G. Perry et al. atrazine was detected in only four children (Arcury et al. Geneva.47(6):503-517. Laws SC. Striley CA. 3/11/09 Laws SC. 2000). Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Tapia J. Maroni M.atsdr. Lioy PJ. Barbieri F. Saiz SG. Cooper RL. Shoemaker DA. Cooper RL. Chen H. Brown KK.. Toxicological profile for atrazine. Fleenor-Heyser DG. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. The geometric mean of urinary atrazine mercapturate was 1. Moseman RF. In a small number of field workers.53(2):297-307. Stoker TE. 1996. Sanborn JR. Mendoza M. Carr WC Jr. Barr DB. Quandt SA. In small studies of Maryland residents in 19951996 (MacIntosh et al.. McElroy WK. In a study of 60 farm worker children. Biagini RE. Simpkins JW. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. Bersani M.

2007. 6/1/09 U. Office of Prevention. 3/11/09 U.S.epa.gov/oppsrrd1/REDs/ atrazine_ired.58(1):50-59. Washington (DC). A risk characterization for atrazine: oncogenicity profile. Needham LL. Pesticides and Toxic Substances. 2003b. Toxicol Sci 2002. Ann Epidemiol 2000. EPA Office of Pesticide Programs. Fenton SE. Stoker TE. Singzoni B.6(1):107-116. Supplemental Technical Information (available on-line only). Tortorelli J. Case No. Stoker TE. Toxicol Appl Pharmacol 2004. Cooper RL. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Toxicol Appl Pharmacol 2002. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function.27(6):599612.S.pdf. Osborne DW.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. 0062.usgs. Lansbergen GW. Perry M. The Quality of Our Nation’s Waters. Pesticides in the Nation’s Streams and Ground Water. J Expo Anal Environ Epidemiol 1999. May 2003a. Breckenridge CB. Available at URL: http://www.9(5):494-501. Timchalk C.10(7):479. Laws SC. A review of epidemiologic studies of triazine herbicides and cancer.67(2):198-206.195(1):23-34. Available at URL: http://www. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Crit Rev Toxicol 1997.pdf. J Toxicol Environ Health A 1999. Cooper RL. Toxicol Sci 2000.S.182(1):44-54. Circular 1291.S. Environmental Protection Agency (U. Geological Survey (USGS). Rayner JL. Laws SC. Urinary biomarkers of atrazine exposure among farm pesticide applicators. March 2006. Environmental Protection Agency (U. Hammerstrom KA. Sathiakumar N.S. MacIntosh DL. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .Herbicides development of a biomarker of exposure. Kastl PE.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. A longitudinal investigation of selected pesticide metabolites in urine. EPA). Ryan PB. 1992-2001. van den Berg M. Wetzel L. EPA). Dryzga MD. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Stevens JT. Dagenhart D. Boerma J. Christiani D. Interim Reregistration Eligibility Decision For Atrazine. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Delzell E. Langvardt PW. revised February 15. Guidici DL.epa.php. Sanderson JT.61(1):27-40. White paper on potential developmental effects of atrazine on amphibians. Environmental Fate and Effects Division. Chem Res Toxicol 1993. U. Toxicology 1990. Guidici DL. Available at URL: http://water. Wood C.56(2):69-109.

70) 1.27 (1. the chlorophenoxy herbicide 2.660) 1.960-1.40) 1.690 (. 2.4-D has low acute toxicity. 1989.EPA.930 (.10 (<LOD-1.670-1.21) 1. Sauerhoff et al. population from the National Health and Nutrition Examination Survey. 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.16) < LOD . 2004).680-1. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness. 4-D.4-D were used in the U.890) < LOD . but at higher levels they are herbicidal. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. Recent estimates of chronic intakes of 2. abdominal pain.440-1.66) < LOD 1. It was first registered with U. dizziness. by direct contact with agricultural and residential areas after applications..250 (<LOD-. MCPA.24 (.310 (. 2.S. agricultural.250 (<LOD-.4-D is rapidly absorbed via oral and inhalation routes.890 (. 94-75-7 General Information Widely used throughout the United States. headache.80) 1.32 (1.490 (. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .EPA in 1948.350) < LOD < LOD < LOD . 2.550-1. It is poorly bound in soils.07 (.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .S. Similar to other chlorophenoxy herbicides. Kohli et al.610 (.10) < LOD 1.S.4-D can be applied either as an aqueous salt or as oil-soluble esters. which may vary for some chemicals by year and by individual sample.420-.08) < LOD . As much as 62 million pounds of 2.490) < LOD < LOD < LOD . General population exposure to 2.00-2.51 (1. It is rarely detected in ground waters (USGS.760 (.210-. it acts as a plant growth hormone. and by consuming food or drinking water contaminated with 2.560-.4-D have been below recommended intake limits (U.22) < LOD .4-dichlorophenoxyacetic acid (2. with a half-life of several days to several weeks.13) < LOD .55 (1.540-.930-1.27 (..02-1.48) < LOD 1. Fourth National Report on Human Exposure to Environmental Chemicals 57 .310) < LOD .27-2. Survey Geometric mean (95% conf.690-1.370-.730 (.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.690 (. At low levels. and mecoprop). and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.260 (<LOD-.30 (<LOD-2.952 and 0. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.4-D may occur during residential applications..EPA.910) 1.43) 1.910) < LOD . hypotension.690 (.740 (. 2005).4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4-Dichlorophenoxyacetic Acid CAS No.10 (<LOD-1. 2007). 1974.560-1. It is not well absorbed through the skin.2.S.810-1.03) 695 659 520 668 589 892 Limit of detection (LOD.37) size 1977 2413 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD .4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. in 2001 (U. these herbicides can enhance plant growth. 1977). nausea. renal and hepatic injury. myotonia.4-D) controls broadleaf weeds in residential.20 (.320) 90th .S.05-2. Human health effects from 2.330 (.20 (<LOD-1. and delayed Urinary 2. and aquatic environments.400) < LOD .610-.420) < LOD .410) < LOD .210 (<LOD-. Once absorbed.4-D or exposed for prolonged periods.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .230 (<LOD-.230-.Herbicides 2. < LOD means less than the limit of detection.60) 1.

U. The acid and salt forms of 2.610-.56) .13 (..08 (. population (Hill et al. 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.550-. 2000). CDC. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.gov/pesticides/.05) . adrenals and gonads (NTP.670 (<LOD-1.26) size 1977 2412 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th < LOD .S.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC. Post-application levels in farmers and home gardeners were dependent on Urinary 2.470) < LOD .16) 1.780 (. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.27-1.380-.S. myotonia.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. Biomonitoring Information Urinary levels of 2.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. 2005.520-. 58 Fourth National Report on Human Exposure to Environmental Chemicals . U. In previous samples of the U. 2005...410) 90th . 1980. 1992).S.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.660 (. 2001.680) < LOD ... in small samples of children (Hill et al. 1985.270-. IOM.330-.980) < LOD 1.270 (<LOD-.S.epa.890-1.39) < LOD 1.590 (<LOD-1.810-1.570) < LOD . Survey Geometric mean (95% conf.14 (. 2..440 (. or teratogenic effects in chronic rodent studies (Charles et al. Additional information is available from U.810-1.890) < LOD 1.930-1. other exposures.08 (. IPCS. Kolmodin-Hedman and Erne.780-1. 1994).670 (.720 (.350 (<LOD-.32 (<LOD-2..990-1. 2006.S. or to contaminants in the herbicide formulations (specifically 2. Acute high doses administered to laboratory animals produced ataxia.490 (.3.560-. Pearce and McLean. Epidemiological studies have reported associations of several types of cancer. Frank et al. 1995.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and of adults and children (Baker et al. 1989).790) 1.850) < LOD .EPA 2005). 2002.380 (<LOD-. 2004).660) < LOD .340-.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .EPA. and evidence of histological injury to the kidneys.380 (<LOD-.700 (.380) < LOD ..920) < LOD 1. 2005.4-D production plant workers and a few forestry workers spraying 2.EPA at: http://www. 2005).EPA.17 (.S. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.590 (<LOD-1.410 (<LOD-. IPCS.640 (.390) < LOD < LOD < LOD .24) 1.4-D levels were detectable in less than a quarter of the individuals studied. IPCS. thyroid. Kutz et al. 2.. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1. U.740 (.580-.Herbicides neuropathy (Bradberry et al.610-.19) . 2005).790) < LOD . 1996.780) . Knopp et al.26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Hill et al. urinary 2. 2005.480 (. It is unclear whether these associations are related to the chlorophenoxy herbicides.410) < LOD < LOD < LOD .4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.41 (1.4-D are eye irritants. liver. 2005). 2. 2003. population from the National Health and Nutrition Examination Survey.13 (. Average post-application urinary levels of 2.4-D reflect recent exposure.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.08 (.340 (. eyes.620-. 2005).560-.820-1. 2002. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. 1995). 1996.73) .670 (.7. U. 1996.35) < LOD .4-D does not have significant reproductive.EPA..410) < LOD 1. developmental.

Reynolds SJ. Kutz FW. TOX-63: TOXICITY REPORT CURVES. Baker S. Selected pesticide residues and metabolites in urine from a survey of the U. Estimation of occupational exposure to phenoxy acids (2. Review of 2. Arch Environ Contam Toxicol 1989. Scand J Work Environ Health 2005. Philbert MA. 2005).4:427-435. Campbell RA.niehs. International Programme on Chemical Safety-INCHEM (IPCS).4-D) epidemiology and toxicology.4.4-D than levels found in the general population. Pesticides residues in food: 1996 evaluations Part II Toxicology.31 Suppl 1:90-97.gov/index. Tables. Veterans and Agent Orange: update 2002. 3/17/09 Institute of Medicine (IOM).5-T). 3/17/09 Knopp D. Ripley BD. Khanna RN. 2005). cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5. Garabrant DH. Kolmodin-Hedman B.4-D): exposure and urinary excretion.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Carter-Pokras OD. Kohli JD. Sanderson WT.. the amount of pesticide applied.31 Suppl 1:98-104.51(3):152-159. Arch Toxicol Suppl 1980. et al. Biomonitoring of herbicides in Ontario farm applicators.60(1):121-131. J Toxicol Environ Health 1992.edu/catalog. Wilson RD. Mandel JS. Scand J Work Environ Health 2005. Holler JS. 2005. Harris SA. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 .15(6):500-508. Shealy DB. et al. Arnold EK. Absorption and excretion of 2.htm. 914. Alexander BH. Arch Environ Contam Toxicol 1985.4-Dichlorophenoxyacetic Acid). Hein MJ. Smith SJ.4-. Sirons G J. Barr DB. Biomonitoring studies of 2.org/documents/jmpr/jmpmono/v96pr04.S. Dichlorophenoxyacetic acid. Developmental toxicity studies in rats and rabbits on 2.4-D). National Toxicology Program (NTP). 2005 Charles JM. Head SL. Needham LL. and the use of protective clothing or equipment (Arbuckle et al. Curwin BD. Chapman P. Beasley VR. Forestry workers involved in aerial application of 2.4-dichlorophenoxyacetic acid and its forms. the number of acres to which it was applied (Curwin et al. 2005. Vet Hum Toxicol 1989. Baker BA. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4-D were highest in the farmers who applied the 2. Tandon JS. Bailey SL. Beeson MD. Cole DC. Finding a measurable amount of 2. TOX-63 Peroxisone Project (2.37(2):277-291. Available at URL: http:// www. Dhar MM. Survival and Growth Curves from NTP Toxicity Studies. Third National Report on Human Exposure to Environmental Chemicals.4-dichlorophenoxyacetic acid (2. Ritter L. Exposure of homeowners and bystanders to 2.4-D and 2. In farm families. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Mandel et al. Crit Rev Toxicol 2002. general population.php?record_id=10603. Frank R.4-dichlorophenoxyacetic acid (2. Barr DB. Available at URL: http://ntp. Gupta BN. Washington (DC): National Academies Press. Hanley TR Jr. J Expo Anal Environ Epidemiol 2000. Heederik D. 2006. Pesticide residues in urine of adults living in the United States: reference range concentrations. Assessment of exposure to 2.4:318-321. Driskell WJ. Gregg M.32(4):233-257. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. et al.inchem. Murphy RS.4-D will result in an adverse health effect.4-D. Xenobiotica 1974. J Environ Sci Health B 1992..27(1):23-38..18(4):469-474. J Expo Anal Environ Epidemiol 2005 Nov. Environ Res 1995. 2. Stephenson GR. Hill RH Jr.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 2.71(2):99-108. Needham LL. Sircar KP. Biomonitoring for farm families in the farm family exposure study. Updated March 7.4-dichlorophenoxyacetic acid in man.Herbicides the time since application. Acquavella JF.nih. Cook BT.. Fast DM. Atlanta (GA). Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Brody D. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. To T. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2003. References Arbuckle TE. Hill RH Jr. Available at URL: http:// www. Bus JS. 1992).4-D in urine does not mean that the level of the 2. Toxicol Sci 2001. Occup Environ Med 1994. Erne K.10(6 Pt 2):789-798. geometric mean urinary levels of 2.4 dichlorophenoxyacetic acid (2.4:97-100. van Ravenzwaay B. Centers for Disease Control and Prevention (CDC). Board on Health Promotion and Disease Prevention. Harris et al. Solomon KR. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Baker SE.nap.31(2):121-125. Honeycutt R.

EPA).Herbicides Sauerhoff MW.2000 and 2001 market estimates.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. 1992-2001. 2004.epa.usgs.epa.4-dichlorophenoxyacetic acid (2. 3/17/09.pdf. Blau GE.4-D RED Facts. S.htm. May.S. Environmental Protection Agency (U.S. EPA 738 F-05-002.gov/oppsrrd1/ REDs/factsheets/24d_fs.S. The Quality of Our Nation’s Waters. 2007. revised February 15.EPA). Office of Prevention Pesticides and Toxic Substances. Braun WH. Supplemental Technical Information (available on-line only).php. Toxicology 1977. Circular 1291. Geological Survey (USGS).8:3-1U. 2. Pesticide industry sales and usage . Environmental Protection Agency (U.S. March 2006.4-D) following oral administration to man.S. gov/oppbead1/pestsales/01pestsales/market_estimates2001. The fate of 2. 60 Fourth National Report on Human Exposure to Environmental Chemicals . Washington (DC): U. Available at URL: http://www. 4/2/09 U. June 2005. 3/17/09 U. Gehring PJ.EPA. Available at URL: http://www. Available at URL: http://water. Pesticides in the Nation’s Streams and Ground Water.

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

200 (<LOD-. Survey Geometric mean (95% conf.240) 679 701 957 Limit of detection (LOD. 62 Fourth National Report on Human Exposure to Environmental Chemicals . 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 . Survey Geometric mean (95% conf.500) < LOD 1192 1345 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Urinary Metolachlor mercapturate (creatinine corrected) Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.740) 679 700 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. < LOD means less than the limit of detection.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. which may vary for some chemicals by year and by individual sample.Herbicides Urinary Metolachlor mercapturate Metabolite of Metolachlor Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 01-02 is 0. population from the National Health and Nutrition Examination Survey.220) < LOD 1192 1346 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 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 .670 (<LOD-.S.440 (<LOD-.

Gillion.S. et al.11(4):353359. Hladik ML. Thurman EM.248(2-3):123-133. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. March 2006. Gilliom RJ). Quistad GB. Geological Survey (USGS).usgs. Feng PCC. Hsiao JJ.ESTfeature_gilliom.pdf. Ward EM. R. 1992-2001.gov/oppsrrd1/ REDs/0001. Biagini RE. Environ Health Perspect 2000. 1999.39(17):6561-6574. Sci Total Environ 2000. Hodgson E. Furlong ET. Burkhardt MR.php. Chem Res Toxicol 1998. Striley CA.37(4):10881093. Barr DB.pdf. Environ Health Perspect 2003. Supplemental Technical Information (available on-line only).S. 3/26/09 U.41:3409-3414. Reregistration Eligibility Decision (RED) Metolachlor. revised February 15. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Pesticides in U. Background document for development of WHO Guidelines for Drinking-water Quality. Feil VJ. 2005. California. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Larsen GL.24(10):1003-1012. acetochlor. 6/1/09 Whyatt RM.who. Available at URL: http://water. usgs. Kolpin DW. 2007. imidazolinone.html. Linhart SM. Deddens JA. Dialkylquinonimines validated as in vivo metabolites of alachlor. Brown KK. Sci Total Environ 2000.epa. Wratten SJ. Centers for Disease Control and Prevention (CDC).pdf 3/30/09 Hines CJ. Environmental Protection Agency (U. April 1995. Thelin GP. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.15(6):500-508. Xenobiotica 1994.108(12):1151-1157. and metolachlor herbicides in rats. Reynolds SJ.47(6):503-517. and other herbicides in rivers. EPA 738R-95-006.usgs. Geological Survey (USGS). Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.S. Kolpin DW. Shoemaker DA. Davison KL. World Health Organization (WHO). Sanderson WT. Casida JE. Environ Sci Technol 2007. Linderman R. Curwin BD. Ann Occup Hyg 2003. Camann DE. Barr JR. Metolachlor in Drinkingwater. U. Kinney PL.111(5):749-756. Coleman S. Environ Sci Technol 2005. Andrews HF. Available at URL: http://www.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. et al.S. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Rose RL. Comparative metabolism and elimination of acetanilide compounds by rat. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Atlanta (GA). streams and groundwater. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Available at URL: http://www. Jefferies PR.int/water_sanitation_health/dwq/chemicals/ metolachlor. Hein MJ. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . reservoirs and ground water in the Midwestern United States.248(2-3):115-122. Available at URL: http://water. EPA). 1998. Sacramento.gov/nawqa/ pnsp/pubs/wrir984245/text. Heederik D. Third National Report on Human Exposure to Environmental Chemicals. 4/2/09 U. Alavanja MC. 98-4245 (by Barbash JE. Barr DB. Circular 1291. 2003. Roberts AL. Occurrence of sulfonylurea. J Expo Anal Environ Epidemiol 2005.S.gov/nawqa/pnsp/pubs/files/051507. Available at URL: http://water. sulfonamide.Herbicides References Battaglin WA. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Peter CJ. J Agri Food Chem 1989.

such as soft tissue sarcoma and non-Hodgkin’s lymphoma. 2007). At low levels.5-T in soil varies with conditions. Once absorbed into the body. Ester forms of 2. dizziness.7. 1986. Nelson et al.4. Epidemiological studies have reported associations of several types of cancer. and concern about contamination with 2. population from the National Health and Nutrition Examination Survey. Chlorophenoxy herbicides act as plant growth hormones. with an elimination half-life of approximately 19 hours (Arnold et al. < LOD means less than the limit of detection. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. Human health effects from 2.3.4..5-T (Holson et al.4..4.4. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD. Mohammad and St.4.5T is rapidly absorbed via oral and inhalation routes.5-T degrades to 2. 2. ranging from several weeks to many months.4.4.5-Trichlorophenoxyacetic acid (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1992.4-D were used as defoliants in the Vietnam War (e.5-T has been rarely detected in ground waters (USGS. 2.. 2. Given the commercial unavailability of 2. 2. which may vary for some chemicals by year and by individual sample.5-T. Kohli et al.4. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.Herbicides 2.5-T is eliminated mostly unchanged in the urine. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness.4. these herbicides can enhance plant growth.5-T and 2.4. renal and hepatic injury. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2..1. 64 Fourth National Report on Human Exposure to Environmental Chemicals .4.S.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.. 93-76-5 General Information 2. 1974).5-T was once applied as either an aqueous salt or as an oil-soluble ester. abdominal pain. Omer. Although 2.5-trichlorophenol and other degradates.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. and delayed neuropathy (Bradberry et al. it is not well absorbed through the skin. 2004). myotonia. Survey Geometric mean (95% conf. headache.2 and 0. The half-life of 2.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2.g. the general population is unlikely to be exposed to it. hypotension.5-T use as a herbicide in 1985. 1992).4. but higher levels are herbicidal.5-Trichlorophenoxyacetic Acid CAS No.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.4. 1989.4..4. nausea. Agent Orange).

2005). similar to results of NHANES II (19761980). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC. 1996. 2002.5-T also were below the limit of detection (Kutz et al.4.EPA. IPCS. Finding a measurable amount of 2. other exposures. population from the National Health and Nutrition Examination Survey.4. Biomonitoring studies on 2. 2003.5-T reflect recent exposure.4. 2004).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-T does not mean that the level will result in an adverse health effect.gov/pesticides/..5-T than levels found in the general population. Mean urinary levels of 2. Biomonitoring Information Urinary levels of 2.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.4.5-T were generally below the limit of detection.4.7. 2005. Fourth National Report on Human Exposure to Environmental Chemicals 65 . U. Pearce and McLean. 1992). 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. Urinary 2.EPA at: http://www. 2.5-T itself is not mutagenic. IOM.S. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. or to contaminants in the herbicide formulations (specifically 2. urinary levels of 2.epa.4.Herbicides or contaminated herbicides.4. Additional information is available from U.4. It is unclear whether these associations are related to the chlorophenoxy herbicides.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.3.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.S. in which urinary levels of 2. 1980).

Toxicol Rev 2004.5-T).4. Arch Toxicol Suppl 1980. McLean D. Selected pesticide residues and metabolites in urine from a survey of the U. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Available at URL: http:// www.4.4. Holson JF. et al. Environmental Protection Agency (U.epa. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. McCallum WF. Behavioral and developmental effects in rats following in utero exposure to 2. Centers for Disease Control and Prevention (CDC). Beasley VR. Arch Int Pharmacodyn Ther 1974.S. Gaines TB. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Sheehan DM. Available at URL: http:// www. Pesticides residues in food: 1996 evaluations Part II Toxicology.19(2):298-306. Sircar KP.5-trichlorophenoxy acetic acid in man. Murphy RS. 3/17/09 Kohli JD. May. Khanna RN. Review of 2.23(2):65-73.5-T in four-way outcross mice. Nelson CJ. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice.5-trichlorophenoxyacetic acid (2.edu/catalog. Third National Report on Human Exposure to Environmental Chemicals. Absorption and excretion of 2. Fundam Appl Toxicol 1992.8(5):551-60. Brody D. Office of Prevention Pesticides and Toxic Substances.4-. 2003. Multireplicated dose-response studies with technical and analytical grades of 2. Gaines TB. Dichlorophenoxyacetic acid.31(2):121-125. Garabrant DH. Available at URL: http://www.32(4):233-257. Philbert MA. Gaylor DW. Board on Health Promotion and Disease Prevention. Tandon JS. LaBorde JB. Atlanta (GA). I. S. 3/17/09 Institute of Medicine (IOM). Scand J Work Environ Health 2005. Washington (DC): National Academies Press. Vale JA. II.5-t mixture. 2004. Nelson CJ. 2005. Neurobehav Toxicol Teratol 1986.4. Pesticide industry sales and usage .Herbicides References Arnold EK. Erne K. Dhar MM. Vet Hum Toxicol 1989. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .4-dichlorophenoxyacetic acid (2.4-D) epidemiology and toxicology. Bradberry SM. Developmental toxicity of 2.inchem. Gupta BN. Developmental toxicity of 2. 210:250-255. Washington (DC): U. Wolff GL. Kolmodin-Hedman B.31 Suppl 1:1825. Holson JF. Crit Rev Toxicol 2002.htm.org/documents/jmpr/jmpmono/v96pr04.4:318-21. Mohammad FK. Pearce N. Veterans and Agent Orange: update 2002. Estimation of occupational exposure to phenoxy acids (2. general population. Agricultural exposures and non-Hodgkin’s lymphoma. J Toxicol Environ Health 1992.S. LaBorde JB.37(2):277-91. Proudfoot AT.5-T). St Omer VE. Poisoning due to chlorophenoxy herbicides. International Programme on Chemical Safety-INCHEM (IPCS).4. 914. Carter-Pokras OD.EPA). Kutz FW.19(2):286-297.4. 2. U. Cook BT.S.4-D/2.4-D and 2.EPA.5-T).4.4.pdf.nap.2000 and 2001 market estimates.php?record_id=10603. discussion 5-7. et al.5-trichlorophenoxyacetic acid (2. Fundam Appl Toxicol 1992.

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

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

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

2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.S.158) .055 (.4) 1007 954 1152 998 01-02 03-04 01-02 03-04 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.9 (13.5) 21.8) 15.130-.130-.0) 21.4) 95th 20.9 (13.098 (.8 (18.50) 15.00-14.120) .9-23. Survey years 01-02 03-04 Geometric mean (95% conf.101) .2-15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.093) .160 (.073-.6 (15.116) .9 (12.049-.7 (<LOD-15.053 (<LOD-.056-.8) 14.8 (9.109 (.160) .7 (14.1) 15.090 (<LOD-.8-17.147) 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 .80-9. which may vary for some chemicals by year and by individual sample.089 (.70 (7.0 (15.5 (<LOD-11. see Data Analysis section) for survey years 01-02 and 03-04 are 10.4) 539 456 484 487 980 885 Limits of detection (LOD.7-22.054-.090-.096-.2) 12.3 (18.140) .139 (.6) 19.130) .130 (.2) 14.30 (8.60-10.070-.9-38.8-24.30 (8.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.054-.149) .075) < LOD .4-18.5-17.083-.064) 90th .50 (8.242) .0 (10.190) .5-17.1) 10. interval) Selected percentiles ( 95% confidence interval) Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * * 50th < LOD < LOD 75th < LOD 9.180) .5 and 7.2) 11.048 (<LOD-.150 (.2) 15.S.120 (.1-18.3 (19.080-.8.0) < LOD 9.6-33.190) .147 (.0-21.40-10.1) 13.00 (8.108-.130) .1) 15.100 (.138 (.110 (.100) .90) 90th 15.130) .182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .0 (11.8-25.9 (14.112-.062 (.120 (.062-.058) < LOD .7 (15.110) .059 (.4) 19.112) 95th .5 (16.4 (12.109-.4) 21.10 (<LOD-16.063-.124) .3-21.110) .170) .077-.080) .084-.180) .090-.0-25.138) .5-15.100) .069) < LOD < LOD .4) < LOD < LOD 16.5) 19.80-10.070 (<LOD-.062 (.1-24.6-24. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4) 20.9-22. population from the National Health and Nutrition Examination Survey.1 (18.100-.1-19.130-.110-.120 (.9 (12.80 (<LOD-10.086-.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.117) < LOD .140 (.090 (.077 (.070) .6 (15.102 (. 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) 19.3 (18.110 (. which may vary for some chemicals by year and by individual sample.3 (13.1-16.064 (.8-19.1 (13.1) 20.103 (.139 (.3 (14.4-17.40-9.080 (. population from the National Health and Nutrition Examination Survey.7) 15.100-.1) < LOD 9.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .120-.140-.054-.060) . Survey years 01-02 03-04 Geometric mean (95% conf.090-.6) 16.150 (.100-.113 (.8 (11.8-17.6) 9.6-24. 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 . Fourth National Report on Human Exposure to Environmental Chemicals 79 .7-19.0 (10.160 (.8) < LOD 8.4) 14.4 (12.5) 15.088-.1) 14.110 (. < LOD means less than the limit of detection.6 (14.103 (.109-.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.

2 Classes of Pesticides. PA. New York. Andersen A. International Programme on Chemical Safety (IPCS). Grajewski B.inchem. Stehr-Green. Lancet 1998. Grandjean P. Song S. In Hayes WJ. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. and lymphocyte sister chromatid exchange. J Occup Environ Med 2005. Pesticides in the Nation’s Stream and Ground Water. Finley B. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease.org/documents/ehc/ ehc/ehc91. plasma dieldrin. Exp Neurol 1998. Demographic and seasonal influences on human serum pesticide residue levels. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. Six high-priority organochlorine pesticides. Carlson JN.150:263-271. Organochlorine insecticides in substantia nigra in Parkinson’s disease. J Toxicol Environ Health 1989. Kanthasamy A. Toxicol Lett 1992. Hartvig HB. Handbook of Pesticide Toxicology. Sanchez-Ramos J.103(Suppl 7):113-122. Chapin RE. 4/21/09 Bates MN.fda. Ginsburg KS. 15.gov/ circ/2005/1291/. Inc. Li AA.47:1059-1087. 6/1/09 Ward EM.91(1):122-126. either singly or in combination. August 2008. Basit A. Chemosphere 2004. et al.109(Supp1):113-139. Facca A. Academic Press.54:1431-1443.usgs. Aldrin and Dieldrin [online]. Wienburg CL. Fernandez MG. Cox. Available at URL: http://pubs. References Agency for Toxic Substances and Disease Registry (ATSDR). Sonnenschein C. J Toxicol Environ Health. and epidemiology in the United States. September 2002. Priestly BG. 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. Frey JM. Vol. Environ Health Perspect 1995. Soto AM. Organochlorine exposure and risk of breast cancer.352:1816-1820.14:95-102. Teta MJ. Environ Health Perspect 2001.html. Daniel SE. 1989. Garrett N. McIntosh LJ. Serrano FO.atsdr. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. 80 Fourth National Report on Human Exposure to Environmental Chemicals . Aldrin and dieldrin: A review of research on their production environmental deposition and fate. Part A 2000. toxicology. are nonestrogenic in transfected HeLa cells. Jr and Laws ER. Reprod Toxicol 2000. No:429-436. Kitzazwa M.gov/~dms/ pesrpts. Narahashi T. Chung KL. Revised Feb. bioaccumulation. Kanthasamy AG. Needham LL. Available at URL: http://www. Anantharam V. 1991. 731-915. Rosellini RA. Buckland SJ.9:1357-1367. Eds. pp. Mann D. Roy ML. Turner W. Smith AG. Mink PJ. United States Geological Survey (USGS).cdc. et al. Jr. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. Shore RF. Psychopharmacology (Berl) 1987. Available at URL: http://www. 2007 [online]. Edwards JW. Environmental Health Criteria 91. Int Arch Occup Environ Health 1994. Tully DB. Olea N. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Schulte P. Mumtaz MM.59:229-234. Neurotoxicol 2005. Patterson DG Jr.66(4):229-234. Corrigan FM.gov/toxprofiles/ tp1.64-65 Spec.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Jorgensen T.htm. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Toxicological profile for aldrin/dieldrin [online].cfsan. Brock JW. 1992-2001. David VL. Cancer Epidemiol Biomarkers Prev 2000. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. Food and Drug Administration (FDA). 4/21/09 Hoyer AP. Patterson DG Jr.26:701-719.html. Ellis H. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Chlorinated Hydrocarbon Insecticides. VT. 4/21/09 Jorgenson JL. Available at URL: http://www.27:405-421. 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.

69-10.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.8) 53.1-65. from the early 1950’s until the mid-1980’s.7 (<LOD-32.7 (32.8-61.3 (<LOD-19.0 (37.2) < LOD 11.9) 37.7-14.Organochlorine Pesticides Chlordane CAS No. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 01-02.6) 48.1-50.9-38.2) 34.9 (11.8-33.3 (25.0-67.2) < LOD 11.3 (28.4) 39. and dairy products are the usual sources of exposure to these chemicals in the general population.8 (42.9) 11.4 (30.5-40. fish.9) 36.5-41.6) < LOD 11.20-11. 57-74-9 Heptachlor CAS No.1 (<LOD-12.7) 35. chlordane was used to kill termites and other insects on agricultural crops.3) 37. 2007).6) 39.1 (11.2 (39.4 (35.9 (17.7 (<LOD-13.3 (27.2 (36.1 (<LOD-12.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.0-12.2-28.7-25.6-53.4) 12.2 (9. Heptachlor and chlordane are somewhat volatile and may be detected in the air and dust of buildings long after treatment for termite or insect control (Whitemore et al.1 (16.8-73.10-11.2 (37.63 (8.2) 33.1 (17.5-43.20 (<LOD-11. Until 1988.9) 13. and 03-04 are 14. Consequently.8 (40.7) 19.6) 20.8 (10.6 (43.4-51.7 (34.3) 10.5 (33.9) 17.. and in soil.9 (29.9 (15.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.7-39.9 (26.10 (8.0-33.S.0 (26.7-70.5) 9.2) 22.9 (21. in addition to trace amounts of numerous other related compounds (ATSDR.5-38. Technical grade chlordane had contained 7% trans-nonachlor.8-33.1 (27.1-15.10-18. see Data Analysis section) for Survey years 99-00. 10.2-21.9) 23.1) * 11.9) 23.0 (20.7) 19. population from the National Health and Nutrition Examination Survey.8-43.2) 37. lawns. the technical grade product of each chemical contains 10%-20% of the other chemical.7) 9.0) 21.9-21.S.36-11. buildings. Survey Geometric mean (95% conf.2-49. Both pesticides are persistent in soils and sediments and have been detected in water from agricultural run-off and near production and disposal facilities (ATSDR.8) 52.9 (26.9 (15.6) 23.5-65.3) 10.2 (28.2-49.8.3) 18.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.4) 22.4 (<LOD-12. Chlordane is not currently produced or used in the U.9) 47.4) 37.4-21.3-49.1 (40.82-11.1-51. respectively.5-42.0) 20.2-56. which results in exposure to the fetus and nursing infant Serum Oxychlordane (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.3 (9.5) 56.2-26.8-20. 1994.0-25.6) 9.1) 30.9-21.4) < LOD < LOD < LOD 23.5-44.5) 793 1049 963 868 1200 1015 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 11.0 (32.7 (17.5 (8.7 (34.6-12.1) 30.8-32. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.0-13.3-45.4 (10.9 (36.5.4 (30.7-12.2 (41.6-18.3 (26. 1994).7 (43.1) * 11.4) 18.0-61.6) 48.1-25.0 (<LOD-12.7 (10.90 (8.3-43.1) 90th 34.5 (34.3) 41.9 (11.S.1 (20.0 (16.3-32.5 (41. and 7.6 (9.3 (11.6 (9.4) < LOD 11.2 (21.1 (25.7) 28.8-23.1-19.0) 31.5) 38.74 (<LOD-10.8-42.6-24.3-24.0) 75th 20.9) 11.6) 11.0-18.5 (<LOD-12. 2007).1 (<LOD-12.1 (15. As a result of the manufacturing process.5-13. < LOD means less than the limit of detection.5) < LOD < LOD 9. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.9) 31.6 (16.5) 10.8 (17.9) 10.70 (<LOD-10.3 (20.20-10.5) < LOD < LOD < LOD < LOD 13.6) 49. Fourth National Report on Human Exposure to Environmental Chemicals 81 .89-10.8 (10.1) < LOD < LOD < LOD < LOD < LOD 8.8) 27.8-31.6) 9.30-11.9) 39.4-40. foods high in fat such as meat.6) 36.1-25. which may vary for some chemicals by year and by individual sample.8 (17.1 (44.7) 42.7 (19.6-45.4 (31.0) 37.3-45.7 (42.7) 31. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.2) 46.6-24.3 (21.4 (22.2 (10.7-56.4-14.5) 44.5-47. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.9-40.8) 18.0) 27.5) 37.8) 44.6 (25.9-42.1) 16.5) 21.37 (8.8) 52.9 (18. Since 1992.9 (31.5-32.5 (31.6) 8.5. heptachlor use has been limited to treatment of fire ants near power transformers.0) 41.3) 18.4-45.2) * 12.1) 22.4) 29.8 (18.2) 36. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.

100 (. 82 Fourth National Report on Human Exposure to Environmental Chemicals .170) . to heptachlor.370 (.315 (. 2007)..310) . 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.082 (. 2002.130) .260-.080) .310) . Elimination of all these chemicals from the body occurs over months to years.286 (.070 (<LOD-.067 (. 1991).108-.150 (.150-.258-.069 (<LOD-.269 (.063 (.165-. 1977b.230 (.049 (<LOD-.140 (.230-.070 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.207) .063) * .110 (<LOD-. and alterations in immune function of offspring.170-.203-.286 (.302) .220-. heptachlor. Acute. characterized by seizures and paralysis.320) .073) < LOD < LOD < LOD < LOD .300 (.066 (<LOD-. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.100-.400) .053-.180) . 1986). In laboratory animal studies.087-.271 (. FDA established allowable residues of chlordane.080) . population from the National Health and Nutrition Examination Survey.S.300) .S.120-.119 (.560) .350) .350 (.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .189-.070 (<LOD-.360) .079) .068) .200-.380) .400) .440) .130-.. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.290-.148) ..208 (.160) .075 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 1996.253-.170) .070 (<LOD-.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .064) < LOD .240) .066-.070 (<LOD-.300) .063 (.130 (.068) 75th . Chlordane and heptachlor are absorbed after oral.140 (.200-.071 (.079) < LOD < LOD < LOD .120-.146) .070) .250 (.063 (.220-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.250 (.290 (.130-.063 (. 1977a.370 (.148-.090-.320 (.074-.168-. neonatal mortality.210 (.115 (.190-.207 (.190-.310 (.270 (.076) < LOD . Shindell and Ulrich.077) .199-.130-. 2007. which may vary for some chemicals by year and by individual sample. and breast milk is a major excretion route in lactating women.330 (.128 (.077) . Rogan.340) .149 (.055-.450) . The U.373) . chronic doses of heptachlor have produced liver enlargement and injury.225 (.348) .047 (<LOD-.058-.140-.136) . Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.242-.260 (.133) 90th .320 (.053-.077) .290) .160) .270 (.077) .260 (.320 (.063) .300-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.290-.430) .200 (.104-.080 (.061-.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 * * * * .140-.410) .340) . EPA has established environmental criteria for chlordane and heptachlor.058 (.150) . 2006).250-. and heptachlor epoxide in foods and bottled water.090) .170) .S.083 (.231) .216-.130-.223) .280-.140 (.080) . 2001.210 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.112 (.320) .050-.070-.100-. 1981).060 (<LOD-. which is also persistent in the body (ATSDR.057 (.230) .110-.066 (.130 (.070-.160) .291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .180-.140 (.140) .230-.180) .260 (.280-.Organochlorine Pesticides (Dallaire et al..068-.150 (. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.092) .240 (. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.080 (.180-.280 (. dermal.146) < LOD < LOD . IARC.073 (. Takahashi et al.227) < LOD .120 (.245-.160 (. Le Marchand et al.062) < LOD .230-.220 (.130 (.057) * . 1991. and inhalation exposure.126 (.048-.210-.280-.189 (.270 (. The major metabolite of heptachlor is heptachlor epoxide.290-.056 (.430) .230 (.287) .190-.065-.070-. Survey Geometric mean (95% conf.106-.510) .290) .170) .115-.246-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide. Smith.130) .090) . OSHA has established occupational exposure criteria.150 (.320 (.350 (. and the U.120-.070) < LOD < LOD < LOD < LOD < LOD .450) .300) .310) .258 (.370 (.240-.104) .066-.240-. 1986).280) .280 (.130-.310-.063-.213) * .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.170) .057-.100 (<LOD-.091) .058-.300) .050 (<LOD-.200-.126) .083) .204 (.

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

9-23.0 (15.7-25.5 (11.8) 19.3 (13.7-18.3) 18.8) 15.8.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.2) 13. 01-02.9-16.9 (15.1) 13.8 (<LOD-23. population from the National Health and Nutrition Examination Survey.4 (<LOD-54.6.0-17.8) 14.8-24.6 (14.7 (16.6 (<LOD-27.2-27.3-18.9 (12.2 (<LOD-25.0-54. and 7.8) 21.9) * * * 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 8.3) 16.20 (<LOD-9.4 (15. see Data Analysis section) for Survey years 99-00.6 (11.6 (16.3) 27. Survey Geometric mean (95% conf.1-16.8 (18.6) 14.8 (18.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8-24.8) 13. 10.2) 20.6-17.8-23.1 (16.2-17.4 (11.6 (8.4) 18.5.6) 22.4 (11.3) 22.3) 18.90 (<LOD-9.8 (15.3) 23.2) 26.5 (<LOD-21.8) 13.0) 13.9) 15.5) < LOD 14.5 (<LOD-32.6 (16.0) 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 13.6-21.8-24. respectively.1-38.2 (<LOD-16. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.3 (<LOD-25.7-19.8) 14.2 (<LOD-62. which may vary for some chemicals by year and by individual sample.6 (13.8 (13.9-29.5 (10. < LOD means less than the limit of detection.1) 23.5 (18.1) 20.40) 15. 84 Fourth National Report on Human Exposure to Environmental Chemicals .4 (<LOD-19.2-27.1-15.0-19.7 (13.6) < LOD < LOD < LOD 27.0-17.8-46.6 (12.9-25.0 (11.5) 19.6) 13.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.5 (11.2 (18.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.8) 20.50) < LOD < LOD < LOD 17.8) 19.8) 16.8 (13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3) 10.0-16.4) 21.2-16.1-29.9-29.2) 15.7 (10.3) 18.10-13.1 (19.S. and 03-04 are 14.

180 (<LOD-.096 (.063) .082-.063) < LOD < LOD < LOD .110 (<LOD-.120 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 85 .100 (.100 (.120-.310) .220) .130) .170) .094 (.150 (.090-.100 (.110) .113-.106-.135 (.104) .077-.110-.087 (.180) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.180) .130-.100 (.140-. population from the National Health and Nutrition Examination Survey.120) .101 (.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 . interval) Selected percentiles ( 95% confidence interval) Sample 95th .110) .094 (.173) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140) .090-.110 (.077-.170 (.069 (.120 (<LOD-.055 (<LOD-.126 (.140) .128 (.098 (.090 (.076-.157) .120 (.170 (.180) .100-.090-.240) .100 (<LOD-.117) .101 (.380) .120) .130 (<LOD-.161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .180 (.190 (.200 (.170 (<LOD-.070-.090-. Survey Geometric mean (95% conf.057 (<LOD-.150 (.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.110 (<LOD-.090 (<LOD-.108-.130) .180) .180) .067-.071-.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 .170) .190) .110-.053-.097) < LOD .310) .200) .130-.130-.135 (.116) < LOD < LOD < LOD .074-.113) .270) .133 (.S.150 (<LOD-.090-.190) . which may vary for some chemicals by year and by individual sample.110 (.090-.190) .100-.170) .170 (.111-.200) .111) .130 (.107-.149) .108) .

6 (32.9 (66.5 (15.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.5) 48.0-93.4 (45.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.8 (15.5 (13.9-58.0) 18.4 (16. population from the National Health and Nutrition Examination Survey.0-143) 112 (68. see Data Analysis section) for Survey years 99-00.1) 78.3) 30.3) 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.8 (11.3 (16.1-126) 67.0 (62.7-160) 86.2) 39.86-13.8 (28.3-74.8 (28.9 (28.1 (22.1-22.7 (35.6 (16.6 (56.5) 90th 55.9) < LOD < LOD < LOD 20.5.Organochlorine Pesticides Serum trans-Nonachlor (lipid adjusted) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.5) 77.3 (45.1) 18.7-17.9-89.6-66.8 (42.6-20.4) 55.0 (19.4-36.7) 17. 10.8 (12.1) 18.7) 35.7-38.7-113) 68.7) 78.8-16.7 (28.7 (16.0 (15.0-23.4 (11.2) 59.3 (56.2 (25.7-77.2-88.4-23.7) 78.8 (13.1 (48.9) 51.5) 9.1 (47.4) 19.5 (44.7-34.2-18.8 (30.2 (19.S.9-65.3) 18.6) 56.7) 59.1) 31.7-20.8-110) 59.2 (64.6) 60.8 (<LOD-20.2 (14.7-35.1-20.3) 16.0) 75th 31. Survey Geometric mean (95% conf.3) 19.2 (7.2) 20.4-22.5.0 (42.3) 32.3) 30.4) 20.7) 56.7) 52.5-19.0 (16.6 (57.6) 84.7 (18.9 (15.0) 40.7-22.0) < LOD < LOD 8.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.0 (13.9) 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 (27.8 (49.3) 18.4-52.5) 22.7 (59.3 (14.8 (71.3-86. and 03-04 are 14.1) 30.8-90.9 (51.6) 25.2) 34.8-41.3 (49.1) 17.6) 10.0 (60.6) 13.6-82.4-62.0 (48.9-35.0 (15.7) 15.2 (36.8 (45.2-18.1 (65.70 (<LOD-12.6) 54.9 (<LOD-14.7 (11.9 (47.5-87.2 (14.3-50.9-69.2-16.2 (60.6 (15.9 (15.3-32.5) 14.6) 34.8-90.1) 16.5) 26.9) 51.9-22.1-34.3) 25.3 (58.3) 15.7 (30. which may vary for some chemicals by year and by individual sample.1 (41.6) 56.8-67.1-55.6-19.8 (26.2 (26.8-129) 74.8) 19.9-36.8 (26.4) 48.1-16.1) 17.0) 19.3-30.8.1) 17. 86 Fourth National Report on Human Exposure to Environmental Chemicals .3-57.9) 14. interval) 18.8 (19.0-68.7-18.0-93.8 (28.5-95.2-23.5 (15.5-69.8) 80.5-20.9-65.5) 36.7-23.1-28.1) 17.2-17. 01-02.6) 82.1) 14.4) 59.7-32.8 (17.8 (16.3-39.4 (12.6-22.8-77.4 (67.9 (29.8-19.0 (13.5 (45.8 (13.0 (14.4 (28.4) 107 (84. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.4 (30.9) 14.5) 20.3) 32.0-23.7) 73.5) 19.0-20.0-113) 68.7 (74.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.4-67.8 (26.4) 16.9 (51.1 (10.7) 28.0 (16.1) 17.8) 51.4-35.2 (15.7-29.0) 13.2) 19.1) 32.10 (<LOD-11.6 (52.8-21.9 (19.1-51.2 (59.9-20.6 (56.6-54.1) 17.5-111) 68.0) 49.8-19.1-16.2) < LOD 10.3 (14.9-64.0-24.3-58.6-88. respectively.5) 30.9 (36.3 (17.6 (12.1) 78. < LOD means less than the limit of detection.1) 62.7 (13.6 (50.0 (42.7) 14.5 (25.3-21.0) 33.5) 35.9-45.0-38.0-59.1 (17.0-22.9 (16.2) 30. and 7.5) 14.4-18.1) 17.8-79.5) 78.1-34.2-21.7 (59.0 (29.0-37.1-18.7-21.5-36.9-40.2-37.2) 17.5-17.6 (<LOD-14.8-16.3) 36.0-123) 74.8) 47.

120 (.470-.250) .060 (<LOD-.630) .060-.450) .470-. interval) .092 (.559) .240-.310) .110 (.400-.540) .470 (.330 (.580 (.190-.470 (.097) .405) .099-.300) .126) .760 (.510-.220 (.120 (.600 (.288-.600) .440-.310 (.286-.210-.098 (.170 (.180-.590 (.220 (.085-.098) .360-.183 (.109 (.070 (.093-.186 (.160-.288 (.110 (.130) .068-.080-.114) .390 (.930) .210-.173-.830) .116 (.S.089 (.130 (.090-.350-.090-.680 (.120-. population from the National Health and Nutrition Examination Survey.550 (.340-.171-.096-.080-.120) .397-.800) .112 (.237) .460-.594) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .127) < LOD < LOD .069) .079-.272-.103 (.110) .220) .047-.594) .320-.370 (.177-.128 (.082) .395-.161-. Survey Geometric mean (95% conf.210 (.371) .242) .480) .234) .390 (.091) .590) .098 (.690) .104 (.150) .122) .109 (.106 (.409-.093-.117) .090) .220 (.237) .090 (.100-.096-.250) .120) .120-.145-.131) .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .490 (.20) .062 (.103 (.380 (.320-.087 (.414 (.090-.116-.190-.081 (.460) .110 (.410-.400) .490-.190-.205 (.111 (.350 (.340-.330-.310-.099-.160 (.390) .084-.100-.095-.640 (.279-.130) .096) .240) .080-.106 (.125) .490) .330-.094 (.081-.211) 90th .232) .651) .135 (.400-.122) .324 (.060) .367) .340) .186-.680) .080-.120) .390-.091-.290-.317 (.573 (.092 (.343 (.500) .420) .220 (.125 (.120 (.141) .085-.113) .119) < LOD < LOD < LOD .105 (.190-.310-.430-.400 (.520) . Fourth National Report on Human Exposure to Environmental Chemicals 87 .054-.510 (.240 (.301-. which may vary for some chemicals by year and by individual sample.417 (.110 (.130) .191 (.180-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .130) .630) .300-.098-.960) .497-.630) .220 (.400 (.113) < LOD .430-.240) .129) .210 (.390) .130) .079-.090 (<LOD-.190-.260) .280) .141) .684) .490 (.590 (.355 (.100 (.690) .840) .108 (.210) .134) .061-.220 (.069-.210 (.210) .090-.130) .410-1.520 (.390 (.093-.106 (.140) .161) .110 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.470 (.580 (.580 (.119) Selected percentiles ( 95% confidence interval) Sample 95th .080 (.210) .390 (.327 (.520 (.220 (.130 (.150) .085-.104-.420 (.120-.190-.310-.440) .180-.285-.461 (.395) .055 (<LOD-.270-.250) .108) 75th .130) .080) .100 (.Organochlorine Pesticides Serum trans-Nonachlor (whole weight) Metabolite of Chlordane Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.230 (.090-.100-.565) .112 (.100-.360-.071 (<LOD-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .078-.110-.460) .124) .093) .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.111-.108) .078 (.202 (.310-.041 (<LOD-.116) .260) .158-.370 (.120) .830) .220 (.458 (.240) .430-.110 (.090-.

Concise International Chemical Assessment Document 70 Heptachlor [online]. maternal serum and milk from Wielkopolska region.pdf. 9/25/07 International Programme in Chemical Safety (IPCS). 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). Organochlorine exposures and breast cancer risk in New York City women. Bioassay of chlordane for possible carcinogenicity.niehs. August 2007. A Report to the Hawaii Heptachlor Research and Education Foundation. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum.inchem. Takahashi W. Stehr-Green P.9:1-109. Environ Res 2000.41:145–148. Voorspoels S. 79. Loo S. Jaraczewska K. Kolonel LN. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Bjerselius R. Environ Health Perspect 2002. 4/21/09 James RA.nih. 4/21/09 Baker DB. Available at URL: http://ntp. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor. Tartter P. Hertz-Picciotto I. Shindell S and Ulrich S. Distribution of polychlorinated biphenyls. Jr and Laws ER. 731-915. 1991 pp. Keller JA. Head SL.gov/toxprofiles/tp31.cdc. Available at URL: http://www. Baker DB.110:617-624. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Sci Total Environ 2004. National Toxicology Program (NTP).372:20-31. Toxicological profile for heptachlor and heptachlor epoxide [online]. Environ Health Perspect 2003. Chlordane and heptachlor [online]. Laliberte C. Eds.html. Vol. Organochlorines in Swedish women: determinants of serum concentrations. 2006. Poland. Available at URL: http://www. LeMarchand L. Darnerud PO. Environ Health Perspect 2002. Saidein D. gov/toxprofiles/tp12. 88 Fourth National Report on Human Exposure to Environmental Chemicals . Smith AG. Wohlleb JC. Aune M. 2 Classes of Pesticides. Bull Environ Contam Toxicol 1981:27:506-511. Bleiweiss IJ. Glynn AW. Academic Press.pdf. Brower S. Dewailly E.gov/ntp/ htdocs/LT_rpts/tr009. Charles MJ. New York. In Hayes WJ.Summaries & Evaluations.330:55-70. Mortality of workers employed in the manufacture of chlordane: an update. Wolff MS.8:1-123.gov/ntp/ htdocs/LT_rpts/tr008. J Occup Med 1986. Ayotte P. et al. Arch Pediatr Adolesc Med 1996. Dewailly E. Siegel BZ. Hawaii Med J 1991. 2001. et al. Organochloride pesticide residues in human milk in Hawaii. Available at URL: http://ntp.heptachlor. Jr. Vol.atsdr. JAMA 1988. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Chashchin V. Drews K. 1979-1980. Dendle WH.htm. 6/1/09 Rogan WJ. Canada). 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Barker J.html. Gilman A. May 1994.50(3):108-118. Senie R. Odland JO.28:497501. 1963-1967. Natl Cancer Inst Carcinog Tech Rep Ser 1977b.259(3):374-377. Lulek J. Berkowitz GS. Toxicological profile for chlordane [online].150:981-990. Available at URL: http://www.110(8):835-838.84:151-161. 1986.inchem. Inc. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii.cdc.org/documents/iarc/ vol79/79-12.html. Bioassay of heptachlor for possible carcinogenicity. Circumpolar maternal blood contaminant survey.htm. et al. Atuma S. 1994-1997 organochlorine compounds. 1993. Chlorinated Hydrocarbon Insecticides.111:349355. Available at URL: http://www. Natl Cancer Inst Carcinog Tech Rep Ser 1977a. Royce W. Covaci A. Lawrence River (Quebec. Arch Environ Health.org/ documents/cicads/cicads/cicad70. Pollutants in breast milk. Wong L. International Agency for Research on Cancer (IARC) . Available at URL: http://www. Van Oostdam JC. Hansen JC.niehs.org/site/foundation/ research/projects2. International Agency for Research on Cancer (IARC).nih. Sci Tot Environ 2006. 6/1/09 National Toxicology Program (NTP). Granath F. Handbook of Pesticide Toxicology. et al. KalubaSkotarczak A. Muckle G. Takei G. Willman E. 4/21/09 Dallaire F.atsdr.

air.9 (<LOD-20.9) < LOD < LOD 9.3-590) 293 (104-541) 48.2 (<LOD-40. These chemicals are highly persistent in soil.90 (<LOD-12.5-36. In the body. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.10 (<LOD-12. particularly for endemic vector and malaria control.3) 21.7.3 (27.4) < LOD 17.6-33.8-23. It was produced and used in the U. population from the National Health and Nutrition Examination Survey.0) 19.0) 20. Gunderson.5-54.0) 40.6 (31.0 (18.4) < LOD < LOD < LOD 61. DDT is converted to DDE and several other metabolites. and 7.5 (23. o. 1991).p’-DDT (65%-80%). Survey Geometric mean (95% conf.6 (9.9) 14. DDT is converted in the environment to other more stable chemical forms.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.6 (25.00 (<LOD-10. and 03-04 are 20. as well as in plant and animal tissues.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 (10.5 (15.0-155) 83. < LOD means less than the limit of detection.3) 22.1’-dichloro-(2.0-37.9 (21.5) 23. 2008. which is a mixture containing p.0 (18. sediments. Food imported from countries that still use DDT may contain the chemical or its residues. and water.7 (15. p. and dairy products.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.8-26. 17.9) 29. 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.S.5 (14.9 (10.3) 28. fish. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. 2002. respectively. Fourth National Report on Human Exposure to Environmental Chemicals 89 .9 (10.50-11. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 (23. although DDT and DDE intakes have decreased over time (FDA.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. resulting in fetal exposure.2-95.70 (8.3 (<LOD-21.1-71. inhalation.6 (<LOD-25. The biodegradation half-life of DDT in soil varies from 2 to 15 years.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. DDT usually refers to the technical product.1 (<LOD-39. Smith.4 (23.0) 26.3 (<LOD-31. In the general U. Only a small proportion of DDT is metabolized and excreted (Smith.2) 155 (59.S.8. It is still used in some countries.10-13.7) 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. Both Serum p.7) < LOD 18.5 (23. or dermal exposure. DDT and DDE can cross the placenta.8-17. see Data Analysis section) for Survey years 99-00. depending on conditions.8) 30. continues to be the primary source of DDT exposure.3-16.6 (22. food.2-bis(p-chlorophenyl) ethane (DDD).5) 25.1) 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 12.0-27.2 (11.1’-(2. population.7 (19. 1991). DDT was used at one time as a treatment for head and body lice.9-34. after World War II until 1972. DDT can be absorbed after ingestion.1 (33.1-27.5) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * 11.5) < LOD < LOD 9.8) 36.0-15.0-53. which may vary for some chemicals by year and by individual sample. when virtually all use of it was banned.8) 15.1) 31.p’-DDT (15%-21%).S.0-35.7) 12.2) < LOD < LOD 9. 01-02.3-236) 24.8-39.p’-DDD (4% or less).4.2) 30.0 (21. particularly meat. and trace amounts of several related compounds. 1988).9) 17.9 (10.9-28.3) 21.7-16.2-65. including 1.

* Not calculated: proportion of results below limit of detection was too high to provide a valid result. In laboratory animals.203) . tremor.240 (. 1956). 2006). Longnecker et al. and altered behavior after neonatal exposure (Eriksson and Talts.p’-DDD and p. resulting in exposure to nursing infants (Rogan.420) .180 (. Animal studies reported reduced fertility.146 (.108 (.086 (.150) .106) < LOD < LOD . 2006).140) . accidental exposures.200 (. 1998).098-.170) . polychlorinated biphenyls.34) ... 90 Fourth National Report on Human Exposure to Environmental Chemicals .130 (<LOD-.. population from the National Health and Nutrition Examination Survey.. and leukemia have also been inconclusive (ADSDR.290) .071 (. 2006.250 (.400 (.. 2004.62 (.260) . overt signs of acute human toxicity include vomiting.150 (<LOD-.150-.00 (. dioxins and furans).150-. Mariussen and Fonnum. and o. have not been consistently demonstrated (Beard.. Gladen and Rogan. premature delivery.051 (<LOD-.230) . 2001). 2002.075) 1.105-.071-. Calle et al.01) . 2002.190 (.180) . 2001).146 (. Gray et al. Hayes et al. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown.530 (..095) < LOD .061) < LOD < LOD < LOD . Jusko et al. Snedeker. although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.p’-DDE can produce anti-androgenic effects (Gray et al. 2001). It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.180 (.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 .079) < LOD < LOD .068-..170 (. and seizures.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 . other organochlorines.180-.189-. fertility.530) .00) .330-4.570-4.059-. 2001). 2006.120 (<LOD-.190-1.080-.160-. 1996).240) . 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. which may vary for some chemicals by year and by individual sample.g..106-.128 (.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.084 (. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al. Beard.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * . 1995. DDT may bind to estrogen receptors (Chen et al.054-.220) .074-. and duration of lactation.069) .063 (<LOD-.. 2002.064 (.400) .120-..132-.201 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 2002. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.130 (<LOD-.627) . 2006). Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.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 .343) < LOD .065-.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. Studies of DDT exposure and pancreatic cancer.130-. lung cancer.114-.142 (.26) 1.078-.313 (. Reproductive effects in humans affecting birth weight. Survey Geometric mean (95% conf.112 (.S.143) < LOD < LOD .. A workplace standard for DDT has been established by Serum p.106) . reproductive organ abnormalities.048 (<LOD-. In high dose.190 (.180) . 2000.150 (<LOD-.250-1.Organochlorine Pesticides chemicals are excreted in breast milk.140-. 2006. Jusko et al.087 (.220) .230) .078 (. 1997).170-.130 (<LOD-.

Smith. population from the National Health and Nutrition Examination Survey. EPA at: http://www. 01-02. population declined by about fivefold to tenfold. 2003. 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. In general...e. 1989). 2003). Fourth National Report on Human Exposure to Environmental Chemicals 91 . mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p.p’-DDT) as a possible human carcinogen. 2004). 2005).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. 8.. 1991).atsdr. compared to levels observed in this Report (Anderson et al.Organochlorine Pesticides OSHA and a guidance established by ACGIH. 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. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR.7-119) 113 (100-140) 93. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels.8. Heudorf et al. 2002. More information about external exposure (i. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al.html.gov/ pestcides/ and from ATSDR at: http://www. Survey Geometric mean (95% conf. 2004). mean serum levels of DDT and DDE in the U.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. respectively. 2002.6 (81. Biomonitoring Information DDE persists in the body longer than DDT.S..6. In a population-based sample of men and women from eastern Slovakia. Declining DDE levels over time have also been observed in the German population. and 03-04 are 18. 1998. Link et al. Compared to females in the NHANES 1999-2000 subsample.S.gov/ toxpro2. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person.cdc. respectively.3. Since the 1970’s.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.epa. IARC classifies DDT (p. NTP considers DDT as being reasonably anticipated to be a human carcinogen... for males and females in the NHANES 19992000 subsample (Pavuk et al. see Data Analysis section) for Survey years 99-00. environmental levels) and health effects is available from the U.. Stehr-Green..S. 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. and 7.

66) 3. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.64) 3. 2004).8 (14.69) 4. interval) 1.32 (1.93 (7.561 (.6) 12.58) 1.51-15.34-3.5) 10.38 (1.47) 3.79) 4.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.68-4.87-16.2 (19.00) 7.04 (6.520 (.09-1.03-4.37-4.66-17.81) 11.14-9..72) 1.00 (.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 .31-12.31 (1.01-1.2-32.01) 1.45 (1.p’-DDT.6) 8.77 (1. less than one percent had detectable serum levels of o.9 (15.29 (1.8-90.726) .82) 1.24 (1.456 (.34) 6.34 (7.4 (8.91 (6.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.55 (2.25) 8.82 (1.8) 15.994-2.41 (1. or p.26-10.11 (2.9-38.49) 8..30 (1.28) 1.49 (1.56-6. serum levels of o.1 (8.0 (12.11-1.430-.76) 1.24-17.71) 32. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.59 (4.51) 1.66-2.69) 8.13-2.76) 1.99) 1.69 (1.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1..07) 1.80) 1.46-2.43-4.07 (5.37-1.75 (8.83 (1.57) 2.25 (.44) 1. High mean levels of whole blood DDT (about 3.71) 12.4-19.488-.0 (9.9 (26.37 (1.48-4.39 (3.05 (3.3) 16.54 (1.02 (2.32) 1.13) 4.91-2.81-18.54) 8.97-4.6) 13.39) 1.66-4.6) 9.59) 3.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.53) 1.66) 1.96) 1.13 (1.92 (3.40-4.557) 1.6) 9.6) 11.730) .88 (2.4) 13.22) .70-3.06) 3.20 (.78 (4.25) 1.p’-DDT.52 (1.27) 3.43 (5.90) 22.5) 22.7-20.68) 2.40-4.54-7.32-9.45 (1.3) 10.76-3.63-15. population from the National Health and Nutrition Examination Survey.46 (1.61-2.85 (1.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.38 (1. In the NHANES 1999-2000.2 (6.36) 3.40-8.72) 1.6) 9.4) 9.51) 3.36 (3.12-1.75) 1.10-5.15-4.59 (1.23 (7.01) 1.5) 5. Finding a measurable amount of p.21) 3.84 (3.43-4.26-2.2 (9.51-8.04-1.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.10-1.80) 1.26) 3.57 (1.57 (3.10) 2.75) 6.611-1.26 (1.870 (.419-.71 (5.05) 1.40 (3.7-19.18-3.8 (13.65) 1.600) .680-1.69 (2.65 (1.17-3.37-16.80) 3.19-14.6) 9.1) 7.49 (6. Serum p.646) .7-48.6 (7.25 (1.25-14.75 (4.7) 16.57-3.84-3.51-49.06) 1.53) 7.71 (6.36-1.16-1.385-.51 (1.01-11.69 (. 1971).01-11.21) 90th 7.965-1. Survey Geometric mean (95% conf.22 (7. 2004).36-2.2) 26.7) 9.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .57-2.31-2.87 (5.97 (3.14) 2.3) 13.14 (1.14-1.4 (12.32-1.12 (6. 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.34) 2.57 (1.01-1.p’-DDT were below the limits of detection.92) 1.18-1.22-1.18) 1.963-1. 1989).50-17.00-1.6 (17.9-17.18 (6.7 (8.9) 7.46 (1.41-12.02-8.8 (13.635) 1.49 (1.53 (2.32 (1.590 (.00 (6.70) 1.63 (1. considerably higher than levels in this Report (Smith.3 (8.90-8.12 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.30 (1.43-8.02) 1.63 (6. o. 2005).07) 1.80 (2.57-13.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.S.75) 2.60-13.33-1.61 (1.18-1.Organochlorine Pesticides nearby agriculture (Botella et al.50 (2.91) 3.01-5.30-1.7) 13.5) 16.56-2.37-10.81-5. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.820-1.81 (1.39-1.10) .500-.85-4.91-3.4) 14.66) 4.59) 6.47 (1.9) 5.58) 75th 3.66) 1.25-16.56-3.88-35. In a subsample of NHANES II (19761980) participants.92 (3.03-1.3 (9.63 (1.85-10. 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.68 (2.62-6.1 (9.17 (3.3-43.860 ng/L) and DDE (about 14.48 (6.14) 2.1) 12.6 (8.76 (2. 1991).36-11.56) 2.30-1.52 (3.0) 2.24) 1.96) .27-1.2 (9.39-2..623 (.64-2.81 (7.32-1.16 (2. 309 versus 268 ng/g lipid.59 (1.53-15.18-4.1) 40.35) 1.8 (9.55-9.19) 4.52-6.796 (.58) 1.6 (9.5) 7.34-11.2) 19.01-15.p’-DDT (Stehr-Green.534-.77 (1.516 (.890-1. 2001-2002 and 2003-2004 subsamples.

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

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

Longnecker MP. FDA total diet study. Neurotoxicol 2000. et al. Environ Res 2005. Brock JW.111:349355. April 1982 to 1984. Kashyap R. Piechotowski I. Calle EE. Hanrahan L. Hurd C.112(17):1761-1767. and dichloro(diphenyl)ethylene (DDE). Botella B.72:261265. Epidemiology 2006. FDA Pesticide Program Residue Monitoring 1993-2006 [online].cdc. Klebanoff MA. Needham LL. Chen CW. Vena JE. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 4/21/09 Gladen BC. Available at URL: http://www.85:504508. Aune M. Eriksson P. and polythelia among male offspring.162:890-897. Vorojeikina DP. Brock JW. DDE. Davis MD. Patterson DG Jr. Environ Health Perspect 2004.205:297-308. Swanson MK. Schulz C. Food and Drug Administration (FDA). et al. and other chemicals. and HCB residues in human blood in Ahmedabad. Wolf CJ. Furr J. selected elements. Kulkarni PK. et al.355:7889.52:301-309. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). dietary intakes of pesticides. Fourth National Report on Human Exposure to Environmental Chemicals 95 . a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Garrett N. Rogan WJ. Environ Health Perspect 2003. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Bates MN.7(3):248-264. Granath F. Levels of DDT. Angerer J.96:34-40. Effects of environmental antiandrogens on reproductive development in experimental animals. JAMA 1956. Talts U. Heudorf U. DDE and shortened duration of lactation in a northern Mexican town.html. Needham LL. et al. dichlorodiphenyldichloroethylene. Savitz DA.206:485-491.1-dichloro2.71(6):1200-1209. and DDD [online].17(6):692-700.97(2):178192. Zhou H. CA Cancer J Clin 2002. Zhou H.106(5):279-289. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Maternal serum level of 1. Environ Res 2004. Gunderson EL. Glynn AW. et al. Bjerselius R. Notides AC. lindane (g-HCH). Koepsell TD. Barr DB. Organochlorines and breast cancer risk. Hum Reprod Updat 2001. Cueto C. Klebanoff MA. 4/21/09 Anderson HA.atsdr. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. hypospadias. et al. Thun MJ. Needham LL. Baker RJ. Gray LE Jr. Available at URL: http://www. Jr. Lancet 2001. Chemosphere 2004.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. Klebanoff MA. Link B. J Assoc Off Anal Chem 1988. Organochlorines in Swedish women: determinants of serum concentrations. Frumkin H. Drexler H. hexachlorobenzene. Biochem Pharmacol 1997. Parks L. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males.58:1185-1201. Int J Hyg Environ Health 2003. Darnerud PO. Atuma S. Greenfield TA. Bhatnagar VK. Paepke O. Crespo J. Bloom MS.53(8):1161-1172. Jusko TA. Henley SJ. Willman EJ. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Burse VW.21(1-2)37-48. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Sci Tot Environ 2006. Bull Environ Contam Toxicol 2004. Zaidi SS. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. India. Ellis H. Ostby J. Environ Health Perspect 1998.html. Olea N. Seiwert M. Buckland SJ. HCH. Katz SH. Zoellner I. et al.. Moysich KB. Falk C. Biomonitoring of persistent organochlorine pesticides. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. DDT and human health.fda. Gladen BC. Herrman T. et al. Lepom P.358:110-114.54:1431-1443. Durham WF. Gray KA. Profiles of ortho-polychlorinated biphenyl congeners. August 2008. Am J Epidemiol 2002. Rivas A.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR).gov/ toxprofiles/tp35. Int J Hyg Environ Health 2002. Toxicological profile for DDT. The effect of known repeated oral doses of chlorophenothane (DDT) in man. September 2002. Maternal DDT exposures in relation to fetal and 5-year growth.cfsan. Exposure of women to organochlorine pesticides in Southern Spain. Charles MJ. Arnold SF. Longnecker MP. Lambright C. Krause C. Am J Public Health 1995. Gabrio T. Beard J. Hediger ML. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Olson J. et al. Becker K. Saiyed HN. Olson JR. Hayes WJ. Chemosphere 2005.gov/~dms/ pesrpts. Cerrillo I. Jr. The Great Lakes Consortium. Olea-Serrano MF.155(4):313-322. Kaus S.

Pollutants in breast milk. PA. J Toxicol Environ Health 1989. Pavuk M. 731-915. Stehr-Green. Lynch CF.27:405-421. Astolfi E.36:253-589. Jr. Jr and Laws ER. Fonnum F. Chemosphere 2004. Petrik J. Snedeker SM. Environ Health Perspect 2001.53:455-477. Comparative pharmacodynamics of CYP2B induction by DDT. Demographic and seasonal influences on human serum pesticide residue levels. Jones CR. Arch Pediatr Adolesc Med 1996. Cerhan JR. Chovancova J. Lubet R. Deichmann WB. Chlorinated Hydrocarbon Insecticides. and dieldrin. In Hayes WJ. et al. New York. Reddy AB. Rogan WJ. Schecter A. Crit Rev Toxicol 2006. Fox S. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Inc.54:1509-520. Radomski JL. Rey AA.Organochlorine Pesticides Mariussen E. Academic Press. 2 Classes of Pesticides. Nims R. Thomas PE.20(2):186-193. Handbook of Pesticide Toxicology. et al. Toxicol Appl Pharmacol 1971. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Eds. Smith AG. Pesticides and breast cancer risk: a review of DDT. J Toxicol Environ Health Part A 1998. DDE. children and newborn infants. 1991 pp.109:35-47.150:981-990. Neurochemical targets and behavioral effects of organohalogen compounds: an update. and DDD in male rat liver and cultured rat hepatocytes. Vol. DDE. 96 Fourth National Report on Human Exposure to Environmental Chemicals .

High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. Ketoendrin is a major photodegradation product (IPCS. 1991). Smith. Kavlock et al.40 (<LOD-6. endrin is converted rapidly to its major metabolite. Endrin was used as an insecticide. 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. population from the National Health and Nutrition Examination Survey. anti-12hydroxyendrin..10 (<LOD-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Endrin does not accumulate in body tissues (IPCS. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. < LOD means less than the limit of detection. 72-20-8 General Information Endrin. and inflammation (Smith. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.70) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5.S. 1996. endrin usually is not detected in serum of exposed individuals. 1981). EPA. Survey Geometric mean (95% conf. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. Fourth National Report on Human Exposure to Environmental Chemicals 97 . or from contact with contaminated soils and sediments in areas where endrin was applied. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al.20 (<LOD-5.S. endrin has been detected with declining frequency in U. which may vary for some chemicals by year and by individual sample. rodenticide and avicide. or discarded. 1987). In the body.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. Depending on soil conditions. All uses of the pesticide in the U. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. a stereoisomer of dieldrin. 1992).S.S. 2008). An epidemic of acute endrin poisoning.. and occasionally at low levels in sediment and surface waters.50) < LOD 5. inhalation or dermal exposure routes.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. Hepatic effects of endrin exposure have included necrosis.Organochlorine Pesticides Endrin CAS No. 1992).09 and 7. have been cancelled by the U. endrin can persist for years.30 (<LOD-6. manufactured. 1979. IPCS. unless the dose is high and the exposure is very recent.60 (5. fatty infiltration.8. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. is no longer manufactured in the U.S. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. 1992). At high doses. see Data Analysis section) for Survey years 01-02 and 03-04 are 5.40-5..10 (<LOD-5. Endrin has been detected in soils. Because it is metabolized so rapidly.30) < LOD 5. 1991).. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. unlike aldrin and dieldrin.20 (<LOD-5. Endrin was not widely used as a termiticide.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. Over time. Endrin is absorbed rapidly after ingestion.50) < LOD < LOD < LOD 5. 1992. total diet surveys (FDA.

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

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

wildfowl.6-19..8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. 31.6-TCP) (To-Figueras et al. Urinary metabolites include pentachlorophenol (PCP). respectively.4.2 (13. 1976).3-26.4 (11.6-33. and 03-04 are 118.1 (14.9) < LOD < LOD 20.5-trichlorophenol (2. 100 Fourth National Report on Human Exposure to Environmental Chemicals .4) < LOD < LOD 18.8 (22. The FDA dietary surveys have shown that over time.4.1) * * 15.3 (20. 1988).7) < LOD < LOD 75th < LOD < LOD 90th * * 15.6) < LOD < LOD 25.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and foods with a high fat content.4 (22.9) < LOD < LOD 15.6) < LOD < LOD 26.0-19. population from the National Health and Nutrition Examination Survey.9 (25.S.7-26.4 (18.7-16.1-20. measuring HCB in serum is a specific indicator of exposure to the parent Serum Hexachlorobenzene (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.9) 19.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.0 (18.6) < LOD < LOD 26. 2008. 01-02.7 (15.5-15. HCB is slowly metabolized. distributes widely throughout the body.9) < LOD < LOD 28.0) < LOD < LOD 15.1 (17.3 (12.7 (15. and elimination occurs by renal and fecal routes.9) < LOD < LOD 16. or game taken from areas with HCB contamination.7-16.4) < LOD < LOD 22.7) * * 14.2-31.5-TCP) and 2.5-14.4. < LOD means less than the limit of detection.6-44.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.7) < LOD < LOD 24.2 (17.2) < LOD < LOD 13.9 (23.7) 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 * * 16.4-15.2 (14. HCB is well absorbed after oral administration.S.2-15.9) < LOD < LOD 20.5-18.1) < LOD < LOD 15.4) < LOD < LOD 19. The general population may be exposed to HCB through diet.3-20.9 (14.8) < LOD < LOD 27.7-30.0-28.7-15. Therefore.6) < LOD < LOD 24. 2002).8-15. Survey Geometric mean (95% conf.4-16. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications. Gunderson.5-15.1-16.S. EPA cancelled its use in 1984.1 (14. and has been detected in soil. see Data Analysis section) for Survey years 99-00.0) * * 15.4) < LOD < LOD 33.0.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.3 (22.7 (27.1 (13.3) < LOD < LOD 20. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.4.6-trichlorophenol (2.3-22. breast milk is an additional route of elimination in nursing women. particularly by consuming fish.3) < LOD < LOD 29.0-25. water.3) * * 15.0) < LOD < LOD 24.2-15. HCB has been detected in fewer foods since the 1980s (FDA. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.4) < LOD < LOD 14. 2005). Although it is not manufactured as an end-product in the U.. and 7.3 (22.8 (15.7 (19.9-32. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.9 (25...0) < LOD < LOD 15.5 (13.5 (14.3) 24.9-24. air.5-14. 1997).Organochlorine Pesticides Hexachlorobenzene CAS No. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides. and accumulates in fatty tissues where it persists for years.4 (18.4) < LOD < LOD 23.7-29. primarily as a fungicide and seed treatment until the U.6-32.9-30.3 (16.9-20.6 (23.5) < LOD < LOD 18.0 (25. which may vary for some chemicals by year and by individual sample.S.0 (14.7-21.0 (18.9-15.2 (24.6 (21.6) < LOD < LOD 14.9) < LOD < LOD 19. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.5-33.7-22.8.0-16.8 (26.5 (13.3 (14.6-26. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.9-17.2) < LOD < LOD 29. 2. and sediment (Barber et al.2 (14.6 (24.

092 (.086-.062-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .098 (. as well as hypertrichosis.157 (.123 (. Biomonitoring Information Serum concentrations reflect the body burden of HCB.099) < LOD < LOD .163) < LOD < LOD .107) < LOD < LOD .114-. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 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.100) < LOD < LOD .085) * * .088-. and liver and thyroid cancers (ATSDR.S.087 (.225 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.203) < LOD < LOD . very high. EPA at: http://www.081 (.123 (.175) < LOD < LOD . and weakness.065 (. 1982.163-. immunologic abnormalities. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.097 (.090 (.095-.069) < LOD < LOD .090 (.090-.073-.html. With chronic exposure.060-.095) * * . 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. 1960).178-.122) < LOD < LOD .Organochlorine Pesticides chemical.107-.147-.e.095 (.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 * * .095) < LOD < LOD 75th < LOD < LOD 90th * * .155) < LOD < LOD .132) < LOD < LOD .094 (. Infants were exposed transplacentally and through breast milk.099) < LOD < LOD .167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .182 (.130) < LOD < LOD . Chronic feeding studies in animals have demonstrated kidney injury.079 (. Schmid.064 (.S.121 (.143-. and many died before 2 years of age (Peters et al. ACGIH has developed workplace exposure limits for HCB.086-.145-.092-.160 (.258) < LOD < LOD . IARC classifies hexachlorobenzene as possibly carcinogenic to humans.118-.gov/pesticides/ and from ATSDR at: http://www.171 (.078 (.140 (. environmental levels) and health effects is available from the U.148-. EPA has established a drinking water standard.156 (.083) < LOD < LOD . The U.118-.089-.118) < LOD < LOD .102) < LOD < LOD . thyromegaly. which may vary for some chemicals by year and by individual sample. and the FDA has established a bottled water standard for HCB.196) < LOD < LOD .113-.190 (. Fourth National Report on Human Exposure to Environmental Chemicals 101 . In humans.086) < LOD < LOD .072-.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.097) < LOD < LOD ..115 (.088-. acute doses produce central nervous system depression and seizures.atsdr.173) < LOD < LOD .176-.114-. More information about external exposure (i.186 (.145-.109) * * .135-.163 (.179 (.082-.095 (.176) < LOD < LOD . reproductive and developmental toxicities.077-.102 (. HCB interferes with normal heme synthesis.081-.167 (.169-. 2002).cdc.157-. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.S.097) .gov/toxpro2.090 (.091-.069) * * .epa.125 (.088-.191 (.159-.111) < LOD < LOD . This condition.129) < LOD < LOD .092 (.126) .085-.141) < LOD < LOD .094) < LOD < LOD .111-.203) < LOD < LOD .212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .089-.092 (.174-. arthritis. anorexia.099) < LOD < LOD .104 (. Survey Geometric mean (95% conf.127-.120 (..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 * * .147 (.123 (.152) < LOD < LOD . population from the National Health and Nutrition Examination Survey.

Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. In Spain. 2002. Sci Tot Environ 2005. Gocmen A. but overall. Sala M. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect.58:1185-1201. Aune M.fda.html. J Assoc Off Anal Chem 1988. August 2008. Dogramaci I. Reference values updated. Kemper FH. 2003). In a representative sample of the 1998 German adult population. Eskenazi B. Glynn et al. 2002).81(2):82-85. 1986. Available at URL: http://www. Ayotte P.349:144. Kaus S. 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.111:349355.135(4):400404. Lackmann.gov/~dms/ pesrpts.. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Holland NT. In the 1976-1980 NHANES subsample. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al..17:388–399. Krause C.. Can J Biochem 1976. Lepom P. Gunderson EL.54(3):203-208. Granath F. Bradman A. Ozalla D..9% of participants had quantifiable levels (Stehr-Green. however. Bryan GT. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Barr DB. et al. 2002) and among children (Link et al. Peters HA.44 mg/L. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. Lawrence River (Quebec. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. levels. Atuma S.cdc.. only 4. Biol Neonate 2002. Herrman T. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. 1989). Jones D. Seiwert M. distribution... than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al.. Bertram et al. more HCB levels were quantified. September 2002. Lecha M. Available at URL: http://www. Schwartz JM. 2002. dietary intakes of pesticides. trends and processes. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Arch Dermatol 1999.110(8):835-838.gov/ toxprofiles/tp90. and the geometric mean concentration of HCB in whole blood was 0. The metabolism of higher chlorinated benzene isomers. 1999).Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. et al. IARC Sci Publ 1986. Darnerud PO. FDA total diet study. Santiago-Silva M. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Link et al. Lackmann GM. Herrero C. Int J Hyg Environ Health 2002. Organochlorines in Swedish women: determinants of serum concentrations. References Agency for Toxic Substances and Disease Registry (ATSDR).. Arch Neurol 1982. 2002. HCB levels were directly related to age. Zoellner I. 2005). Jones KC. van Wijk D.atsdr. 4/21/09 Glynn AW. Environ Health Perspect 2002. et al. April 1982 to 1984.cfsan. As a result of the lower limit of detection in NHANES 2003-2004. selected elements. Food and Drug Administration (FDA). Piechotowski I. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Dallaire F. 2005). Otero R. Kohli J. Lackman.. Bjerselius R. Safe A. 4/21/09 Barber JL. et al. Canada). Laliberte C. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. HCB detection in serum also was proportional to age. 2002. Fenster L. 2005. Biomonitoring of persistent organochlorine pesticides. Gabrio T. Muller C. J Exp Sci Environ Epidemiol 2007. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Toxicological profile for hexachlorobenzene update [online]. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Bradman et al. Becker K. Link B. Schulz C.77:173182.html. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al.205:297-308. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Muckle G. and other chemicals. Dewailly E.. Bertram HP. Chemosphere 2005. Cripps DJ. respectively. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. 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. Sweetman AJ.39(12):744-749. Over the past two decades.71(6):1200-1209. 2006). Environ Health Perspect 2003. Hexachlorobenzene in the global environment: emissions. Paepke O.

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

each result has been multiplied by 1.7 (13.9-24. 58-89-9 General Information Hexachlorocyclohexane (HCH).9 (40.04-10.8-54.4) 27.6) 16.6-62.6) 50.5) 90th 42.1 (16. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.90-8.2-42.8-19.43 (<LOD-9.4-50.2 (48. 104 Fourth National Report on Human Exposure to Environmental Chemicals . so they can accumulate in fatty tissues of animals. see Data Analysis section) for survey years 99-00.1 (30.7-96.7) 32.1-15.7) 56.5 (8.8-16.7-166) 70.1-36.2 (29.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.5) 40.1 (9.8) 12.8) 7. 319-85-7 gamma-Hexachlorocyclohexane CAS No.4 (11.6) 653 758 589 1240 1533 1370 20 years and older 10.3-56.0-34.3-38. It is no longer produced or sold in the U.6-47.8) 39.7) 18.2) 9.1 (12.9 (9.0 (33.8 (9.0 (<LOD-12.5 (37.70 (8.1-49.7) 10.0) 17.4-73.6-42.5-123) 49.7) 27.5 (14.7 (30.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.0) 7.9-81.4) 21. the U.7 (53.4) < LOD < LOD < LOD 46.1) 12. Technical grade HCH is a mixture of all four isomers.0) 41.5528. See the section “What’s New” at the beginning of this Report for details.2) 142 (99.S. exists in several isomeric forms.4) 51.9-178) 48.9-56.6 (22.1-32.2-20.7-96. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.6) 35. interval) 9. which may vary for some chemicals by year and by individual sample.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14. formerly referred to as benzene hexachloride.4) < LOD 9. beta.2-98.6-18.5 (43.0-20.7-20.8) < LOD 10.8 (32.7 (25.6) 47. commonly known as lindane.4) 44.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.1-16. < LOD means less than the limit of detection.9) 17.2 (18.4 (12.2) 36.70-19.0-70.0-21.6 (16. particularly alpha and gamma have been detected widely in air.6-37.2) 13.68 (<LOD-10. The gamma isomer.70-12.0-70.4 (50.9 (11.90-8.1 (9. 2005). HCH isomers. 608-73-1 beta-Hexachlorocyclohexane CAS No.90) 7.7 (35.2 (50.9 (62.S.5 (11.2-46.3 (42. gamma.6 (33. The other isomers can be formed during the synthesis of lindane. In 2006.4 (8.9) 81. population from the National Health and Nutrition Examination Survey.0 (35.6) 18. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.8) 27.0) 71.80 (<LOD-14.8) 95th 68.5) 16.9 (50. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.60-13.36.Organochlorine Pesticides Hexachlorocyclohexane CAS No. environmental levels declined.7 (62.89 (<LOD-9. containing about 64% alpha and 10%-15% gamma isomers.0-23.2-87.7) 23.9-14.1-27.1 (18.70 (6.2) 62.3) 14.5 (24.1 (11. 6.6-14.4) 901 1067 952 992 1224 1007 Females 11.9) 15.5) 67.1) 71. and 03-04 are 9.7 (<LOD-16.5) 11.6 (17.7) 10.8) * * * * * * 15.2-17.4) 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 21.9 (30.9-21.1 (27.2 (34.3 (42.0 (8.4-111) 84. **In survey period 2001-2002.7-26.56-12.50) 8. and 7.2-22.5) 29.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19. EPA cancelled agricultural uses of lindane (ATSDR. As pesticide applications of HCH were increasingly restricted or eliminated. HCH isomers are lipophilic.7-69.5-29.5) 22.8 (23.6-20.2-55.4 (16.0 (14.4 (52.1-32. Lindane has a half-life of about two weeks in soils and water.20-16.8 (21.4) 11.8.7-69.0-111) 70. soil. respectively.8 (10.3 (13.S.1 (21.0) 8.0) 35.8) 52. General population Serum beta-Hexachlorocyclohexane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6 (40.4) 10.8-87.46-11. 01-02.2 (9.8 (33.5 (16.3) 34.87 (9. 2005).6) 36.5) 14.8 (64.0 (19.80 (6. and delta. including alpha.2-67.4-45.9 (32.1-37.6 (10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3 (62.30-11.3 (26.7) 97.2-52. and sediment as a result of historic production and use. water.9 (26.8-68.6-89.8-199) 134 (85.66-12.61-12.3) 37.3-85.3) 25.1) 12.0 (37. and have been used either as fungicides or to synthesize other chemicals.9) 45.9-51.3) 51.8 (17.1) 13.1) 31.7 (29.6-135) 69.76. However.7) 73.2 (31.

1996.600) .37) 1.290 (.260) . respectively. Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.150) .287 (. tremors.080) . probably by blocking inhibitory neurotransmitters in the central nervous system.350 (. When animals were chronically fed lindane at high doses.370-.250-.244-.070 (..090 (.382-.160) .092 (. U.120) .068-.470 (.103 (. each result has been multiplied by 1.110) .100 (. 2002). 2008.090-. EPA has established a drinking water standard.442 (.281 (.410) .710) .120-.210 (.100) .254) 95th .210) .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.680) .070-.130 (.150 (.140) . ingestion.240-.050-.059-. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.260) .065 (.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .290 (.125) < LOD < LOD < LOD .360 (. population from the National Health and Nutrition Examination Survey.062 (.310) .058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .560 (.331 (.140 (.120 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.. enlarged livers.118 (.110) .5528.404) .067 (.216 (.050 (<LOD-. See the section “What’s New” at the beginning of this Report for details.412 (. and nephropathy developed (IPCS.070 (. or dermal exposure.100-.100) . Saxena et al.372 (.120) .086) < LOD < LOD < LOD < LOD < LOD < LOD . 1971.170-.200-.050-.050-.070) .050-.190-.330 (.160-.190) .330-.210 (.077) < LOD .308-.587) 653 758 589 1240 1533 1370 20 years and older . from 6% of samples in 1982-1984 to 2% in 1994 (FDA.056-.S.521 (.191-.310) . **In survey period 2001-2002.060) .056-.910 (.580 (.139 (.073-.01 (.057-.700) .167 (.290) .214) .057-.077) < LOD .360) .080-.400) . Fourth National Report on Human Exposure to Environmental Chemicals 105 .360-.230-.280-.150-. HCH isomers are absorbed after inhalation.400) .190) .460) . and seizures. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown. which may vary for some chemicals by year and by individual sample.064) .057 (<LOD-.220 (.080-.840) .180-. for lindane.305) .S.051 (<LOD-..234 (. OSHA and ACGIH have established workplace standards and guidelines.070-.S.250 (.350) .190-1.32) .270 (.051-.174) . resulting in a half-life of about seven years.130-.050) .510) .410) .160 (.090 (.103) 90th .120-.380 (.210-. Workers who directly handled HCH have complained of headache.120 (.320 (.221-.064 (.140) . HCH crosses the placenta and is also excreted in breast milk (Radomski et al.091) . Gunderson 1988). hepatic enzyme induction.250 (.280-.620) .290) .260-.290 (.220) .069) . FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.089-.450) .081-.100 (. Rogan..080 (.048 (<LOD-. interval) .450 (.130) . 1977).175 (.050 (<LOD-.089) . After dermal application of lindane 1% lotion. and memory loss (Nigam et al.083 (.340-.070-.191-.146-.058 (<LOD-.144 (.620-1. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.294-.065 (.220-.080-. 1986).110) .Organochlorine Pesticides exposure to HCH is through the diet.390-.340) .062 (.200 (. and FDA has established a bottled water standard and food residue tolerances for lindane. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 1981). 1983).470) .150) . Distribution is mainly to fatty tissues.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 .120-.040-.100-.200-.173-.090 (.222 (.05) .118-.410 (.140) . Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.170-.390 (.240 (.319) .080 (. 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.560) .690) .480 (.096) .050 (.050 (.119) .103-.297-.220-.120 (.814) .460 (.098 (.420-.480) . The beta isomer accumulates in fatty tissues and is metabolized more slowly.047-.072 (.310 (. ataxia.450-.661) 901 1067 952 992 1224 1007 Females .480 (.124-.250 (.067) .250) . paresthesias.100-.080) * * * * * * . the serum half-life was about 20 hours among children (Ginsburg et al.570 (. The U.083) .131-.250-.580-1.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .501) .410-..300-.078 (.110-.

In an earlier (1996-1997) sample of German children. and 03-04 are 14. 1989).. the maximum and 95th percentile beta-HCH values. Biomonitoring Information Because of its longer half-life. 1991..8. respectively. Additional factors associated with higher beta-HCH levels include rural residence. 106 Fourth National Report on Human Exposure to Environmental Chemicals . Bates et al..epa. beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. 1998). 2005. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. 2005.html.. Stehr-Green. 1971. and a diet that includes meat (Becker et al. Link et al.S. 01-02.. 1991. which may vary for some chemicals by year and by individual sample. respectively.cdc. 2001-2002. More information about external exposure (i. In recent years. older age.e... environmental levels) and health effects is available from the U. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR.5. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. Survey Geometric mean (95% conf..gov/toxpro2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Stehr-Green. serum levels of lindane were generally below the limits of detection. and 2003-2004.. 1998. 2004.. 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. In NHANES 1999-2000. Becker et al. Kutz et al. In populationbased studies of New Zealand adults and German adults and children. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al. EPA at: http://www. 2004) and India (Bhatnagar et al. 1989.5. Sturgeon et al.atsdr. 2002).. were similar to the 95th percentiles in this Report. < 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. Radomski et al.gov/pesticides/ and from ATSDR at: http:// www.S. Kutz et al. and 7. 10. population from the National Health and Nutrition Examination Survey. 2004). see Data Analysis section) for Survey years 99-00. male sex. 2002.Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. aged 9-11 years.

Radomski et al. population from the National Health and Nutrition Examination Survey. 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. 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.. 2005). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1799 2280 1960 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 660 758 593 1139 1522 1367 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 863 1060 952 936 1220 1008 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 631 563 461 380 509 490 646 1045 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. 1998). 1986.S. 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. 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). 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.. 2003). 1971).. Fourth National Report on Human Exposure to Environmental Chemicals 107 . in this Report (Nigam et al. In a small study of adults who consumed sport fish from the Great Lakes. Finding a measurable amount of HCH isomers in serum does not mean that the level of HCH isomers causes an adverse health effect.Organochlorine Pesticides 2001-2002 survey period (Link et al. respectively. the median beta-HCH levels were similar or slightly higher than the 95th percentile in this Report (Anderson et al...

Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Brinton LA. Toxicological profile for hexachlorocyclohexanes update [online]. Environ Res 2004.fda. Needham LL.205:297-308. et al. Bai KM. Siddiqui MKJ.27:405-421. Botella B. Saxena MC. Available at URL: http://www.html. Rogan WJ. Becker K. Seiwert M.96:34-4Food and Drug Administration (FDA). Karnik AB. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Rivas A. selected elements. Arch Pediatr Adolesc Med 1996. Majumder SK.cdc. HCH. org/documents/jmpr/jmpmono/2002pr08. Crespo J.gov/~dms/pesrpts. J Pediatr 1977. Visweswariah K. children and newborn infants. Biomonitoring of persistent organochlorine pesticides. Bottimore DP. 4/21/09 Ginsburg CM. Atuma S. Brock JW. Lepom P.57(4):315-320. et al. August 2008. Burse VW. August 2005. Raju GS.106(5):279-289. Reisch JS. Levels of DDT. Bjerselius R.inchem. Olea N.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 4/21/09 Kutz FW. Environ Health Perspect 1998. and HCB residues in human blood in Ahmedabad.71(6):1200-1209. Arch Toxicol 1981. Sturgeon SR. Organochlorines in Swedish women: determinants of serum concentrations. Granath F.html. Schulz C. Herrman T. Int J Hyg Environ Health 2002. Absorption of lindane (g benzene hexachloride) in infants and children.cfsan. Needham LL.20(2):186-193. Needham LL. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. gov/toxprofiles/tp43. Patterson DG Jr. and other chemicals. Environ Health Perspect 2003. Lowry W. Nigam SK. Garrett N. International Programme on Chemical Safety (IPCS).58:1185-1201. Glynn AW. et al. Falk C. Stehr-Green. Aune M. et al. Kaus S. J Assoc Off Anal Chem 1988. Astolfi E. available at URL: http://www. Pollutants in breast milk. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Metabolism of gammahexachlorocyclohexane in man. Krishna Murti CR. Krause C. India. Buckland SJ.72:261265. Heinrich R. Rev Environ Contam Toxicol 1991. Link B.91:998-1000.54:1431-1443.120:1-82. Placental transfer of pesticides in humans. Ellis H. et al. FDA total diet study. Olea-Serrano MF. Demographic and seasonal influences on human serum pesticide residue levels.atsdr. Wood PH. Exposure of women to organochlorine pesticides in Southern Spain. Cancer Causes and Control 1998. Lindane. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Toxicol Appl Pharmacol 1971.52(1):59-67. Darnerud PO. Available at URL: http://www. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Rothman N. Gabrio T. The Great Lakes Consortium. Angerer J. Chemosphere 2004. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. Maass R. Piechotowski I. Kutty D. Gunderson EL.htm. Deichmann WB. Bhargava AK. et al. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Cerrillo I. Occupational exposure to hexachlorocyclohexane. Bates MN. Hanrahan L.150:981-990. Rey AA. VI. 2002. Radomski JL. 4/21/09 Anderson HA. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Zaidi SS. Kashyap R. Bull Environ Contam Toxicol 2004. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. et al.111:349355. dietary intakes of pesticides. Kulkarni PK. April 1982 to 1984. Paepke O.9(4):417-424. Int Arch Occup Environ Health 1986. Bhatnagar VK. PA. Potischman N. Saiyed HN. Olson J. J Toxicol Environ Health 1989. Int Arch Occup Environ Health 1983. Chemosphere 2005. Zoellner I.48:127-134.

see Data Analysis section) for Survey years 99-00.2) 51. mirex was detected in human adipose samples. Mirex can cross the placenta and be excreted in breast milk.5. and 03-04 are 14.1 (8.4 (8.6-305) 15. 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. where it has a half-life of 12 years. which may vary for some chemicals by year and by individual sample.6 (<LOD-31. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.2 (7. and 7.7 (<LOD-47.1 (<LOD-65. 1995). resulting in exposure to newborns and nursing infants.4) < LOD 63.6 (<LOD-23. In studies conducted in the 1970’s and 1980’s.0 (14.5-82.0) * * * 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.40 (<LOD-13. Formerly.1 (<LOD-104) < LOD < LOD < LOD < LOD 39. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.4-230) 18.Organochlorine Pesticides Mirex CAS No.S.6.10-37. and foods.10 (<LOD-15. especially those from persons living in the southeastern U. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex.70-24.7) 8. Some states and the U.7) < LOD 66. it is a highly persistent chemical in the environment.S.. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. (Kutz et al. Mirex has been detected in air.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. Occupational exposure is limited to workers at sites where mirex contamination is present. animals. disposal.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.3) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.3-225) 15. since 1977. Mirex is not metabolized in the body.90-29.70 (<LOD-15.3 (15.1) 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 16.8.8 (12.2-230) 13.8 (<LOD-73.7 (12.S.4) < LOD 15.6 (<LOD-108) 9. 01-02. sediments.5 (<LOD-115) 153 (30. 1991). after which it is widely distributed in the body and stored in fat. 2385-85-5 General Information Mirex has not been produced or used in the U. where it was applied directly to soil and by aerial spraying. respectively.0 (<LOD-108) < LOD < LOD 50.S.5 (9. or pesticide application. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 109 .0 (12. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.70-40. soil. 1985.6) 9.5 (<LOD-42. Mirex binds strongly to soil. 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.3 (15.S.0-374) 11.1 (13.6) < LOD < LOD < LOD < LOD 71.5-291) 11.5-425) 40. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8) < LOD 15. < LOD means less than the limit of detection. water.. aquatic organisms. 10. Mirex is absorbed through the skin and from the gastrointestinal tract.

which is approximately twofold to threefold lower than the 90th percentile for females in the NHANES 20012002 subsample but similar to 95th percentile for females in the NHANES 2003-2004 subsample (Van Oostdam et al.470 (.. Smith.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .110 (<LOD-..093 (. environmental levels) and health effects is available from the ATSDR at: http://www.054 (<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 .atsdr.077 (<LOD-.102) < LOD < LOD < LOD < LOD .090-1. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.370 (.106) < LOD .450 (.510) < LOD < LOD .055-.062-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .8. More information about external exposure (i. 7.090-1. 2004). which may vary for some chemicals by year and by individual sample.02) .106 (.37) .064 (<LOD-.170-3.080-1. and 4. 110 Fourth National Report on Human Exposure to Environmental Chemicals .41) .220) .e.92) . and NTP classifies mirex as reasonably anticipated to be a human carcinogen. serum mirex levels were generally below the limits of detection (Stehr-Green. Biomonitoring Information In the NHANES 1999-2000.090 (<LOD-.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th . population from the National Health and Nutrition Examination Survey.268) < LOD . Fishermen in New York who consumed Great Lakes sport fish had median levels of lipid-adjusted serum mirex that were lower than the 95th percentile value among males the NHANES 2001-2002 subsample (Bloom et al.070-1.410 (.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.Organochlorine Pesticides exposures are unknown.79) .470) . 2005).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 . The geometric mean mirex levels of the Inuit mothers were 8.089-.08 (.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 .220 (<LOD-.080-1. 1991).052-.140 (<LOD-.470) . In samples obtained between 1994 and 1997.S.7 ng/g of lipid. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.635) < LOD .090 (<LOD-.079 (<LOD-. In addition.100 (<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.100 (<LOD-.690) . reproductive toxicity included decreased fertility and testicular damage.256 (. and 2003-2004 subsamples.79) .090 (<LOD-. 1989).310 (. 2001-2002. EPA has established environmental standards for mirex.S. as well as in a subsample of NHANES II (1976-1980) participants. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..cdc. Laboratory animals fed high doses developed liver enlargement and liver tumors.gov/toxpro2.73) .html.108 (.059 (<LOD-. Inuit mothers from three Arctic areas had geometric mean serum mirex levels that were threefold to sevenfold higher than nonInuit mother from other Arctic regions. The U.112 (.090-1. 1995.170) < LOD .450) 1. IARC classifies mirex as possibly carcinogenic to humans.053-.430 (. Survey Geometric mean (95% conf.610) < LOD < LOD < LOD < LOD .

2 Classes of Pesticides. Vol. Kutz FW. Odland JO. Inc. Profiles of ortho-polychlorinated biphenyl congeners. Jr and Laws ER. Eds. Jr.97(2):178192. Van Oostdam JC. Stehr-Green. Swanson MK. Rev Environ Contam Toxicol 1991.html. New York. Available at URL: http://www. 1994-1997 organochlorine compounds. et al. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue.gov/toxprofiles/ tp66. Smith AG. Handbook of Pesticide Toxicology.Organochlorine Pesticides effect. Academic Press. J Toxicol Environ Health 1989. Kutz FW. Bottimore DP. Carra JS.27:405-421. 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. et al. Olson JR.330:55-70. Leininger CC.atsdr. Hansen JC. August 1995. Moysich KB. References Agency for Toxic Substances and Disease Registry (ATSDR).cdc. hexachlorobenzene. Strassman SC. Environ Res 2005. J Toxicol Environ Health 1985. Wood PH. The human body burden of mirex in the southeastern United States. In Hayes WJ. 1991 pp. 731-915.15:385-394. Dewailly E. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. Circumpolar maternal blood contaminant survey. Toxicological profile for mirex and chlordecone [online]. PA. dichlorodiphenyldichloroethylene. Watts DL. Chlorinated Hydrocarbon Insecticides. Stroup CR. 4/21/09 Bloom MS. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Gilman A.120:1-82. Demographic and seasonal influences on human serum pesticide residue levels. Fourth National Report on Human Exposure to Environmental Chemicals 111 . Vena JE. Sci Total Environ 2004. Chashchin V.

950 (<LOD-1.4.4.60-8. and polychlorinated benzenes (Kohil et al.5-TCP) and 2.00-3.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.60 (2.40 (.40 (1.4..6-TCP were used as intermediates in the production of certain pesticides.4.30-40.60 (.03) 9.90-33.0) 2.S.S. Formation of 2.4.0) 14.0) < LOD 11.63) 18.6-Trichlorophenol CAS No.0) < LOD 11.9 and 0.30 (.0) 5.50-25. Historically.0 (4.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.0 (5.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .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 1.40 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30-11.30-27.27) 696 661 521 696 603 939 Limit of detection (LOD.Organochlorine Pesticides 2.80) < LOD 1.940-3.50 (.60-18.4.980-3. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols.30) < LOD 4. population from the National Health and Nutrition Examination Survey.0) < LOD 5.920-3. Exposure to trichlorophenols also may result from metabolism of lindane.7) 24.80-41.40-11. other organochlorines.0) 2.40-18.S. public drinking water systems did not detect 2.31 (<LOD-9.0) 2.4.900-2.71 (<LOD-8.0) 2. 2.6-TCP).60 (4. usually at herbicide production or waste incineration facilities.6-TCP in any of the samples (U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Occupational exposures.00 (2.4. 2.40) < LOD 6.42 (<LOD-8. < LOD means less than the limit of detection.0) < LOD 21.50-16.4. Survey Geometric mean (95% conf. 1976).9.20) < LOD 90th 5.40 (2.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR. 1999).50 (2.40 (.0) < LOD 5. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.0) 2.40) < LOD 1.10-3.30-3.5-Trichlorophenol CAS No.57 (<LOD-15. soils. including hexachlorobenzene and hexachlorocyclohexanes.7. are metabolites of several organochlorine chemicals. 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.4. EPA.0) 2.71 (<LOD-8. Both chemicals have been detected in air.5TCP and 2.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4. 112 Fourth National Report on Human Exposure to Environmental Chemicals .19 (<LOD-6. Such workers would probably Urinary 2.20 (4.0 (8.50 (1.80 (1. 2006). 2.9 (<LOD-121) 9.20) < LOD 1.0 (4.0 (4. hexachlorobenzene. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16. which may vary for some chemicals by year and by individual sample. recent sampling of U.0) < LOD 5.30-44. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.30) < LOD < LOD < LOD < LOD < LOD 1. however.20-36. and sediments. surface water.00-8. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.30-27.6-trichlorophenol (2.40 (1. 95-95-4 2.3.0 (3. Trichlorophenols are no longer manufactured commercially. 1999).8) 21.72) < LOD 1.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.60) < LOD 8.40) < LOD 4.5-trichlorophenol (2.80 (2. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.00-3.50) < LOD 1.980-3.30-27.4.50-63.20) < LOD 5.5-trichlorophenol.0 (3.42 (<LOD-12.40 (2.20-71.00 (3.40 (2. may occur by inhalation or dermal routes.

4) < LOD 3.00-19.60-3.3 (5. 7.. Neither 2.75 (<LOD-6.80 (1.4.3 mg/L reported in German adults aged 18-69 years (Becker et al. urinary 2.00-29.0 mg/L.81 (<LOD-9. 1995) and up to 19 times higher than the 95th percentile value of 1. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.8 (5.2) < LOD 5. Fourth National Report on Human Exposure to Environmental Chemicals 113 .82 (<LOD-32. and other chlorinated compounds.1) 2.37) 16.cdc. animals showed hepatocellular abnormalities.43 (2.11) 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. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.17) 9.4.4) < LOD 3.88-16.68-4.920-2.86 (3.9 (5. Laboratory animals chronically fed high doses of 2.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.1 (<LOD-58. which includes trichlorophenols.93-11.5) < LOD 12.980 (<LOD-1. Human health effects from 2.5-TCP or 2. 1989).83-12.8) < LOD 9.31) < LOD 2. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.4. 1989).6) 4.33) < LOD < LOD < LOD < LOD < LOD 2.. population from the National Health and Nutrition Examination Survey.57 (<LOD-7.69-18.19-12.6-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.4.2) 2.64 (4.24-11.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.67 (1.27-17.74) 11.S.24) < LOD 6.6-TCP as reasonably anticipated to be a human carcinogen..6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.43) < LOD 12.62-20.02-3.73 (<LOD-8.37-11.4.4.8) 4.75 (3.7 (4.Organochlorine Pesticides be exposed to mixtures of chlorophenols.19-4. the 95th percentile urinary 2.6) 4.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.820-2.5-TCP. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples. However.02) < LOD 7.6-TCP had increased rates of hepatic tumors.67 (1. 1995) were similar.4.50) < LOD 2. environmental levels) and health effects is available from ATSDR at: http://www.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.24 (3.4.00) < LOD 4.9) 12. leukemias.15) < LOD 2.4. Survey Geometric mean (95% conf. Radon et al. the 95th percentile urinary 2.4.79-4.16 (.90 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.28-25..29 (1. furans. In the same 2-6 year old children.atsdr.4) 5.4.78-19. in addition to dioxins..05-8.5) 11.49 (1.0) 7.55 (4.47-8.05-17.57 (3.2 (2.78 (3.e. More information about external exposure (i.4. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.gov/toxpro2.57 (<LOD-7.24) < LOD 5.68 (<LOD-8.5-TCP nor 2.46 (1.6) 4.53-3. 2003.69 (2.. At lower doses.20-6. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.44 (1.6-TCP levels at the 95th percentile were up to eight times higher than 3.6-TCP.36 (1..html.13-13.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..4 (6.16) < LOD 90th 5.95 (3. NTP classifies 2. IARC classifies combined exposures to polychlorophenols.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. 2003).24) < LOD 1.53-3..78) < LOD 1.4. 2004).3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . as being possibly carcinogenic to humans.5-TCP and limited for 2.44 (. Among 6-11 year old children in NHANES 1999-2000. The 95th percentiles for 2.32) < LOD 4. 2003). Urinary 2.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). and lymphomas.

Mean values of 2.47 (3.75 (8.80-6.1-25.0-37.4.57 (<LOD-2.7-16.89-6.6 (12. Biomonitoring studies on levels of 2.8 (9.74-3.28) * 2.23) 3.45) < LOD 11.0 (8.0) 7.4.4.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002. 0.07 (<LOD-3.2-0.54) 6. respectively.4.6-19.52-3. population from the National Health and Nutrition Examination Survey.10) 6.3 (11.0) 17.0) 13. Urinary 2.51-12.00-4.0-44.98-11.44) 75th 4.8-24.4.3) 37.60-3.0-54.78 (2.0-38.59) 4.4.36 (1.00-21. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.6) 21.5-TCP level of 0.50 (2..02) 2.4.40 (2.7-3.0) 12..0) 7.80-20.85) * 3.30-2.46-3.40) 2.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.9 (13.60 (3.7 mg/L.20) 4.3 (11.4.50-5.40) 4. Survey Geometric mean (95% conf.40) 3.23-2.95 (4.5-TCP or 2.30-33.60) < LOD 5.3) 23.10) 2.S.0 (9.70-6.69 (3..68 (<LOD-2.0) 13. which may vary for some chemicals by year and by individual sample.0 (14.00 (4.0 (15.6) 26.31) * 2.36-5.90 (3. Urinary 2.12) 2. 1998).72-10.31 (3.0 and 1.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.0 (6.65 (5.7) 21.25-11.40-32. < 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 harbor workers exposed to chlorophenol-contaminated river silt.36 mg/g creatinine.53) 2.7 (9.4.9) 13.6-17.8) 32.00 (2.70) 5.5 mg/g creatinine) were similar to the limit of detection for 2.0 (11.0-68.9) 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 2.6 (11.0 (14.3-17. the median urinary 2.0 (8.0 (12.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.0 (6.23) 2.0 (13. 2004).0) 15.08 (2.52 (2.4.78 (2. Biomonitoring data will also help scientists plan and conduct research about 2.0) 19.70 (2.0 (7. similar to the limit of detection for this Report (Anderson et al.0) 11.48-26.4..5-TCP or 2.80) 1.4.40-2.79 (5.80 (2.70) 1.95-6.10-3.4. interval) 2.6TCP causes an adverse health effect.3-26.0 (4.9) 694 677 519 696 602 931 Limit of detection (LOD.66 (8.0) 11.0-41.0-18.0) 17. 1991). 114 Fourth National Report on Human Exposure to Environmental Chemicals .53) 4.1 (10.0) 6.73-9.40-7.0) 14.56 (3. Finding a measurable amount of 2.80-7.5-TCP or 2.6-TCP level.6-TCP in urine does not mean that the level of 2.7 (13.6-22.67) 4.2 (14.0-38.20 (3.0) 10.90 (4.5-TCP and 2.4.32) * 3. 2003).9 (11.4.45-9.0 (6.00 (1.0-43.10-2.5-46.8-13.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.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 2.35-3.65) 15.70) 3.58 (1.5-TCP (0.0) 9.95) 3.40-2.20-3.8) 18.60-37.01-6.0 (16.98-7.90) 2.45 (2.60) 6.6TCP values. was about six times lower than the median urinary levels for males in this Report (Radon et al.99) 6.04) 2.0 (20.4 (8.0 (15.6-TCP exposure and health effects.4-17.0) 9.40) 2.0 (14.58-3.0) 14.84) 2.0) 13.76) 3.49 (6. for males in NHANES 19992002 (Agramunt et al.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.70) 5.90-8.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.55-3.6-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 (20.70-3.59-6.1 (8.60-21.4.4.33-4.28) 24.1) 16.20-6.4 (17.4 (9. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.10-3.32-4.67-12.40 (2.60 (3.7) 33.18-3.6-TCP (0.60 (2.74 (2.3) 20.80 (2.32) 3.30-11.85 (2.70 (2.5-TCP or 2.3.0) 10.30) 4.0-50.26 (2.63) 90th 15.4.09-7.24 (2.40-14.45 (5.92 (2.20 (3.5-TCP and 2.0) 13.6-TCP than are found in the general population.4 (10.14 (2.87-14.0) 19.80-25.8-15.2) 25.20-23.4.89 (3.2) 12.80 (3.10 (5.4.6 mg/g creatinine) and 2.09) 15.06) * 2.5-TCP and to the median 2.91-4.70-6.40-4.30-2.

63 (<LOD-2.5-28.63-13.2 (13.5 (10.77-4.Organochlorine Pesticides Urinary 2.08-2. Survey Geometric mean (95% conf.68) 2.7-36.88) 4.06) 11.05 (6.5 (7.14-13.40 (2.3-23.09-3.53) 4.22 (<LOD-2.40 (7.4) 4.38-5.55-2.8 (7.30-2.6 (5.35 (3.44 (3.02) 3.89-2.5) 11.6) 8.43 (2.10-9.18-2.6-31.21-11.76) 4.9) 7.81) 2.25-15.58 (4.2 (12.4.33 (7.83-6.29 (6.2) 19.00 (2.78) 90th 12.76-8.9 (9.1-32.56-5.22 (3.9-29.50-8.13-6.0) 10.82) 2.65) 18.25-17.77) 2.22 (1.6) 12.51-21.3) 8.49-3.76) 2.33-2.65-21.52) 2.2 (7.1 (13.06-2.4 (11.18-4.99-2.3-37.73) 5.25 (3.88) 4.20-2.63) 4.88 (2.68) 2.59 (2.11) 10.72-16.32 (2.78) 2.87 (3.51) 18.6 (12.83-6.7) 6.90) 2.32-19.88) 5.43-7.29-4.28-4.15 (1.87) * 2.81-9.16-10.60-2.87) 2.79-17.1 (8.7) 25.52 (5.6 (10.8) 12.8) 21.53-11.42) 2.91 (3.38 (4.8 (8.98 (1.67-17.17) 13.0 (6.56 (7.05 (3.88) * 2.43 (<LOD-2.56) < LOD 11.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.89) 10.90 (1.71 (3.0) 8.6 (9.10 (6.29-4.52 (3.63-15.14-2.33 (1.62-15.53 (3.63) * 4.38 (2. Fourth National Report on Human Exposure to Environmental Chemicals 115 .46-14.17-4.60 (4.52) 2.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.54 (2.13 (1.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.41 (3.6) 13. population from the National Health and Nutrition Examination Survey.98) 10.1-21.23 (1.9) 19.8) 19.3 (9.23) 4.95-2.33) * 2.63 (2.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.83-5.53) * 2.49) 4.26-13.06) 4. interval) 2.83 (3.26 (6.65) 2.51 (2.02 (1.94-13.76) 1.19-5.87-6.92) 4.04-16.41-6.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.22-9.7 (14.65-2.50 (2.S.96) < LOD 4.4) 8.78 (2.5) 8.01 (3.38) 22.6) 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 2.25 (3.9) 8.25-2.22-2.48-2.17) 2.00 (3.6 (9.6 (6.15 (6.04-2.42 (2.91 (7.91-2.8) 11.72) 32.9) 8.1) 11.82 (3.88-7.0 (11.5) 9.5) 12.9-64.00) 4.00) 4.66-4.27-9.24 (1.9-34. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.82-2.87-7.4) 9.88) 1.70-9.75) 75th 4.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.5 (8.9-32.2 (8.47-5.4 (12.0 (9.1) 14.5) 11.82 (8.9 (9.10) 4.6 (22.73-22.

Domingo JL. 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].146:83-91. Falk C. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Aitio A. December 2006 Draft. Seifert B.45:440-445.71:99108. Luotamo M. Radon K. Environ Health Perspect 1998. Jarvisalo J. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Becker K. Poschadel B. Wegner R. Schulz C. Toxicol Lett 2003. Heinrich-Ramm R. Jones D. et al. Burse VW. html. Hanrahan L. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. 206:15-24.63:57-62.54(3):203-208. U. Seiwert M. Needham LL. Hill RH Jr. Corbella J. et al. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Baker S. Available at URL: http://www.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Gregg M. Int Arch Occup Environ Health 1991.epa. July 1999. Baur X. Safe A. The Great Lakes Consortium. Shealy DB. Domingo A. Hill RH Jr. Szadkowski D. The metabolism of higher chlorinated benzene isomers. Chlorophenol exposure in harbor workers exposed to river silt aerosols. Head SL. Am J Ind Med 2004. Arch Environ Contam Toxicol 1989. To T. Urinary excretion of chlorinated phenols in saw-mill workers. S. Smith SJ.atsdr. Can J Biochem 1976. Kohli J.EPA).gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Kaus S. Available at URL: http://www.gov/toxprofiles/tp107. 4/21/09 Agramunt MC.106(5):279-289. Olson J. et al.18(4):469-474. Bailey SL. Lindroos L. Anderson HA. Int J Hyg Environ Health 2003. Environmental Protection Agency (U. Pesticide residues in urine of adults living in the United States: reference range concentrations. Toxicological profile for chlorophenols [online]. Pekari K.pdf. Needham LL. Environ Res 1995. Fast DM. Holler JS.cdc.S.

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

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

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

2 (14.93-24.94) * * .8 (12.623-1.30-6.2 (9.80) 2.4) 20.80) .2.0 (8.80) .32 (.00 (5.0 (7.1 (9.01) * * 1.10 (2.10) < LOD < LOD 4.9) 8.8) 7.76 (2.82) 10.5-17.55-8.11 (.0) 10.40 (.00-12.21 (.20-7.60 (5.00-7.0 (5.39 (3.61) 4.80) 3.48-7.70-11.46) 10.890 (<LOD-2.4 (9.15) 14.20 (. respectively.05-7.58 (3.2 (7.90) 3.29) * * 1.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.55-6.50) 2.28) 1.89) 9.40-5.27-3.981 (.4 (9.1.56 (4.70 (4.12) 4.95) 5.13 (2.63) 1.44 (2.0) 5.0) 11.80 (4.6) 18.70 (2. interval) 1.47) * * 1.1) 95th 13.290 (<LOD-.42-3.52) 6.50 (2.700-1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.53) 4.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80) 2.757-2.38-5.579-1.40-16.37 (3.20-4.0) 11.42) .80-22.90 (1.74 (8.5-16.20 (.0) 10.15-12. and 03-04 are 0.60) .0) 15.30 (2.08 (<LOD-2.57-7.290 (<LOD-1.19) 9.21) 9.780) < LOD 3.40-1. population from the National Health and Nutrition Examination Survey.0-27.71-9.10-7.02) 4.13-2.2.0 (7.30-4.00) 3.50-5.97) 8.2) 14.50-36.79 (5.9-18.0 (6.0) 6.60-18.03 (. which may vary for some chemicals by year and by individual sample.6) 7. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7) 11.70-14.39 (8.0 (9.23-5.47) 5.9) 14.0) 10.2) 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 1.81) 11.0) 11.8 (8.7 (12.93 (4.3) 16.1-17.44-38.70) < LOD < LOD 75th 3.5 (8.22 (.79-7.80-4.8) 11.30 (2.12-19.13 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2-20.830 (<LOD-3.2) 16.3) 14.2 (7.0 (4.70-23.0) 5.4) 18.00-27.0) 7.72) 5.2) 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 1.717-1.670-1.80) 2.490-2.52) * * 1.02-5.73) * * .00-27.1) 10.70) .86-15.97) 90th 7.0 (8.1-23. 0.66) * * 1.860-2.0) 10.4) 17.0 (7. see Data Analysis section) for Survey years 99-00.740-2.60 (1.43-12.36-4.4 (7.0) 6.1 (10.S.0 (12.96-3.00 (1.32) 1.68-7.1) 13.14) * * . < LOD means less than the limit of detection.81) 1.00) 3. and 0.970-2.0) 6.599-1.20 (.80) 11.16 (2.0 (8.620-1.2 (9.20 (.35-11.00-12.16) 4. 01-02.80 (2.5) 20.3-15.56 (6.33 (5.98-12.2) 16.26-8.30 (4.94) 3.90) 2. 120 Fourth National Report on Human Exposure to Environmental Chemicals .71 (2.0) 20.26 (5.20-30.0 (6.82-12.50 (.0) 5.99 (5.86 (1.35-12.840-1.80) 4.8 (9.08-15.758-1.5 (11.530 (<LOD-2.27-15.51) 2.60-25.07-10.58 (2.40-11.56-13.0) 12.0) 11.4 (7.50 (4.10 (2.90-4.0) 10.0 (9.70) < LOD < LOD 1.00 (4.955 (.00-19.08-2.20 (2.810-1.35-16.61 (3.3) 17.8-32.60-11.2 (7.8) 7.33-18.80-24.10 (.5) 15.34-3.9 (8.70-19.58 (5.83 (5.17-3.0) 9.0-28.52-11.81) 11.26-6.45 (2.60) < LOD < LOD 4.954 (.74 (8.34-7.40-19.2 (14.85 (3.7 (14.0 (7.600 (<LOD-1.56 (1.54 (3.9) 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 1.44-3.98-5.8 (14.2 (11.90-5.750-1.40-14.91) 4.67) 3.10 (.04) < LOD 1.8) 19.10) < LOD .

710 (<LOD-1.900 (.37) 9.2) 13.855 (.5) 8.5) 11.53) 9.75) 14.4) 4.62) . interval) .8) 8.8) 16.67) 4.56) .7) 5.5) 7.3) 15.03-6.02-14.549-1.30 (1.924 (.4 (4.996 (.540-1.75) 2.09-11.28) 10.43 (3.42) 12.81-5.35 (1.620-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.54-15.7) 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.80 (2.64-5.95) 2.54-4.69-10.36) * * 1.790 (.89-3.54-11.9-28.00 (4. Fourth National Report on Human Exposure to Environmental Chemicals 121 .00-13.57) 4.98-5.87 (1.80 (7.1 (6.570-1.31 (3.500-1.32-12.60-9.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.6) 13.54) .430-1.94-22.90-8.46-5.47 (3.66 (2.07 (.44 (2.533-1.40-5.94-10.79-9.883 (.02 (2.52) 4.830-1.94-9.3) 16.0) 7.15-10.8 (10.67-19.1 (10.633-1.28 (4.37 (5.67) 1.2 (8.1) 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 1.06-2.8) 12.05) .2) 7.45-5.2 (10.860 (.1 (8.69) 2.03) 2.5-13.53-11.05 (.40) < LOD < LOD 75th 2.57-10.71-2.68-4.7) 18.7 (10.34 (6.932 (.88) 2.88-10.98-22.870-2.9) 16.9 (9.0 (8.7 (8.1-15.57 (4.00) 8.6) 9.40-12.19 (4.34 (6.71) 10.75-7.98) .61-29.62-5.02 (7.7) 12.25) 6.960 (<LOD-2.21-23.1) 4.92-2.98) 9.76) < LOD .1 (9.45-5.40-14.2) 95th 12.02-2.2) 5.60) 2.960 (.53 (6.780 (<LOD-1.4) 4.04 (1.54-2.58) * * 1.51-5.43 (.47) 2.88-15.94 (4.28-9.1 (7.61 (1.98 (3.47) * * .03 (2.93-9.66-34.650-1.01-2.6 (10.3) 12.28 (2.00-17.90-5.13) 4.75 (3.60) * * .82-14.30) 2.0) 6.41-12.29 (2.43) 2.4 (9.87 (3.2 (6.68) < LOD < LOD 3.56-13.55-20.8) 6.5) 7.3) 5.61-13.9) 11.5-16.83 (7.79-3.5) 12.66 (1.38) .45-11.89) * * 1.820 (.4) 13.85 (6.78 (2.2) 5.41) .890 (<LOD-1.93-5.00 (4.47 (3.440 (<LOD-2.6 (9.75 (7.9) 12.750 (<LOD-1.14 (3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.56) 7.9 (5.84 (5.7) 471 576 308 664 821 699 814 1122 921 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .77 (6.94-23.10-13.18 (.95 (3.S.24-3.37-3.83) 8.23) 4.28 (5.03) 2.11-6.23 (4.920 (.82-14.76-4.38 (1.5-20.37 (4.40-3.82-26.560-1.85) 2.5 (4.6) 11.00-19.35) < LOD < LOD 3.61 (1.82-6.81 (1.87-5.74) 90th 7.39 (2.69) 4.05 (1.40) 4.9 (9.74) 4.608-1.37-5.88 (5.72) 11.80) 9.818 (.2) 9.57 (6.69 (4. population from the National Health and Nutrition Examination Survey.27) < LOD 2.773-1.1 (11.3) 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 1.03 (7.8) 7.26) * * .1) 4.56) 4.84) 7.40-28.94 (2.09) 2.2) 8.04-6.98) .566-1.31-14.09 (.34) * * .66-15.6) 8.50) 7.10 (3.47 (1.25) < LOD .93) 9.40 (3.5-32.46) 2.80 (6.574-1.41) Selected percentiles ( 95% confidence interval) Total * * 50th .29) * * .510-1.34) < LOD < LOD .20-8.73 (1.92-5.66 (5.42 (3.890 (<LOD-1.7 (9.

3 (9.90 (6.40) < LOD < LOD 75th 2.0) 11.1-23.39-13.80-21.67-10.46-28.90-31.70-8.82) 8.910 (<LOD-2.90 (5.73) 7.22 (6.3) 14.30) 8.0 (5.10) 6.9-17.67) 4.97-4.80 (2.5) 21.10 (<LOD-1.00) 3.80) .0) 23.80-12.00-9.650-1.95-9.00) 8.2 (7.25 (2.33-11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30) < LOD < LOD 4.31-12.42 (1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.35-3.S.6) 11.39 (5.8) 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 1.30) < LOD < LOD .30) 3.37 (3.34-10.63-14.20) 3.80-14.5.14 (6.5.3) 22.10 (.04 (3.52 (6.86-10.15-2.95 (5.740 (<LOD-1.70-9.80-3. see Data Analysis section) for Survey years 99-00.61-32.74) * * * * * 1.90 (2.2) 14.90-9.4) 7.35 (6.27) 4.53 (3.9) 9.40 (2.90) 4.51) < LOD 1.790 (<LOD-1.90 (6.0 (14.60 (2.28 (7.31) 1.20) .9 (7.0 (15.22) 8.0) 14.680 (<LOD-1.80 (2.70) 2.29) < LOD < LOD < LOD < LOD 3.9 (12.00-4. 0.0) 12.9-14.20-4.5 (9.0) 14.670 (<LOD-1.95 (2.670 (<LOD-1.64) 10.0-29. which may vary for some chemicals by year and by individual sample.66) 4.18 (3.0) 18.0 (13.80-6.96) 90th 7.20) 3.970 (<LOD-2.8-20.80) 5.01 (2.0) 9.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.4 (10.12 (4.11-6.46-4.00) 7.7) 16.17 (7.0) 7.50-4.90-15.10-4.00-18.80-4.34-5.75 (2.75 (3.67) 3.7) 22.8-21.0) 12.3) 8.29-4.0 (9.50) 3.8-20.20-18.60 (5.24 (2.6) 18.90 (1.8 (12.5) 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) 19. and 0.37) 2.3 (9.77-14.8) 9.1) 11. population from the National Health and Nutrition Examination Survey.4-17.10-15.20-8.98-9.20 (<LOD-2.90 (6.5-26.0 (10.4 (10.92) 9.7) 14.50-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 01-02.0) 13.3 (11.22-12.16-1.5 (8.90-15.80 (5.99 (3.0 (7.72) 2.0) 9.3 (6.00-18.3 (12.34 (6.670 (<LOD-1.50) 5.70-9.6 (10.6 (10.27 (3.00) 3.30) 3.59-3.22 (6. respectively.35) 4.7 (10.9) 16.80) .6-41.7 (11.45 (3.58 (1.90) 8.80-8.40 (2.6-19. 122 Fourth National Report on Human Exposure to Environmental Chemicals .88) 10.89 (2.31-7.70 (1.5 (8.34-3.58.66-13.96) 3.1 (10.00-16.9) 10.78) 5.4 (14.0-24.50) .27) .4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90 (6.00-4.81-6.0-24.4) 11.89) 2.10-10.0) 6.0-19.0 (8.24-5.84-4. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .9) 95th 14.60 (6.7) 10.18) * * * * * * * * 1.49-4.8 (12.3) 10.41-5.2 (9.27 (7.62-17.88) 3.27) 9.60) < LOD < LOD 2.0) 11.6) 14.61 (3.70-5.3) 20.77-3.47-6.06 (2.7-21.670 (<LOD-1.0) 13.580-2.90 (2.6) 14.0) 12.1 (10.3 (7.8) 8.00 (. and 03-04 are 0.9-15.0 (10.7) 15.92-17.8-17.7-19.0 (9.00) < LOD .15-6. < LOD means less than the limit of detection.41) 3.0-33.90 (2.70 (8.

1) 13.20-3.89 (2.55) .33-10.88-7.74-4.27-13.71 (1.760 (<LOD-1.0 (8.86-3.29) 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 * * * * * * .3-15.7) 9.2-15.9 (9.06) .6 (11.0 (11.89-3.29 (5.11 (5.00 (<LOD-1.5) 8.54) 9.00 (5.30) 2.0 (10.6) 13.920 (<LOD-1.95) 90th 8.28-12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.54-5.45) 3.83 (7.74-19.0-19.6 (11.61 (2.03) 3.1 (19.50 (6.34-18.89 (3.48 (2.77 (2.70-2.3) 9.4) 15.81 (7.53-8.6-19.21-21.7) 14.68-19.96-10.00) 8.93 (6.68) .89-3.67 (7.87 (3.34) < LOD < LOD < LOD < LOD 3.37-5.75-3.973 (.52-3.2) 10.9 (9.82-8. population from the National Health and Nutrition Examination Survey.36 (2.39-17.0) 14.3-21.810 (<LOD-1.95) 3.63 (2.80) 3.51-7.91-9.9) 16.25 (4.2) 19.6 (13.05-3.7 (10.33) 3.4) 9.29 (2.1 (8.2) 672 678 497 509 694 578 595 948 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.1) 20.11-3.89) 5.04) 9.00) 2.82-11.51-10.950) .1) 10.86) 9.29-2.4-16.94 (5.06 (<LOD-1.6) 7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.38 (.59-3.78 (4.2) 12.4) 16.5 (15.2-30.37) 3.95 (2.590 (<LOD-.4-15.67 (1.7) 14.9-25.30) 7.99) 2.6 (10.68-10.910 (<LOD-1.780-1.8 (8.42) 7.85-8.9) 19.5) 10.58 (4.530-1.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.09-11.07) 2.78) 4.88 (1.55) 16.1 (13.85-17.2 (9.00 (3.42-19.940) < LOD < LOD 1.4 (11.6) 6.5 (11.7 (11.6 (13.27) 5.30) 8.38 (2.6) Sample size 1949 2518 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.7 (10.4-18.64-11.16-14.16 (3.99 (4.15) < LOD < LOD 75th 2.4) 6.6) 95th 16.25-9.44-6.2 (9.73 (5.8) 16.97-4.00 (2.9 (9.63 (6.79-6.72) 4.02-4.42) 8.54 (7.2) 12.79-9. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .7) 15.9-17.5 (9.5) 22.96-11.2) 8.27) * * * * * * * * 1.7-23.27) 1.4) 7.6 (12.6) 12.71) < LOD < LOD 2.2) 16.07) 2.890-2.77 (2.23-3.12 (7.S. Fourth National Report on Human Exposure to Environmental Chemicals 123 .41 (7.690 (.6) 14.01-5.89-13.68-4.0 (13.30-5.00 (<LOD-1.4) 7.38-13.3-34.93 (2.5) 13.28) 6.5-17.07-3.3-17.93-10.38) 1.8) 14.78 (6.0-21.3 (7.43 (2.78-10.09-11.3) 8.21) * * * * * 1.3) 6.12) < LOD < LOD 4.47-9.27) < LOD .5 (10.32-8.18) 2.50-17.45) 6.8) 11.69-11.2) 12.14 (2.4-16.28 (1.75-3.03 (6.07 (5.83 (6.91) 3.32) 2.93 (<LOD-2.92) 3.2) 15.4) 7.00 (7.86 (3.15 (1.77) 3.72-4.3-17.850 (<LOD-1.7) 12.89-10.94-14.92 (5.19) 3.7 (8.38 (1.7-19.8 (10.70-35.3) 12.03 (2.6) 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 * * * .5 (8.55 (2.620 (<LOD-.97) < LOD .

50) 1. 01-02.960 (.710 (.810) .359-.350-. 0.17) 1.10-1.70-2.09.680-1.560-.83) 1.00) 1.04) 1.45 (1.20) 3.910 (.10) 1.910) 1.70-7. respectively.54 (2.820 (.69-4.570-1.850) < LOD .79) .01-3.50 (1.78) 952 1187 907 997 1332 998 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .57 (2.690) .30 (.90) 3.95-5.63 (1.467 (.94 (2.20 (1.20-3.48 (1.970) . which may vary for some chemicals by year and by individual sample.597) * .790 (.90-4.47) 2.49) 2.26) .45 (2.08 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.15) 2.01) .457 (.32-1.425 (.390-.388-.840 (.30-3.60) 3.98-3.650-.10) 3.64 (1.58 (1.22-3.18 (.980) 1.690-1.29) 1.47 (1.710) .42-2.49) .70 (1.73-5.29-2.620-1.13) .380-.720 (.98 (2.2. 124 Fourth National Report on Human Exposure to Environmental Chemicals .09 (.S.80 (1.587) * * .657) * * .680-1.60) 2.89) .740-1.570 (.10) 1.96-3.60-4.03) 1.30-3.510 (.83) 2.880) < LOD .22-2.86) 3.740-.68-5.70 (1.88) 1.540 (.90) 2.33-2.11-3.46 (2.960) .01-1.930-1.20-2.79) .760 (.749 (.880) < LOD 75th .960) 1.11-3.780) .77 (1.592) * .600-.31-3.700) .30) 4.820 (.16-3. and 0.20 (2.32 (1.50-2.20) 2.80) 3.949) .353-.750-1.94) .27 (3.32) 3.20-1.76-6.690-. see Data Analysis section) for Survey years 99-00.83 (2.14-1.570 (.26 (2.00 (1.960-1.21) 3.17-4.780 (.97 (2.505 (.30) 4.30 (1.18 (1.91) 2.700) .27 (2.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.75-2.90 (1. interval) Selected percentiles ( 95% confidence interval) Total * .40 (1.54) .950) 90th 1.490 (<LOD-.20) 1.910-1.585) * * .280-.580-.17) 1.98) .30 (.780 (.22-3.618) * .940) < LOD .20 (1.240 (<LOD-.13) 2.55 (3.76 (1.89) 1.46-3.592) * 50th .70 (1.880 (.15) 2.60 (2.57 (1.450 (<LOD-.77-2.08 (2.74-5.46 (1.1.930) 1.73 (2.87-3.94 (3.00) 2.440-.59-6.549 (.570) * .860) < LOD < LOD .74) 3.710 (.95) 2.20 (1.95 (2.550 (.720-1.80) 3.500 (<LOD-. < LOD means less than the limit of detection.54-2.16) 2.584) .05-2.25-1.730) .340-.90) 2.303-.380) .600 (<LOD-.83 (2.930) < LOD .46) 1.14 (1.800 (.20) 3.05-3.201-.83) .31) 95th 2.34) 2.210 (<LOD-.160 (<LOD-.22-8.20-2. population from the National Health and Nutrition Examination Survey.40 (1.830 (.390-.50 (1.570 (<LOD-.380-.23-3.382-.41 (2.10) 1.930 (.80) 2.78) .460-.75 (2.19-1.16) 1.550 (.510 (<LOD-.30-1.65 (2.37-2.50 (1.50-2.86 (1.96-5.398-.48 (2.30) 1.343 (.31-3.45 (1.570 (<LOD-.580-1.35) 1.20) 1.10-1.00-4.61 (1.39) 2.455 (.970) 1. and 03-04 are 0.34) 2.600-1.740 (.36-4.670) .89-6.22 (1.690 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.592-.80) 2.38) 1.759) * .590-.73 (1.449 (.720-1.750) 1.31) 2.350-.45-4.260 (<LOD-.30 (.41-5.20) 2.740 (.990-1.30) 2.50 (1.04) .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 * .80) 3.453 (.59-2.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.960) .459 (.00-2.80) 5.400) .80 (2.336-.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 * .50 (1.

61 (3.43) 2.05-2.136-.00-3.447 (.850) 1.350) .750 (.380-.72) 1.470) .710 (.444-.412-.22-3.88 (1.55 (1.820) .840) .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 * .990-1.550-.300-.22) .97 (1.550-.640 (.08 (2.82) 2.400) .72 (1.25-3.65) 2.47 (1.310 (<LOD-.07) 1.490 (.58 (1.560-.280 (<LOD-.71) .640 (.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 * .07) 1.19 (1.30-2.42) .84-6.33) .23) 1.97) 1.23) 2.870 (.38 (1.53) .510 (.880) 1.540-.57-2.91 (1.16-2.50) 1.08-2.67) 1.94) .930-1.32-1.64 (2.49-4.760) < LOD 75th .530 (.97) 2.50 (1.372 (.28 (1.285-.591 (.06-2.33 (1.63 (1.92-8.440-1.02-3.485) * * .790 (.515) * * .645) .82 (2.740) .520 (.60) 1.07) 1.05 (1.310 (<LOD-.03-1.36) 3.520-.72 (2.950-2.710 (.55-3.07) 5.89 (1.39 (1.00 (3.42-8.471-.58) 3.820) 1.535 (.31-1.760) .49 (1.740) < LOD 1.57-4.95) 1.42 (.87 (2.900) 1.739) * .590-1.11) 1.32) 5.42-6.81) 2.04-1. Fourth National Report on Human Exposure to Environmental Chemicals 125 .90) 2.690) < LOD < LOD .393 (.72-4.270-.30) 3.480) .04) 95th 2.720-1.305 (.08-3.22) 4.47 (1.390-1.02-6.76) 1.460-1.300 (<LOD-.07-3.29-4.250 (<LOD-.790) .73 (2.05) 1.700 (.330 (<LOD-.17) 2.590 (.370-.34 (1.08-3.11-2.270 (<LOD-.870) .84 (2.742) * * .552 (.69 (1.700 (.840) 1.44) 2.08) 1.580 (.60) .60 (2.80) 2.710 (.470 (<LOD-.70 (2.67-3.89-3.750 (.597) * .390) .270-.57 (3.980-1.320-.13 (1.52) 3.660-.920) .234 (.67) .45 (1.24) 4.348-.830 (.510-.940-1.57 (1.335-.23) 3.79) 1.590) * 50th .61-3.60 (1.580) .75 (1.32 (.230 (<LOD-.08-2.77-4.16-1.99) 2.688) * .70 (3. interval) Selected percentiles ( 95% confidence interval) Total * .43) 2.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.510 (.453 (.18-2.800-1.23) 2.41 (.560 (.62 (2.39) 2.08-2.20-2.98) 1.69 (3.38-3.400-1.75-3.580-.05) < LOD .97 (1.79 (1.380-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.08) 2.38 (2.800) < LOD .04-5.05-4.22) 1.71) 2.43 (1.66) .640 (.250 (<LOD-.75) 6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.73-3.16) 1.52 (1.S.23 (.03-2.730) .17) 2.07-2.700 (.43) 1.77-3.403) .67 (1.61) 2.550-1.58-6.07 (.11 (.45 (2.88) .61-3.75 (2.910) < LOD .06) 4.22-2.318-.460 (. population from the National Health and Nutrition Examination Survey.22 (2.72) 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 * .630) * .92 (1.320-.00-1.448 (.500-.377-.71 (1.180 (<LOD-.08-3.509 (.460) .32) 2.09) .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.08-3.550) .92) 3.44-2.10) 2.20) 1.840) 1.480-1.67 (1.830) 90th 1.02-3.310-.720 (.380) .62 (1.78) 3.22-3.670 (.66 (2.368) * .99) 1.17-2.253-.64 (2.47-4.680 (.14 (2.32) 1.20-7.08 (.330-.77 (3.560-.

9 (27.0-31.2-62. interval) 1.4-76. 01-02.14) 5.1-20. which may vary for some chemicals by year and by individual sample.19) 2.77 (1.3 (12.80-2.9) 18.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80-18.660-2.10-4.0 (38.70) 1.2 (19.10 (1.77) 38.0) 6.830-4.8 (26.05) 1.20) 1.0 (38.53) 40.85) * 2.0) 17.30-14.0-39.26 (.79 (1.0) 17.8-21.6-22.4 (19.30 (.93-3.18) 6.29) 2.4 (10.0) 31.97) 6.0) 18.0) 8.23-2.10) .0 (13.71) 5.610 (<LOD-1.40-4.7 (12.0 (33.79-2.05-3.2) 31.0) 3. population from the National Health and Nutrition Examination Survey.41) 1.0) 4.0 (26. 0.6-27.0) 32.1-46.48-2.61-2.9-51.0) 20.95 (5.2-27.70 (1.10-13.46-2.65 (4.23) 9.80) < LOD 1.8 (22.00-24.0-110) 42.92) * 2.43-7.2-27.82 (1.81-2.0-92.0) 45.10 (1.18) 14.50 (2.98 (1.25-3.69) 2.05) * 2.59 (1.8) 32.0) 13.0 (38.44) Selected percentiles ( 95% confidence interval) Total * 2.4 (15.6-45.64-3.58-2.40) < LOD 1.0 (8.0) 15.94 (1.1 (26.1-40.88) 1.06 (1.64-8. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0-41.41 (1.53 (1.0) 28.0) 16.87-7.2-80.53) 1.90 (1.3 (10.21 (3.53) * 2.59 (1.0 (32.6 (11.0-69.1) 38.27-6.48-2.90) 11.44) 2.4.41) 1.40) 50th 2. and 0.23-2.07-5.76 (2.0-39.0 (6.3 (23.690-3.5) 69.04-8.7 (28.0) 33.83 (3.29-4.45) 2.0) 16.41-4.S.76 (2.58) 16.41) 5.2) 16.9 (19.0) 30. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5-27.8) 62.0) 3.0 (24.6 (26.06) * 2.75-14.0-62.0-52.1-25.19-2.16) 2.09 (4.1 (25.0-41.3) 26.13 (1.98) * 2.10 (7.0) 5.1 (10.1-47.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.0) 3.50-20. < LOD means less than the limit of detection.20-4.0-43.92-5.6) 52.83 (1.16) * 1.70) 5.12 (3.4) 19.99 (2.3) 38.00 (.0 (21.33 (5.70-17.04) 3.7) 47.57-2.50-7.8) 41.35-6.63-6.86-3.9-21.2-39.1 (22.17-2.2 (12.54 (1.40) < LOD 2.50-17.7-22.0-50.44) 3.45) 2.31-6.6-54.80) .26) 75th 11.830-3.0) 3.0) 4.50-5.46-6.8-24.7-41.6 (9.1-19.90 (1.0-62.0 (38.8) 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) 28.1 (25.10 (1.1 (11.86 (1.44-7.3 (24.0 (40.8 (12.70-6.12) 1.0) 20.50-2.5-45.57-2.78 (1.5-74.40-16.54 (3.72 (1.0 (38.71 (4.11 (4.0-110) 34.0 (20.600-2.5.13 (1.83-2.0 (7.0-47.0-49.0-58.61 (1.3) 31.9) 48.7 (12.1) 38.0 (38.21 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0-41.0 (20.48) 5.60) < LOD 1.0-53.9 (10.30) 11.90-8.1) 95th 48.0) 4.0-230) 35.52 (4.71-2.00 (.5) 30.3 (14.60 (2.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.9 (19.0) 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 2.1) 18.0 (38.0 (19.78) 9.30) 4.80) 1.0 (8.9) 38.470 (<LOD-1.5-20.11) 2.0-29.6 (15.67 (1.20 (2.32 (2.10) 39.3) 33.3 (12.0 (17.70 (1.29-9.18. respectively.530-4.0) 19.0) 15.74-2.0 (8.3) 28.4-22.2-26.36-2.5 (24. and 03-04 are 0.0-53.13) 12.81-3.2-47.0 (37.7) 20.79 (2. see Data Analysis section) for Survey years 99-00.0-260) 34.0 (25.9 (23.70) 1.46 (.0 (11.0-58.18) 20.88) 3.66-5.2-33.80) 90th 38.85 (1.83-2.21 (1.1) 140 (46.70 (7.70 (.8 (12.10 (1.8) 39.49-2.42) 1.5-40.4) 38.02 (2.9) 17.91 (4.96) 5.04 (<LOD-2.

9 (7.38) 5.67-16.5) 70.54-2.52 (1.25-3.51) < LOD 1.62 (2.0) 48.8) 11.1) 17.95-16.60 (.23) < LOD 2.46-6.7 (18.40 (2.17-3.0-71.64 (1.15 (.9) 24.16 (1.1-22.95 (2.6-32.0 (6.35) .3) 28.3-22.07-2.01 (.91 (6.27 (6.44) 9.0) 25.8 (7.79-17.16 (1.59-2.19-6.0-40.2-28. population from the National Health and Nutrition Examination Survey.20-5.6 (27.80-8.38-5.26-2.95-16.17) 2.22 (2.7) 23.76-2.27) 10.67 (1.4 (5.71 (1.4 (9.4) 12.3) 13.68 (1.96) 2.38-1.36-13.22 (.6-51.56) 1.24 (1.35) 1.19 (1.670-1.46) 1. Fourth National Report on Human Exposure to Environmental Chemicals 127 .5 (8.0 (17.1) 13.4-67.7-43.1-60.1 (34.82) 1.5 (15. interval) 1.75 (1.69-18.9) 12.35 (2.1) 13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2) 36.99-4.23) 37.39 (1.9-52.0) 10.30) 28.7) 34.14 (.6-38.8-34.9) 24.36 (4.1) 25.4-39.1) 25.69-5.08) 1.5 (15.32 (3.28 (1.12) 3.71) 8.6) 3.66 (1.02 (.7 (11.19-14. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7 (10.7-19.88 (1.8) 23.7) 95th 51.95) 90th 32.9-18.57 (6.31) 2.9 (39.4-34.9 (26.1) 36.41 (2.3 (8.06) 1.6) 3.930 (<LOD-1.3 (10.22-2.899-2.7) 66.83 (.2-34.8) 31.83) .5-97.6-49.8) 32.1 (50.9-36.1 (33.11) < LOD 1.40-4.94-20.46-5.4) 14.56 (2.37 (1.86) * 3.7 (24.5-190) 30.2) 4.00) 1.96-16.32-3.9 (13.47-17.48 (4.2) 13.50-5.00) 6.8-45.21 (4.86) * 2.07-2.2-38.61-2.93) 5.70 (1.0 (23.4 (19.58-17.5) 27.8) 3.59-2.4) 3.00 (4.4) 12.2) 671 678 497 509 694 578 595 947 756 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.7-47.3-42.45-1.2-70.8-37.870-3.7-109) 22.870-3.2) 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 2.75-6.55 (2.33-5.9-37.40 (5.7-37.43-12.67-3.9) 54.27) 50th 2.6) 19.7 (18.6) 11.07) 9.59-15.7) 15.23-1.06) 1.7-20.28) 1.16 (1.2 (8.1-63.4 (12.9 (10.0 (19.3 (10.08 (1.75) * 1.14-8.82 (2.19) 5.5 (13.50 (2.62) 4.06-1.12 (1.2 (15.27-3.18) 3.91-2.5 (41.88 (4.00-16.94) 1.0-70.88 (1.S.20) Selected percentiles ( 95% confidence interval) Total * 1.03-2.1) 27.61 (1.7) 26.02) * 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 1.36) 10.9-95.8-26.68) 47.860 (<LOD-1.3 (20.54-15.1 (25.2 (21.1) 52.34) * 1.80 (1.09 (5.0-118) 29.7-38.6 (7.33) < LOD 1.46-22.02) 1.9) 3.6) 23.5-36.0) 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 1.6) 112 (40.7) 61.53) 1.6 (11.8) 15.26-4.4-71.90 (.51) .37-2.1) 15.0 (39.2) 33.06) 75th 9.66 (1.97 (1.9) 3.58-2.79 (2.4 (11.38 (3.47 (1.18) * 2.0) 3.63-5.1 (12.5 (34.48) 1.9-41.40-7.2) 13.67 (1.1 (39.33) 2.03) 1.0 (32.47 (3.4-21.4 (21.0 (25.16-2.18-1.0) 30.2 (9.6 (24.2) 41.3 (9.84-13.5 (6.7) 30.88 (4.43-2.66) 8.6) 7.61-22.75 (1.0 (14.43) * 2.2-47.57) 4.22-3.52-4.0) 13.60) 4.71-2.70-4.0) 47.11-2.9 (19.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.4 (25.750 (<LOD-1.8-43.94) 19.1) 27.2 (22.680-4.19) 5.890-4.0 (23.2 (16.888-1.5 (17.5-43.33) 1.72) 2.29-5.4 (25.3-19.45 (1.3-27.870-3.

730) .370-.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 * * * * * * .830 (.1.10 (. which may vary for some chemicals by year and by individual sample.440-1.130) .260 (.410-.100 (.120-. respectively.640-1.03) .130-.940 (.540) .360-.084-.310) < LOD < LOD < LOD < LOD .850 (.090 (<LOD-.130-.162) * * * * * .760) < LOD .400-.630 (.290 (<LOD-.860-1.820 (.860) .720 (.30) .650 (.390) < LOD < LOD .220 (<LOD-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.410-.090 (<LOD-.42) .180) .130-.190 (. see Data Analysis section) for Survey years 99-00.830 (.190 (.830) .10) .60) 1.650-1.510-1.350) < LOD < LOD < LOD < LOD .12 (.210 (.230) .630 (.320-.15) .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.30) . and 0.160) .640 (.680 (.460 (.090 (<LOD-.680-1.870 (.470-1.140-.13) .130) .640) .230-.870 (.430 (.310 (.090 (<LOD-.58) . 128 Fourth National Report on Human Exposure to Environmental Chemicals .420-.540) .870) < LOD .32) .610 (.05.080 (<LOD-.120 (<LOD-.780) < LOD 1.720-1.240 (<LOD-.650-1.10) .870 (.680-1.610 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.220 (.360-.410-1.117 (. 01-02.640) .870 (.150 (<LOD-.850 (.210 (.930 (.490 (.36) .20) .310) < LOD < LOD < LOD < LOD .110-.900 (.150) .740) < LOD .700-1.120-.600 (.390 (.830) < LOD .990) .650) . and 03-04 are 0.S.690-1.720) .310-.160-. 0.550) .140) .290) < LOD < LOD < LOD < LOD 90th .840) .370-.730-.380-.700-1.090 (<LOD-.310 (.10) .460-.090 (<LOD-.170-.700-1.40) .280) < LOD < LOD < LOD < LOD .290) < LOD < LOD < LOD < LOD .450 (.850) < LOD .190 (.320 (.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .200) < LOD < LOD .450 (.430-.410) < LOD < LOD < LOD < LOD .300-1.080 (<LOD-.1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.380-.870 (.620 (.140-.650) .050-.610-1.160) .42) . population from the National Health and Nutrition Examination Survey.140-.990) .300-. < LOD means less than the limit of detection.450 (.330-.700-1.30) .530-.840) .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 * * * * * * * * * .540 (<LOD-.470 (.380-.560 (.770 (.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 .570) .099-.350) .610-.130 (.270 (.00) .820 (.990 (.171) * * .660 (.560 (.770) < LOD 95th .680) .

600) .870) .280) < LOD < LOD < LOD < LOD .38) 1.400) .150-.580) < LOD .710-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .330-.520-.970) .500-1.67) .230) < LOD < LOD < LOD < LOD .110) .110-.360-.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.86) .740 (.24 (.860 (.440 (.880 (.410 (.390-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.650) < LOD .78) .330-.300-.110) .580 (.780) < LOD 1.990) .057-.700 (.500 (<LOD-.03 (.070 (<LOD-.03 (.990) .210 (.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 * * * * * * .940) .170 (.200 (.510-.161) * * .500) .090 (.550 (.300-.960) .730) .070 (<LOD-.270 (.084-.580 (.03) .60) .560 (.140-.120) . Fourth National Report on Human Exposure to Environmental Chemicals 129 .410-.300 (.410) < LOD < LOD .810 (.09) .36 (1.290) < LOD < LOD < LOD < LOD 90th .380-.43) .260) .730) .02) .580-1.700 (.440-1.570-1.410) .220) < LOD < LOD < LOD < LOD .470 (<LOD-.730 (.86) .450) .570 (.12) < LOD .170 (.740) < LOD 1.670 (.570-.360-.340-.670-1.720 (.670 (.200 (.760) .700-1.050 (<LOD-.860 (.730) .140-.550 (.370 (<LOD-.380-.320 (<LOD-.260-.650-1.190-.00) < LOD .116 (.380-1.230-.660-1.410-. population from the National Health and Nutrition Examination Survey.410 (.19 (.330-.720 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.190 (.640-1.310) < LOD < LOD < LOD < LOD .070 (<LOD-.070 (<LOD-.01 (.390-.890 (.330 (.080 (.62) 1.850 (.29 (.780 (.170) < LOD < LOD .110) .230 (<LOD-.610-1.240-.14) 1.111) * * * * * .110) .66) 1.330 (.380-.140-.02-1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethyldithiophosphate (DEDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.190 (.700) .20) 1.140-.490-1.400 (<LOD-.140) .100-.060-.460 (.600-1.080) .380 (.100 (<LOD-.540) .220 (.540 (.940) .860-2.360) < LOD < LOD < LOD < LOD .180-.270) < LOD < LOD < LOD < LOD .800-1.540 (.140-.250-.880-1.640) 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 .520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .750) < LOD 95th .24) .03 (.120) .S.360 (.450 (.58) 1.090 (<LOD-.580) .080 (<LOD-.510) Sample size 1949 2515 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .

0-38.0 (6. population from the National Health and Nutrition Examination Survey.510-.720) 2.10 (3.840 (<LOD-1.70-50.0) 2.0 (5.52 (1.30 (1. and 03-04 are 0.62-8.00-17.86) 4.640 (.0) 5.03 (.63) 32.6) 5.0-38.0 (3.0) 5.07 (1.12) * * * * * * * * .47 (3.42) .67) .0) 3.580 (.48) 13.30 (.00-17.690 (.21) 3.55-8.35-10.590 (.110 (<LOD-.600 (.36-3.00 (1. see Data Analysis section) for Survey years 99-00.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.850) 16.90) .51-8.0) 5.76 (1.750-2.40 (1.0 (4.94-3.14) 2.170-1.94 (1.20-4.40-7.51 (2.45 (2.74) 5.30-7. 130 Fourth National Report on Human Exposure to Environmental Chemicals .87) 12.080-1.97) 20.210-1.11) .01) 5.70-17.0) 2.23-6.0-39.67 (2.70-3.350-. and 0.07) 1.13 (3.05 (2.99) 11.0 (17.0) 2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.11 (1.52) 5.770) 2.1.07 (3.0 (4.0-40.0 (5.00) .0) 4.49 (1.750-1.31) .00 (.250 (<LOD-.14-5.65) 1.880) 5.59-5.08.0-40.640 (.40-20.0 (17.610 (.190-1.0 (17.70) 2.10-9.14) .15) 14.0 (5.0) 2.52 (1.85-3.0) 2.68) 2.99 (1.870) < LOD < LOD .0 (5.40) 1.480-.840-3.50) .53) 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.15) 19.43-4.70-30.30-3.83) 2.55-4.0 (17.35) 5.31-10.49) 17.740 (.67 (1.3) 952 1187 935 997 1331 995 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .0 (5.610) < LOD < LOD < LOD < LOD < LOD 2.0 (13.0) 2.0-44.60) .20) < LOD < LOD < LOD < LOD < LOD 1.900 (.42) 2.30) .0) 4.40-8.24-7.26 (2.29-10.07-3.1.840 (.97) 20.425-1.05-3.30 (1.83-3.60) 1.39 (2.88-3. 01-02.890 (.30-6.10 (.30 (2.33 (4.80 (4.830 (.35) 11.38-3.10-3.28-9.50) 2.360-1.350-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.53 (2.05 (3.18) 1.20-17.74 (3.800) 17.99) 19.10 (3.07 (3.32-9.90-20. < LOD means less than the limit of detection.90) .83-3.96 (1.20-4.00) .28) . which may vary for some chemicals by year and by individual sample.82-4.36-3.40 (1.87) 5.40-4.800-4.39) .10-3.90-9.691 (.40) 2.960 (.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 .260-. respectively.12-1.0 (16.620-1.370-.910) 2.20 (1.53-7.61 (1.66) 4.49 (1.90-37.00) 1.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.62) 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 * * * * * * .90-28.0-38.960 (<LOD-1.770 (<LOD-1.90 (1.37) .90) .380-.20 (1.63 (3.70-7.30) 95th 19.800) 90th 13.0) 2.48 (2.90 (2. 0.28) 1.730 (.0) 7.0 (17.S.07-3.0) 4.400-1.330 (<LOD-1.0) 4.30 (1.32 (1.94-8.0) 5.46 (1.0 (7.11) 13.21-3.

40-12.64-4.36 (.57 (.96-8.12 (4.7) 5. population from the National Health and Nutrition Examination Survey.17) 5.8 (20.340-.07-21.340 (.650 (.77 (.28-6.00-19.23-7.86) .11) .06 (.90-6.32-6.540-1.33-5.1 (7.30 (4.5-40.8) 4.620-3.98 (4.61) 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 .48-42.39) 20.50) .0 (4.800-2.970-3.48-7.1) 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 * * * * * * .660) < LOD < LOD .33-3.40) 1.7) 3.57) 1.31) .850-3.770) .75) 5.740-1.85-3.96) 2.81-17.53) .890 (.48 (4.04-16.580-1.8) 2.748 (.630-1.51-44.450 (.310-.820) .580 (.580) 16.04 (1.47) 5.24) 3.02-4.50) 11.4 (4.670 (.82-11.540 (.11-5.250 (<LOD-.690-5.49-2.80 (.71 (2.05) .56) .830 (.91) 2.590) 2.1 (5.190-1.83 (4.10-3.69-7.57) 8.57-40.1) 2.67) 1.35 (.700) 6.01 (1.25-9.8-33.65 (2.7 (6.03) 16. Fourth National Report on Human Exposure to Environmental Chemicals 131 .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 * * * * * * * * * .29 (4.08) .55) 21.74 (2.5 (11.960 (.18) 1.5) 2.15) 9.88-3.3) 2.55 (3.31) .340-.150 (<LOD-.14-6.22-27.79 (.53) 27.840-3.33 (1.67-6.97) .710 (<LOD-1.67) 2.270-.07 (2.5) 2.47-10.430) 1.31-18.9 (11.91-4.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethyldithiophosphate (DMDTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.03) 2.370-1.60 (1.44) .470 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600 (<LOD-1.860-2.4-34.64) 30.560 (.340-.00) .14 (1.32) 9.240-.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.73 (4.13 (2.430 (<LOD-.27 (2.370 (.5 (8. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.62 (1.8) 7.88 (.0) 4.66-47.43) .41 (4.62-17.92 (2.5 (9.930) .88 (2.270 (<LOD-.47) .9) 6.83-11.500 (.89 (2.50 (4.33-4.12-4.44-11.29-4.474-1.80) 3.45 (1.85 (1.25 (1.790 (.7) 4.0 (9.21-3.5) 7.7) 6.360 (.9) 5.700) < LOD < LOD < LOD < LOD < LOD 1.31-7.320-1.790) 11.02) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.71 (.51-4.56) 2.3) 3.69) 2.940-4.580) 1.41) 18.25-38.260-.8) 7.22) 2.55) 21.330-1.02 (.7 (12.50 (2.02 (1.56 (1.370) < LOD < LOD < LOD < LOD < LOD 1.260-.38 (2.84) 9.830-3.59 (1.40 (.10 (2.4) 2.33 (3.47-10.650) 90th 10.2 (8.780-4.2-38.390-.86 (3.88) 17.730-3.37) 4.96-25.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.40-2.09-3.17 (1.67 (2.8) 1.52 (.8) 2.S.18) 95th 21.820 (.10) 2.18) * * * * * * * * .

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Gladstone EA. U. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Lasarev M. Keefe TJ. Am J Ind Med 1987. Visuthismajarn P. Environmental Protection Agency (U. et al. Buccafusco JJ. et al.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Available at URL: http://www. National Academy of Sciences. Weerasekera G. 1993 [online]. Barr DB. Rohlman D. Bradman A. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Spurgeon A. Available at URL: http://books.338(8761):223-227. Burcar PJ. Frasca G. 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. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. J Toxicol Environ Health A 2005. Jenkins B.345(8958):11351139. Prendergast MA. Pedersen L.44(4):352-357. Lu C. Savage EP. Stokes L. Lancet. Effects of long-term organophosphate exposures on neurological symptoms. Calvert IA. Effects of chronic.12(2):153-172. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. McCauley L. Buchanan D. Muniz J. Keifer M.php?record_id=2126&page=1. low-level organophosphate exposure on delayed recall. Neurotoxicology 2005. Levy LS. Masala G. Bravo R. Neurotoxicity among pesticide applicators exposed to organophosphates. Smit LA. National Research Council (NRC). Kidd M. Dinoff TM. 1991. Rosenstock L. Schenker M.epa.nap. 2004. Eskenazi B. Muniz J. Takamiya K. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand. Rothlein J. Hore P. London L. Petchuay C. Occup Environ Med 1995. Arch Environ Health 1975. Aprea C. Caltabiano LM. Environ Health Perspect 2006.edu/ openbook. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Daniell WE.20(2):115-22. Robson MG. Pesticides in the Diets of Infants and Children. Ruberu DK. Weisskopf C. Lancet 1995.52(2):190-195. and cholinesterase status of date dusters and harvesters in California. Sci Total Environ 2004. Washington (DC). vibration sense and tremor among South African farm workers.52(10):648-653. Russo J.S. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Hansen S. Jamal GA. J Occup Environ Med 2002. A behavioral evaluation of pest control workers with short-term.pdf. Nell V. metabolite clearance. Occup Environ Med 2001. McConnell R. Bull Environ Contam Toxicol 1994. Berry H. Claypoole K. Rothlein J. Vitayavirasak B. Wickremasinghe AR. Office of Prevention Pesticides and Toxic Substances.38(4):546-563. Int J Occup Environ Health 2006.84(5):731-736. Myers JE. Pesticide industry sales and usage .2000 and 2001 market estimates. O’Malley M. et al. low-level exposure to the organophosphate diazinon. Steenland K. and spatial learning in monkeys and rats. Neurotoxicol Teratol 1998. Stark A. Tumino R. Heaton RK. Scand J Work Environ Health 1998. Malathion deposition. Gillham R. Stephens R. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. et al. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). et al. Johnson C. The Pesticide Health Effects Study Group. Seiber J. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. Lewis JA. 4/7/09 Young JG. Chronic neurological sequelae of acute organophosphate pesticide poisoning. EPA). Marshall E. Terry AV Jr. Scherer J. Salvini S.58(11):702710. Chrislip D. Lambert WE. Samuels S. gov/oppbead1/pestsales/01pestsales/market_estimates2001.24(1):18-29. Mounce LM.332(1-3):71-80.30(2):98-103. Saieva C.114(5):691-696. Arch Environ Contam Toxicol 2000. Ames RG.S. discrimination. Rodnitzky RL. Irish RM. Beach J. 1/12/09 Peiris-John RJ. May.43(1):38-45. Washington (DC): U.26(2):199-209. Pilkington A. Am J Public Health 1994. Santana J. Phillips J. Lasarev M. Narang A.68(3):209-227 Maizlish N. Chronic neurological sequelae to organophosphate pesticide poisoning. S. EPA. van der Hoek W.12(2):134-141. Environ Health Perspect 2005.113(4):504-508. Thompson ML. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Arch Environ Health 1988.

These metabolites differ from the dialkyl phosphate metabolites because each specific metabolite derives from one or only a few parent insecticides. see the section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites.Organophosphorus Insecticides: Specific Metabolites Organophosphorus Insecticides: Specific Metabolites General Information The specific metabolites of the organophosphorus insecticides discussed in this section are those that are often measured in biomonitoring studies.” Organophosphorus insecticide (CAS number) Chlorpyrifos (2921-88-2) Chlorpyrifos-methyl (5598-13-0) Coumaphos (56-72-4) Diazinon (333-41-5) Malathion (121-75-5) Ethyl parathion (56-38-2) Methyl parathion (298-00-0) Pirimiphos-methyl (29232-93-7) Primary urinary metabolite (CAS number) 3. the level may reflect exposure to the environmental degradation products of these pesticides. In addition to reflecting exposure to the parent insecticide. parathion and methyl parathion are metabolized to para-nitrophenol. For general information about the organophosphorus class of insecticides. For example.6-Trichloro-2-pyridinol (6515-38-4) 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol 2-Isopropyl-4-methyl-6-hydroxypyrimidine (2814-20-2) Malathion dicarboxylic acid (1190-28-9) para-Nitrophenol (100-02-7) 2-(Diethylamino)-6-methylpyrimidin-4-ol/one 134 Fourth National Report on Human Exposure to Environmental Chemicals . malathion is metabolized to malathion dicarboxylic acid.5. The table below shows the parent organophosphorus insecticides and their metabolites measured in this Report.

05) 1.36 (4.50 (1.0) 10.4 (10. pre.0 (9.13 (1. 5598-13-0 General Information The chemical 3.28-3.000 pounds are used per year.80) 4.9-18.50-2.80-8.50-8.EPA. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.52-12. applied to structures to kill termites.5 (8.20-14.37) 5.10) 2.92 (1.70-11.44 (3.61-7.02 (1.0 (7.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.35) 2. and sprayed to kill mosquitoes.76 (1. although some tolerances for specific food crops have been reduced in the past to avoid exceeding recommended intake limits for total dietary intake in special groups (U.51) 1.00) 2. 2007).50-14.50 (2.52-2.90) 7.90-2.00) 1.71 (2. and is infrequently detected in ground water (IPCS.04-10.13-3. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.3 (10. staying bound to soil particles.39-2.03) 1.59-2.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.0) 6.37 (1. Fourth National Report on Human Exposure to Environmental Chemicals 135 .0) 10.45 (1.60-4.57 (2.and post-construction structural applications for termite control were to be phased out by 2005 (U. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.5.04-10.27 (7.20-3. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.97-7.38 (3.80-10.40 (5.9 (9.50 (2. Chlorpyrifos is Urinary 3.26) 7.0) 11.63 (2.8) 10.25) 1. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.30) 4.3 (8.21) 3.10 (1.66-15. Survey Geometric mean (95% conf. 2921-88-2 Chlorpyrifos-methyl CAS No.87-6. Approximately 21-24 million pounds per year were used domestically from 1987-1998. USGS. and on plants for days to several weeks.77) 1.44-2.70-15.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1. and dust.90 (3.S.47-13.53 (1.10 (3.0) 8.68 (7.35) 1.S.0) 9.47-9.83) 1.22) 2.91 (1.6) 7.10 (5.63 (8.0-28. For instance.9 (10.40-2.84) 1.37 (4.40) 9.20) 2.40 (6.70-5.1) 5.97) 4.67 (2.00) 3.01) 1.32) 2.63 (1.09 (2.60 (4.77 (1.1-16.0) 12.40 (5.5-24.90 (1. The general population may be exposed to chlorpyrifos via oral.30-11.55-5.9) 11. It also has been applied directly on animals to kill mites.9) 697 660 521 701 602 947 Limit of detection (LOD.60 (5.4-15.80) 1.40-10.40) 2.97) 7.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00-8.47-11.29-1.30-2.0 (7.32-1.71 (1.10) 6.80 (7.4 (8.3) 8.0 (10.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.99-4.62-2.24-1.90-8.80) 12.9 (7.0) 15.29) 90th 7.90 (2.72) 2.0) 12.88 (1.05-5.10-17.0 (7.43-2.S.19-3.72-4.5.60) 5.50 (2.50-4.81-2.20-2.61) 75th 3.0 (7.90 (6. 2002).4.64) 3.96) 3.40-26.30) 5.7) 13.77-15.90 (1.0) 18.40-13.EPA.95 (4.77-6.20-11.25) 3.89-2.68-2.0) 12.10 (4.67 (2.97) 2.51-2. After 2001.02 (7.97) 2.16) 2.51 (1.47) 1.74-9.47 (4.20 (2. air.17 (1.90-7.0) 14.74 (1.. Exposure can also result from contact with contaminated surfaces.70-17.4 and 0.20-16. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn. Estimated intakes from diet and water have not exceeded recommended intake limits.09 (3.50-5.3 (11.59) 2.30-9.7-23.02) 1.80) 2.94 (4.24-3.4 (9.43-2.8) 9.3) 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 1.60-2.7) 8.0 (13.22 (1.0) 7.20) 10.20-4. 2002). see Data Analysis section) for Survey years 99-00 and 01-02 are 0.60 (2.70-16.20) 4.90) 3.7) 9.5) 7. in 142 urban homes and preschools in North Carolina.0) 12.30 (2.91) 16.95) 7.70) 1.20) 2.67 (1.98-15. chlorpyrifos was no longer registered for indoor residential uses in the United States.30-1.20 (4.15 (1.00-24.34) 1. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.70 (1.78 (7.28) 2.50-2.19 (1.30) 4.60-3.90-4.76 (1.80 (1.30-5. interval) 1.60-3.46-2. 1999.31-2. It has low leachability. dermal.30 (4.0 (7.0) 10. population from the National Health and Nutrition Examination Survey.0) 12.31-2.2 (10.50-4.8-15.30-12. but can be detected in streams receiving runoff from application sites.66-4.79-2.50 (1.86) 4.0) 8.03) 99-00 01-02 99-00 01-02 99-00 01-02 2. and inhalation routes.70 (1.44-5.61 (1.71 (6. Approximately 80. 2005).89 (2.39) 4.30 (2.

45 (1.31-1.44-6.57-2. TCPy is more persistent in the environment than chlorpyrifos itself (U.92) 3.0) 12.00-13.24-1.14-8.86 (3.22 (4. 2006. Survey Geometric mean (95% conf.97 (3.98 (6.77) 1.42 (6.94-14.59-2.95 (3.88-8. Howard et al.27-1.47 (1.71 (1.91) 10.41 (1.49 (1. Based on animal data and human cholinesterase monitoring during occupational exposure.80-4.91 (3.93 (2.24) 5. cholinergic effects.20 (2.54 (2.34-1.00-8.46 (2.17-4. 2000).12-3.06 (5.53-5.58) 5.60-3.47 (1.69 (1.24) 75th 2.06-4.83-11.12) 1.91 (4.62-7.33-7.15 (4.6) 9.48 (1.6) 10.24-4.91-13.97 (2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).50 (4.05-1.45-1.06 (1.24 (1.1-38.99-8.90-9..25-11.82) 8.89) 4.14) 1. Roy et al.97) 3.32) 1.43-10.03) 1.S.05-3. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.23) 14.11 (2.16) 6.07) 5.07) 1. 2005.09 (1.58 (4.26-14.16 (4.73 (1.76 (3.72) 2.80-6.08) 6.58 (1. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.7) 7.85 (3.56 (4.95 (1..0) 16. 2005.83-2.65-15.86 (1.87-3.62) 1.01) 3.44 (5.39 (2. Once absorbed. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.S.44 (1. neurotransmission.88 (1.59) 3. and producing acute symptoms such as nausea.19-2.42-2. 2005.02 (5.0) 10.93) 5. paralysis.49-2. Metabolic hydrolysis leads to the formation of TCPy. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.96) 3.63 (4.63-2.53 (2.62) 90th 5.56-2. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.76 (2. Urinary 3.80) 3.39) 6.85) Selected percentiles ( 95% confidence interval) Sample 95th 8. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.44 (1.11-9. 2006b).7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .47 (5.85) 4. Ricceri et al.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 1.99) 1.64-7.31) 1.47-2.68) 6.57) 9.25-1.71) 3.17-4. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.98 (7.09-3.57) 2.46 (1.1-21.57-2.35) 2.52 (5.72) 1. Thus.33 (5.58) 1.8) 9.63 (5.49-2.35) 1.0) 6.2) 6.39 (4.48 (2.30-4.28) 2.28) 2.09-1.85) 1. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.24-24.85-4. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide. and seizures. Betancourt et al.35-1.30-1.80-11.21-1.75) 6.81 (3.44 (5. interval) 1.55 (1.1 (7. 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.44 (6.75 (1.. In pesticide applicators.02) 7.55 (4.49-2.36) 1.55) 1. 2006a.56) 5.19) 6.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1. 2006. vomiting. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.31-4.9 (12.88-10.01) 3.22 (6.66-11.66) 1.33 (1.20-1. Slotkin et al.85 (2.82 (3.09-2.72-2..11) 7.21-6.51 (1. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.2 (7.05-4.58 (1.92-2.37 (1.00 (7.29 (3.74) 1.82-4..88-8.93) 2.19) 3. TCPy can also occur in the environment from the breakdown of the parent compounds.3) 8.86 (1.25-12.05-8.60 (1.68) 1. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.940-1.78 (1. and other metabolites.88-9.5.82 (2.94-12.40) 1.00) 1.88) 6.23-1.97) 3.91-4.43 (4.97-3.65-11.91) 2.33 (.56) 2.91) 1.22) 1.81) 2..27-7.11 (2.70-4. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.88 (1.01) 1.54) 5. population from the National Health and Nutrition Examination Survey. resulting in excess acetylcholine at nerve terminals. weakness.83) 1.64 (1.3 (7.91) 1.19-1..39-1.93 (1.24-5.66 (1.1 (10.92 (1.4) 4.84-6. 2002).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.5 (6..58-5.3) 9.12-1. 1984).EPA.64-2.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.56 (1.42 (5.05) 3.38) 3.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion..79-13.22-6.5) 5.33) 2.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.3) 8.93 (4.

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

Bucelli R. Environ Health Perspect 2000. Fortuna S. Lu C. Neurologic function among termiticide applicators exposed to chlorpyrifos.10(4):327-340. Wartenberg D. et al. Weltzien E. Herrick RF. et al. Ann Occup Hyg 2007.nih. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Lein PJ.org/documents/jmpr/jmpmono/ v99pr03.niehs. Honeycutt R. Sharma V.207(2):112-124. Head SL. Fenske RA. Barr DB. Seidler FJ. Hammerstrom KA. Pellizzari E. Environ Health Perspect 2003.6-trichloro-2-pyridinol.15(4):297-309. Environ Health Perspect 2006a. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites.114(2):260-263. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). et al. J Expo Anal Environ Epidemiol 1999. Toxicol Appl Pharmacol 1984. Croghan CW.5.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Venerosi A. Hines CJ. 2005.108(4):293-300.51(1):53-65. Baker S. Kinney P. Sheldon LS. Bravo R. Kromhout H. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Slotkin TA. Third National Report on Human Exposure to Environmental Chemicals. Heederik D. Ryan L.5. et al. Dick RB. Biomonitoring for farm families in the farm family exposure study. 4/7/09 Koch HM. Robson M. Capone F. Toxicol Appl Pharmacol 2005. Edwards RD. Toxicol Sci 2006. Levin ED. Lioy PJ. et al. Ryde IT. Yang D. Environmental Protection Agency (U. Toepel K. Levin ED. 4/7/09 Perera FP. Zhang J. Morgan MK.S. Barr DB. 1999. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application.15(3):271-281. Cometa MF. February 5. Jett DA. Hill RH Jr. Roy TS. Environ Health Perspect 2005. Eskenazi B. International Programme on Chemical Safety-INCHEM (IPCS). Bailey SL. Robertson GL. Scand J Work Environ Health 2005. Hein MJ.111(2):201-205.114(5):746-751. Freshour NL. Meeker JD. Howell RJ. Interim registration eligibility decision for chlorpyrifos. EPA). mothers and fathers living in farm and non-farm households in Iowa. Brain Res Dev Brain Res 2005. National Toxicology Program (NTP). Int J Hyg Environ Health 2001. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Irish R. Angerer J. et al.155(1):71-80. J Expo Anal Environ Epidemiol 2005.71:99108. Alexander BH. Curwin BD.31 Suppl 1:98-104. Tsai WY. Sanderson WT. 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EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Seidler FJ.114(10):1542-1546.93(1):105-113. Barr D. J Expo Anal Environ Epidemiol 2000. Steenland K. Freeman N. Chapman P. 1992. Available at URL: http://ntp. Hore P. Pesticide residues in urine of adults living in the United States: reference range concentrations.6-trichloro 2-pyridinol in their everyday environments. Tate CA. Bruun D. chlorpyrifos. Chrislip DW. Needham LL. Bennett DH.htm. Environ Health Perspect 2004. U. A longitudinal investigation of selected pesticide metabolites in urine. Rauh V. Seidler FJ. Lorenzini P. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Bravo R. Environ Health Perspect 2006. 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. Striley C.113(2):211-219. Chuang JC. MacIntosh DL. Barr DB. Slotkin TA. Environmental Health Criteria 198.73:8-15. Ozkaynak H.inchem. et al.S. Available at URL: http://www. Harley K. 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. Slotkin TA. Environ Res 1995. Rick DL. Jewell NP. gov/ntpweb/index. Camann D. 2921-882.9(5):494-501. et al. Saunders JH.

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

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

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 . < 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. population from the National Health and Nutrition Examination Survey.200 (<LOD-.S. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey.670 (<LOD-1. 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.380 (<LOD-.270) < LOD 659 701 920 Limit of detection (LOD.560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.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 . see Data Analysis section) for Survey year 01-02 is 0. which may vary for some chemicals by year and by individual sample.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. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.2.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Fourth National Report on Human Exposure to Environmental Chemicals 141 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200 (<LOD-.

EPA). Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies.pdf. Centers for Disease Control and Prevention (CDC).gov/oppsrrd1/ REDs/0018tred. 2005. Reprod Toxicol 1998.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. Sadowski MA. Eigenberg DA.epa. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . Nguyen JV. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos.S. Freshwater KJ. Available at URL: http://www. Environmental Protection Agency (U. U. Olsson AO.12(6):619-645. Anal Bioanal Chem 2003.S. September 2000. Barr DB. Atlanta (GA). A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. EPA 738-R-00-010.376(6):808-815. Third National Report on Human Exposure to Environmental Chemicals.

05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine.EPA. Before these restrictions.S. Most granular formulations. which may vary for some chemicals by year and by individual sample.2 and 0. but these uses have been phased out. diazinon was widely used in residential and garden application. aerial. 2004). Diazinon is not well-absorbed through the skin.EPA. and forage crops. see Data Analysis section) for Survey years 99-00 and 01-02 are 7.S. diazinon produced wild bird kills before use restrictions were in place. fruits.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. Prior to 2000. 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. population from the National Health and Nutrition Examination Survey.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. Once absorbed. 1998). It is toxic to birds. an organophosphorus insecticide that is used to control insects on nuts. and particularly when it was ingested in granular form. in some pest strips. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. vegetable. It is also used for cattle ear tag applications to control flies and ticks and.49 (<LOD-2.7. in the past. 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. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). Fourth National Report on Human Exposure to Environmental Chemicals 143 . 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. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. 2007). 1998.45 (<LOD-3. but is rapidly absorbed orally (IPCS. Survey Geometric mean (95% conf. Estimated intakes from diet and water do not exceed recommended intake limits (U. Inhalational and dermal routes of exposure can be significant for pesticide applicators. since 2004. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS.S. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. and other metabolites. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. USGS. 2004). seed and foliar applications are planned to be phased out (U. diazinon cannot be sold for residential use. < LOD means less than the limit of detection. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity.

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

Diazinon.epa.9(2):117-131. Interim reregistration eligibility decision (IRED. Oloffs PC. Barr DB. Kruse RL. Environ Health Perspect 2006. EPA 738-R-04-006. 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. Dumas P. et al. Baker SE. Available at URL: http://www. 1998. 1/14/09 U. Barr DB. Effect of sublethal levels of diazinon: histopathology of liver. References Anthony J. Seifert J. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. J Expo Anal Environ Epidemiol 2000.50(5):505-515. Nguyen JV.usgs. Rajendra W. Carrier G. Ann Occup Hyg 2006. 1992-2001.376(6):808-815. Environmental Protection Agency (U. Toxicol Lett 2002. Environ Health Perspect 2003.org/documents/ehc/ehc/ehc198.S. Atlanta (GA). urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al.gov/ oppsrrd1/REDs/diazinon_ired. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Cocker J. Diazinon. March 2006. 2005. Banister EW. 2007 [online]. Needham LL. Geological Survey (USGS). Noisel N. Third National Report on Human Exposure to Environmental Chemicals. Brunet RC.37(4):501-507. Olsson AO. Liu F. In a small number of men visiting fertility clinics in Missouri and Minnesota. Garfitt SJ. U.gov/circ/2005/1291/.pdf.htm. 4/7/09 Lu C. Jones K. Pesticides in the Nation’s Streams and Ground Water. In 23 children. May 2004. revised February 15. International Programme on Chemical Safety-INCHEM (IPCS). Biochem Pharmacol 1992. Swan et al. Bouchard M. Fenske RA. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Drobnis EZ. Drug Chem Toxicol 1986. Redmon JB. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses. Centers for Disease Control and Prevention (CDC).10(6 Pt 2):789-798. 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. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers. The Quality of Our Nation’s Waters.44(11):2243-2250.Organophosphorus Insecticides: Specific Metabolites 2005). Irish R.inchem. In 54 Canadian greenhouse workers. 2006). 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Pewnim T.111(12):1478-1484. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Sadowski MA. Bull Environ Contam Toxicol 1986. Semen quality in relation to biomarkers of pesticide exposure. Barr DB.. Toepel K.S.. Banister E.114(2):260-263. Available at URL: http://pubs. Driskell WJ.S. Beeson MD. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Environmental Health Criteria 198. Available at URL: http://www. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Oloffs PC. Anal Bioanal Chem 2003. 2006). EPA). Bravo R. Mason HJ. Barr DB. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.134(1-3):105-113. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Swan SH. Study for Future Families Research Group.

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

S. Additional information about external exposure (i. EPA at: http://www. IARC considers malathion not classifiable as a human carcinogen.0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. Toxicity from unprotected bystander exposure during applications is rare (U.gov/pesticides/. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2006). Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect.EPA. but cholinesterase activity was not affected. 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. Fourth National Report on Human Exposure to Environmental Chemicals 147 . 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.html and from U. Giri et al.e. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. and it is not considered an animal teratogen or a reproductive toxicant. 1996.cdc.. 2005).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. Lu et al.. Thomas et al. A study of agricultural workers reported preshift urinary levels of malathion dicarboxylic acid that were twofold to eightfold higher than detection limits in the NHANES 1999-2000 subsample (Krieger and Dinoff.. Human studies of single oral doses between 0. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. 1999. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid.S. 2000). Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. population from the National Health and Nutrition Examination Survey. Pluth et al. environmental levels) and health effects is available from ATSDR at: http://www. 2005). interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 1920 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 50th < LOD < LOD 75th < LOD 90th * 99-00 99-00 99-00 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al.S. 2006). 1999). 2005.S.5 and 5. 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..gov/toxpro2.74 (<LOD-5. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample.. 2003). median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC. but isomalathion. 2001.. 2002. Of 382 pregnant women living in an agricultural community. Survey Geometric mean (95% conf.EPA. 1993. Malathion itself has not been considered genotoxic (U.epa..S. 1987. 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. Flessel et al. 1990).. CDC. representative subsample from NHANES 19992000 (Adgate.atsdr.. 2004).Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions. 2006)...

114(2):260-263. Flessel P.514(1-2):223231. metabolite clearance. Gosselin NH.pdf. 4/7/09 Kissel JC. Eskenazi B.9(5):494-501. Centers for Disease Control and Prevention (CDC). Clayton CA. Mutat Res 1999.38(4):546-553.74(2):following table of contents. htm. The Quality of Our Nation’s Waters. et al. Available at URL: http://www. Arch Environ Contam Toxicol 2000.gov/circ/2005/1291/. Goldhaber M. Environmental Protection Agency (U. Geological Survey (USGS). Krieger RI. Swan SH. Sharma GD. Giri A. Carrier G. Neutra R. Erratum in: Toxicol Sci 2003 Aug. Ryan PB. Malathion (addendum). Grether JK. International Programme on Chemical Safety-INCHEM (IPCS). Griffith W. J Expo Anal Environ Epidemiol 2005. Albertini RJ. Am J Epidemiol 1990. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Petitti D. Environ Health Perspect 2001. A longitudinal investigation of selected pesticide metabolites in urine. March 2006.445(2):275-283. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Needham LL. Environ Mol Mutagen 1993. Toxicol Sci 2003 May. Szyfter K. Reproductive outcome in women exposed to malathion. Barr DB. Nicklas JA. Prasad SB. Available at URL: http://www. 6/1/09 U. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. Hammerstrom KA. Bouchard M. Pluth JM.inchem. Rappaport E. Available at URL: http://pubs. July 2006. Barr DB. Third National Report on Human Exposure to Environmental Chemicals. Am J Public Health 1987. 2005. Toepel K. Genetic toxicity of malathion: a review. Jewell NP. Environ Health Perspect 2004. Mutat Res 2002. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers.132(4):794-795.S. Giri S. Environ Health Perspect 2006. Blasiak J. Eberly LE.77:1009-1010. Atlanta (GA). Dumoulin MJ.S. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Lioy PJ.112(10):1116-1124. Weltzien E. Lu C. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues.56(10):2393-2399. revised February 15.15(2):164-171. 2007 [online]. Thomas D. et al. J Expo Anal Environ Epidemiol 1999. EPA 738-R06-030. Brunet RC. U. Jaloszynski P. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals .22(1):7-17. Barr DB.Organophosphorus Insecticides: Specific Metabolites References Adgate JL.73(1):182-94. EPA). et al. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.epa. Malathion deposition. Curl CL. Dinoff TM. Irish R.109(6):583-590.usgs. Cancer Res 1996. Harris JA. Kedan G.gov/oppsrrd1/REDs/ malathion_red. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. Reregistration eligibility decision (RED) Malathion. Fenske RA. Freeman NC. O’Neill JP.S. Harley K. 1992-2001. MacIntosh DL. Hooper K. Hertz-Picciotto I.org/documents/jmpr/jmpmono/v2003pr06. Pesticides in the Nation’s Streams and Ground Water. Trzeciak A. Quintana PJ. Samuel O. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Lu C. Bradman A. Bravo R. Barr DB. and cholinesterase status of date dusters and harvesters in California.

and of the chemical nitrobenzene.50-14.0 (3.70-3.19 (.60 (4.70-6.40-3.01) 4.11-4. was once a restricted-use insecticide with limited applications on certain agricultural crops.00 (2.33) 2. 2006).80) 2.40 (1.50) 3.0) 3. Increased risk of exposure via dermal.80 (1.300-. first registered in 1948.. and eliminated rapidly from the body after absorption (Kramer et al.49 (1.80 (2.30-5. population from the National Health and Nutrition Examination Survey. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol. and has a short half-life in soils and on plants.37) 2.37-4. Given its limited use.85 (2. ethyl parathion.45 (1.10-11.50 (1.44) 2. more slowly absorbed through the skin. Fourth National Report on Human Exposure to Environmental Chemicals 149 .18-3.74) 5. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. and aquatic invertebrates.80 (2. Methyl Parathion.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .EPA.67) < LOD 1.72 (3.60-19. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. binds tightly to soils resulting in low leachability.21-1.S.71 (2.860 (<LOD-1.61) < LOD 1.850) < LOD .62 (1.50 (2.940 (<LOD-2.01-4.41-4.0) 3.90 (1.70) 2.10 (3.298-00-0 Ethyl Parathion CAS No.02-6.0) 3.50) 2.92) 5. Estimated intakes from diet and drinking water have been below recommended limits. Methyl parathion is not registered for residential use in the United States. but by 2003.21 (2. 2000).30 (1.22-3. 2002. Once absorbed.28 (1.40-4.50) 3.50 (1. 2007).26 (1. which may vary for some chemicals by year and by individual sample.40) 2.910) < LOD < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.00) 3.S.60) 1.. Many previous registered agricultural uses of methyl parathion have been cancelled (U.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .40) 4.16) < LOD 1.60-36.50 (1. In the 1990s.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 1.20 (<LOD-2.20 (2. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.70 (3.S.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.66 (2.20) 5. on cereal grains.30 (2. fish.57-4.46 (3..30-3. Both are toxic to birds. In animal studies.91-3.10-1. Methyl parathion has low water solubility.28 (1.50 (1.32 (1.58) 3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.990-1.57) 1. 1977).11) 2.12) < LOD < LOD 1.0) 2.69) 4.70 (<LOD-3.90-9.700 (<LOD-.50) 1.61) < LOD 1.0) 3.0) 3. Methyl parathion use is highly restricted.40) 1.37-2.45) 5.0) 4.71 (3.32-3. with limited applications in agriculture.40-4.70-6.50-9.10) 4.27) 2. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.70-6. It had been applied to cotton.20-5.48) 90th 2. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. all registered uses were voluntarily cancelled (U.13-1. 2003). methyl parathion was rapidly absorbed after ingestion.70 (2. pulmonary.1.EPA.70 (2.33 (1.60-5. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.28-4.01) 695 660 518 679 603 941 Limit of detection (LOD.30-16.05) 4.79) 4.15-3.70 (2. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low.00 (2.70) 2.09-1.89 (2.910) < LOD . peak domestic use was as high as 5-6 million pounds per year.10 (<LOD-6.32-1. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.32-1.67 (1.50 (2.910) < LOD < LOD < LOD 1.47) 2. < LOD means less than the limit of detection.730 (<LOD-.36-1.70-3.37-4. Ethyl parathion.90-11. and oral routes can occur in pesticide and agricultural workers (Muttray et al.34 (3.8 and 0.69 (2. Morgan et al.70) 2.790 (<LOD-. and to a lesser extent.92-2.10 (3.10) 22.770 (.60-24. Survey Geometric mean (95% conf.

. 2006.940 (<LOD-1. 1990.78-2.67 (3.35-3.61) 4.76-14. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate. and unintentional acute or chronic high-level occupational exposure (Hill et al.440 (<LOD-.91 (1.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .30-1.08) < LOD .790-. Jaga and Dharmani.830-1. vomiting.44-3.400 (<LOD-.01-3. paranitrophenol.78-2.epa.930 (.79 (1. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.41-2. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.96 (1. Karanth and Pope et al.730-1.04) 1.04 (2. environmental levels) and health effects is available from ATSDR at: http://www. 1995).55) 2. 1995. Parathion and methyl parathion have high acute toxicity in animal testing. Orsorio et al.e. 150 Fourth National Report on Human Exposure to Environmental Chemicals .980 (.500) < LOD < LOD . 2006.17-4..29) 1.95) 1.01 (.05) 4.720-1.26 (1.90 (1.950) < LOD . 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.4 (3.89 (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 .26) 17. but lists ethyl parathion as a possible human carcinogen.92 (2. 1978.2) 2.16-4.84) 3.88 (1.88) 1.S.57-7. Zurich et al.91) 1.850-1.77-7.39) 1.30) 3.73 (1.23) 1. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens. and seizures.13) 4.59 (1.540) < LOD . Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.89 (2.97 (<LOD-4.930 (.38-3.96 (1. Methyl Parathion. and other metabolites.. cholinergic effects.93 (2.43) 4.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD . weakness. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .720 (<LOD-. does not inhibit acetylcholinesterase enzymes. The metabolite.97 (2.. Survey Geometric mean (95% conf. In addition to being a metabolite of methyl and ethyl parathion.310-.71 (1.21) 1.60 (1. At high animal doses of methyl parathion. teratogenic.98-7.87 (1. Slotkin et al.57) 6.20) 3.09) 2. EPA at: http://www.82 (2.00) 2. and producing acute symptoms such as nausea.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. ethyl parathion. 2003.html and from U. population from the National Health and Nutrition Examination Survey.56-2.07) 2.79) 1.82) < LOD .530) < LOD < LOD < LOD .14-3.31) < LOD .680 (<LOD-1.60-2.S.94-4.78) 2.08 (1.80 (1.37-1.2) 2.S. 2005.11) 1..880 (.57-2. 1991).80 (1.25 (2.11-4..29) 2.790-1.70) 3.690-1.15) 3.08-3.800-1. 2004).94-47.01 (2.25) 1.21-21. 2004)..60) 2.430 (.78 (2.33-3.970 (.48-4.Organophosphorus Insecticides: Specific Metabolites Metabolites”).370 (<LOD-. In large doses.55 (<LOD-3.33-6.71) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.39 (1.20) .7) 3.640) < LOD < LOD 1. methyl parathion.10 (1.1) 2. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.31-3.72-2. gov/pesticides/.. paralysis.00 (1.15-10.atsdr.97-10.67-2. resulting in excess acetylcholine at nerve terminals.840 (. Lores et al.17) . Thus.35-3. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.9) 1.83 (1. U.970 (.cdc.20 (3.EPA considers methyl parathion unlikely to be carcinogenic to humans.870) < LOD .86 (2. accidental exposure.10) 90th 2.07 (1.00 (1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.13-12.33-3.29 (2. gov/toxpro2. WHO.44-3. Additional information about external exposure (i. Methyl parathion is not considered genotoxic.3) 2.

Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Pesticide residues in urine of adults living in the United States: reference range concentrations. Needham LL. Eskenazi B. 1995..71:99108. 2004). 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. Lu C. J Anal Toxicol 1990. Head SL. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. et al. Rev Environ Health 2006. Neurotoxicol Teratol 2003. Bradway DE. et al. Environ Health Perspect 2002. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum. Head SL. McCann KG. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion.. Barr DB. Laboratory investigation of a poisoning epidemic in Sierra Leone. Bradman A. Karanth S. Pharmacokinetics of methyl parathion: a comparison following single intravenous. 2005). a range of values several hundred times higher than levels found in the U.56(7):449553. Clark JM. Moomey CM. Environ Res 1995.S. Morgan DP. Rubin et al. Wellman SE. 1995). Alley CC. Pope C. International Programme on Chemical Safety-INCHEM (IPCS). Harley K. Curl CL. Environ Health Perspect 2002. Hetzler HL. population (Olsson et al. Costa LG.112(10):1116-1124. general population (CDC. Griffith W. et al. Levels of para-nitrophenol in the NHANES 1999-2000 and 2001-2002 subsamples were similar or slightly lower than those in a nonrandom subsample of NHANES III (19881994) participants (CDC. Bailey SL. Hill RH Jr.33(5):270-276. et al.110 Suppl 6:1085-1091.inchem. Arch Environ Contam Toxicol 1977.6(2-3):159-173. Lores EM. 1999). Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects..110 Suppl 6:1075-1078. Baker S. 4/7/09 Jaga K. Arch Environ Health 1978. Jewell NP. Toxicology 2005. References Barr DB. McClure PC. Leng G.org/documents/jmpr/jmpmono/v95pr14. ACGIH recommends a BEI of 0. Giordano G.15(2):164-171. Methyl parathion: an organophosphate insecticide not quite forgotten.. Atlanta (GA). 2005. Baker RC.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Environ Health Perspect 2004. 2002). Kissel JC.S.21(1):5767. Guizzetti M.5 mg (500 µg)/g creatinine for workers at the end of shift. Hill et al. Turner WE. In a study of workers who handle parathion. Runkle KD. 2005. Pathak S. 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.25(5):599-606.9:311-320. Lin LI. oral or dermal administration. Fourth National Report on Human Exposure to Environmental Chemicals 151 . J Expo Anal Environ Epidemiol 2005. Cline RE. Chicago area methyl parathion response. Gregg M. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. et al. CDC. Hill RH Jr. Dharmani C. Third National Report on Human Exposure to Environmental Chemicals. Barr DB. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.. Role of individual susceptibility in risk assessment of pesticides. Occup Environ Med 1999. Pesticide workers may have much higher levels following pesticide applications.14(4):213-216.. McCann et al. Available at URL: http:// www. 2002. Kedan G. Shealy 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. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Lewalter J. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Baker SE.htm. Hryhorczuk DO. Barr DB. and many residents were symptomatic (Barr et al. and levels were similar or slightly lower that those in a small convenience sample of the U. J Biomed Sci 2002. Weltzien E.. Rockhold RW. Moseman RF. 2005. 2005). Barr JR. Parathion-Methyl (addendum). Centers for Disease Control and Prevention (CDC).215(3):182-190. 2002. Ashley DL. DiPietro E. Kramer RE. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Slach EF. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation.

Osorio AM.D.Organophosphorus Insecticides: Specific Metabolites Muttray A. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos.04/106.pdf. 2007 [online]. EPA). Methyl parathion in drinking water. 1/14/09 U. Am J Ind Med 1991. Ohio. Pesticides in the Nation’s Streams and Ground Water. EPA). 5/19/09 Zurich MG. Jung D.pdf. Dunlop B. R. Nguyen JV. Monnet-Tschudi F. Levin ED. 1995-1996.gov/circ/2005/1291/. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Ethyl parathion. Costa LG. 6/1/09 World Health Organization (WHO). gov/oppsrrd1/REDs/methylparathion_ired. Slotkin TA. Available at URL: http://www.S. Barr DB.114(10):1542-1546. Honegger P. Investigation of a fatality among parathion applicators in California. Available at URL: http://www.162(2-3):219-224. September 2000.gov/oppsrrd1/REDs/factsheets/0155fct. 152 Fourth National Report on Human Exposure to Environmental Chemicals . 0153. Hill RH Jr.E. Sadowski MA.20(4):533-546. Esteban E. March 2006. 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. Hill G. Ames RG. Ryde IT.376(6):808-815.usgs. Interim reregistration eligibility decision (IRED) for Methyl Parathion. Case No. Olsson AO. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County.S. Kieszak S. Anal Bioanal Chem 2003. Environmental Protection Agency (U. Available at URL: http://www. WHO/SDE/WSH/03. Geological Survey (USGS). Environmental Protection Agency (U.201(2):97-104. U. Toxicol Lett 2006. May 2003. Environ Health Perspect 2002.110 Suppl 6:1047-1051. 1/12/07 U. pdf.S. Environ Health Perspect 2006. Rubin C. 1992-2001. Facts. Toxicol Appl Pharmacol 2004.S. The Quality of Our Nation’s Waters. et al. External and internal exposure of wine growers spraying methyl parathion. Rosenberg J.epa. Available at URL: http://pubs.int/water_sanitation_health/dwq/chemicals/ methylparathion. revised February 15. EPA-738-FOO-009. Yacovac R.epa. Backer G. Mengle DC. Seidler FJ.S.who. Letzel S. Schilter B. Tate CA. 2004.

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

700-1.740 (.210-.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 .08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .700-.820) < LOD < LOD . Survey Geometric mean (95% conf.27) .880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .17 (. population from the National Health and Nutrition Examination Survey.430 (<LOD-. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample.950) < LOD < 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.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.210-1. 154 Fourth National Report on Human Exposure to Environmental Chemicals .210 (<LOD-.31) .740-1.55) .680 (<LOD-.580-1.760 (<LOD-.250 (<LOD-.500 (.21) < LOD .2.670 (<LOD-1.94) . see Data Analysis section) for Survey year 01-02 is 0.780 (.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.470 (.840 (.780 (<LOD-1.780 (.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 .300-1.15) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .S.07) .610 (<LOD-1.850 (.780 (<LOD-1.64) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .200-. Survey Geometric mean (95% conf.840) 669 687 929 Limit of detection (LOD. Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one (creatinine corrected) Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.410 (<LOD-1.

org/documents/jmpr/jmpmono/v92pr16. 1/14/09 Fourth National Report on Human Exposure to Environmental Chemicals 155 . Barr DB. Available at URL: http://www. Pesticides residues in food: 1992 evaluations Part II Toxicology. gov/oppsrrd1/REDs/pirimiphos-methyl_ired. Sadowski MA.S. Market Baskets 91-3-01-4.gov/~acrobat/tds1byps. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.pdf. July 2006.inchem. Third National Report on Human Exposure to Environmental Chemicals. 2535. Anal Bioanal Chem 2003. 4/7/09 Olsson AO. Nguyen JV. Pirimiphos-methyl. Available at URL: http://www. EPA). Available at URL: http://www.pdf. Case No. Total Diet Study: Summary of Residues Found Ordered by Pesticide. Environmental Protection Agency (U.S. 850.Organophosphorus Insecticides: Specific Metabolites References Centers for Disease Control and Prevention (CDC). cfsan. U.epa. 4/7/09 International Programme on Chemical Safety-INCHEM (IPCS).htm.fda. Finalization of interim registration eligibility decision for pirimiphos-methyl. Food and Drug Administration (FDA). 2005.376(6):808-815. June 2003. Atlanta (GA).

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

Agrawal AK. tremor. Kuhn K.. 2005). Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Lazarini et al.atsdr. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Hu et al. Biochem Biophys Res Commun 1998.300(3):161-165. Pogo BG. Ose K. 2006.. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Leng G.atsdr. Lewalter J. Chen JH.. Fredriksson A. Garey J. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Wieseler B.8(1):197-202.205(6):459-472.. Hu JY. motor activity. 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. Neurotoxic effects of two different pyrethroids.. Florio JC. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats. Richardson JR. Wolff MS. 2000.50(2):245-255. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Bernardi MM. and seizures (ATSDR.. Varoli FM. Toxicological profile for pyrethrins and pyrethroids. 2005). Soderlund et al. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Abell AD.. Sunami O. 2002).. Ray et al. J Environ Monit 2006. Seth PK. Song L. and striatal dopamine levels in male and female rats. Idel H.html.. et al. 2001. Wolff MS.gov/toxprofiles/ tp155. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Neurotoxicol Teratol 2005. 2003. Go V. salivation.107(3):173-177. Moniz et al. Kamita Y. Pyrethroid pesticide-induced alterations in dopamine transporter function. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. September 2003. McCarthy AR. Elwan MA. Leng G. Kim IY. Adhami VM.62:101-108. J Reprod Dev 2004. Additional information about pesticides is available from U.. 2002). Effects of prenatal exposure to deltamethrin on forced swimming behavior. Ranft U. 1999. Idel H. Lazarini CA. Shukla Y.gov/pesticides/ and from ATSDR at: http://www. Kunimatsu et al. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Bull Environ Contam Toxicol 1999. 2005). McCarthy et al. Okuno Y. Kang IH. Leng A.27(12):1273-1283.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. cdc. Spinosa HS. Environ Health Perspect 1999. Generally. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Miller GW. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Lemonica IP. et al. Garey J. choreoathetosis. 2006. Toxicol Appl Pharmacol 1991.27(4):609-614. Pauluhn J.gov/toxpro2. 2006). 2002. Kim HS. 2003.S.cdc. Eriksson P. Bernardi MM. Neurotoxicol Teratol 2001.1/15/09 Aziz MH. neurochemical changes in cholinergic. Shaw IC.8(1):18-21. Eriksson and Fredriksson. Zhao RC. Regul Toxicol Pharmacol 2002.html.35(2 Pt 1):227-237. EPA at: http://www.23(6):665-673. Wang SL. Go et al. dopaminergic. Shin JH. In developing rodents. et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Estrogenicity of pyrethroid insecticide metabolites. fenvalerate. 1998. Lee SJ. Kunimatsu T. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Kim TS. Int J Hyg Environ Health 2002. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation.108(1):78-85. Yamada T. Available from URL: http://www. Leng G. Kuhn KH. Toxicol Appl Pharmacol 2006. Garey and Wolff. Sugiri D. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Shafer. bioallethrin and deltamethrin. Cruz-Casallas PE. 2005). Indoor pyrethroid exposure in homes with woollen textile floor coverings... Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. 1991. WHO. and permethrin) in the Hershberger and uterotrophic assays. 2001. et al. Moniz AC. 2003. Yang J. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Xenobiotica 1997. Neurosci Lett 2001. Levsen K. Elwan et al. Salzgeber SA. Caudle WM. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. 2004. Kim et al. epa. In California.. 2003. Guillot TS.211(3):188-197. Thomson BM. Berger-Preiss E. hypersensitivity.251(3):855-859.

gov/oppsrrd1/REDs/ factsheets/permethrin_fs.10. Environmental Protection Agency (U.S. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment. sumithrin synthetic pyrethroids for mosquito control.S. Environmental Protection Agency (U. Reregistration Eligibility Decision for Cypermethrin.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005.pdf. 5/26/09 U. Pesticides in the Nation’s Streams and Ground Water. Laird WJ.38:95-101. et al.htm.S.htm. Pyrethroid illnesses in California. 1992–2001. Available at URL: http://whqlibdoc. pdf. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals .S. J Toxicol Clin Toxicol 2000. Spencer J.S.epa. Available at URL: http://www.who.S.gov/ circ/2005/1291/. Available at URL: http://www. Environmental Protection Agency (U.Pyrethroid Pesticides Ray DE. 2005.22(8):983-991. Piccirillo VJ. 5/26/09 U. 5/26/09 Woollen BH. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration. Available at URL: http://pubs. June 2006a. Toxicology 2002. U. Rev Environ Contam Toxicol 2006. 19962002. Permethrin. Pyrethroid insecticides: poisoning syndromes. 2007. Sargent D. Geological Survey (USGS). April 2002. Available at URL: http://www.186:57-72. Revised February 25.S.epa. Marsh JR. resmethrin.epa. EPA). Safety of pyrethroids for public health use. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). Crofton KM. EPA). March 2006.gov/oppsrrd1/REDs/cypermethrin_red. Environ Health Perspect 2005. Sheets LP. synergies. Soderlund DM. Meyer DA.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Lesser JE.113(2):123-136. Mullin LS. Shafer TJ. Clark JM. Pesticide and Evaluation Scheme. O’Malley M. World Health Organization (WHO). Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. EPA). June 2006b. Forshaw PJ. 5/26/09 U. and therapy.usgs. Xenobiotica 1992.171:3-59.

. 2003). 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. Thus.. 2005.. Following an indoor application exposure. representative 2001-2002 NHANES subsample (CDC.95 µg/L. 2004). Fourth National Report on Human Exposure to Environmental Chemicals 159 .S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. Leng et al. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). Biomonitoring studies of 4-fluoro3-phenoxybenzoic acid in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of cyfluthrin than levels found in the general population. 2003). Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. Seven individuals participating in floor exercises on cyfluthrin treated carpet demonstrated a rise in the urinary excretion of 4-fluoro-3-phenoxybenzoic acid in the 72 hours following the activity (Williams et al. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0. representative subsample in NHANES 2001-2002 (CDC. 2006). 2005). Cyfluthrin is rapidly metabolized and eliminated from the body. Studies in Germany of 396 children and adolescents (Becker et al. 2001. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002.2 μg/L) in the U. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin.Pyrethroid Pesticides Cyfluthrin CAS No.. Baker et al.68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. 2005). 2003). 2006) and 1177 urban adults and children (Heudorf et al. most of which were dermal and respiratory irritations (Spencer and O’Malley.. but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment.. Urinary levels for adults and children in these studies were similar (Heudorf et al. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. 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..S.

S. < LOD means less than the limit of detection. Survey Geometric mean (95% conf. 160 Fourth National Report on Human Exposure to Environmental Chemicals . 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. * 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. population from the National Health and Nutrition Examination Survey.2 and 0.2.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. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.

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

Arch Environ Contam Toxicol 2004. Int J Hyg Environ Health 2006. Int Arch Occup Environ Health 2004. Heudorf U. Atlanta (GA). Krieger RI. J Expo Anal Environ Epidemiol 2003. Bernard CE. Angerer J. Pyrethroid illnesses in California. Heudorf U. Heudorf U.209(3):221-233. Becker K. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Idel H. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.13(2):112-119. Human exposure to indoor residential cyfluthrin residues during a structured activity program.Pyrethroid Pesticides References Baker SE. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Butte W. Angerer J. Barr DB. Rev Environ Contam Toxicol 2006. Sugiri D. Angerer J. Centers for Disease Control and Prevention (CDC). Ball M.186:57-72.206(2):85-92. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. et al. Seiwert M. Int J Hyg Environ Health 2003. Third National Report on Human Exposure to Environmental Chemicals. Ranft U. Hadnagy W. 19962002. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Schulz C. Drexler H. Hoppe HW.77(1):67-72. Kolossa-Gehring M. O’Malley M.209(3):293-299.46(3):281-288. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. 2005. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Spencer J.109(3):213-217. Williams RL. Angerer J. Environ Health Perspect 2001. Berger-Preiss E. Leng G. Int J Hyg Environ Health 2006. Olsson AO.

the presence of trans-3-(2.110-.960 (.200) < LOD < LOD < LOD .80) .160 (<LOD-.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .770) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.32) .600 (.640 (.370-.2dichlorovinyl)-2. and trans-cyfluthrin.160 (. transcypermethrin and trans-cyfluthrin.350) .53) .910-5.270-.740) 1.240) . 52315-07-8 CAS No.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .270 (.. Generally.140 (<LOD-.54) . The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.2-dichlorovinyl)-2. 1999).1 and 0.44 (.890 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .35) 1.47 (.280-.120-. The chemical trans-3(2.200 (.120-.2-dichlorovinyl)2.210) .11) .340) .150 (.2-dichlorovinyl)-2.690) . Kuhn et al.330 (.790 (.430-.440 (.220-. 1999).570 (.410) .262) * * * < LOD < LOD .380-.380 (.230) .2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.740 (.510 (.200) .500 (.110-.670-1.10) 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 .202 (.490-1.900 (.570-. cis-permethrin.510 (.460-1.. Similarly. which may vary for some chemicals by year and by individual sample.24) 1.630-.68) . The presence of cis-3-(2.08) .1.or trans-3-(2. trans-cypermethrin.740-2.200-.850 (.180) .600) .270 (.380) .220) .490-.S.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.700) .155-. more of the trans-metabolite than Urinary cis-3-(2.200-.220-.550) . Cyfluthrin.370 (.880 (.68359-37-5 Cypermethrin Permethrin CAS No.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.530 (.200) .260 (.77 (.68 (.740-1.15) .330) .790-1. Kuhn et al. 1985.710-1.710) .and trans-isomers.680-3.490-1.460-. and ciscyfluthrin.790) .220-.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.43) .580-1.890 (.770-1.610) . Biomonitoring Information Urinary levels of cis.670-1.820 (.2-dichlorovinyl)-2.730 (.730 (. cis-cypermethrin.310) .520) .670 (.270 (.180 (.470 (.110 (<LOD-. but it can also reflect exposure to cis-3-(2. Fourth National Report on Human Exposure to Environmental Chemicals 163 .460 (.630) .300 (.12 (.340) .2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.500 (.160 (.2dichlorovinyl)-2.13 (.300-.250-.600-1.490-.630) .220-.2-dichlorovinyl)- CAS No.380-. population from the National Health and Nutrition Examination Survey.580) 1.340-.410) .420-.400-.120-.730 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300-.650-1.610) .780) .140 (.670-2.2-Dichlorovinyl)-2.300 (.50) .250 (.28) 671 680 518 701 591 957 Limit of detection (LOD.68) .920) 1.240) .510 (.630 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.120-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.210) 90th .170 (.950-2.21) .470-1.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.870) 1. but can also reflect exposure to trans-3(2. ciscypermethrin and cis-cyfluthrin. cis-3-(2.680 (. trans-permethrin.110-.07 (.200-. < LOD means less than the limit of detection.280 (.790-1.35) .210-.380-. In the body. 1985.

280-.220) .830) . 2006.550-1. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.130-.150-.33) .390-.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.240 (<LOD-.200-.59) .270-.2-dichlorovinyl)-2.500 (.11) .2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.840 (.840 (.410) . median urinary levels of trans-3-(2.2-dichlorovinyl)-2.230-.350 (.180 (.200-.900 (. 2006). 2005).680-1.300 (..550 (. the median and 95th percentile of urinary levels of cis-3-(2..560) 1.2dichlorovinyl)-2..340-.080-.710 (.270) .260 (.59) .21) . representative NHANES 2001-2002 subsample (CDC.29 (.640-.250-.360-1.320-.150-.290-.400 (.and trans-3(2.350) .680 (. Schettgen et al.270 (.750-1..120 (. 2004).49) .S.250) 90th .890 (.Pyrethroid Pesticides 2. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U. urinary trans-3-(2. 2001) showed urinary levels of cis.11) 1.450-1.580) .80) .03) 1.640-1.260 (.430-.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . 2005) In a small group of indoor pest-control operators.540 (.340) .290) .230 (.450 (. In these volunteers.880) .260 (..300-.640) 1.700) .440 (. 2003).2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.180-.800 (.S.37) .590) .210-.640-1. Survey Geometric mean (95% conf.390 (. 2004.150-..138 (. 2001.380) .440-.540 (. 2006). Studies in Germany of 396 children and adolescents (Becker et al.300 (. Lu et al.12 (.2dichlorovinyl)-2.104-.24) .340) .300) .890) . population from the National Health and Nutrition Examination Survey.370-.700-2.450-.290) .430 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.250) .420 (.260) .190) .530 (.780 (.250) .250-.390-.750 (. In a study of volunteers. In a study of urban residents in Germany (Berger-Preiss et al.710-3.170 (.220 (.33 (. 2002).230-.320) .640 (.550) . urinary levels of cis-3-(2.690-1.170) < LOD < LOD < LOD .250-.230-.200 (.370-.550) ..290 (.2-dimethylcyclopropane carboxylic acid did not increase. Cyfluthrin.380-.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.11) .580-1.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.600 (.250 (<LOD-.430-1. post- Urinary cis-3-(2.67) .680-1.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .530 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.160 (<LOD-. 164 Fourth National Report on Human Exposure to Environmental Chemicals .440 (.182) * * * < LOD < LOD . 2005). 2006. Other studies have provided evidence that urinary levels of cis. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.510-1.560) .700) .220 (.200) . and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.570) .540) . 2006) and 1177 urban adults and children (Heudorf et al.590 (. 2005).2-Dichlorovinyl)-2.400-1.2-dichlorovinyl)-2. 2005)..and trans-3-(2.920 (.260-.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.190 (..12-2.08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .370-..470-1.. 2002). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.300) .170 (.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 .190) . Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al. 2003).270) .810 (.59 (1.140-.2-dichlorovinyl)-2.780) 1.280 (.380 (.440-.67 (.11 (. In the same residents.550-1.31) .

69) 1.76-3.49-5.500 (.17 (.490 (<LOD-.Pyrethroid Pesticides application median urinary levels of summed cis.27 (1.68-2.95) 2.60-4.4.820) . and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.440 (<LOD-.28 (2.16) 1.580 (.07-3.910-1.5) 2.560 (. Fourth National Report on Human Exposure to Environmental Chemicals 165 .520) .03-1.95) 3.19 (3.68) 1.400-.55-3.20 (.S.25-3.14-2.66) 691 680 518 690 595 954 Limit of detection (LOD.26 (.910-1.43) 2.66) .620) < LOD 2.28 (1.94 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.41-14.680-1.68-3.55-4.76-4.23) 2.760) .or trans-3-(2.56 (1. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.4 and 0.89 (2. trans-Cypermethrin. Survey Geometric mean (95% conf.54) 4.77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .69 (1.460-.42) 1.10) 2.84 (1.97-11.22 (1.410-.60) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3. Finding a measurable amount of cis.970 (.19 (2. which may vary for some chemicals by year and by individual sample.64-4.77) 1. population from the National Health and Nutrition Examination Survey.570) 90th 1.03-1.and trans-3-(2.11-2. however.710 (.7) 2.54 (1.77 (1.23 (.810-1.780 (.56) 2.77) 2.750) .60) .56) 2.17 (.660) 1.13) .25 (1.68) 1.410-.730) .2dichlorovinyl)-2.400 (<LOD-.90) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.550 (.42 (2.470 (<LOD-.37 (1.11-1.20 (.48) 4.70) 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 . 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.40 (1.470 (.91 (1.14-6.2-dichlorovinyl)-2.420 (<LOD-.81) 2.39 (1.08-4.490-1.670) .49-3.480-.63) 1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin. The maximum post-application urinary levels.520-.14) 1.460-.610) 1.920-1.55-5.700) .08-6.830-1.17-1.35) 1.50 (1.20 (.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.12-6.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.63) 1. 2005).87 (1.07 (1.68) 2.940 (.01 (1. Urinary trans-3-(2.560 (.39-5.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .59 (1.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.860) .500-. 2005).19) 1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .49-3.410 (<LOD-. < LOD means less than the limit of detection.2-dichlorovinyl)-2.530) .01) 4.09 (.2-Dichlorovinyl)-2.85) 4.08) 1.850-1.800-1.62 (1.500) .410 (<LOD-.560 (.56 (1.700-1.670) . Biomonitoring studies on urinary levels of cisor trans-3-(2.41 (1.840-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

89) 2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.35) 1.61) 1.640) .13) .98 (1.730) .39) 1.30-3.36 (1.850-3.07-2.22-2.16 (1.3) 2.42) 1.26 (1.22-1.780 (<LOD-.08 (.11) .27-2.880 (<LOD-1.880-1.67 (2.12-1.55 (2.750) .57) 3.91) 1.22) 1.56 (1.440-.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.68) 3.00) 1.13) 1.12 (.39 (1.00-5.00 (1.820-2.760 (.02-1.87) 1.60 (1.Pyrethroid Pesticides Urinary trans-3-(2.15) 2.56-2.900 (<LOD-1.540) .87) 1.56-5.15-3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.07-3.64 (1.740) .55 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.34-3.720-1.34-4.47-2.35 (1.47 (1.47-2.880 (. trans-Cypermethrin.470-.660) .11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .45 (1. population from the National Health and Nutrition Examination Survey.610-.87-8.470 (.570 (.57 (1.700 (.91-11.07-1.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.48-2.28) 2.850) .65 (2.65) 1.570-.31) 1.970 (.780) 90th 1.800-1.15-3.530 (.19) .520 (<LOD-.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 .87 (1.33 (1.720-1.500-.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .480-.30-6.00) 1.780) .800-1.74) .36) 2. Survey Geometric mean (95% conf.37 (1.60) 2.31 (2.670) .86 (2.720 (<LOD-.770) < LOD 2.20 (1.74) 2.07) 2.41) 1.48 (1.40-2.33-2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.91 (1.33-1.580) .S. 166 Fourth National Report on Human Exposure to Environmental Chemicals .700-.930-1.42 (.850) 1.29) 1.75 (1.81 (2.45-2.80) 1.08 (.19 (1.27-2.530 (<LOD-.70 (.2-Dichlorovinyl)-2.07) 2.87-3.700 (.15) 3.560 (.20-2.31 (.570 (<LOD-.00) 5.15 (1.580 (.60) 2.410-.55 (2.15-3.44) 2.

Sugiri D.206(2):85-92. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Third National Report on Human Exposure to Environmental Chemicals. Heudorf U. Idel H. Int J Hyg Environ Health 2002.114(9):14191423. Atlanta (GA). et al. George DA. Drexler H. Heudorf U. Leng G. Drexler H. Berger-Preiss E. Butte W. Environ Health Perspect 2001. Seiwert M. J AOAC 1985.209(3):293-299. Angerer J. Bartell S. Idel H. Ranft U. Hoppe HW. Permethrin and its two metabolite residues in seven agricultural crops. Angerer J. Hardt J.Pyrethroid Pesticides References Becker K. Idel H. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int J Hyg Environ Health 2006.205(6):459-472.77(1):67-72. Angerer J. Angerer J. Int Arch Occup Environ Health 2004.76(7):492-498.109(3):213-217. Kuhn K. Berger-Preiss E. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Int J Hyg Environ Health 2003. Environ Health Perspect 2006. Barr DB. Int J Hyg Environ Health 2006. Leng G. Ranft U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine.134(1-3):141-145. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Heudorf U. Lu C. Schettgen T.209(3):221-233. Angerer J. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Sugiri D. Hadnagy W. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. 2005. Levsen K. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Schulz C. Wieseler B.62:101-108. Angerer J. Int Arch Occup Environ Health 2003. Kolossa-Gehring M. Biological monitoring of workers after the application of insecticidal pyrethroids. Ball M. Centers for Disease Control and Prevention (CDC).68(6):1160-1163. Bravo R. Leng G. Pearson M. Bull Environ Contam Toxicol 1999. Heudorf U.

2005).2-dibromovinyl)-2. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.2-dibromovinyl)2.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al. Baker et al.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Pyrethroid Pesticides Deltamethrin CAS No. in some situations replacing the use of DDT.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0.2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. 2005). in detection of cis-3-(2.2dimethylcyclopropane carboxylic acid formed in the environment.3-0. Biomonitoring Information Urinary levels of cis-3-(2. 168 Fourth National Report on Human Exposure to Environmental Chemicals .2-dibromovinyl)-2. 2006) and 1177 urban adults and children (Heudorf et al.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate.2-dibromovinyl)-2..2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. 2001.2-dibromovinyl)-2. 2001) showed that urinary levels of cis-3-(2. Urinary levels for adults and children in these studies were similar (Heudorf et al. 2004).. 1990). The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample..2-dibromovinyl)-2.2-dibromovinyl)-2. (2004) reported a geometric mean concentration of cis-3(2. Outside the U. mean peak urinary levels of cis-3-(2. urinary levels of cis-3-(2.1 μg/L) for the NHANES 2001-2002 subsample (CDC. Following residential spraying with deltamethrin for malaria protection in Mexico.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid of 0.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2. Thus. deltamethrin has been used against mosquitoes that carry malaria.5 μg/L) than the detection limit (0. 2005). 52918-63-5 General Information Cis-3-(2. Finding a measurable amount of cis-3-(2. Deltamethrin can degrade to cis-3(2. In the NHANES 2001-2002 subsample.. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population.2-dimethylcyclopropane carboxylic acid in the environment (IPCS. Studies in Germany of 396 children and adolescents (Becker et al.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.S.39 µg/L..

Survey Geometric mean (95% conf. Fourth National Report on Human Exposure to Environmental Chemicals 169 .2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin 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.1. < LOD means less than the limit of detection. 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.S.2-Dibromovinyl)-2.1 and 0. 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.Pyrethroid Pesticides Urinary cis-3-(2.

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

Angerer J. [online] 1990. Heudorf U. Angerer J. Atlanta (GA). Int Arch Occup Environ Health 2004. Seiwert M. Drexler H. Angerer J.209(3):293-299.77(1):67-72. Batres LE.113(6):782-786. et al. Available at URL: http://www. 5/26/09 Ortiz-Perez MD. Int J Hyg Environ Health 2006.209(3):221-233. Torres-Dosal A. et al. Schulz C.Pyrethroid Pesticides References Becker K. Heudorf U. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Lopez-Guzman OD. toxicokinetics. Environ Health Perspect 2005. Environ Health Perspect 2001. Angerer J. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Grimaldo M.htm. Heudorf U. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. International Programme On Chemical Safety (IPCS). Deltamethrin. Environmental Health Criteria 97.org/documents/ehc/ehc/ ehc97. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Hoppe HW. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.inchem. Int J Hyg Environ Health 2006. Third National Report on Human Exposure to Environmental Chemicals. Kolossa-Gehring M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.109(3):213-217. Centers for Disease Control and Prevention (CDC). Butte W. and genotoxicity in exposed children. 2005. Ball M. Carranza C.

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. CDC. representative NHANES 2001-2002 subsample (CDC.52315-07-8 CAS No. the presence of 3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of any of the six pesticides listed above. 2006. 2005).. Following residential spraying with deltamethrin for malaria protection in Mexico...Pyrethroid Pesticides Cyhalothrin CAS No. 52918-63-5 use and house dust levels (Lu et al. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. Hardt and Angerer. 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 . Median levels of urinary 3-phenoxybenzoic acid were 67-fold higher in 307 pregnant New York City women who used indoor pesticides compared with the median levels for adults in the NHANES 2001-2002 subsample (Berkowitz et al. 2005)... Thus. Biomonitoring Information Urinary levels of 3-phenoxybenzoic acid reflect recent exposure to the parent pyrethroid pesticides. In the New York City study. but can reflect direct exposure to 3-phenoxybenzoic acid formed in the environment from the degradation of these pesticides. 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.. 2002. 52645-53-1 Tralomethrin CAS No. The mean peak levels in these children were 83-fold higher than the geometric mean for children in the NHANES 2001-2002 subsample (CDC. 39515-41-8 CAS No. 2005). A study of 396 German children (Becker et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 2005). 2005. 2004).S. 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. 2003. Fenpropathrin Permethrin CAS No. 2005). 2003). In a small group of indoor pest-control operators.. 2003.. Becker et al. (2004) reported geometric mean levels of 3-phenoxybenzoic acid that were approximately sixfold higher than levels for adults in the NHANES 2001-2002 subsample (CDC. Baker et al. CDC. Biomonitoring studies of 3-phenoxybenzoic acid provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of pyrethroids than levels found in the general population. Finding a measurable amount in urine does not mean that the level will result in an adverse health effect. 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. 2005). 68359-37-5 Cypermethrin Deltamethrin CAS No. In one study of 145 urban residents in 80 private homes in Germany. a temporal variation in levels was observed and considered to correspond to seasonal spraying of pesticides. 2005. 2006). urinary 3-phenoxybenzoic acid levels at the 95th percentile were about threefold lower than the levels at the 95th percentile in the 2001-2002 NHANES subsample (Berger-Preiss et al. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides. CDC. median urinary levels of 3-phenoxybenzoic acid were slightly less than median levels in the NHANES 2001-2002 subsample (Leng et al. Saieva et al. 66841-25-6 General Information The chemical 3-phenoxybenzoic acid is a metabolite and an environmental degradate of the six pyrethroid pesticides listed above.

44) 5.940) 1.35) 2.13) .18 (1.49 (1.800 (.33 (1.S.830-2.601) . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.288-.63-3.230 (.233-.21 (2.01 (1.328 (.27-2.25-1.38 (2.507 (.34 (2.190-.36) 1.250 (.54) 1.300 (.56-5.76 (1.510-.510-.750) .246-.352-.12) .190-.230-.360) .220-.78) 1.330) .650 (.25-4.23 (2.79) 3.60) .16-1.48-2.180-.586) .43) 3.32 (1.25-7.384) .820) .345) Selected percentiles ( 95% confidence interval) Sample 95th 4.39) 2.320) .640 (.265-.353 (.434) .35) 2.260 (.710 (.240 (. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.26-2.276-.440) .12 (.830) 90th 1.820) .51-3.850) .1) 3.730 (.238-.55 (1.320 (.49-2.390) .760 (.590-.46) 2.417 (.430-.34) 8.750-1.8) 3.321 (.200-.28) 1.41 (1.32-21.260 (.26) 2.288 (.570-.64) 697 680 524 701 603 957 Limit of detection (LOD.570-1.350-.369) .870 (.260 (.610) .520 (.14-6.266-.530-.48-2.160-.42-2.62-8.490) .75 (1.280 (.336 (.300 (.86 (1.49-2.30 (.38 (2.311 (.990) .292-.340) 75th .73) 1.700-1.250-.340) 1.630) .960 (.253-.34-6.740 (.450 (.320) .62) 5.230-.53) 1.290 (.53-3.300 (.314) .72 (1.62-6.490-.92-3.325 (.33 (2.90) 1.05) .670 (.271-.65-2.550-.370) .454 (.210-.27-11.320) .710 (.374) 99-00 01-02 99-00 01-02 99-00 01-02 .160-.850) .41-3.226-.406) .470-.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .78) 6.41) 3.530-.427) .05) 1.45-5.25 (2.1 and 0.78) 1.190-.81 (1.33) .295) .78 (1.267 (.700 (.297 (.13 (. population from the National Health and Nutrition Examination Survey.26) 2.277-.315 (.200-.51-6.1) 3.227-.69) 3.270) .780) 4.200-.25 (2.430-.1) 3.590 (.30 (1.240 (.04-5.52-4.83-11.49 (1.25) 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 .12) 4.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .355) . Fourth National Report on Human Exposure to Environmental Chemicals 173 .420) .02-6.65 (1.41-2.298 (.03 (3.29-1.560-1.600 (.210-.32 (2.800) 1.428-.292 (.810) 1. interval) .840-1.300) .35 (2.69 (1.1.50 (2.740 (.620-1.320) .330) .373) .35 (1.89-71.35) 1.260-.63 (3.250 (.52-5.230 (.250 (.387) .750) .27-2.273 (.71 (1.46) . Deltamethrin.247-.93 (1.04) .314 (.364) .190-.560-.18 (2.362) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.680 (.230-.340) .16) 1. Survey Geometric mean (95% conf.595) .45 (2.560-.270 (.30) 3.

500) .86 (1.423 (.35) .930) 1.49 (1.270) .530-.860-1.280 (.52) 2.510 (.04 (.0) 3.550 (.329) .13-1.270 (.275 (.240 (.460-.43 (2.44 (1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.09 (.309 (.11 (.760) .238-.49) 1.290) .350 (. population from the National Health and Nutrition Examination Survey.91 (2.83) 1.37 (1.860 (.13-1.190-.51-7.670) .63-3.25-2.25) 2.480 (.410) .27) 1.72 (1.49-2.490 (.19-6.200-.04 (3.200-.67 (1.280) .280 (.09-2.88) 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 .272) .378 (.446) .226-.460-.380-.54 (1.216-.234 (.43 (1.730) .05-3.534) .55 (1.510 (.310) .36 (1.210 (.06-3. Deltamethrin.350) .400) .420-.90) 3.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .60) 1.840-1.84 (1.210-.173-.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .253) .230-.21 (1.73-4.329) .380 (. Survey Geometric mean (95% conf.480-.00) 1.37) 1.240-.36-6.43-64.160-.202-. interval) .35 (1.94 (1.35) 1.25-5.11 (.19 (2.43) 1.S.200-.930) .178-.250 (.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.250 (.09) 3.720) 90th 1.365) 99-00 01-02 99-00 01-02 99-00 01-02 .387) .328) .52 (1.510 (.320) .810) 1.264 (.750-1.96 (1.440-.610 (.75-8.61-2.490 (.630) .200-.280 (.225-.74) 3.590) .224-.35-3.17-1.39) 1.240 (.227 (.670) 3.580 (.32 (2.261-.00) 1.720 (.62) .88-5.274-.401) .440-.370-.190-.550 (.91) 9.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .580) .290) .311 (.290-.02-1.540 (.400-.299-.07) 2.590-1.570) .330) .09-2.91-4.40) 2.22 (1.330) 75th .229-.321-.210 (.270 (.03-1.280-.560 (.15-2.81 (1.590) .41) 1.590) .357) .240 (.21-4.02 (2.49) 3.312 (.410-.64-5.740) .230) .55) 3.150-.323 (.860-1.220 (.440-.270) .677) .640 (.240 (.330) 1.62) 1.280) .40 (1.16-4.490-.450 (.261 (.330 (.67 (1.390-.372) .44) 2.60-4.335-.309) .240-.240-.67) 1.19) 2.316 (.95) 1.190 (.550 (.530-.650) .700-1.80) 4.10 (2.41-4.400-.300-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.640 (.278) .300-.03 (.13 (.53 (1.330) .07-5.730-1.00) 5.960-1.63) 1.91) .48 (1.250) .240-.370 (.730) .246 (.230-.362 (.17 (.83 (1.274 (.220-.271-.272 (.73) 1.270-.437) .

Lu C. Leng G. Torres-Dosal A. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Lapinski R.209(3):221-233. Hardt J. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Bravo R. Exposure to indoor pesticides during pregnancy in a multiethnic.206(2):85-92. Sugiri D. et al. et al. Third National Report on Human Exposure to Environmental Chemicals. Int J Hyg Environ Health 2003. Ranft U.46(3):281-288. Angerer J. et al. Int J Hyg Environ Health 2002. Godbold J.113(6):782-786. Berkowitz GS. Idel H. Liu Z. Fourth National Report on Human Exposure to Environmental Chemicals 175 . Centers for Disease Control and Prevention (CDC). Berger-Preiss E. Bartell S. Barr DB. Obel J. Ranft U. Kolossa-Gehring M. Lopez-Guzman OD. Levsen K. Olsson AO. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Environ Health Perspect 2003. Pearson M.111(1):79-84. Batres LE. Ball M. toxicokinetics. Int J Hyg Environ Health 2006. Int Arch Occup Environ Health 2003. Barr DB. Biological monitoring of workers after the application of insecticidal pyrethroids.Pyrethroid Pesticides References Baker SE. Atlanta (GA). Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Environ Health Perspect 2005. Idel H. Berger-Preiss E. Leng G. Angerer J.76(7):492-498. Hoppe HW. 2005. Sugiri D. Grimaldo M. Hadnagy W. urban cohort. and genotoxicity in exposed children. Ortiz-Perez MD. Becker K. Arch Environ Contam Toxicol 2004.114(9):14191423. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Deych E. Environ Health Perspect 2006. Carranza C.205(6):459-472. Seiwert M.

300-.144) .120 (.390-.530) .400 (. and refuse incinerators that process or release antimony. see Data Analysis section) for Survey years 99-00.250-.190 (.110-.190-.160 (.360) .220-. often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.210) .197) .180 (.220) .088-.103) .120 (.095 (.150) .270 (.137) .350) .200) .130 (.270) .270) .134 (.230) .230 (.100 (.470) .210 (.114) .133) * .400) .370-. ammunition.190-.119-.260 (.098-.190 (.120) .170 (.099 (.070 (<LOD-.141-.150-. It is also used in paints.160) .140 (.230 (.220 (.310) .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 .080-.176 (.120-.310 (.150 (.210-.150) . 0.100-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.350) .154) .460 (.280 (.390) .230-.108-.130-.170-. water.310 (.110) . 01-02.300-.210 (.184) .115-.140) .170-.350 (.120 (.080) .146 (.161) . Antimony enters the environment from natural sources and from its use in industry.180 (.490) .320 (.390-. and pewter.470) . Workplace exposures can occur at smelters.200-.220-.180 (.200 (.157) .270-.150 (.330) .137) .140) .120) .290 (.490 (.180-.240 (.110-.220-.300 (.330 (.220) .500) .170-.410) .130) .250-.100) .250 (.136) * .150-. coal-fired plants.110-. and 03-04 are 0.240-.090) 75th .180 (.220) 95th .136-.430 (.260) .280) .330) .109-.220 (.350-.134-.156-.160) .370) . Urinary excretion appears to be greater for pentavalent antimony Urinary Antimony Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.190 (.140) .170) .180-.131-.200) .360-.290-.400) . The absorption.070 (<LOD-.117-. or other substances containing antimony is another means of exposure. respectively.140-.260-. and +5.240 (.330-.150-.120-.130 (.178) .240) .160) .090-.300) .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 .230 (.190) .250) .440 (.120-.260) . from air and drinking water.280) .440) .130) .220) .190-.087-.200) .210) .430 (.210) .070-.330-.200 (.130-.190 (.123 (. population from the National Health and Nutrition Examination Survey.240 (. 0.132 (.230) .126 (.S.280) .460 (.170 (.200 (.140) .310-. ceramics.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 .120-. distribution.200 (.250-.460) .360 (.390) . storage batteries.280-.160-.250 (.350-.07.100 (.120) .190) .200-.079-.120-.160-. 7440-36-0 General Information Antimony is found in ores or other minerals.164-. to a lesser extent.190 (.120-.240-.230-.180 (.560) . sheet and pipe metal.400-.160-.143 (. < LOD means less than the limit of detection.150 (.090 (<LOD-.140 (.230-. which may vary for some chemicals by year and by individual sample.220-.190) .100-.128 (.130 (.340 (.140) .310) .115) .200) .410) .400) .280-.270 (.105 (.122 (.320 (.130-.390 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.270 (.200 (.260 (.230-.108 (.210) .250 (.190) .130-.160) .280 (.300) .145) Selected percentiles ( 95% confidence interval) 50th .090-.350 (. and glass.280-.390) .190-. Dermal contact with soil.120-.145 (.280) .360) .130-.170-.320) Total .150-.130 (. interval) .190) .250-.600) . 176 Fourth National Report on Human Exposure to Environmental Chemicals .125 (.350 (.220-.410-.360 (.150) .180-.140 (.310-.270 (.154) .330 (. and as a fire-retardant in textiles and plastics.260) .330) .180-.710) .Metals Antimony CAS No.175 (.135) * .340) .117-.320-.350 (. castings. enamels.230) .420) .180) .120-.160) .200 (.240 (.400 (.310 (.510) .280-. It is used in metal alloys.126-.260 (.158 (.095-.080) . People are exposed to antimony primarily through food and.350) .112-.330 (.130-.280-.240 (.130-.093 (.320) .142 (.210-.160 (.110 (.130 (. +3.330) .260-.148-.190-.320-. Stibine is a metal hydride form of antimony used in the semiconductor industry.460 (.200-.300-.310 (.220-.119) .120-.160-. solder.350-.207) . fireworks.470 (.400 (.180) . and excretion of antimony vary depending on its oxidation state.140) . metal bearings.350 (.120) .132 (.200-.180 (.230-.300 (.130) .210) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.160 (.300) .160) .440) .04.390) .500) .140 (.169 (.340 (.154-.290-.090 (.150-.130 (.080 (<LOD-.320-.150) 90th .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Antimony can exist in one of four valences in its various chemical and physical forms: -3.350) .170-.430 (.120 (.320-.130 (.570) .120 (. and 0.130) < LOD .130 (.128 (.390-.180-.04.110-.

097-.310) .086) 75th .333-.163 (.109 (.178 (.263-.208-. skin.082) .119-.128-.228-.333 (.146-.084) .098-.320-.Metals than for trivalent compounds (Elinder and Friberg.281-.256 (. abdominal pain.235-.116-.230-.079 (<LOD-.417) .217 (.405) .129) * .149-.107-.181) .214) .148-.294) Total .195 (.147) .317) .137 (.421) .238 (.127) .069-.247) .200-.119-.333-1.076-.068 (. 1995).129) .298 (.417) .147-.255-.117-.135) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.080 (.120 (.112 (.308-.391) . Histopathologic inflammatory and degenerative changes in the lung. 1953).333 (. population from the National Health and Nutrition Examination Survey.138 (. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.126-. diarrhea.159-.272) .320 (.149) .250-.107-.193 (.092-.300 (.108-.087) .069-.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.109-.315) .195-.277 (.104-.225) .103-.278 (.357) . 1958) and occupational exposures (Briegner et al.140) < LOD .163 (.178-.167 (.266 (.241-.112-.263 (.224 (.105-.447 (.089) .120 (.187) .115 (.076-.156-.074 (. liver.228 (.124) .131 (..160 (.124-.164 (.086 (. and eyes.255) .276 (.204-.114 (.242-.130) .192) .121 (.116 (.135) .133) .213 (.151) .209 (.106-.113) .119 (.156 (.120 (.122 (. 1962).143) Selected percentiles ( 95% confidence interval) 50th .267) .167-.471 (.121 (.391) .230) 95th .171) .257) .082) .233-.192 (.196 (.364 (.185-.310) .244-.139 (.183) .268) .115-..132) .135 (.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 .286 (.444) .373) .192-.131-.161) .081 (<LOD-.211) .317) .173) .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 . 1954).121) .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 .146-.095-. 1944).241-.114 (.146-. Inorganic antimony salts irritate the mucous membranes.265-.153-.135) .185 (.107-.143) 90th .127) .118 (.30) .444) .225 (.300) . Fourth National Report on Human Exposure to Environmental Chemicals 177 .113-.429) .173 (.131) .227-.080 (<LOD-. interval) .195-.144-.172-. and route of exposure (Elinder and Friberg.352 (.209-.429 (.338) .129 (.333) .250-.115 (.061-.138-.068-.321) .106-.430) .206-.269 (.179-.338 (.228 (.203) .115 (.077) .117-.371 (. Ming-Hsin et al.208 (.099-.098) .098-..118 (.164) .248-.102-.136) .099-.259 (.267-.134) .130) .108-.120 (.173-.143) .103-.162-.338 (.229-.318-.143 (.253 (.222 (.320) . and gastrointestinal symptoms such as vomiting.146) .209) .185 (.414) .250 (.130) .135 (.126) .167 (.265 (.333 (.152) .250-. 1973).209) . The toxicity of stibine after acute inhalational exposure is similar to that of arsine.170 (.081) .288 (. and ulcers (Werrin.226 (.125 (.261) .400 (.500) .145) .308) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.176 (.480) .245) .352) .150-.113-.111 (. 1986).313-.333-. and kidney have been demonstrated in high dose animal studies depending on the dose.173 (.148-.176-.200) .318-.075 (.082 (<LOD-.109 (.096-.280-.741 (.114 (..253-.159-.188) .207) .139 (.164-.S.425) .182 (.125-.741) .357-.095-.127) .317) .123 (.148) * .198) .127 (.300) .124 (.123) . 1986).727) .126 (.200-.186) .250-.111-.085) .248) .143) . 1988.194-.078 (. Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman. Acute antimony poisoning may cause a metallic taste. resulting in hemolysis with abdominal and back pain (Dernehl et al.188-.112 (.333-.191 (. myocardium.115) .250 (.438) .485) . An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.129 (.239-.271-.127) ..310 (.205-.343 (.320 (.181) .071-.181) .203) .267 (.108 (.100 (.233) .117-.161) .124-. 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.175 (.385 (.278) .140) . Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.138-.108-.236 (.220) .280 (.233 (.238) .159-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown. species.122 (.092) .471) .154-.138) * .167 (.320-.102-.130 (.200-.132 (.193) .115-.075 (.238) .176 (.150-.250) .380 (.199-.153 (.295 (.152) .189 (.104-.364 (.

Cheng-Wei L. Sabbioni E.16: 33-39. Carelli G. Ju-Sun P.S. External and internal antimony exposure in starter battery production. Suchenwirth R.cdc. Element reference values in tissues from inhabitants of the European community. Konings J. 1998. Semisch CW. Cordasco EM. Dezateux C. Atlanta (GA). VI. even when exposure levels were below workplace air standards (Bailly et al. gov/toxpro2. 1997). EPA. Friberg L. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals .521-523. Dezateux et al. Alimonti A. Chemotherapy for leishmaniasis: Biochemical mechanisms. Roland H. Fuchs A. Matthews T. Pietra R.. eds. Kuo-Juie Y. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Gebel TW. 26-42. and a drinking water standard has been established by the U. et al. 1987). Stone FD.67:119-123. Antimony in blood and urine of infants. Vouk VB. J Occup Environ Med 2004.. Apostoli P. Arsine... Ho C-K.. Hamilton EI. O’Regan M. 20012002. 1998) or compiled reference ranges (Hamilton et al. Sci Total Environ 1994. and antimony in optoelectronic industry workers. Cullen A. 2nd ed. stibine. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. clinical efficacy. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Sabbioni E. Pilgrim L.76:432436. Industrial Medicine 1944. Int Arch Occup Environ Health 1987. Bailly R. Biological monitoring of exposures to aluminum. 1986. et al. Earlier measurements in general populations (Minoia et al. Yu H-S. arsenic. Stead FM. Nordberg GF. 1995. 1994) have reported values slightly higher than those in this Report. Centers for Disease Control and Prevention (CDC). Review of elements in blood.e. Chin Med J 1958. Mayer P. Minoia C. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure.. Elinder CG. pp. In: Friberg L.. Weltle D. Yang C-Y.46:931-936.48:93-97. and future strategies. Delves HT. 1990. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Ming-Hsin H. Industrial antimony poisoning. Delves HT. Industrial Medicine and Surgery (Dec.atsdr.html. Stocks J.158:165-190. gallium. and 2003-2004. Buchet JP. et al. and hydrogen sulfide.13:361-362.. Rev Infect Dis 1988. Ludersdorf et al. Costeloe K.59:469-474. indium. Biological assessment of exposure to antimony and lead in the glass-producing industry. Bolten C. Wade A. Kentner M.. HH. Shao-Chi C. Antimony.76(2):103-115. 2004. Nau CA. Paschal et al. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Schacke G. Chia-Yu H. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. J Clin Pathol 1998. Dunkelberg.. Leinemann M. Urinary antimony in infancy. Antimony trioxide is rated by IARC as a possible human carcinogen. Dernehl CU. Handbook on the toxicology of metals. environmental levels) and health effects is available from ATSDR at: http://www. Chest 1973. Environ Health Perspect 1998. 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. Chen J-R. Caroli S. Information about external exposure (i. Arch Dis Child 1997. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al.64(2):182-185. Schaller KH. which may be due to methodologic. Liao Y-H. References Berman JD... Iavicoli et al. Iavicoli I. Kentner et al. Int Arch Occup Environ Health 1995. Biomonitoring Information Levels of urinary antimony reflect recent exposure. or exposure differences. Mahieu P. Trace element reference values in tissues from inhabitants of the European community I. Piatnek DA. Gallorini M. Wu M-T.)1954. 1998). Briegner H. Liao Y-H et al. respectively. Van der Venne MT. Br J Ind Med 1991.106:33-39. Mayne P. 2005. Kiberd B. Petrucci F. Third National Report on Human Exposure to Environmental Chemicals. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Pozzoli L.10(3):560-586. Biomonitoring of a worker population exposed to low antimony trioxide levels.51:238-240. Lenert G. Skulsukai G. 1991. 2002. population. Pulmonary edema of environmental origin. Stasney J. New York: Elsevier. Lauwerys R. Luedersdorf R. J Trace Elem Med Biol 2002.Metals to antimony have been established by OSHA and ACGIH.

Jackson RJ. Trace metals in urine of United States residents: reference range concentrations. 27:38-45. and serum of Italian subjects. Sampson EJ.99-108. Renes LE. Paschal DC. Fourth National Report on Human Exposure to Environmental Chemicals 179 .Metals in urine. Environ Res 1998. Werrin M. Morrow JC. Antimony poisoning in industry. Industrial Hygiene and Occupational Medicine 1953.95:89-105. Pirkle JL. blood. Sci Total Environ 1990. et al. Chemical food poisoning. Quarterly Bulletin of the Association of Food and Drug Officials 1962.76(1):53-59. Ting BG.

2) 46. arsenic as elemental metalloids may be used in some ammunition. it is found in over 200 crystalline or mineral forms.5) 41.41 (7.Metals Arsenic CAS No.4 (48. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.34-9. referred to as inorganic arsenic compounds.2-93.2 (51. grain.30 (6. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste. lead.7 (11.4 (31. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides. Arsenic is measurable in most soils.70 (6.0-60. In nature.1) 7.S.90-8.29 (8.2 (12. 2001).0 (14. solders. sodium arsenite. Gallium.6) 11.5-41. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.2) 15. such as arsenopyrite (FeAsS) and realgar (As4S4).9) 21. and in lead-acid storage battery grids.00-9.20 (8. lead hydrogen arsenate. mostly for use in wood preservation (ATSDR.13-8.2-20.6) 618 722 1074 Limit of detection (LOD.10) 10. ocean and fresh waters.90 (7.7-95. Also.66-8.2 (41.57) Selected percentiles ( 95% confidence interval) 50th 7.7) 90th 37.74.30) 17. arsenites. and as homicidal poisons.3-19. and indium arsenides are used in the semiconductor industry. semiconductors.5 (14.30 (7.5) 43.3-111) 78. cacodylic acid.2-61.90 (5. Arsine (AsH3) is a reactive. Arsenic trioxide is approved to treat acute promyelocytic leukemia.0 (22. psoriasis. meats.7) 65.7-83. population from the National Health and Nutrition Examination Survey.80 (5.84) 8. though in some locations arsenite may be prevalent (WHO. Survey years 03-04 Geometric mean (95% conf.19-9. see Data Analysis section) for Survey year 03-04 is 0.10-10.1) 1281 1276 03-04 03-04 03-04 9.8 (48.2 (13. Since the 1940s.8-77.4 (24.6-141) 53.4) 40.8-61.5 (23.90-7. and arsenates (oxidation states of -3.000 metric tons annually. and as a cosmetic to lighten complexion. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed. were used as treatments for syphilis. black. 180 Fourth National Report on Human Exposure to Environmental Chemicals . The United States no longer produces arsenic from mining but imports about 22. alloys. and foods.80-9.4) 13.5 (36. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. gaseous hydride manufactured in small quantities for use in the semiconductor industry. Although it is still widely used in the United States.4) 60.84) 8.8) 30. and.9-62. copper arsenates.97) 8.02-8.6 (32.0 (11.08 (5.90) 16.6-43.1) 15. interval) 8. Various arsenic compounds were used in paint pigments and for tanning animal hides.25-9. and other metals.8) 7.3) 10.00 (6.3) 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 7.5) 66. Before the 20th century.9 (8.5 (40.90) 75th 16.27) 9. pesticides.5 (34. and play sets.7) 24. from coal burning.40) 7. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.4 (7.10 (6.9-46.9-34. particularly arsenic trioxide.8) 33. and gray forms).6-35.1) 290 725 1542 03-04 03-04 9. and produce.8) 7.34-10.1 (38.12-10. Water sources contain mostly inorganic arsenate.4-65. to a lesser extent.1-40.5) 95th 65.5-52.90-11.70) 8.0 (43.0 (15. aluminum. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.5-178) 46.6 (9.2-17.70-9.3-15. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.55 (7.1-18.90 (7.50-14.4 (26. In the last century.9 (17. Arsenic trioxide (As2O3. and arsenosugars.5-19.9) 68. arsenic compounds.50 (8. trimethylarsine oxide. to a lesser extent.12 (6.90-14. cancers.10-7.80) 6. the smelting of copper.8) 29. retaining walls. mental disorders. or rarely as elemental metalloids (yellow. arsenocholine.8) 34. General population exposure to inorganic arsenic can occur through consumption of drinking water and.0-19.6 (13. 2005).6 (15. +3 and +5).90-8. Arsenic and its compounds have had many uses in the past and present as medicines.8) 17.1 (32. as alloy in metal bearings.77) 6.

WHO.04) 7.6-17.0) 1281 1276 03-04 03-04 03-04 8. 1988). dose level. 2001. 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.7) 28. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.25 (6.50 (6.5) 290 725 1542 03-04 03-04 8.93-9.8 (21. trimethylarsine oxide (TMAO).5-120) 40. Children may have additional exposures from ingestion of contaminated soils (e.6 (35. In aquatic organisms. 2006.86-17.8) 27. Extremely high groundwater arsenic levels. population from the National Health and Nutrition Examination Survey.88 (5.58-10. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. and folate status (Chen et al.7-35. Some studies suggest that variation in the degree of methylation among persons is related to the susceptibility of arsenicinduced disease and may involve consideration of genetic polymorphisms.6) 45.25-9. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al.66 (7. 2007.0-69.4 (40. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC. and some other seafood can contain organic forms of arsenic including arsenobetaine. 2001).g. Direct exposure to DMA and MMA may result from use of the two pesticides.5-17.99-9.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.4-64.10-8.9) 53.. cacodylic acid and monosodium methyl arsenate.04 (5.8) 22. U. Steinmaus et al.8 (11.20-9. dust.9-56. inorganic arsenic is widely distributed within the body.5 (9.. mine tailings).1) 6.4 (12.40) 8. and arsenosugars. and contact with CCA-preserved wood structures.7-18.1-36.7-188) 27. interval) 8.44-11.2) 15.0-18.0) 26.23-7.33-10.0 (31. The semiconductor dopants.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 ..01) 11.0) 42.4 (26. gallium arsenide and indium arsenide.96) 12.66-8.2) 40.. as observed in Bangladesh where millions of people have been exposed.59) Selected percentiles ( 95% confidence interval) 50th 7.9 (45.7 (9. 2001). 2007. 2006.61 (7.47 (6.3-53. Gamble et al.8-62.4 (11. age.8 (12.1 (11. arsenic does not show biomagnification in the food chain (WHO.6 (10.2 (12. shellfish.47-6.11 (5.S.0) 12.5) 17.4) 54.1) 7.35) 7.10-16.75 (5. 2001). 2001).3-62. Smoking tobacco is also a source of inorganic arsenic. so exposure to the general population is extremely limited.S.8 (20.7-34.75) 13. Fish. organic arsenic can be converted back to methylated and inorganic arsenic. 2001).S. Chowdhury et al.3) 6. After absorption.45) 5.7 (11.4 (42.64 (7.32 (5.4) 32.7-17. but is poorly absorbed dermally (WHO.7) 95th 50. Though modest bioconcentration occurs in some aquatic life.88) 7.38-10.01) 7.18 (5. Inorganic forms of arsenic demonstrate high acute toxicity.3-41.66-8.6 (17.1 (14.28-7.06 (4. Survey years 03-04 Geometric mean (95% conf.3 (24.1) 58.47 (7. 2001. have caused clinical arsenic poisoning.76 (6.2) 90th 30.93-8. arsenocholine. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.13) 8.2-15. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established. NRC.0-26.5) 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. 2001).8 (27. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.1) 24. EPA.0-38.41) 6.24 (7.3) 9.. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC. WHO.9) 13. kelp. Arsenate is reduced in the body to arsenite (oxidation state +3).51) 75th 14. In aquatic sediments. though some reduction may occur in the gut prior to absorption.2-46.3-64.30-9. Tseng.0) 33..0) 14.07-9. are used in enclosed ultraclean operations within the semiconductor industry.81-9.33 (6. 2007.12-10.8-75. selenium. EPA’s maximum contaminant level (Hughes.00 (6. 2001).31 (6.1) 8.3 (27. 2003.4 (24. 2001).8-32. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.44) 6.7 (25.0 (17.

and it also will inhibit succinate dehydrogenase.EPA.. which can lead to dehydration and shock. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. 2001).50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.S. including inhibition of numerous enzymes. 2004. 2007.EPA has established drinking water. U. Although arsenate is reduced in the body to arsenite. With chronic exposure. 2007). some of these effects may take years to develop.10 (<LOD-1.. gluconeogenesis.20 (<LOD-1. apoptosis. arsenic trioxide) includes hemorrhagic gastritis with nausea. 2006.S... Such actions may lead to decreased energy production.g. cytotoxicity. 2007.10 (<LOD-1.S.10 (<LOD-1. 2001). and production of glutathione may be affected as well. see Data Analysis section) for Survey year 03-04 is 1. population from the National Health and Nutrition Examination Survey. hypertension. which may vary for some chemicals by year and by individual sample.0. Raml et al. and bladder cancer (IARC. hematocytopenias. 2006. NRC. 1998. and childhood neurodevelopmental effects in observational human studies. 2004). Acutely. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. lung. hyperkeratosis.g. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. Bangladesh. WHO. 2004).. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. respectively. Survey years 03-04 Geometric mean (95% conf. 2001).30) 1... 2000. 182 Fourth National Report on Human Exposure to Environmental Chemicals .. interference in signal transduction pathways. can cause peripheral sensorimotor neuropathies.20 (<LOD-1. WHO. Cellular glucose uptake. 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. < LOD means less than the limit of detection..50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1.. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. 2001). Arsenic has many actions demonstrated in cellular studies. 2001. 2006. WHO.S. Chronic elevated arsenic intakes have been associated with diabetes.60) 1. 2001). Chronic arsenic exposure in humans is considered to be a cause of skin.60) 1. Cohen et al. Cardiac arrhythmias. 2006) or when exposure occurs in smokers (Chen et al. drinking water have not been associated with increased cancer rates (Schoen et al. and DNA repair inhibition (Cohen et al. Laboratory studies using inorganic arsenic have shown chromosomal aberrations.. hepatotoxicity.50) 621 725 1078 Limit of detection (LOD. cell transformations. Taiwan. food residue. fatty acid oxidation.. Chronic human intake of arsenic at less than acutely toxic doses. peripheral vascular disease. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. Studies of arsenic at levels typical of U.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. and altered gene expression. Chile). and hyperpigmentation of the skin (NRC. and by uncoupling oxidative phosphorylation (NRC.10 (<LOD-1.50) 1. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. noncirrhotic portal hypertension. vomiting. renal failure. The U. substitution in phosphate metabolism.20 (<LOD-1. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. NRC. including drinking water sources with elevated arsenic levels (e. Bredfeldt et al. 2001. and diarrhea.80) 1.10 (<LOD-1. but additional or confirmatory research is needed (Kapaj et al. and endothelial injury (Kumagai and Sumi. 2001). interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. WHO.20 (<LOD-1. The organic forms of arsenic occurring in seafood have little known toxicity. increased oxidative stress. leading to a decrease in adenosine triphosphate energy production.

S. 2006.41) 3. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD Sample size 3.80 (<LOD-4. Valenzuela et al. and the FDA has established a bottled drinking water standard.. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. 2000. 2006. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.69 (<LOD-3. 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.. 2004. 2007.. 2007. population (Rubin et al. 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. 2008).33 (<LOD-3.S. arsenic has been fetotoxic and teratogenic. Meza et al.75 (<LOD-2.. 2004. 2006). In a Nevada town where groundwater levels were naturally elevated.. 2006). In animal studies... 1986). environmental levels) and health effects is available from ATSDR at: http://www. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. Pellizzari and Clayton.. 2001). had decreased since the prior 1990– 1992 survey.. 1999.cdc. Calderon et al. 1999.atsdr.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2..S. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. and were about two-fold lower than those for the U. Survey years 03-04 Geometric mean (95% conf. Pellizzari and Clayton 2006). Offergelt et al.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Fourth National Report on Human Exposure to Environmental Chemicals 183 . 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. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens.. 2008. 2006. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2008).70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. Vahter et al.61 (<LOD-3.00) 1. Levels of total urinary arsenic in the U.. Shalat et al. Biomonitoring Information Urinary arsenic levels reflect recent exposures and are moderately to highly correlated with arsenic intakes from drinking water and dietary sources (Ahsan et al.. Additional information about external exposure (i. Caldwell et al. DMA produced bladder cancer in some chronic rat studies (Cohen et al.18 (<LOD-3.04 (<LOD-3. Josyula et al.33 (<LOD-3.18) 3.. 1999). gov/toxpro2. but generally only at maternally toxic doses (WHO..50) 1. Consequently. although urinary arsenic levels were not associated with CCA contact (Shalat et al. Pellizzari and Clayton.html.. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 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.. population from the National Health and Nutrition Examination Survey. Shalat et al... Caldwell et al. 1992. 2003. 2001).19) 3. 2006). 2006).. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. population in NHANES 2003–2004 (Schulz et al.. median urinary total arsenic levels in 4052 adults varied with seafood intake. Though CCA-treated wood contains several thousand times more arsenic than untreated wood.75 (<LOD-2. 2001). In the German Environmental Survey III of 1998.e. 1998. 2000).Metals compounds.. WHO. Compared with this Report..S.

.1) 18. arsenocholine.600 (. 184 Fourth National Report on Human Exposure to Environmental Chemicals .55 (1.8-50.800 (. geometric mean levels were about 70-fold higher than for the U. After recent seafood ingestion.43-1.3) 35. 2006).00 (1. 2005.30 (1.11-1.8 (17. population from the National Health and Nutrition Examination Survey. 2000. see Data Analysis section) for Survey year 03-04 is 0. vasospasm.30) 10.30) 2.70-21. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. population (Sun et al.48-2. Caldwell et al. 2000. and 0. These associations are stronger at higher urinary levels. 1990. In most human studies.50) 90th 16.9 (7.1) 45.83) Selected percentiles ( 95% confidence interval) 50th 1. Some noncancer effects of arsenic (e.e..g. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.37 (1.80-5. Also.31-1. in NHEXAS 1995–1996.. When seafood intake is avoided.S.70-21. arsenite.Metals other areas of the world (Ahsan et al. arsenite.40-6.7 (13.93) 1.74 (1.70 (3.45 (1. 2005.2-35. 1996. < LOD means less than the limit of detection.29 (1.3 (9. with DMA.9-23. interval) 1.19 (. 2008).900 (.80 (4.20 (2. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.5) 292 728 1548 03-04 03-04 1.40) 5.90-7.S. which may vary for some chemicals by year and by individual sample.66 (1.60) 1. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.3) 95th 35..3 (21.0 (26.6 (25. Pellizzari and Clayton. and TMAO were detected in only 7.20-25.4-35. 2008).1-94.5) 32.700-1.20 (4.6) 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.S.80 (.10) 4.68) . Arsenate. 1...700-1.30 (2.. Blom et al.20) 18. Valenzuela et al.400-. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i. 2007). 2008.20 (1.. 2008). population showed a higher contribution of arsenobetaine (Caldwell et al. 2003). respectively. Caceres et al..0) 4.20-190) 31. 2008).0 (27.00-1.00-6.1-25.50-6.8. 2000.3-39.800) 1.871-1.90-29..20 (.62) 2..28) 1. Sun et al.1-51. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.. dermal keratosis.800-1. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. In the late 1980s. methylation capacity. 2005. and duration of exposure are also considered important. MMA. Measurable organic arsenic species in this Report are three biologically generated environmental forms.S.500-1.5) 621 725 1078 Limit of detection (LOD.00) 3.05) < LOD . arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.7) 13.8-40. The higher percentiles of total urinary arsenic levels in the U. 2007) with higher levels of arsenic in the drinking water.7) 15..70 (5. Survey years 03-04 Geometric mean (95% conf. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.9 (6.20) 3.40-7.0-23.. 2001.60-3. China. 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.7 (21. Chowdhury et al.800 (.50) . DMA and MMA.4) 23.00-12.6 (13.5 (26..17-1. Individually measurable species resulting from inorganic arsenic exposure are arsenate. and other factors such as nutrition.40) 75th 5. 4. population in the NHANES 2003–2004 subsample...2 (6. Aposhian et al.800-4.900-1.10) 8.0) 29. when seafood organic arsenic is subtracted). In the residents of a Chilean town who consumed water with high levels of arsenic.. and two methylated metabolic products.3% of a representative sample of the U..10 (4.50) .5 (14. arsenobetaine.2-38.4) 31. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. Caldwell et al.80) 1.00 (. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.7-22. 2008.. and TMAO.6 (11.00-4.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) 7. population (Ahsan et al. arsenocholine.5) 29.80 (3. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 1985.8) 35. 2001). Tseng et al.9) 13. WHO. For residents of Inner Mongolia.6.8 (12.4 (16. Caldwell et al.4. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.20-3.3) 1284 1284 03-04 03-04 03-04 1.6-44.6. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.70) 6.

13-39.67) 4.2 (13. 2001).6 (6.91) 90th 16. 1998.4-21. The 95th percentile of the U..80-153) 17.8) 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.73-6.51-2.18-1.9) 32.65 (1.82) 4.959-1.400-. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.638) 1.4) 32. population from the National Health and Nutrition Examination Survey.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.877 (.2 (12.30) 1. In recent years.9) 14.25 (.05) 1.7) 17. 2008).39-3.21) 5. Offergelt et al.76-27. Survey years 03-04 Geometric mean (95% conf.70) 5..47 (2.40 (1. Sun et al.5) 26. 2006.4-82.14 (1. The American Conference of Governmental Industrial Hygienists (ACGIH) provides an occupational biologic effect index (BEI) for urinary inorganic arsenic plus metabolites equal to 35 μg/L (ACGIH.5-20.28) 1.83) 2.6-32. population for the sum of inorganic related species was 18. 2008).4 (11.6-46.11 (.78-5.4) 292 728 1548 03-04 03-04 1.9-18.40) 1..3-24.29-14.2 (12.786-1.1 (26.88) 2..44 (1.93 (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 * * 1.12) < LOD . 2007).53 (.50-15. 1992.32-7.00 (1.78 (3.68 (1.1-36.7) 9.612-1.51) 5. 1986.19-2.. which is below the ACGIH BEI (Caldwell et al.6 (9.10 (.36) 2.50-7.00 (3.45) 1. 2001).43) 75th 5.909-1.901-2.4) 13. Caldwell et al..9 (13. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.05 (.72) 12.15-1.80) ..9 μg/L.7) 30.29 (4.82) Selected percentiles ( 95% confidence interval) 50th 1.83) 8.5 (18..54 (1. 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.S.Metals as with DMA.55) 1. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.15-4. not to imply a safety level for general population exposure.S.5 (18.2 (4.531 (.30-1.938-1.61-6.37-2.81 (4.91 (4.58 (3.3 (10.88 (5.4 (24.62-6.9 (25.1) 26.4-28.15-1.64-29.3 (10. Biomonitoring studies of urinary arsenic can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of arsenic than are found in the general population.43) 14.25-7.3) 1284 1284 03-04 03-04 03-04 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1-18. Information about the biological exposure indices is provided here for comparison.6) 19. 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. WHO. interval) 1.16 (. 2003. Vahter et al.3) 95th 29.0-36.67) 1.47 (1.833-1.6-29.5) 17.0 (9. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect. Fourth National Report on Human Exposure to Environmental Chemicals 185 .79 (1.

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

Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40 (<LOD-1. population from the National Health and Nutrition Examination Survey.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Fourth National Report on Human Exposure to Environmental Chemicals 187 .S. * 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.08 (<LOD-4. which may vary for some chemicals by year and by individual sample. Survey years 03-04 Geometric mean (95% conf. see Data Analysis section) for Survey year 03-04 is 1.70) < 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 2.00) 1. < LOD means less than the limit of detection. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. 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 1.00 (<LOD-3.80) < LOD 621 725 1078 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.20 (<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 3.2.44) 2.00 (<LOD-2.95 (<LOD-2. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey years 03-04 Geometric mean (95% conf.S.

18 (6.1 (8.74) 90th 9.00-4.11) 4.94-3.9) 5.00-7.60-6.82) 3.00) 4.88 (4.74 (2.34-4.45) 8.00) 6.9) 13.44) 5.0) 95th 16.00-4.95-6.05) 10.0-17.90) 2.0) 621 725 1078 Limit of detection (LOD.95 (4.00-3.80-5.31) 4.71-4.0-17.00-11.03 (3.00-7.45 (8.82-5.17-4.78 (4.39-3.12 (3.65-6.6) 292 728 1548 03-04 03-04 3.91) 75th 5.46 (4.71) 3.50-5.95-3.20) 11.7) 1284 1284 03-04 03-04 03-04 4.30 (7.38 (3.92-12.48 (2.80 (4.69 (3.67) 8.25 (4.1-15.00-11.6) 1284 1284 03-04 03-04 03-04 4.0) 11.0 (12.00) 9.48 (3.16 (4.0) 11.00-15.0) 17.15) 4.00 (4.0 (9.7. population from the National Health and Nutrition Examination Survey.0 (13.85 (3.19) Selected percentiles ( 95% confidence interval) 50th 3.95-4.0-18.00-15.0 (9.69 (3.24) 3.6 (9.17 (2.00-13. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.50 (4.77 (3.80-6.70-12.00-12.86-21. interval) 3.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.32 (8.0) 9.5) 12.50-15.12-4.00) 75th 6.84-18.29-4.00-5.00) 12.28) 2.33-4.00-4.00 (6. Survey years 03-04 Geometric mean (95% conf.00) 5.0) 17.60-4.84-8.00-4.7) 13.16 (2.2) 10.33) 3.00 (5.0) 13.0) 292 728 1548 03-04 03-04 4.90 (3.7) 12.37 (3.81 (5.70) 5.80) 7.0 (10.0) 16.00 (5.11 (3.08 (2.8) 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 3.94) 3.0 (10.00 (5.10) 6.00) 3.0 (13.00-9.09 (7.0 (9.0 (10.0-12.62) 4.00) 7.57-5.34-4.22) 4.20-12.67) 9.14) Selected percentiles ( 95% confidence interval) 50th 3.9 (7.71 (4.03-6.71 (3. population from the National Health and Nutrition Examination Survey.0 (8.73) 6.80) 2.31-4.0-16.89 (3.0) 12.60-3.34 (3.27-2.49-4.0 (11. see Data Analysis section) for Survey year 03-04 is 1.0-19.00) 90th 11.00 (3.00) 3.86 (2.70-4. interval) 3.42) 3.00 (3.78) 4.32 (4.0) 13.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.00-22.27-5.59 (6.44 (2.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .0 (10.70-3.52) 3.6-18.14) 3.00 (7.34 (3.37 (2.16-11.79 (3.57 (3.32-10.00) 6.97-3.00 (7.69-3.00 (5.9) 11.17-6.55 (2.0-16.0) 9.00 (3.8) 7.0 (8.49) 10.00 (3.92) 3.00-12.00-7.61-16.7-16.00 (5.05) 3.06) 5.10) 3.3 (7.00-15.73 (3.72 (4.70 (3.5) 95th 13.1-18.8) 7.7 (10.00-4.0 (14.00) 4.60-7.00 (3.00 (6.00-3.69-6.61-11.1-22.5 (11.0 (12.9 (11.S.98) 4.0) 16.90) 5.0) 10.9) 12.3 (8.00-10. Survey years 03-04 Geometric mean (95% conf.80-3.00 (6.0) 14.05) 5.00) 6.00 (3.27 (3.00-7.24-4.45) 3.20-4.3 (8.00-8.30) 3.S.0-25.4 (7.82-9.13-4.27 (2.00) 6.34) 3.00-11.86-7.65-8.00-4.0) 9.

96-2.60-2.30-1.28 (1.40) 2.10 (.00-2.70) 2.30-1.20-3.77) 1.40-2.31 (1.33 (1.90) 1.86 (2.61) 2.14-1.73-2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.46 (1.S.82-2.90) 2.50-2.22) 3.10 (.23) 1.54) 90th 2.00-4.50 (1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.40) 1.90 (1.58) 2.20 (1.88 (1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.71-2.45) 3.00 (1.53 (1.20 (1.30) 1.70-3.40-3.20-1.80-2.40-3. see Data Analysis section) for Survey year 03-04 is 0.60) 2.60) 2.10 (<LOD-1.86) 2.79) 2.40) 1.00 (2.17) 2. population from the National Health and Nutrition Examination Survey.80 (1.33 (1.985) 1.S.00 (2.30-2.20 (1.50 (<LOD-1.80 (1.30 (1.05-1.43-3.853-1.20 (1.61-3.63 (<LOD-1.30 (1.10) 2.07) 2.00) 1.30) 90th 1.88-2.70-2.00) 1.07 (1.00) 1.10) 95th 2.80) 1.16 (2.50) 1.52 (2.57) 95th 2.80 (1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .70-2.00 (<LOD-1.22 (1.90 (2.86) 3.60 (2.84-3.80) 1.18-1.11-1.18-1.30) 2.28 (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 1.00) 2.70-2.53-2.20 (1.00-1.50 (2.10-1.62) 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.88 (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 1.10-1.00-1. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.90) 2. Survey years 03-04 Geometric mean (95% conf.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.00-2.20) 2.10 (1.80 (1. < LOD means less than the limit of detection.36) 1.40 (1.30 (2.10-3.40-2.60 (1.35-3.900-1.36 (1.80-2.50) 621 725 1077 Limit of detection (LOD.50 (1.00) 2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.30) 1.40 (2.00 (<LOD-1.9.10 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.85) 1.93) .31-3.80 (2.34) 2.60) 1.30 (1.86 (2.816 (<LOD-.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.37 (1.07-3.46-2. which may vary for some chemicals by year and by individual sample.70-2.82-2. population from the National Health and Nutrition Examination Survey.81) 1.20 (1. Survey years 03-04 Geometric mean (95% conf.85) 2.15-1.

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

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Monomethylarsonous acid induces transformation of human bladder cells. International Agency for Research on Cancer (IARC). Perrin M. Bredfeldt TG. Environ Health Perspect 1990. Kalman DA.

Zhang H. Pellizzari ED. Arsenic methylation.30(5):293-301. EPA).113(3):250-254. 3rd Ed. Environ Health Perspect 2006. Arsenic in Drinking Water. Garcia-Montalvo EA. Morton J. Relation between airborne arsenic trioxide and urinary excretion of inorganic arsenic and its methylated metabolites. Rey OA.115(4):648-652. J Anal Toxicol 2006. Solo-Gabriele HM. Ferreccio C. Lauwerys RR. Valenzuela OL. Toxicol Appl Pharmacol 2005. Kolossa-Gehring M. Suzuki KT. Friberg L. Borja-Aburto VH. Xu Y. Lauwerys R.epa. Urinary trivalent methylated arsenic species in a population chronically exposed to inorganic arsenic. Lu X. Shipp M. Naranmandura H. 1998 [online].inchem. Chung CJ. Becker K. urinary arsenic metabolites and human diseases: current perspective. Guidelines for Biological Monitoring. Int Arch Occup Environ Health 1986.Metals Kwon E. Gandolfi AJ. Liaw J. National Research Council (NRC).htm. Arsenic in drinking water-2001 update. J Environ Sci Health C Environ Carcinog Ecotoxicol Rev 2007. Available at URL: http://www. et al. Toxicol Appl Pharmacol 2007. Airborne arsenic and urinary excretion of metabolites of inorganic arsenic among smelter workers. Arsenic.htm.206(3):299-308.36-37. 8/7/07 U. Yuan Y.K. using a routine LC-ICP-MS method. Rahnster B.S.S.gov/iris/subst/0278. 2001.20(8):1120-1125. Kopplin MJ. Boeckx M. html. 8/8/07 192 Fourth National Report on Human Exposure to Environmental Chemicals . Tseng CH. Urinary arsenic metabolites in children and adults exposed to arsenic in drinking water in Inner Mongolia. et al. Environ Health Perspect 2005. Huang YK. Tseng CH. Lewis Publishers. Mason H. Environmental Health Criteria 224. Sun G. et al. Goessler W. Li L. Chem Res Toxicol 2007. Garcia-Vargas GG. Speciation of arsenic compounds in urine from occupationally unexposed and exposed persons in the U. Conrad A. Hoet P.211(2):175.57(2):79-91. inorganic. EPA). In:Industrial Chemical Exposure. Wang Z. and peripheral vascular disease in blackfoot disease-hyperendemic villages in Taiwan. Assessing the measurement precision of various arsenic forms and arsenic exposure in the National Human Exposure Assessment Survey (NHEXAS).210(3-4):271-297. Environ Health Perspect 2006. Schulz C. Kieszak SM. Environ Health Perspect 2007. Biggs ML. Increased mortality from lung cancer and bronchiectasis in young adults after exposure to arsenic in utero and in early childhood. et al. Vahter M. Black K. Sonora. Available at URL: http://www. and metabolism of arsenic. Flanders WD.112(14):1375-1380. Ibata K.25(1):1-22. Arsenic drinking water exposure and urinary excretion among adults in the Yaqui Valley. Washington (DC) National Academy Press. Toxicity of dimethylmonothioarsinic acid toward human epidermoid carcinoma A431 cells. Chen CJ.96(2):119126. Belson MG. Steinmaus C. von Ehrenstein O. Fleming LE. Environmental Protection Agency (U. 2nd ed.114(8):1293-1296. Huang YL. Nolinder P. Twenty years of the German Environmental Survey (GerES): human biomonitoring--temporal and spatial (West Germany/East Germany) differences in population exposure. Moore LE. GSTM1 and T1. Erratum in: Toxicol Appl Pharmacol 2006. Li B. Meza MM. Fact Sheet: Drinking Water Standard for Arsenic. China. World Health Organization (WHO). Arsenic exposure. Yang MH. 2001. Clayton CA.367(1):80-88. Seiwert M. Shalat SL.115(1):151-157.114(2):220-227. Integrated Risk Information System. Jhangri GS. Arsenic on the hands of children after playing in playgrounds.gov/safewater/arsenic/regulations_factsheet. Fok N. Burgess JL. Arsenic. Sun X. J Toxicol Environ Health A 2007. Buchet JP. Br J Ind Med 1992. Rubin CS. Jimenez M. et al. Kalman D. January 2001 [online]. Smith AH. pp. Environ Health Perspect 2007. Vahter M. Francesconi KA. Investigating childhood leukemia in Churchill County.70(2):159-170.org/documents/ehc/ ehc/ehc224. Li X. Environ Res 2004. Jones RL. Roels H. Mexico. CruzGonzalez MB. urinary arsenic speciation.epa. Genetic polymorphisms in MTHFR 677 and 1298. Holmes AK. et al. Environ Health Perspect 2004. Raml R. Sci Total Environ 2006. Jin Y. Offergelt JA. Geneva 2001. et al. Ochi T. Seifert B. Marshall G. Environmental Protection Agency (U.222(3):374-380. Available at URL: http://www. Buckley BT. Nygren A. Int J Hyg Environ Health 2007. Thio-dimethylarsinate is a common metabolite in urine samples from arsenic-exposed women in Bangladesh. Calderon-Aranda ES. Rumpler A.S.49(6):387-393. A pilot study of children’s exposure to CCAtreated wood from playground equipment. U. Arsenic and Arsenic Compounds. 8/7/07. Nevada. EPA 815-F-00-015.S. Boca Raton (FL).

38 (1.78) 1.52 (4.50 (1.00-8. and 03-04 are 0.22-1.30 (5. and food.35) 5.63 (5.18) 3.75) 2.26) 2.87-9.85 (2.70-2.10 (2.40 (5.54) 1.66 (4.12 (2.32-7.63) 1. Barium compounds are used by the oil and gas industries to make drilling muds.14-1.80 (1. it combines with other chemicals such as sulfur or carbon and oxygen.55-3. barium sulfate and barium carbonate).15-11.34 (1.08-8.00-76.73 (6.57 (5.67) 6. 7440-39-3 Medically.46) 1.31.70) 5.01-7.59) 3. and ceramics.47-1. Barium salts have also been available as rodenticides.34 (2.30 (3.90) 4.00) 4.18-1.12) 6. bricks.56 (1.80) 1.20 (1.88) 7.12.56 (6.61 (1.31-2.50) 1.15 (6.11 (3.20-1.71) 2.40) 7.76-2.1) 9. 2001).82) 2.07 (2.36 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50 (4.40 (5.50 (1.51 (1.19-1.50 (1.64 (1.50 (5.04-2.4) 6.21-2.4) 9.49-1.72) 4.63 (1.00) 1.12 (2.32) 8.73 (5.24-1.74-2.60) 3.43) 2.16) 5.80 (1.86) 6.36-1.48 (6.19) 2. tiles.14 (6.68 (1.20-8.29-5.30-5.99 (4.30) 4. such as brazil nuts.50) 2.40 (1.76-7.00 (1.82) 1.80) 6.53-5.85) 1.65) 1.85) 1.35 (2.06-1.26-1.30) 3.63 (2.20 (4.49) 4.41) 1.65-1.51) 2.48) 1.56) 4.50 (3.8) 9.56 (2. The general population can be exposed to low amounts of barium in air.95 (4.54) 2.25 (1.88 (5.04-6. interval) 1.56) 1.92) 2.47-1.99-5.26) 5.15 (1.39 (1.76-3.30) 2.86 (4.36-1.41-3.31 (2.39-1.27) 2.35 (1.18 (6.70-3. are high in barium (Genter.62 (1.15 (2. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.73) 3.86 (4.30-2.80 (1.71) 95th 6.10-5. fireworks.40) 7. 0.40-13.62) 1.37 (4.37) 1.40) 3.40 (1.49) 8.35-1.16 (1.54 (2.4) 7.35 (3.53) 2.12-1.35-4. 01-02.60-10. Certain foods.43 (1.90 (6.98) 1.35-1.46-1.50 (2.22) 6. In nature.48-4.g.8) 5.15-1.00-3.80 (2.71 (2. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.20-1.50 (4.40 (5.11 (2.55-7.43 (1.90) 2.54-8.93-2.21 (1. Some barium salts are freely soluble in water.45 (1.80-7.05% of the earth’s crust.20-1.88) 4.61-8.72) 1.54-1.20-5.37) 5.93 (4.87 (5.62 (1.41-1.94-6.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.30) 5.43) 6.27 (1.39) 4.90-13.30-3.26-7.93-8.97 (1.73) 1.15-1.44-5.90) 1.78-2.71-9.80-3.61 (1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.48-4.. population from the National Health and Nutrition Examination Survey.09 (2.60-6.71) 1.50-1.06-2.22-1.48) 1.80 (5. see Data Analysis section) for Survey years 99-00. and 0.87 (6.61 (5.80-5.65-8.50) 2.50-1. respectively.82-6.76) 1.65) 1.54 (6.60) 1.49-9.30) 8. glass.57) 3.38) 2.39 (1.70 (1.70) 3.00) 6.Metals Barium CAS No.64-3. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).38 (1.20-8.25-1.54) 1.30 (1.78-3.34) 2.70) 7.24-1.20 (3.63) Total 1.28-1.70 (5.65 (5.63 (8. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.96-2.60) 1.02 (7.70-8.20-1.76 (3.20-8.50 (1.50 (6.49) 2.53) 1.46) 1.87) 7.50) 4.70) 1.65) 3.2) 6.90-9.25-11.64) 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 2.32-1.90-2.60) 4.08 (6.59-11.73-5. soluble forms of barium.61 (3.49 (1.70-6.72) 75th 3. whereas others are practically insoluble (e.17-1.8 (6.56 (1.30-1.52 (1.10) 1083 1335 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.70-2.81-3.43 (5.10 (4.S. Small amounts of barium can be released into the air during mining and other industrial processes.90 (4.11-1.10) 5.70-5.86-4.28) 90th 5.11 (3. Fourth National Report on Human Exposure to Environmental Chemicals 193 .74) 3.21 (1.30) 5.77) 1.87-7.20-6.34 (1.47) 4.12) 7.49) 11.01 (4.95-6.9) 5.70) 4.87-3.44 (1.40 (4. Workers employed by industries that make or use barium compounds can be exposed to barium dust.30 (2.30 (5.80-2.39) 1.78) 1.84) 5.86-5.21-8.57-7.00) 1.27 (1. water. depilatories.36) 5. rubber.54-1. In single dose animal studies.10-4.24 (4.10) 3. Barium compounds are also used commercially in paint.91) 2.60-6.51) 7.81-2.75-3.61 (2.36 (4.33 (1.77-3.15) 5.29-1.80 (2.44-2.00 (2.42 (1.50-6.45) 7.91 (2.81-2.62) 1.70) 1.87-14.30) 5.14-6.37-8.09 (1.60 (2.60-3.12.51) 1.88) 1.65-5.69 (1.90 (1.50 (4.29) 5.30-1.90) 2.20) 2.40 (1.50 (1.38) 8.80) 7.66) Selected percentiles ( 95% confidence interval) 50th 1.74-3.60 (1.63) 1.77 (3.30-2.37-1.60-2.91) 6.50-6. such as barium chloride.05-2.03 (1.10 (3.

57-7.52) 7.43-6.42) 1.00 (5.67-6.48-5.47 (5.2 (3.69 (5.76 (3.76 (4.62) 2.00) 1.73-2.16) 11.31 (4.13-2.84-5. weakness.69-9.72 (2.50) 2.34-5..76-3.05-1.49-1.777-1.24) 3.68 (3. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves. population from the National Health and Nutrition Examination Survey.26-1.79) 1.20-2.50 (4.19-1.24-3.22-1.16-1.26-1.38-7.54) 2.74) 1.48 (1.44-2. paralysis.40 (1.76) 2.37-1.38 (4.75-3. vomiting.46-22.46 (2. Chronic high doses in animals resulted in kidney damage (McCauley et al.81-7.32 (2.29-4.0) 6.56-3.59) 1.83) 2.25) 4.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.84 (3.03-1.72) 4.4 (5.53 (2.04) 5.36-2.45) 95th 6.46) 2.25 (1.57) 2.24-6.03-1.92 (4.36 (5.74 (5.03) 2.710-1.91-2.40 (1.22-2.48 (1.754-1.28 (1.30 (1.39-5.82) 1.27-3.24-6.33) 1.85-5. Perry et al.3) 6.2) 5.96) 4.64) 7.36-1.27-1.963 (.97-3.28-7.58 (2.703-1.68) 1.91) 2.18 (1.01) 1.50) 1. are not absorbed when administered.39 (2.51 (1.36 (3.33-1.73) 2.61 (4.39-1.66 (1.64 (1.51 (1.48 (1. 2001).49 (1.76 (2.02-5.905 (.55 (5.77) 1.37-2.44-2.40 (1.32 (1.31 (1.45) 1. Wones et al.33 (5.96) 4.16 (1.8) 4.53-21.31-1.86-7.29-4.20 (1.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .32 (1.92) 2.00-1.45-1.71 (5. Toxicity from soluble barium salts is rare.80) 3.19-2.52) 2.75) 2.52 (3.73-4. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.56 (1.38) 4.77) 1. in urine.62 (2.23-5.2) 6.06) 2.00) 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 1.57 (6.43) 1.38-5.59) 2.55 (1.11-2.42 (4.40-1.75) 2.29-7.11) .60 (2.38 (1.36 (1.10-2.10) 3.38 (4.51) 4.26-4.88 (2.34) 1.47) 1.56) 4.41 (2.39) 4. Barium is not rated for human carcinogenicity.4) 5.87) 1.00 (2.52-10.41) 5.70) 1. 1985.21 (1.51) 4.37 (1.08-2.28) 5.01 (4.10 (6...00 (3.59-7.00) 6.44 (1.03) 3.29-1.3 (6.68 (2.39-10. and cardiac dysrhythmias.32) 2.64 (1. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.33) 6.58-6.77) 5. Following intravenous injection in animals.48-1.28-1.51 (3.48-3.31) 5.55-5.04) 1. Symptoms following acute high dose include perioral paresthesias.64 (1.62 (1.36 (3.22-4.38-1.02 (3.47) 4. 1986).46) 1.86 (2.97-4.59 (1.26) 4.86) 5.39-1.27) 7.77-5.99) 1.65 (5.09) 6. such as those used in medical radiographic procedures.30 (1.75) 1.45-8.880-1.34-1.63-4.37) 2.91 (3.29 (1.54 (2.45 (3.61) 2.64) 7.49-1.41) 4.31-1.58) 75th 2.60 (1.56 (1.81-6.68) 3.20-8.03) 1. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.39 (2.10-1.96-6.97 (5.34-3.18 (1.00-7.62 (4.14-2.52) 1.08-1.38) 1.65 (2.00) 4. water solubility.81-6.26-1.42) 1.31-1.77) 1.96) 4. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.38 (1.04 (2.33 (1. diarrhea.37 (1.24-1.97 (4.72) 6.22-1.74) 1.915 (.57-5.13-3.51) 6.35-1.75) 1.57-10.00 (3.51-3.60 (1.0) 7.52-4.24-1.45 (1. chemical form.06) . Barium blocks cellular efflux of potassium resulting in profound hypokalemia.26-1. and route of exposure.39 (3.28-11.56) Selected percentiles ( 95% confidence interval) 50th 1.60 (2.58) 4.79-5.97) 1.24 (3.82) 1.35-1.70) 10.75-22.36 (1. hypertension.84-2.49-1.68-3. The health effects of exposure to barium compounds depend on the dose.33-4.90-2.55 (4.891 (.34 (1. 1984.36-1.0) 5.15-4.881 (.47) 1.01 (5. 1994.30) 2. NTP.41 (1.49 (1.58 (4.96) 7.02) 4.832-1.84) 2.70) 4.47 (2.68 (3.47) 10.83) 3.64 (1.98 (2.88 (6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.48) 2.12) 2. 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.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. 1989).Metals was eliminated primarily in feces and to a lesser extent.50) 1.921 (.99 (2.33 (1.96 (4.54) 1.55 (1.35-3.55-6.24 (5.28-6.96 (4.60 (5.19-1.91 (3.45-1. 1990).20) 4.59) 1. Insoluble barium salts.68-3.11) .80-6.77) Total 1.80) 4.38) 1.59 (1. interval) 1.32) 2.27 (2.46) 3.20-1.99 (4.02) .53) .25-11.78 (2.29) 1. a benign condition that may occur among barite ore miners.29-3.63) 1.10) 6.76) 2.54 (1.19-1.76) 1.58) 1.89) 90th 4.23-1.41 (1.29 (3.24-11.47-8.39 (2.89 (2.23-2.55) .45-6.

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

Beryllium compounds are commercially mined. bertrandite and beryl. and machine-parts industries. which may vary for some chemicals by year and by individual sample. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. or drinking water containing the metal. are mined for commercial recovery of beryllium. < LOD means less than the limit of detection.130 (<LOD-. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames.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. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes.13. beryllium is used in instruments.130 (<LOD-. and can be found in mineral rocks.S. electrical.13. coal. 196 Fourth National Report on Human Exposure to Environmental Chemicals . and refined beryllium is used in mirrors and special metal alloys for the automobile. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. Low-level beryllium exposure in the general population can occur through breathing air. and dental bridges. and 0. population from the National Health and Nutrition Examination Survey. near some hazardous waste sites. eating food. nuclear. see Data Analysis section) for Survey years 99-00. 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 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. soil. computer. respectively. the lightest of all metals. x-ray machines.13. In medicine. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Exposure to beryllium occurs mostly in the workplace. 01-02.150) < 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 . 0.Metals Beryllium CAS No. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. aircraft.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 . 7440-41-7 General Information Pure beryllium is a hard gray metal. and volcanic dust. and 03-04 are 0. Two types of minerals.140 (<LOD-. and from breathing tobacco smoke. In studies of laboratory animals.

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

Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. 1990. Costa R. Howerton K. Hamilton et al. Clin Chim Acta 2000.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. blood. Sci Total Environ 1990. Minoia C. Sampson EJ.S.13 μg/L. population are lower than levels in workers. In other studies. Beryllium [online]. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. 2000.S. Third National Report on Human Exposure to Environmental Chemicals. 1990. Pietra R. They reported urinary beryllium levels ranging from 0. Trace metals in urine of United States residents: reference range concentrations.S. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. et al. Trace element reference values in tissues from inhabitants of the European community I.. References Apostoli P. Pirkle JL. less than 0. plasma and urine and a critical evaluation of reference values for the United Kingdom population. HLA-DPB1 and chronic beryllium disease: a HuGE review..23:827-839. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure.htm. Minoia et al.74:162-166. 106.html. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Maier L. population were generally undetectable in NHANES 1999-2000. Sabbioni E. International Programme on Chemical Safety (IPCS).1 μg/L). and the fact that most NHANES participant levels were undetectable.76(1):53-59. Andrew M. Environmental Health Criteria. Ash KO.95:89-105. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. it is likely that urinary beryllium levels in the U. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure.296(1-2):71-90. Genetic and exposure risks for chronic beryllium disease. Given these results. Paschal et al. 2001).158:165-190. 0.e.cdc. Sabbioni E.12 to 0. and serum of Italian subjects. Am J Epidemiol 2003. 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. Weston A. et al. Comparison of representative ranges based on U. Available at URL: http://www. Gallorini M. Element reference values in tissues from inhabitants of the European community. McCanlies EC. Levels of beryllium in urine for the U.atsdr. Jackson RJ. 1998).org/documents/ehc/ehc/ ehc106. Schaller KH. 3/27/08 Komaromy-Hiller G.inchem.. Int Arch Occup Environ Health 2001. and the 95th percentile for males in NHANES 2001-2002. Morrow JC. Centers for Disease Control and Prevention (CDC)..e. Hamilton EI. Pozzoli L.. A study of 46 elements in urine. Ting BG.gov/toxpro2. Environ Res 1998. VI. patient population and literature reference intervals for urinary trace elements. Kriess K. 20012002.157:388-398. Sci Total Environ 1994. which approximate this Report’s limit of detection.Metals (i. environmental levels) and health effects is available from ATSDR at: http://www. Review of elements in blood. Paschal DC. Van der Venne MT. and 2003-2004. Apostoli P. Clin Chest Med 2002. Atlanta (GA) 2005.

500 (.400 (.400 (.30-1.400 (.600 (.50) 1.00 (.500) .10 (.366) * * .400) . Fourth National Report on Human Exposure to Environmental Chemicals 199 .326 (.500-.700) .600 (.70) 1.400) .200 (. U.20) 1.600 (.600 (.300) .400) < LOD .50-1.600 (.300) . interval) .300-.300-.10) 1.60-1.500 (. cadmium use has declined in response to environmental concerns (http:// minerals.20-1.300) .300 (<LOD-.403 (. and incineration of municipal waste materials.900 (.900-1.900-1.10) 1.20-1.80) 1.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .800-1.80 (1.300 (.300) .300-.00 (.50) 1.00 (. Since 2001. and nonferrous alloys.500 (.00-1.700 (.400) .300 (.400) < LOD .400 (.382 (.900-1.20) 1.10 (1.700) .800 (.00-1.10) 1.600-.10) 1.900-1.70) 1.00 (1.50 (1.386-.gov/minerals/pubs/commodity/cadmium).500) .20) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.400 (.60) Total * .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 .378 (.460) .313 (. and 03-04 are 0.00-1.30-1.20 (.60) 1.283 (.3.300-.00-1.600 (.700) .10 (1.700) .70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.900-1. Other uses include pigment production.400) .304 (. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.300-.216-.500 (. or copper smelters (U.400 (.513) .500 (.300-.30-1.00 (.00) .600 (.900-1. lead.600 (.10 (1.300 (.00-1.50-1.20) 1.00-1.30) .50 (1.40) 1.425 (.400-.00 (.20-1.600-.300-.3.00 (1.500) .600) 90th 1.20 (1.500-. coatings and plating. plastic stabilizers.500-.300-.50-1.300-.20-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.40 (1.600-.400) < LOD .30-1.337) . see Data Analysis section) for Survey years 99-00.800-1.300 (.300-.300-.40) 1.200 (<LOD-.400-.304 (. and 0.50 (1.500 (. during refining of lead and copper from sulfide ore.800) .00 (.289-.700) .600-1.300) .70) 1. < LOD means less than the limit of detection.40-1.468 (.500-.900-1.20) 1.275-.368-.362-.00-1.367-.900-1.50-1.10) 1.400-.449) Selected percentiles ( 95% confidence interval) 50th .600) 1.200 (.20-1.90) 723 898 910 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .00 (.400-.200 (<LOD-.30 (1.700-1.500-.30) 1.304-.309-.300-.500-.10 (1.900-1.S.393 (.300) 75th .70) 1.300-.400) . 0.296-.30) 1.500-.400-.400) .10 (1.40 (1.300 (.500-.10 (1.20) 95th 1.200-.20) 1.Metals Cadmium CAS No.600) .398) < LOD < LOD < LOD < LOD < LOD < LOD .400 (.376-.200) .300 (<LOD-.600) .20-1.300-.400 (.700) .600) .40 (1.424) * .300 (.400) < LOD < LOD < LOD .400 (.900 (.600) .420 (.427) * .700-1.40 (1.200-.20) .200) .333 (.266-.80) 1.395 (.00-1. population from the National Health and Nutrition Examination Survey.255) .00 (.500) .200-.00-1.500-.441) * .700) .300-.300) .300-.200-.400-.10 (1.378-.300-.300-.412 (.500) .300) .200 (.300 (.300) .400) .30) 1.300 (<LOD-.20) 1.300) .00 (.300) 1.40 (1. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.700-1.500) .60 (1.361-.426-.40 (1.400) .300 (.900-1.500 (.60 (1.400 (.300-.300-.200-.300 (.usgs.500-.400 (.500-.470) * .00) .300-.421 (.500) . 7440-43-9 General Information Cadmium is a soft.600 (.452) .600 (.S.300-.800) .500-. malleable.344) .30-1.359-.500 (.400-.S.300) .300 (.500-.300) .800) 1.400 (.300 (.300) .400-.60) 1.40 (1.90) 1.10) 1.400) .600) .400) .331) .600 (.403) .50) 1.50 (1.600) .400 (.400) .500-. which may vary for some chemicals by year and by individual sample.500-.20) 1.600) . EPA.500-.300 (.400-. as zinc sulfide) and to a lesser extent.600) .500 (. The predominant commercial use of cadmium is in battery manufacturing.00 (.300) .600 (.400 (.235 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.600 (.700) .700) 1. respectively.800 (.40-1.20) .60 (1.400-.400) .10) 1.400) .20-1.500-.300 (.60) 1.400 (.500-.300 (<LOD-.14.60 (1.10) 1.400 (.600) .600 (.300 (.400-.400) .60 (1. 01-02.400 (. Cadmium also may be emitted into the air from zinc.

680 (.087-.550 (.20 (1.208-.235) .153-.209 (.302 (.067-. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.150) .065-.210 (.51 (1.263) .300 (.179-.700-.972 (.890 (.520-. and various seeds.20) 1.766 (.249) .820) 1.200 (.763-. Cadmium in soil is absorbed by plants. Horiguchi et al.475 (.640) .220) Selected percentiles ( 95% confidence interval) Sample 95th 1.17) .354) .790 (.300) .890-1.173) .284) .977) . wheat.326) .450 (. drinking water is a source for cadmium intake.818 (.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.231) .730-.423-. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.272-. 2001).686-.880) .351-.607) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170-.255) .141 (. 0.200 (.169-.28 (1.366-.227 (.130 (.733) .199 (.436-.061-.210 (.530 (.482) .279 (.336) .17 (.462 (.13) .980) .700-.875 (.180 (.171-.092 (.203) . Cadmium absorption may be increased with iron deficiency (Berglund et al.198) .310) .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 .306 (.43) 1.458 (.57) 1.41 (.06.157-.445 (.492 (.167-.238) .151-.219 (.430) .03) .241) .253-.519) .886) .193 (.705-.813 (.28-1.551 (.01 (.203 (.289-.. copper) and protein.190-.210 (.285-..433-..222) .255) .892 (.918-1.313) .596) ..717-.238-.190-.160) .919) . **All results are corrected for molybdenum oxide interference in the ICP-MS method.82) 1. Inhalation of cigarette smoke is a predominant source of exposure in smokers.190-.800-.S.255) .836-1.839 (.107-.200-.714-1.206 (.330-.246) .06.817 (.980) .320) .20 (1. 2004a.06-1.545 (.187 (.170-.234 (.260 (.202-. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.388-.339) .262) .12-1.232) .412) .860) 1.480) .283 (.447 (.990) .34) 1.800 (.22 (1.220-.273 (.220-.308) .229) .121 (.450 (.243-.322 (.280 (.07-1.135 (.221 (. Cadmium is absorbed via inhalation and ingestion.456-. 2003).623) .219 (.081) .400-.114-.01) .350 (.178-.177-.148-.170 (.207-.189) .633 (.100-.394-.299) .092) .790 (.493-.194-.52 (1.498-.290-.090) .72) 1.20 (1.282 (.181 (.633-1. rice.060-.440 (.277 (. 1994). The kidney is a critical target and shows the earliest sign of cadmium toxicity.193-. Kikuchi et al.196-. and 0.120 (.490) .204 (.713) . 01-02.06.25 (1.426 (.25) 1.360) . The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.316 (.150-.233) .445 (. including many food crops such as cereal grains.38) .261-.366) . zinc. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.589 (.112-.20-1.390-.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 .700-.257) .30-1.219 (.270 (.400-.470-.270 (.126) .10 (1. Diamond et al.28) 1.310 (.229-. To a lesser extent. With chronic exposure.989-1.230) .160-. see Data Analysis section) for Survey years 99-00.74) 1.38) 1.15) 1.135-.733-.191 (. an inducible metal binding protein.817 (.479) .200-.430-.17 (.265) .115-.175 (.221) . 2003). calcium.261-.530) .17 (. ingestion through food is the largest source of exposure.741-1.191-.820-1.610) .230) 75th .500) .257-. population from the National Health and Nutrition Examination Survey.080 (.160) .387) .362) .372) .189-.128 (.211 (.559 (.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th .109 (.12 (.806) .220) ..24) 1.251) .892-1.507) .067-. respectively.510) .753-.239 (.963-1.01-1.230 (.329 (.210 (.157) .519) .265 (.191-.870) .390-.452 (.327 (.551) . interval) .220 (. 2003.980-1.15) .184-.848 (.136) .233) .455 (.210) .216 (.201 (.281 (.148) .247) .820 (. 2003).580) .500) 90th .101) .858 (.886-1.02-1.211-.15 (.229) .36) 1.510-.249-.843-1.206) .440 (.06) .38) 1.366-.. Renal tubular and glomerular damage.22 (.440-.183-.476-.237-.481) .077 (.19) 1. however.83) 1. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.393-.466 (.223 (.06-1.980 (.540) .390 (.110-.810-1.214-.539) .165-.226) .48 (1.960 (.980-1. and 03-04 are 0.260-.077 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .240) .175 (.875) .295) .240-.260-.192-.04 (.04 (.078 (.47) 1.109-.090) .202 (.960) 1.381-.09-1.160 (.13-1.940-1.855-1. For nonsmokers who are not exposed to cadmium in the workplace.490) 1.13 (.232 (. 200 Fourth National Report on Human Exposure to Environmental Chemicals . potatoes. whose body burdens of cadmium can be approximately twice that of nonsmokers.134) .38) .Metals 2000).32 (1. 1999.189-.061 (<LOD-.210 (.210) .195-. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.192-.** Survey Geometric mean (95% conf.748-1.140 (.

876-1.158-.418-.722-.078 (. 2004). interval) .084-.185) .404) .084 (.204-.247-.075 (<LOD-. 1999).998) .826-1.266-.884) .157-.194-.470) .537-.247-.280 (.051-.296 (.086 (.795) 1.614) .173 (.446) .473 (.622 (.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 .802 (.757) . 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.607) ..865 (.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 .826-1.631) .481 (.418) .501 (.17) . Horiguchi et al.377-.38) .962) .094) .126 (.181 (.650-.297) .05) 1.209) Selected percentiles ( 95% confidence interval) Sample 95th .229) .687 (.917 (.414 (.106) .278) .191-.221-.163) .183 (.931 (. 1999).256-.100 (.083-.171-.421 (.156-.281) .382-.438) 90th .234 (.559-.178-.135) . 1996.404 (.331 (. Olsson et al.727-.449) .336-.839) .136-.177) .112) .830) .253) .215 (.267 (.757 (.154-.** Survey Geometric mean (95% conf.196 (.691-.874-1.189-.674-1.754) .210) .104) .663 (.536 (.516-.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .440) .150-.364) .185 (.700) .182) .288) .235) .16) .343-.531 (.856) .426-.423 (.716) .335 (.687-.122 (.538) .104) .253 (.168-..316 (.767 (.950) .917) .412 (.740 (.067-.784) .077-.789 (..293-. 2002.273 (.441-.850) .182) .388-.176 (.16) 1.02 (.484 (.218) .096) .873 (..228-.140-.827) .431) .198) .252 (.289) .221 (.329 (..10) 1.245 (.350) .716-.075-.063-.444-. 2002.433-.304) .154 (.828) .700 (.159 (.236-.667) .227-.123-.208-.391-.792 (.779 (.941 (.187) .187-.098) .250) .156 (.909-1.162 (.200 (.222-.725-1.338 (.541) . 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.440) .240) .340) ..985 (.07 (. During the 1950’s and 1960’s.708-1.311) .719 (.647-.211 (.630-. Staessen et al.156) .143-. can result from high dose chronic exposure.919 (.238-.352) .270 (.184) .183) .282 (.191) .806-1.090 (.678-.906) .232) .266) .300-.091 (.288 (.143-.192) .07) . most often a result of occupational exposure (Roels et al.767) .268 (.071 (.929) .168 (.668-.12) 1.168-.261) .274) 1.490 (.173-.507-.212 (.783 (.242) .206-.292) .381-.085 (.163 (.223) .308) .174-.166 (.382) .161-.09 (.487 (.617 (.111-.181 (.783) .143) .325 (.472) .08) .06 (.199-.208 (. 2002.130-..00 (.226) 75th .693 (.175 (.123-.545) .207) .157-.220 (.191 (.140-.813-1..175 (.181) .170 (. Noonan et al.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.261 (.224 (.176 (.940-1.261-.318 (. 2003.107) .479 (..199 (. 1999).170-.00 (.316) .210 (.438-.232) .146-. 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.533) .233 (.113-.690 (.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.470) .927-1.219 (.238) .201-.813-.147-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.690-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.247-. Jarup et al.718 (.303) .414-.207-.423-.239-.202 (.085-.591 (.500-.304-.091 (.686 (.562-.078-. 2000.131-.159 (. At lower environmental exposures.137 (.136-.518) .225) .940 (.S.308 (.147-.209) .267 (.398-.560-.856 (.321) . 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. Fourth National Report on Human Exposure to Environmental Chemicals 201 .197-.415) .093 (. population from the National Health and Nutrition Examination Survey.074-.148 (.712 (.387-.255-. 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.432 (.190 (.234) .190 (.144-.289) .850) .979 (.178) .769 (.818) .147 (.491-.288-.184-.137-.234-.551) .184-.263-.833-1..205 (. 2004b).091) .653) .729 (.666-.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .175-.210 (. However.225) .281) .688-.678 (.690-.263 (.219 (.240) .645-.182) .434 (.830-1.818) .283 (.696-.101) .097) .181-. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.476) .13) .216-.241) .387 (.

2003. Olsson et al. 2005. 2002.html. Jarup et al. 2003). 2003. 1988).. 2002). 2005. 2002. 2002).1 mg/L (Alfven et al. Information about external exposure (i. Olsson et al.S. 2003.. 2004. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al.. 1999... Women had higher blood and urine cadmium levels compared to men of similar ages. with peak values observed in the fifth to sixth decades (CDC. 2002.S.. 2000.. 2006. Jarup et al. 2002).. Staessen et al. Horiguchi et al. intermediate in former smokers and lower in never-smokers (Becker et al. In adults aged 60 years and older. Becker et al.. respectively. 2003. However. Mannino et al.. 2005).. 2002. Olsson et al. 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 Information Blood cadmium reflects both recent and cumulative exposures. 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). 2003.atsdr.. Ezaki et al. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1. Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. 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). 2003. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. 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. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. 2000. 2005. Noonan et al... 2002. environmental levels) and health effects is available from ATSDR at: http://www. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH.. Creatinine-corrected urine cadmium values in U. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.. data (CDC.. 2006).. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al. as may occur from welding cadmium-alloyed metals. Moriguchi et al.cdc. Occupational standards are provided here for comparison only.26 and 3. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . Suwazono et al. 2004b). Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. In postmenopausal women.. approached these values associated with subclinical changes in renal function and bone mineral density. Komaromy-Hiller et al. 2002). not to imply a safety level for general population exposure.. respectively. CDC. 2002).. 2000). Zhang et al.. In the typical environmental exposure. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al.. Ezaki et al. 2006). Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al. 1999). Staessen et al. EPA. Salpietro et al. Acute and heavy exposure to airborne dusts and fumes...gov/ toxpro2. 2004b.. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect. Wennberg et al. maternal blood or maternal urine and birth weight (Nishijo et al. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood.... 2006. Wilhelm et al.S.. Further research is needed to address the public health consequences of such exposure in the United States. 2002. 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.. Wennberg et al.e..... potentially fatal pneumonitis (Fernandez et al. Staessen et al. 1996). Becker et al.. and drinking water and environmental standards have been established by U. 2005.46 mg/gram of creatinine) (Ezaki et al. 1996. Jin et al... blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. Friedman et al... 2000. Both IARC and NTP consider cadmium a human carcinogen. Animal studies have demonstrated reproductive and teratogenic effects. 2004. 2002) and length at birth (Nishijo et al.. For NHANES 19992000. 2004. Cadmium can produce lung. has resulted in severe. 1999). 2004.. Becker et al.

Sasaki S. Jin T. et al. Miyamoto K. Grubb A.000 women in the Japanese general population: a nationwide large-scale survey. Vahter M. Howerton K. Thayer WC. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Komaromy-Hiller G. Uemura T. Akesson A. Environ Health Perspect 2005. Horiguchi H. Kaus S. Ezaki T. Mucha A. Fukui Y. et al. Schulz C. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Hellstrom L. Davison AG. Lancet 1988. Toxicol Appl Pharmacol 2004a. Consonni D. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. Fayers PM. Persson B. possibly better than b2microglobulin. Savage-Brown A. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Bregante G. et al. Tsukahara T.Metals with reference values so they can determine whether people have been exposed to higher levels of cadmium than are found in the general population. Environ Health Perspect 2002. Seiwert M. Lauwerys R. Sasaki S. Environ Res 2004. Bellerup P. Kumagai N. patient population and literature reference intervals for urinary trace elements. Kundiev YT. Atlanta (GA).45:43-52. 196:114-123. Fernandez MA. Becker K. environmental. et al.24:717-724. Machida M. Machida M. Becker K. Centers for Disease Control and Prevention (CDC). Agency for Toxic Substances and Disease Registry (ATSDR). Krause C. Gadea E. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Toxicological profile for cadmium update. Darbyshire J. Moriguchi J. Occup Environ Med 2000.57:668-672. Venables KM. Zhu G.95:20–31. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. et al. Stock AL. References Akesson A. Fatal chemical pneumonitis due to cadmium fumes. Choudhury H. Anthropometric. diabetes mellitus. Available at URL: http://www. Takebayashi T.110:699-702. Hotz P. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Lancet 1999. Buchet JP. Bo M.96:353-359. Holguin F. Tsukahara T. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Third National Report on Human Exposure to Environmental Chemicals. Chislovska NV. population. Nomiyama T. Environ Res 2004b. et al. Ash KO. 2005.59:497]. 4/8/09 Alfven T. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Comparison of representative ranges based on U. Environ Health Perspect 1994. Comprehensive study of the effects of age.46:372-374. Greves HM.html. J Toxicol Environ Health 2003. Cadmium fume inhalation and emphysema. Sanz P. Int J Hyg Environ Health 2003. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Jones RL. Fukui Y. Lidfeldt J. Lepom P. Schulz C. Clin Chim Acta 2000. Nordberg G. Okamoto S. 206:15-24. Lundh T. Wang H. Pickering CA. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Jarup L.gov/toxprofiles/tp5. Seifert B. Furuki K. Friedman LS. Ikeda Y. Toffoletto F.148(1-2):11-20. Moriguchi J. Ukai H. Ye T. Oguma E. Kikuchi Y. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. iron deficiency. Nermell B. et al.76:186-196. Oguma E. Diamond GL. Jarup L. Bernard A. Chiappino G. Occup Med 1996. Seiwert M. Mascagni P. Ezaki T.354:1508– 1513. Elinder CG. Taylor AJ.59:194-8. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Mannino DM. Kaus S.cdc. Costa R. Serra J. Lison D. Vahter M.102:83-89.13(11):1627-1631. 1999 [online]. Thorax 2004.66(Pt A):2141-2164. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Alfven T. Lukyanova EM. Berglund M. Fourth National Report on Human Exposure to Environmental Chemicals 203 .1(8587):663-667. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group.S. Toxicol Lett 2004. Int Arch Occup Environ Health 2003. Miyamoto K. Olfactory function in workers exposed to moderate airborne cadmium levels. 102:10581066. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. J Occup Health 2003. Environ Res 2006.205:297-308. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. et al.atsdr. ShkiryakNizhnyk AZ. et al. Carlsson MD. Nerbrand C.S. Int J Hyg Environ Health 2002. Neurotoxicology 2003.296(1-2):71-90. et al. Horiguchi H. Ikeda Y. Furuki K. Dekio F. Palomar M.

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0) 12.55-11.49 (5.94) 4.99) 9. interval) 4.53-11.64) 4.1) 11.59-5.60 (7.2-12.79 (4.40-5.97 (7.12) 5.5) 12.12 (4.80-13.9 (11.94 (4. Whether cesium compounds are carcinogenic is unknown.17 (6.3) 12.30) 7.90) 7.09-5.50-7.90-12.3 (8.40-11.84 (4.05) 5.70) 5.3-15.69-6.9 (11.08) 7.20) 7.62 (5.81) 4.4) 12.4) 9.59) 7.63 (4.70-5.08-5.2) 11.25-5.10-9.8-13.16-6.2 (9.80-10.1 (11.12-11.20) 5.03 (4.14. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.83) 6.13-8.99-6.47-4.74-5.82) 5.22 (4.21 (4.54) 4.47-8.80-10.4) 10. although cesium was generally of low toxicity when given to animals.00-8.56-11.42) 7. photographic emulsions.7) 11.0) 12.39-4.1) 10.31-8.9 (11. Little is known about the health effects of this metal. see Data Analysis section) for Survey years 99-00.84-5.26) 7.49) 4.86-11. and high-power gas-ion devices.87 (4.87-7.0-15.05) 5.98 (7. diarrhea.7 (9.93 (4.70) 7.6 (9.26) 4.71 (4.60) 5.20) 8.90-10.32) 4.10 (8.35 (4.5 (8.8 (10.25) 4.64-5.43-8.20-7.23-4.56 (4.33 (5.54-11.9) 12.50 (4.68) 9.7 (8. cesium hydroxide is corrosive and irritating at high concentrations.45-8.70 (5.46) 7.21) 90th 9.5 (10.73-5.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.84-9.30 (6.5-14.6 (11.59-5.70) 5.87 (4.52) 7. population from the National Health and Nutrition Examination Survey.5) 10.4) 95th 11.40-5. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.80 (4.0) 10.76-6.29) 4.70 (6.81) 4.81) 9.13 (8.20 (6. nausea.60 (8.52-9. semiconductors. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.44 (8.50 (4.0-13.4) 11.01-8.80-6.05-5.2 (9.97) 4.3-13.74 (4.35-5.61) 7.08 (7.20 (4.61-6.3) 10.50 (4.80-10.70 (9.59 (5. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.30) 5.3) 10.80 (8.81-14.56 (4.4-13.4 (9.04) 7. and clay.5-16. respectively.82-4.5) 9.50 (6.00-4.8) 9.81 (4.4) 10.94 (4.33-5.90 (6.83-4.84) 8.34 (4.99-11.00) 4.8) 11.60) 7.60-7.8) 9. and 0.0) 12.64) 5.9) 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 4.8) 12.67 (4.91-8.9 (10.80 (8.3) 10.40) 7.00-9.38) 5.0) 9.32 (3.1-12.55 (4.23) 9.22-4.42-7.64) 5.25 (3. Fourth National Report on Human Exposure to Environmental Chemicals 205 .60-6.89-5.27) 4.70 (6.6 (9.72) 4.9 (10.72-7.97-7.70 (8.34) 9.6 (9.7 (10.64 (4.36 (3.00-8.40-11.57-5.74) Selected percentiles ( 95% confidence interval) 50th 4.59-5.53 (6.00-10.49 (4.14 (4.2-13.60-5.90 (4.89) 4.66 (7.10 (6.64-10.7) 10.03-4. soil.50) 5.94-4.1 (10.95-4.27-5.0) 11.8 (11.43 (5.9 (11.9) Total 4.80) 7.42) 6.0) 11.50) 9.2-13.13 (7.7) 10.0 (9.55 (7.40-7.12-5.2.30-5.1) 9.90) 5.4) 12.08-5.3-13.36 (6.71-5.08 (6.35 (4. 2004).40) 5.7) 11.77 (9.10 (6.40-5.24) 4.14.8) 12.3) 9.90) 9.8 (10. and 03-04 are 0.68 (7.40-5. and cardiac arrhythmia (ATSDR. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.86 (7. infrared lamps.3) 10.8) 11. Most human exposure to cesium occurs through the diet.33 (6.02 (4.26-11. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.45-5.1) 9.40 (4. the body half-life is estimated to be 70-109 days based on 137Cs exposures.6 (11.10-7. For absorbed cesium salts.29 (4.77-8.5-14.2) 12.01) 7.60-12.7 (9.10 (8.32-5.8) 12. and as polymerization catalysts.60-7.07-11.0 (10. 0.20-4.1-12.6) 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 4.20) 4.7 (9.62) 4.1-13.27 (7.17-6.13 (5.77 (9.7 (10.16-6.90) 4.71-8.2-14.80 (4.40) 5.4 (9.00) 7.01-6.99-11.95) 5.92-13.50 (7.62 (5.00 (7. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.00) 6.71-9.S.03 (4.39) 7.05-5.30 (6.56) 5.90-8.5-13. 01-02.87) 5.26 (3.2-13.71) 4.60-6.10-8.4 (10.7 (10.09) 5.86-12.70 (8.84) 5.63-4.1) 11.91 (7.99) 7.95 (3.89) 5.9) 11.98 (7.80 (8.71 (8.6) 11.9) 8.90-10.96 (6.60) 7.20-8.70 (4. Radioactive 137Cs has been used medically to treat cancer.73-11.36) 3.Metals Cesium CAS No.15-8.70-8.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.87 (4.6 (9.7-14.30-10.1 (9.6) 10.90-10.37) 7.37) 5.07) 4.04 (4.88 (8.49) 75th 7.63) 6.80 (4.90-12.3 (8. However. scintillation counters.80-11.20-5.7 (11.17) 4.90) 5.77 (4.10-5.

91 (5.53 (4.08 (5.09 (4.18-7. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.83-7. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.41) 4.04) 5.81 (4.63-6.58-5.22 (3.41 (4.71 (7.28 (5.15 (7.87) 5.06) 4.80) 6.50 (7.72 (4.94) 7.3) 11.30 (3.15) 95th 8.20-4.03) 5.76-9.30-4.67 (5.70 (7.07) 8.S.84-11.95 (3.35-7.58) 3.89-4.63-6.58 (4.39 (5.51 (4.62-8.98 (6.81 (4.17-4.56) 4. Two small studies of European populations reported urinary cesium levels similar to U.29-3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.53) 6.66-6. and were also roughly similar to those in this Report.25) Selected percentiles ( 95% confidence interval) 50th 4.3) 9.51 (7.03-6.44-5.68-11.74) 3.98) 5.00) 6.33-3.35-11.5) 9.36-3.50) 4.14-6.59) 4.47) 6. (2000) found urinary cesium levels that were slightly lower than those reported for the U.37) 4.00-5.55) 4.95 (5.36-6.30 (7.20-4.22-11.08-7.28 (4.10 (3.3-15.95) 8.77-5.18) 8.1) 11.67 (6.50-5.14) 4.99-4.46 (7.93-7.13-9.40) 6.64) 4.43 (4.88-10.55-5.04-5.42-4.14-7.2 (8.53 (6.0) Total 4.38-7.S.2) 11.87-4.17) 4.45-6.41 (5.79) 4.08 (3.90-8.43) 8.0) 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 .79) 9.72-5.13 (3.51 (4.20-8.14-4.54 (4.16-8.84-9.84-7.50) 4. Using clinically submitted specimens..91) 5.77 (7.86 (4.47 (4.75-11.40-5.36-10.14 (6.35 (3.45 (4.60-20.46-8.48-6.95) 10.48) 90th 7.9) 10.78) 4.43 (4.50 (6.3 (10.08 (6.42 (4.38 (3.27) 4.56) 4.08) 3.90 (7.S.00-10.77) 4.68) 6.41) 9.59-8.5 (9.37-3.91-9.47) 6.43-11.26-6.63) 6.95) 4.24-4.14) 4.58) 8.52-5.66 (6.8) 10.50) 8.60) 3.29) 5.04-11.94 (5.16) 5.60 (3.95-6.0 (7.68 (4. Komaromy-Hiller et al.87 (5.90-8.44 (4.63 (6.64 (8. 1990).41 (8.63 (4.17) 9.64-6.74) 75th 5.3 (8.88-4.06 (3.04) 6. 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.65-4.12) 3.96 (4..28) 8.83-6.56-10.38) 10.39) 5.03) 6.66 (5.68) 4.29-3. population from the National Health and Nutrition Examination Survey. 2004).31-6.28) 7.30) 10.84-7.49) 3.30 (4.73 (3.20-4.09) 8.35 (4.79 (5.64 (4.91-7.75 (6.30) 10.93-9.10-4.67) 5.64) 5.3) 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 3.46 (8.98 (7.4) 10.46) 6.42-6.06 (5.83) 8.84-9.98) 5.68) 3.66 (5.08) 4.21 (2.47) 4.97-5.79-5.82) 7.43 (8.90-3.24-10.87) 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 5.23 (7.05-3.19-3.08-3.0) 7.10 (5.8) 6.13-9.99 (3.95-12.16-5.33 (5.75 (7.10) 7.82-4.38 (3.85) 5.54 (4.54 (3.50 (5.6 (9.99) 4.42-4.17 (6.56 (4.62) 5.73-4.61-3.78 (3.51 (3.33-8.18 (7.02 (5.3 (9.5) 9.21-4.8 (9. interval) 4.06) 5.35) 3.27 (6.26 (3.43 (3.65 (6.21-3.15-4.61 (7.7) 10.65-3.03-5.19-6.2 (8. Minoia et al..44) 3.33 (5.99-9. population.20) 5.40) 7.01-8.13) 7.34 (5.22) 6.31 (4.64) 9.05 (4.27 (6.55 (3.53) 3.57) 3.74 (5.16-8.85) 4.00-9.07) 8.77 (6.09) 4.39) 8.42 (5.05) 6.21-5.60 (5.85-4.58 (6.27-6.29) 4.24 (3.7-12.00 (8.00-4.41-4.46-4.43-6.25) 4.96) 4.05) 3.18-6.47 (7.91) 5.9 (9.05-4.41-7.48) 7.44 (8.70) 7.78) 4.27 (8.00-5.77 (4.92 (5. population results shown in this Report (Alimonti et al.02-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.6 (9.44-9.99-9.08) 4.70) 6.11 (5.38-12.76-6.11 (5.6) 6.63 (7.51 (3.91) 4.29) 4.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.00-8.72) 4.74 (4.97-4.9 (10. 2005.31 (4.05-3.79) 6.27-4.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.56) 3.15-11.54 (5.07 (5.12 (3.78 (3.96-4.50) 4.47) 7.26 (4.10 (3.5) 7.12-6.91 (5.31-4.51) 4.71) 6.74-11.97) 8.91-6.30-4.60-10.07-4.92) 3.96-4.96) 4.8) 5.7) 10.

Fourth National Report on Human Exposure to Environmental Chemicals 207 .19:3131-3138. Wolfe MI. Toxicological profile for cesium. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium.cdc. et al. Ash KO. Available at URL: http://www. Spezia S. A study of 46 elements in urine.Metals References Agency for Toxic Substances and Disease Registry (ATSDR). Gatti A. New Mexico. Mott JA. Sabbioni E. Clin Chim Acta 2000. Howerton K. Apostoli P.14:120-128. Gallorini M. Centers for Disease Control and Prevention (CDC). J Expo Anal Environ Epidemiol 2004. Pozzoli L. Forte G. patient population and literature reference intervals for urinary trace elements. antimony and tungsten. Ronchi P. Paschal D. 2000. et al. blood.S. Atlanta (GA) 2005. cesium. Sewell CM. Sci Total Environ 1990.296(1-2):71-90. Minoia C. Rapid Commun Mass Spectrom 2005. Komaromy-Hiller G. 4/8/09 Alimonti A. Pietra R. Assessment of urinary metals following exposure to a large vegetative fire.gov/toxprofiles/tp157. and serum of Italian subjects.atsdr. Third National Report on Human Exposure to Environmental Chemicals.html. et al.2004 [online]. Mincione G. Comparison of representative ranges based on U. Wood CM.95:89-105. Voorhees RE. Costa R. Trace element reference values in tissues from inhabitants of the European community I.

700) .42) 1.372) .13) 1.850) 1.371 (.450) .23-2.590) .09 (. automobile airbags.04-1.26-1.760) .340-.870-1.359 (.348-.360-.338-.410-.600 (.930) .660) .380 (.430 (.540-.890-1.520) .379 (.316-.570) .500 (.570-.500) .390 (.340) .19) .04 (.660) .331-.670-.540-.390 (.343 (. shiny.369 (.410) .790-. and magnetic recording media.333-.24 (. Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.07.375 (.15-1.300 (.620-.404) .520 (.700) . and in synthesizing polyester and other materials.03) .502) .06 (.17 (.05) 1.890-1.519 (.560 (. Usual human exposure is from food sources.07-1.367 (.550-.440-.650 (. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.67) 1.370-.370-.399) .670-.680) .710) .26-2.680) .950 (.270-.420 (.550) 90th .670 (.980-1.50) 1.08.830-1.320 (.890) 95th 1.520-.20 (1. blue-colored pigments.940-1.930 (.640) .810) .620-.820 (.950-1.496) . population from the National Health and Nutrition Examination Survey.434 (.68 (1. Cobalt compounds are used as catalysts in producing oil and gas.28 (1.386) .640) .870 (.520 (.350) 75th .580 (.17 (1.09 (.01 (.620-.740-.16 (1.750 (.24 (1.316 (. 208 Fourth National Report on Human Exposure to Environmental Chemicals .680 (.06-1.630 (.373) .430 (.810) .460 (.570 (.900) .32 (1.880-1.690-.280-.393-.16) 1.350 (.600) .39) 1.620) .374 (.390-. large appliances.380-.410-. see Data Analysis section) for Survey years 99-00. 0.23) .980) .06 (. 01-02. respectively.48) 1.590 (.427-.450-.410 (.340-.405-.03) 1.355-.73) 1.52 (1.600-.01-2.820 (.470 (.364-.870 (.740 (.379 (. steel-belted radial tires.470) .640) . and 0.419) Selected percentiles ( 95% confidence interval) 50th . and kitchenware. Cobalt occurs naturally in airborne dust.590-.37-1.430-.99) 1.530 (.920) 1.04) 1.670 (.460 (.520) .430) .02-1.26) Total .373-.900-1.630-. varnishes.305-. seawater.523) .540-.400-.420) .350-.463-.380 (.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 .564) .21) 1.469-.390 (.900) .570) .910-1. hard metal or in combination with other elements.32 (1. It is emitted into the environment from burning coal and oil and car and truck exhaust.340) .26) 1.47) 1.490-.291-.540-.480-.880 (.790) .530) .430 (.03 (.550 (.410-.940-1.33-1.452 (.460) .380 (. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.370) .543) .710) 1.92) 1.00) .22) 1.53) 1.340 (. industry is imported or obtained by recycling scrap metal that contains cobalt.81) 1.290-.12) 1.890) .950) .480 (.510) 1.410 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.360-.81) 1.650-.890-1.760 (.07 (.790 (.270-.22 (1.454 (.350-.03-1.313) .900) .330 (.56) 1.418 (.670 (.Metals Cobalt CAS No.850-1.60 (1.450) .428-.710 (.465) .14-1.424) .44) 1.73) 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .01-1.310-. hard metal (alloys of cobalt and tungsten carbide).16-1.940 (.330-.690-.15 (1.750-.490-.45 (1.680 (.630 (.377-.300-.430) .390) .650 (.370 (.S.398 (.417) .960-1.16 (1.16) 1.33 (1.740-.410) .03 (.800-.50 (1.450) .850) .580 (.08) .520 (.75 (1.420) .414) .840) . Cobalt compounds are also used in manufacturing battery electrodes. and fertilizers.820 (.487) .29 (1.294 (.05 (.25-1.360-.950-1.435 (.301 (.17-1.28-2. The cobalt used in U.05 (.930-1.334) .352 (.730) 1.590-.410 (.380-.460) .450-.394) .750 (.07.319) .800) .26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.416) .398) .270-.46 (1.461 (.336-.480 (.515 (.660-.339 (.460-.800-.900-1.327-.47) 1.520-.48) 1.860 (.450) .S.370-.259-.08-1.348-.770) .810-.388-.28 (1. and 03-04 are 0.520-.530-.610) . diamond-polishing wheels.12) 1. and soil.540) 1.47 (1.410 (.28 (1.07-1.22-1.64) 1.431) .36) 1.460) .03) 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.410 (.570-.330) .580 (.32-2. Cobalt is used as a drying agent in paints.499 (.17 (1.09) .333-.520-.32) 1.690 (.16 (.850-1.310 (.47 (1.16-1.308-.950 (.350-.610-.285 (.750 (.01 (. It is also a component of porcelain enamel applied to steel bathroom fixtures.610) .65) 1.59 (1.581) .920-1.610 (.04-1.343) 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 .04-1.520 (.431) . interval) . and inks.583) .14) .32) 1.

388 (.582-.55) .352) .329-.44 (.35) .346 (.316 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.33) . Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.400 (.27) 1.313-.467-.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 .503-.10) .963) .425-.495 (.911-1.704-.00 (.380-.879-1.419) .792 (.290 (. respectively.02 (.306 (.29 (1.16 (1. population from the National Health and Nutrition Examination Survey.282 (.895-1.344-. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.23 (1.S.955) .365-.481) 90th .396) .600-.24) .700 (.554 (.848 (.310) .329 (.505) .57) 1.50 (1.608 (.469-..337) .313-.821 (.362-.15 (.319-.626-. or using diamond-polishing wheels that contain cobalt metal.25 (.727 (.426 (.847) .404-.638-1.479-.562) .471-.327 (.508-.861-1.17) .662) .393-.609) . 1972).851 (.407) .792-1.990-1.533 (.952 (.277-.03 (.574-.581) .534-.417) .54) 1.257-.298 (.850 (.248-..471 (.435-.28) 1.449) .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 .291 (.632-.547 (.964 (.19) .804) 1.313-.542 (.838 (.552 (.03-1.29 (1. cobalt is excreted predominantly in the urine.707) . 2003).361 (.378-. 1972).738 (.286) .438) .378-.523 (.257 (.363) .679-.750) . Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.06 (.384) .386 (.616-.358 (.548 (.331-.334) .328) . interval) .335 (.850-1.895-1.04-1.786-.983-1.294-.243-.740-1.595) .278 (.585) .563-. Smith et al.937 (.669) .976 (.594) . Exposure in the workplace may come from electroplating.777-.409) .00 (.10 (.917) .281) .36) 1.234 (.250) .611) .324-.476-.324) .550-.381) .606 (.634-.00) .457-.392 (.280-. in the feces.455 (. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.309) .673-.932-1.857-1.599) .461) .343-.14 (.314 (.872 (.306) 75th .353 (.302-.644 (.750-.323) .328 (.417 (.00 (.333 (.733-1.562) .500 (..694) .960 (.756 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).611) .50) 1.829) .753) 1.975 (.760-1.522) .407 (.278-.488) .297) .949) .487-.378 (.475 (.391 (. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.09) 1.689 (.543) .929) .29) 1.237-.282-.513 (.394) .561) .327-.00-1.683-.11-1.333-.12 (.938) .378-. Once absorbed and distributed in the body.349) .560-.737 (.500-.442-.830 (.463-.304) .362) .361 (.368 (.271 (.826-1.905) .785) .15) 1.247 (.60) 1.33) 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .554 (..703-.353-.301-.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 . and to a lesser extent.421) .275-.29 (1.462) .408 (.500-.529 (.256-.376 (.640) .337 (.753-.303-. A portion of cobalt retained for long periods is concentrated in the liver.00) . 1994).11-1.393 (.313 (.296) .83) 1.667-1.955) .700 (.36) 1.449-.821-3.444 (. with pulmonary clearance half-lives of from one to two years (Hedge et al.738 (. using hard metal cutting tools.382-.248-.317 (.368) .534 (.25 (.457 (.635 (.275-.900-1.360) .50) 1.471-.49) 1.844 (. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.30 (1.615) .29) .352 (.439) . an essential human nutrient. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.723 (.429) 1.757-1.00 (.515 (.304-.829-1.259-.537 (.833-1.434-.387) .774 (.273 (.963) .289) .04 (.963-1. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.362 (.33) 1.355) .963-1.215-.736-.513-.60) 1.10-1.348) .396) .938-1.630-.293 (.279 (.12-1.708) .781) 95th 1.593) .268 (.274-.73) 1.647) .402 (.259) .898 (.983) .468) ..301) .365) .667-1.479) .10) Total .691 (.487-.343 (.372) .452-. Cobalt is absorbed by oral and pulmonary routes.990) .435 (.290 (.290 (.598 (.297-.296-.388 (.16 (.630-.272-.428-.425) .16) .27) 1.391) Selected percentiles ( 95% confidence interval) 50th .842) . 1994.368) .352 (.523 (.513) .361-.300) .251-.369 (.35) 1.239-. 1979).342-.861 (.660-.728) .433) .457) .333-.Metals fabricated from cobalt alloys (Lhotka et al.728 (.313-.361-. refining or processing alloys.339-.591 (.313-.16 (.279) .328 (.824 (.333-.744) 1.326-.781-1..259 (.

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

Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Zweymuller K. Edmonds CJ.148:241-248. Zhuber K. salt. Palmroos P. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Heki S. Cannon SR. Fujimura N. et al. Dunstan E. Robinson C. Sci Total Environ 1994.95:29-37. Lison D. Industrial Chemical Exposure: Guidelines for Biological Monitoring.(1-3):133-139. Health Phys 1979. and hard metal dust. Swennen B. Thabe H. DeSantis V. Int Arch Occup Environ Health 1997. Absorption and retention of cobalt in man by whole-body counting. Kristiansen J. Peltier A. Schank M. Wild P. 3rd ed. Swennen B. J Occup Med 1992. Thomassen H. Lison D.242:1412-1415. Oksa P. et al. A report of two cases from mineral assay laboratories and a review of the literature. Sabbioni E.87(5):628-631. Thakker DM.22:359367.50(9):835-842. Sci Total Environ 1994. Ichikawa Y.55(4):269-276. and cobalt metals. Lisi P. Kiilunen M. Ghat IS. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Lauwerys RB.20(1):25-31.533:135-152.157:117121. Trace element reference values in tissues from inhabitants of the European Union. Christensen JM. Buchet JP. Lung cancer risk in hard-metal workers. Buchet JP. Occupationallyinduced “isolated cobalt sensitization. Chest 1989. Bunn HF. Kuska Y. 1985. J Bone Joint Surg Br 2006. Roto P. Zedda S. Lauwerys R. Hoet P. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Schaller KH. Angerer J. Science 1988. Radulescu M. Br J Ind Med 1993.204:147-160. Lhotka C. Goto S. Boca Raton (FL): Lewis Publishers. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements.88(4):443448. Kusaka Y.406:282-296. Sabbioni E. HoffmannB. De Boeck M.48:172-173. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. Mutat Res 2003. Contact Dermatitis 2003. Iversen BS. Shirakawa T.150. Sci Total Environ 1998. Schramel P. Zobelein P.69(3):193-200. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Clin Orthop Relat Res 2003. Kriss JP. Vitali MT. Biological monitoring of workers exposed to cobalt metal. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Molders J. Cobalt cardiomyopathy. Blunn G. et al. Bourne RB. Cobalt and antimony: genotoxicity and carcinogenicity. Tilley S. Meyer zum Buschenfelde K-H. J Bone Joint Surg Br 2005. Sci Total Environ 1997. Am J Ind Med 2003. J Rheumatol 2001.51(7):447450. Long-term clearance of inhaled 60Co. Uitti J. McCalden RW. Mosconi G. Kraus T. Pradhan C. Diepgen TL. Gross RT. Hoher T. Salvatori S. MacDonald SJ. Hedge AG.21(2):189-195. X. Ziaee H. Dickel H. Kirsch-Volders M.150(1-3):167-171. Meier R. Cleland D. Hammon E. Alessandrelli M. J Trace Elem Med Biol 2006. Weber A. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Goto S. Barnaby CF. Goldberg MA. Romazini S.58(10):631-634. Chess DG. Int Arch Occup Environ Health.Metals effects of cobalt. Cresti R.216:253-270. Stanescu D. White MA. Epidemiological survey of workers exposed to cobalt oxides. Dunning SP. Linnainmaa M. Outcome of occupational asthma due to cobalt hypersensitivity. Co-sensitivity between cobalt and other transition metals.34:620-626.45:246-247. et al. Pisati G. Smith T. Bozec C. Unwin P. Linna A. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Bacis M. Steffan I. Weyher I. Kato M. J Orthop Res 2003. Rorabeck CH. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. cobalt salts. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. McMinn DJ. Carnes WH.44:124-132. Occup Environ Med 1994. 2001.36:732-734. Laippala P. Moulin JJ. Sanghrajka AP. Lauwerys R. oxides. Occup Environ Med 2001. et al. The release of metals from metal-onmetal surface arthroplasty of the hip.” Contact Dermatitis 2001. Szekeres T. Respiratory health of cobalt production workers. Daniel J. Lasfargues G. Falcone G. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Salama A. Arch Intern Med 1990. Lison D. et al.28(5):1121-1128.150:177-183. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Leghissa P. a study of 13 elements in blood and urine of a United Kingdom population. Iavicoli I. Am J Epidemiol 1998. Sabbioni E. Health Phys 1972. Jarvis JQ.

60) 5.10) 3.878-1.60) 3.60 (1.10-8.60) 3.20) 3.91) 1.60) 2. such as lead phosphate and tetraethyl lead.80-4.30 (2.90) 2.70-2.20-2.37 (1. In the past.60) 2.25 (1. respectively.20) 1.00) 2.20) 3.30 (3.00) 2.00 (1.10 (2.20) 90th 3.43) 1.90-2.30 (2.40-3. the main source of lead exposure for the general U.40 (5.80-5.87) 1. and 0.60-3.20) 2.70) 1.31) 1.10 (1.56 (1.30-1.22 (1.37-1.32-1.70) 1.30 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.60) 1.90) 2.80 (2.70 (2.30 (2.90-2.20 (1.3.00 (2.90) 3.60 (1.81) 1.50) 3.20-3.30-4.10-3.60) 4.30 (2.70 (3.19 (1.40 (1.80) 1.50-1.60-1.51) 1.90 (1.10-2.30) 2.80-3.90 (3.900-1.50-2.20 (3.70-1.10 (3.37 (1.60 (2.90) 1.S.50-6.20-6.60-4.40) 2.14-1.60 (1. antique-molded or cast ornaments.60) 1.43) 1.30-5.g. 01-02.75 (1.30) 2. malleable.80-4.10 (2.80 (1.45-1.80-3.77 (1.10) 1.00 (1.50) 7.946 (.10) 4.50) 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 2.43 (1.69 (1. 7439-92-1 General Information Elemental lead is a soft.90-4.90-4.90-6.17) .25) 1.40) 1.70) 4.00-1.50 (2.00-2.20 (1.00) 4.10-2.70-1.90 (3.50) 2.60) 4.40) 2.80-3.60) 4.S.00-6.20 (3.89) 1.23 (1.71-1.70 (5.10 (2.60) 2.40-2.70-2.942 (.30 (4.40-3.10) 3.60 (4.10) 3.40-1.70 (2.34-1.00 (3.75-1.50-1.70) 3.75-2.10-4. Elemental lead can be combined with other elements to form inorganic and organic compounds.40 (1.70) 3.10-4.70 (1.80) 2.50-1.90-2.40 (2.00) 5.70-6.90 (3. interval) 1.50) 5.80-4.50-1. plastics.36-1.40) 5.60 (1.50-4. metal alloys (e.60 (2.70) 2. Lead has a variety of uses in manufacturing: storage batteries.20-3.80-2.00 (6. Lead was used in plumbing for centuries and may still be present.50) 75th 2.40 (1.60) 1.69 (1.55-1.20 (2.60-1.90-4. leaded glass.40 (4.50-2.30-1.20 (2.40-1.70) 1.00) 3.00-1.50 (2.80) 2.60) 2.62) 1.20 (3.30 (1.00) 4.52-1.70) 1.95) 1.48) 1.43-1.40 (2.00-4.60 (3.80 (4.50 (2.20-1.50 (1.60-1.30-1.70) 4.10) 2.80 (2.52 (1.40) 2.14-1.10) 1.30-2.30) 2. ammunition.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 2.60 (1.30-2.00) 6.60 (2.60 (3.70) 1.10-3.50 (1.30) 5.60-1.30 (1.43 (1.66) 1.90) 5.50) 1.90 (2.52-1.53) 1.70 (1.62 (1.00-4.40 (3.00) 1.90) 2.60) 1.66 (1. see Data Analysis section) for Survey years 99-00.69) 1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.10-2.10-2.60 (3.70 (3.72) Selected percentiles ( 95% confidence interval) 50th 1.68-1.78 (1.60 (3.50) 1.39-1.70 (2.62-1.10-6.70-1.10-1.90) 2. population was aerosolized lead emitted from combustion engines that used leaded gasoline.10) 2.70) 4. solders.90 (2.20 (3.30 (2.70 (1.50 (4. and 03-04 are 0.90) 1.90) 3.01 (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.10 (1.30-2.80 (1.39) 1.986) .40) Total 1.60-6.90 (3.50-5.40-1.Metals Lead CAS No.90-4.20) 3.80 (1.80) 2.70-4.80) 2.20 (1.20 (1.50) 4.50-2.50) 2.30 (4.20 (4. 212 Fourth National Report on Human Exposure to Environmental Chemicals .60 (1.50) 5. ceramic glazes.49-1.90 (3.50 (1.20 (3.60) 5.00) . blue-gray metal that occurs naturally in soils and rocks.20) 4.50) 4.50-2.10-1.80 (2.20) 5.75) 1.70-2.55-1.20) 3.40) 1.30-2.50 (4.87 (1.30 (2.50 (3.20) . Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.90 (1.80) 1.60-2.28.50-4.90-3.50) 1.80) 1. and for radiation shielding.900 (.51 (1.83 (1.50-3.20) 4.00) 1. population from the National Health and Nutrition Examination Survey.80-3.60) 3.09) 1.3.40 (1.800-1.900 (. Before the 1980’s.20-3. Since lead has been eliminated from gasoline.80 (4.02) 1.30 (2.04-1.50-5.30-6.40-1.40-2.40-6.90) 1.10 (1.30) 1.20 (3.20-1.55 (1. 0.40) 3.50 (1.00) 2.50) 1.60 (1.14-1.80) 3.93-2.20-4.40-2.25 (1.80) 1.00) 3.60) 2.10) 1. brass.30-1.32-1.00) 1.00) 1.65 (1.00 (4.00-5.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.40) 4.80) 1.90 (4.20 (3.80 (3.36-1.10-1.40) 2.60) 4.80) 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 1.50 (3.30-1.60 (2.30) 95th 5.60) 3.00 (4.96-2.20 (1. Lead is most often mined from ores or recycled from scrap metal or batteries.80 (5.00) 1.10-3.60) 1.12-1.30 (4.30 (1.10-6.10-2.45 (1.90-2.00 (5.70-3.36) 1.90) 2.50 (2.69) 1.10 (4.10-2.50-1.899-.10-3.80 (1.00) 2.10) 5.40) 1.40-6.46 (1.70-5.80 (1.20-3.00-4.70 (1.80 (5.40-4.60 (2. bronze).40-3. dense.60 (2.60-4.30-1.50-3.20-2.40-1.40-5.60-2.80 (1.70) 4.86) 1.50 (2.70) 3.40-1.

00) .600) .535-.773) . the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.710-1.82 (1.40-2.17 (1.21 (2.795 (.30 (3.20-2.00-1.915-1.579-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.10) 2.90 (1.729-.700-.40 (1.828) Selected percentiles ( 95% confidence interval) 50th .40) 2.00) 1.00 (.610 (.900 (.560-.30) .80-2.40-1.920 (. 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.24-1.766 (.00-2.30) 2.800) .40) 2.573 (. lead-contaminated dust in indoor firing ranges.40 (2.70-2.650) 1.40) 1.90-4.677 (.637-.695 (.10-5.13) .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 1.590 (.90) 2.40) 1.40) 2.40-3.822-1.10) 2.718) .82 (2.850 (.680) .78-2.70) 3.700 (.00 (1.04-2.30-2.10-1.674) 1. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.30) 2.970-1.620 (.600-.14 (1.628) 1.44-2.60-2.70) 2.18-1.600-.50-2.80-3.808 (.52-1.04) 2. Fourth National Report on Human Exposure to Environmental Chemicals 213 .97) 4.80) 2.30-1.64) 2.900) .990) 2.745-.960 (.40) 2.620) 1.59-2. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.10-1.500-.40) 3.710-.50) 1.800) . However.10 (1.90-2.30 (2.80) 2.700) 1. and contact with soil.790 (.40) 1.29 (2.800 (.31-3.580-.700 (. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.60-3.800 (.680-.40 (2.910-.630 (.900) .09) 1. 1991). or after soluble lead compounds are ingested.570-. lead-containing folk remedies and cosmetics. or water contaminated by mining or smelting operations.810-1.700-1.13-3.02 (.60) 2.10 (1. stained glass framing.10) .940 (.833-1.19 (1.91) 2.30-5. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.20) 1.90 (2.688 (.848 (.22) 1.931) .23) . which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (2.66 (2.900-1.00 (1. Approximately half of the absorbed lead may be incorporated into bone.613) .1. 2007. pewter utensils and drinking vessels.955-1.800-.800-1.595-.10) 1.480-.20-2.20) .Metals occupational (e.40) 1.27 (1.30) 1.900 (.616) .66 (2.20) .52-1.10-1.700-.60 (1.50-3. 2000). population from the National Health and Nutrition Examination Survey.600-.900 (.90-3.00-2.579-.900) .506-.10-1.31 (1.00) 2.11) 2.749) .00-1.70) 1.70-3.14-1.80 (1.04 (.564 (.941) . imported children’s trinkets and toys.30-3.986) .80 (2.72) 1.50 (2.g.75) 3.10-3.27) 1.800-1.857) .78-2.700 (.49 (1.40) 1.00 (2.80) 1.20-1.00 (1.800 (.20 (1.10-3.50) 1.556-.90 (1.04) .900) .00 (1.62-4.50) 2.815 (.52 (1.80) 3.671-.642 (.10 (.757-.90-2.50) 3.840 (.S.80) 3.20-1.20 (1.03-2.731 (.553-. CDC. battery and radiator manufacturing) and recreational sources. 0.50 (1.558 (.700-.700-.738) .03 (1.651) .80) 2.800 (.818) .700 (.60 (2.50 (2.62) Total .640-.00-1.660) .990) 1.30) 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 1.14 (1.10 (.35 (.90) 2.659 (.90 (2. In the blood.700 (. lead-based painted surfaces undergoing renovation or demolition.20 (1.40 (1.89) 2.20 (1. see Data Analysis section) for Survey years 99-00.90-2.10-1.70) 3.30 (1.10 (1.820-1.90 (2.900-1.40 (2.30-1.862) .70 (2.752 (.40-5.20) 1.59) 1.33.20 (2.30) 1.700) .11 (1.900-1.730 (.701) .02) 1.50 (1.591 (.900) .540 (.800-.23-4.30-1.636 (.600-.923 (. 01-02.600-.80) 1.20 (1.680-.86-2.90) 2.935) 1.20 (1.07 (.30-1.60 (1.80) 2.70 (2.753 (.540-..86) 1.600) .51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. and 0.10 (1.40 (1.00) 2.86 (1.07-1.800) .04 (.50) 2.20 (3.625 (.80-2.920 (.900-1.80) 1.10-3.40-1.60 (1.30) 2.700 (.700-. interval) .12) 90th 2.40 (1.70) 1.20) .70 (2.960-1.90) 1.661-.800) .90-2.625-.70 (2.708-.50 (2.690) 75th 1. respectively.40 (1.640 (.73 (1.604 (.50-1.526-.86) 95th 2.00) .33 (2.78-2.60-2.90-3.75) 4.691-.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 .40 (2.40-1.10) .80) 2.60-3.06) .20-1.00) .600 (.30) 1.70) 1. older plumbing systems with leaded pipes or lead soldered connections.40-1.41) 2.70 (1. bullet fragments retained in human tissue.60 (1.960-1.20) 1.900) .641-.20 (2.800) .785) .50-2.90 (1.33-2.00) .32 (1.50) 1.29) 2.00-2.589-.20) .30) 1.80 (1.10 (.50-2.572-.30) 1.605) .600 (.. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead. and 03-04 are 0. dust.1.833 (.60-1.

722 (. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.47 (1.03) 2.594-.765) .05-1.02-1.15) 1.27 (1.508) .635 (.569 (.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 .730) 1.615 (.98 (1.725) .37-1.43) 2.50-2.51) 1.700-.70 (1.933) .571-.03) 1.66 (1.18) 1.698) .428) .668-.709 (.49 (1.46 (1.98-2.667) .68 (1.07) .56-2.03 (.800-.85) 1.69 (1. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al. through the inhibition of certain enzymes.00 (1.639 (.551-.03-2.898) .541-. 1995).34-1. zinc.71 (1.670) 1.20) . based on prospective population studies.703) .64-2.11 (.790) .88) 1.632 (.940 (.44 (1.607-.S.436) .38 (2. In 1991.701 (.03 (1.25-1.683-.593 (.83 (2.28) .11 (1.50-2.492-.31) 1. abdominal pain.639 (.79 (1.887 (.380-.31 (2.63) 1. 1996).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 .702) .686) .96 (1.853-1.763) .988-1.988 (.22-1.41 (1.673) .644) .26) 2..35) 2.44) 1.841-1.667-.15-3.688) .659-.583-.609 (.39-1.962 (.Metals 90% of the body lead burden in most adults.739) .408-.00 (.15-2.588-.01 (.18) 2.677-.606-.52) 1.657) 1.73) 2.641 (.10 (.796-1.612-. BLLs and associated toxic effects differ in children and adults. The toxic effects of lead result from its interference with the physiologic actions of calcium.61) 1.03) 90th 1.61) 1.342-.63) 4.731-.89-5.79) 1.11-1.718) 1.97) 1.677 (.851) .432 (.645-.639 (.72) .957-1. and nails (Leggett.561-.56 (1.918 (.33-1.992-1.946-1. interval) .47 (2.810 (. and through binding to ion channels and regulatory proteins. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.603 (.08-2.43) 1.404-.622 (.38 (2.529-.652 (.62-3.893) .48 (1. population from the National Health and Nutrition Examination Survey.975-1.918-1.50) 1.914-1.04) 2.53) 1.838) . Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.85 (1.88) 2.26) Total .718) .469 (.701) .22-2.28) 2.662) 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 1.92) 2.12-1.20-3.638 (. encephalopathy.09-1.667-.25-1.758) .979 (.50-1.94 (1.655-.496 (.97-18.64) 95th 2. with a half-life of years to decades.876-1.696 (.722 (.404 (.72-2.900 (. hair.97) 1.603-.681-.61) 1. Staessen et al.01) .671 (.971 (. kidney injury.08) . Nash et al.926 (.702-.33) 2.03) 2.655) 75th 1.29 (1.08) .571-.746) .633 (.793-1.05 (1.594-.677) .990 (.693 (.75-2.79) 2.98) 2.88) 2.648 (.882-1.09-1. and iron.46 (2.64 (1.22) 1.644 (.917-1.676) .707 (.77) 2.74 (1. 2003. 1993).658 (.623 (.94-2.07-1.19) 1.963-1.43 (1.62-2.59-3. For instance.977) 1.698) .774 (.33 (1.19-5.00 (1.870 (.88-2. with lesser amounts eliminated via the feces.781-1.933-1..61) 3.05 (.22) .02) 1.11) 1.33) 1.85-2.41) .20) .50-2. 2007).14 (1.725) .03) .31) 1.586-.11 (.03 (.0) 3.920-1.03 (.588-. 1993.992-1.625 (.605-.400) .812-1.679-. Schwartz. scant amounts are lost through sweat.72-2.06) .58) 1.679) 1.17 (.828) .28-1. seizures.14) 1.31 (1.18) 1.24 (1.71-2.755 (.712 (.43-1.45 (1. Approximately 70% of lead excretion occurs via the urine.603-.11) .601-. Large amounts of lead in the body can cause anemia.375 (.61) 1.88 (1.05-1.828-1..55 (1.52 (1. 2004.40-1.65 (1.18 (1.618 (.53-1.73-2.36-2.86 (1.18) .997-1. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.47) 1.78 (2.23 (1.43 (2.938 (.06) 1.587-.62) 2. 1991.62-1.37-1.75 (2.66 (1.31 (1.78-4.742) .85-2.03) 1. and paralysis.742) Selected percentiles ( 95% confidence interval) 50th .87) 1.09-1.621 (.04-3.65-2.721 (.460-.510-.55 (1.535) .708 (.38 (2.702) .734) .51 (1.22) 1.89-2.64) 2.41-1.09) 1.00) .862-.03) .649 (. Lead can cross the placenta and enter the developing fetal brain.06 (1.97 (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 . 1995.50 (1.645-.608-.720 (.655) .981-1.938-1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects. O’Flaherty.623 (.914 (.06 (.17-1.83) 1.639) .66) 2.15-2.682) .753) .579-.11 (1.404 (.44 (1.592-. The skeleton acts as a storage depot.608 (.461) .00 (1.720 (.56-3.67-4.604-. CDC.383-. 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.559-.56) 3.617-.82) 1.10) 1.914 (.07 (.615 (.681-.15) 1.654) .710) .10 (1.

2005a)... urban residence. In occupationally exposed adults. and low family income (CDC. environmental levels) and health effects is available from ATSDR at: http://www. IARC considers inorganic lead compounds probable human carcinogens.21% of approximately 3.6% in NHANES 1988-1991 to 1. 2001). Schwartz et al.atsdr. 2005b).0 µg/dL in females (Soldin et al. when the geometric mean BLL was 2..4% in NHANES 1999-2004. At low environmental exposures. The U.S.g.e. though there is greater individual variation in urine lead than in blood and greater potential for contamination.. 1995.cdc. which is an 84% decline. CDC. Bellinger 2005..4% of children had BLLs of 10µg/dL or higher (CDC. 2003.xls).5 per 100.. Telisman et al.75 µg/dL in U.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1.6%) were lower than those from NHANES 1991-1994.S. 1996. Korrick et al... 1998). both the geometric mean (1. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. and peripheral neuropathy generally occurring at much higher levels (e..S..S...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. 1999). including minority race or ethnicity. Overall. Schwartz.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006. Information about external exposure (i. In NHANES 1999-2002 in children 1-5 years old.. 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. Muntner et al. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. with overt encephalopathy.07 µg/dL (Becker et al. 2002).cdc. 1991. 2003. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. 1996. 2005b. 2003. 2003). 2006).S. 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. 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. EPA. Staessen et al. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.S.. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. almost double the geometric mean of 1. and decrease fertility (Alexander et al. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al. Lanphear et al. 2007). However. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC.. and organic lead compounds not classifiable with respect to human carcinogenicity. subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. and spontaneous abortion (Baghurst et al.. 1994). residing in housing built before the 1950’s.gov/toxpro2. High dose occupational lead exposure. A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. adults in the 19992000 NHANES sample (Apostoli et al. 2000). 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. Payton et al. Data submitted through state public health programs from 2006 showed that 1.. 1984. reduce sperm count.html. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. particularly in the skeleton. 1996. 1987. premature delivery. 2009)... usually with BLLs greater than 40 mg/dL. 2000). 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. BLLs reflect both recent intake and equilibration with stored lead in other tissues. More recently.7 µg/dL and 4. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR..3 million children tested had BLLs of 10 mg/dL or higher (http://www. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. Jones et al. 2002. adult residents. Borja-Aburto et al. approximately 11.. Urine levels may reflect recently absorbed lead. 2006). Surveillance data reported by U. 2002a).Metals µg/dL or higher as the level of concern in children. higher than 100-200 µg/dL). For example. 1999). respectively.000 adults. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. Both drinking water and ambient air standards for lead have been established by the U. the geometric mean BLL was 3. the prevalence rate has declined annually since 1994 (CDC. seizures. may alter sperm morphology. lead in women may be associated with hypertension during pregnancy.2 µg/dL in males and 3. adults in the 1999-2000 NHANES sample.. Pirkle et al..

Baj A. et al. Atlanta (GA). Angle CR. Jacobson JL.gov/nceh/lead/publications/ books/plpyc/contents. Toxicological profile for lead. Age-specific kinetic model of lead metal in humans. Roberts RR. Lead. et al. Weiss ST. Bellinger D. Rios C. Wigg NR. Robertson EF. Am J Public Health 1999. Teratogen update: lead and pregnancy. Available at URL: http://www. Krause C.cdc. Borja-Aburto VH. Neri A.113(4):1016-1022. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Environ Res 2000. Henderson CR. Pirkle JL. et al. Rotnitzky A. Cox C. Hu H. Manton WI.275:1177-1181. Sparrow D. 2005b. Korrick S. Lead and hypertension in a sample of middle-aged women. Lepom P. Korrick SA. Ronchi L.htm. Apostoli P. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Pediatrics 2009. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Speizer FE. JAMA 1996. Kaufman JD. Coresh J. Atlanta (GA). Blood lead levels measured prospectively and risk of spontaneous abortion. Neurotoxicol 1987. Scand J Work Environ Health 1984. McMichael AJ. Neurotoxicol Teratol 2004. 1991 [online].cdc. Dietrich K. Am J Epidemiol 1999. Rotnitzky A. Sci Total Environ 2002. Available from URL: http://www. Kim R. Semen quality of men employed at a lead smelter.atsdr. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . CDC. Blood lead reference values: the results of an Italian polycentric study. Available at URL: http://www. Weiss ST. Available at URL: http://www. et al. Blanco J. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. doi:10. The relationship of bone and blood lead to hypertension.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. MMWR Morb Mortal Wkly Rep 2006. Int J Hyg Environ Health 2002.287:1-11.73:409-420. Jacobson SW. Payton M.10:43-50. Occup Environ Med 1996. 4/14/09 Centers for Disease Control and Prevention (CDC).87:1-471.cdc.gov/nceh/lead/ CaseManagement/caseManage_main.8(3):395-401. Reese YR. Vupputyuri S.cdc. Hu H. Available at URL: http://www. Cory-Slechta DA. Chiodo LM. Luukkonen R. Kaus S. Blood lead levels—United States. 4/14/09 Alexander BH.348:15171526. 1988-2004. Hunter DJ. Rojas LM. Jones RL.55(32):876-879. Hu H. van Netten C. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Birth Defects Research (Part A). gov/mmwr/preview/mmwrhtml/mm5420a5.53:411-416. Muntner P.htm. Stanek KL.html. Environ Health Perspect 1993.82:60-80. Cox C. Vimpani FB.cdc. Bavazzano P. 2002 [online]. Third National Report on Human Exposure to Environmental Chemicals. Schulz C. Hänninen H. Centers for Disease Control and Prevention (CDC). Hertz-Picciotto I. Jusko TA. Seiwert M. Adult blood lead epidemiology and surveillance—United States. Farias P. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas. Baghurst PA. Hernberg S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Managing Elevated Blood Lead Levels Among Young Children. Caldwell KL. Ewers TG. 2003-2004. et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Lanphear BP. Bellinger D. Kuehnemann TJ. Canfield RL.123:e376-e385. Atlanta.26:359-371. IARC Monogr Eval Carcinog Risks Hum 2006. Meyer PA. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. Auinger P.101(7):598-616. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.54(20):513-516. MMWR Morb Mortal Wkly Rep 2005a. Sparrow D. JAMA 1996.htm. Preventing Lead Poisoning in Young Children. 4/14/09 Centers for Disease Control and Prevention (CDC). Lanphear BP. 4/14/09 Centers for Disease Control and Prevention (CDC). Homa DM. Checkoway H.htm. Muller CH.205:297-308.gov/toxprofiles/tp13. Acquisition and retention of lead by young children. Becker K. 4/14/09 Centers for Disease Control and Prevention (CDC). Leggett RW. Inorganic and Organic Lead Compounds. Brody DJ.1542/peds:2007-3608. Neurodevelopmental effects of postnatal lead exposure at very low levels.gov/mmwr/preview/mmwrhtml/ mm5532a2. 1999-2002. Batuman V.115:521-529. Ganzi A. Aug 2007 [online].275(15):1171-1176. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Aro A.89:330-335. Wager C. Pediatrics 2004. Public Health Rep 2000. 2005. Mantere P. N Engl J Med 2003. Ga.150(6):590-597.

S. Staessen JA. Gunter EW. Exposure of the U.63:1044-1050. Kaufmann R. Revised and new reference values for arsenic. Pizent A. zinc. J Hum Hypertens 1995.140:821-829. Kinetics of lead disposition in humans. et al. Flegal AR. Kidney Int 2003. Payton M. Environ Health Perspect 1996. Gavella M. Telisman S. Soldin SJ.209:301305. Blood lead. dimercaptosuccinic acidchelatable lead. blood pressure. Weiss ST. Paschal DC. JAMA 2003. Pirkle JL. Amery A. Magder L. Lustberg M. Schwartz J. Am J Epidemiol 1994. Lee GS. Clin Chim Acta 2003. Osterloh JD. Schulz D. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Sherwin R. Lead. IV. Arch Environ Health 1995. Environ Health Perspect 1998. and copper in men.104(1):60-66. Toxicol Appl Pharmacol 1993. cadmium. Soldin OP. Use of endogenous. Hickman T. Blood lead concentrations in children: new ranges. Cvitkovic P. Brody DJ. cadmium. Am J Epidemiol 2001. Stewar WF. Int J Hyg Environ Health 2006. Environ Health Perspect 2000. Kaufmann RB. O’Flaherty EJ. Schwartz BS. Fourth National Report on Human Exposure to Environmental Chemicals 217 .327:109-113. Roels H. stable lead isotopes to determine release of lead from the skeleton. Lauwerys RR.106:745-750. Low-level lead exposure and renal function in the Normative Aging Study. Hu H. and tibia lead with neurobehavioral test scores in South Korean lead workers. Lee BK. Rubin R. Jurasovic J.289(12):1523-1531. et al. Wilhelm M. Low-level lead exposure and blood pressure. Sparrow D. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. blood pressure and cardiovascular disease in men. Hanak B. Lee SS. Rocic B.153(5):453464. Physiologically based models for bone-seeking elements. 50:31-37. Hwang KY. Smith DR. and hypertension in perimenopausal and postmenopausal women.108(1):45-53.Metals results from NHANES III.118:16-29. Nash D. Schwenk M. lead. Association of blood lead.9:303-327. population to lead: 1991-1994.

900) 75th 1.40-2.00) 3. which create an episodic potential for volatization and inhalation of mercury vapor.00 (.60 (2.20 (2.70 (1.S. thermometers.. and mining and smelting. to form inorganic mercury compounds or salts. synthetic organomercury compounds were once used in pharmaceutical applications.886) .655-.00) 1. thimerosal.50-1.70) 911 856 2081 4525 03-04 03-04 .20-4.90) 90th 3.S.10) . merbromin). an organic form of mercury.900 (.800-1. Atmospheric elemental mercury can be deposited on land and water..20-4.Metals Mercury CAS No.00) 4. have often required public health intervention (Zeitz et al.2. Poorly absorbed from the gastrointestinal tract.30) 5.80 (1.00) 1..797 (.80 (1.700) .90 (1. Apart from methyl mercury. constitutes the main source of dietary mercury exposure in the general population.919) .30) 1.814 (. see Data Analysis section) for Survey year 03-04 is 0.40-2.90) 3.800 (.70 (1.800-1..372) .00 (2.30 (2...600) 1.30-5.400-.30) 1. 1980. Accidental spills of elemental mercury.700) .979 (.80) 1. or oxygen.500-. solid-waste incineration. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.285-.90) 95th 4. thermostats and switches).30) 3.903) Selected percentiles ( 95% confidence interval) 50th .50-2.781 (. inorganic. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic). The ingestion of methyl mercury.877 (.00 (2.40-1. electrical lamps. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.900) 1.12) .800-1.40) 3. predominantly from fish and other seafood.00 (1.00-5. and mercury compounds are still used as preservatives (e.500-. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.60-5. Survey years 03-04 Geometric mean (95% conf.60) 1. and is distributed to most tissues.500 (. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore. with the highest concentrations occurring in the kidneys (Barregard et al. population from the National Health and Nutrition Examination Survey.40 (4.490 (.700-.70 (4.800-1.g.363-.50-3. elemental mercury is absorbed mainly by inhaling volatilized vapor. and organic forms. Some cosmetic skin creams from countries other than the U. sulfur.700 (.400 (.40 (4.40 (3. Other major uses include electrical equipment (e.60-6.700-.. 1999 . Kingman et al. phenylmercuric acetate) or topical antiseptics (e. mercuric chloride).g. interval) .500 (.90 (1. Woods et al.40-3. sphygmomanometers and barometers. Hursh et al.50) 1.00-1.00 (.40 (3.927) .00 (.419 (. The kinetics of the different forms of mercury vary considerably. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. 1994.00) .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 . such as chlorine (e.00 (2.80) 4.60) 2085 2293 3478 Limit of detection (LOD. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.20-3.10-3.689-.50) 5.60-2.60 (1. 2002). IARC. 2007).703-.30-6.70-2. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.30) 3. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.700-. which can bioaccumulate in aquatic and terrestrial food chains.400-. 1998. After elemental mercury is absorbed.600 (.60) 1.90 (4.80 (3.326 (.60-6.714-. In addition. 218 Fourth National Report on Human Exposure to Environmental Chemicals . Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.472-.300-.02) .g. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).60-3.20) 2.700-. Also.753-1.90-3.500) .800 (.30 (1.800 (.80) 3. 1993).900) .300) .776 (.900) 1.40-1.50) 4.700-.60 (1.484) .800-1.30-4. Elemental mercury is a shiny..900) 1.418-.00 (.50) 2..g.563 (.800 (.30) 4132 4241 03-04 03-04 03-04 .860-1.70 (3.672) . may contain inorganic mercury.30-2.300 (.574) . and dental amalgam.40) 1.80 (1.

944 (.300) .60) 1..700 (. 1993).30 (1.90 (4. Fourth National Report on Human Exposure to Environmental Chemicals 219 .0) 4.S.800) 1.10-3.500-.200-. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.60 (2. with most elimination occurring through in the feces (Sherlock et al.300) .297-..70-3.20-11.40 (1.200-. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury. National Health and Nutrition Examination Survey.256-.800 (.50-2.700 (.800) 75th .400-. 1995..90 (4.00) 4.50) 2. Miettinen et al.90) 90th 1.90) 3.825-1.7) 4. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.20-3.500-1.317 (.30-4. 2003).200-. 1992).23) .318 (.700 (.40) 1.475) .50-3.20-3.300 (.50) 3..500 (.369) 1.20) .919) .50 (2. After exposure to elemental mercury.00) 6.269-.Metals the tissues to mercurous and mercuric inorganic forms.40) 5.700-.824) 1.200 (.800-1.697-..00) 2. population. 1998).3) 4.871-1.70) 4.541-. 1971). 1993).00-6.10-1.800) .500-.300) .30) 1.30) 3..73) 1.268-.664-1.407) .00) .. Excretion occurs by renal and fecal routes.30-2. 1990).00-2.307 (.265-. 1984.200-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.20-2. 1969. 1998).14 and 0.29) .50 (1. thereafter.900 (.30) 1.500-.738-.374) .30-4.70-6. interval) Selected percentiles (95% confidence interval) 50th . 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . Smith et al.90 (3.60 (3.. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.300) ..90 (1.40-2.700 (. Jonsson et al. Suzuki et al. 2004.00 (2..60) 2.60 (1.700-1.60) 3. and a useful marker of exposure in epidemiologic studies (Grandjean et al..377) . 2005). excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al.200-. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al. Geometric mean Survey years (95% conf.27) .30-11..80) 1.20-3.300 (. 1992.700-1. 1996).35 (1.70 (1. 1992 and 1999.. a measure of accumulated dose (Cernichiari et al. 1999-2002.00-3.300 (.700-.40-2.00) 7..00-2.. 1999).00 (1.800-1.70) 1.50) 95th 2. 2003). Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.40-1.300) .500-.60 (1.00 (3.06-1.00-2. 1994).10) .500-.30-3.10) 1.833 (. 1975.80 (3.70) 4.06 (.900 (.01) .10 (3..02 (.70-5.10 (.90) 2.10 (1..60 (1.395) .00) 1.00-1.14.10 (5.800 (.940) Race/ethnicity (females. McDowell et al.60 (3.299-. 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. Sandborgh-Englund et al.80-3.00 (2.300) . Vahter et al. 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.30 (1.20 (.30 (1. Vimy et al.10 (1. 1991.667 (.80 (1. Myers et al.200-. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.40 (1.300 (.800) 1.50) 1. Methyl mercury enters the brain and other tissues (Vahter et al. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.726-1.90) 5.30-5.. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.. 1994) and then undergoes slow dealkylation to inorganic mercury.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 .40) 2.900 (. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.30 (.600) .60) 1.30-6.700) 2..70-5.200 (.50-12.900-1. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.70-3.600 (.20) . and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.329 (.600) .800) .20 (2.800-1.70 (1.10 (.90 (1.820 (.500 (.343 (. 1973).10) .30-6.30-6.800 (. Smith and Farris.00 (2.10 (1.20) 1. 1996..90) 2. for both acute and chronic exposures.50) 1.70 (1.00) 1.377 (. Methyl mercury is incorporated into growing hair. 1994..900-1.80) 579 527 370 436 588 806 Limit of detection (LOD.

700 (. anorexia. ataxia. 2000.600) .. < LOD means less than the limit of detection. 1993). and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. Acute.. Sakamoto et al. cerebellar ataxia.700 (. 1998. The constellation of findings may include anorexia.600) . Inorganic mercury exposure usually occurs by ingestion. 2002.600) . 2004..800) . Smith et al.700 (. DeRouen et al. sensory impairments. the existence of a causal relation is unresolved (Chan and Egeland. 2006. overt signs and symptoms of chronic inhalation may include tremor.600) . Vupputuri et al... 2004. dysarthria. Rissanen et al. and progressive constriction of the visual fields.600 (...600 (.500-. see Data Analysis section) for Survey year 03-04 is 0. and neurocognitive and behavioral disturbances.600) . 2005.600-.600-. 2000. 2000).. 1983). 2004). Smith et al.500-.. Drexler and Schaller.600) . and sleep disturbance (Bidstrup et al. particularly irritability. pain in the extremities.500 (. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas 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 . which may vary for some chemicals by year and by individual sample.700-. dysarthria.. 1995. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.600-. 2004).500 (.500-. 1970. hypertension. Once absorbed. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..600 (.600 (.600) .500-.500-.. depression. 1951.700) .. In recent epidemiologic studies. 2006.. typically after a latent period of weeks to months. Overt poisoning from methyl mercury primarily affects the central nervous system. Bellinger et al...700-. 220 Fourth National Report on Human Exposure to Environmental Chemicals .800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .800) . 1987).500) . maculopapular rash.500-. Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH.42. and cerebral palsy (NRC. 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. and pinkish discoloration of the hands and feet (Tunnessen et al. Stern 2005. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. limb deformities.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. Salonen et al. short-term memory loss.600 (.Metals may be more efficient for inorganic mercury (Grandjean et al.600) .800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .600) .700) 2007 2240 3406 Limit of detection (LOD.500-.700-. 2003). hearing impairment. Factor-Litvak et al. Sakamoto et al.600 (.500 (<LOD-. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 2005).600-. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.. 1995. 1996).700 (. 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. population from the National Health and Nutrition Examination Survey. Rice. insomnia. altered physical growth..700 (.500 (<LOD-. causing parasthesias.500-. 1963).S. gingivitis.600 (. irritability.600 (. At levels below those that cause acute lung injury. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. Oskarsson et al.700 (.500-. fatigue.

200 (. Among the three racial/ethnic groups.epa.700 (.433 (.870-1. 1998).e.S.460 (.476 (. 1995.280-. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.160-.700-1. Biomonitoring Information In the general population.88-3.14) 90th 2. 2003).840-1. 2001.42) 95th 3. Kingman et al. military veterans (mean age 52.34-3.58 µg/L for 4645 adults.S.360 (.416 (.495 (..cdc.405-.46 µg/L for children.39-3.31) 2.420 (. During the same survey periods..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 . 2000).12 (.96 (1.16 (.9 years). In NHANES 19992002.08 (1.13-2..313-.99-6.28) 1.65) 1.840-1. interval) .8 years.33 (2.530) . EPA.770-1. 2001.01 (.330-..52) 2.14.08 (1.840) 1.530-.441 (. the total blood mercury concentration is due mostly to the dietary intake of organic forms..406-. 2003). aged 18 to 69 years.254 (.340-. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity. Information about external exposure (i..509) .382-. 1998). particularly methyl mercury.460) .90) 2. A cohort of 1127 U. Schober et al. These distinctions can help interpret mercury blood levels in people.408) .430 (.76-3.20 (1.. population from the National Health and Nutrition Examination Survey. 2009). et al. total blood mercury increased with age. 2004. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning. total blood mercury geometric mean levels in females aged 16-49 years did not change. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.. Over the NHANES 1999-2006 survey periods. slightly higher total blood mercury levels were found in U.413-.68 (2.870-1.930-1. However.330 (..358 (.213-.330-.atsdr.447 (.440 (.67-2. average age 33 years.480 (. and the age-related changes differed across the groups (Caldwell et al.05) 1.29) 1.96 (1.430) .55 µg/L.66) 3.24) 1.61) 1.26 (1. who participated in a 1998 representative population survey (Becker et al.16 (1. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. EPA at: http://www. 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.05) 3.00) 1...360-.03-4.23) .555) .442-.89) 3.580) .46) 3. Survey years 03-04 Geometric mean (95% conf.85-2. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al. and increased slightly in non-Hispanic white children (Caldwell.24 (2.890 (.18) 2. Benes et al. average age 9. 2009).60) 619 713 1066 Limit of detection (LOD.78 µg/L for adults and 0..492) Selected percentiles ( 95% confidence interval) 50th .330-.54 (2.530) .63-2.250) .549) .19 (1.420 (.534) .09 (2. Sanzo et al.14-2.76-3.400 (.gov/mercury and from ATSDR at: http:// www.509) . 758 children.360-. 2006).610-1.07 (. 1997.396-.19 (2.76-4.93 (1.67-3.570) .Metals standard for inorganic mercury has been established by U.290-.88) 287 722 1529 03-04 03-04 . Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.370) .S.23) 2. Total blood mercury levels increase with greater fish consumption (Dewailly et al.. see Data Analysis section) for Survey year 03-04 is 0.S.304) . Grandjean et al.480) 75th 1. From 1996 through 1998. adult women in several ethnic subgroups (Hightower et al. In Germany the geometric mean for blood mercury was 0.77-2.31) 1266 1272 03-04 03-04 03-04 .88 (1. Fourth National Report on Human Exposure to Environmental Chemicals 221 . although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.97) 2.S.00 (.410-.940 (. environmental levels) and health effects is available from the U.gov/toxprofiles.. 2002).350-. the median concentration of blood mercury was 0. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.520) .960 (.78-2. Mahaffey et al.430 (.30) 3.60 (1. range 40 years to 78 years) had an average total blood mercury concentration of 2.60-2.463) .

486) Selected percentiles ( 95% confidence interval) 50th . and on average.400-. not to imply a safety level for general population exposure. Langworth et al.11) 1.40 (1.455-.455-.225-.18-1.11) 2. Information about the biological exposure indices is provided here for comparison. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.400) .588) .. An expert-panel report recently prepared for the U.. Department of Health and Human Services noted that several studies have observed a modest.784) 1.276 (. 2006).443 (.652) . Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect. 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.64-2.32 (1.46-2.309-.800-1.03) 2. et al.88 (1.376-.307-.714-1.217 (..63) 1.13-2.30) 1.472-. reversible increase in urinary N-acetyl-glucosaminidase.12-3. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al. Levels in U. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.30) 2..39) 1.65 (1.537) .508 (.385-..208-.768 (.587 (.32-2.67 (1.480) ..00) 90th 1.365 (.532 (.404-.79 (1. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.343 (.358) .297 (.391-.384 (.196-.616) . Urine mercury and the number of dental amalgams were correlated.54 (2.255 (. 1998). military veterans with dental amalgams.88-2. Survey years 03-04 Geometric mean (95% conf.620-.07) 1. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.417) . 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.S.464 (.969-1. Urinary mercury levels in recent German (Becker et al.265-.44) 1.535) 1.455) .875-1.04-3.246-.88-2.306 (.87 (1.362 (..87) 2.391) .35 (1. mean urinary mercury was 3.79) 1. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.51-2.463 (.40-1. the urine mercury increased by approximately 0. 2003).687) . 2009).485 (.62 (1.566) .28 (. 2006. 2009).S.447-.964-1.970 (. DeRouen et al.S..56) 1266 1271 03-04 03-04 03-04 .909 (.301-. 1988. et al.78-4.06 (. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects. women of childbearing age have generally been much lower than these levels (CDC.347) .599) .522-.77 (2.280-.368) .09) 1. In the study of U.525 (.275) ..365 (.630) .S.289) .447 (. 1992). Czech (Benes et al..25 (.67 (1. 2002).990) .16) 1.392-. a biomarker of perturbation in renal tubular function.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 .21) 1.1 µg/L. 2002) adult population surveys were similar to those in a U.545 (. and Italian (Apostoli et al.785-1.476 (.06 (.31 (1.86) 95th 2.Metals 2000). interval) .667-1.696 (.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .498) 75th .S.01) 2. 2005).00 (.61) 1.13 (1.1 µg/L for each surface with a dental amalgam (Kingman et al.619-.333-.76 (1. population from the National Health and Nutrition Examination Survey.00) 286 722 1529 03-04 03-04 .11-2.23-2.41-2.

723 (.65) 1.650 (.21 (1.639 (.45-3.656-.41 (1.560-.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .00 (2.99) 1.569-.70 (2.31 (1.94) 1.79) 3.35) .99-2.00) 2.30-2.27-1.59-5.21 (2.27 (2.806) .55-3.00 (3.605-.85-3.691) .870) .810) .526-.10-4.37 (1.50 (2. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.709) .631-. National Health and Nutrition Examination Survey.62 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.582-.3) 5.632 (.52) 3.92) 4.62 (4.565 (.25) 2.966) .41-6.799) .520-.09-1.16) 5.23-1.45 (1.24) 6.45) 2.655 (.475-.69 (1.42) 90th 2.553-.46) 3.450-.32) 2.580-.57-4.79) 1.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.S.833) .65-4.21-3.710) 1.709) 75th 1.502-.07-2.31-1.516 (.650) 1.616-.97) 2.69-3.824) .95 (2.54) 595 531 381 442 594 826 Limit of detection (LOD.92) 2. Geometric mean (95% conf.38) 4.77) 2.410-.522 (.622-. interval) Selected percentiles (95% confidence interval) 50th .53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 . 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U. National Health and Nutrition Examination Survey.636-.97) 2.43-1.83-3.42) 2.22-3.560 (.32-3.55) 90th 3.98 (5.62 (3.16-5.22 (.15-1.14) 3.14.76-5.772 (.61-6.832-1.09-1.47) 1.04-1.10-2.606 (.686) .46 (1.91 (2.774) .14-2.426-.06 (.910) .41 (1.578-.580 (. population.387-.37) 1.28 (1.670) 75th 1.657 (.14-1.68 (3.84 (2.592 (.45) 2. interval) Selected percentiles (95% confidence interval) Survey years 50th .624-.13-4.05 (2.500-.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.13 (2.07) 1.76 (1.56 (1.46-4.92) 3.97 (1.89 (2.930) .77) 1.706 (.831) .664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 . population.721 (.892) .50-4.420-.809) .05 (3.520-.18 (3.740 (.508-.909-1.24-1.91-7.03-2.710 (.699) 1.53-3.710 (.620 (.600 (.831) .99 (2. 16-49 years) 99-00 01-02 .14 and 0.846) .18) 3.61) 1.658 (. 16-49 years) 99-00 01-02 .72) 1.664) .32 (1.39-3.596 (.68) 3.42-3.03 (.03) 1.610-.Metals Urinary Mercury−Females Aged 16-49 Years Old. 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.501-.41 (2.790) .742-1.51) .540 (.87-4.719 (.30 (1.47) 1.S.97) 2.76) 2.557-.45) 95th 3.44) 3.50 (1.56) 4.665) .07-5.68-3.17) 95th 5.48 (2.03 (.27 (1.85) 4.615 (.30 (2.81-6.650 (.84 (2.724 (.23-1. 1999-2002.579-.760 (.30 (2.850-1.56) 3.637) .35 (1.51 (3. Geometric mean Survey years (95% conf.04-10.45-2.540-.744) 1.685 (.81 (3.99 (3. 1999-2002.15 (2.

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Farris FF. Turner MD. Bolger PM. Toxicol Appl Pharmacol 1996. Sinks TH. Amiano P. Whittle K.48(4):221229. Leroux BG. Orr MF. Tunnessen WW. Azpiri MA. Toxicol Appl Pharmacol 1994.40:413-419. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Longnecker MP. Vupputuri S.79:786789. Pediatrics 1987. Allen PV. Am J Physiol 1990. Smith RG. Stern AH. Guo S. Topping G.97(2):195-200.110:129-132. 1999-2000. Am Ind Hyg Assoc J 1970. Imai H. Stern AH. Smith JC. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. et al. Sandler DP.4(5):981-988. Schober SE.289(13):1667-1674. Lind B. Public Health Nutr 2001. JAMA 2003. Daniels JL.98(1):133-142. Friberg L. Leitao JG. Hum Toxicol 1984. Newton G. Environ Health Perspect 2007. McMahon KJ.31:687-700. Smith AE. Hall LL. Woods JS.37:245-252. The kinetics of intravenously administered methyl mercury in man. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. DeRouen TA. Mottet NK. et al. Effects of exposure to mercury in the manufacture of chlorine. Patil LS. Hongo T. Mooney TF. Martin MD. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Aguinagalde FX. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Blood mercury levels in US children and women of childbearing age.258(4 Pt 2):R939-945. Kaye WE.Metals Sanzo JM. Matsuo N. Vimy MJ. Baser M. Methyl mercury pharmacokinetics in man: a reevaluation. Hislop D. McDowell M.115(10):1527-1531. Nakazawa M. Goldberg J. Smith PJ. Most B. Toxicol Appl Pharmacol 1994. Burbacher T. Environ Res 2005. Environ Health Perspect 2002. Environ Res 2005. Shen DD. Suzuki T. Sherlock J. et al. Environ Health Perspect 2003. Yoshinaga J. Zeitz P. 1993-1998. Osterloh J. Vorwald AJ. Jones RL. Acrodynia: exposure to mercury from fluorescent light bulbs. Arch Environ Health 1993.124:221-229. Amurrio A. Effects of occupational exposure to elemental mercury on short term memory. Dorronsoro M. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings.2:117-131. Langolf GD. Br J Ind Med 1983. Lorscheider FL. The contribution of dental amalgam to urinary mercury excretion in children. Fisher HL. Smith JC. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. The hair-organ relationship in mercury concentration in contemporary Japanese.111(12):1465-1470. Bernardo MF. Takahashi Y.128(2):25125-25126. Vahter M. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish.

5-52.2 (56.3 (55.7-51.4 (34.7-105) 69. interval) 45.8.5-91. and paints.6 (40.0 (43. which exert homeostatic regulation over molybdenum balance.2 (83.9 (73.7) 75th 84. Compounds of molybdenum are also used as corrosion inhibitors.3-44.2 (49.7-39. Fourth National Report on Human Exposure to Environmental Chemicals 227 . 1997). More recently.2-91.7 (51.7) 78.3 (38.0-53.8 (42.0) 60.5) 80.7) 77.8) 39.8) 46. inks. 0.0-77.0) 97.7) 46.2-59.2-53.0-101) 82.3 (46. 1996).9 (34.9-55.2) 52.0 (42.5 (48.1-63.7 (73.5-46.8-94.0) 84.7 (71.2) 178 (147-259) 169 (138-197) 138 (127-152) 146 (112-171) 145 (129-159) 118 (105-125) 126 (114-134) 114 (103-124) 105 (98.0-38.8-106) 88.5 (37.1 (38.6-62.4 (79.2 (63.4 (48.0 (48.6 (55.7 (44.9) 62.6-72.1 (91.3) 85.S.0) 54.0) 55. semiconductor and battery industries have begun to use molybdenum.2) 53.6-46. urinary excretion over six days CAS No.5 (67.4) 45.0-65. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.2) 79.1) 35.6 (73.1-59.1 (71. and 1.2) 40.9 (78..0) 39.6) Selected percentiles ( 95% confidence interval) 50th 50.3) 41.5-52.7-50.1) 126 (106-147) 109 (94.7 (37.4-61.3-115) 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. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.5 (74.1) 59.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.5 (81.5 (41.2 (38.4 (80.2) 48. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.3 (47. lubricants.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 52.9-85.1) 46.1) 82.7 (58.3 (55.7 (36. hard metal widely used to add strength and hardness and retard corrosion in metal alloys. aldehyde dehydrogenase.3-47.7-41.3-75.7-96.4) 52. WHO. population from the National Health and Nutrition Examination survey.8) 40.6 (40.9 (44.4) 42.7-73.4) 56.9-56.7) 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 78.9-83.8.5) 47.6) 71.1 (34.3 (84.8 (82.7) 78.5-66.7) 51. 01-02.1-52.8 (67.0-62.4-52.6) 71.0-56.2-59.2) 37.5) 44.0 (42.5 (43.5) 60. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.6) 53.6) 93.5-68.9 (40.7) 45.6 (52.6 (55.6-55.2-79.5 (49.0-100) 63.5) 85.0 (46. At a daily oral molybdenum dose of 24 µg.3 (64.3 (71.2 (69.9-109) 97.9) 67.3 (73.2) 41.8) 44.8-46. and 03-04 are 0.4-82.6-82.2 (49.4) 41.3-91.4) 49.8 (85.9-55. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.7 (50.5-124) 108 (92. 2001. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day. In humans.Metals Molybdenum or ore deposits.2-37.3) 65.9 (32.8-108) 87.7-92.6-96.1-51.9) 34.4) 76.3) 54. and in pigments for ceramics.1-52.0-110) 90.7) 57. see Data Analysis section) for survey years 99-00.3-108) 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 47.5) 80.0) 45.2-70.0 (76.5-41.8-49.7 (45.6) 51.2 (40.0-85.3 (53. respectively.9 (33.1-55.4 (72.0 (81.4 (48.7-91.5.8-90.1) 57.0-71.9-82.1-88. chemical reagents in hospital laboratories.2 (61.8) 48.5-65.7-47.1-48.3 (37.1-44.3) 83.3 (79.6-42.3) 37.5 (41.6-58. 2001). 7439-98-7 General Information Elemental molybdenum is a silver-white.1) 60.9 (52. Excretion occurs predominantly via the kidneys. and xanthine oxidase (Kisker et al.7) 86.9 (37.0) 62.7-84.4-75.7-60.7-122) 93.2-42. hydrogenation catalysts. 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.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.6) 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 (99.2 (55.0 (41.7-68.3) 47.8) 75.6 (43.

2) 42.5 (35.3) 44.6) 36.6-61.3-43.5 (79.3-45.4-106) 85.3 (58.3 (55.9-118) 91.9 (64.3 (51.6-76.1-43.9-41.9-61.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.1 (54. Molybdenum is generally considered to be of low human toxicity.8-52.4) 58.7) 45.2-103) 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 42.5) 73. population from the National Health and Nutrition Examination survey. respectively.2 (40.2-65.6 (36.5) 71. and urinary levels reflect intake from all sources.4) 77.9 (49.4 (67. of the ingested dose (Turnlund et al.7) 53. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5 (39.7-62.5-99. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.2-49.6-63.7-137) 129 (109-155) 112 (97.0 (80.0-46.4) 60.7-38.3-141) 109 (81.4 (56.6 (57. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.8-42. 1997).5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.0) 33.1-41..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 40.6) 43.1-100) 86.7 (30. and clinical or epidemiologic evidence of adverse effects is limited.4) 89.5 (80.1-40.8) 79.5-119) 90.2) 39.9-117) 57.S.4 (37.5 (39.3 (83.Metals was 18% of the ingested dose.3) 41.5 (40. interval) 43.7-44.1-39.0 (35.9 (40.4-118) 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 .9) 92.7) 57.5-70.03 mg/kg/day in humans (IOM.6 (36.8) 71.1) 37. but available epidemiologic data are scant.4-107) 85.5 (34.7) 42.3 (71.6-88.4) 116 (101-126) 104 (88.8-65. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.1 (44.0 (74.1 (33.2) 58.0) 39.7) 41.7) 62.0-38.5-92. 1995)..1-112) 78.6-61. 1961. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.1-34.0-56.3-115) 98. In industry.2-40. 2001).3-56.5-69.7-93.9 (39.1-45.9-96.2) 38.1 (42.1) 40.3) 40.9-87.4 (44.2 (43.3 (36.5 (50.8) 37.5) 63.2-96.5-97.6 (42.1-67.4-76.4-66.7 (66.0) 62.5 (40.0) 53.1 (40.8-66.2 (36.7-40.3 (37.8) 45.1) 101 (83.0) 72.0) 88.0-103) 103 (90.9) 79.4) 44.5 (83.2) 39.1-79.8) 38.6) 48.6-45.5) 90th 108 (97.4) 40.4-185) 106 (94.1-39.3-46.3) 61.9-45.5 (59.4 (55.5 (35. Based on studies finding adverse reproductive effects in rats and mice.5) 72.1-109) 89.2-47.7-100) 77.3) 57.8 (56.0-133) 119 (88.3) 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 85.1 (38. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.1-43.8) 62. at daily oral doses of 95 µg and 428 µg.6) 39.8-67.5 (36.1-81.2-121) 107 (92.2-46.3 (71.5 (65.6) Selected percentiles ( 95% confidence interval) 50th 41.5-46.0) 38.8) 38.2-96.5 (78.6 (71.5 (65.1 (39.7) 75th 63.1) 43.5-50.5 (38.9 (64.6-41.0) 36.1 (38.4) 122 (107-133) 109 (99. Biomonitoring Information Molybdenum is an essential element for health.4-39.2 (52.9) 44.2 (40.9-40.9-71.7) 112 (95.0-46.6) 39.1) 37.2-80.6-63.4-42.8 (36.8 (57.1 (82.0 (58.1) 56.2 (50.8 (75. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9 (36.3-52.8 (90.9) 40.9 mg/kg/day and established a tolerable upper intake level of 0.2) 55.1 (30.2) 37.4-120) 101 (84.4 (78.2 (57.5 (37.3 (36.0) 39.7 (75.4 (59.4 (53.8-46.1-38.9 (35.2) 43.7 (77.2) 42.6 (38.2 (33.1) 65.S.9-45..7-43.2 (37.5-62.5-48. 1999).5-35.0-120) 85.1-127) 90.4-41.0) 44.7) 115 (93. 1993).8) 39.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.7-52. U.8 (37.9 (39.4) 61.5 (41.1 (37.4) 48.3) 64.5 (54.2 (73.3) 56.3-59.0-41. EPA.2) 37.7-120) 87.4 (40.8-118) 81.5-44.2 (69.8-47.5 (37.3 (37.5-60. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.3) 37.9 (73.8-47.3-44.6 (59.2 (40.1 (49.3-68.9-68.9-42.8-84.9) 41.8) 61. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.6-78.2-41.3 (53.5 (41.9 (79.5) 60.9) 31.3) 43.4) 47.5-45. urinary excretion over six days rose to 50% and 67%.

cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. boron. 420-441. 4/14/09 Sievers E. Molybdenum-cofactorcontaining enzymes: structure and mechanism. Sci Total Environ 1998. Weyler JJ. Available at URL: http://www. Ann Rev Biochem 1997. Peiffer GL. Dietary reference intakes for vitamin A. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Sabbioni E. White MA.niehs. 2001. Molybdenum. pp.Metals in urine for the U. nickel.gov/iris/ subst/0425.gov/index. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. White and Sabbioni. Geneva: WHO. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect..S. A study of 13 elements in blood and urine of a United Kingdom population. 2002. and zinc: a report of the Panel on Micronutrients.66:233-267. Keyes WR. Institute of Medicine (IOM). 2001).S. Washington. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al.. 1998. Van Meerbeeck JP. manganese. 56:322-327. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. J Trace Elem Med Biol 2001. Occup Environ Med 1999. Sciarra G. Rees DC. Yarovaya GA. 1996. Kristiansen J.15(2-3):149-154. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Turnlund JR. 4/14/09 White MA. Zhurnal Obshchey Biologii 1961. Menne C. chromium. Available at URL: http://ntp. Ronchi A. iron. Trace element reference values in tissues from inhabitants of the European Union. Occupational risk factors of lung cancer: a hospital based case-control study. Molybdenum in infancy: methodical investigation of urinary excretion. 144-154. 2005. Schaub J. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. iodine.S. (DC): National Academy Press. copper. Food and Nutrition Board. Vermeire PA. excretion. Molybdenum absorption. Droste JHJ. arsenic. et al. Gatti A. Biomonitoring studies on levels of molybdenum can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of molybdenum than are found in the general population. silicon. Environmental Protection Agency (U. van Sprundel MP. Schleyerbach U. Kisker C. References Centers for Disease Control and Prevention (CDC). Minoia C. X.. Shmavonyan DM. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. U. Koval’skiy GA. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. Minoia et al. Available at URL: http://books.123(1):81-85. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al.nap. Analyst 1998. Atlanta (GA). 1998). National Toxicology Program (NTP). Christensen JM.php?record_id=10026&page=420. In: Trace elements in human nutrition and health. Molybdenum 1993 [online]. Aprea C. pp. vanadium.22(3):179-191. Turci R. Sabbioni E.216:253-270.nih. Fourth National Report on Human Exposure to Environmental Chemicals 229 .htm. 4/14/09 Iversen BS. 2005). vitamin K.62(4):790-796. Rapid Comm Mass Spectrom 2002. Schindelin H. edu/openbook. TR-462. Am J Clin Nutr 1995. 16:1313-1319. EPA). World Health Organization (WHO). molybdenum.epa. Third National Report on Human Exposure to Environmental Chemicals. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC.

Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. see Data Analysis section) for Survey years 99-00. however.. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. dental alloys. and iron. which may vary for some chemicals by year and by individual sample.04. and as drugs (e. population from the National Health and Nutrition Examination Survey. 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. 01-02. carboplatin) in the treatment of cancer. 230 Fourth National Report on Human Exposure to Environmental Chemicals .. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. 0.04. jewelry. and high catalytic activity. and 0. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. Important properties of platinum are resistance to corrosion. strength at high temperatures. < LOD means less than the limit of detection.S. thick-film circuits printed on ceramic substrates. copper.g. 7440-06-4 General Information Platinum is a silver-gray. Platinum compounds are used in electrodes. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Metals Platinum CAS No. 1998). and 03-04 are 0. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. cisplatin. 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. as oxidation catalysts in chemical manufacturing. respectively.07.

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

Urinary excretion of platinum from platinum-industry workers. Hall L. osmium. Neuendorf J. palladium. Fruhmann G. Petrucci F. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Cohrssen B. Several studies have shown that background concentrations in general populations were usually less than 0.inchem. Seifert B. van de Weyer C. Ruff F: Histamine release by sodium cholorplatinate. 2003. Huber R. Fries HG. References Becker K. Platinum concentrations in urban road dust and soil.005 µg/L (Iavicoli et al. Gromiec JP. Saindelle A. Kavanagh P. and in blood and urine in the United Kingdom. eds. Schierl et al. Biomarkers 1999.org/documents/ehc/ehc/ehc125.. rhodium.123(3):451-454. Schulz C. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Saindelle A. Raab W. Hysell D. 3/31/08 Moore W Jr. Influences on human internal exposure to environmental platinum. et al. 2003). Int Arch Occup Environ Health 1997. Herr et al. Iavicoli I. Alimonti A. Hysell D. Turfeld M. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. 289-380. Herr et al. 1998).13(1):24-30.htm. Patty’s Toxicology. Boos KS. Thornton I. Analyst 1998. Allergy and histamine release due to some platinum salts.76(1):5-10. 206:15-24. Pethran et al. Biomonitoring of traffic police officers exposed to airborne platinum. Schierl R. Seiwert M. Pethran A. Wilhelm M. Occup Environ Med 1998.35:313-321. Ewers U. Bocca B. and platinum. Nowak D. Jankofsky M. Senofonte O. Duneman L:Long-term urinary platinum. Begerow J. International Programme on Chemical Safety (IPCS). 1999.. population were below the limit of detection (0.inchem. Czerczak S. 2000. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. 2004). Wilhelm et al. Powell CH.Metals the International Programme on Chemical Safety at http:// www. Parrot JL. 5th ed. Int J Hyg Environ Health 2004. Arch Environ Health:1969. 2001). Environmental Health Criteria 125. Herr CE.. Ruff F: Platinum and platinosis.55(2):138-140. Levels of platinum in urine for the U. 2003. Environ Health Perspect 1975b. Farago ME. 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. Crocker W.. et al.19:685-691. Br J Pharmacol 1969. Arch Environ Health 2001. In: Bingham E. Schulz C. Schierl R. Kulka U.. Blanks R. Hebert R. and gold excretion of patients after insertion of noble-metal dental alloys. Grimm CH. Angerer J. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Pethran A. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect.. pp. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. 1998). Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine.70(3):205-208. Urinary platinum levels associated with dental gold alloys. ruthenium. Occup Environ Med 2004. Nickel. Environ Res 1975a.207(1):69-73. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. Campbell K. which elevate urinary platinum by five to twelve-fold (Begerow et al. Kaus S..S.4(1):27-36.. Kelly J. J Expo Anal Environ Epidemiol 2003. 2004) or less than 0. Ensslin AS. et al. Int Arch Occup Environ Health 2003. Moore W Jr.01 µg/L (Becker et al. Stilianakis NI.9:152-158. Kazantzis G. Gieler U.04 µg/L) in this Report. International Journal of Hygiene and Environmental Health 2003. et al. Part 1: monitoring of urinary concentrations. Platinum.htm. 1997.. Hauff K. Available at URL: http://www. 2003.. Biomonitoring Information Urinary platinum levels reflect recent exposure. palladium.org/documents/ehc/ehc/ ehc125. 1991 [online].61(7):636-9. 2004. Kuster W. Schierl R.. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Rommelt H. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. New York: John Wiley & Sons. Uptake of antineoplastic agents in pharmacy and hospital personnel.10:63-71. Carelli G. Schierl. 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.56(3):283-286. Schierl R.

330) .400) .170-.190 (.330-.173) . representing distribution into other tissues.410 (.220-.160-.217 (.410-.220 (.430 (.300) .175) .280-.490 (.171 (.480) .320) .360) .460) .178) .200-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.270 (.640) .320) .400-.590) .500) .420) .340-.270-.02.500 (.340 (.173) .260) .210 (.220 (.410-.190 (.S.430 (.410-.260-.135-.350 (.215) .390-.480) .190 (.400) 95th .240) . 2005).160-.153-.400) .370-.218) .550 (.240-.410 (.250-.300 (.290 (.480) .250-.210 (.250-.290) 90th .200) .230-.350-.170 (.380-.360 (.202) .200 (.440 (.184 (.510) .188) .420-.370 (.370-.360 (.380 (.147-.200 (.370 (.340-.210-.590) .560) .290 (.280) .420-.520) . respectively.176 (.430) .200-.220) .300) .172 (.280 (.290) .165 (.260 (.260-.230-.290-.159 (.162-.390) .180 (.185 (.149 (.400 (.134-.270 (.410-.260-.200) .147-.180-.470) .400 (.450 (.179-.196) .190 (.390) .230) . 01-02.220 (.145 (.440) .310 (.330-.250-.340-.440 (. In the United States.310 (.180) .181-.150-.167-.200-.200 (.160-.145-.197-.500) .173-.144 (. population from the National Health and Nutrition Examination Survey.270 (.330-.420-.440) .500) .460-. it has not been specifically mined or refined in the United States since 1984.250-.370-.202 (.310 (. thallium readily crosses the placenta and also distributes into breast milk.280) .340) .190 (.260 (. thallium was obtained as a by-product of smelting other metals.370 (.180-.190 (.200) . and 03-04 are 0.200) .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 .218) .330) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.330) .180) 75th .400-. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.360-.163) .320-.410) .280 (.420-.360 (.450 (.200-.201 (.350-.360-. however.200 (.350 (.520) .520 (.200 (.420) .220) .220) . thallium has been restricted from use in rodenticides and Urinary Thallium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.370-.239) . and 0.350-.440 (.440) .290-.187-.370) .147-.450 (.490) .185-.160 (.360-.196) .490) .400) . In the past.470) .180 (.420) .430 (.220 (.158) .190-.350-. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.157-.280-. the latter being the current major industrial consumer of thallium in this country. Thallium disappears from the blood with a half-life of several days.430-.410 (.350-.170) .240) .290) .290 (.230-.159 (.460 (.260 (.183) .350) .250 (.490) .410-.320 (.370 (.370) .410 (.330-.177) .167 (.420) .250-.370 (.520) .170-.260-.154-.170-.220) .390) .260-.160 (. interval) .690) .430) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .510 (.160 (.300) .430 (.240-.390 (.270) . It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.150-.145-.380) .450 (.243) .230) .320) .330-.230) .400-.170) .450 (.159 (.270-.230 (.430-.470) .140-.170-.350) .280 (.470 (.450 (.167-.02.170-.170-.200) .270) .410 (.200 (.450 (.420) .430-.390) .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 .220) .270-.220) .330) .480) .290) .390-.420 (.180 (.217) .172 (.240-.310-.400-. From these and other sources.400 (.490) Total .350-.400 (.250) .148-.155 (.400 (.Metals Thallium depilatory cosmetics. In addition.210) .450 (.160-.300 (.180-.156) .170-.183) .380 (.330-.360-.240) .290 (.340) .150-.182-.330-.02.170 (.150-.202 (.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.150-.300) .225) . thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.180-.250 (.370 (. Human health effects from thallium at low environmental CAS No.170 (.380-.410 (.300 (.410-..400-.201 (.250-.420) .191 (.290 (.133-.156-.230) .280) .160 (.197 (.360 (.270 (.450) .150-.390-.290) .206) .390-.290 (.370 (.480) . 0.200) .450 (.160-.440-.220 (.390 (.270 (.137-.310) .192) Selected percentiles ( 95% confidence interval) 50th .146 (.340-.420) .300-.250-.630) .440 (.470 (. see Data Analysis section) for Survey years 99-00.172) .170) .400) .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 .160 (.360-.156) .

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

1992 [online]. Trace element reference values in tissues from inhabitants of the European Union. A study of 13 elements in blood and urine of a United Kingdom population. Cassot G. White and Sabbioni. Challeton-de Vathaire C.html. 1990. Centers for Disease Control and Prevention. Paschal et al. References Agency for Toxic Substances and Disease Registry (ATSDR). Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L.. Int Arch Occup Environ Health 1980. Sci Total Environ 1998. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Jackson RJ. et al. Gallorini M. Boisson P. 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. Martin J-C. Investigations of thallium-exposed workers in cement factories. Valentin H. with concentrations ranging up to 76. Marcus RL. 2005. blood. Ting BG. et al. X.1 mg/m3 (Marcus. Trace element reference values in tissues from inhabitants of the European community I. Brockhaus et al. Pietra R. Schaller KH. Minoia C. Schaller et al. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Wiegand H. Brockhaus A. 7/15/09 Blanchardon E. Sci Total Environ 1990. Sabbioni E. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Available at URL: http://www. A study of 46 elements in urine.S.cdc. (1981) studied 1. Trace metals in urine of United States residents: reference range concentrations. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Schmidt M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Kramer U. Fourth National Report on Human Exposure to Environmental Chemicals 235 . Apostoli P.gov/toxprofiles/tp54. Third National Report on Human Exposure to Environmental Chemicals. and serum of Italian subjects. White MA. 1981. Raithel HJ.35(1):4-9.. Buhlmeyer G. Pozzoli L. 1980. Morrow JC.113(1):47-53. J Soc Occup Med 1985.95:89-105. 1985). Sampson EJ. Sabbioni E. et al. Ewers U. Atlanta (GA).265 people living near a thallium-emitting cement plant in Germany. 2005) and are shown with results from NHANES 2003-2004 in this Report.48(4):375-389.76(1):53-59.5 μg/L. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Int Arch Occup Environ Health 1981. Manke G. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Paschal DC. Pirkle JL. Minoia et al.. Soddemann H. Toxicological profile for thallium. 2005. 1998)..Metals (CDC. Investigation of a working population exposed to thallium.47(3):223-231. 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. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Celier D.216:253-270. Environ Res 1998. Dolger R. Radiat Prot Dosim.atsdr.

110) .069) .105 (. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.090-.810) .450-.082 (.370 (.160) .180) .060-.092) .180-.080 (.360-.250) .120-.070) .510 (.110 (.500 (. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.190-.087) .107 (.150 (. and 03-04 are 0.260 (.460) .071 (.084-.400 (.090 (.120) .560 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.270 (.056-.090-. Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.100) .380 (.070-.116) .062 (.320) .580) .280-.670) .100) .430 (. see Data Analysis section) for Survey years 99-00.160 (.090) .180-.300 (.180) .300 (.130) .220) .360) .500) .260-.220-.080) .590) .120) .560) .180 (.150-.078-.380 (. respectively.120 (.050-.830) .320-.530 (.090-.123-.270-.130-.140) 90th .460 (.350) .250) .310-.070-.800) .130-.120-.220) .068) . which are used in rock drills and metal-cutting tools.410-.170) .130-.090-.290-.073-.240-.060-.090) .280 (.550) .210) .096 (.110-.290-.095-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.100-.350) .00) .069-.290) .210 (.790) .126) .090-.330-.510-.210-.070-.110) .080) .050-.137 (.380-.160-.170-.160-.270 (.360 (.430 (. Little information is available on the toxicity of tungsten.S.400) . mainly as scheelite (CaWO4).550) .071-.170) .380-.320-.090) .320 (.060-.450 (.170 (.300-.53) .110-.135) . Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.064-.180-.100 (.090) .390 (.060-. population from the National Health and Nutrition Examination Survey.620 (.230) .650) .133) .270-.370) .620) .180 (.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 .060 (.150 (.060 (.092 (.490) .090 (.120) .530 (.200-.170) .110 (.310) .410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.140 (.460 (.088) .170) .430-.800) .400-. Tungsten is used mainly for producing hard metals.640 (. 01-02.340-.070 (.111-.270 (. Tungsten compounds are used as lubricating agents.080 (.120) .190 (.520) .04.060 (.380-.060-.230) . which is used in the steel industry.130) .480) Total .080) .109) .074-.180-.320 (.130-.390) .230-.101-.300 (.190 (.360-.100) .097-.260) .082 (.210 (.080-.310 (.160) .070-. and 0.250-.080 (.560) .080-.060-.060 (.122) .560) .400 (.440) .084) .120-.073) .130 (.082) .210 (.095-.370-.950) .160-.100 (.430-.250) .070 (.370 (.520) .420-.240 (.080-.110 (.130) .082-.160 (.130) .490 (.470 (.470-.310-.460) .380-.100) .132) .093 (.280 (.065-.090-.056-.470 (.260 (.140 (.430 (.470) .310-.120) .630) .110 (. bronzes in pigments. 0.050-.065 (.690) .090-.204) .160 (.100) Selected percentiles ( 95% confidence interval) 50th .210 (.070) . and as catalysts in the petroleum industry.158 (.Metals Tungsten CAS No.380) .100 (.310-.350-1.160 (.290-.330) .180) .510-1.220) .080 (.080) 75th .500 (.220 (.140 (. filaments for incandescent lamps. interval) .270-.370 (.151) .290 (.120-.340) .160-.340-.060 (.350 (.130 (.340-.250-.150) .310-.190-.096-. 236 Fourth National Report on Human Exposure to Environmental Chemicals .140 (.160 (.190) .300) 95th .530 (.570 (.113 (.066-.104) .050-.090 (.620) .091) . and for producing ferrotungsten.110-.550) .070 (.100-.073 (.113 (.400 (.330 (.190-.210 (.04.081 (.093-.073-. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).190-.105) .560) .250) .230-.260-.370-.086 (.062 (.270-.058-.520) .092 (.120-.770 (.460 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.250) .088 (.230-.087-.140-.084 (.076 (.120-.120) .260-.410 (.100) .180) .100-. Evidence is lacking for the carcinogenicity of tungsten.360 (.300) .230-.360 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.350) .110 (.077-.250) .093) .420-.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 .070) .130) .101 (.060 (.070-.430) .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 .570 (.290) .113 (.470) .140-.330) .113 (.400 (.150 (.550 (.070) .04.170 (.090-.330-.200 (.200) .100 (.230 (.076 (.080 (.

116) .339 (.109-.130-.062 (.167) .057-.056-.301) .075 (.216 (.130 (.065-. interval) .727) .279 (.061-.233-.293 (.158) .074-.069-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.108) .279 (.211 (.120) .071 (.065-.089 (.176-.216-.082) .360 (.317 (.078 (.148 (.121-.179-.301) .267) .133) 90th .065 (.198-.200-.255 (.180-.075) .439) Total . (1987) found possibly due to methodologic.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 .145 (.300) .333 (.426) .084) . 1997).081 (.333-.315-.070 (.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 .150 (.237-.095) Selected percentiles ( 95% confidence interval) 50th .161) .214-.098-.329 (.098-.079) .306) .103-.412 (.300 (.482 (.074-.181 (.250-.157) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.111 (.272-.084 (.067-.231 (.200-.174 (.353 (.158) .109 (.067 (. 2001).059-.060 (.116 (.067 (. Patients with medically-inserted tungsten found at increased levels in drinking water.117) .061-..153) .073 (.797) .275 (.119 (.072 (.341 (.253-.302-.124-.146 (.364 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.484) .059-. population.231-. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U..094) .086) .392) .203-. Nicolaou et al.300-.136-. 2003.333-.188-.358) .086) .146 (.253) 95th .086-.431) .060-.088) .258 (.082 (.347 (.359 (.164 (.077) .100) .081 (.065-.054-.073 (. population (CDC.055-.283) .148) .064-.139 (.383 (.074) 75th .255-.073 (.070 (.216-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.077) .121 (.080 (.091 (.197-.085) . population from the National Health and Nutrition Examination Survey.331-.093) .301) .245-.167-.167) .081-.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 .120) .465) .092) .088) .375) .176-.078) .217-.072-.074) .091) . Using neutron activation analysis to 2000.538) .453) .090-.201) . 2001-2002.333) .190) .187) .353 (.497 (.083) .122-.073 (.059 (.084) .068 (.080-.287) .061-.197 (.071) .208-.136-. or exposure that a control group of non-metal workers had mean levels differences. measure urinary tungsten.605) .158) .124 (.250 (. 1998).119-.214) .484 (.150-.308) .205-. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.144-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.S.168 (.169) .197) .063 (.436) .091) .152-.823) .174) .344-.197) .317) .107-.075-.136-.065 (.206-.069 (.267-.146) .138) .090-.431) .079 (.381) .167-.117 (.082) .237) .075) .108-.131-..098-.265 (.085-.179-.122-.091) .217-.063-.072-.087 (.170-.066 (.071 (.083 (.354-.340 (.224) .071) .410-.216-.054-.270 (.634 (.150-.218 (.286-.071-.084 (.155-.091) .079) .059-.077-.199 (.063 (.098 (.058-.057-.582) .880) .462) .28) .739) .064-.069 (.125 (.144 (.222) .138 (.105 (.125) .237) .136 (.S.317-. 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.333) .253 (.126-.080 (.153-.184 (.439 (.326) .049-.093-.199 (.186 (.122 (.(Kraus et al.465) .075 (.240-.169 (. similar to those in this Report (Schramel et al.216 (.077-.379 (.143-.094-.105 (.078) .068-.333 (.099-.083-.308) .554) .555 (.154) .201 (.198) .063-.086) .053-.066 (.074 (.143 (.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 .080-.079) .258-.081) .667) .300-.087) .056-.S.431) .104-.151 (. and 2003-2004 (Paschal et al.079 (.078-. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.071) .215) .255 (.060-.436-1.329-. 2005).386) .261-.133) .215 (.285) .100 (.158 (.075-.065) .278-.333 (.294 (.414) .063-.333 (.426) .078 (.133) .136-.299 (.452-.439 (.116-.459) .083) .139-.284) .165) .385 (.106 (.154) .359 (.500) .250 (.085 (.667 (.063-.222-.139) .089) .100) .096) .094) .083 (.071 (.209-.095-.138 (.302-.098) .354) .279 (.079) .091 (.339 (.

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

038) . In workplaces that involve uranium mining.024-.011) .008 (.037-.008-.035) .006-.008) .158) . Fourth National Report on Human Exposure to Environmental Chemicals 239 . including nuclear weapons.013 (.020-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.013 (.008 (. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).007) .023) .018) .036-.023 (.009) Selected percentiles ( 95% confidence interval) 50th .009 (.008 (.049) .008) .027-.040-.031-. Depleted uranium (DU) refers to uranium in which the proportions of 235U and 234U isotopes have been reduced compared with the proportion in natural uranium.056) .010 (.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.067) .019-.008-.067) .008 (.015 (.006-.034-.008) .007-.006-.006 (.022) .012-. Thus.014 (.013-.Metals Uranium CAS No.017) .012-.014 (.036 (.127) .012) .023-.013-.053 (.007-.037) .006-.023) .017-.039-.018) .010) .019-.009-.041 (.016-.026 (.020-.005-.037) .054) .017-. Since the 1990’s.015 (.007) 75th .114 (. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.031 (. 01-02.013) .027 (.020) . interval) . see Data Analysis section) for Survey years 99-00.006 (.030) .016) .013 (.011-.009) .009) .012) .018) .024 (.045) .017-.023) .033-.009-.014 (.020) .017-.007-.72%).041 (.073) .012-.009-.052 (.026) .013) 90th . human exposure occurs primarily by inhaling dust and other small particles.021 (.054) .016 (.008-.030 (.007 (.024-.056) .010 (.011) .034-. Variable concentrations of uranium occur naturally in drinking water sources.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 .023 (.043) .006-.040 (.021) .031 (.009-.006-.027) .023 (.048 (.010-.009) .016) .007 (.016-.026) .015 (.008 (. respectively.016) .007-.030-.007-.007 (.046) .007-.046 (.060 (.022-.008-.009) .011-.021) .028 (.013 (.007-.007-.008-.021 (.010-.066) .008) .027 (.036 (.018 (.023-.050) .021) .022-.027) .069) .018-.004.009-.053) .004. 235U (about 0.039) .036-.009) .047 (.017) .021-. DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.054-.026) 95th .008 (.010-.043 (.008 (.018) .009) .008) Sample size 2464 2690 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .006-.019-.036) . population from the National Health and Nutrition Examination Survey.055 (.017) . and as an aid in electron microscopy and photography.017) .005-.026-.007 (.022-.020-.013-.007-.012 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.015) .009) .015 (.021 (.011 (.020-.029 (.031 (.064 (.010 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.040 (.009-.008 (.010) * .006-.011) .037 (.010 (.006-.046-.012 (.012-.016-.008 (.046 (.008-.027 (.063) .008 (.012 (.009 (.028 (.005.017-.040) .019-.007-.012-.011 (.029-.031 (.027) .015-.034) .011-.016) .015) .008) .014 (.009) .009 (.007) .007 (.030 (.029-.010 (.027-.020 (.033 (.011-.006 (.050) .007) . 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.009 (.028 (. Uranium has many commercial uses.005-.010-.046 (.011) .048) .006-.014 (.033) .009 (.006 (.038 (.042) .027) .008 (.013 (.012 (.045) .009-.009 (.026-.007-.010) .072) .009) .026 (.030 (.009) .009) .028-.007 (.042 (.012 (.023-.009 (.033 (.035-.005-.007-.006-.007) .009-. or processing.016) .010) .065) .023-.009-.026 (.010-.037) .017 (.020-.032 (.016) .009) * .009-.012-. nuclear fuel.006-.011-.007 (.022 (.025-.010) .007-.009) .039) .028-.062) .008 (.009 (. 0.010) .011) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.046 (.007 (.010-.040-.012) . in some ceramics.010) * .008 (.017) .008 (. and 0.051) .019 (.024-.007-.008 (.008 (.011-.011) .038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .010) .011) .035) .027-.037) Total .044 (.007-.013 (.027 (.008-.010) .007 (.014 (.007 (.021-.010) .005-.017 (. milling.008-.007-. and 03-04 are 0.006-.040) .031 (. and 234U.088) .012 (.049) .279) .008 (.011-.012) .009 (.007) .036) .S.007-.065) .007-.017-.013 (.009 (.007 (.018 (.009) .

080) .014) .024) .006) .007-.015-.008 (.053) .013) .006) .009) .042) .016 (.021-.006-.017-.013 (.045 (.008-.048) .018 (.027 (.011 (.039) Total .012) .008) .012 (.024) .012 (.027-.022-.017) .009 (.010-.039) .014 (. 0.024-.019) .016-.027 (.010-.051) .007-. After inhalation.008-.010-.006-.008 (.008) .010-.016) .034 (.019 (.022) . population from the National Health and Nutrition Examination Survey.019-.018-.009 (.016) .041) .029 (.019) .028) . Depending upon the specific compound and solubility.010-.020 (.020 (.007 (.025-.050) .005-.024-.008 (. After exposure to soluble uranium salts.013) .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 .009) .009 (.006 (.023-.008) 75th .007 (.007-.007-.007 (.029) .007 (.006-. 2003).006-.030) .029 (.012 (.028 (.024) .025) 95th .007) .009-.012 (.007 (.007-.016-.033 (.008-.007 (. 2005).005 (.015-.007 (.027-. Uranium is eliminated in feces and urine.008-. liver.013 (.006-.025-.004-.019-.028) .006-. the shrapnel acts as a source of chronic.006) .018-.013 (. interval) .021 (.006-.007-.031 (.024 (.019 (.010 (. 240 Fourth National Report on Human Exposure to Environmental Chemicals .007 (.014) .027) .020-.040 (.051) . and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.025 (.014) .010) .058) .028 (.016) .018-.009) .013) .010) .006) .006-.037 (.054) .077) .008-.014-.051 (.034) .010-.006-.009-.010 (.051) .007 (. Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.035 (.Metals impact.028) .048) . Health effects from uranium exposure result from chemical toxicity to the kidney.024 (.013 (.012 (.008) . Radiation risks from exposure to natural uranium are very low.028) .011-.010-.034 (.007) .063) .013 (. about 50% of the absorbed dose is eliminated in the urine within the first 24 hours.015) .008) .034 (.006 (.042-.007 (.008) . the initial half-life of uranium is about 15 days (Bhattacharyya et al.006 (.015 (.009-.032) .067) .006-.008) .019 (. low level exposure. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.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-.005-.013 (.012) .020-.010-.017) .015-.016) .027-.012 (.022 (.146) .033) . In cases of retained DU shrapnel.016-.050 (.042) .010 (.013 (.011-.021 (.015-..007 (.020-.016) .009 (.007-.008-.007-.007-.008 (.021) .058) .005-.008) .022 (.015 (.017 (.013-.008 (.008) .015 (.026 (.025-.008 (.029) .059 (.010-.024) .034 (.012-.011-.011 (. 1992).030 (.029 (.011-.009) * .007 (.004-.022 (.027) .015) .061) .006) .039) .010) .1%-6% of an ingested dose may be absorbed.033 (.044) .007 (.053) .011-.026) . Inhaled uranium-containing particles are retained in the lungs.008) Sample size 2464 2689 2557 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .006-.009) .025-.006-.020) .011-.020 (. which represents distribution and excretion.012-.013 (.010-.026 (.024) .009) .034-.021 (. After long term or repeated exposure.008) .028-.006 (.038) 340 368 289 719 762 725 1405 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .008) .009) Selected percentiles ( 95% confidence interval) 50th .056) .018-.030-.011) .034-.008 (.006-.043 (.026 (..015) .011) .011) * .006-.019-.029) .008) .006-.017-.006-.039) .047) .006-.006-.035 (. where limited absorption occurs (less than 5%).013 (.015) .005 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.033 (.010) .010 (.014 (. with much slower elimination from bone.012) .016) .016-.010-.016) .007 (.006-.007 (..018-.005-.007 (.020-.032) .005-.019-.005 (.011) .017) . kidneys.007 (.008 (.011-.007 (.030) .007-.024 (.008 (.030 (.010) .017 (.014) 90th .005-.027-.S.005 (.006 (.006-.009 (.009) .007 (.009) .010) .009) .100 (.021 (.007 (.017-.009-.074) .005-.011-.270) .007 (.009) .012 (.010 (.006-.006-.031-. 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.008 (.022-.015-.006-.030-.022-. which can occur occasionally from high occupational exposure.026-.015 (.009-.033 (.024-.007) .018) .013 (.009) .034 (.011-.010) * .027 (. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.016) .017-.006-.029) .025 (.050) .014-.019-.006 (.030 (.009) .009-.

Fourth National Report on Human Exposure to Environmental Chemicals 241 . the geometric mean urinary uranium concentration was 0. 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. Ejnik JW.62:562-566. and 2003-2004 (Dang et al. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Tolmachev et al.S. Zimmerman I. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. 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.. 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. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU.168(8):600-605.78:143-146. Dang HS. pp. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect.65 μg/L). McDiarmid M. Information about external exposure (i.. Centers for Disease Control and Prevention (CDC). Kent (England): Nuclear Technology Publishing. Squibb K. 2004). Hamilton MM. 2001-2002. Muggenburg BA. 1991.. Stradling GN. Health Phys 2000.110 to 45 μg/L (Ejnik et al. EPA. Radiation protection dosimetry. urinary levels of uranium were as high as 9. Mil Med 2003. had a mean urinary uranium concentration of 0. McDiarmid et al. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. Pillai KC. although slightly increased during and after deployment. Volf V. respectively.1996. et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.S. Breitenstein BD. Thomas RG.. 2004). 28 soldiers who may have been exposed to DU by inhalation. 2006). 2004). Determining the normal concentration of uranium in urine and application of the data to its biokinetics. 2006). Benedik L. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. Vol. In the same study. 1994. or wound contamination. during. In a study of 105 persons exposed to natural uranium in well water. Dietz LA.. in that the levels were below their respective detection limits (Byrne et al. In 17 U. Third National Report on Human Exposure to Environmental Chemicals. NRC. 2000).html.Metals injury associated with elevated urinary uranium levels (Kurttio et al. eds. 2002.162 μg/L) (Orloff et al.. but in whom no shrapnel was embedded. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis.S. ingestion. 2003. Byrne AR.011 μg/L (McDiarmid et al. soldiers evaluated before.. 1-49.55 μg/L (median 0. 2006). Guidebook for the treatment of accidental internal radionuclide contamination of workers.atsdr. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. environmental levels) and health effects is available from ATSDR at: http://www.. In two studies of a Finnish population with high natural uranium concentrations in their drinking water.61 μg/g creatinine. Carmichael AJ.. 2004). Durakovic A. A cohort of 46 U.. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U.. 2006). 41 (1). In: Gerber GB. 1992. 2002). The U. Metivier H. soldiers who had been injured and had embedded DU shrapnel for as long as eight years.S. Six workers in a depleted uranium program showed concentrations of 0. Estimate of the time zero lung burden of depleted uranium in Persian Gulf War veterans by the 24-hour urinary excretion and exponential decay analysis..078 μg/L (ranging up to 5. Pullat VR.gov/ toxpro2.e. Karpas et al.. population. Sci Total Environ 1991. Atlanta (GA). IARC and NTP have no ratings for uranium human carcinogenicity. Drinking water and other environmental standards have been established by U. (May et al. Hamilton et al.. Uranium content of blood. Galletti.066 μg/g creatinine (Gwiazda et al.. and no consistent effects on multiple endpoints of kidney function were found. 2000). 1978).S. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. the median urinary uranium concentration was 2..1992. Boyd P. Health Phys 1992. with emphasis on quality control. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. (Kurttio et al. 2005. Komaromy-Hiller et al. 2006. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH...107:143-157.cdc. the median urinary concentration was 0. Horan P. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population. References Bhattacharyya MH.S.

Health Phys 1996.S. Auvinen A. Orloff KG. Sabbioni E. Jarrett JM. J Toxicol Environ Health A 2004.S. Smith D. Biokinetic modeling of uranium in man after injection and ingestion. concentration and daily excretion of uranium in urine of Japanese. Englehardt SA. rapid. Karpas Z. Salonen L. U. Paretzke HG. Cordero S.79(1):11-21. Jackson RJ.85:228-235. Andrews WS. D’Annibale L.82(4): 527-532.87:51-56. Oberbroekling KJ. Makelainen I. Howerton K. Radiat Environ Biophys 2005. Katorza E. Health Phys 2006.67(8-10):697-714. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Nuclear Regulatory Commission (U.158:165-190. Environ Res 1999.71(6):879-85. Saha H. Metcalf S. Hollriegl V. Salonen L. U.S. Comparison of representative ranges based on U. Halicz L. Am J Kidney Dis 2006. Kurttio P. Clin Chim Acta 2000. Wilson PD. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Health Phys 2004. et al. Marko R. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. VI. Pinto V. patient population and literature reference intervals for urinary trace elements. Marino R. Squibb K. Review of elements in blood. et al.94:319-326.86:12-18. Washington (DC): NRC. Karpas Z. Pekkanen J.47(6):972-982.44:29-40. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Charp P. NRC). Kidney toxicity of ingested uranium from drinking water. et al. Hamilton EI. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Biologic monitoring for urinary uranium in Gulf War I veterans. Ough EA. Shelly T.91(2):144-153. Lewis BM. Ash KO. Inductively coupled plasma mass spectrometry as a simple. Kane R. Nuclear Regulatory Commission (NRC) Guide 8. Heller J. Int Arch Occup Environ Health 2006. May LM. Van der Venne MT. Scott K. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Hancock RG. Sci Total Environ 1994.296(1-2):71-90.Metals Galletti M. Gwiazda RH. Health Phys 2002. McDiarmid M. Element reference values in tissues from inhabitants of the European community. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Sampson EJ.81:45-51. Uranium daily intake and urinary excretion: a preliminary study in Italy. Kurttio P. McDiarmid MA. Oeh U. Saha H. Costa R. Roiz J. et al. Squibb K. Kalinsky V. Wahl W. Gucer P. Komaromy-Hiller G. Uranium and thorium in urine of United States residents: reference range concentrations. Ting BG. July 1978.22–Bioassay at uranium mills. Health Phys 2004.S. Komulainen H. Li WB. Renal effects of uranium in drinking water. Health Phys 2003. Environ Res 2004. Roth P. et al. Tolmachev S. Harmionen A. Human exposure to uranium in groundwater. Engelhardt SM.110(4):337-342. Pirkle JL. Ejnik J. Mistry K. Noguchi H. Bennett LG. Auvinen A. et al. McDiarmid MA. Kuwabara J. Lorber A. Environ Health Perspect 2002. Paschal DC. Cremisini C. Oliver M.

22-5.76 (3.10-11.0-19.80-4.0 (11. 1998).10-4.90 (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.11) 3.32 (3.0) 10.0 (11.21 (2. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.0) 13.80) 12.80-6.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.70 (3.70-5. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.20-11.10 (6. 2005). 2007).70-11.20 (2.10 (5.44-4.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.60 (4.0-17.0) 9.0) 13.0-17.60 (7.0 (12.70-7.50) 5.50) 11. but has strong oxidant properties in the presence of concentrated acids.20 (5.90 (5.29-3.84) 14.0) 8.60-6. 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.0) 11.0) 95th 14.60-7.0 (9.0) 11.90-11. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.40) 3.51 (3.51 (3.0) 9.74-3.60) 3.16) 3.20 (8.81-16.30) 6.40 (4.40 (4.40-4. potassium. and limited applications in pharmaceutics. and reducing agents.70-9.S.30 (5. certain catalytic metals.96 (3.08-3.66) 3.10-11.02 (3.0 (11.60 (4.80) 3. laboratory analysis.05 (2.30-6.0 (11.50-4.80-4.0) 9.30-17.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.20-3.70-12..00) 3.54 (3.00) 4. leather tanning.93-4.60) 5.56) 3.31) 2.10-7.75 (3.01 (2.50 (5.50 (3. It is normally found and produced as the anion of a sodium.40-4.89-3.0) 10.40-7. 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.35 (3.26 (2.75-3.90 (2. Survey years 01-02 03-04 Geometric mean (95% conf.0 (8.50-7. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.50 (8.93-3.0 (11.70-3.50-11.03) 3. Other manufactured uses include fireworks.80 (3.90 (5.62 (3.0 (11.g.10) 3.. or ammonium salt.0 (11.80 (7.0-17.0-17.10) 12.0) 9.0-17. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.70 (3.90-11.0) 13.10 (6.30 (2.20 (4.40-6.67-5.00) 7.90-10. 2005).10 (7.0-14.S.90) 5.50-4.0) 15.0) 9.40) 3.0 (12.50) 6. and electroplating.88) 3.50) 5.0 (9.0 (11.40 (5.40-13.0 (9.40) 6.0) 13.90-6.30-7.90-12.70-6.30) 6.40) 90th 10.EPA.40-11. population from the National Health and Nutrition Examination Survey.07-4.68) 4.0) 9.60) 8.0-17.0-18.0 (11.0 (11.11) 4.10-12. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .40 (3.93 (4. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.40 (5.70-3.0-18.20) 4.46) 3. and certain plants with high water content (e.12) 3.80-12.45-4.0) 13.81) Selected percentiles ( 95% confidence interval) 50th 3.0 (12.20-12.20-4.20 (7.50-3.0 (8.0-15.18-3.49-3.0) 708 617 681 652 1228 1092 Limit of detection (LOD.80-8.0-18. lettuce) can be the main sources of intake for humans (FDA.05. In addition.0) 16.38) 5.30 (2.0) 12.0-23.90 (5.76) 4.09) 3.0) 13.0 (8.0) 14.0) 15. Perchlorate was added to the U.S.90 (4.39-4.10 (2.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.40 (5.0 (10.90) 6.0 (8.00) 3.79 (2.19-4.20 (2.0 (13.0 (9.0 (9.40 (3.40) 3.80 (3.20 (6.70) 3.0) 14.40 (8.0 (12.Perchlorate Perchlorate (Urbansky.70 (3.0) 13.30-19.30-7.0) 11. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS. matches.10) 5.30 (5.90-9.0) 10.00-5.90-3.5 hours and has a small estimated volume of distribution (Crump and Gibbs.65) 3.20) 3.00-6.80) 75th 6.50) 3.0-15.0) 13.05 and 0. Drinking water. Perchlorate is stable under most environmental and physiological conditions.87-3.40) 2.00) 5. interval) 3. milk.20-4.0 (8.22 (2.90-3.19 (3.80-15.0) 8.40-5.47-4.40) 4.0 (9.0-29.20 (4.80 (6.80) 7.00-6.10) 5. 2002).10) 3. fabric dyeing.0) 19.0-20.0 (9.20) 7.0) 14.90-9.

12-2.30 (3.29) 2.99-3.20) 8.6) 20.43) 6. and the presence of other substances known to affect thyroid function (e. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.0 (11. levels.. although iodine intake was higher than U.00) 9.8 (11.6) 12.50-9.50) 2.50) 95th 12.80-3.05 (4..36 (8. medications).0) 4.33-12.0 (9.0 (9.83 (5.40) 3.20 (4. U.51 (3.0) 9.71 (5.16-3.47) 2. gender. 2005).90-15.30-10.0) 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 3.4-16.0) 14. 2007). 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.90-2. Lamm and Doemland.35 (2.0 (10.0) 11.37-13.70-5.72 (3.50 (6. in a representative sample of U.S.60) 8. In the U.S.44-6.60) 10.30) 5.09) 3.. However.00) 3.22-4. 2006.0) 12.40) 5.22-6.76-3.54 (3.60) 3..42 (3.41-9..20 (2.50) 6.60-6. Greer et al.70 (2.90-9.0) 9.70-4. Li et al.5 (13.60-3.80) Selected percentiles ( 95% confidence interval) 50th 3.S.81-3.98) 3. 2005).20 (3.93-5. altered thyroid function was not found in Chilean pregnant women or their newborns with mean urinary perchlorate levels about 40-fold higher than average U.20-4.20-3.0 (11.20 (6.4 (8.0-14.1 (8.96) 2.S.00-11.64-3.93-5.0 (11.80 (7.89 (2.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.80 (7.82 (5.14 (2.1-13.39-4.0) 10.60 (3.84) 2.30) 3.0-44.0) 13.08) 3.10) 3.25 (3.35) 3. congenital hypothyroidism is a condition for which nearly all newborn blood is screened... 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. Also.80 (4.0) 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 .64) 5.10-3.0) 13. dietary iodine intake.90 (4.53 (2.6-17.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.60-15.39) 2.37 (4.EPA.56 (3.0 (9.3) 11.95 (2.89-3.99 (5. 1999.19-6.S. During gestation and infancy.35 (4.45-2. Steinmaus et al.70 (2.70) 2.52-9.32) 5.30 (6.5) 8.0 (8.87 (5.60-11.09 (7.S.1) 8.40 (4. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.20-3.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.60-5.4 (10.33-6.19-10.25) 5.87) 2.70-15.EPA.30) 75th 5.4 (11.18-3.91) 4.g.25) 5.08 (3.10 (2. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.61-5.21 (2.20-9.93) 3.1-16. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.90) 5.30 (5.10 (4..0) 12.93-7.10 (1.90-20. Many factors may be important in consideration of perchlorate action on the thyroid: dose.52 (8.70-3.90-11.3-14. interval) 3.3) 8.90-3. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.40) 17.60-11. levels and sufficient in most participants (Tellez et al. NAS.87) 7.7 (11.50 (3. 2005.00 (4.10) 6.22 (2.2) 8.50-3.50-5.Perchlorate inhibition (RUI).59) 3..10) 4.12 (6.61-10.40 (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.25) 5.34-3.3) 12.75) 3.30-5.10) 13.20-10..1-22.04-3.00-2.54 (2.90 (2.2) 8.24 (4.20 (7. Lawrence et al. age.40-10.66) 3.44) 3.07 (2.46-13.60-8.0-14.00 (2.22-4.00 (6.15-12.0-19.S.40 (3.1 (11.0) 7. population from the National Health and Nutrition Examination Survey.80-3.39 (3.0-17.70 (4.46 (3.0) 6.60-8.26 (3.74) 7. 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) 2. women with urinary levels of iodine less than 100 micrograms per day.60-5. perchlorate is negative in most genotoxic assays (U.00) 4.30-5. 2001.10 (4.76 (3.02-4.29-6.50) 9.1-14.67) 5.45) 3.90 (7.77 (3.4) 8. chronicity of exposure.10 (6. 2002).33 (7.70) 10.02) 3.56-3.46-4. nitrate.0 (8.4) 13. Survey years 01-02 03-04 Geometric mean (95% conf. 2003.10-7.30) 90th 9.58) 2.0) 12. 2000).0) 12.00-3.24-2.04-3. 2005.4 (11. 2002.97-5.50) 5. thiocyanate. 2005).86) 4.90 (2.03 (2.87-3.61 (5. 2002.87 (7. up to 68% RUI has been demonstrated.26) 4.3 (10.73) 3. menopausal status.20) 3.40 (7.51-4.93-8.

Lawrence J. Goodman G. Tellez RT. 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. Rutherford GW.114(12):1865-1871.41(5):409-411. Lamm SH. Byrd D. Mauldin JP. Washington (DC): National Academy Press. CFSAN/Office of Plant & Dairy Foods. Abarca CR. Pino S. et al. thiocyanate.S. 2005). Jackson WA. Barnard JC. Blount BC. Landingham CB. J Occup Environ Med 2003. Environ Health Perspect 2007. Pirkle JL. Doemland M. The effect of short-term low-dose perchlorate on various aspects of thyroid function. Braverman LE. Available at URL: http://www. Li Z. Valentin-Blasini L.cdc. Gibbs JP.110(9):927-937. Thyroid 2000.113(11):A732. Caldwell KL.90(2):700-706. Additional information about exposure and health effects is available from the U. Lamm SH. J Occup Environ Med 2000. Health Implications of Perchlorate Ingestion.html. Perchlorate Exposure of the US Population. Analysis of relative source contributions to the food chain. Environ Health Perspect 2002.115(9):1333-1338. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. Lamm S.gov/safewater/ccl/perchlorate/perchlorate.. Pino S. Erratum in: J Occup Environ Med 2004. Lau EC.11(3):295. J Clin Endocrinol Metab 2005. Blount et al. Dyke JV. (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. newborn thyroid function.113(8):10011008.10(8):659-663. Kirk AB. Steinmaus C. epa. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. et al. Crump KS. Lawrence JE. Food and Drug Administration (FDA). Benchmark calculations for perchlorate from three human cohorts.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis.EPA at: http://www. May 2007. 2005.htm. Environ Health Perspect 2005.S. Pleus RC. Lamm SH. et al. Biomonitoring studies of urinary perchlorate provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of perchlorate than levels found in the general population. Braverman LE. Environ Health Perspect 2006. Perchlorate in the United States. Pirkle JL. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. and nitrate on thyroid function in workers exposed to perchlorate long-term. Biomonitoring Information Urinary perchlorate levels reflect recent exposure.fda. 2007). 6/2/09 Greer MA. Blount BC. Also. Li FX. Valentin-Blasini L.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Erratum in: Environ Health Perspect 2005. Dasgupta PK. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. most of the population is considered to be below the U. Environ Sci Technol 2006. He X. population.46(5):509. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water.40(21):6608-6614. Daaboul JJ. Chacon PM. Magnani B.45(10):1116-1127. Page Last Updated: 05/28/2009. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Richman K. EPA reference dose (Blount et al. The effect of perchlorate. Howd R. Miller MD. 2001-2002. J Expo Sci Environ Epidemiol 2007.. National Academy of Sciences (NAS). Neonatal thyroxine level and perchlorate in drinking water. National Research Council of the National Academies. 2005). Skeels MR. Braverman LE.gov/toxpro2. Kelsh MA. Osterloh JD. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. Sesser DE. Cross M. Low dose perchlorate (3 mg daily) and thyroid function. Crump KS. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999.17(4):400-407. 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.. and environmental perchlorate exposure among residents of a Southern California community.42(2):200-205. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 .atsdr. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Osterloh JD.html and from ATSDR at: http://www. Greer SE. Deyhle GM. References Blount BC. Thyroid 2001. Buffler PA. et al. Primary congenital hypothyroidism.S.

1988.15(9):963-975.gov/iris/quickview. cfm?substance_nmbr=1007. Available from URL: http://cfpub. EPA). Environmental Protection Agency (U. U. EPA).S. EPA/600/F-98/002 Washington (DC).S. Perchlorate. Environmental Protection Agency (U.1/15/06 U. Doc. 246 Fourth National Report on Human Exposure to Environmental Chemicals .epa. Thyroid 2005. Integrated Risk Information System (IRIS).Perchlorate pregnancy and the neonatal period.S. No.S.9(3):187-192. Revised 2/11/05. Drinking Water Contaminant Candidate List. Urbansky TF. Perchlorate as an environmental contaminant. Environ Sci Pollut Res Int 2002.

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

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

500 (<LOD-1. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. the potential to estimate risks to humans from animal doses is uncertain. EPA.10) . see Data Analysis section) for Survey year 03-04 is 0.400-1.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. 2003a.S... reproductive.500) 90th . 1999.500-1.800 (.. hepatotoxicity... 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.600 (.700) . In comparing three separate reports on adults.300 (<LOD-.900 (.400-.700 (. 1992. 2007.400-1.S.500-1. 2007a.500 (.500) . U.800 (.. 2004.400 (<LOD-.20) . 2007b). population.400-..00) . 2004). possibly related to lung immaturity (Lau et al. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. At high but non-toxic maternal doses of PFOS.. 2003. However.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .. 2003a).80) 640 1454 03-04 03-04 * * < LOD < LOD . EPA. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.500-3.. PFOA. 2004b).. 2003a).10 (. At doses causing maternal toxicity. 2003a. Thibodeaux et al.80) 485 538 962 Limit of detection (LOD. Harada et al. 2005). Cook et al. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. Survey Geometric mean (95% conf. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U.00) .S. In such studies. 2003. 2003). Fei et al. elderly and children.. monkeys. 2005). thyroidal). 2003. 2004.500 (. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.400) . Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.10) * 03-04 03-04 * * < LOD < LOD < LOD .. the median PFCs values tend to be roughly similar in these age categories (Olsen et al.400 (<LOD-.. 2004a. 2001. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality. 2003).800 (.400-1.600 (.108 times higher than background serum levels in humans (Butenoff et al. Olsen et al.3.. interval) Selected percentiles ( 95% confidence interval) Sample 95th .. 2007). population from the National Health and Nutrition Examination Survey. Olsen et al. 2003a.. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. Animal studies of PFOS have demonstrated weight loss. development in offspring was stunted and hypothyroxinemia was observed.500-1. Olsen et al. U.. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. and humans. Lau et al. PFOS.800) 1. 2004). PFOS.40) .400 (<LOD-. perfluorohexanesulfonate (PFHxS). and changes in thyroid hormone concentrations (Grasty et al. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear.900 (.00 (. PFOA. 2007b.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 .500-.500) .00) . Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years.600-2.. developmental and teratogenic effects were demonstrated in offspring. Kennedy et al. Serum PFOS levels associated with toxicity in test animals were 310-1550 fold higher than 95 percent of the levels found in a study of adults (Olsen et al. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.400-1.S.300-1. 2007a. or increased cancer rates (Alexander et al.300 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 249 . 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.900 (..10) .600 (.50) .800 (.400-1. and there was no clear evidence of excess all-cause or diseasespecific mortality.300 (<LOD-.500) ..500-1. 2003).500) .800) 1.

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

400) .900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0.900) < LOD .3.300 (<LOD-.400 (<LOD-.300-. population from the National Health and Nutrition Examination Survey.600) < LOD .Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.600 (.300 (<LOD-. Survey Geometric mean (95% conf.S.400 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (<LOD-.400 (<LOD-.0. Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample. which may vary for some chemicals by year and by individual sample.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 .500) 485 538 962 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey year 03-04 is 1.S.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th . Fourth National Report on Human Exposure to Environmental Chemicals 251 .500-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < 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.

40) 1.0) 1053 1041 03-04 03-04 03-04 1. see Data Analysis section) for Survey year 03-04 is 0.80-4.826-1.40) 640 1454 03-04 03-04 1.40) .721-1.60) 3.60-7.90) 8.20 (6.70) 13.20-3.50) 6.20-2.50 (1.73-2.30) 03-04 03-04 .40 (1.42 (1.50 (4.03) 1.20) 1.861 (.70) 3.67-2.80) 3.16) Selected percentiles ( 95% confidence interval) Sample 95th 8.80-8.90 (4.10-5.30 (6.10) 1053 1041 03-04 03-04 03-04 .20) 1.00 (.10 (4.30 (1.40) 640 1454 03-04 03-04 2.5) 8.08) 2.963 (.50 (1.12) .00) 3.697-1.20 (1.80-3.600-.80-4.90 (1.20-1.87-2.40 (1.40) 1.00-1.60) 9.00 (1.835-1.51) 1.00) 1.40 (1.700 (.60-8.00-7. 252 Fourth National Report on Human Exposure to Environmental Chemicals .30 (2.40 (2.10) 1.800 (.80) 4.10 (.70) 2.40-1.70) 1.90-2.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.900-1.70-10.20 (6.80 (4.90 (1.10 (4.86 (1.60-4.900-1.809) 1.30-12.10) 6.00) 1.70-2.92 (1.20-1.40-1.10-9.10) 6.26) 2.S.50 (4.0) 8.60-3.3.30) 3.20) 2.72 (1.90) 1.40) 2.10) 4.90-19.70 (2.00 (1.40) 4.20 (1. interval) .50 (6.30-9.70 (1.17 (1.1.689 (.834-1.20) 485 538 962 Limit of detection (LOD.30) 3.00 (1.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.09 (.80 (1.80-12.80-2.90 (1.56-1.5) 5.00 (2.50 (6.3 (9.60) 2.20) .80-7.77-2.50-10.93 (1.10) 75th 1.1) 485 538 962 Limit of detection (LOD. Survey Geometric mean (95% conf.60-2.60 (1.30) .14 (.60) 1.44 (2.900-1.90) 90th 5.80-8. population from the National Health and Nutrition Examination Survey.90 (2.27) 1.00-8.50-6.50) 2.90) 1.6) 7.30 (1.62-2.60 (1.912-1.60 (1.70-6.30 (3.816-1.80) 5.10) 5.90) 3.00 (.30 (7.90) 1.16) .30) 3.70) 1.30 (1.50 (1.10) 75th 3. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20-1.40-3.50 (2.20 (1.60-3.17-1.80-6.90 (1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.50-6.30 (1.586-.10-9.900 (.00) 2. interval) 1.05-2.90 (4.60-2.20) 03-04 03-04 2.40 (1. see Data Analysis section) for Survey year 03-04 is 0.20-1.00-1. population from the National Health and Nutrition Examination Survey.80-7.70) 2.80 (1.01 (1.900-1.70-2.S.10 (.900) 1.900-1.80) 90th 2.10 (1.50-3.04) .30 (2.10) 1.20 (1.30-6.900-1.984 (.60-2.966 (.30-2.90-10.10) 4.900 (.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.60 (6.80-3.80-4.54) .700-1.852 (. Survey Geometric mean (95% conf.00-6.10 (.800-1.50) 2.70-7.80) 1.00 (5.60-4.10) 8.70-5.72) 1.50 (1.00 (1.91) 2.

7 (35.70 (5.6) 1053 1041 03-04 03-04 03-04 3.1 (23.4) 75th 30.40 (6.37 (2.5 (28.5) 19.82) 4.20-9. population from the National Health and Nutrition Examination Survey.30-6.7 (35. Fourth National Report on Human Exposure to Environmental Chemicals 253 .0-66.00) 3.80) 8.9-38.9 (19.85-4.30-3.9 (13.9-19.1-35.40-14.30) 6.5) 32.8) 46. Survey Geometric mean (95% conf.0) 90th 41.90-4.7) 39.8-22.3) 28.2 (18.0) 36.90-4.6) 21.35) 3.8) 27.6-24.5) 57.70-9.50 (4.5-23.7 (7.4 (17.7-30.53) 3.30-11.9) 22.5) 18.2 (16.8-35.2 (21.89 (3.4-42.6-50.90 (7.60) 8.1 (24.50-6.20) 5.1-25.9-23.0-70.27) 4.3 (35.20) 10.1) 15.3 (35.60 (4.40) 75th 5.4. see Data Analysis section) for Survey year 03-04 is 0.0) 03-04 03-04 19.70-5.96 (3.1-33.4) 20.4) 56.8 (45.40-10.40-17.6 (42.90) 6.2) 640 1454 03-04 03-04 4.9 (17.8-22.40) 90th 7.2 (27.2) 45.6) 7.0) 21.1 (19.6-45.60) 03-04 03-04 3.1-52.8-81.90 (5.0-16.70) 6.50-13.20) 7.65-4.4 (23.20 (4.2-57.2-22.8 (37.5-21.5) 8.1-36.3 (28.5) 1053 1041 03-04 03-04 03-04 14.7-23.5) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 21.9) 9.20 (4.3 (44.7-33.9) 22.80-12.70-10.1-24.4) 21. interval) 20.2) 30.60 (6.60-9.0) 43.90 (7.2) 30.6 (44.20) 5.1) 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 4.00 (5.6) 62.30) 7.5) 9.40) 5.7 (43. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.7-69.3-61.50) 4.3-22. interval) 3.8-78.S.30 (3.80 (7.80-9.4 (19.70) 4.60 (3.8-30.00 (5.70-7.60-6.60-13.1) 57.10 (6.7-49.2 (28.5-62.40-6.0 (27.6 (35.7 (43.4-25.30-8.90-12.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.7 (13.4 (19.6 (19.3) 42.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.3 (17. population from the National Health and Nutrition Examination Survey.80 (6.40) 3.60-14.80 (6.1.30-5. Survey Geometric mean (95% conf.3) 485 538 962 Limit of detection (LOD.70 (5.70-7.0) 23.18 (3.50-4.90 (7.21-3.00 (3.07-4.4-17.30 (5.3) 41.6) 18.0) 485 538 962 Limit of detection (LOD.47-4.10 (3.50 (3.30 (3.40 (4.0-20.2 (19.5 (28.10) 5.8) 32.84-3.5-33.80-4.91) 3.6) 9.10-3.20) 4.S.95 (3.70) 3.8-22.20-5.9 (22.0) 21.47 (4.80 (5.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.6) 42.4 (28.50) 7.40-6.7-53.60 (6.5) 7.99-3.8 (34.9) 27.7 (19.67-4.20) 7.6) 35.60 (7. see Data Analysis section) for Survey year 03-04 is 0.20-4.11 (2.70 (3.4) 640 1454 03-04 03-04 23.10 (3.60 (5.0 (20.79) 4.

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 (.4.300 (.300 (.200-.200-.300) .300) .300) .300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .200 (<LOD-.2. 254 Fourth National Report on Human Exposure to Environmental Chemicals .300 (.300 (.300-. < LOD means less than the limit of detection.S.300 (.300) . population from the National Health and Nutrition Examination Survey.300-. * 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.200-.200-.500) < LOD 485 538 962 Limit of detection (LOD. < LOD means less than the limit of detection.500) . see Data Analysis section) for Survey year 03-04 is 0.300) . Survey Geometric mean (95% conf.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.300-.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th . interval) Selected percentiles ( 95% confidence interval) Sample 95th .300) .500) .300 (.400 (<LOD-.300 (.300 (.500) . 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) 485 538 962 Limit of detection (LOD.200-.200-.300 (.300 (. which may vary for some chemicals by year and by individual sample.300) .200-.300-.Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.200-.200-. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample.300 (.S.300 (. see Data Analysis section) for Survey year 03-04 is 0.200-.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .

10) 1.80) 1.700) 1.00 (.300 (<LOD-1.900 (<LOD-1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.500 (<LOD-.700) .700 (<LOD-.60) 640 1454 03-04 03-04 * * < LOD < LOD .700 (<LOD-.00-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 1.700) 1. Survey Geometric mean (95% conf.900-1. population from the National Health and Nutrition Examination Survey.10) * 03-04 03-04 * * < LOD < LOD .10 (.40) 1.40) < LOD < LOD .80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .700) 90th 1.10) . Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.900-1.10-1.00 (.30 (1. < LOD means less than the limit of detection.Perfluorochemicals Serum 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300-2. population from the National Health and Nutrition Examination Survey.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .30) 1.10-1.400 (<LOD-.50 (1.20-1.30 (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 .600 (<LOD-1.700 (<LOD-.10 (.600 (<LOD-1.S.00) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 255 .800) .00 (.400 (<LOD-1. which may vary for some chemicals by year and by individual sample.20) 1. which may vary for some chemicals by year and by individual sample.800 (<LOD-.10 (1.3.900-1.900) .900-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .10) .10) 1.800) .300 (<LOD-.600) .30) 1.600 (<LOD-1.70) 1.900) 485 538 962 Limit of detection (LOD.900-1.700 (<LOD-.700 (<LOD-2.60) 485 538 962 Limit of detection (LOD.900) 1.900-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.10 (.10-1.900-1.10-1. see Data Analysis section) for Survey year 03-04 is 0. see Data Analysis section) for Survey year 03-04 is 0. Survey Geometric mean (95% conf.00 (.900 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6.50 (1.700 (<LOD-.600 (<LOD-.S.10-1.700 (<LOD-.20 (1.30) .90) .30 (1.

Reidy JA. Cook JC. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Polyfluoroalkyl chemicals in the U. Environ Sci Technol 2004. McLaughlin JK. Reidy JA. et al. Biegel LB. Environ Health Perspect 2007. Kuklenyik Z. Toxicol Sci 2001. Rogers JM.99(2):253-261. Yoshinaga T.and perfluorinated acids. Jarnberg U. Suzuki E. Yun SH. 2007b. Fillmann G. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Environ Sci Technol 2006a. Butenhoff JL. et al. Hurtt ME. Androgenic deficiency in male rats treated with perfluorodecanoic acid. brominated. Chem Biol Interact 2000. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. The influence of time. Inoue K. Cook JC. Olsen GW. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Hurtt ME. Fei C. et al. Tarone RE. Keller JM. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Grey BE. Taniyasu S. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. J Environ Monit 2005.60(10):722729. Environ Res 2005. Calafat AM. Halden RU. Yamashita N. Fluorotelomer alcohol biodegradation yields poly. Butenhoff JL. Reidy JA. Witter FR. Environ Sci Technol 2005. Hekster FM. Environ Sci Technol 2005. Calafat AM. et al.46(2):141-147. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Murray SM. et al.1968--2003. Toxicol Appl Pharmacol 1990.124(2):119-132. Falandysz J.38(10):2857-2864. Perkins RG. Chlorinated. Seneviratne HR. Environ Sci Technol 2005.40:21282134. 256 Fourth National Report on Human Exposure to Environmental Chemicals .115(11):1677-1682. Loganathan BG. Herbstman JB. Taniyasu S. Needham LL. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Lau CS. Tully JS. Kennedy GL Jr. in vivo. Perfluorinated chemicals in selected residents of the American continent. et al. Rev Environ Contam Toxicol 2003. Burris JM.S. Needham LL. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Laane RW. and perfluorinated contaminants in livers of polar bears from Alaska. Holmstrom KE. Rodricks J. Ye Y. Mohotti KM. Dinglasan MJ. Frame SR. Wong LY. Inoue K. Mandel JH. Koizumi A.104(2):322-333.S. Caudill SP. Kannan K.115(11):1670-1676. Environ Sci Technol 2004. Wijeratna S. Toxicol Appl Pharmacol 1992. O’Connor JC. Harada K. Yoshinaga T. Day RD. Environ Sci Technol 2007a. Peterson RE. Morikawa A.41:2237-2242.134(1):18-25. Mandel JS.7(4):371-377.68(6):465-471. Seacat AM. Saito N. Kamiyama S. Grasty RC. Frame SR. Edwards EA. Kuklenyik Z. Characterization of risk for general population exposure to perfluorooctanoate. Kuklenyik Z. Guruge KS. Calafat AM. The toxicology of perfluorooctanoate. Olsen GW. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Olsen GW. Regul Toxicol Pharmacol 2004.34(4):351-384. Watanabe T. Environmental and toxicity effects of perfluoroalkylated substances. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Mandel JH. Needham LL. Gaylor DW. Harada K. de Voogt P.113(2):209-217. Kudo N.39(23):9057-9063. Biegel LB. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Cook JC. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Olsen J. Saito N. Calafat AM. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Ingall GB. Apelberg BJ. Tully JS. Corsolini S. Bignert A. Kawashima Y. Environ Health Perspect. Kumar KS. Yamashita N. J Occup Health 2004.39(23):9101-9108. Bandai N.39(1):80-84. Katakura M. et al. and ex vivo studies. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. Liu RC. Kuklenyik Z. Sasaki S. Kannan K. Aguilar-Villalobos M.60(1):44-55. Needham LL. Mabury SA. Crit Rev Toxicol 2004. Evans TJ. Occup Environ Med 2003. Birth Defects Res B Dev Reprod Toxicol 2003. Moore RW.38(17):4489-4495. Environ Health Perspect 2007.39(3):363-380. Caudill SP. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Arendt MD. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Calafat AM. Reidy JA. Hurtt ME. O’Connor JC. Toxicol Appl Pharmacol 1995.63:490496. Chemosphere 2006b. Bookstaff RC.Koizumi A.179:99-121.115(11):1596-1602. Kannan K.Perfluorochemicals References Alexander BH. Moore JA.

Chemosphere 2004a. Larson EB. Toxicol Sci 2003. Burris JM.54(11):1599-1611. Yamashita N. Half-life of serum elimination of perfluoroo ctanesulfonate.Perfluorochemicals Kudo N. J Occup Environ Med 2003b. Miller JP. Ellefson ME. Cao XL et al. Froehlich JW. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Gamo T. II: postnatal evaluation. Thibodeaux JR. Grey BE. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. et al.41(9):799-806.51(8-12):658-668. Coordinate induction of acyl-CoA binding protein. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Olsen GW. Mar Pollut Bull 2005. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Environ Sci Technol 2006. Environ Health Perspect 2003a. (Erratum in: Toxicol Sci 2004. Olsen GW. Hanson RG. 2003a. Butenhoff JL. Mair DC. U.74(2):369-381. Peterson RE.S.1177(2):183-190.perfluorohexanesulfonate.74(2):382-392. Environ Sci Technol 2003. Sources. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Washington. et al. Sterchele PF. Biochim Biophys Acta 1993. Ehresman DJ. Yamashita N..epa. fish. Chemosphere 2007b. Lau C.gov/opptintr/pfoa/pfoara. Olsen GW. EPA). Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Church TR. Butenhoff JL.45(3):260-270. Toxicol Sci 2003. Burris JM. Burris JM.82(1):359. et al. Olsen GW. Olsen GW. fish. Burris JM.111(16):1892-1901. Thomford PJ. Toxicol Appl Pharmacol 2004. perfluorooctanoate andother fluorochemicals in human blood. (Erratum in: Environ Health Perspect. Hanson RG. Mandel JH. Pepper K. Lundberg JK. Olsen GW. Hansen KJ. Mandel JH. Mandel JH.68(1):249-264. Butenhoff JL. Taniyasu S. J Ag Food Chem 2007. Prevedouros K. Hansen KJ. Church TR. 2007a. Grey BE. Reagen WK.55:3203-3210.68:105–111. htm. Olsen GW. and food items prepared in their packaging. Helzlsouer KJ. and humans from Japan.) Tittlemier SA. Hansen KJ. Barbee BD. 1/15/06 Vanden Heuvel JP. Lau C. Thibodeaux JR. I: maternal and prenatal evaluations. Huang HY.198(2):231-241. Richards JH. Horii Y. Church TR. Butenhoff JL. Historical comparison of perfluorooctanesulfonate. Taniyasu S. Environ Health Perspect 2005. J Children’s Health 2004b. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Burlew MM. Ehresman DJ.113(5):539-545. Kawashima Y. fate and transport of perfluorocarboxylates.37(12):2634-2639. Petrick G. Toxicol Sci 2002. Hansen KJ. Environmental Protection Agency (U. Case MT. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Seymour C. Kannan K. Moisey J. et al. Hansen KJ. A global survey of perfluorinated acids in oceans. birds. Rogers JM.111(16):1900) Olsen GW. Seacat AM. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Nesbit DJ. Butenhoff JL. 2003. et al.2(1):53-76. Buck RC. Rogers JM. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Rogers JM.S. Olsen GW. fast foods. Fourth National Report on Human Exposure to Environmental Chemicals 257 .40(1):32-44. Kannan K. Burris JM. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. J Occup Environ Med 1999. Environ Health Perspect. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. and perfluorooctanoate in retired fluorochemical production workers. The developmental toxicity of perfluoroalkyl acids and their derivatives. Mandel JH. Butenhoff JL. Cousins IT. et al.26(1):47-51. Stanton ME. Bronson R. Seacat AM. van Belle G. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Korzeniowski SH. Lundberg JK. Biol Pharm Bull 2003. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Available from URL: http://www. Zobel LR.115(9):1298-1305. Hanari N. Horii Y.

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

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

Koch HM. 6/2/09 Okubo T. Jobling S. et al. J Androl 2004. Park MG. Harris CA. Meeker JD.nih. Kano K.niehs. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Hauser R. et al. Environ Health Perspect 1997. Research Triangle Park (NC). Kano I. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. Albro PW. Milligan SR. Pan G. Int J Hyg Environ Health 2007. 2000a [online]. Kalita JC. Skakkebaek NE. Giwercman A. 6/2/09 NTP-CERHR.112(17):1740].html. Suzuki T. McKee RH. Research Triangle Park (NC). Rylander L. Filser J. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP).64(8):555-560. Duty SM. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.nih. Boehmer S. gov/chemicals/dehp/dehp-eval.103:582-587. The estrogenic activity of phthalate esters in vitro. Andersson A-M. Hartle RW. Jacobsen H. Kessler W. Butala JH. Scand J Work Environ Health 1985. Silva MJ. Singh NP. Decreased serum free testosterone in workers exposed to high levels of di-n-butyl phthalate (DBP) and di-2-ethylhexyl 260 Fourth National Report on Human Exposure to Environmental Chemicals . Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.11(5):381-387. 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Balasubramanian AV. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Park S. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Chahoud I. Int Arch Occup Environ Health 1993.110(5):515-518.210:21-33. Available at URL: http://cerhr. Epidemiol 2005. 6/2/09 NTP-CERHR. Hauser R.niehs. Brock JW. Sumpter JP. Lovekamp-Swan T. White R. Environ Health Perspect 2002. Environ Health Perspect 2004. Nielsen J.112(17):1734-1740.html. Reprod Toxicol 2004.niehs. Anal Bioanal Chem 2005. Richthoff J. Yoshimura M. Parker MG. Available at URL: http://cerhr. Am Ind Hyg Assoc J 1985. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). David RM. Hum Reprod 2007. Ladefoged O. Research Triangle Park (NC). Akesson B. NTP-CERHR. et al. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Zhang S. Reproducibility of urinary phthalate metabolites in first morning urine samples. Environ Health Perspect 2003. Toxicol Appl Pharmacol 2004. Bolte G.gov/chemicals/dehp/dehp-eval. Yokoyama Y. Hoppin JA. Grote K.18(1):122.nih. Biol Pharm Bull 2003. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Csanády G. 2000c [online].19(4):505-515. Drexler H. Davis BJ. Brock JW. Reynolds T.195:142-153. Duty S. Tsukino H. Meeker JD.105:802-811. Jarfelt K.niehs.gov/chemicals/ phthalates/dbp/dbp-eval. Henttu P. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Baird DD. Main KM. Leffers H.Phthalates in human urine samples. and infant formula by tandem mass spectrometry (LC-MS-MS). Skerfving S. Jonsson BAG. 2000b [online]. Silva MJ. 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Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Cunningham ML. Environ Health Perspect 1986.65:299-308.58:339349. Peck CC.36:459-479. Fielden MR. Batten PL.45:11-17. Barr DB. Zacharewski TR. et al.112(3):331-338. Hodge CC. Caudill SP. Environ Health Perspect 2006. Pratt IA. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. et al. Silva MJ. Albro PW. Clemons JH. Meek MD. Abbott BD. Klinefelter GR. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Ostby JS. Wu ZF.46:282-293. Matthews JB. Urinary levels of seven phthalate metabolites in the U. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Crit Rev Toxicol 2006. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Orton TC.S.Phthalates phthalate (DEHP): a cross-sectional study in China. Parks LG. Peters JM. Jackson SJ. Environ Health Perspect 1982. Barlow NJ. Toxicol Sci 2000. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Rusyn I. Toxicol Sci 1998.114(11):1643-1648. Environ Health Perspect 2004. Rhodes C. Reidy JA. Bratt H. Malek NA. 112(5):A270]. et al. Lambright CR.

8-16.2) 66.1 (14.6 (12.0) 32.4 (32.8-18.8-98.8 (28.6) 14.7-119) 99.5) 82.9 (12.0 (33.1) 31. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.7 (53.1) 14.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93. can produce developmental and reproductive toxicity in rodents.4 (10.1-214) 166 (116-191) 145 (110-213) 88.5) 15.6-150) 94.2 (14. 2000).3-18.1 (13.3 (13.8-48.8 (21.8 (71.8-14.1 (14.7 (80.3) 54.0-106) 58.2 (47.4-62.3 (30.Phthalates Benzylbutyl Phthalate CAS No.2) 14.2) 69.5-62.4-25.6 (13.5-40.9 (16. car care products. and 0.7-17.8-72.1) 67.6 (41.5 (13.0 (27.9 (11.7-15.3-74.6-92.1 (20.5-36. particularly male animals (McKee et al.8-14.7-13. 2001-2002.7-16.6-39. it can be released into the ambient air during use or disposal of the products.8-76.3 (54.2) 14. 262 Fourth National Report on Human Exposure to Environmental Chemicals .2) 32.4-24.9) 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. 0.5 (76.6) 14.8-16.3) 63.5-94.1 (10.9) 11.0-85.6 (13.8-35.5) 16.1-38.0) 70.7) 38.4 (63.9 (39.6-38.0 (11. see Data Analysis section) for Survey years 99-00.9) 14.4) 71.8 (53.7-16.7-58.0) 24.4 (13.2) 17.5-35.0) 23.4) 35. population from the National Health and Nutrition Examination Survey.6 (66.7 (13.9) 43.1) 12.1) Selected percentiles ( 95% confidence interval) 50th 17.6) 16.9 (13.9-27.4-15.2-39.6) 67.2 (25.9 (22.4) 35.6) 24.5-18.1-61.2 (11.7-170) 169 (134-198) 152 (99.4) 80.4 (53.4) 108 (96.4) 81. sealants.9-30.4) 51.9 (21.6) 95th 103 (94.2-16.9-87.9 (28.8) 33.6 (13.1-90.8-17.3-27.5-97.2 (19.3-161) 99.1 (58.2-155) 91.3 (33.0 (30.7 (82.6 (32.6-92.3 (12.8) 14.1. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.9-49.0 (14.7-35.1 (13.5-25.3 (44. including MBzP.6) 13. and diet is the major source for general population exposure. interval) 15.4 (32.8-17.8 (86. and 2003-2004 were generally similar those reported in U.6-72.5 (57.4-120) 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 13.2-20. High dose BzBP and its monoester metabolites.9-28.2 (19.5-41.5 (55.2) 12.0 (20.6) 15.8 (38.9-190) 86. and 03-04 are 0. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.6) 13.3 (22.7) 40.0) 20.5) 55.1 (32. BzBP can be released into the environment during its production and.1-120) 52.0) 90th 67.3) 23. some personal care products.4 (53. vinyl tile.7) 23.7-14.9-14.2-116) 122 (102-143) 101 (84.8) 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. NTPCERHR.3 (29. respectively.0 (30.8 (71.1 (55.3 (29.1-116) 122 (93.1-39.6) 35.7 (15.6 (13.3-75.0 (12.3-130) 122 (88.1 (19.7-82. 01-02.2-183) 101 (78.3-21.0 (34.8) 28.0-130) 101 (86.9-16.5-33.3-12.5-36.2-38.0) 34.7-16.9) 14.0 (43.4-127) 80.5) 65.3) 94.6-79.4 (31.9 (12.4) 65.5 (67.8-121) 79.6-29.3 (12.4) 75th 35.0 (15.9) 12.9 (70. and to a lesser extent.7 (70.3-43.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5) 27.5) 15.4 (10.8 (14.8 (30.9) 18.3-34.4 (27. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.3) 37.4 (59.4-16..4) 12.9) 15. because it is not bound to products in which it is incorporated.7 (11.8 (12.9) 13. residents (Blount et al.6-17.2 (10.S..7-25.8) 63.4) 38.2) 13.5-145) 138 (106-241) 143 (127-179) 120 (99.3-82.2-17.1-15.2-19.8 (50.6) 25.4) 129 (98.1-16.6) 50.0-55. IARC considers BzBP not classifiable with respect to human carcinogenicity.0-26.3) 13.2-31.0 (55.4 (48.6) 37. 2000).9) 49.3) 15.0 (26. Food crops take up BzBP.4-92.8.8-41.2 (43.6 (53.1-15.2-16.6-43.2) 15.1-16.3-88.7-172) 103 (74.5) 23. 2004.1) 32.5-14.1) 29.0 (15.1-35.6-132) 103 (84.6-116) 122 (102-142) 101 (85.2-40.5 (26.5 (47.9-62.4) 98.2-115) 113 (91.4 (68.0) 16.9-47.3-18.6-18. 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.6) 63.4) 33.1-43.4 (29.2) 22.0 (23.1-18.1) 68.3) 13.5 (66.5 (61.8-13.5 (27.3.8-133) 89.7 (12.5) 30.4) 49.8-64.S.2-33.0) 33.6) 35.5-84.8 (10.3-125) Total 15.6) 29.6 (21.1) 13.4) 14.3-91.8 (80.2) 33.2) 78.8) 24.1) 76.7 (51.3 (12.

5 (10.0-15.7) 25.2-21.4 (34.1 (13.2-78.2 (40.9-28.2) 11..6 (57.8-13.2 (41.0 (49. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.8) 53.9) 64.6) 58.4-27. adolescents compared with adults. Hauser et al.6-12.4-142) 134 (116-176) 136 (85.1 (21.4-14.8-13.Phthalates York City (Adibi et al.1) 17.3) 55.0 (10.4-90.9 (22.9) 11.8-173) 195 (121-305) 229 (99.1 (21.6-116) 74.7 (19.6 (11.9) 12. interval) 14.8) 33.4) 15.7-15.8-16.6-81.1 (18.8) 71.4) 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 12.0) 49.6 (34..8-42.5 (56.4-93.8) 33.2-12. 2003).4) 17.4) 14.8) 53.4 (12.3 (38.3-11.9-14.5-79.4) 44.5) 46.6 (36.5-26.6 (15.6) 25. in young Swedish men (Jonsson et al.0) 13.0-109) 65.3-16.8) 46.1) 80.8 (69.5-23.69-11.6) 73.3) 18.1-79.2-15.1 (14. 2005.8) 13.8 (12.7 (14.4) 104 (89. and in a small sample of German residents (Koch et al.8 (64.4-116) 73.4 (63.9-13.0-90.1) 24. Hoppin et al.9 (10.1) 39.8 (13.1-29.7 (13..8-13.8 (50.3 (12.1 (13. 2002.6-26.4-99.2) 67..6 (30.8) 34.0 (33.6 (11.5) 17. In an annual sample of German university students.5 (11.2-26.5 (49.0 (13.2-51.7-61.8-14.9 (29.7-123) 77.4) 90th 50.4) 13.4) 28.7 (38.2-17.9 (15.1 (43.9 (10.9 (12. 2003). in men attending a Boston infertility clinic (Duty et al.4 (46.1 (19.2 (69.9 (54.0) 12. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.7) 46.0 (12.6) 75th 25.3) 73.9) Total 14.2) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 12.0-53.3 (15..6 (19.6 (11.8 (49.8-64.3-38.9) 100 (80.1-125) 86. 2007).6-47. 2004.5-57.6-40.8) 11.4-60.3 (39.6) 30.2-49.9-69.9-104) 62.5-42.4 (21.9-40.7-14.1 (11.9) 24.3) 29.1) 27.2) 11.4-15. 2005).0) 60.4-14.9) 11.7-19.8-27.5) 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 .7 (23.1 (23.7-20.4-19.8-80.1) 24.7-20.7 (21.1-27.7-56.8) 16.3-34.4 (11.2) 26.2-13.S.1 (41. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.7-31.3 (23.8) 15.3 (60.3 (35.5) 41.6 (30. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7) 56.5) 20.7-69.7) 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 40.5) 78.3) 16.8-60.8-15.6) 53.1-120) 77.8-15.4 (26.4 (25.2) 32.3 (13. population from the National Health and Nutrition Examination Survey.6) 12.0-51.6) 38.0 (11.7-90.3) 67.0) 24.9 (9.9) 52.8 (10.0) 11..5 (12. In NHANES 1999-2000.7 (18.8-85. 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.2 (27.1 (46.9-23. 2006).4 (11.8) 80.5) 95th 77.2) 12.5) 16.9) 12. Weuve et al.5-99.8) 56.5 (35.8 (30.7-12.0 (38. A small study of African-American women in Washington.2) 11.1) 35.7-397) 70.5-31.1-35.8-39.6-15.4) 13.4) 25.9-13.6-20.4 (74.1 (9.0 (12.3) 37.4) 12.5) 13.4 (69.0 (41.1 (53.5-13.9 (12.7 (11.4-17.9-83.7-29.5) 10...8) 108 (75.1 (21.6 (22.1-14.2-13.0 (62.3) 14.7) 38. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.9-16.7 (55.3) 12.3) 90.0) Selected percentiles ( 95% confidence interval) 50th 13.9 (24.6) 13.6 (14.4 (10.9 (24.5-213) 49. and females compared to males (Silva et al.2-15.6-86.4) 51.7 (54.3) 14.2-117) 95.9) 42.4 (13.5-76.3) 89.9 (39.0 (67.5 (9.8 (46.8 (57.6-99.4-79.7) 11.7-14. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.9 (51.5-29.5-61.4) 60.3) 13.7-19.0) 24.9 (43.6-13.73-12.4 (33.0) 15.. 2002).7) 19.3 (24.3) 13.2 (56.5 (42.9 (15.9 (55.95-14.8) 24.1-12.6) 12.8) 54.5 (10.5) 23.0 (41.0-48.9) 12.6 (24.1 (25. 2004).7 (13.1 (15.5 (48.5-16.4) 50. 2007).1 (21.8 (11.9-62.3-73.4-42.3) 21.1-58.5-58.4 (60.5-38.1) 12.7-15.5-26.8-34.7 (11.4 (11.3) 36.5-58. 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.4) 21.7 (11.3-64.8) 68.3) 13.4-102) 70.4-23.2) 15.8-69. 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.4-18.6 (51.1) 142 (99.7 (59.8-14.0-27.9-115) 57.0-26.7 (12..5) 14.1) 23.1 (34.8-48.2-57.8) 26.1-12.

Baird DD. et al. Wiesmuller GA. Perera FP. Blount BC. et al. Angerer J. Green RA. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Drexler H. Research Triangle Park (NC). Prenatal exposures to phthalates among women in New York City and Krakow. Malek NA.16(4):487-493. 2005. Needham LL. Calafat AM.22(3):688-695. et al. Chen Z. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction.112(3):331-338. Hilborn ED.210(3-4):319-333. Environ Health Perspect 2000. et al. Singh NP. et al. Atlanta (GA). Hodge CC. Wittassek M. Koch HM. Duty S. Schettler T. Rylander L. Hum Reprod 2007. Sanchez GN. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Int J Hyg Environ Health 2007. Ryan L. Needham LL. 112(5):A270].114(9):1424-1431. Reidy JA.html. Gans G.nih.18(1):122. 2000 [online]. et al. Hauser R. Pirkle JL. Caudill SP. Caudill SP. Calafat AM. Rossbach B. Reprod Toxicol 2004. Ryan L. Dobler L. Poland. Third National Report on Human Exposure to Environmental Chemicals. Meeker JD.93:177-185. Duty SM. Davis BJ. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Reproducibility of urinary phthalate metabolites in first morning urine samples. J Androl 2004. Caudill SP.niehs. Silva MJ. Giwercman A. Hagmar L. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Bull Environ Contam Toxicol 2002. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Hu H.110(5):515-518. Richthoff J. Urinary levels of seven phthalate metabolites in the U. Environ Res 2003.108(10):979-982. Levels of seven urinary phthalate metabolites in a human reference population. Eckard R. Phthalate monoesters levels in the urine of young children. Butala JH. Brock JW. Environ Health Perspect 2006. Koch HM. Barr DB. Jonsson BAG. 4/20/09 Silva MJ.111(14):1719-1722. Weuve J. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites.S. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Hoppin JA. Available at URL: http://cerhr. Sampson EJ. Helm D. Jacek R. Camann DE.Phthalates References Adibi JJ. Jedrychowski W. Silva MJ. 264 Fourth National Report on Human Exposure to Environmental Chemicals .gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Environ Health Perspect 2002. Environ Health Perspect 2003. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. et al. Epidemiol 2005. David RM.25(2):293-302. Centers for Disease Control and Prevention (CDC). McKee RH. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Silva MJ. Barr D. Silva MJ. NTP-CERHR. Brock JW. Environ Health Perspect 2004. Brock JW.68:309-314.

2000).4 (20. 2004.63) 3.0-14. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.40-5.6) 16.6-14.43) 6. mostly as MnBP (Anderson et al.6 (10.40-12.0-18.40-3.20 (6.97-7.6) 26.. and insecticides.2 (11.00) 6.33 (2.5 (17.00 (7.00-4. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.55) 2.5) 22.2-22.90 (3.48 (2.5) 14.10 (4.5-29. interval) 2.9 (16.3 (11.6) 17.6) 16. population from the National Health and Nutrition Examination Survey..3 (16.6-18.6 (11.5) 25.68 (2.00) 7.46 (2.20 (3.90) 12.5-16.10 (4.1) 22. Survey Geometric mean (95% conf..60) 3.20 (7.30-6.70 (2.40) 5.00-9.1 (13. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.9) 10.50) 2. 2000.7) 14.3-18.30 (1.6) 17.8) 21. and also in some printing inks.5-16.82-3.2 (12.3 (13.0) 13..40-4.00) 10.4) 22. 2005).60 (2.6-20.6 (13.60 (8.0) 12.0 (19.30-2.7 (18.1-12. in a small sample of pregnant women in New York City (Adibi et al.3-19.4-27. they have been referred to as monobutyl phthalate (MBP).50) 90th 12.84) 4.90-2.3 (19.66) 2.97) 4.50) 18.4-12.0-38.3-24. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.6-26.0) 20.4 (14.90 (6.80-5. OSHA has established a workplace air standard for external exposure to DBP. Studies of children found age-related differences in urine MBP levels.2 (8.00 (5. 84-74-2 Di-isobutyl Phthalate CAS No.90-4.4) 12.. 2005).6 (14.91) 4.40-3. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.3-43. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.20-6. residents (Blount et al.40 (6.90 (4. Biomonitoring Information Median concentrations reported in the NHANES 19992000.5) 18.30) 5.3-30.80) 75th 5. Following oral administration of DBP to humans.00-11.8) 677 652 703 699 1216 1088 Limit of detection (LOD.3) 3.5) 12.6 (10.50) 7.30-3.3-20.30) 6.4) 5.10) 8.00) 4. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.30-6.22 (3. 2003). 2001).37) 6..5 (11.3) 18.80-5.30 (3.2-33.6 (29.40 (3.70) 3.67 (5.3 (16.3.8) 40.80 (3.50-6. In addition.5-24.44-2.40-17.81 (3.59) 3. CDC.50-10.07 (3.90 (4.5 (27.1) 16. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.30-7.7 (16.7-31.0) 9. Fourth National Report on Human Exposure to Environmental Chemicals 265 .7) 7.70-4.7-20.90-4.80 (5.30) 2. 2004.6) 10. DBP can produce reproductive toxicity in male rodents (McKee et al.80 (5. pharmaceutical coatings.50-4.. and in a small sample of Japanese adults (Itoh et al.10-2. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.5) 18.90-7.9 (16.40 (2.10) 11.5 (20. 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.49-2.0-25.50) 8.70 (5.1-25.50) 5.24-8.40-4.73 (2.6) 12.20-2.60 (4.10-9.8 (9.20-12...17) 4.0 (13.7 (7.20-9.70-8. NTP-CERHR.3-48.28-5.02) 4. in men attending a Boston infertility clinic (Duty et al.50 (3.70-4.85-6.0) 24.60-6.6 (14.46) 2.22) 3.6-34.00-6.80 (2. Hauser et al.40-9.00-6.20-12.2-14.S.73-5.7 (17.20) 4.96) 3.17 (2. 2005.46-5.7) 15.1-17.56 (5. 2007).56-4.5 (10.72-3.30) 10.0 (13.55 (3.7-18.0) 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. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.10) 2.60 (5.71 (2.50 (6.3 (13.6 (13.0 (11.10 (3.9-23. When total DBP metabolites have been measured.97) 2. 2003).5) 19. 2005).9) 15.3 (18.70) 5.S.20) 7.7 (9.50-2.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.30-13.7 (17.00) 4.46 (3.11-3.7-31.1-20.10) 9.30) 10.40 (2.30-11.1 (8.Phthalates Di-n-butyl Phthalate CAS No.56 (3.7) 18.3) 33.10-9.1) 25. about 65% to 80% of a dose is eliminated in urine within 24 hours. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.2) 5.7) 4.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.40 (7.26 (2.19-3.30 (4.10) 3.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.9-14. Koch et al.0 and 0.56) 3.80 (2.5) 23.6 (9.

96 (3.52 (2.S. up to four and 13 fold.1-12.69-7.1) 11.56-15.32) 7.47 (3.65 (4.89-5.9-16.7 (13. samples from German university students had consistently higher median urine levels of MnBP and MiBP.26-2.55-6.11-2.8 (8.81 (3.62-12.85 (2.1 (10.32 (7.01-2.66 (8.20 (2.81 (6.. 2007).76-3. 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.5 (9.83 (2.81) 4.1) 15.84 (8.00-7.27-12.11) 5.4) 23..33) 3.76-15.18-10.6-19..37) 3.0 (12.41 (2. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al.7) 3. than adults in NHANES subsamples during the same time period.04-5.17) 90th 8.02 (7.1-24.28-13.64-7.35) 3.18) 4.66) 4.91-6.0) 7..00) 01-02 03-04 01-02 03-04 01-02 03-04 4.76 (3.29-3.29-8.76-3.61-3.2) 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 2.17-12.3) 18.44 (3.69) 4.30) 2.38 (6.94-12.42) 2.33 (2.2 (10.6 (15.20 (7. Between 1998 and 2003.1) 7.5) 15.8 (10. An analysis of NHANES 2001-2002 showed similar age.51) 15.74-3.03 (5.15-4. 2005).0 (10.58-4. respectively.99) 7.80) 7.4) 7.98 (2.05) 2.13 (2.20-3.82) 4.47-12.68) 3.18) 3. ranging from more than one-tenth the NHANES median (Itoh et al.8-13.18 (1.58-3.69) 6.56-4.17 (2.31 (2.64-10. 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. Survey Geometric mean (95% conf.79-8.46-11.86) 6.52-3.28 (4.5 (11.8-18.75 (4. Over this time.9 (11.2-13.6 (9.94) 6.0) 15.and gender.62 (6. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.52) 3..53-4.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.75 (6.53-5.54) 2.79 (4.03-11.95) 10. 2005).2) 24.1) 13.9) 12.93-6.7) 10.6-19.2-15.1) 10.9 (15.10-5. 2006). In an analysis of NHANES 1999-2000.46 (2.6 (12.7) 19. 2002.45) 3.04) 7.0) 3.86-4.65-4.3) 16.04) 3.21 (5.8-36.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2..07-5.54 (4.03-7.14 (4.73 (5.24) 3.07 (2.4) 15.33-9.19 (2.5) 13.6 (8.39) 5.92 (7.20-4.1) 4.1 (11.57-4.15) 3.66) 2. while MnBP declined (Wittassek et al.1-15.78) 8.7) 11.74 (4.7 (21.80-3.51) 5. the students’ median values for MiBP levels remained relatively unchanged.09-2.52-20.3 (13.64-7.7 (9.11 (5.56) 5.8-18.5-19.4 (12.9 (9.99-4.51) 2.97-2.80 (3.65-11.57 (3.08-2.25) 5.69 (2.08) 75th 4.89 (3. to about two to fourfold higher (Fromme et al.9-26. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.95-3.00-3.72-7.72) 5.30 (6.89) 6. Weuve et al.33 (3.18 (4.6 (10. 2004).13-6.6) 11.56) 2.0 (8. 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.0) 11.81) 9.31) 2.68) 5.36-2.88 (2.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .78-8.31) 2.54 (2.34 (3.20-2. 2004).32 (3.22 (2.31 (7. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.02-10.7 (11.66) 10.68 (2.47-5.53-3.3) 13.7-28. 2007).00 (3.2 (11.21) 10.0-18.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.3 (17.3) 28.6) 13.18-4.2) 9.82 (4.6 (8.84 (4.20 (2.36-7.39-3..38-10.26 (2.79-6. interval) 2.95) 2.43) 3.78) 9.8 (9.43) 3.9-40.3) 13.8) 10.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.67-5.4-16.00-3. population from the National Health and Nutrition Examination Survey.94 (5.1-25.43) 3.46) 3.57 (3.59 (4.

2 (74.4 (71.3) 26.0-32.5-60.4 (35.2-93.2 (20.0) 27.1-22.4) 52.4.4) 22.0 (18.5) 37.0-58.1 (19.5-53.7) 74.2 (78.1 (21.4 (35.0) 117 (104-131) 112 (84.8) 48.1) 23.9.9) 29. and 0. respectively.5) 24.6 (55.6 (22.1 (19.4 (36.5-47.1-82.7-34.7) 28.6) 38.4-44.2-21.6 (26.2-22.8-119) 90.1-92.7-116) 95.4-20.3 (36.7-124) 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.2) 26.4) 20.4 (19.1 (19. see Data Analysis section) for survey years 99-00.7 (28.3-21.4 (84.9) 36.5 (29.2-24.2 (58.4-25.1) 31.4 (23.9-79.8) 19.6-29.6-24.1-29.0 (23.6 (48.3-96.9) 46.9 (20.3) 19.6) 46.9-101) 77.5) 85.7-20.6-49.8-22.6) 35.3-136) 137 (107-162) 119 (90.9) 18.2-114) 73.7-53.0 (30.7-42.7 (22.3-145) 85.5-42.0 (78.9-33.8) 43.1 (31.6 (61.8 (19.1) 47.1) 36.2) 68.8-123) 101 (90. Fourth National Report on Human Exposure to Environmental Chemicals 267 .3 (60.8) 23.6-37.6-20.9 (79.9-22.2 (79.2 (59.7-42.3 (23.6) 21.0 (17.5) 36.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.5) 78.8-29.5-27.0) 38.7) 42.1.0 (36.3) 36.8-132) 95.3-24.2) 90th 98.9 (17.7-91.7-26.0-26.3 (51.5 (30.6) 20.3 (23. Survey Geometric mean (95% conf.7-92.S. referred to as monobutyl phthalate (MBP).0) 31.1-27.5) 65.3) 40.1-75.1 (17.6 (65.3) 18.2 (75.7) 52.1) 25.2) 38. 01-02.5) 34.9) 75.2-56.6 (44.6 (90.3-60.7) 92.3) 23.3-85.Phthalates Urinary Mono-n-butyl phthalate (MnBP) Metabolite of Dibutyl phthalate (DBP) and Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.9 (17.2) 62.7-127) 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 22.6-113) 108 (90.2 (25.3) 21.7 (24.0-51.8) 58. 1.4-26.5 (74.5) 95.1 (16.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89. *In the 1999-2000 survey period.6-69.1 (51.6 (16.1) 17.3 (56.7-34.6) 80.1 (36.3 (37.9 (79.0-19.4 (21.0 (45.4 (25.7-117) 118 (108-143) 93.3-40.1-80.6 (32.5 (28.6-48.1-51.5) 21.4-18.2-87.2-23.5) 17.0) 21. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.7 (38.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.0-19.5 (59.1 (28.5-121) 106 (94.5) 36.7-121) 97.7 (19.2 (21.1) 20.4-42.2) 32.5-43.1) 23.1) 19.9-28.8-25.4 (72.1 (58.1 (54.2 (17.5) 19.7 (18.9) 71.3 (30.7 (33.9-114) 116 (97.4 (35.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.7 (16.5-117) 95.7-111) 64.3 (42.0) 120 (98.6 (19.4) 64.3 (30.4 (38.6-31.5) 26.9-22.2) 20.7 (64.0 (72.7-106) 69.8) 62.6-29.7 (18.9-92.2 (21.1 (18. interval) 24.6-33.3-67.6) 39.2-63.9-53.4-31.3-76.2 (18.8) 75th 51.1 (26.7) 124 (98.1-20.1-24.8-111) 167 (143-223) 121 (106-136) 137 (122-156) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 23.5) 20.2-32.2-49.5) 40.5) 31.0 (20. and 03-04 are 0.2-33.0) 30.1) 23.9) 21.3 (17.6-36.8-42.1) 30.9-42.6) 17.4-159) 107 (84.8 (57.4) 59.1 (41.1) 46.0) 84.6-143) 127 (99.2 (19.5-44.5-47.0 (25.3-79.0 (31.7 (51.1 (19.0 (15.6-44.0-24.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.4-60.4 (35.0-73.6) 71.9) 26.7 (43.2-159) 92.0-21.9-87.1 (34.7 (70.0) 20. population from the National Health and Nutrition Examination Survey.1 (62.5) 47.5 (59.7-24.0-24.2) 42.3) 24.6-40.

6-92.0 (69.0) 94.4 (17.3-81.7 (43.0) 108 (71.2-179) 84.9 (21.9-34.3-40.6-53.5 (18.3) 35.3 (17.7-26.9 (30.2-48.1) 21.1 (34.5-37.S.9 (73.4-131) 81.0) 53.2-22.7-39.0 (61.6-50.3 (24.4) 19.8) 75th 38.7 (14.6 (19.5 (14.2) 74.5-22.9 (56.6-155) 91.7-19.9 (35.0) 28.0-19.4-103) 117 (83.1-128) 97.9) 49.8 (17.8) 17.1-23.8) 30.2-73.3-39.2-108) 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.1) 20.9-68.8 (18.2) 31.2-21.2) 65.8) 63.1) 35.5-30.0) 26.2-28.8) 28.3) 21.2-16.1-62.6-43.0 (26.5-70.5 (15.4 (68.3) 67.8) 40.3) 18.8) 35.0) 19.6) 65.3-20.0) 70.6 (29.5) 84.5-142) 89.7 (12.2-22.4 (16.3) 33.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.5-41.3-78.6) 24.9) 91.2 (19.9 (30.5) 17.1-83.8 (13.5-16.5-15.4-24.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.4) 51.8-235) 137 (108-198) 88.9) 24.6) 31.8) 17.9-26.6) 37.3) 33.6-44.0 (43.5-23.4 (13.1) 17.1) 53.7 (27.9-84.0) 29.9) 39.3 (76.6 (41.9) 14.8-43.7) 20.0) 35.4-61.3 (16.1-99.7-78.6) 38.1) 37.4) 53.4-47.9) 62.3 (55.4 (56.7) 19.0 (18.3) 19.1) 44.0) 25.7 (16.0-38. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.1) 61.7) 42.2) 159 (102-263) 147 (93.3-26.9-68.0 (50.0) 81.6) 34.9 (16.8) 20.4-65.6-23.7-37. population from the National Health and Nutrition Examination Survey.9) 28.5 (30.7 (19.7-21.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.6 (25.0-90.6 (25.5-21.8) 19.1) 42.6-24.2-61.7-19.5 (18.7 (57.8 (18.8-24.6) 23.6-24. 268 Fourth National Report on Human Exposure to Environmental Chemicals .6 (61.4 (33.3 (21.9) 30.0 (27.1) 22.0-113) 104 (83.9-56.2-22.2-86.9-70.5) 21.6-28.3 (69.6-74.9-38.1 (61.3-38.9 (39.7-51.7 (60.2 (16.0-92.6) 14.4 (31.4) 20.5) 90th 68.6 (57.6-23.9 (35.1-32.0 (20.6 (72.0-60.2) 59.7 (73.5) 91.3 (48.0 (71.3 (60.5 (64.4) 62.1-99.3 (19.4 (37.4-135) 71.6-27.8) 13.3-17.6-139) 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) 19.3-32.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.2-18. Survey Geometric mean (95% conf.8 (18.0 (19.5 (81.6) 83.1) 20.8-24.0 (70.3-49.1 (21.7-80.6) 25.5) 39.9-36.3 (46.8 (22.1) 50.4) 16.6-44.4-72.4) 15.2 (35.5) 60.4-164) 96.9-14.9) 20.3-106) 74.3) 20.7 (60.5-64.0) 41.9 (37.0 (34.4) 15.5-76.7-28.8 (33.2-85.4 (16.3 (52.6) 24.4 (47.2-106) 64.0-41.9 (20.3) 17.1-21.3 (28.7) 36.6) 39.1 (56.3) 19.0 (16.6-26.3 (17.2) 21.9-100) 86.6-42.4) 21.2-27.0 (52.8 (16.8) 23.0-75.8-23.1 (29.6) 64.9-105) 85.0) 75. interval) 22.7 (28.3-21.8 (65.9-49.6-128) 96.3-18.9 (30.0 (18.6) 18.8) 17.8) 34.8-32.4 (17.4 (19.6 (17.7 (20.5-18.0) 55.4 (31.3 (71.1-18.6 (27.0 (15.3 (17.3) 52.1 (32.7-42.4 (23.4 (45.7-23.6-19.1 (15.8) 34.5) 134 (93.5-142) 81.1 (46.2 (83.3 (42.9 (58.0-47.8 (50.3 (52.6 (31.4 (53.0) 59.2) 16.3-21.3) 59.9 (64.6-16.7-20.4 (31.4 (20.4 (18.8 (25.9) 52.4-34.7 (54.3-71.4 (50.3-114) 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 17.8) 20.9 (19.3-23.2 (19.6-119) 63.6-22.7 (81.0-17.8) 22.6-32.2 (38.4 (50.6 (74.5) 82.4-76.

Urinary phthalate metabolites and biomarkers of reproductive function in young men. Blount BC. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Eckard R. Richthoff J. Third National Report on Human Exposure to Environmental Chemicals. et al. McKee RH. Castle L. Drexler H. Int J Hyg Environ Health 2005. Needham LL.16(4):487-493. Weuve J. Calafat AM. Dobler L. Yoshida K.18(12):10681074. Scotter MJ. Ryan L. Reprod Toxicol 2004. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Koch HM. et al. Atlanta (GA). Environ Health Perspect 2003.html. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Occurrence and daily variation of phthalate metabolites in the urine of an adult population.114(9):1424-1431. Singh NP. Wittassek M. Jacek R. Needham LL.18(1):122. Bull Environ Contam Toxicol 2002. Helm D. Food Addit Contam 2001. Giwercman A. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Itoh H. et al. Masunaga S. Pirkle JL. Bolte G. David RM. Barr DB. Reidy JA. Duty S. Barr D. Perera FP. Environ Health Perspect 2006.93:177-185. Hu H.niehs. Poland. et al.111(14):1719-1722.nih. Angerer J. Malek NA. Rossbach B.S. Koch HM. Centers for Disease Control and Prevention (CDC). 2000 [online]. Rylander L.210:21-33. Caudill SP.25(2):293-302. Hum Reprod 2007. Ryan L. et al. Hagmar L. Epidemiol 2005. Environ Res 2003. Prenatal exposures to phthalates among women in New York City and Krakow. Research Triangle Park (NC). National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. 2005. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Butala JH. Fromme H.22(3):688-695. Massey RC. Camann DE. et al.68:309-314. et al. Angerer J. et al. Wiesmuller GA. Silva MJ.Phthalates References Adibi JJ. NTP-CERHR. Caudill SP. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine.108(10)979-982. 112(5):A270]. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Levels of seven urinary phthalate metabolites in a human reference population. Int J Hyg Environ Health 2007. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). Duty SM. Meeker JD. Silva MJ. Sanchez GN. Silva MJ. Hodge CC. Available at URL: http://cerhr. Brock JW. Green RA. Brock JW.gov/chemicals/ phthalates/dbp/dbp-eval. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Drexler H. Hauser R. Environ Health Perspect 2004. Gans G. Springall C. Boehmer S. Calafat AM. Silva MJ. Caudill SP. Koch HM. Jedrychowski W. Int J Hyg Environ Health 2007.208:237-245. Chen Z. Sampson EJ. Phthalate monoesters levels in the urine of young children. Schettler T. Jonsson BAG.210(3-4):319-33. J Androl 2004. Urinary levels of seven phthalate metabolites in the U. Hilborn ED. Anderson WA. 4/20/09 Silva MJ. Environ Health Perspect 2000.112(3):331-338. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.

300-.400 (.500 (. and 03-04 are 0.400-. polyvinyl acetate.600) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600) . Biomonitoring studies on levels of urinary MCHP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DHCP than are found in the general population.200-. including nitrocellulose. Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.300 (.300-.400 (.500 (.00-2.300-. population from the National Health and Nutrition Examination Survey. respectively.S.10 (<LOD-2.300 (.200-.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .600) .500) .70) .300-.300 (. 270 Fourth National Report on Human Exposure to Environmental Chemicals .400 (.00 (<LOD-1.400-.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.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 . see Data Analysis section) for Survey years 99-00.400-.400 (.600) .200-.2.700) .300 (. 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.500) 1. only levels at or above the 90th percentile could be characterized.300 (.200 (<LOD-.500 (. 01-02.500) < LOD 1.400) 1.400) < LOD 1.300 (. which may vary for some chemicals by year and by individual sample.400 (.600 (.00-3.500) .10 (<LOD-1.00 (<LOD-1.500) < LOD < LOD .400 (<LOD-.400) 1.400 (.300) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300-. and polyvinyl chloride.400 (<LOD-.600) .Phthalates Dicyclohexyl Phthalate CAS No.300 (<LOD-.400 (<LOD-. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.300-.400) < LOD < LOD .70) .50) .10 (. Survey Geometric mean (95% conf.500) . People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.500) .400 (<LOD-.500) 1.500-.500 (.300 (.500) < LOD < LOD . < LOD means less than the limit of detection.300-.90) . and 0.700) . Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.300) < LOD .10) .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 1.500 (. 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.400 (.00) .500 (.500 (.500 (.400-.400-.00 (<LOD-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 .200-.3.600) < LOD . resins.400-.700) . 0. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers. In this Report.200-.400-.300-. and polymers.500) 1.50) .200-.70 (1.900-1.10 (<LOD-1.20) .500 (.80) .300-.70 (1.9.300-.

380 (.740) .14 (<LOD-3.54) .16) .310) < LOD .43 (1.82 (1.490) .350-.630 (<LOD-.36-1. Fourth National Report on Human Exposure to Environmental Chemicals 271 .690-1.500-.18) .33 (<LOD-3.620) < LOD .420-.330 (.910 (.290-.530 (.830) 1.910 (.220 (<LOD-.44) .670-1.590) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .940 (.590 (<LOD-.470 (.420-.33) .770) < LOD 2.530-.450 (.240-.500) 3.800-1. population from the National Health and Nutrition Examination Survey.74) .670 (<LOD-.330 (.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 .53) .360-.530) 1.00 (<LOD-3.00) .770-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.Phthalates Urinary Mono-cyclohexyl phthalate (MCHP) (creatinine corrected) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.11) .510 (.34) .400-.410 (.370 (<LOD-.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .54 (<LOD-2.950 (.480 (.10) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.06) .67 (1.260-.710) .54-6.250 (.630 (<LOD-.770-1.910 (.17) .690) < LOD < LOD .22 (<LOD-1.170-.400-.310-.690) < LOD 2.590 (.16 (<LOD-3.390 (.610 (.530-1.880 (.05) .510-.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.770 (.270) < LOD .06) .470) 3.560) 1.500 (.450 (.770-1.660) .12-1.380-.82) . Survey Geometric mean (95% conf.910 (.740) < LOD < LOD .690) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.660) < LOD < LOD .420-.S.53) .790-1.690 (.

3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75.. deodorants. particularly those containing fragrances. respectively. and also in men attending a Boston infertility clinic (Hauser et al.5) 81.3 (74. In contrast. 2002).3 (82. 0.S. 2001-2002. 2007).8-111) 85.9. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples.2. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. 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. and hand lotions.1 (71. Products that may contain DEP include perfumes. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. soaps. and 03-04 are 1.7) 71. shampoos. 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. colognes. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.Phthalates Diethyl Phthalate CAS No.4 (62.2-102) 95. see Data Analysis section) for Survey years 99-00. 2003) and African-American women in Washington.1-93. and 0.9-92. Biomonitoring Information MEP levels in the NHANES 1999-2000.4.9 (61.7 (70. 272 Fourth National Report on Human Exposure to Environmental Chemicals .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 2003-2004 subsamples were similar to median or geometric mean levels in small samples of pregnant women in New York City (Adibi et al. 01-02. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH.. DC (Hoppin et al.. population from the National Health and Nutrition Examination Survey.

Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. interval) 163 (149-178) Selected percentiles ( 95% confidence interval) 50th 141 (129-157) 148 (133-162) 153 (137-177) 75th 360 (307-422) 388 (330-435) 452 (386-504) 90th 905 (753-1180) 969 (805-1180) 1110 (889-1290) Total 167 (150-185) 181 (163-202) Sample size 1950 (1670-2310) 2536 1840 (1450-2200) 2782 2040 (1640-2540) 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 92. Analysis of NHANES 2001-2002 showed similar findings. Median MEP levels found in a small sample of German residents (Koch et al.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. 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.S. 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.2 (66. 2003) were slightly lower than levels found in NHANES 2001-2002. 2004)..9-110) 96. 2002). Other population estimates also differed by sex and race ethnicity (Silva et al.. 2005).9 (82. This age-related trend is opposite the direction seen for other phthalates.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 .7-110) 81. 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.3-105) 87.6 (77.Phthalates 2002 (Brock et al.5-113) 122 (93. In an analysis of NHANES 1999-2000.0 (66.5-114) 101 (87.6 (65. with adjusted geometric mean levels of urinary MEP that increased with age (CDC. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.. 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. population from the National Health and Nutrition Examination Survey.

Ryan L.112(3):331-338. Drexler H. Environ Res 2003. Jedrychowski W. Prenatal exposures to phthalates among women in New York City and Krakow. Third National Report on Human Exposure to Environmental Chemicals. Jacek R.110(5):515-518. Atlanta (GA). Camann DE. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.22(3):688-695. 112(5):A270]. Hodge CC. Hoppin JA. et al. Barr DB.93:177-185. Brock JW. Environ Health Perspect 2004. Caudill SP. Poland. Rossbach B. et al. Bull Environ Contam Toxicol 2002. Caudill SP. Silva MJ. Brock JW. Angerer J. Urinary levels of seven phthalate metabolites in the U.68:309-314. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. 274 Fourth National Report on Human Exposure to Environmental Chemicals . Needham LL. Baird DD. Singh NP. Hum Reprod 2007. Barr D.111(14):1719-1722. 2005. Phthalate monoesters levels in the urine of young children. Reidy JA. Duty S. Meeker JD. Perera FP. Silva MJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Environ Health Perspect 2003.Phthalates References Adibi JJ. Hauser R. Davis BJ. Koch HM.S. et al. Hilborn ED. Centers for Disease Control and Prevention (CDC). Malek NA. Silva MJ. Reproducibility of urinary phthalate metabolites in first morning urine samples. Environ Health Perspect 2002.

9 (17.70) 2.50-16. and in humans.2-35.5 (25.31 (3.00-3.31-4.0 (19.10 (3.S. DEHP is metabolized to more than 30 metabolites which are rapidly eliminated in urine.10) 8.0-84.00-5.3-49.0 (14.83) 2.4-20.62) 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 5.20 (1. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).35) 4.80-3.4-20.0) 35.50-6.30-13.6 (10.30 (4.90-4.70) 7.70-4.8) 15.2) 29.16-3.1 (11.90) 4. population from the National Health and Nutrition Examination Survey.4) 6.4) 22.10-11.40) 2.39) 3.70 (5.80) 9. 1982.6 (11.50 (8.6) 14.7) 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 3.60) 3.7-18.4 (21.70 (1.50) 4.1-48.80 (8.5) 43.5-28.70-6.00 (7.9 (26.82) 3.15 (1.4) 33.3 (11.9) 13. mainly polyvinyl chloride.5) 31.00) 3.27) 2.26-2.40) 4. 1.9-55.80 (8.50-3.80-4.90) 4. as glucuronide conjugates (Albro et al.6 (12.00 (5.6) 15. DEHP has been removed from or replaced in most toys and food packaging in the United States.70-5.Phthalates Di-2-ethylhexyl Phthalate CAS No.3 (15.6-25.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.50-6.34 (2.20 (3.50-5.03-2.4 (13.6-38.70 (8.7) 22. interval) 3.20 (3.60) 4.1982). Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40-12. Fourth National Report on Human Exposure to Environmental Chemicals 275 .7) 27.9) 5.8-50.80-5.7) 37.0) 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 3.00 (4.5 (18.12 (4.5) 21.5-41.1) 19.40) 8.80 (1.4) 20.00-4.60) 7.6 (16.20 (1.40 (4. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.3) 13.30-6.9) 27.9-29.6 (9.2 (29.3 (10.1) 25.1 (8.5 (20.9-57.00) 11.1-17.80) 6.10-5.2-28.10-2.5-40. and 03-04 are 1.90-3.70 (3.69) Selected percentiles ( 95% confidence interval) 50th 3.3-57.6-28.1) 29.98) 2.50-20..50 (3.5) 37.80-9.35 (1.5-28.51) 4.3-25.0) 23.4-53.3 (24. Albro and Lavenhar.6) 39.40 (6.40-8.6 (41.2. Concentrations in plastic materials may reach 40% by weight.4) 5. 01-02.3-26.82 (3.42-5.10-11.40-8.40 (4.80 (4.0-19. Peck and Albro.40) 4.9) 18.40-8.42) 3.5) 40.3) 52.7 (17.50-5.10-5.63-4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.1-29.20 (4.0 (9.5 (30. Following ingestion.10) 3.41 (3.1 (8.0 (19.4-40.2 (31.9 (29.50 (7.9 (7.4 (16.00) 1.85) 4.4) 7.54) 4.00) 19.2 (11.5) 23.4) 15.10 (4. and blood product storage and intravenous delivery systems.23 (2.0 (18.5 (18.57-7.30 (3.37-4.9-19.10) 3.9-48. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP)