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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Paradichlorobenzene) 1.4’.4'.4'-Tetrabromodiphenyl ether (BDE 66) 2.2'.4.2'.2’.4.2'.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2'4.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.4.4.1-Trichloroethane (Methyl chloroform) 1.1.2-Dichlorobenzene (o-Dichlorobenzene) 1.3'.2'.6'-Hexabromodiphenyl ether (BDE 154) 2.4'.4.4'-Tribromodiphenyl ether (BDE 28) 2.4.4'. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.3.cdc.1-Dichloroethane 1.What’s New in this Report What’s New in this Report In this Fourth Report.4'.2-Dichloroethane (Ethylene dichloride) 1.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .4.4’.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.4.1-Dichloroethene (Vinylidene chloride) cis-1. 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 (2.3.html.5.2.2'.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.4'-Tetrabromodiphenyl ether (BDE 47) 2.2'.2'.1.3-Tetramethylbutyl] phenol) Triclosan (2.2-Trichloroethane Trichloroethene (Trichloroethylene) m.5'-Hexabromodiphenyl ether (BDE 153) 2.3’.5'-Tetrachlorobiphenyl (PCB 44) 2.4'-Pentabromodiphenyl ether (BDE 85) 2.2-Dichloroethene Dichloromethane (Methylene chloride) 1.4-Tribromodiphenyl ether (BDE 17) 2.3.5’.gov/exposurereport/chemical_selection. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.5'.5-Pentabromodiphenyl ether (BDE 99) 2.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.4.3-Dichlorobenzene (m-Dichlorobenzene) 1.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.1.4.4-Dichlorobenzene (p-Dichlorobenzene. The process for selection is described at http://www.5.3.4.5.6-Pentabromodiphenyl ether (BDE 100) 2.5'-Tetrachlorobiphenyl (PCB 49) 2.1.2'3.6.2'.2-Dichloropropane 2. Table 1.6-Heptabromodiphenyl ether (BDE 183) 2.2'.4'.5.2-Dichloroethene trans-1.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.4.

Some results reported previously have been changed or removed due to improvements in analytical measurement or recognition of an analytical issue (e. urinary 2. 2003-2004 data for these other pesticides will be provided on this website as soon as they are available. Data for other pesticides are included only for 1999-2000 and 2001-2002.4-dichlorophenol and 2. and these data will be included in the next release of the Report. Explanations for each change are provided in Appendix B. Fourth National Report on Human Exposure to Environmental Chemicals 3 . 2003-2004 data for the organochlorine pesticides and the dialkyl phosphate organophosphorus insecticides are included in the Report.g. Percentiles for all three NHANES survey periods (1999-2000.g..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. Details of this procedure are provided in Appendix A. five results that all have the value 90..5-dichlorophenol for the 1999-2002 survey periods. 2001-2002. 2003-2004) have been re-computed by use of this improved procedure. the presence of an interference) that produced results of inadequate quality. Only slight differences should be noted when one compares the recomputations to previous releases of the Report.1). 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.

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

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

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

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

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

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

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

and cosmetics (NTP-CERHR. or to glutathione conjugates (Calleman et al.4 (59. the main source of exposure is from the diet.5 (79. Recently.1) 55..9-52.1-64.7-60.0 (67.3) 70.7 (65.2-118) 98.7-64. and from dermal contact with products that contain residual acrylamide.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59.7) 75th 79. EPA.6-61.2-67. 2005).0) 57. 2004). 1990.5) 66.Acrylamide Acrylamide CAS No.1) 101 (95.6) 73. and binding agents.7) 54.4 (51. widely distributed in tissues.2-70.8 (52.4 (54.3-2. and well below doses known to cause nerve damage or carcinogenicity in animals.1 (52.0-104) 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 61.9) 63.2-114) 163 (147-191) 96.9) 57. Fourth National Report on Human Exposure to Environmental Chemicals 11 .S.2-93. In humans.4-76.0-58.0-49. acrylamide has produced upper airway irritation following inhalation of high levels.2) 57. (NTP-CERHR. Acrylamide is not thought to accumulate in the body at environmental doses.2 (62.8-57.4) 100 (89.0) 85. in permanent press fabrics.1 (47. soil conditioners. 2005).0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.4-83.3) 86. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U..S. but are generally above the U. In the general population.6-104) 82.2-59. Elimination occurs mainly in the urine as mercapturic acid conjugates. EPA reference dose of 0. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. as an absorbent in disposable diapers.4) 57. 2005). interval) 61.9 (60. Foods such as french fries and potato chips can contain acrylamide at levels up to 100 times greater than levels found in cooked fish or poultry (DiNovi and Howard.0-66. it was discovered that acrylamide is formed when starch-rich foods. 2005). Since acrylamide has limited volatility and high water solubility. such as potatoes and some grains. Survey Geometric mean (95% conf.1-57.6) 90.3-71. 2002).0 μg/kg for adults (FAO/ WHO. 2005).7 (63. glycidamide.0-108) 152 (139-175) 126 (111-142) 108 (86. FDA.5-80.1-61.1 (83.1 (73.6-65.9) 75.6 (51.0 (53.1) 46. pulp and paper production. 2006. smoking.5 (52. mineral processing. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging.7) 58.0. 2005. are heated at temperatures used for frying and baking. Estimated intakes in children are about twice that of adults (DiNovi and Howard.7) 96. and in the synthesis or compounding of dye materials. Tareke et al.2-91.4) Selected percentiles ( 95% confidence interval) Sample 95th 192 (168-217) size 7101 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 54.9-61. drinking water.7 (58.1) 62.6-108) 61.4-60.2-77. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR.9) 58.7 (55. see Data Analysis section) for Survey year 03-04 is 3.2 (75. 2004. Polyacrylamides are useful water-compatible polymers used in water treatment.0 (57.6) 71. 217 million pounds of acrylamide were produced commercially in the U. in some sealing grouts.2 (58. population from the National Health and Nutrition Examination Survey.1-64.3 (53.8 (81.. and is either metabolized to the reactive epoxide.S. EPA.S. Animal studies indicate that acrylamide is well absorbed.6-75.8 (57.6) 50.1) 53.5 (44.9 (69.6-66. Natural substances in the food are converted to acrylamide.9 (54.S.6 (81. Fennell et al. 2006). ocular and dermal irritation from direct contact with acrylamide containing materials.6 (56.1 (88. and an average daily intake is estimated as 0. In 1997. acrylamide is synthesized and used in the production of polyacrylamide polymer.2) 57. 1994).7-64.0 (69.4-89.8-55.3) 63. These estimated intakes are hundreds of times lower than occupational exposures. but can covalently bind to form adducts with proteins.4-60. gels.8 (91.7) 73.4 (54.5 (74.9-105) 86. People may be exposed to acrylamide from foods.2 μg/kg/day (U. FAO/WHO.3 (55.5-85.5) 58. and in some cosmetics. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U.4 (53.4) 57. Commercially.

2006). 2006). U. 2005).5-66. 2005) have been demonstrated in animals.9 (81. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U..3) 59.9-78. EPA at: http://www..2 (56.9) 87.4-103) 79. 2005).5) 87.3 (56. IARC classifies acrylamide as probably carcinogenic to humans.0-62.7-86.5) 75th 85. 2009).S. respectively) are markers of integrated acrylamide exposure over the preceding few months..2) 55.. although different analytic methods can affect results.1) 62.5) 71.0.7 (84. Schettgen et al.9-138) 143 (130-159) 96. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. and neuronal DNA reactivity (Doerge et al.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.3) 85.. 2005.1-70. see Data Analysis section) for Survey year 03-04 is 4.pdf. male germinal cell injury. reproductive effects (reduced litter size. 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. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.4 (61.. 2008).1 (66. Hagmar et al. AHA levels have been shown to increase with dietary intake (Hagmar et al. 2005. 2001). 2005.4 (81.0 (52.. 2005). 2008). 2002.5-94. 2006) have been demonstrated after acrylamide dosing.6 (66. 2005).1 (57. EPA.7) 74.0-103) 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 64.8-61.. fetal death.4) 53. 2004).8) 45.9 (58.7-64. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al. Additional information is available from U. scrotal..3) 59...0 (75.4) 83.9) 59. Vesper et al.0-93.9-76. 2005.1) 60.7 (87. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers. Animal studies have shown that acrylamide can cause nerve damage (neuropathy).9-62.0) 118 (103-126) 121 (112-134) 113 (94.2) 87.1 (56.7) 61. 2005. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA.5 (56.3) 59.3-101) 95.4 (57.4 (56. In addition.5-92.5 (59.9) 65. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood.1-56. Mucci et al. 2005.8 (44. 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. Glycidamide has been shown to react with DNA (Doerge et al. Maniere et al.7-62. Rice.7) 60. 2005. population from the National Health and Nutrition Examination Survey.6-90.2-91. EPA. Klaunig et al..who. uterine. 2002.7 (57.0 (80. presynaptic nerve terminal binding (LoPachin.2) 65.. dominant lethality).5-64. 2005.2-68. glycidamide (NTP-CERHR.7) 90.4-65. Survey Geometric mean (95% conf. 2003.4 (51.S..4-59.8-49. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.. interval) 59.2 (72.6-64.. Acrylamide is clastogenic and can produce dominant lethal mutations.1 (70.Acrylamide occupational exposures. 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. 1997.5 (83.9) 75.4) 46. thyroid.6-62. 2005. Puppel et al. most non-smokers had levels less than about 100 pmol/gram hemoglobin. 12 Fourth National Report on Human Exposure to Environmental Chemicals . 1997.epa.S. 2005) and sperm DNA adducts (Xie et al.7 (61. Puppel et al. probably through its epoxide metabolite.int/ ipcs/food/jecfa/summaries/summary_report_64_final. U.9-77..1) Selected percentiles ( 95% confidence interval) Sample 95th 167 (153-181) size 7278 Total Age group 3-5 years 6-11 years 12-19 years 20-59 years 60 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 59.9 (57. Vesper 2005) and smoking (Bergmark..6 (90.5 (42. altered gene expression in testicular tissues (Yang et al.4-98.8 (51. Axonal degeneration.0 (70. Schettgen et al. adrenal.1 (82.1-62.3-78.S. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www. NTP-CERHR.8) 60.4 (90. 2005.0) 94.. 2006. After exposure ceases.1-60.1) 56. 2004.8-48.9-64.2 (63.2-90. and cancer (mammary.. and other sites) (FAO/WHO.

et al. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake.561:21-37.cfsan.126(2):361-371. Cheong HK. 2/3/09 Klaunig JE. 2/3/09 Hagmar L. 2001. 2001). DiNovi M and Howard D. NIH Publication No.10(1):78-84.27(4):219-226. et al. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. 2009 Jan 8. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. Mutat Res 2005. Nordander C. Churchwell MI.43:365–410.85:447-459. Beland FA. 2004 Acrylamide in Food Workshop: Update Scientific Issues. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Calleman CJ. Aprea P. Perez et al. Kautiainen A. National Toxicology Program.. Survey data on acrylamide in food: individual food products.Toxicol Appl Pharmacol 1994.561:49-62. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). Granath F. Rome.580(1-2):119-129. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Hagmar et al. smoking habits and gender. Toxicol Appl Pharmacol 1993. Illinois. Chem Res Toxicol 1997 Jan. Available at URL: http://www.who. 6013-6019. gov/~dms/acrydata. Calleman CJ. Axmon A.pdf. Acrylamide neurotoxicity: neurological. Mucci LA.fda. Food Chem. Adv Exp Med Biol 2005. Italy. 1993. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Chicago. 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. Metabolism and hemoglobin adduct formation of acrylamide in humans..html#u1004. CFSAN/Office of Plant and Dairy Foods. Laurentie M. Bjellaas T. Mutat Res 2005. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide.3:406-412. Churchwell MI. 054472. February. The Updated Exposure Assessment for Acrylamide. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes.120(1):45-54. Fennell TR. Zhang S. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. 2005. In another study. Tornqvist M. Maniere I. 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.gov/chemicals/ acrylamide/Acrylamide_Monograph. 2006.580(1-2):131-141. He F. Doerge DR. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation. Rosen I. Available at URL: http://www. Wu Y. July. DNA adducts derived from administration of acrylamide and glycidamide to mice and rats. Farmer PB. Yang JS. Human exposure and internal dose assessments of acrylamide in food. Bergmark E. Toxicol Sci.Acrylamide In occupational settings. J Agric Food Chem 2008. 1994). Godard T. Mechanisms of acrylamide induced rodent carcinogenesis. Toxicol 2005. smokers and nonsmokers. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al.. Paulsen JE. Kamendulis LM.nih. Duale N. Paulsson B. Food and Drug Administration (FDA). Hagmar L. Uncertainties. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Tornqvist M. da Costa GG. Bergmark E.. April 13-15. Burgess J. References Bergmark E. et al. Magnusson AL.580(1-2):157-165. Guffroy M. Wilson KM. Costa LG. LoPachin RM. Malmberg B. Twaddle NC. et al. Available at URL: http://cerhr. Andersen M. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. Tian G. He F. Mutat Res 2005. Summer SCJ. Joint FAO/WHO Expert Committee on Food Additives. Acrylamide intake through diet and human cancer risk. and Research Strategies. Fennell TR. Adv Exp Med Biol 2005. McDaniel LP. 2004.pdf. Snyder RW. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. 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. Spicer R. 64th Meeting: Summary and Conclusions (FAO/WHO). Toxicol Sci 2005. Calleman CJ. Wirfalt E. Bridson WE.int/ipcs/ food/jecfa/summaries/summary_report_64_final. [Epub ahead of print] Dybing E. 1999).. Osterman-Golkar S. 2/3/09 Perez HL. Doerge DR. et al. Haugen M. Bruze M. 8-17 February 2005. morphological and molecular endpoints in animal models. Chem Res Toxicol 1990. Bergmark E. Scand J Work Environ Health 2001. Becher G.niehs. Alexander J. Costa LG.56.

Washington (DC).163(2):101-8. Ding X.gov/chemfact/s_acryla. Tjønneland A.274(1):59-68. Gray JG. Angerer J.htm. Available at URL: http://www. propylene oxide. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Reprod Toxicol 2005. Eriksson S. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells.580(1-2):3-20. September. Ospina M. Rydberg P. Jin Y. Karlsson P. Mutat Res 2005. Fu D. Chemical Summary for Acrylamide. Ingham L. Marko D. Myers GL. Office of Pollution Prevention and Toxics. Licea-Perez H.50(17):4998-5006. J Agric Food Chem 2008. 2/3/09 Vesper HW. 1994. EPA).206(1):9-14.19(4):527-34. 2/3/09. Angerer J. Toxicological effects of acrylamide on rat testicular gene expression profile. Slimani N. Sun H. Weiss T. Rapid Commun Mass Spectrom 2006. Kutting B. Toxicol Lett 2002. Tjaden Z. J Agric Food Chem 2002. Tareke E. Han DU. Benetou V. Int J Hyg Environ Health 2003.gov/iris/subst/0286.Acrylamide glycidamide by gas chromatography-mass spectrometry. Rice JM.580(1-2):71-80.epa. U. Environmental Protection Agency (U. Letzel S.S. Hemoglobin adducts of ethylene oxide. Chae C. Liu K. Adv Exp Med Biol 2005. et al.txt. EPA).epa. Smith A. Lee SH. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Broding HC. Environmental Protection Agency (U.561:89-96. Vesper HW. et al. Lee MH.207(6):531-9.20(6):959-64.S. Integrated Risk Information System (IRIS). Available at URL: http://www. U. Tornqvist M. Hallmans G. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure. The carcinogenicity of acrylamide. Han CH. Xie Q. Int J Hyg Environ Health 2004. Mutat Res 2005 Feb 7. Agudo A. Acrylamide. Drexler H.S. Liu Y.56(15):6046-53. Schettgen T. Vesper HW. Yang HJ. Drexler H. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Schettgen T. revised 1/3/06. Angerer J. Drexler H. Choi JH. Rossbach B. Fueller F. a carcinogen formed in heated foodstuffs. Analysis of acrylamide. Meyers T. Puppel N. Ospina M.S. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Toxicol Lett 2006.134(1-3):65-70. Schettgen T. Anal Biochem 1999. Meyers T.

060) .35 (2.193) .710 (.071) .840) 3.49) 1.015 ng/mL.059-.50) 3.00) .360) .960-1. < LOD means less than the limit of detection.950 (.230 (.12) 1.175 (.63 (2.110 (.187) .080-.190-.060-.198) * . 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.505 (.188) .050 (.052 (<LOD-.060-.320) .54 (1.620 (.770) .370-. 1998).506 (.15 (2.088-.054 (.160 (.570-1. acute respiratory infections.04 (1.480-1.66-3.997-3.050) .060-.38-2.39 (1.76 (1.S.39) 3.87-3. ** In the 2001-2002 survey period.020-.110 (.96) 2.75) 1.62) 2.310) .540 (.087) < LOD < LOD .92 (1.42-4.96 (1.12 (2.43 (1.153-.580) .70) 2.052 (<LOD-. and various other disorders (U.68) .180) .620-1. ear problems. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.09-2.990 (.047-.139) * .Cotinine Cotinine CAS No.111-.310-1.533-.300) .077) .110-.19-2.180) .12 (1.34 (1.216 (.120-.53 (1.200) 1.140 (.53-4.910-1.302) .55 (1.160) .630 (.061) < LOD .66) 1.160 (.17) .500 (.089) Age group 3-11 years 99-00 01-02** 03-04 .053 (<LOD-.100-.78) 2.131 (.220) .140-.280 (.21-1.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * . which may vary for some chemicals by year and by individual sample.49) 1.790) .630 (.240 (.600-1.01 (1.030-.20 (.120 (.350-.137-.77 (1.50-4.310-1.066-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.40) .076-.071 (.062 (.030 (.120) .430-1.060 (.230) .01) 3.077) .950-1.77 (2.30) 2. cardiovascular disease.110 (.77 (1.33-2.68 (1. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.110-.310) 90th 1.14) .580 (.63-2.770) .059-.32-2.28-1.30) 2.124 (.09-3.050-.197) .66 (1.900-1.65 (1.88 (.00) 1.066 (.120 (.058 (.770-1. 83% of measurements had an LOD of 0.726) .84-3.260) 1.080) < LOD .130) .154-. emphysema.670) .075 (.080 (.11) .50-1.080-.02 (.063) .23 (1.220-.145) .110-.070-.120 (.060 (<LOD-.137 (. and 0.050 (<LOD-.93) .930 (.54 (1.60-2.160 (.83-2.57) 2.040 (. 2004).70-2. Children exposed to ETS are at increased risk for sudden infant death syndrome. DHHS. 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. and 17% had an LOD of 0.073) < LOD .080 (.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.570 (. see Data Analysis section) for Survey years 99-00.28) .740-1.S. respectively.48-3. maternal exposure during pregnancy can result in lower birth weight.44 (1.400-.115-.120 (.16) .087-.580-1.142-.163) .040 (.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 . Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.20 (1.54) 1.470-.79) 3.860 (.106-.85 (1.148-.05 ng/mL.043-.120-.350 (.05) 1.540-.047-.350-.14) .22) 2. acute respiratory illness.167 (.21-1.068) . 2004).45) 1.110 (.94) 1.163 (.54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .030-. 2006).820) .50 (1..234) .108) * .21 (.126) .68) 2. stroke.180) .015.17 (.308 (.96-4.164 (.42 (1.660) .030-.050-.180 (.070 (<LOD-.087 (.99) 2.30) * .040-.110) .150) .920 (. and exacerbated asthma (U.20) 1.201) .19) 1.110 (.094) .160-.110) .190-.090-.190-.057-.180 (.740-1.410) .44 (2.32) 1.040 (.090-.164 (. and 03-04 are 0.080-.060 (<LOD-.89) 1.066) .213) .070) .520 (.260-1.14-1.990) . and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP.730 (.050 (<LOD-.050 (<LOD-.02) 1.15) 2.88 (1. Cigarettes contain about 1.47-3.19) .690 (.26-1.050 (<LOD-.5% nicotine by weight (Kozlowski et al.060 (.850 (.140 (.20-2.220) .23 (2.480-. DHHS.130 (.180) .070) .23 (.62 (2. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.050) .44) 2. population from the National Health and Nutrition Examination Survey.510 (.086 (.120 (.48-2.05.150) .428-.090-.32-2.44) 2.12-4. Fourth National Report on Human Exposure to Environmental Chemicals 15 .104-.080) < LOD < LOD .450-.800 (.17 (1.55-2.210 (.630 (.180) .23-2.160) .S.140-.02) 1.18-3.95) 1.070) 75th .040-.312) .080-.81-2.99) 2. Survey Geometric mean (95% conf.144 (. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.625) .621-1.20) .068) .09-3.084) .

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

Brody DJ. Vogler GP. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Fong I. Absorption and metabolism of nicotine from cigarettes.56:483-493. Pirkle JL. JAMA 1998. 1988-1991. et al.275:1233-1240. Tobacco Smoke.pdf.cancer. Clin Pharmacol Ther 1994. 4/13/09 International Agency for Research on Cancer.S.S. Metabolism of nicotine to cotinine studied by a dual stable isotope method. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children.cdc. 1988-1991.S Department of Health and Human Services (U. Racial/ethnic differences in serum cotinine levels among adult U. Turner DM. Benowitz NL. Jarvis MJ. June. In Report on Carcinogens. Benowitz NL. 2004.114(6):853-858.280:135-140.S. Metabolism and disposition kinetics of nicotine. Centers for Disease Control and Prevention. U. Strauss WJ. Coordinating Center for Health Promotion.gov/library/ secondhandsmoke/. Maurer KR. Vol 38. Jacob P. Ethnic differences in N-glucuronidation of nicotine and cotinine. 4/13/09 Centers for Disease Control and Prevention (CDC).fr/ENG/Monographs/allmonos90. 11th ed. Exposure of the U. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Kozlowski LT.S. Etzel RA. Mehta NY. Available at URL: http://www.S Department of Health and Human Services (U. JAMA 1998. Tobacco related exposures. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Sweeney CT. Jacob P III. National Center for Chronic Disease Prevention and Health Promotion. DHHS). Pharmacol Rev 2005. [online]. Schwartz SS. Cotinine as a biomarker of environmental tobacco smoke exposure. Tob Control 1998. Flegal KM. Giovino G. U. and the United States. 4/13/09 U.nih. Third National Report on Human Exposure to Environmental Chemicals. Sosnoff CS. Int Arch Occup Environ Health 1991. Trends in the exposure of nonsmokers in the U. Benowitz NL. Pirkle JL.94(2):314-320.291(3):1196-1203. Lewis PJ. U. Smoking and Tobacco Control Monograph 10 [online].gov/ntp/roc/eleventh/profiles/ s176toba.18:188-204. Office on Smoking and Health [online] 2006. Herrera B. Tobacco Smoke and Involuntary Smoking. J Pharmacol Exp Ther 1999. Caraballo R. Available at URL: http:// cancercontrol. International Agency for Research on Cancer.S.surgeongeneral. Nicotine metabolism and intake in black and white smokers. Kira S.niehs. Coordinating Center for Health Promotion.gov/tcrb/monographs/10/. Giovino GA. Houseman TH. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Modin G. Centers for Disease Control. Benowitz NL. 1999. Available at URL: http://ntp. Vol 83. Curtin LR. DHHS). IARC Monogr Eval Carcinog Risks Hum. the United Kingdom.iarc. Herrera B.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. IARC Monogr Eval Carcinog Risks Hum. 4/13/09 Perez-Stable EJ. Pickett MA. Tob Control 2006. Centers for Disease Control and Prevention. Benowitz NL.fr/ENG/Monographs/ allmonos90. 4/13/09 Iwase A. Available at URL: http://monographs. JAMA 1996. Dollery CT. National Toxicology Program (NTP). Warner K. Summary of Data Reported and Evaluation [online] 1986.15:302-307. Aiba M.63:139-43.7:369-375. Caudill SP. References Armitage AK. Respiratory nicotine absorption in non-smoking females during passive smoking.php. Hukkanen J. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Pollack HA. 1991. Schober SE.niosh. 1999-2002.4:313-316.pdf. 4/13/09 National Cancer Institute (NCI). National Institute for Occupational Safety and Hygiene (NIOSH). Epidemiol Rev 1996. available at URL: http://mtn. cigarette smokers: the Third National Health and Nutrition Examination Survey. George CF. Atlanta (GA): 2005. Am J Public Health 2004. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. Bernert JT. Jacob P III. Bernert JT. Available at URL: http://monographs. Soliman S. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary.S.57(1):79115. Brody DJ. et al.S. Mowery PD. Pechacek TF.280:152-156. Pechacek TF. Summary of Data Reported and Evaluation [online] 2004. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency. Jacob III P. iarc. Perez-Stable EJ. population to secondhand smoke: 1988-2002. Richter PA.php. Environ Health Perspect 2006. Department of Heath and Human Services. Department of Heath and Human Services.gov/eid/rmca/critdocs/ criteriadoc/33. BMJ 1975. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 .

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

S.130-. DEET is not genotoxic. DEET is not a developmental or reproductive toxicant in animals (U.S.100-.epa.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 .S.N. About 3-8% of dermally applied DEET is absorbed.180 (.110 (<LOD-.EPA at: http://www.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130 (.130-. Additional information is available from U.170 (.140) < LOD .. EPA. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. and it has not been rated by IARC or NTP with respect to human carcinogenicity. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.180 (. After absorption. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure.110-. 1998). DEET is also used in combination with dermal sun screens (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 .180) < LOD . Survey Geometric mean (95% conf.130-.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). 2002). 2003).S. DEET is not registered for use on agricultural commodities. There are over 225 insect repellents brands containing DEET. 134-62-3 General Information N. population from the National Health and Nutrition Examination Survey.190) < LOD . DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.250) < LOD .100-. One survey detected DEET in 74% of sampled streams in the U.110 (<LOD-.1.160) < LOD . General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.gov/pesticides/. 2002).449 and 0.110 (. Fourth National Report on Human Exposure to Environmental Chemicals 19 .520) < LOD .180 (.140) < LOD .120-.100 (<LOD-. Its use is recommended for prevention of several vector-borne diseases. and they range in concentration from 4% to 100%.N-Diethyl-meta-toluamide (DEET) CAS No.100-. including seizures and encephalopathy. DEET can be applied to clothing and the skin to repel biting insects. (Kolpin et al.130-. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.130) < 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.110 (.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. 2003). which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .170 (.110 (. Neurological effects in humans.100-..140) < LOD ..100-. (U.270) 688 678 518 700 598 956 Limit of detection (LOD. 1995.560) < LOD .210 (.S.140-.220 (.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.110-. DEET has low acute toxicity.130) < LOD .150) < LOD .EPA.130 (.120-.110 (.EPA.S. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Urinary N. have been reported as result of self-poisoning by ingestion or excessive dermal application. Sudakin and Trevathan.130 (.240) < LOD .140 (.N-Diethyl-meta-toluamide (DEET) N.100-. 2005).

240) < LOD .320 (.93) < LOD . 20 Fourth National Report on Human Exposure to Environmental Chemicals . DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.440) < LOD ..270) < LOD .410 (.N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.150-.N.300 (.250) < LOD .270-. Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.350-. Urinary DEET levels as high as 5.230-.280 (.350) < LOD .S. 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 . 2005).190 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.140-.580) 964 1191 1013 1343 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200 (.370-.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 ..150) < LOD .390-.290-.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.280-1. Urinary N.480 (.250-.370) < LOD .S. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .190 (.410-.300) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.130 (<LOD-.270 (<LOD-.270 (. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U.250 (.490) < LOD .410 (.190-.240-.330 (.320) < LOD . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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.170-. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.500 (.630) < LOD .690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al. 1992).350) < LOD .230-.230) < LOD . In this survey period.330 (. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC. 2007).190 (.

Quandt SA. Third National Report on Human Exposure to Environmental Chemicals. Zaugg SD. metabolism. pdf. Washington (DC): U.N’-diethyl-mtoluamide (m-DET): analysis of an insect repellent in human urine and serum by high-performance liquid chromatography. streams. Barber LB.2:341352.pdf.25:95-100. 1999-2000: a national reconnaissance. Tapia J. Chen H. and excretion of N. Absorption. U.36(6):1202-1211. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Toxicity and Exposure Assessment in Children’s Health. Diethyltoluamide (DEET). September 1998. Furlong ET. 2005. Environmental Protection Agency (U.S.N. Available at URL: http://www. Thurman EM. Schoenig GP.gov/oppsrrd1/REDs/0002red. pp.S. Sudakin DL. Atlanta (GA). Hartnagel RE Jr. U. Gabriel KL. Grzywacz JG. Barr DB. Available at URL: http://www. Bell JW. Trevathan WR. et al. EPA 738-R98-010.41(6):831-839. J Toxicol Clin Toxicol 2003. Centers for Disease Control and Prevention (CDC). 4/9/09 U. 1-118.EPA.S. DEET: a review and update of safety and risk in the general population. Meyer MT.epa. Environmental Protection Agency (U. Osimitz TG.N-diethyl-mtoluamide insect repellents reported to the American Association of Poison Control Centers.epa.115(8):1254-1260.S. Lowry LK.EPA). N. 1993-1997.EPA).16(1):10-13. Smallwood AW. DeBord KE. EPA. and other organic wastewater contaminants in U. Pharmaceuticals. Environ Health Perspect 2007. Selim S.S. Chemical Summary.N-diethyl-mtoluamide following dermal application to human volunteers. 2005 Kolpin DW. 4/9/09 Fourth National Report on Human Exposure to Environmental Chemicals 21 . Fundam Appl Toxicol 1995. Page BC. Human exposures to N. Int J Toxicol 2002. hormones. Veltri JC. Environ Sci Technol 2002.S.N-Diethyl-meta-toluamide (DEET) References Arcury TA.gov/teach/chem_summ/ DEET_summary. Reregistration Eligibility Decision (RED): DEET.S. J Anal Toxicol 1992.

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

Barber LB. Joskow R. Calafat AM. Koh WS. Available at URL: http://ntp. 1999-2000: a national reconnaissance. Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. August 2001.niehs. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Han SS. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. Regul Toxicol Pharmacol 2002.35(2 Pt 1):238-254. Hara K. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A. In vitro and in vivo interactions of bisphenol A and its metabolite.113(4):391-395. 2/4/09 Fujimaki K. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. Ye X. Meyer MT. Gray GM. Wong LY. Calafat AM. Keimowitz AR. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants.J. 4. Calafat AM. Kroes R.116(1):39-44. Reidy JA.69(22):2611-2625. Timms BG. 2/4/09 Ouchi K. bisphenol A glucuronide. Needham LL. Needham LL. Caudill SP.S. with estrogen receptors alpha and beta. Kim YH. Kawamura N.europa. Han SY.149:988-994. Zacharewski TR. Kiguchi M. Toxicol Sci 2002. Department of Health and Human Services. Watanabe C. Available at URL: http://ecb. Biochem Biophys Res Commun 2003.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. National Toxicology Program. 2/4/09 European Commission. Chung MK. J Am Dent Assoc 2006.. MacLusky. Thomas BF. Doull J. Ecotoxicity and the Environment (CSTEE). 5: 505-523. NC. Exposure of the U.102(19):7014-7019. Tsugane S.14(2):149-157. Life Sci 2001.nih. streams. Thurman EM. vom Saal FS. Arakawa C.Scientific Committee on Toxicity. National Institute of Environmental Health Sciences.59(9):625-628. Bradley S. Available at URL: http://ec. Barton L. Reidy JA. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). N.S. hormones.gov/chemicals/bisphenol/bisphenol. U. and other organic wastewater contaminants in U. Richter CA.pdf .59(4):403-408.eu/ health/ph_risk/committees/sct/documents/out156_en. Fujii S. Belgium.780(2):365-370. Zaugg SD. Brussels. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. DirectorateGeneral Health and Consumer Protection. Twomey K. Endocrinology 2008. Brine DR. Yoshinaga J. Lynch BS. Italy. An evaluation of the possible carcinogenicity of bisphenol A to humans. Imai H. 2008. Hughes C. European Commission.145:592-603. Park S. 2007. Cunha G. Matthews JB.36(6):1202-1211. McConnell EE. Barr DB. Hlywka JJ. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy.jrc.137(3):353-362. Shin HC.nih. Reprod Toxicol 2001. Myers CB. Rubin C.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Klinefelter GR. Cha SW. Ispra. Watanabe S. Marr MC.Environmental Phenols References Akingbemi BT. September. Occup Environ Med 2002. Haighton LA. Rhomberg et al. et al.312(2):441-448. November 26. Ikka T. Available at URL: http://cerhr. Hum Ecol Risk Assess 2004.pdf. Koulova AI. Available at URL: http://cerhr. Howdeshell KL. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.pdf. Kuklenyik Z. Leranth. et al. Proc Natl Acad Sci USA 2005. Bisphenol A.pdf . Furukawa M. K. and Hardy MP. and Hajszan. May 22. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Yang M.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325. Cohen JT. Environ Health Perspect 2008.nih. Harazono A. Gender differences in the levels of bisphenol A metabolites in urine. Furlong ET. 32 Fourth National Report on Human Exposure to Environmental Chemicals . Research Triangle Park. Endocrinology 2004. Human Health.gov/chemicals/bisphenol/BPAFinalEPVF112607. Environ Sci Technol 2002. et al. Tyl RW. Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra.. Joint Research Centre Institute of Health and Consumer Protection.10:875-921.S. Kim JC. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Ema M. T. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Pyo MY. Environ Health Perspect 2005. Kim CS. Rat two-generation reproductive toxicity study of bisphenol A. Nippon Eiseigaku Zasshi 2004. Barr JR. niehs. niehs. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Pharmaceuticals. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. National Institutes of Health. Szigeti-Buck. 2003.. Munro IC. Kolpin DW. 2002.68(1):121-146. Ekong J. 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. C. Chem Res Toxicol 2001. Serizawa S. Hanaoka T. Needham LL. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population.pdf. Sottas CM.

Chang SS. Biological monitoring of bisphenol a in a Korean population. Dekant W.147(6 Suppl):S56-69. bisphenol-A. Jang JY. Food Chem Toxicol 2002. Environ Health Perspect 2005. Wilson NK.15:12811287. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. Sheldon LS. Morgan MK. Csanady GA.44(4):546-51. vom Saal FS. Yang M. Nagel SC. Chem Res Toxicol 2002. Chuang JC. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure. et al. Lordo RA. Environ Res 2007. Lee SM. III. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Vom Saal FS. Kawamoto T. Hughes C. Filser JG. An observational study of the potential exposures of preschool children to pentachlorophenol.113(8):926-33.103(1):9-20. and nonylphenol at home and daycare.Environmental Phenols Volkel W. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Arch Environ Contam Toxicol 2003. Fourth National Report on Human Exposure to Environmental Chemicals 33 . Witorsch RJ. Large effects from small exposures. Welshons WV.40(7):905-12. Colnot T. Kim SY. Endocrinology 2006.

40) 1.80 (1.20-2.20) 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 . The alkylphenols can bioaccumulate in some fish.900 (.10) 1. an alkylphenol.60) 613 652 1092 Limit of detection (LOD.600-1.500) .900 (.50) 1. 34 Fourth National Report on Human Exposure to Environmental Chemicals .20) 1.300-. which are anionic surfactants used in detergents. over 500.50 (1. In rats.40) 2. which may vary for some chemicals by year and by individual sample.40) 2. fish) and drinking water. Survey Geometric mean (95% conf.S.357 (.90) 2.389 (..10-2.. and some personal care products.200-.30-2. industrial cleaners.600) .400 (.Environmental Phenols 4-tert-Octylphenol CAS No.2. 2000. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses. through sewage.60) 1.369 (.900 (. 2006. impaired steroidogenesis. 2002). 1996). Katsuda et al. 2002)..500) .60-3.700-1.500 (.20) 314 715 1488 03-04 03-04 * * . During the 1980s and 1990s. Saito et al.600-1.5% of 139 U.000 tons of alkylphenol ethoxylates were produced annually worldwide. orally administered 4-tert-octylphenol was well absorbed.10 (1.10 (. Laws et al.10 (. 2004). Several alkylphenols..500-1.10) 2.50-3. altered estrus cycles and reproductive outcomes.299-. see Data Analysis section) for Survey year 03-04 is 0.70 (1.60-3.300 (<LOD-.600-1. streams in 30 states (Kolpin et al.400 (.50) 1. 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.. In 1999-2000.40 (1.90) 2.600) 1. Disposition in humans has not been studied sufficiently.300 (<LOD-.30 (1. is used to manufacture alkylphenol ethoxylates. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2. 140-66-9 General Information 4-tert-Octyphenol.477) . Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.600) .60-3.20-2. 1997.300 (<LOD-.20 (1.30) 2. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers. population from the National Health and Nutrition Examination Survey. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression.g.30) 90th 1.20-2.40) * 03-04 03-04 03-04 . 1995.300-.70 (1.300 (<LOD-. and through manufacturing waste streams (Warhurst.50) .g.30 (1. pesticides.600-1.268-.20-2.80 (1. Bian et al. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins.50-2.3.30 (.60-3. including 4-tert-octylphenol. did not bioaccumulate. 2003..497) * .30 (1.900 (.60-3.800-1. testicular atrophy.50) .50) 1. the various alkylphenols have also been used as emulsifiers and modifiers in paints. and the polyethoxy chain may consist of up to 50 ethoxy units.274-. altered neonatal sexual development.300 (<LOD-.. and impaired spermatogenesis (e. Urinary 4-tert-Octylphenol (4-[1.600-1. In the 1990s.30 (1.600) .S. leading to inhalation as another potential exposure route (Rudel et al.1.70 (1. Less frequently.00 (.20-2.60) .00) 1229 1288 03-04 03-04 03-04 * .400) 1..500-1.500) .3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and emulsifiers.20) 2. have demonstrated estrogenic effects particularly when injected at high doses in animals. Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.30) 1. 2000.20-2.40) 1. Ying et al. textiles. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. The alkylphenol ethoxylates enter the environment through human use of products containing them. and was quickly eliminated from the blood (Certa et al.80) 2.. 4-octylphenol monoethoxylate was detected in 43. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.00 (1.500) 75th . < LOD means less than the limit of detection. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol). to shorter chain alkylphenol ethoxylates. and from contact with some personal care products and detergents. and to alkylphenoxycarboxylates.400 (.70 (1.507) * < LOD .00 (.900 (.600-1. Blake and Boockfor..80 (1. Indoor and to a lesser extent.200-. and some of their degradation products are toxic to aquatic life.60-3.

00 (. 2001.850 (. Kawaguchi et al.11) 1.910 (..25) 2.53-3.3.630-1.06 (2.S.31 (1.269 (.40-4.00) 1.450) . 2001).410 (.276 (.170-. 2005.02-4. 2004. population from the National Health and Nutrition Examination Survey.68-2.570) .25) 90th 1.470-1. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.270 (. Fourth National Report on Human Exposure to Environmental Chemicals 35 . at lower or environmentally relevant doses (Blake et al.22) .740 (.67-2. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Urinary 4-tert-Octylphenol (4-[1.620) .50 (2.71) 2.280-.41) .207-.40 (1.29) 2..380 (<LOD-.81 (1. Survey Geometric mean (95% conf. 2003.540-1.435 (.00 (.11) 2. Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure.59 (1. 4-tert-Octylphenol is not considered directly genotoxic.530) .14) 314 713 1487 03-04 03-04 * * .05-2.78) 1228 1286 03-04 03-04 03-04 * .11-2.470) 75th .78) 3.62 (1.420) .76 (2. Nagao et al.65-3.03 (1.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.62) .320 (<LOD-. IARC and NTP have not rated octylphenol. nonylphenol.500-1.54) * 03-04 03-04 03-04 .860 (. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.450) 1.64 (.470-1.337-.31-2. or their corresponding ethoxylates with respect to human carcinogenicity.20 (1.349) * < LOD .18-4.384) * .300 (<LOD-.1.33 (2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.560) .460 (.260 (<LOD-.17 (.S.00) 2.620-1. 2000.00) 2..43-3.00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .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..770 (.10-2. It is unclear if estrogenic or other effects occur in animals through oral dosing.400) .740 (. representative subsample of NHANES 2003-2004.08) 1.270-.62 (1. In a small number of adult Japanese volunteers.550-1.78 (1.610) .270 (. Calafat et al.Environmental Phenols Myllymaki et al..15) 1.43) 1.96-4.199-.68) 2.33) 3.85 (1.03 (1..640-1.730-1.25-2.59) 1.03-6.370 (<LOD-. 2004).36-3. Sweeney et al. Yoshida et al. Tyl et al.160-.890-2.43) 1. 1999).60 (1.

Xu L. Blake CA. Yoshimura S. Exposure of the U. Indoor Air 2004. hormones.15(6):683-692. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Ono H. Brine DR. Spengler JD. Nicol L. Brooks AN. Laws SC.uk/resource/reports/ethoxylates_alkylphenols. Regul Toxicol Pharmacol 1999. Boockfor FR. Nair-Menon JU. Maekawa A. Taya K. Inoue K. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone.S. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Yoshimura Y. Toppari J. prolactin. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression. and testosterone. Biol Reprod 1997. et al. Katsuda S. Taya K. Zaugg SD.37(20):4543-53. Toxicol Appl Pharmacol 2000. 2/4/09 Ying GG. et al. Watanabe G. Yoshida M.folliclestimulating hormone. Bodman GJ. Qian J. Anal Chim Acta 486:41-50. polybrominated diphenyl ethers.141(7):2667-2673. Yoshida M. Calafat AM.36(6):1202-1211. Okada F. Bolt HM.207(1):59-68. Kookana R. Izumi S. nonylphenol. Seto H. Reprod Toxicol 2001. Tyl RW. Kolpin DW. Environ Sci Technol 2002. Arch Toxicol 1996. Endocrinology 2000.116(1):39-44.799(1):119-125. Ferrell JM. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Environ Health Perspect 2008. Chen J.Environmental Phenols References Bian Q. Haavisto TE. testis size. Phthalates. Takai N. Marr MC.28(3):215-226. Cooper RL. Ye X.18(1):43-51. Needham LL. Karjalainen M. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. Available at URL: http:// www. Certa H. Song L. Katsuda S.71(1-2):112-122. 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. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Food Chem Toxicol 2006. McCoy GL. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Indoor air pollution by alkylphenols in Tokyo. Horie M. Carey SA.44(8):1355-1361. Camann DE. Reprod Toxicol 2004. 2003.121(1):21-33. Sweeney T. Saito Y. Watanabe G. Toxicol Appl Pharmacol 2005. et al. Environ Int 2002. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Furlong ET. Wang X. Kawaguchi M.54(1):154-167. Environ Sci Technol 2003. Onuki A. Raychoudhury SS. bisphenol A and methoxychlor in rats. Williams B. Brody JG.14(5):325-332. 1995. Rudel RA.30(2 Pt 1):81-95. Blake CA. Maekawa A. Paranko J. and other endocrine-disrupting compounds in indoor air and dust.57(2):255-266. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats. et al. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Thurman EM. Muller AM. Usumi K. Pharmaceuticals. Reidy JA.pdf. Myers CB. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion. Millette CF. Takenaka A.co. Estrogenic activity of octylphenol. Fedtke N. Korn LR. Inoue K. Boockfor FR. and sertoli cell number. Wong LY. Toxicol Sci 2000. streams.S. Saito I. and other organic wastewater contaminants in U. Meyer MT. Warhurst AM. Nagao T. Nakagomi M. Two-generation reproduction study with para-tert-octylphenol in rats. Seely JC. Fail PA. 1999-2000: a national reconnaissance. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Myllymaki SA. Barber LB. Toxicol Lett 2001. Wiegand HJ. Sakui N. Roche JF. alkylphenols. Makino T.165(3):217-226.foe. Ito R. pesticides. Kawaguchi M.

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

40-17.5 (11.8 (21.3-67.4) 357 (225-456) 203 (87.11-11.4.9 (33.1 (45.8-112) 30.48-10.2 (37.6) 12.2-58.9-236) 193 (90.16 (6.6 (12.9 (50.2 (27.6) 39.5) 20.74 (5.1) 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 (26.90-10.45-13.5) 11.0 (11.0-15.30-14.2-14.1) 11.8-60.8-127) 37.4-19.20-10.6 (9.6) 90th 212 (172-241) 03-04 03-04 03-04 9.0 (34.2 (11.55 (4.S.4.3 (11. see Data Analysis section) for Survey year 03-04 is 2.50-10.20-11.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.9) 75th 47.10-9.7 (39.8) 14.9 (11.Environmental Phenols Urinary Triclosan (2.43-13.72-13.29-12.5-86.1) 13.4) 90th 249 (188-304) 03-04 03-04 03-04 8.2-46.6-15. Urinary Triclosan (2.3-31.2 (13.3) 10.6) 31.4 (38.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4) 7.3) 47.50) 10.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.5) 13.7) 292 (151-432) 132 (78.4-18.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.6-14.1 (8.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.1-39.1) 9.4 (11. interval) 12.2 (10.10) 84.00 (4.3-15.89-11.0-19.6) Selected percentiles ( 95% confidence interval) Sample 95th 461 (383-522) size 2517 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 9.3-35.4 (12.4) 317 (231-433) 144 (96. Survey Geometric mean (95% conf.7 (11.6-111) 33.9 (8.3 (8.54 (8.70-16.1) 7.00-8.1) 9.2 (25.0) 9.7) 123 (36.80 (5.22-10.1) 50.0-73.60 (6.2) 12.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.0 (26.1) 9.9) 7.6-20.1 (15.4) 73.86-12.0-15. Survey Geometric mean (95% conf.7 (14.20 (7. interval) 13.9-61.6) 10.20-13.3) 6.7) 10.48 (8.45-10.6-14.3.0 (8.8) 7.2-58. population from the National Health and Nutrition Examination Survey.6-37.4) 51. population from the National Health and Nutrition Examination Survey.21 (6.93 (7.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.0) 49.6-65.18 (5.4) 25.S.5-14.60 (8.7 (9.4 (32.5) 66.3 (9.40-11.0 (36.6 (30.0) 65.8-85.6 (10.45 (5.8-63.9) 8.7 (28.8) 116 (39.0-213) 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 .94 (7.2) 9.8) 9.9) 32.92-12.4) 75th 43.1) 14.20 (7.2) 13.38-18.32-14.82 (8.1) 9.

Bhargava HN. Arch Environ Contam Toxicol 1988.83(1):84. Kaneshima H. Photolytic degradation of triclosan in freshwater and seawater. Pinney SM. Gilbert RJ.S. 4’-trichloro-2’-hydroxydiphenyl ether. Kolpin DW.116(3):303-307. Wolff MS.36(6):1202-1211. Biol Pharm Bull 2005. et al.17(5):637-644. Matsumura N. Ekstrand J. et al. Kanetoshi A.67(4):532-537. et al. Chemosphere 2007. Ogawa H. Erratum in: Aquat Toxicol 2007. Gomez MJ. Aranami K. Larson EL. Okui T.24(3):209-218. Shiratsuchi H.Environmental Phenols References Aiello AE.7/2. Katsura E. Zaugg SD. Pharmacokinetics of triclosan following oral ingestion in humans. Urinary concentrations of triclosan in the U. Chelimo C. Environ Sci Technol 2002. Pilot study of urinary biomarkers of phytoestrogens.45 Suppl 2:S137-S147. Benson WH. Mar Environ Res 2000. Levy SB.50(1-5):153-156. Aguera A. Readman JW. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Gunderson MP. Calafat AM. Britton JA. streams. Nagao Y. Environ Health Perspect 2008. Pharmaceuticals. Evidence of 2. Toxicology of 2. Leonard PA. 1999-2000: a national reconnaissance. Developmental evaluation of a potential non-steroidal estrogen: triclosan. IMS Ind Med Surg 1969. Hirano M.524:241-247. The oral retention and antiplaque efficacy of triclosan in human volunteers. Wigmore H.115:116-121. Williams FM. Am J Infect Control 1996. Hong HC. Food Chem Toxicol 2000.23(5):579-583. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development.. Needham LL. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Environ Health Perspect 2007.69(20):1861-1873. Mezcua M. Aquat Toxicol 2006. Ebersole R. Furlong ET. Reidy JA. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Meyer MT. 4. Williams PE. Skirrow RC. Clapson DJ. Sandborgh-Englund G. Fernandez-Alba AR. phthalates. Howes D.66:1052-1056. Triclosan: applications and safety.80(3):217-227. Percutaneous penetration and dermal metabolism of triclosan (2. Barber LB. Watanabe N. population: 2003-2004. Anal Chim Acta 1004. Wong LY. Ishibashi H. Foran CM. Bodey GP.4’-trichloro-2’hydroxydiphenyl ether). Osachoff H.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007. Ferrer I. hormones. Br J Clin Pharmacol 1987. Veldhoen N.38(2):64-71. Fourth National Report on Human Exposure to Environmental Chemicals 39 . and other organic wastewater contaminants in U.28(9):1748-1751. Adolfsson-Erici M. J Toxicol Environ Health A 2006. Furia T. Thurman EM. Lyman FL. and phenols in girls.38(4):361370. Teitelbaum SL. et al. Odham G. Moss T. Bennett ER. Hernando MD. Ye X.S. J Invest Dermatol 1976.4. Windham G.

990-2.53) 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-.990 (<LOD-2. PCP is eliminated over a few days (Braun et al. and dermal contact with PCP-treated products. The parent compound and conjugates.390 (.00 (.65 (.350 (.350-1.33) .890 (.70) . Survey Geometric mean (95% conf.350-2.10 (. bactericide.660 (.350 (. Since 1984.860-2.350) < LOD .. PCP cannot be used on wood in residential or agricultural buildings. 1976. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.00) 1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.350) < LOD .98 (1.350 (. ingestion of contaminated food or water. Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. so it is relatively non-persistent. water and sediments because of the large amounts that were produced and used historically. mollusicide.350 (.g. General population exposure to PCP may occur by inhalation of contaminated air.350 (.58-2.30) 1. After a single dose.350-.33-2.10 (1.47-5.37 (.45-2.30 (1.350) .980 (.350-1.42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . herbicide.5.350-.500-2.94 (1.680-1.09) .350-2.350-.75) 2.32 (.350) < LOD . other polychlorinated benzenes. Human exposure to PCP has become less common. air.90) 1.350 (.83 (2.850-2. which may vary for some chemicals by year and by individual sample.10) 1.04) 1.23 (.10 (<LOD-1. PCP use in the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350-2. PCP is degraded by sunlight and metabolized rapidly by microorganisms.350) < LOD .350 (. and it is used primarily as a preservative for wood to be used outdoors (e.350-1.350-. Kohli et al.350 (.650 (.480-2.350 (.60) 1.350 (.350 (. PCP has been detected in soils.350-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.350-.48-2.64) 1.73 (1.350) < LOD .650) 1.350) < LOD . 1986).350-.350-.51) 1. < LOD means less than the limit of detection. algaecide and insecticide.350-. and possibly of lindane (IPCS.350) < LOD . has been restricted.510-5.76) . and animals.350) < LOD . 2002.350) < LOD .30) 1.350) < LOD .350 (.350 (.350-2.350-.890-1.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * ..48 (. PCP is absorbed rapidly and well by all exposure routes.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.S.90) 2.25 and 0.40 (.350) < LOD < LOD 75th .350-.350-.67) 1.18 (<LOD-1.S.10) 1.350) < LOD .350 (. population from the National Health and Nutrition Examination Survey.08-3. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.350 (. 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.94 (1.630 (. hypertension. Acute. plants.960) 1.37) .80) . PCP is distributed to most tissues and is not extensively metabolized.350-.30) .50) 1.47-3.62 (.78) 1. 1997). and metabolic acidosis were observed in CAS No.350 (. To-Figueras et al.350 (. along with small amounts of tetrachlorohydroquinone and conjugates.76) 1. In the environment.350 (. Effects including hyperthermia.350) < LOD . 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.00) 1.350 (.350-. utility poles and fence posts).350 (.350-.30 (.42) 696 680 521 696 603 951 Limit of detection (LOD.350-.00) 2.350-.350-2.350) 90th .350-.350) < LOD .. with repeated or chronic exposure. 40 Fourth National Report on Human Exposure to Environmental Chemicals .70) 2.350-1..60) 1.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .350 (.590-1.54-2. the elimination half-life may be a week or more (Uhl et al.91 (1.30 (.58-2.. After absorption.350) < LOD .65 (.350-.530) 1. are eliminated in the urine. 1979).350) < LOD .510-3.350-.90 (1.01 (<LOD-1.350-.770 (.390 (.350) < LOD .

220-.78) 1. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.00) 1.S.52 (<LOD-1.950-1.830) < LOD .. environmental levels) and health effects is available from the U.18) .500-1.35) 1. 2004.56) 1.590-1.30) 1..40) 1.67-3. Death can result from seizures and cardiovascular collapse.52) 1.84) 1.69 (1. or skin absorption.S. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.250 (.10 (1.360-. 2003).67 (1.Fungicides adults and children severely exposed to PCP through ingestion.S.94-3.300 (.95) 3.500 (. 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. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.560-.99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .35-2.19) 2.gov/ pesticides/ and from ATSDR at: http://www.40) 1.67-3. In animals.06-3. In a small sample of U.270-.340-.580-.atsdr.78) 1.09-1.epa.900-1. Among adults in the NHANES 1999-2000 subsample. 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.560) < LOD .290-.26 (1.300 (.25) 1.75 (<LOD-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.800-1.S.990 (. and the FDA has established a standard for bottled water.83 (1.67 (1.25-2. Survey Geometric mean (95% conf.11) 2.440 (.19) 2.84 (1.710-1.S.650 (. More information about external exposure (i.82) 1.510-. 1989).16 (.10-2. 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. van Raaij et al.920 (.500-. 1995).75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * ..82 (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.560) < LOD .EPA. 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.590) < LOD .570 (. The U. 1991).e.94 (1.760 (.630 (.780-1.08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.79) 1.36) .25-2.55) 1.320) < LOD .320) < LOD .73 (1.09) size 1994 2527 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .910-1.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .21 (.25 (1. respectively) (Seifert et al.360 (.510-.700-2.html.470 (.09 (<LOD-2.25-1. and adversely affected thyroid function (U.34 (.67-2.35-2. children in the 1980’s.57 (1. population from the National Health and Nutrition Examination Survey.40) 1.25 (1.250 (.52 (1.30-2. 2003).650) 90th 1.51) 1.610 (. carcinogenic.490) < LOD .430-... Pentachlorophenol is not mutagenic or teratogenic. 2000).40) 1.240-.800) < LOD 1. OSHA has established an occupational standard.310) < LOD .430) < LOD .30 (.310-.06) 1.260 (.370 (.67 (1. In NHANES 2001-2002 subsamples.00-1.75) 1. Urinary levels of pentachlorophenol in the general population are far below (hundreds of times lower than) urine levels reported for workplace exposure to PCP or among people living in PCP-treated log homes (Cline et al.950-1.730) < LOD .29-3.cdc.320) < LOD < LOD 75th .48-2.94 (1.21-2. inhalation.26 (1.9 mg/L.00-1.35) 1.18 (1.380-.280) < LOD .40-2.06 (..40) 1.320 (.330-. respectively) (Becker et al.420) < LOD .650 (.350) < LOD .780) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 41 . EPA has developed standards for PCP in drinking water and the environment.0 mg/L.08 and 5..400 (.52 (<LOD-1.84-4.67 (1.gov/ toxpro2.92) 1.850 (.57 (.19 (1.220-. EPA at: http://www.30) 1. chronically administered high doses of PCP were hepatotoxic.290) < LOD .67 (1.13 (.6 and 14.290-.300 (.270-.16-1.19) 2.950-1. 1989).90) 1.

S. Fast DM. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Hill RH.105(1):78-83. Needham LL. Environ Res 1995. To-Figueras J.18:475-481. Phillips DL. Environ Health Perspect 1997. et al. Gregg M. et al. Uhl S. Schulz C. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. Shealy DB.71:99108. Schmid P. Pentachlorophenol measurements in body fluids of people in log homes and workplaces. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Arch Toxicol 1986. drinking water and indoor air. Blau GE. EPA).S. Needham LL. Safe A. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Kaus S.58:182-186. Cline RE. Head SL. et al. Otero R. Smith SJ. 4/21/09 van Raaij JA. Pesticide residues in urine of adults living in the United States: reference range concentrations. Santiago-Silva M. Bragt PC.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Krause C. 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. Holler JS.inchem. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Notten WR.18(4):469-474. Barrot C. available at URL: http://www. 4/21/09 Kohli J. Schlatter C. References Becker K. 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. J Expo Anal Environ Epidemiol 2000. Pharmacokinetics of pentachlorophenol in man. Bailey SL. 2002. The metabolism of higher chlorinated benzene isomers. Hill RH Jr. Int J Hyg Environ Health 2003.54(3):203-208. Seifert B.org/documents/jmpr/jmpmono/2002pr08. Seiwert M. Becker K. U. Lindane. Chenoweth MB.4:289296. hair. Hill RH Jr. Braun WH. van den Berg KJ. r e g u l a t i o n s . Environmental Protection Agency (U. To T. house dust. Toxicology 1991: 67(1):107-16. Available at URL: h t t p : / / w w w. Dev Toxicol Environ Sci 1979. PCP: Human Risk Characterization [online]. Can J Biochem 1976. International Programme on Chemical Safety (IPCS). Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Arch Environ Contam Toxicol 1989. Seiwert M.10:552-65. Rodamilans M. Helm D. 11/30/2004. Seifert B. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. 206:15-24. Jones D. Schulz C. Engel R. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Baker S. Sala M. urine. htm. Arch Environ Contam Toxicol 1989.

880-2.3. In the past.621) * . sodium ortho-phenylphenate (SOPP).19 (.60-3.600-1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.90 (1. Most agricultural food applications have been revoked.61) 2. Survey Geometric mean (95% conf.742) * .710-2.00) < LOD . 1998). 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.30) < LOD .00 (1.30-7.00) . EPA. Timchalk et al.450 (<LOD-.570 (..600) < LOD 75th .490 (<LOD-.EPA.10) 1. 2006). small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley. 2006).S.3 and 0. and sanitizers.840-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. or apply these chemicals may be more highly exposed than the general population. Fourth National Report on Human Exposure to Environmental Chemicals 43 . inhalational. 90-43-7 General Information Ortho-phenylphenol (OPP. 2006).30) 1.10) 2.890 (. and it has limited water solubility.20 (1.14 (<LOD-3.860) * 99-00 01-02 99-00 01-02 99-00 01-02 . General population exposure can occur via dermal.88) 1.00 (1. or 2-phenylphenol) and its water-soluble salt.590-2.690-1.600) < LOD 1.20) < LOD 2.22 (.433-.60 (1.09) 2.10 (1.76) 1.90) 2. fungicides.50-4.508 (.50) .23) 695 680 520 695 603 953 Limit of detection (LOD.85) 2.696) * .750-2.610 (. 1998.30) < LOD 1.497 (.950) < LOD .10) 1.580-1.40-5.389-.. on ornamental plants and turfs.930 (. and it is eliminated rapidly from the body as OPP glucuronide and sulfate conjugates (Bartels et al. Human health effects from OPP at low environmental doses or at biomonitored levels from low environmental exposures are unknown.770 (.90) .389-. OPP is volatile.60-2.830 (.50 (1. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.386-. OPP is still used as a disinfectant fungicide for industrial applications. population from the National Health and Nutrition Examination Survey. leaving the chemical residue OPP.370-.40-5.509 (. Estimated human intakes have been below recommended intake limits (U.470 (<LOD-.03) 1.800-3.624) * .20 (.890) 1.780) < LOD .23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .490 (<LOD-.420 (<LOD-.610-1.02) 1.10 (1. however.636) * .50) < LOD .07 (.370-. whereas SOPP is not volatile and is more water soluble.50) 1.890 (.10) .28 (.410-.645) * .20) < LOD 1.30 (1.S.50) < LOD .80) 1.496 (. Cnubben et al.80) 1.670) 2.570-.40-7. 1989).Fungicides ortho-Phenylphenol CAS No.790) 2.490 (<LOD-.560-8.850 (.540-2. interval) .552 (. OPP is efficiently absorbed from the gastrointestinal tract and through the skin.390-.836) * .20-3.S.490 (<LOD-.50) < LOD .550-1.17 (.600) < LOD . 2002. are antimicrobial agents used as bacteriostats.498 (. it was used in home sanitizers for surfaces.00 (1.640) < LOD .10-2.27 (.820 (.630) < LOD .10) .80 (2.00 (1.EPA..520 (.92 (.60 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.30) < LOD 90th 1.600-1.40-2.00-2.91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 .60 (1.450 (<LOD-.567 (. which may vary for some chemicals by year and by individual sample.90) .493 (.50-3. in paints.480-1.760-2.50 (1.33 (. 2006).50-2.20 (1.350-1.600-1. formulate.50 (1.860 (.28-3. and as a wood preservative.10-1. OPP is considered to be moderately toxic after acute oral doses in animal studies.20) 2.600) < LOD .30-2.970 (.40 (. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.10) .740 (.22) 2.370-.638) * .770 (. < LOD means less than the limit of detection. such as fruits and vegetables.364-.402-. SOPP is applied topically to the crop and then rinsed off. Available evidence suggests that OPP does not accumulate in the body.80-3.00) . Both chemicals degrade within hours to weeks in the environment (U. Both have been used in agriculture to control fungal and bacterial growth on stored crops.570 (. but OPP and SOPP are still used on pears and citrus (U.90 (1.570-1.570-2.20-2.90) 1.S.466 (.490 (<LOD-.710) 3.34) 1.85) 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 .450 (<LOD-. Workers who manufacture.500-2.349-.690) < LOD .

.25-6. U.96 (1.550-.29) 1.382 (. Ito et al.840 (.46) < LOD 1.43 (1. Smith et al.470) < LOD .38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 .910-1.38-3. 1986).78 (2.. Murata et al.13) 1.496 (. 1984.93) .21-2. Additional information is available from U.18) 2.440 (.74 (1.EPA at: http:// www.301-.61 (2.33) . 44 Fourth National Report on Human Exposure to Environmental Chemicals .S.61 (1.510-.02 (.568) * .06-4. Brusick.S.59) 1.00 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.09 (1.910 (<LOD-1.06 (1.84 (1.320 (<LOD-. by possible genotoxic mechanisms (Hagiwara et al.17) * 99-00 01-02 99-00 01-02 99-00 01-02 . reproductive.670 (.17 (.EPA 2006).08-1.470 (<LOD-. Bomhard et al.580) < LOD . 1998. 2005).670) < LOD .07) 2.580-1.62) .21 (.990) < LOD .473) * .43-2.453 (.770-2.S.500) < LOD .12-2. Pathak and Roy. 2002).980 (. 2000.44 (1.508) * .4 mg dermally had urinary levels of OPP that were several hundred times higher than median levels found in NHANES 1999-2000 and 2001-2002 (Bartels et al.810-1.33) size 1991 2528 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th . 2002.248-. Biomonitoring Information Urinary OPP levels reflect recent exposure.860 (. 2005).69 (1.11 (.08) 1. leading to production of two metabolites.08-2.810) < LOD . Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.89 (1.455-.600-1.S. interval) .360 (<LOD-.550 (.780-14.28 (<LOD-4.59) .52 (. OPP was not found to be mutagenic. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.20) < LOD 3. 1999. 1997.51-3.33-2.32) 1.21) 1.40-13.650-1.11 (.670 (.560-2.00 (1.88-4. population from the National Health and Nutrition Examination Survey.58) 2..940-2. Survey Geometric mean (95% conf.96-4. 1993.43) 3.38) 1.560) < LOD 75th .361-.81) 1.17) 2.38) 2.444 (. Zhao et al.53) 1. less likely..860 (.47) .09-3.29) 1. 1999.97 (2.910 (.24-2.970) 1.270-.Fungicides anemia.09-6.17 (. or.950) < LOD .S. U. 2005.800-1.750-2.780 (.93) .590) * ..64 (2. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.91 (1.550) < LOD .880-1.gov/pesticides/.353-.311-.750 (.28 (2.558) Selected percentiles ( 95% confidence interval) Sample 95th 2.900-1.514 (. Kwok et al.43-2.403-.32) 3. Detectable levels were seen in over half the U.75 (1.510 (<LOD-. 2002.620-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.750 (.11) 4. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.791) * .460-.480-. but no neurologic.900) < LOD . ortho-phenylhydroquinone and ortho-phenylbenzoquinone. IARC has classified SOPP as a possible human carcinogen.980 (<LOD-1.570) < LOD 1.690 (.04-4. or developmental toxicity was observed (Bomhard et al. Nakagawa et al.291-.24-2.11) < LOD 90th 1.27) < LOD .385 (. In high dose animal studies. and it has classified OPP as not classifiable with respect to human carcinogenicity.91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.05-2.343 (.420 (<LOD-.11-1.06-5. 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.329-.640-1.610) < LOD 1.484) * .EPA 2006).61 (. CDC.12) < LOD 1.. These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.410 (<LOD-.656) * .epa. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.666) * ..30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 ..410 (<LOD-.420 (<LOD-.26) 1.01) 1.0) 1.4) 3.96 (1. 1992.31) < LOD . Volunteers exposed to 0.. 1984.380 (.93) 1..620-1.86 (1.75 (1.93 (1.96) 1.

703(12):97-104. Vogel JS.S. Smith RA.32(6):551-625. J Agric Food Chem 2002. EPA). Tayama S. Turteltaub KW. Bartels MJ. Hagiwara A. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Eastmond DA. Christenson WR. McNett DA. Nakagawa Y. rat and man.gov/ntp/htdocs/LT_ rpts/tr301. Toxicol Appl Pharmacol 1999. J Agric Food Chem 2006. EPA 739 R-06004.150(2):402-413. Mendrala AL. Regul Toxicol Pharmacol 2002. Stanley JS. Identification of SARA compounds in adipose tissue. March 1986. Moore GA.74(2):61-71. Fourth National Report on Human Exposure to Environmental Chemicals 45 . U. Arch Toxicol 2000. Richter M. Herbold BA. Fukushima S.epa. 2006.gov/oppsrrd1/REDs/ phenylphenol_red. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Bomhard EM..22(10):809-814. Bromig KH. National Toxicology Program (NTP). EPA-560/5-89-003. Meuling WJ. Buchholz BA. Eadon G. food additives and natural products as promoters in rat urinary bladder carcinogenesis. Carcinogenesis 1999. Hum Exp Toxicol 1998. Available at URL: http://www. The carcinogenicity of the biocide ortho-phenylphenol. Brendler-Schwaab SY. Food Chem Toxicol 1984. Bartels MJ.S. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Brusick D. Hakkert BC. Shibata M. Leser KH. Environmental Protection Agency (U. J Chromatogr B Biomed Sci Appl 1997. July 28. Bormett GA. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Inoue S. Environ Mol Mutagen 2005.286(2):309-319. Gierthy J. Elliott GR.45(5):460-481.EPA). Biochem Pharmacol 1992. Timchalk C. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Selim S. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Xenobiotica 1998. Bartels MJ. St John MK. Zhao S. Christenson WR. Shirai T.54(16):5731-5735. Narang A. Available at URL: http://ntp.(56):399-407. Freyberger A. Moldeus P. Kawanishi S.20(5):851-857.17(8):411-417. Roberts AL. Kwok ES. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. et al. 2005. Drugs. Cnubben NH. U. Third National Report on Human Exposure to Environmental Chemicals. Sangha GK. Timchalk C. Imaida K. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Ito N. Hirose M.35(2 Pt 1):198-208. Brzak KA. 4/13/09 Onstot JD.43(7):14311437. Ito N. Fukushima S. Pathak DN. van de Sandt JJ. Crit Rev Toxicol 2002.159(1):18-24. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol. Roy D. Murata M. Atlanta (GA). Office of Toxic Substances. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. 4/9/09. Hagiwara A. Moriya K. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. et al.pdf. Environmental Protection Agency (U.Fungicides References Appel KE. Comparative metabolism of orthophenylphenol in mouse. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Toxicol Appl Pharmacol 1998.50(11):3351-3358. 1989.S. Glas K. 90-43-7) in Swiss CD-1 mice (dermal studies).28(6):579594. Coelhan M.pdf. Bartels MJ.niehs. Sangha G. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry.S. Mutat Res 1993. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats.nih. Arnold LL. Centers for Disease Control and Prevention (CDC). IARC Sci Publ 1984. Cano M. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP).

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

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

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

cce. Burkhardt MR. Barr DB.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. Volume 65. Barr DB. Whyatt RM.11(4):353359. Peter CJ. pages 3682-3690. Coleman S. Kier L. Thurman EM. Hsiao JJ. Hodgson E. Kinney PL. acetochlor. Heederik D. J Expo Anal Environ Epidemiol 2005. Andrews HF. Roberts AL. et al. reservoirs and ground water in the Midwestern United States. Hines CJ. Barr JR. Chem Res Toxicol 1998. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. U. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Comparative metabolism and elimination of acetanilide compounds by rat. Feng PCC. epa. Bravo R. Hein MJ. Lefevre PA. Sanderson WT.pdf. imidazolinone. Number 15.39(17):6561-6574. Furlong ET.S. Hum Exp Toxicol 1996. Deddens JA. EPA 738-R-00-009. EPA). Available at URL(non U. Curwin BD. Available at URL: http://www. Olsson AO. Alavanja MC. Quistad GB.S.248(2-3):115-122. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Barr DB. Reynolds SJ. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. Feil VJ.37(4):10881093. 5/30/06 U. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. J Agri Food Chem 1989. Environ Health Perspect 2000. Atlanta (GA). Tinwell H. Battaglin WA. EPA). Environ Health Perspect 2003.S.17(6):559-566. Larsen GL. Camann DE. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor. et al. Jefferies PR. Environmental Protection Agency (U.24(10):1003-1012.108(12):1151-1157. Rose RL. Federal Register: January 24. Linderman R.S.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Wratten SJ.cornell. and other herbicides in rivers. March 2006. Wilson AG. Environmental Protection Agency (U.15(9):702-735. Fourth National Report on Human Exposure to Environmental Chemicals 49 . 5/30/06. sulfonamide. et al. 2000. Occurrence of sulfonylurea. Sci Total Environ 2000. Acetochlor (Harness) Pesticide Petition Filing 1/00. 2005.248(2-3):123-133.15(6):500-508. Casida JE.Herbicides References Ashby J. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.111(5):749-756. 1998. Centers for Disease Control and Prevention (CDC). J Expo Sci Environ Epidemiol 2007. Sci Total Environ 2000. Davison KL. Green T. Kolpin DW. Ward EM. and metolachlor herbicides in rats. Xenobiotica 1994.html. Striley CA. Hladik ML. Linhart SM.S. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Third National Report on Human Exposure to Environmental Chemicals. Environ Sci Technol 2005.EPA): http://pmep. Dialkylquinonimines validated as in vivo metabolites of alachlor.

. In chronic animal testing. and uveal degeneration.EPA. 2005. about 20-25% of the U. IPCS. WHO. mean values of urinary concentrations of alachlor metabolites. Finding measurable amounts of alachlor mercapturate in the urine does not mean that the levels of alachlor mercapturate cause an adverse health effect. and on non-crop land for general weed control.. 2000.EPA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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. 1995.S.. Alachlor has low potential for acute toxicity.S. as measured through conversion to deethylamine. Urinary levels of alachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC..S..EPA.. 1997. 1988.6-diethylaniline and its reactive metabolite. 50 Fourth National Report on Human Exposure to Environmental Chemicals .2% of a reference population had detectable alachlor equivalents by immunoassay in their urine. In animals. People exposed to alachlor will excrete alachlor mercapturate in their urine (Driskell et al. 1995). Hill et al.S.Herbicides Alachlor CAS No. alachlor is quickly absorbed after oral doses and mostly excreted as metabolites within a week (IPCS. Human health effects from alachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. EPA at: http://www. 1998).1 mg/L at various collection times (Sanderson et al. It is absorbed by plants and inhibits plant protein synthesis. but not likely at low doses. 2000. Hines et al. Additional information about is available from U. 2003). Animal carcinogenicity studies have demonstrated tumors of the nasal turbinates. the dermal exposure route is potentially significant for applicators. 1994. though positive genotoxic results are reported for several metabolites of alachlor (Brown et al. In animal studies. Because it can be absorbed through skin. hemosiderosis. Tessier and Clark. Since the late 1980s alachlor use has been declining. It is both metabolized in plants and degraded microbiologically in agricultural soils into as many as 19 metabolites and degradates. corn cropland was treated with alachlor. 1996). Alachlor is highly toxic to freshwater fish and slightly toxic to birds and some invertebrates. NTP and IARC do not have ratings regarding human carcinogenicity. 2003). ranged from 0.S.. 1996. but has not shown developmental or reproductive toxicity in mammalian systems (U. 15972-60-8 General Information Alachlor is a chloroacetanilide type herbicide with restricted usage for preemergent control of grasses and broadleaf weeds on agricultural cropland. Biomonitoring Information Urinary levels of alachlor mercapturate reflect recent exposure. WHO. the latter may account for some observed effects (Davison et al. 1996. Alachlor has a soil half-life of a few weeks. U. General population exposure to alachlor may occur through consumption of contaminated food or drinking water. 1998. Jefferies et al. Hladik et al. 2003).epa.EPA considers alachlor to be a probable human carcinogen at high doses. 1998). 1998).gov/pesticides/. Kolpin et al. (2003) showed that 2.1 to 1. and field workers. but another metabolic pathway can produce 2. formulators.. WHO. and thyroid only at either maximum tolerated doses or related to species-specific pathways (Heydens et al. Alachlor itself is not considered mutagenic. U. 1989.EPA. alachlor has demonstrated hepatotoxicity. 1998. peanuts and other crops.. Estimated human intakes have been below recommended limits (U. U. 1999 and 2007. including corn. 2005). Feng and Wratten.S.S. whereas 60% of applicators had detectable amounts. USGS. In a study of applicators and workers exposed to alachlor.S. 2003). 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. but this metabolite is not a marker of exposure to most plant metabolites or environmental degradates which are often more prevalent in the environment. stomach. 1999. In 1993-1995. WHO. mercapturate conjugates were predominant metabolites.EPA. but shows little bioaccumulation.. 1998. soybeans. U.

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

Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Davison KL. Chem Res Toxicol 1998. Wratten SJ. Xenobiotica 1994. Third National Report on Human Exposure to Environmental Chemicals. Occurrence of sulfonylurea.php. Quistad GB. 1992-2001. Geneva. and other herbicides in rivers.epa. International Programme on Chemical Safety (IPCS). Henningsen G. December 1998. EPA).pdf. U.47(6):503-517. Biagini R.htm. Biagini RE. Striley CA. Atlanta (GA). Burkhardt MR. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Sci Total Environ 2000. Comparative metabolism and elimination of acetanilide compounds by rat.37(4):10881093. Barr DB. Environ Health Perspect 2003. Hull RD. World Health Organization (WHO). Environ Sci Technol 2005. Jefferies PR. sulfonamide. 2007. Kolpin DW.111(5):749-756. 1997. imidazolinone. Available at URL: http://www.Herbicides References Battaglin WA.43(9):2504-2512. Kier LD. Shealy DB. Geological Survey (USGS). An evaluation of the carcinogenic potential of the herbicide alachlor to man.org/documents/pds/pds/pest86_e. 2/27/09 U.39(17):6561-6574. Centers for Disease Control and Prevention (CDC). Andrews HF. 1998. Camann DE. Background document for development of WHO Guidelines for Drinking-water Quality. 1999. et al. Geological Survey (USGS). Sacramento.24(10):1003-1012.pdf. Hsiao JJ. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Life Sci 1988. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Casida JE. Heydens WF. Casida JE. Brown MA. Wilson AG. Furlong ET. revised February 15. Kimmel EC. J Agri Food Chem 1989. Thake DC. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Kolpin DW. Available at URL: http://www.18(6):363-391.44(18):1325. ALACHLOR.S. Available at URL: http://water. 2003. Erratum in: Life Sci 1989. Environmental Protection Agency (U. Tessier DM. Casida JE. Brown KK.S. Peter CJ. 2005. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Kinney PL.56(6):853-859. Mutat Res. Gilliom RJ). DNA adduct formation by alachlor metabolites. Driskell WJ. EPA 738R-98-020. Shoemaker DA. MacKenzie B.S. Roberts AL. Feil VJ. Reregistration Eligibility Decision (RED) Alachlor. Thelin GP. Thurman EM. 86. Martens MA. Sanderson WT. Feng PCC.11(4):353359. and metolachlor herbicides in rats. Dialkylquinonimines validated as in vivo metabolites of alachlor. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Available at URL: http:// www.gov/oppsrrd1/ REDs/0063. World Health Organization.S. Hill AB. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. Hines CJ. No. Ann Occup Hyg 2003.usgs. WHO/ FAO Data Sheets on Pesticides. 2/27/09 Jefferies PR. 1999. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. acetochlor. 4/2/09 U.int/water_sanitation_health/dwq/chemicals/en/alachlor. Hum Exp Toxicol.inchem. J Ag Food Chem 1995.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Alachlor in Drinking-water. March 2006. et al. Deddens JA. who. Hill RH Jr.248(2-3):115-122.248(2-3):123-133. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals . Circular 1291.395(2-3):159-171. California. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Hines CJ. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Linhart SM. Bull Environ Contam Toxicol 1996. Sci Total Environ 2000. 1996. Tolos W. reservoirs and ground water in the Midwestern United States. Lau H. Hladik ML. 98-4245 (by Barbash JE.43(25):2087-94. Larsen GL. Quistad GB. Whyatt RM. Supplemental Technical Information (available on-line only). Barr JR. Am Ind Hyg Assoc J 1995.56(9):883-889. Clark JM.

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

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

Eberly LE. Stoker TE. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. 2003. Seiber JN. Shoemaker DA.cdc. 2005). Reynolds SJ.. Sanderson WT. Eldridge JC. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Vonk A. WHO/ FAO Data Sheets on Pesticides. Pest Manag Sci 2005. Lioy PJ. A risk assessment of atrazine use in California: human health and ecological aspects. 2001).99(8):5476-5480. Deddens JA. Pfeifer KF. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function.43(2):155-167. Simpkins JW. 2007). Stoker TE. et al. Available at URL: http:// www. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. atrazine was detected in only four children (Arcury et al. Stoker TE.115(8):1254-1260. Blewett C. Tyrey L. Curwin BD. 2001 [online]. Third National Report on Human Exposure to Environmental Chemicals. Chen H.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al.58(2):366-376. Carr WC Jr. Quandt SA. Agency for Toxic Substances and Disease Registry (ATSDR). In small studies of Maryland residents in 19951996 (MacIntosh et al. Brown KK.. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample... Clayton CA. 3/11/09 Laws SC. World Health Organization. Breckenridge CB. Saiz SG.. 82.76(1):190-200. Striley CA.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. et al. Toxicol Lett 1993. Cooper RL. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.61(4):331-355. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al. No. Moseman RF. Tapia J.org/documents/pds/pds/pest82_e. Fleenor-Heyser DG. diamino-S-chlorotriazine and hydroxyatrazine. Barbieri F.. Stevens JT. Wetzel LT. et al.. In the NHANES 2001-2002 subsample. 2005). Ferioli A. Grzywacz JG. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.15(6):500-508. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect. In a small number of field workers. Stuart AA.gov/toxprofiles/tp153. 2000). References Adgate JL.30(2):244-247. Wetzel LT. Toxicol Sci 2000. Barr DB. Hein MJ. Biagini RE. 2005. Mendoza M. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households.html. et al. Catenacci G. et al.inchem. Eldridge JC. Lee M. Environ Health Perspect 2007. Gillis JH. Biological monitoring of human exposure to atrazine. Steroids 1999. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Lucas AD. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Sanborn JR. Toxicological profile for atrazine. Barr DB. International Programme on Chemical Safety (IPCS).43(2):155-167. Goldman JM. J Expo Anal Environ Epidemiol 2005. Maroni M. Barr DB.htm. Bradway DE. Heederik D. Cooper RL. Hermaphroditic.atsdr. In a study of 60 farm worker children. Gammon DW. Schmid J. J Toxicol Environ Health 1994. levels of atrazine mercapturate were generally not detectable (CDC. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate).109(6):583-590.47(6):503-517. Proc Natl Acad Sci USA 2002. Extrom PC. Collins A. Laws SC. Toxicol Sci 2000. Ferrell JM. Ann Occup Hyg 2003. ATRAZINE. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Aldous CN. Ferrell JM. 3/11/09 Arcury TA. J Agric Food Chem 1982. Cooper RL. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. J Toxicol Environ Health 1994. Noriega N. Hines CJ. Toxicol Sci 2003. Gillis JH. Freeman NC.64(9):672-678. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Goodrow MH. Jones AD. McElroy WK. Geneva. Perry et al. et al. The geometric mean of urinary atrazine mercapturate was 1. urinary concentrations ranged from 5-1756 μg/L (Lucas et al. Cottica D. Environ Health Perspect 2001. 1996. 1993). Atlanta (GA). Hayes TB. Centers for Disease Control and Prevention (CDC). Available at URL: http://www.53(2):297-307. Bersani M. Atrazine disrupts the hypothalamic control of pituitary-ovarian function.69(2):217-222.

S.pdf. 6/1/09 U. Wetzel L. Toxicology 1990. Hammerstrom KA. J Toxicol Environ Health A 1999. Chem Res Toxicol 1993.67(2):198-206.pdf.10(7):479. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function.gov/oppsrrd1/REDs/ atrazine_ired. Guidici DL. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .9(5):494-501. Toxicol Sci 2002. A longitudinal investigation of selected pesticide metabolites in urine. Urinary biomarkers of atrazine exposure among farm pesticide applicators. Tortorelli J. Available at URL: http://www. Case No. van den Berg M. Stoker TE. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Sathiakumar N. Dagenhart D.S.epa. Guidici DL. 3/11/09 U. Environmental Fate and Effects Division. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Sanderson JT. Toxicol Appl Pharmacol 2002.S. A risk characterization for atrazine: oncogenicity profile. Environmental Protection Agency (U.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Dryzga MD. March 2006. Office of Prevention. Cooper RL. Fenton SE. Delzell E.epa. Stevens JT. EPA).Herbicides development of a biomarker of exposure. The Quality of Our Nation’s Waters. Circular 1291. Pesticides in the Nation’s Streams and Ground Water.61(1):27-40. Rayner JL. Available at URL: http://water. Crit Rev Toxicol 1997. EPA Office of Pesticide Programs. Singzoni B. Available at URL: http://www. Ryan PB. Pesticides and Toxic Substances. Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Wood C.58(1):50-59. revised February 15. 2007. Osborne DW.6(1):107-116. Cooper RL.php.usgs. Ann Epidemiol 2000. Interim Reregistration Eligibility Decision For Atrazine. A review of epidemiologic studies of triazine herbicides and cancer.195(1):23-34. Needham LL. EPA). Christiani D.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. Boerma J. May 2003a.182(1):44-54. Langvardt PW. Supplemental Technical Information (available on-line only). Laws SC. White paper on potential developmental effects of atrazine on amphibians. 2003b. Laws SC. Environmental Protection Agency (U. Kastl PE.27(6):599612. 1992-2001. Timchalk C. Toxicol Sci 2000.S. U.S. MacIntosh DL. Lansbergen GW. Perry M. Stoker TE. Washington (DC). J Expo Anal Environ Epidemiol 1999. 0062. Toxicol Appl Pharmacol 2004. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Breckenridge CB.56(2):69-109. Geological Survey (USGS).

310 (. It was first registered with U. dizziness.51 (1.610-.4-D is rapidly absorbed via oral and inhalation routes.210-.370-.02-1.Herbicides 2.890) < LOD .490) < LOD < LOD < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0. 1977).4-D or exposed for prolonged periods. 1974.4-Dichlorophenoxyacetic Acid CAS No..16) < LOD .952 and 0. and aquatic environments.03) 695 659 520 668 589 892 Limit of detection (LOD. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba. Similar to other chlorophenoxy herbicides. nausea. 1989. 2.40) 1.440-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.810-1.560-.S.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.690-1.730 (.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 . 2.690 (. Recent estimates of chronic intakes of 2.EPA in 1948.48) < LOD 1.760 (.66) < LOD 1. agricultural.00-2.10 (<LOD-1.24 (.80) 1.27 (.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . MCPA. Kohli et al.08) < LOD .410) < LOD . 4-D.250 (<LOD-.230 (<LOD-. 2007).420-.S. It is poorly bound in soils.20 (<LOD-1.13) < LOD . Fourth National Report on Human Exposure to Environmental Chemicals 57 .4-D can be applied either as an aqueous salt or as oil-soluble esters. 2004). At low levels. Survey Geometric mean (95% conf.10) < LOD 1.30 (<LOD-2. in 2001 (U.690 (. It is rarely detected in ground waters (USGS.22) < LOD . and delayed Urinary 2. renal and hepatic injury. and by consuming food or drinking water contaminated with 2. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.320) 90th .350) < LOD < LOD < LOD .4-D were used in the U.4-D have been below recommended intake limits (U.20 (. 2. Human health effects from 2.680-1.540-. hypotension.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD . < LOD means less than the limit of detection.21) 1.. 2.930-1. but at higher levels they are herbicidal.490 (.4-dichlorophenoxyacetic acid (2.07 (. population from the National Health and Nutrition Examination Survey.910) < LOD .330 (.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .EPA.05-2. It is not well absorbed through the skin.60) 1.670-1.560-1.27-2. and mecoprop).EPA.230-. 2005).10 (<LOD-1.S.S. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.960-1.S. Once absorbed.310) < LOD .4-D) controls broadleaf weeds in residential.2. it acts as a plant growth hormone. 94-75-7 General Information Widely used throughout the United States. the chlorophenoxy herbicide 2.400) < LOD .890 (.32 (1. headache. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1..930 (. General population exposure to 2.55 (1.660) 1. Sauerhoff et al.550-1. abdominal pain. myotonia.420) < LOD .260 (<LOD-.43) 1.4-D may occur during residential applications. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.690 (. As much as 62 million pounds of 2.910) 1.610 (.210 (<LOD-.70) 1. by direct contact with agricultural and residential areas after applications. which may vary for some chemicals by year and by individual sample.740 (.27 (1. these herbicides can enhance plant growth.250 (<LOD-. with a half-life of several days to several weeks.4-D has low acute toxicity.

1995.820-1. 2002. thyroid. 2005). In previous samples of the U.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.32 (<LOD-2. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. 2006. 2005. developmental.610-.270 (<LOD-.3.330-.720 (.340-.780) .810-1. liver.4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..890) < LOD 1.620-..S.380 (<LOD-.08 (.590 (<LOD-1.S. 2003.S.19) .39) < LOD 1.790) 1.27-1. Epidemiological studies have reported associations of several types of cancer. 2005. U.8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert. Pearce and McLean.780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 1992).890-1.470) < LOD . 2000). 1995).13 (.810-1.. 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 . other exposures.S.410) 90th .13 (.380) < LOD .790) < LOD .4-D reflect recent exposure.4-D are eye irritants.05) . 58 Fourth National Report on Human Exposure to Environmental Chemicals .14 (. or teratogenic effects in chronic rodent studies (Charles et al.580-.56) . Hill et al. 2005.26) 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 .270-.920) < LOD 1. U.73) . 2005).440 (. 2002. IPCS.4-D does not have significant reproductive. Post-application levels in farmers and home gardeners were dependent on Urinary 2.08 (.. Survey Geometric mean (95% conf.560-.990-1. and evidence of histological injury to the kidneys. U.epa.670 (.390) < LOD < LOD < LOD .35) < LOD . 1994).4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.4-D levels were detectable in less than a quarter of the individuals studied..gov/pesticides/.4-D production plant workers and a few forestry workers spraying 2.. or to contaminants in the herbicide formulations (specifically 2. Kutz et al.410) < LOD < LOD < LOD . CDC. 1989). 2.780 (.380-..16) 1. in small samples of children (Hill et al.670 (..550-.670 (<LOD-1.EPA.570) < LOD . IOM. 1996. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2001.850) < LOD . adrenals and gonads (NTP.EPA. It is unclear whether these associations are related to the chlorophenoxy herbicides.740 (. Average post-application urinary levels of 2.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2005).29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .41 (1. 1996. 2005.17 (.S.930-1.Herbicides neuropathy (Bradberry et al. population (Hill et al. 1980.490 (.EPA 2005). 2005). U.380 (<LOD-. 2.S. The acid and salt forms of 2.08 (.640 (.. 1985. myotonia. 1996.410) < LOD 1.610-.560-.520-.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. and of adults and children (Baker et al. 2004).660) < LOD . population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.590 (<LOD-1.340 (. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.410 (<LOD-.. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. Additional information is available from U.24) 1.EPA at: http://www.780-1.700 (.680) < LOD .EPA. Kolmodin-Hedman and Erne. 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. urinary 2. IPCS. IPCS.S. Biomonitoring Information Urinary levels of 2.7. Frank et al.980) < LOD 1.660 (.480 (.350 (<LOD-. 2. eyes. Acute high doses administered to laboratory animals produced ataxia.

Gupta BN. Harris et al.5-T).edu/catalog. Barr DB. and the use of protective clothing or equipment (Arbuckle et al. TOX-63 Peroxisone Project (2. Crit Rev Toxicol 2002. Exposure of homeowners and bystanders to 2. Hill RH Jr. Holler JS. Shealy DB. Hill RH Jr. Environ Res 1995. Arch Environ Contam Toxicol 1989. Available at URL: http:// www.4-D). Erne K. Pesticide residues in urine of adults living in the United States: reference range concentrations.nih.31 Suppl 1:98-104. Garabrant DH. References Arbuckle TE. Cole DC. Beasley VR. 2006.10(6 Pt 2):789-798. Sircar KP. J Environ Sci Health B 1992. Baker BA. Driskell WJ. Smith SJ. Philbert MA. Cook BT. general population.4-D than levels found in the general population. Atlanta (GA). van Ravenzwaay B. Bailey SL. J Expo Anal Environ Epidemiol 2005 Nov.. Curwin BD. 2005. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Finding a measurable amount of 2. Survival and Growth Curves from NTP Toxicity Studies. Pesticides residues in food: 1996 evaluations Part II Toxicology. Reynolds SJ. National Toxicology Program (NTP).htm. Scand J Work Environ Health 2005.4:427-435. Barr DB..18(4):469-474. Ritter L.4-. 2005). Selected pesticide residues and metabolites in urine from a survey of the U. Scand J Work Environ Health 2005. Kolmodin-Hedman B. Vet Hum Toxicol 1989. 3/17/09 Institute of Medicine (IOM). Head SL. Available at URL: http://ntp. et al. Arch Toxicol Suppl 1980. International Programme on Chemical Safety-INCHEM (IPCS). Arch Environ Contam Toxicol 1985.inchem. Veterans and Agent Orange: update 2002. Biomonitoring for farm families in the farm family exposure study. Murphy RS. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. geometric mean urinary levels of 2. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Khanna RN.Herbicides the time since application.4-Dichlorophenoxyacetic Acid). Bus JS. Board on Health Promotion and Disease Prevention..4-dichlorophenoxyacetic acid (2. Sanderson WT. 2005.60(1):121-131.31 Suppl 1:90-97.S. et al. 2. J Toxicol Environ Health 1992.4:318-321. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.31(2):121-125. Honeycutt R. TOX-63: TOXICITY REPORT CURVES. Review of 2.4-dichlorophenoxyacetic acid and its forms. Updated March 7. Ripley BD. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.php?record_id=10603. Xenobiotica 1974. Dichlorophenoxyacetic acid. Biomonitoring of herbicides in Ontario farm applicators. Absorption and excretion of 2. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.4-D): exposure and urinary excretion. Fast DM. Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Arnold EK.32(4):233-257.4-D) epidemiology and toxicology. Kohli JD. Baker S. Brody D. 3/17/09 Knopp D.gov/index. Sirons G J. Mandel et al. Alexander BH.niehs. 2003.4-D will result in an adverse health effect.51(3):152-159. To T. Assessment of exposure to 2. Baker SE. the number of acres to which it was applied (Curwin et al. J Expo Anal Environ Epidemiol 2000. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.4. Washington (DC): National Academies Press.. et al. Needham LL. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Mandel JS.4-D in urine does not mean that the level of the 2.37(2):277-291. 2005 Charles JM.4 dichlorophenoxyacetic acid (2.4-D were highest in the farmers who applied the 2. Acquavella JF. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Tandon JS. Hanley TR Jr. Carter-Pokras OD. 2005). Estimation of occupational exposure to phenoxy acids (2. Toxicol Sci 2001.4-D in urine provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of 2.4:97-100. Hein MJ. Kutz FW. Gregg M. Occup Environ Med 1994. the amount of pesticide applied. Chapman P. In farm families. Available at URL: http:// www. Wilson RD. 1992).org/documents/jmpr/jmpmono/v96pr04.nap. Beeson MD. Heederik D.4-D and 2. Tables. 914.4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Frank R. Biomonitoring studies of 2.27(1):23-38.4-dichlorophenoxyacetic acid (2. Needham LL.4-D. Harris SA. Developmental toxicity studies in rats and rabbits on 2. Stephenson GR.15(6):500-508.71(2):99-108. Dhar MM. Campbell RA.4-dichlorophenoxyacetic acid in man. Solomon KR. Forestry workers involved in aerial application of 2.

Environmental Protection Agency (U.usgs.gov/oppsrrd1/ REDs/factsheets/24d_fs.S. Available at URL: http://www. Blau GE.4-dichlorophenoxyacetic acid (2.S.S. Available at URL: http://www. Supplemental Technical Information (available on-line only). S. Available at URL: http://water.4-D RED Facts. Washington (DC): U.EPA. 1992-2001.EPA).epa.4-D) following oral administration to man. The fate of 2.php. Braun WH. 2004.EPA). Toxicology 1977.htm. 2007. Pesticide industry sales and usage . 3/17/09. 3/17/09 U. 4/2/09 U. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Gehring PJ. March 2006.epa. May. Office of Prevention Pesticides and Toxic Substances. Environmental Protection Agency (U. 2.8:3-1U. EPA 738 F-05-002. Circular 1291. Pesticides in the Nation’s Streams and Ground Water.pdf.Herbicides Sauerhoff MW.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. Geological Survey (USGS). 60 Fourth National Report on Human Exposure to Environmental Chemicals .2000 and 2001 market estimates.S.S. The Quality of Our Nation’s Waters. revised February 15. June 2005.

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

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

Biagini RE. Xenobiotica 1994.pdf.gov/nawqa/ pnsp/pubs/wrir984245/text. Third National Report on Human Exposure to Environmental Chemicals. Jefferies PR. Sci Total Environ 2000.11(4):353359.248(2-3):123-133. Deddens JA. Comparative metabolism and elimination of acetanilide compounds by rat. Centers for Disease Control and Prevention (CDC).Herbicides References Battaglin WA. Available at URL: http://www. Camann DE. Available at URL: http://water. Available at URL: http://water.php. 1992-2001. Wratten SJ.41:3409-3414. Davison KL. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. April 1995. usgs. reservoirs and ground water in the Midwestern United States. 6/1/09 Whyatt RM. Kinney PL. Roberts AL. Environ Health Perspect 2003. U. and metolachlor herbicides in rats. Hladik ML.47(6):503-517.248(2-3):115-122. Sanderson WT. California.37(4):10881093. Coleman S. 1999. Peter CJ. EPA 738R-95-006. Thelin GP. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. 2007. Feng PCC. Reregistration Eligibility Decision (RED) Metolachlor. Metolachlor in Drinkingwater. Occurrence of sulfonylurea. Hein MJ.pdf 3/30/09 Hines CJ.S. Shoemaker DA. Chem Res Toxicol 1998. 2003. Pesticides in U. Available at URL: http://water. Ann Occup Hyg 2003.epa. Dialkylquinonimines validated as in vivo metabolites of alachlor. EPA). Environmental Protection Agency (U. J Expo Anal Environ Epidemiol 2005. Reynolds SJ. revised February 15.usgs.111(5):749-756. Brown KK. Barr DB. 3/26/09 U. Sacramento.gov/nawqa/pnsp/pubs/circ1291/ supporting_info.gov/oppsrrd1/ REDs/0001. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No.108(12):1151-1157. Environ Sci Technol 2005. 98-4245 (by Barbash JE. World Health Organization (WHO). Atlanta (GA). Background document for development of WHO Guidelines for Drinking-water Quality. Kolpin DW. imidazolinone.usgs. Geological Survey (USGS). Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Circular 1291. Gillion.S. Barr JR. Barr DB.html. Burkhardt MR. J Agri Food Chem 1989.int/water_sanitation_health/dwq/chemicals/ metolachlor. Striley CA.ESTfeature_gilliom. Feil VJ. Heederik D. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . Geological Survey (USGS). Linhart SM.S.15(6):500-508.gov/nawqa/pnsp/pubs/files/051507.who. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.S.pdf. Larsen GL. and other herbicides in rivers. Andrews HF. Alavanja MC. 1998. sulfonamide. Supplemental Technical Information (available on-line only). Quistad GB.S. et al. 4/2/09 U. Hsiao JJ. Thurman EM. acetochlor. R. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Hodgson E. March 2006.24(10):1003-1012. Sci Total Environ 2000. Environ Sci Technol 2007. Furlong ET. Kolpin DW. Linderman R. Gilliom RJ). Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Ward EM. et al. Available at URL: http://www.39(17):6561-6574. streams and groundwater. 2005. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Environ Health Perspect 2000. Curwin BD. Casida JE. Rose RL. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.

myotonia.Herbicides 2.2 and 0.5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown.4. Human health effects from 2. Given the commercial unavailability of 2.5-T use as a herbicide in 1985.5-T in soil varies with conditions. 2. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. Chlorophenoxy herbicides act as plant growth hormones. 1992). 93-76-5 General Information 2. abdominal pain. Omer..5-T has been rarely detected in ground waters (USGS. and delayed neuropathy (Bradberry et al.5-T (Holson et al. Ester forms of 2. Although 2. dizziness.4.5-Trichlorophenoxyacetic Acid CAS No. the general population is unlikely to be exposed to it. 1992. ranging from several weeks to many months.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. Survey Geometric mean (95% conf. 1974).4.5-T degrades to 2. it is not well absorbed through the skin.5-T and 2. 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD.4.5-trichlorophenol and other degradates. Once absorbed into the body.4.5T is rapidly absorbed via oral and inhalation routes. Agent Orange). and concern about contamination with 2.4. The half-life of 2. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. these herbicides can enhance plant growth. headache.5-T is eliminated mostly unchanged in the urine. renal and hepatic injury. < LOD means less than the limit of detection. with an elimination half-life of approximately 19 hours (Arnold et al. 64 Fourth National Report on Human Exposure to Environmental Chemicals .5-T.4. Mohammad and St. nausea.4.4. 1986.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.3. 2.. but higher levels are herbicidal. hypotension.. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. At low levels.7.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-T was once applied as either an aqueous salt or as an oil-soluble ester. 2007).4.4. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2.g. 1989.4.4.4-D were used as defoliants in the Vietnam War (e. Nelson et al.S. 2004).4. which may vary for some chemicals by year and by individual sample.4..1. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2.. Epidemiological studies have reported associations of several types of cancer. 2. Kohli et al.5-Trichlorophenoxyacetic acid (2.4.

4.S.4.7.EPA at: http://www. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.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. population from the National Health and Nutrition Examination Survey. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Biomonitoring Information Urinary levels of 2.gov/pesticides/.4. Fourth National Report on Human Exposure to Environmental Chemicals 65 . U. 2002. urinary levels of 2.5-T reflect recent exposure. 1996. IPCS.4. in which urinary levels of 2. It is unclear whether these associations are related to the chlorophenoxy herbicides.5-T does not mean that the level will result in an adverse health effect.3.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.. 2005.epa. similar to results of NHANES II (19761980). 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. Finding a measurable amount of 2.S. other exposures. Survey Geometric mean (95% conf. Mean urinary levels of 2.4.Herbicides or contaminated herbicides.4. Biomonitoring studies on 2. 2. 1992).5-T itself is not mutagenic. IOM. Additional information is available from U.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.5-T also were below the limit of detection (Kutz et al. 1980).5-T than levels found in the general population. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans.5-T were generally below the limit of detection.4. or to contaminants in the herbicide formulations (specifically 2.4.EPA. 2003. 2004). Pearce and McLean.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. 2005).4.

Third National Report on Human Exposure to Environmental Chemicals. Board on Health Promotion and Disease Prevention. Available at URL: http:// www. Mohammad FK. Arch Int Pharmacodyn Ther 1974. Nelson CJ.31 Suppl 1:1825. general population.32(4):233-257. Review of 2. Environmental Protection Agency (U. Pearce N. Proudfoot AT. Fundam Appl Toxicol 1992.S. International Programme on Chemical Safety-INCHEM (IPCS). Vale JA. Behavioral and developmental effects in rats following in utero exposure to 2.5-T). S.19(2):298-306. 2003.4. Poisoning due to chlorophenoxy herbicides. Crit Rev Toxicol 2002.4. Kutz FW.php?record_id=10603.4. Toxicol Rev 2004. gov/oppbead1/pestsales/01pestsales/market_estimates2001.19(2):286-297. Nelson CJ. et al. Neurobehav Toxicol Teratol 1986. Fundam Appl Toxicol 1992.4-dichlorophenoxyacetic acid (2.4-. 2. U. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice.S. Gupta BN.8(5):551-60.5-T). Murphy RS.4-D and 2. Carter-Pokras OD.4-D/2. Developmental toxicity of 2. Dichlorophenoxyacetic acid. Tandon JS. Holson JF.4.S. 2005. Dhar MM. Khanna RN. I. Selected pesticide residues and metabolites in urine from a survey of the U.37(2):277-91. Garabrant DH. May.5-T in four-way outcross mice.nap.4-D) epidemiology and toxicology. LaBorde JB. McLean D. Available at URL: http://www. Atlanta (GA). J Toxicol Environ Health 1992.epa. Washington (DC): U. Pesticides residues in food: 1996 evaluations Part II Toxicology. Estimation of occupational exposure to phenoxy acids (2.5-trichlorophenoxyacetic acid (2. Centers for Disease Control and Prevention (CDC). 210:250-255. Sircar KP. Erne K.5-trichlorophenoxyacetic acid (2. Absorption and excretion of 2. Gaines TB.EPA). St Omer VE. Veterans and Agent Orange: update 2002. et al.5-t mixture. Holson JF. Developmental toxicity of 2.23(2):65-73. Pesticide industry sales and usage .2000 and 2001 market estimates. Brody D. Cook BT.org/documents/jmpr/jmpmono/v96pr04.Herbicides References Arnold EK. Sheehan DM.pdf. Bradberry SM. 2004. 914. Beasley VR. LaBorde JB. Multireplicated dose-response studies with technical and analytical grades of 2. 3/17/09 Kohli JD. Office of Prevention Pesticides and Toxic Substances. Scand J Work Environ Health 2005. Gaylor DW. McCallum WF. Kolmodin-Hedman B.5-trichlorophenoxy acetic acid in man.EPA.4. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update.inchem. Philbert MA. discussion 5-7. Gaines TB.4. Vet Hum Toxicol 1989.edu/catalog.31(2):121-125.htm. Washington (DC): National Academies Press. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals . Arch Toxicol Suppl 1980.4. 3/17/09 Institute of Medicine (IOM). Agricultural exposures and non-Hodgkin’s lymphoma. Available at URL: http:// www. II. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. Wolff GL.4:318-21.4.5-T).

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

Carbamate Insecticides

Carbofuran

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 827 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1340

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

* * * * * *

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

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

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

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

696 680 521 696 603 953

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

68

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 826 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1339

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

* * * * * *

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

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

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

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

696 680 521 695 603 953

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

Fourth National Report on Human Exposure to Environmental Chemicals

69

Carbamate Insecticides

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

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Carbamate Insecticides

Propoxur

CAS No. 114-26-1 General Information 2-Isopropoxyphenol is a metabolite of propoxur, a carbamate used to control ants, roaches, hornets, and similar pests in residential areas and around commercial food-handling establishments. Propoxur has also been used in pest strips and pet flea collars. Like several other pesticides, propoxur has been used outside the U.S. as a replacement for DDT in malaria vector control. Propoxur may remain in the environment for weeks to several months, longer than most carbamates (U.S.EPA, 1997b). Despite its mobility in soil and its potential for leaching into groundwater, propoxur has been rarely detected in U.S. surface or ground waters (Gilliom, 2007; USGS, 2007). Although propoxur is toxic to birds and aquatic life, ecologic exposures are unlikely due to current outdoor use restrictions. General population exposure to propoxur through the diet is likely to be limited because of usage restrictions (U.S. EPA, 1997a). Estimated human intakes have been below recommended intake limits (U.S.EPA, 1997b). Pesticide applicators are likely to have the highest exposures. Propoxur can be absorbed through the skin, lungs, and gastrointestinal tract. Propoxur does not accumulate in blood or tissues and is eliminated rapidly from the body (Leenheers et al., 1992; WHO, 2003). In animal and human studies, 2-isopropoxyphenol was one of several urine metabolites (U.S.EPA, 1997b). Human health effects from propoxur at low environmental doses or at biomonitored levels from low environmental exposures are unknown. In animal studies, propoxur has moderate acute toxicity consisting of anticholinesterase effects (U.S.EPA, 1997b). 2-Isopropoxyphenol does not inhibit acetylcholinesterase enzymes. Propoxur is not considered mutagenic, embryotoxic, or teratogenic (WHO, 2003). U.S. EPA considers propoxur to be a probable human carcinogen, based on bladder tumors in male rats (U.S. EPA, 1997b). The human carcinogenic potential of propoxur has not been evaluated by IARC or NTP. Additional information is available from U.S.EPA at: http:// www.epa.gov/pesticides/. Biomonitoring Information Urinary 2-isopropoxyphenol levels reflect recent exposure. The level of this metabolite in urine may reflect exposure to propoxur or to 2-isopropoxyphenol as a degradation product in the environment or food (U.S.EPA, 1997b). In the U.S.

representative subsamples from NHANES 1999-2000 and 2001-2002, most 2-isopropoxyphenol levels in urine were below the limit of detection (CDC, 2005). In a nonrandom subsample from NHANES III (1988-1994), the 95th percentile level of 2-isopropoxyphenol was 1.7 µg/L (Hill et al., 1995). Higher urinary levels of 2-isopropoxyphenol have been measured in a few pesticide applicators, with a range of 45-306 µg/g creatinine (Hardt and Angerer, 1999). Finding a measurable amount of 2-isopropoxyphenol in urine does not mean that the level of 2-isopropoxyphenol causes an adverse health effect. Biomonitoring studies on levels of 2-isopropoxyphenol provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of propoxur than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.

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Carbamate Insecticides

Urinary 2-Isopropoxyphenol
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2503

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 820 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1325

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

* * * * * *

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

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

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

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

664 677 500 696 585 931

Limit of detection (LOD, see Data Analysis section) for Survey years 99-00 and 01-02 are 1.1 and 0.4. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

Urinary 2-Isopropoxyphenol (creatinine corrected)
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2502

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 819 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1324

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

* * * * * *

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

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

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

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

664 677 500 695 585 931

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

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Carbamate Insecticides

References Centers for Disease Control and Prevention (CDC). Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA). 2005. Gillion, R. Pesticides in U.S. streams and groundwater. Environ Sci Technol 2007;41:3409-3414. Available at URL: http://water. usgs.gov/nawqa/pnsp/pubs/files/051507.ESTfeature_gilliom. pdf. 4/9/09 Hardt J, Angerer J. Gas chromatographic method with massselective detection for the determination of 2-isopropoxyphenol in human urine. J Chromatogr B Biomed Sci Appl 1999;723(12):139-145. Hill RH Jr, Head SL, Baker S, Gregg M, Shealy DB, Bailey SL, et al. Pesticide residues in urine of adults living in the United States: reference range concentrations. Environ Res 1995;71(2):99-108. Leenheers LH, van Breugel DC, Ravensberg JC, Meuling WJ, Jongen MJ. Determination of 2-isopropoxyphenol in urine by capillary gas chromatography and mass-selective detection. J Chromatogr 1992;578(2):189-194. U.S. Environmental Protection Agency (U.S.EPA). RED Facts. Propoxur. August 1997a. EPA 738 F-97-009. Available at URL: http://www.epa.gov/oppsrrd1/REDs/factsheets/2555fact.pdf. 4/9/09 U.S. Environmental Protection Agency (U.S.EPA). Reregistration Eligibility Decision (RED) Propoxur. August 1997b. EPA 738R-97-009. Available at URL: http://www.epa.gov/pesticides/ reregistration/REDs/2555red.pdf. 4/9/09 U.S. Geological Survey (USGS). The Quality of Our Nation’s Waters. Pesticides in the Nation’s Streams and Ground Water, 1992-2001. Circular 1291. Supplemental Technical Information (available on-line only). March 2006, revised February 15, 2007. Available at URL: http://water.usgs.gov/nawqa/pnsp/pubs/ circ1291/supporting_info.php. 4/2/09 World Health Organization (WHO). WHO Specifications and Evaluations for Public Health Pesticides. Propoxur. FAO/WHO Evaluation Report 80/2003. 2003. Available at URL: http:// www.who.int/whopes/quality/en/propoxur_eval_spec_WHO_ October_2005.pdf. 4/9/09

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Organochlorine Pesticides
General Information Organochlorine pesticides, an older class of pesticides, are effective against a variety of insects. These chemicals were introduced in the 1940s, and many of their uses have been cancelled or restricted by the U.S. EPA because of their environmental persistence and potential adverse effects on wildlife and human health. Many organochlorines are no longer used widely in the U.S., but other countries continue to use them. Hexachlorobenzene has been used primarily as a fungicide or biocide. Organochlorine pesticides can enter the environment after pesticide applications, disposal of contaminated wastes into landfills, and releases from manufacturing plants that produce these chemicals. Some organochlorines are volatile, and some can adhere to soil or particles in the air. In aquatic systems, sediments adsorb organochlorines, which can then bioaccumulate in fish and other aquatic mammals. These chemicals are fat soluble, so they are found at higher concentrations in fatty foods. In the general population, diet is the main source of exposure, primarily through the ingestion of fatty foods such as dairy products and fish. Usage restrictions have been associated with a general decrease in serum organochlorine levels in the

U.S. population and other developed countries (Hagmar et al., 2006; Kutz et al., 1991). Contaminated drinking water and air are usually minor exposure sources. Infants can be exposed through breast milk, and the fetus can be exposed in utero via the placenta. Workers can be exposed to organochlorines in the manufacture, formulation, or application of these chemicals. The FDA, U.S. EPA, and OSHA have developed standards for allowable levels of certain organochlorines in foods, the environment, and the workplace, respectively. Attributing human health effects to specific organochlorine chemicals is difficult because exposure to multiple organochlorine chemicals occurs often and these chemicals may have similar actions. The table shows selected parent organochlorines and their metabolites that can be measured in serum or urine. Measurements of these chemicals can reflect either recent or cumulative exposures, or both. Some of the metabolites can be produced from more than one pesticide. The level of a metabolite in a person’s blood or urine may indicate exposure to the parent pesticide as well as to the metabolite itself.

Organochlorine Pesticides and Metabolites in this Report
Organochlorine Pesticide (CAS number) Serum pesticide or metabolite(s) (CAS number) Urinary pesticide or metabolite(s) (CAS number)

Aldrin (309-00-02) Chlordane (12789-03-6)

Aldrin (309-00-02) Dieldrin (60-57-1) Oxychlordane (27304-13-8) trans-Nonachlor (3734-49-4) p,p’-DDT (50-29-3) p,p’-DDE (72-55-9) o,p’-DDT (789-02-6) Dieldrin (60-57-1) Endrin (72-20-8) Heptachlor epoxide (1024-57-3) Hexachlorobenzene (118-74-1) Pentachlorophenol (87-86-5) 2,4,6-Trichlorophenol (88-06-2) 2,4,5-Trichlorophenol (95-95-4) Pentachlorophenol (87-86-5) 2,4,6-Trichlorophenol (88-06-2) 2,4,5-Trichlorophenol (95-95-4)

Dichlorodiphenyltrichloroethanes Dieldrin (60-57-1) Endrin (72-20-8) Heptachlor (76-44-8) Hexachlorobenzene (118-74-1)

Hexachlorocyclohexanes Mirex (2385-85-5) 2,4,5-Trichlorophenol (95-95-4) 2,4,6-Trichlorophenol (88-06-2)

beta-Hexachlorocyclohexane (319-85-7) gamma-Hexachlorocyclohexane (58-89-9) Mirex (2385-85-5)

2,4,5-Trichlorophenol (95-95-4) 2,4,6-Trichlorophenol (88-06-2)

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Organochlorine Pesticides

References Hagmar L, Wallin E, Vessby B, Jonsson BA, Bergman A, Rylander L. Intra-individual variations and time trends 1991-2001 in human serum levels of PCB, DDE and hexachlorobenzene. Chemosphere 2006;64(9):507-513. Kutz FW, Wood PH, Bottimore DP. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Rev Environ Contam Toxicol 1991;120:1-82.

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Aldrin

CAS No. 309-00-02

but dieldrin has been detected in meats, dairy products, and in crops grown in soils that have been contaminated, usually by application, manufacturing, or disposal. General population exposure to these chemicals occurs through the diet, and detection of dieldrin residue in foods has decreased over time (FDA, 2008). Inhalation exposure may occur among people living in residences where aldrin was applied historically as a pesticide. Aldrin and dieldrin are absorbed following ingestion, inhalation, and dermal application. After absorption, aldrin is metabolized to dieldrin so rapidly that aldrin is rarely detected. Dieldrin accumulates in fatty tissues, and its metabolites are excreted in bile and feces (ATSDR, 2002). It is also excreted in breast milk and can cross the placenta. The elimination half-life of dieldrin is approximately 1 year (IPCS, 1989; Jorgenson 2001). Human health effects from aldrin and dieldrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown. At high doses, aldrin and dieldrin block inhibitory neurotransmitters in the central nervous system (Narahashi et al., 1992). This blocking action can cause abnormal excitation of the brain, leading to symptoms such as headache, confusion, muscle

Dieldrin

CAS No. 60-57-1 Also a Metabolite of Aldrin General Information Aldrin and dieldrin are no longer produced or used in the U.S. From the 1950s to 1970, both chemicals were applied mainly as a soil insecticide or seed dressing for food and commodity crops. Dieldrin was also used for mothproofing clothes and carpets. In tropical countries, dieldrin was used as a residual spray in residential dwellings to control vectorborne diseases such as malaria. The U.S. EPA cancelled agricultural uses of both pesticides in 1970; termiticide uses were cancelled in 1987. Aldrin is readily converted to dieldrin in the environment and in plants that take up the chemical. Aldrin volatilizes after agricultural soil applications or is converted to dieldrin, which volatilizes more slowly. These chemicals persist in the environment and bioaccumulate in foods (Jorgenson 2001; USGS, 2007). Aldrin is rarely detected in plants or animal tissues,

Serum Aldrin (lipid adjusted)
Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.S. population from the National Health and Nutrition Examination Survey.
Survey Geometric mean
(95% conf. interval)

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 2275 1946

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

years 01-02 03-04

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

756 588 1519 1358

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

1057 946 1218 1000

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

* * * * * *

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

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

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

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

559 456 512 485 1045 881

Limit of detection (LOD, see Data Analysis section) for Survey years 01-02 and 03-04 are 5.94 and 7.8. < LOD means less than the limit of detection, which may vary for some chemicals by year and by individual sample. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

Fourth National Report on Human Exposure to Environmental Chemicals

77

Kanthasamy et al. nausea. and seizures.. 78 Fourth National Report on Human Exposure to Environmental Chemicals .. dieldrin at higher doses caused irritability. 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. 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. In samples obtained between 1973 and 1991 from Norwegian women..gov/toxpro2.. 2005. both aldrin and dieldrin caused liver enlargement and liver tumors. seizures (Smith. but no estrogenic effect was noted in a study that used cultured cells (Tully et al. in which only 10. Survey Geometric mean (95% conf. Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples.. 2004). Epidemiologic and animal studies have not conclusively associated dieldrin exposure with risk for developing Parkinson’s disease (Corrigan et al. 1987). 2000.6% of the subsample had dieldrin levels above the limit of detection (Stehr-Green 1989). 1995).atsdr.e. EPA has established environmental standards for aldrin and dieldrin.S.html. 1998) and behavioral changes (Carlson and Rosellini. serum aldrin levels were below the limit of detection. When dieldrin was fed to pregnant rodents.. environmental levels) and health effects is available from ATSDR at: http://www. Studies done in vitro showed that dieldrin binds to estrogen receptors (Soto et al. similar to results in a subsample of NHANES II (19761980) (Stehr-Green. 2005). 2000). 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. IARC has determined that aldrin and dieldrin are not classifiable with regard to human carcinogenicity. 1991). the offspring had altered CNS neurotransmitter levels (Sanchez-Ramos et al. 1998). 2004).. Serum dieldrin levels at the 95th percentile in NHANES 2001-2002 and 2003-2004 subsamples were approximately ten times lower than the corresponding percentile measured in NHANES II (1976-1980). The median 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.. Information about external exposure (i. and occasionally. 2000).. the median serum dieldrin level was generally similar to the 90th percentile for females in this Report (Ward et al. vomiting. Levels of aldrin also were not detectable in 1996-1997 pooled samples from New Zealand adults (Bates et al.Organochlorine Pesticides twitching. population from the National Health and Nutrition Examination Survey.. The U. When fed to experimental animals. 1989). In a study of pesticide applicators with occupational exposure to aldrin.S..cdc. 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. and the FDA monitors foods for pesticide residues. Li et al. OSHA has established workplace exposure standards for aldrin and dieldrin. tremors.

116) .110 (.080) .1 (18.1) 13.1-18.110) .9 (13.2) 14.4) 14.140) .8) < LOD 8.8) 14.0 (10.00 (8.130 (.077-.0) 19.1) 15.117) < LOD .202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.108-.170) .090 (<LOD-.073-. 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 .60-10.140-.180) .8-17.102 (.7 (<LOD-15.5 (<LOD-11.138 (.112) 95th .5) 21.80-9.124) .4) 95th 20.100-.190) .064 (.109-.9 (12.0 (10.0) < LOD 9.7-22.3 (18. 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.150 (.6 (15.120-. see Data Analysis section) for survey years 01-02 and 03-04 are 10.8 (18.40-10.9 (13.070-.160 (. Fourth National Report on Human Exposure to Environmental Chemicals 79 .4 (12.139 (.130) .070 (<LOD-.5 (16.109-. population from the National Health and Nutrition Examination Survey.4) 21.9-23.149) .190) .130-.147 (.113 (.7 (14.130-.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.00-14.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.3 (13.30 (8.090 (.30 (8.S.158) .109 (.7 (15.054-.059 (.090-.112-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.5) 19.054-. which may vary for some chemicals by year and by individual sample.5) 15.053 (<LOD-.8 (9.50) 15.098 (.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .1) 14.120 (.6-24.160 (.3 (14.0 (11.120 (.048 (<LOD-.160) .8-17.096-.080-.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 .090-.110) .100 (.1-19.110 (.8-19.4) 539 456 484 487 980 885 Limits of detection (LOD.049-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.6 (14.140 (.70 (7.6 (15.080 (.4) < LOD < LOD 16.40-9. which may vary for some chemicals by year and by individual sample.9 (12. Survey years 01-02 03-04 Geometric mean (95% conf.4-17.054-.8-24.101) .7-19.070) .069) < LOD < LOD .3 (19.089 (.100-. population from the National Health and Nutrition Examination Survey.4-18.4) 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 8.090-.100) .086-.6-24.0-25.8-25.8 (11. < LOD means less than the limit of detection.5-17.9-22. 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 9.075) < LOD .6) 19.10 (<LOD-16.2-15.055 (.138) . Survey years 01-02 03-04 Geometric mean (95% conf.5-17.103 (.4) 20.7) 15.1-16.80 (<LOD-10.084-.110 (.1) 20.062 (.062 (.100-.6) 16.4 (12.093) .1) 15.8) 15.060) .110-.1-24.8.120 (.103 (.6-33.1) < LOD 9.5-15.139 (.120) .90) 90th 15.0 (15.056-.0-21.088-.064) 90th .242) .130-.2) 12.150 (.062-.1 (13.5 and 7.7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.063-.130) .50 (8.083-.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .100) .180) .3 (18.0) 21.058) < LOD .80-10.077 (.4) 19.130) .2) 11.6) 9.9-38.1) 10.2) 15.9 (14.3-21.

Soto AM. Neurotoxicol 2005. Patterson DG Jr. Rosellini RA. 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.26:701-719. Aldrin and dieldrin: A review of research on their production environmental deposition and fate. August 2008. 2 Classes of Pesticides. In Hayes WJ. Reprod Toxicol 2000. Eds. Six high-priority organochlorine pesticides. International Programme on Chemical Safety (IPCS). Available at URL: http://www.fda. Stehr-Green. Tully DB. Olea N. are nonestrogenic in transfected HeLa cells. Food and Drug Administration (FDA). Garrett N. Ginsburg KS. Sonnenschein C.91(1):122-126. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. Handbook of Pesticide Toxicology. Exp Neurol 1998. Smith AG. Toxicol Lett 1992. J Occup Environ Med 2005.html. Revised Feb. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Demographic and seasonal influences on human serum pesticide residue levels. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. David VL. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. and epidemiology in the United States. Chapin RE. 4/21/09 Bates MN. Facca A. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis. 731-915. et al. Shore RF.gov/ circ/2005/1291/.54:1431-1443. Frey JM. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women.html. Available at URL: http://www. 80 Fourth National Report on Human Exposure to Environmental Chemicals . and lymphocyte sister chromatid exchange. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Andersen A.150:263-271. 1991.103(Suppl 7):113-122. Lancet 1998. Effect of occupational exposure to aldrin on urinary D-glucaric acid. New York. Available at URL: http://pubs. Environmental Health Criteria 91. J Toxicol Environ Health.64-65 Spec. Part A 2000. No:429-436. Jr. Fernandez MG. Organochlorine exposure and risk of breast cancer. References Agency for Toxic Substances and Disease Registry (ATSDR). 1992-2001. Sanchez-Ramos J. Mumtaz MM. Cox. Patterson DG Jr. VT. United States Geological Survey (USGS). Pesticides in the Nation’s Stream and Ground Water. Narahashi T.109(Supp1):113-139. toxicology. Brock JW. Grajewski B. Environ Health Perspect 2001. Chung KL. 1989. Kitzazwa M. McIntosh LJ. Hartvig HB.66(4):229-234.9:1357-1367. Kanthasamy AG. Jorgensen T.27:405-421.gov/toxprofiles/ tp1. Corrigan FM. Roy ML. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994). Priestly BG. Kanthasamy A. Song S. 6/1/09 Ward EM.352:1816-1820. PA. Finley B. Organochlorine insecticides in substantia nigra in Parkinson’s disease. bioaccumulation. Int Arch Occup Environ Health 1994.atsdr. either singly or in combination.47:1059-1087. 2007 [online]. Vol.cfsan. Aldrin and Dieldrin [online].org/documents/ehc/ ehc/ehc91. Academic Press.gov/~dms/ pesrpts. Cancer Epidemiol Biomarkers Prev 2000. Daniel SE. Mann D. et al. 4/21/09 Jorgenson JL. Basit A. Inc. 15. Edwards JW. Carlson JN. Ellis H. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. J Toxicol Environ Health 1989. Environ Health Perspect 1995. Toxicological profile for aldrin/dieldrin [online]. Chlorinated Hydrocarbon Insecticides. Grandjean P. Li AA. pp. Needham LL. Jr and Laws ER. plasma dieldrin. Available at URL: http://www. September 2002.htm. Wienburg CL.59:229-234. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants.14:95-102. Schulte P.inchem.usgs. 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. Anantharam V. Psychopharmacology (Berl) 1987. Buckland SJ. Turner W. Teta MJ. Serrano FO. Chemosphere 2004. Mink PJ. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population.cdc. 4/21/09 Hoyer AP.

1 (16. Technical grade chlordane had contained 7% trans-nonachlor.5 (33.1 (44.6) 39.0-61.9 (26.3) 18.4 (30.4-14.9) 39.8. 01-02.9 (36. Heptachlor and chlordane are somewhat volatile and may be detected in the air and dust of buildings long after treatment for termite or insect control (Whitemore et al.3) 18.9) 36.8-33.1) 30.0-33.9) 47.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.8) 18.9 (15.6 (9.2 (36. As a result of the manufacturing process.5-47.9) 17.6) 23. < LOD means less than the limit of detection.5-13. which may vary for some chemicals by year and by individual sample.6-24. and 03-04 are 14.10 (8. lawns.4) 39.7 (19.6 (9.9-21.2) 46.9-21.5-32.1 (17.4-21.7) 28.2 (10.5) 37.7) 42.5) 21.2 (41.5) 56.8-43.3 (11.2 (9.5) 38.7) 19.7 (32.6-24. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.9-42.4) 37.9 (21. and 7.2-21.9 (11.0 (16.3 (20.36-11.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8 (17.4 (31. heptachlor use has been limited to treatment of fire ants near power transformers.8-61.5) < LOD < LOD < LOD < LOD 13.4-40.0-67.6 (16.1-15.3) 37.9) 31.5-65.7 (<LOD-32.10-11.5 (41.9 (18.0) 75th 20. 1994). 2007).9-40. Since 1992. 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.5.5-44.0 (26.89-10.7 (34.1-50.3-45.4-45.2) < LOD 11. Fourth National Report on Human Exposure to Environmental Chemicals 81 . Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk. Survey Geometric mean (95% conf.20-11.2-26.0-12.2-28.1 (<LOD-12.3-49. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.7-56.5 (34.4) 18.8 (17.74 (<LOD-10.4) < LOD < LOD < LOD 23.4 (35.6) 11.3) 10.1 (<LOD-12.8) 44.2 (28.5) 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 * * * * 11.9 (31.5) 44.5 (8. see Data Analysis section) for Survey years 99-00.5.3 (<LOD-19. Chlordane is not currently produced or used in the U.8) 27.9) 23.9 (11.3 (27.1) < LOD < LOD < LOD < LOD < LOD 8.9) 13.6) 9.8-23.5) 10.8 (18.7-70.6) 20. and in soil.2) 37.2) 34.8 (40.5-38.2 (21.30-11.7 (34.1 (27.S. the technical grade product of each chemical contains 10%-20% of the other chemical.6) 9. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues. Consequently.0) 21.1-25.8) 52.5-42.9) 11.S. 1994.8-73.5-41. foods high in fat such as meat.70 (<LOD-10.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.2-49.S.0-13.Organochlorine Pesticides Chlordane CAS No.9 (26.0-18.7) 9. population from the National Health and Nutrition Examination Survey.7) 19.1) * 11.3 (26.8 (10.9 (15.9 (17.7-25.7 (10.8 (10.1-19.1 (<LOD-12. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.8) 52. buildings.5 (31.6) 48.9-38.7 (42.1 (20.3 (9.9) 37.4-51.3) 10.8) 53.20-10.1 (25.5) < LOD < LOD 9. 2007).0-25.8-31.0 (37.1) 22.5-40.2) 33.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11.9) 10.4) < LOD 11.8-33.9) 23.2-49.6-18.6) 48.4 (<LOD-12.5-43.2) * 12.6) 36. 10.8-20.2) < LOD 11.7 (<LOD-13.1 (15.4 (22.3-45. from the early 1950’s until the mid-1980’s.6-53..1 (40.4) 22.2) 36. 57-74-9 Heptachlor CAS No.6) 8. Both pesticides are persistent in soils and sediments and have been detected in water from agricultural run-off and near production and disposal facilities (ATSDR.1) * 11.82-11.4 (30.0) 31.37 (8.0 (32.3-24.1-51.8 (42.5) 9.8-42.1 (11.20 (<LOD-11.3-32.4) 29.7 (17.6) 49.7-39.6 (43.2 (39.9 (29.63 (8.1-25.1) 90th 34.2-56. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44.7) 35. fish.6-12. in addition to trace amounts of numerous other related compounds (ATSDR.3) 41.7-14.2 (37.2) 22.4 (10.0) 41.0 (<LOD-12.8-32.90 (8.6-45.69-10.0) 27. chlordane was used to kill termites and other insects on agricultural crops.10-18.5 (<LOD-12. and dairy products are the usual sources of exposure to these chemicals in the general population.1) 16.7 (43.6 (25.1) 30.7) 31.1-65. respectively.0) 20.7-12.3 (28. Until 1988.0 (20.3-43.3 (25.4) 12.0) 37.3 (21.6) < LOD 11.9) 11.

210 (.068) 75th .047 (<LOD-. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.258-.136) .068) .220 (.320 (.060 (<LOD-.250 (. and inhalation exposure.090) .160) . Shindell and Ulrich.140) . neonatal mortality.112 (.091) .133) 90th .170-.070-. Acute.053-. EPA has established environmental criteria for chlordane and heptachlor.079) . 1991).120 (.260 (.066 (.200 (.066-.400) .320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .350) .061-.220-.290-.079) < LOD < LOD < LOD .120-.380) .058-.330 (.290 (. The U.070) < LOD < LOD < LOD < LOD < LOD . 1986).300) .290-.120-.063-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.104) .430) .216-.310-.227) < LOD . FDA established allowable residues of chlordane.271 (.120-.110-.189-.230) . 1981).290-. 1977a.225 (.320 (.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.370 (. 82 Fourth National Report on Human Exposure to Environmental Chemicals ..320 (.080 (. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.140 (.165-.223) .400) .050 (<LOD-.090-.315 (.180) .106-.287) .280-.340) .130-.300) .150-.170) .300-.230-.053-.242-.073) < LOD < LOD < LOD < LOD .063 (.062) < LOD .150 (.075 (.370 (.210 (.070 (<LOD-.087-.110 (<LOD-.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD .115 (.062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .069 (<LOD-.510) .146) < LOD < LOD .150 (.230-.258 (. and alterations in immune function of offspring.140 (. 1986).204 (.148) .130 (. Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility. chronic doses of heptachlor have produced liver enlargement and injury..063 (.180) .074-.250-.130) . OSHA has established occupational exposure criteria. 2007).360) .140-.300) .160) .168-.280-.190-.240) .070 (<LOD-.230 (.148-.058-. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf.189 (.063) .082 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .126) .260 (.068-.130-.373) .119 (.348) .126 (. Takahashi et al.S.290) .149 (.058 (. and breast milk is a major excretion route in lactating women.240-.207) .100-.049 (<LOD-.203-.083 (.055-.280) . high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.057-. 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. heptachlor.073 (.063 (.130-.140 (. Chlordane and heptachlor are absorbed after oral.S.108-.560) .208 (.065-.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 * * * * .070 (<LOD-.104-.077) .064) < LOD . Elimination of all these chemicals from the body occurs over months to years.070 (<LOD-.067 (.200-.286 (.140-.080 (.130 (.280-.146) .190-.180-.115-.077) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.170) .310 (.320 (.320) .066-. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.130) .230 (.450) .260-.170) .180-. 1991.350 (. to heptachlor. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.190-.240-.057 (.140 (.080) . 2002.270 (.083) ..290) .260 (.410) .440) ..220-.340) .450) .310) .170) . dermal.150) .213) * .300 (.270 (.128 (. 1996.063) * .070 (. 2001.240 (. Rogan.076) < LOD .253-.160 (. and heptachlor epoxide in foods and bottled water.092) .100-.056 (.170) .280 (.207 (.071 (.320) .160) .100 (.269 (.280 (.230-.090) .S.310) .070) . Smith.300) .302) .057) * .246-.231) .063 (.286 (. Le Marchand et al.130 (.430) . Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al. In laboratory animal studies. which is also persistent in the body (ATSDR.199-. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.077) .Organochlorine Pesticides (Dallaire et al.250 (. 2006).070-.066 (<LOD-. and the U.270 (. 1977b.080) .310) .350 (. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.200-.130-.050-.210-.370 (.070-. characterized by seizures and paralysis. IARC.130-.245-.048-.200-.150 (.100 (<LOD-. The major metabolite of heptachlor is heptachlor epoxide. population from the National Health and Nutrition Examination Survey.080) .077) . 2007.

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

5) 19.5 (18.0-19.3) 18.4 (11.1-15.8-24.4) 18.8-46. 01-02. and 7.2 (18.6) < LOD < LOD < LOD 27.0 (11.5.6.6 (16.2) 26.1 (16.3-18.3 (<LOD-25.8) 14.7-19.10-13.2) 15.6 (14.2-27.8) 13.8) 15.5 (<LOD-32. population from the National Health and Nutrition Examination Survey.6 (8.7 (16.2 (<LOD-25. which may vary for some chemicals by year and by individual sample.9 (12.2 (<LOD-62.7 (10.6) 14.5) < LOD 14.3) 18. 84 Fourth National Report on Human Exposure to Environmental Chemicals .3) 22.1 (19.1-16.4) 21.4 (<LOD-19.6-21.9) * * * 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 (13.9-23.4 (15.0) 13.40) 15.20 (<LOD-9.0) 638 741 592 951 1518 1371 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13.8 (15.6 (16.6) 13.2 (<LOD-16.6) 22.8) 14. Survey Geometric mean (95% conf.1-38.1) 13.0-16.2) 13.1) 23.8 (13.0-17. and 03-04 are 14.8) 21.4 (11.0 (15.8 (18.2-17.8) 16. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.2-27.9-29.8) 13.9 (15.9-29.1) 20. see Data Analysis section) for Survey years 99-00.8-24.5 (10.6-17. < LOD means less than the limit of detection.5 (11.8 (13.8 (<LOD-23.90 (<LOD-9.2) 20.4 (<LOD-54.8 (18.8) 19.5 (11.9) 15.7-25.7-18.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.7 (13.9-16.3) 18.2-16.0-17. 10.3) 16.6 (13.5 (<LOD-21.3) 27.8.6 (12.Organochlorine Pesticides Serum Heptachlor epoxide (lipid adjusted) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. respectively.8-23.3) 23.8) 19.5) 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.S.3) 10.0-54.50) < LOD < LOD < LOD 17.6 (<LOD-27.9-25.6 (11.1-29.8-24.8) 20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.

074-.135 (.100 (.180) .063) < LOD < LOD < LOD .120) .076-.055 (<LOD-.140-.100-.120) .149) .130) .180) .082-.087 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .094 (.101 (.180) .097) < LOD .100 (.180 (<LOD-.108-.310) .133 (.090 (<LOD-.090-.096 (.053-.130 (.130) .090 (.180) .200) .110 (.190 (. Fourth National Report on Human Exposure to Environmental Chemicals 85 .170) .090-.106-.090-.070-.110 (<LOD-.173) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .110 (.100-.090-.150 (.120-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.126 (.063) .111-.090-.190) .108) .100 (.140) .098 (.150 (<LOD-.157) .170 (.116) < LOD < LOD < LOD .135 (. population from the National Health and Nutrition Examination Survey.190) .310) .380) .111) .110) .110) .071-.113) .120 (<LOD-.180) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.057 (<LOD-.150 (.110-.200) .101 (.069 (.130 (<LOD-.108) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130-.090-.161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .200 (.220) .190) .140) .S.117) .130-.100 (<LOD-.128 (.130-.110 (<LOD-.110-.240) .170 (.130-.120 (.270) .113-.170) .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.170 (. which may vary for some chemicals by year and by individual sample.180 (.100 (.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 .077-.094 (.120 (<LOD-.170) .170 (<LOD-.107-. Survey Geometric mean (95% conf.067-.104) .077-.

70 (<LOD-12.2-16.8 (12.8 (19.4-52.2-18.3-58.4-18.1) 17.2) 19.0 (15. and 7.1 (47.0 (29.9 (29.7-18.5) 9.3) 18.1 (65.1) 31.7 (16.8 (45.0-59.2 (26.3) 19.7-77. < LOD means less than the limit of detection.2 (15.3 (16.8 (30.4) 107 (84.8 (13.0-143) 112 (68.1) 18.9 (15.7) 35.8-67.3 (58.2-23.6 (32. 01-02.6-22.8 (26. 10.8-90.7) 15.9 (15.7-17.3-21.3) 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.1 (22.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.0 (19.6-88.3) 36.5-87.9 (28.5) 20.1-34.7 (35.8) 19.6) 56.8-79.1-20.5) 35.7-38.8 (26.4) 55.0 (13.1) 14.8) 51.7 (30.7-29.0) 40.6 (56.9 (66.5) 48.9) 14.6) 13.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.0) 13.9) 51.1) 17.5 (13.4-35.0-37.5 (15.3) 25.3) 32.2) 20.2) 34.8-21.8 (26.4-22.3-86.8 (16.8-41.0) < LOD < LOD 8.4) 19.6 (57.4 (45.1-34.3 (14.7) 73.0-93.1-51.2) 39.7) 78.2 (27.5-36.6 (<LOD-14.5) 77.7 (59.2-88.1 (41.1) 17.4 (12.5) 19.8-19.9) 51.6) 10.3 (49.0 (48.2) 30.6-20.5-17.8 (11.7) 14.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.0-68.6) 25.0-23.5-95. see Data Analysis section) for Survey years 99-00.3) 32. Survey Geometric mean (95% conf.2 (64.9-58.0 (42.9-35.3) 18.86-13.7-21.7) 59.9-69.7) 52.7-22.9-40.9 (36.3) 30.5-19.0 (16.2-37.7) 28.3 (14.1) 17.4-62.5.1) 78.1-22.5) 14.2) 17.0-113) 68.1-16.9-64.8-129) 74. interval) 18.4 (16.10 (<LOD-11.5 (45.5) 22.1) 17. population from the National Health and Nutrition Examination Survey.8 (28.5-111) 68.7-20.0) 49.7 (13.3-30.9-20.0-24.6-19.6) 54.4) 48.0-20.0 (13.7 (18.4-36.2) 59.1 (48.9 (51.2 (14.5) 26.3 (56.6) 56.7-113) 68.0-38.0 (16.9 (47.7) 56.7) 17.8 (15.6-54.3) 15.9 (<LOD-14.8 (28.3-74.1) 30.8.9 (51.0 (62.4) 16.2 (60.1) 78.8 (13.5-20.0-123) 74.0 (42.0) 18.0) 75th 31.8-77.0) 19.8 (42.9 (19.5 (25.5) 30.4 (67.8-19. which may vary for some chemicals by year and by individual sample.8-110) 59.1) 17.4 (11.5 (44.4) 20.3) 30.8 (71.2 (19.8) 80.1-16.2 (59.6 (56.8-16.0-93. and 03-04 are 14.2-17.0 (15.8-16.0-23.8-90.6) 84. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8 (49.2 (14.1-28.5 (15.1) 17.5) 78.S.9-65.3-50.1) 16.2 (7.7 (59.1-126) 67.3) 16.2 (36.3-32.1-18.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.3-57.8 (<LOD-20.1 (17.7-32.7-160) 86.3 (17.5.6) 82. respectively.1 (10.1) 32.9-36.6 (16.7-35.5) 90th 55.6 (52.3 (45.8 (28.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17.9) 14.4-67.6) 34.6 (12.7 (11.0 (14.9-22.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11. 86 Fourth National Report on Human Exposure to Environmental Chemicals .8) 47.4-23.0-22.6) 60.7-23.2-18.7-34.6 (50.3-39.9-89.7 (74.6-66.1) 18.6-82.9-65.1-55.9 (16.4) 59.9) < LOD < LOD < LOD 20.6 (15.2-21.1) 62.0 (60.2) < LOD 10.8 (17.0) 33.9-45.7) 78.7 (28.5-69.4 (30.5) 14.5) 36.4 (28.2 (25.

371) .090-.092 (.085-.047-.420) .210) .310) .100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .470-.186-.119) Selected percentiles ( 95% confidence interval) Sample 95th .594) .210 (.120) .125 (.090-.117) .350 (.109 (.830) .300-.340) .130) .093) .490-.288-.090-.150) .091-.105 (.093-.190-.177-.301-.684) .110 (.096-.104 (.840) .220) .125) .098-.110 (.081-.112 (.100-.237) .390 (.120 (.190-.116) .100-.108 (.651) .580 (.093-. population from the National Health and Nutrition Examination Survey.060) .300) .240) .173-.550 (.390-.108) 75th .576) 650 558 457 404 514 486 722 1052 889 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 03-04 < LOD means less than the limit of detection for the lipid adjusted serum level.116-.130) .210-.600 (.630) .417 (.400-.079-.360-.288 (.370 (.113) < LOD .130) .183 (.085-.100 (.080-.110) .460) .690) .310-.400 (.100 (.130 (.120-.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.108) .370 (.190-.240-.350-.080-.960) .640 (.120-.111-.400 (.497-.078 (. interval) .414 (.220 (.210 (.930) .120 (.390) .097) .090-.490 (.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 .104-. Survey Geometric mean (95% conf.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .103 (.220 (.460-.327 (.180-.520 (.461 (.190-.081 (.680 (.069) .395-.161) .210 (.098) .430-.128 (.220 (.092 (.600) .286-.061-.145-.272-.410-.080-.110 (.054-.060 (<LOD-.330-.113) .120 (.310 (.590) .134) .242) .068-.110 (.120-.202 (.220 (.109 (.470-.355 (.210-.094 (.237) . Fourth National Report on Human Exposure to Environmental Chemicals 87 .S.120) .099-.317 (.510-.060-.340-.120) .480) .170 (.380 (.141) .130) .400-.090 (<LOD-.490 (.390) .590 (.110 (. which may vary for some chemicals by year and by individual sample.220 (.110 (.141) .397-.400) .129) .510 (.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .830) .091) .090-.250) .082) .055 (<LOD-.210) .409-.111 (.260) .110-.360-.405) .090-.158-.191 (.071 (<LOD-.150) .440) .800) .211) 90th .240) .114) .119) < LOD < LOD < LOD .460) .096-.190-.490) .320-.069-.124) .230 (.099-.190-.220 (.420 (.540) .062 (.690) .310-.098 (.240 (.080-.234) .565) .260) .630) .180-.093-.324 (.580 (.573 (.135 (.090) .130) .290-.070 (.078-.280) .232) .089 (.130 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.390 (.760 (.410-1.180-.367) .390 (.131) .096) .130) .084-.080) .205 (.090 (.440-.127) < LOD < LOD .450) .285-.095-.210) .130) .430-.171-.106 (.220 (.250) .240) .470 (.098 (.330-.343 (.430-.100-.160-.103 (.122) .041 (<LOD-.330 (.106 (.20) .590 (.279-.520) .580 (.080 (.186 (.116 (.250) .270-.160 (.559) .395) .122) .106 (.470 (.112 (.630) .126) .470 (.320-.100-.085-.520 (.120) .310-.079-.500) .680) .310-.390 (.340-.220 (.087 (.161-.458 (.140) .

Lulek J. Bleiweiss IJ.150:981-990. 2001.niehs.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 1993. et al. Dewailly E. Muckle G.8:1-123.html. Canada). 2006. Berkowitz GS. Vol. et al. Concise International Chemical Assessment Document 70 Heptachlor [online]. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. Organochlorines in Swedish women: determinants of serum concentrations. Available at URL: http://www. Drews K. Wohlleb JC.htm. Available at URL: http://www. et al. Baker DB. Keller JA.cdc. Hansen JC. Available at URL: http://www. Available at URL: http://www.Summaries & Evaluations. Lawrence River (Quebec.cdc. Siegel BZ.org/site/foundation/ research/projects2.gov/ntp/ htdocs/LT_rpts/tr009. maternal serum and milk from Wielkopolska region. Dewailly E.org/ documents/cicads/cicads/cicad70. Mortality of workers employed in the manufacture of chlordane: an update. 9/25/07 International Programme in Chemical Safety (IPCS). gov/toxprofiles/tp12. Chashchin V. Brower S. Eds. 79. Bjerselius R. Natl Cancer Inst Carcinog Tech Rep Ser 1977a.84:151-161.110:617-624. Takei G. Odland JO. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Toxicological profile for chlordane [online]. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii. Aune M. Dendle WH. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor.htm. Academic Press. JAMA 1988. 731-915. Hertz-Picciotto I. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. 1963-1967. Chlorinated Hydrocarbon Insecticides. Atuma S. Tartter P. Inc.niehs.41:145–148. Environ Res 2000. 4/21/09 Dallaire F. Vol. Environ Health Perspect 2002.50(3):108-118. May 1994. Darnerud PO. Laliberte C. Charles MJ. Granath F. Bull Environ Contam Toxicol 1981:27:506-511. Loo S.inchem. 1991 pp. Arch Pediatr Adolesc Med 1996. Toxicological profile for heptachlor and heptachlor epoxide [online]. National Toxicology Program (NTP). 6/1/09 National Toxicology Program (NTP). 6/1/09 Rogan WJ. Takahashi W. 2 Classes of Pesticides.atsdr. Arch Environ Health. Kolonel LN. August 2007. Stehr-Green P.org/documents/iarc/ vol79/79-12. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Smith AG. Royce W. KalubaSkotarczak A. Organochloride pesticide residues in human milk in Hawaii. A Report to the Hawaii Heptachlor Research and Education Foundation. Available at URL: http://www.gov/toxprofiles/tp31. Wong L. Pollutants in breast milk. Gilman A. Glynn AW. Sci Tot Environ 2006.nih. Saidein D.heptachlor.nih.372:20-31. Willman E. Wolff MS. Jr and Laws ER. In Hayes WJ. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Available at URL: http://ntp. Sci Total Environ 2004.html. J Occup Med 1986. Shindell S and Ulrich S. Poland. 1986.330:55-70. 88 Fourth National Report on Human Exposure to Environmental Chemicals .28:497501. 4/21/09 James RA. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States.110(8):835-838.atsdr. International Agency for Research on Cancer (IARC). 4/21/09 Baker DB. Distribution of polychlorinated biphenyls.259(3):374-377.111:349355. Hawaii Med J 1991. Covaci A.gov/ntp/ htdocs/LT_rpts/tr008. Bioassay of chlordane for possible carcinogenicity. Ayotte P. 1994-1997 organochlorine compounds. Jr.inchem. et al. New York. Handbook of Pesticide Toxicology. Organochlorine exposures and breast cancer risk in New York City women. Environ Health Perspect 2003.9:1-109.pdf. LeMarchand L. Available at URL: http://ntp. Barker J. Voorspoels S.html. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Bioassay of heptachlor for possible carcinogenicity. Van Oostdam JC.pdf. Chlordane and heptachlor [online]. Head SL. Circumpolar maternal blood contaminant survey. Senie R. 1979-1980. International Agency for Research on Cancer (IARC) . Environ Health Perspect 2002. Jaraczewska K.

which may vary for some chemicals by year and by individual sample.6 (22.5-54.5 (23.0-15.7) < LOD 18.1) 31.1 (23.8-39. 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.8) 36.3) 22.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. It was produced and used in the U. and 03-04 are 20. DDT and DDE can cross the placenta.7) 12.8) 15.5) < LOD < LOD 9.p'-Dichlorodiphenyltrichloroethane (DDT) (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. sediments. resulting in fetal exposure.2-65.S. Only a small proportion of DDT is metabolized and excreted (Smith. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28.3 (27.0-37.0-155) 83.7-16. In the general U. 2002.6 (25.0) 26. as well as in plant and animal tissues.3 (<LOD-31.00 (<LOD-10.2) < LOD < LOD 9.1 (33. see Data Analysis section) for Survey years 99-00. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.1 (<LOD-39. In the body.8-26.3-590) 293 (104-541) 48.6-33.2-bis(p-chlorophenyl) ethane (DDD). respectively.3) 28. DDT can be absorbed after ingestion.3 (<LOD-21. 1991).0-27.2 (<LOD-40.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1.p’-DDT (15%-21%). air. 17. Fourth National Report on Human Exposure to Environmental Chemicals 89 .5 (15.3-236) 24.5) 25. and water. particularly for endemic vector and malaria control.9) 17. food.8.7.5 (23. fish. Both Serum p. depending on conditions. population.1-71. particularly meat.8-17.p’-DDD (4% or less).9 (10.9) < LOD < LOD 9. and dairy products.0 (18.7) 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.S.0) 19.0 (21.1) 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 12.1-27.8-23. population from the National Health and Nutrition Examination Survey.6 (31.2) 30.9 (<LOD-20.70 (8.9 (10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2-95. although DDT and DDE intakes have decreased over time (FDA. DDT was used at one time as a treatment for head and body lice. p. Survey Geometric mean (95% conf.9-28.0) 20. These chemicals are highly persistent in soil.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.S.6 (<LOD-25.4) < LOD 17.5) 23.50-11.90 (<LOD-12. It is still used in some countries.0 (18.9) 29.9) 14.9 (21. and trace amounts of several related compounds.6 (9. DDT usually refers to the technical product.7 (19. Gunderson.7 (15.2) 155 (59.3-16. including 1. inhalation.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No.9-34.0-35. 1991).0) 40. when virtually all use of it was banned.0-53.4. and 7. DDT is converted to DDE and several other metabolites. 2008.1’-dichloro-(2. or dermal exposure. DDT is converted in the environment to other more stable chemical forms.10 (<LOD-12. after World War II until 1972.5 (14.1’-(2.5-36.p’-DDT (65%-80%).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. Food imported from countries that still use DDT may contain the chemical or its residues.3) 21. o. 01-02. 1988).8) 30.4) < LOD < LOD < LOD 61. which is a mixture containing p.9 (10.10-13.3) 21.0 (10.2 (11.4 (23. < LOD means less than the limit of detection. The biodegradation half-life of DDT in soil varies from 2 to 15 years. continues to be the primary source of DDT exposure. Smith.

143) < LOD < LOD .078 (. In high dose.00 (. lung cancer. 1956). 1997). although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al. 2006.080-. 2002. 2006.146 (.146 (.160-. Reproductive effects in humans affecting birth weight.p’-DDE can produce anti-androgenic effects (Gray et al. and altered behavior after neonatal exposure (Eriksson and Talts. 1995. reproductive organ abnormalities. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2006).190 (. 2002.063 (<LOD-. overt signs of acute human toxicity include vomiting. 2004.132-.. DDT may bind to estrogen receptors (Chen et al. 2006). have not been consistently demonstrated (Beard..260) .167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * . 2001).p’-DDD and p.180-. Beard. fertility. Studies of DDT exposure and pancreatic cancer. A workplace standard for DDT has been established by Serum p.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 .170) . Gray et al. Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR.061) < LOD < LOD < LOD .079) < LOD < LOD . which may vary for some chemicals by year and by individual sample. Snedeker.570-4. Gladen and Rogan.. both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.106) < LOD < LOD . and duration of lactation.120-.048 (<LOD-.180 (.106) .130 (<LOD-.087 (.106-.230) . 2002.220) . and o.201 (.150) .098-.120 (<LOD-. population from the National Health and Nutrition Examination Survey.240) .130-. 2006.g.190-1. 2006). accidental exposures. Jusko et al. Calle et al.074-. Survey Geometric mean (95% conf. In laboratory animals.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.250 (..075) 1.230) .26) 1.530) .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.150 (<LOD-.084 (. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.150-.189-.054-.114-.400 (.203) .065-. polychlorinated biphenyls.. premature delivery.071-.530 (. dioxins and furans).330-4. 90 Fourth National Report on Human Exposure to Environmental Chemicals ..068-.343) < LOD . 2000.420) ..627) .078-.108 (.62 (. and seizures. Longnecker et al. other organochlorines. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.112 (.086 (.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 .290) . Mariussen and Fonnum.051 (<LOD-.150 (<LOD-.142 (..34) . 1998). 2001).130 (<LOD-.128 (. Hayes et al.200 (. tremor. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.Organochlorine Pesticides chemicals are excreted in breast milk.180) .071 (. resulting in exposure to nursing infants (Rogan.097) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .150-.180 (.00) . 2001). 2001).130 (<LOD-.170 (.. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e.220) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .400) .170-.. and leukemia have also been inconclusive (ADSDR.S.180) . Jusko et al.064 (..240 (.313 (.059-.069) .. Animal studies reported reduced fertility. 2002.140) .250-1. 1996).095) < LOD .105-.01) .190 (.140-.

. 2005).6 (81. In general.epa. levels of DDT and DDE increase as a person ages as a result of cumulative exposure (ATSDR. compared to levels observed in this Report (Anderson et al.S. 1998.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. Link et al. mean DDE levels were about fivefold higher among women of southern Spain exposed by virtue of Serum p. and 03-04 are 18. Smith. 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. NTP considers DDT as being reasonably anticipated to be a human carcinogen. 1989). population from the National Health and Nutrition Examination Survey.7-119) 113 (100-140) 93. and the most recent median levels for German adults and children are similar to levels in this Report (Becker et al. population declined by about fivefold to tenfold. respectively.gov/ pestcides/ and from ATSDR at: http://www. Biomonitoring Information DDE persists in the body longer than DDT... 1991). environmental levels) and health effects is available from the U. More information about external exposure (i.Organochlorine Pesticides OSHA and a guidance established by ACGIH.6.. 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. 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.cdc. 8. 2002.8. see Data Analysis section) for Survey years 99-00. and 7. Compared to females in the NHANES 1999-2000 subsample.. In a population-based sample of men and women from eastern Slovakia. 2004). IARC classifies DDT (p.atsdr.S.html.7-129) 297 (256-344) 338 (303-376) 268 (217-332) 108 (97. Heudorf et al. Survey Geometric mean (95% conf.e. 2003).3. Stehr-Green. mean serum levels of DDT and DDE in the U. the lipid-adjusted geometric mean levels of DDT and DDE were each fivefold to tenfold higher than the 95th percentile and geometric mean levels. 01-02. 2004). EPA at: http://www.p’-DDT) as a possible human carcinogen. Fourth National Report on Human Exposure to Environmental Chemicals 91 . 2003. 2002. Since the 1970’s. for males and females in the NHANES 19992000 subsample (Pavuk et al....gov/ toxpro2. respectively.0-114) 269 (213-323) 285 (249-337) 233 (175-314) 185 (141-237) 213 (172-253) 167 (123-240) 608 (530-693) 695 (595-798) 557 (420-734) 339 (243-479) 319 (282-389) 341 (211-586) 1260 (1030-1550) 1480 (1310-1700) 1270 (877-1800) 528 (339-812) 456 (343-722) 522 (313-1430) 2020 (1520-2730) 2550 (1980-3080) 1990 (1500-2470) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 249 (220-283) 285 (252-323) 235 (193-288) 270 (226-322) 305 (273-341) 241 (193-301) 223 (182-262) 248 (222-285) 200 (164-262) 234 (184-302) 256 (219-297) 207 (161-281) 494 (380-578) 520 (441-627) 466 (331-653) 601 (492-711) 708 (567-844) 539 (386-735) 1010 (789-1130) 1160 (937-1360) 1000 (763-1400) 1350 (1040-1720) 1480 (1410-1710) 1250 (813-1900) 1430 (1080-2160) 1900 (1580-2490) 1610 (1210-2320) 2210 (1570-2810) 2670 (1940-3300) 2010 (1500-2450) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 674 (574-792) 652 (569-747) 444 (362-545) 295 (241-362) 324 (262-400) 262 (233-295) 217 (189-249) 253 (226-284) 208 (165-263) 624 (545-701) 561 (455-690) 373 (283-522) 251 (199-313) 248 (223-296) 216 (173-267) 194 (162-238) 225 (203-254) 177 (148-238) 1350 (1090-1660) 1400 (1050-1950) 875 (608-1170) 668 (492-874) 762 (583-999) 589 (453-747) 438 (355-507) 463 (402-558) 417 (302-564) 3090 (2040-4950) 4110 (2520-6550) 2150 (1520-2470) 1850 (1040-2220) 1620 (1180-2980) 1620 (1130-2310) 825 (647-1010) 1150 (878-1340) 907 (574-1480) 4950 (3070-9350) 7080 (3080-15600) 3290 (2380-9240) 2300 (1560-5680) 3260 (1270-6900) 2860 (1880-3440) 1160 (1010-1350) 1640 (1410-1940) 1490 (909-2300) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites Limit of detection (LOD.S. so serum DDE levels may be an indicator of historic exposure and may be higher than DDT levels in the same person. Declining DDE levels over time have also been observed in the German population.

68 (2.75) 6.77 (1.16-1.55 (2.06) 1.16 (2.488-.39 (3.965-1.84 (3.37-10.20 (.88 (2.43-4.2 (9.85 (1.25 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.58) 75th 3.85-4.00 (.46 (1.8 (14.22-1.4) 9.p’-DDT.07 (5.83 (1.7) 13.62-6.55-9.30 (1.57-3.18-4.8 (13.69) 4.38 (1.69) 8.71) 12. Finding a measurable amount of p.29 (1.39-1.43-4.79) 4.4-19.21) 3.39-2.02) 1.27-1.6) 9.50-17.36-2.64-2.0 (9.14-9.18) 1.3 (9.02-8.81) 11.2 (19.49 (1.6 (8.46-2.600) .88-35.4 (8.68-4.87-16.12-1.01) 1.37-16.5) 7.54) 8.18-1.2 (9.646) .72) 1.92 (3.54-7.76 (2.57) 2.34-3.4) 14.59) 3.25 (1.36-1.71 (6.81 (7.31-12.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.6 (17. population from the National Health and Nutrition Examination Survey.870 (.93 (7.10) 2.56-3.66) 1.18-3.41-12.81 (1.p’-DDT were below the limits of detection.520 (.26) 3.11 (2.32 (1.26 (1.36 (3.19) 4.557) 1.890-1. 1971).1) 40.31-2. Serum p.82 (1.01-15.p’-DDT..66-4. 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.23 (7.30-1.14) 2.10-1.40 (3.32) 1.36) 3.561 (.5) 22.51-8.24 (1.66) 3.7) 16.57 (1.05) 1.56) 2.66-2.02 (2. High mean levels of whole blood DDT (about 3.57-13.52-6.51 (1.994-2.76-3.10) .37-1.53) 7.72) 1.61-2.5) 16.59 (1.92 (3.456 (. 1991).1 (9.30 (1.91 (6.32-1.19-14.0 (12.91-2.40-4.04 (6.00) 7. In a subsample of NHANES II (19761980) participants.49 (1.75) 1.36-11.516 (. 2001-2002 and 2003-2004 subsamples.00-1.77 (1. 1989).796 (.40-4.69 (.9 (15.39) 1. considerably higher than levels in this Report (Smith.24-17.45 (1.69 (1.6) 12.65) 1.25-14. 2005).14-1.53 (2.25) 1.7-20.820-1.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.28) 1.92) 1.49 (6.76) 1.32-1.57-2. 309 versus 268 ng/g lipid.6 (7.37 (1. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.50 (2.9 (26.9-38.56-2.6) 9. serum levels of o.385-.6) 11.56-6.24) 1.09-1.53) 1..5) 5.34) 2.2 (6.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.07) 1.68) 2.0) 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 .534-.3 (8.75 (8.01-11.04-1.635) 1.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.78 (4.22 (7.6) 8.S. less than one percent had detectable serum levels of o. Survey Geometric mean (95% conf.41 (1.430-.45 (1.680-1. In the NHANES 1999-2000.40-8.13) 4.34 (7.14) 2.76) 1.32 (1.00 (6.47 (1.60-13.84-3.0) 2.01-1..p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.12 (.30-1.1 (8. o..58) 1.17-3.8 (9.6) 13.43-8.Organochlorine Pesticides nearby agriculture (Botella et al.63 (1.10-5.3-43.25-16. interval) 1.57 (3.49) 8.57 (1.35) 1.860 ng/L) and DDE (about 14.48-4.59) 6.9) 5.6) 9.85-10.3) 16.25) 8.51-15.7-19.p’-DDT (Stehr-Green.5) 10.63 (6.4) 13.26-10. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.96) 1.7 (8.6) 9.64) 3.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.66-17.66) 4.90) 22.69 (2.44) 1.34-11.15-4.59 (4.59 (1.82) 1.51) 3.8 (13.87 (5.2) 19.9) 7.47) 3.46 (1.43 (5.6 (9.81-5.12 (6. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.96) .32-9.97-4.03-4.27) 3.26-2.38 (1.590 (.71 (5.65 (1.03-1. 2004).623 (.21) 90th 7.80) 3.63 (1.7-48.80) 1.9-17.54 (1.18-1.33-1.80) 1.17 (3.01-11.80 (2.730) .22) .99) 1.13-2.70) 1.419-.2) 26.14 (1.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .97 (3.75 (4.611-1.3) 13.11-1.01-1.8-90.52 (1.34) 6.48 (6.70-3.51) 1.90-8. 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.1) 12.4 (12.37-4.61 (1.52 (3.2-32.63-15.18 (6.71) 32.58) 1.1) 7.726) .05 (3.8) 15.53-15. or p.3) 10.91) 3.01-5.75) 2.91-3.81-18.07) 1.51-49.31 (1.963-1.06) 3.7) 9.01) 1. 2004).13 (1.500-.66) 1.

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. and 03-04 are 20. population from the National Health and Nutrition Examination Survey. < LOD means less than the limit of detection. Fourth National Report on Human Exposure to Environmental Chemicals 93 . and 7. see Data Analysis section) for Survey years 99-00. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf.Organochlorine Pesticides Serum o.8.7. 01-02. which may vary for some chemicals by year and by individual sample.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. respectively. 17.

Survey Geometric mean (95% conf.Organochlorine Pesticides Serum o. 94 Fourth National Report on Human Exposure to Environmental Chemicals . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD < LOD size 1669 2279 1946 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 667 756 588 1002 1523 1358 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 796 1059 949 873 1220 997 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 632 565 458 354 507 486 560 1045 880 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey.p'-Dichlorodiphenyltrichloroethane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study.205:297-308. Organochlorines in Swedish women: determinants of serum concentrations. Int J Hyg Environ Health 2003. Klebanoff MA. Garrett N. Darnerud PO. Seiwert M. Gabrio T.111:349355. Food and Drug Administration (FDA).112(17):1761-1767. Schulz C. Baker RJ. Epidemiology 2006. Zoellner I. Available at URL: http://www. Botella B. Gray LE Jr. April 1982 to 1984. Piechotowski I. Becker K. Paepke O.162:890-897. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Needham LL. Furr J. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Lepom P. Ostby J. Jusko TA. Zhou H. Talts U. India. Olea-Serrano MF. lindane (g-HCH).cdc. Drexler H. Angerer J. Bull Environ Contam Toxicol 2004. Am J Public Health 1995.72:261265. Granath F. Needham LL. Kulkarni PK.52:301-309.106(5):279-289. Effects of environmental antiandrogens on reproductive development in experimental animals. Olea N. Needham LL.96:34-40. Biomonitoring of persistent organochlorine pesticides.. Toxicological profile for DDT. Gray KA. Frumkin H. Calle EE. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population.17(6):692-700. et al. Lambright C. Thun MJ. Int J Hyg Environ Health 2002. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Greenfield TA. Bates MN.gov/~dms/ pesrpts. Hediger ML. Wolf CJ. Durham WF.85:504508. HCH. et al.53(8):1161-1172. Zhou H. Herrman T. 4/21/09 Anderson HA. Chemosphere 2004.58:1185-1201. and HCB residues in human blood in Ahmedabad. Olson J. Rogan WJ.7(3):248-264. et al. selected elements. Chen CW.fda. Buckland SJ. Beard J. Hanrahan L. Bhatnagar VK. Eriksson P. dietary intakes of pesticides. et al. Patterson DG Jr.355:7889.155(4):313-322. Aune M. Parks L. Brock JW.cfsan.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. hypospadias. Vorojeikina DP. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Olson JR. Link B. Gunderson EL. Environ Health Perspect 2003. Krause C. Moysich KB. Environ Res 2005. Glynn AW. Falk C. Longnecker MP.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Burse VW. 4/21/09 Gladen BC. Zaidi SS.358:110-114. Chemosphere 2005. Hum Reprod Updat 2001. Kaus S. Jr. JAMA 1956. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Cerrillo I. Lancet 2001.html. and dichloro(diphenyl)ethylene (DDE). et al. Crespo J. Longnecker MP. Saiyed HN. Swanson MK. Charles MJ. hexachlorobenzene. Arnold SF. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Davis MD.21(1-2)37-48. Organochlorines and breast cancer risk. Biochem Pharmacol 1997. Exposure of women to organochlorine pesticides in Southern Spain. Bjerselius R. Heudorf U. DDE.atsdr. Katz SH. Bloom MS. Brock JW. et al.gov/ toxprofiles/tp35.206:485-491. Jr. Sci Tot Environ 2006. Cueto C.71(6):1200-1209. Klebanoff MA. The Great Lakes Consortium. Neurotoxicol 2000. et al. Atuma S. Environ Health Perspect 1998. DDT and human health.html. Hayes WJ. Henley SJ. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Maternal DDT exposures in relation to fetal and 5-year growth. Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Ellis H. Hurd C. DDE and shortened duration of lactation in a northern Mexican town. Kashyap R.1-dichloro2. Levels of DDT. Savitz DA. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Fourth National Report on Human Exposure to Environmental Chemicals 95 . and DDD [online]. September 2002. Barr DB. August 2008. Available at URL: http://www. Klebanoff MA.97(2):178192. Koepsell TD. and polythelia among male offspring. dichlorodiphenyldichloroethylene. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Willman EJ. et al. J Assoc Off Anal Chem 1988. Notides AC. Gladen BC. et al. CA Cancer J Clin 2002. Profiles of ortho-polychlorinated biphenyl congeners.54:1431-1443. and other chemicals. Rivas A. Vena JE. Environ Res 2004. Am J Epidemiol 2002. FDA total diet study. Maternal serum level of 1. Environ Health Perspect 2004.

PA. Fonnum F.53:455-477. 2 Classes of Pesticides. Petrik J. Stehr-Green. Eds. Reddy AB. Deichmann WB. Academic Press. Schecter A. Jr.54:1509-520. DDE.27:405-421. and dieldrin. Toxicol Appl Pharmacol 1971. Fox S. et al. Radomski JL. J Toxicol Environ Health 1989. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults.150:981-990. Astolfi E. Arch Pediatr Adolesc Med 1996. children and newborn infants. In Hayes WJ. Pollutants in breast milk. 96 Fourth National Report on Human Exposure to Environmental Chemicals . J Toxicol Environ Health Part A 1998. Jr and Laws ER. and DDD in male rat liver and cultured rat hepatocytes. 1991 pp.109:35-47. Rogan WJ. Thomas PE. Lynch CF. Demographic and seasonal influences on human serum pesticide residue levels. Chovancova J. Handbook of Pesticide Toxicology.36:253-589. Snedeker SM. Environ Health Perspect 2001.20(2):186-193. Chlorinated Hydrocarbon Insecticides. Nims R. Chemosphere 2004. Inc. New York. Rey AA. DDE. Jones CR. et al. 731-915. Comparative pharmacodynamics of CYP2B induction by DDT. Neurochemical targets and behavioral effects of organohalogen compounds: an update. Pavuk M. Vol. Lubet R. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Crit Rev Toxicol 2006. Pesticides and breast cancer risk: a review of DDT. Smith AG. Cerhan JR.Organochlorine Pesticides Mariussen E.

1981). Over time. a stereoisomer of dieldrin..S.. 1991). Fourth National Report on Human Exposure to Environmental Chemicals 97 . All uses of the pesticide in the U. is no longer manufactured in the U. anti-12hydroxyendrin. < LOD means less than the limit of detection. see Data Analysis section) for Survey years 01-02 and 03-04 are 5.40) < 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.S. 2008).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.S. Endrin does not accumulate in body tissues (IPCS. 1992).10 (<LOD-5. 72-20-8 General Information Endrin. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown.40 (<LOD-6.50) < LOD < LOD < LOD 5.20 (<LOD-5. or discarded. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used. 1979.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. endrin has been detected with declining frequency in U. 1992. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. At high doses. and occasionally at low levels in sediment and surface waters.8. unless the dose is high and the exposure is very recent.30) < LOD 5. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals.. Because it is metabolized so rapidly.20 (<LOD-5. IPCS. Ketoendrin is a major photodegradation product (IPCS.. Endrin was used as an insecticide. have been cancelled by the U. Endrin has been detected in soils. Depending on soil conditions. 1992). Endrin is absorbed rapidly after ingestion. An epidemic of acute endrin poisoning.S. 1991). endrin usually is not detected in serum of exposed individuals.50) < LOD 5. 1992). which may vary for some chemicals by year and by individual sample.09 and 7. 1987). 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. endrin is converted rapidly to its major metabolite. Survey Geometric mean (95% conf.Organochlorine Pesticides Endrin CAS No. Hepatic effects of endrin exposure have included necrosis.60 (5. Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al. population from the National Health and Nutrition Examination Survey. 1996. endrin can persist for years.S.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. Endrin was not widely used as a termiticide.30 (<LOD-6. Smith. manufactured. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. EPA. fatty infiltration. In the body. total diet surveys (FDA.40-5. Kavlock et al. inhalation or dermal exposure routes. rodenticide and avicide.10 (<LOD-5. unlike aldrin and dieldrin. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. largely the result of historical agricultural application or run off from contaminated soils (ATSDR. and inflammation (Smith. 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.

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

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

see Data Analysis section) for Survey years 99-00. or game taken from areas with HCB contamination.9-20.S.2 (13.0) < LOD < LOD 15. Therefore.0.7-15. 1997). 2002).2) < LOD < LOD 13.3 (12. water.4.5 (13.0-19.0) < LOD < LOD 24.4) < LOD < LOD 33.5) < LOD < LOD 18. and has been detected in soil. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.3) < LOD < LOD 29. EPA cancelled its use in 1984.9) 19.1-20.9) < LOD < LOD 20.3 (16.5-15.9 (25.3) * * 15.9-15.4.9-32.0-16. and 7.9) < LOD < LOD 16. which may vary for some chemicals by year and by individual sample.7-16.6-26.1 (14.7-21. The general population may be exposed to HCB through diet. Gunderson.8.2 (17.4-16.3 (14.5 (14.8-15.6) < LOD < LOD 24. 100 Fourth National Report on Human Exposure to Environmental Chemicals .4.7-30. measuring HCB in serum is a specific indicator of exposure to the parent Serum Hexachlorobenzene (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.6-19.4) < LOD < LOD 23.3 (22.9-24.8 (26.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13.6-32.7 (15.0) < LOD < LOD 15.7-29. The FDA dietary surveys have shown that over time.9 (25.7) < LOD < LOD 24. < LOD means less than the limit of detection. and foods with a high fat content. 2.1) < LOD < LOD 15.8 (15. 01-02. distributes widely throughout the body. 2008. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al. population from the National Health and Nutrition Examination Survey.4.S. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U.9) < LOD < LOD 15. 2005). HCB is well absorbed after oral administration.5-TCP) and 2. and sediment (Barber et al. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.0-25.5-18.6) < LOD < LOD 26.2-15. Urinary metabolites include pentachlorophenol (PCP). Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications.5-trichlorophenol (2.2-15. Although it is not manufactured as an end-product in the U.2 (14. respectively. and 03-04 are 118.6-trichlorophenol (2.7) 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 * * 16.0-28.7 (15.1 (17.9) < LOD < LOD 19.6 (24.1-16.4-15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.6 (23.6) < LOD < LOD 25.7-22.2) < LOD < LOD 29.3 (20.0 (14.9 (23.3) < LOD < LOD 20.Organochlorine Pesticides Hexachlorobenzene CAS No.3-20.4 (18.3) 24.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5 (13.3-22.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.6) < LOD < LOD 14.S.6-33.7-26.4 (22..9) < LOD < LOD 28. primarily as a fungicide and seed treatment until the U.4) < LOD < LOD 22. particularly by consuming fish. wildfowl.3-26..5-15.4.S.9 (14.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14..5-14.4 (11.0 (18.7-16. Survey Geometric mean (95% conf. 31. and elimination occurs by renal and fecal routes. HCB has been detected in fewer foods since the 1980s (FDA.5-14.5-33.7 (19.6-44. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides.0 (25.9) < LOD < LOD 20.6) < LOD < LOD 26.2-31. and accumulates in fatty tissues where it persists for years.9-17. 1976).1 (14.4) < LOD < LOD 19.4 (18.8 (22.1 (13.1) * * 15.6 (21.2 (24.7) * * 14.7 (27.8) < LOD < LOD 27. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR. air. HCB is slowly metabolized.0) * * 15.4) < LOD < LOD 14.3 (22. breast milk is an additional route of elimination in nursing women. 1988).4) < LOD < LOD 18.6-TCP) (To-Figueras et al.2 (14.9-30.0 (18..

203) < LOD < LOD . were seen in an epidemic of poisoning in Turkey that occurred from 1955 to 1959 when HCB-treated seed grain was diverted for bread production.086) < LOD < LOD .123 (.163-.081-.090 (.175) < LOD < LOD . Chronic feeding studies in animals have demonstrated kidney injury. arthritis.085) * * .169-.083) < LOD < LOD .120 (. reproductive and developmental toxicities. EPA has established a drinking water standard.135-. With chronic exposure.062-.111-. Survey Geometric mean (95% conf.079 (.099) < LOD < LOD . very high.090 (. IARC classifies hexachlorobenzene as possibly carcinogenic to humans.060-. immunologic abnormalities.152) < LOD < LOD .163) < LOD < LOD .145-.126) .097) < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD .113-.097) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. EPA at: http://www.095 (. Schmid.167 (.089-.S. Biomonitoring Information Serum concentrations reflect the body burden of HCB. and weakness. acute doses produce central nervous system depression and seizures. 2002). environmental levels) and health effects is available from the U.218) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.077-.212) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD .088-.109) * * .130) < LOD < LOD .114-.094 (.102 (.225 (.223) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * .065 (. as well as hypertrichosis.073-. and the FDA has established a bottled water standard for HCB.118) < LOD < LOD .078 (.121 (.118-.094) < LOD < LOD .090-.epa.087 (.147-.Organochlorine Pesticides chemical.111) < LOD < LOD .092-..081 (.S.069) < LOD < LOD .092 (. and NTP classifies hexachlorobenzene as reasonably anticipated to be a human carcinogen.100) < LOD < LOD . anorexia.258) < LOD < LOD .191 (.069) * * . which may vary for some chemicals by year and by individual sample.159-.122) < LOD < LOD .086-.114-. The U.104 (.086-.064 (. 1982.097 (. In humans. 1960).160 (.atsdr.092 (.gov/toxpro2.127-.102) < LOD < LOD .html. a consequence of these heme abnormalities is a condition known as acquired porphyria cutanea tarda.e.095 (.157 (.171 (. Human health effects from HCB at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Fourth National Report on Human Exposure to Environmental Chemicals 101 . thyromegaly.176-. More information about external exposure (i.115 (.089-.173) < LOD < LOD .167) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * .155) < LOD < LOD .095) * * .118-.072-.186 (.082-.092 (.S.174-.182 (. 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.147 (. which is manifested by increased deltaaminolevulinic acid synthase activity and decreased uroporphyrinogen decarboxylase activity.098 (.196) < LOD < LOD .157-.163 (.143-.099) < LOD < LOD .090 (.132) < LOD < LOD .176) < LOD < LOD .085-. and many died before 2 years of age (Peters et al.179 (.099) < LOD < LOD . ACGIH has developed workplace exposure limits for HCB.091-.123 (.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 * * . HCB interferes with normal heme synthesis.203) < LOD < LOD . This condition.088-.123 (..125 (.148-.gov/pesticides/ and from ATSDR at: http://www.140 (.178-.095-.190 (.095) < LOD < LOD 75th < LOD < LOD 90th * * . Infants were exposed transplacentally and through breast milk.cdc. and liver and thyroid cancers (ATSDR.107-.156 (.088-.129) < LOD < LOD . population from the National Health and Nutrition Examination Survey.107) < LOD < LOD .145-.141) < LOD < LOD .

2002. Granath F.html. Toxicological profile for hexachlorobenzene update [online]. 1989). levels. Herrero C..71(6):1200-1209. however. 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. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. Kaus S. van Wijk D.9% of participants had quantifiable levels (Stehr-Green. Lawrence River (Quebec. Int J Hyg Environ Health 2002. Bradman et al. Bryan GT. Lackmann. Krause C. Laliberte C. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Arch Dermatol 1999. Schulz C. Available at URL: http://www. Environ Health Perspect 2003.cdc. Bertram HP. 2002). Fenster L. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. and other chemicals. et al. 1986. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. 4/21/09 Barber JL. dietary intakes of pesticides. Hexachlorobenzene in the global environment: emissions.html. Otero R. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area.. J Assoc Off Anal Chem 1988.fda. Safe A. Jones KC.205:297-308.. and the geometric mean concentration of HCB in whole blood was 0. Paepke O.. HCB levels were directly related to age. 4/21/09 Glynn AW.gov/ toxprofiles/tp90. In a representative sample of the 1998 German adult population.81(2):82-85. more HCB levels were quantified. Muller C. Piechotowski I. Lackman. In Spain.gov/~dms/ pesrpts. Muckle G. Link et al. only 4. September 2002. Seiwert M. Biomonitoring of persistent organochlorine pesticides. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher.110(8):835-838. Gabrio T. In the 1976-1980 NHANES subsample. Biol Neonate 2002.135(4):400404. Dogramaci I. Gocmen A. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Santiago-Silva M. Bjerselius R.. 2002. respectively. trends and processes. et al. Aune M. Bertram et al. Gunderson EL. Lepom P. Reference values updated.cfsan. J Exp Sci Environ Epidemiol 2007. but overall. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Eskenazi B. Kemper FH. Lecha M. distribution.349:144.. References Agency for Toxic Substances and Disease Registry (ATSDR). Food and Drug Administration (FDA). Becker K. Ozalla D. 2002) and among children (Link et al. selected elements. Sala M.atsdr. Dewailly E. 2002. Organochlorines in Swedish women: determinants of serum concentrations. As a result of the lower limit of detection in NHANES 2003-2004.17:388–399.58:1185-1201. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. Peters HA.77:173182. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Over the past two decades. 2005). Available at URL: http://www.. The metabolism of higher chlorinated benzene isomers. Atuma S. 2002. Herrman T. Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al. Can J Biochem 1976. Bradman A. Glynn et al. HCB detection in serum also was proportional to age. Chemosphere 2005. Environ Health Perspect 2002. Link B. 2005. Zoellner I. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. the more recent values in these studies were similar to the lipid adjusted limit of detection in NHANES 1999-2000 and 2001-2002 (Dallaire et al. 1999).Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. Barr DB. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. Ayotte P. Dallaire F. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. 2006). FDA total diet study. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. et al. April 1982 to 1984. Jones D..44 mg/L. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. IARC Sci Publ 1986. Arch Neurol 1982. Schwartz JM.54(3):203-208. but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al..39(12):744-749. Kohli J. August 2008. Sci Tot Environ 2005.. 2003). Darnerud PO. 2005).111:349355. Cripps DJ. Holland NT. Lackmann GM.. Sweetman AJ. et al. Canada). PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003.

Sala M. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Environ Health Perspect 1997. Barrot C.27:405-421. Santiago-Silva M.Organochlorine Pesticides Schmid R. To-Figueras J.263:397-398. Stehr-Green. Otero R. PA. Demographic and seasonal influences on human serum pesticide residue levels. Rodamilans M. Cutaneous porphyria in Turkey. Fourth National Report on Human Exposure to Environmental Chemicals 103 . N Engl J Med 1960. et al. J Toxicol Environ Health 1989.105(1):78-83.

01-02.90-8.4) < LOD < LOD < LOD 46.8) < LOD 10.0-111) 70.20-16.5-123) 49.6-47. and 03-04 are 9.7) 97.1-27.0) 17.61-12.6 (10.1 (18.8) 12.1-16.1-49.6) 18.3 (42. **In survey period 2001-2002.6-18.0-21.3-38. environmental levels declined.0-70.70-12.80 (<LOD-14.1-15.89 (<LOD-9.0-23. each result has been multiplied by 1.7-20.0 (33.2 (34.7 (53. soil. population from the National Health and Nutrition Examination Survey. so they can accumulate in fatty tissues of animals.46-11.0 (14.8 (33.8 (10.2) 9. gamma. and have been used either as fungicides or to synthesize other chemicals.4) 10.6-37.6 (40. 104 Fourth National Report on Human Exposure to Environmental Chemicals .1) 12. water. 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.9 (32.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.9-24.1) 71.56-12.4 (16.9-14.0-34.90) 7. beta.4) 11. EPA cancelled agricultural uses of lindane (ATSDR.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 21.2 (48.7 (62.5528.1 (9.66-12. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.70 (6.0) 71.5 (14.1-37.04-10.5) 16.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.5 (43.7) 18.7 (29. formerly referred to as benzene hexachloride.S.2-52. The gamma isomer.2-98. The other isomers can be formed during the synthesis of lindane.9) 17.6-89.3) 25.7-69. interval) 9. exists in several isomeric forms.9-178) 48.2) 142 (99.0 (35.2-46.9 (26.1) 12. It is no longer produced or sold in the U.5 (37.7 (30.1 (9.6) 50.7-166) 70.9-21.36. 6.5 (8.50) 8.4 (11.43 (<LOD-9.6-42.0 (19.9-81.2-20.9) 15.5 (24. including alpha.7) 56.8-54.8-87. < LOD means less than the limit of detection.5) 67.6-62.7 (13.3 (26.8 (64.2-55.8 (21.0) 8.2 (50. However.7 (35.2-22.7 (<LOD-16.1 (12.9 (40. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.1) 31. the U. containing about 64% alpha and 10%-15% gamma isomers.1) 13.8) 95th 68.3 (62. 2005).0 (37.5) 22.9 (11.1-32.4) 27.7) 23.3-56.7 (25.4-73.87 (9.3) 14. 58-89-9 General Information Hexachlorocyclohexane (HCH). and delta.68 (<LOD-10. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR. and sediment as a result of historic production and use.1-36.7-26.8-68.1 (21. which may vary for some chemicals by year and by individual sample.0) 35.3 (13.3-85.8) 7.6) 36.6-20.7-96. HCH isomers. HCH isomers are lipophilic. 608-73-1 beta-Hexachlorocyclohexane CAS No.3) 34.6 (17.9 (9.4-111) 84.60-13.4 (8.8) 39.2 (9.S.5-29.1-32. see Data Analysis section) for survey years 99-00.8-19.5 (16.5) 90th 42. Technical grade HCH is a mixture of all four isomers.9) 81.2) 62.5) 11.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD. commonly known as lindane.2-42.1 (30.4 (52.2) 36.7) 27.90-8.8-199) 134 (85.0-70.6-135) 69.S.2 (31.4-50.9 (30.0) 41.2-67.5 (11.8-16.9) 45.80 (6.70-19. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7) 10.6) 47.6-14. As pesticide applications of HCH were increasingly restricted or eliminated.4) 51.3) 37.9 (62.7-96.8) * * * * * * 15.6) 16.2-17.4 (12.4-45.8) 27.6 (22.5) 29.7) 73. Lindane has a half-life of about two weeks in soils and water.0) 7.0-20.7) 32.8 (32.2 (18.6 (16.7) 10. and 7.4) 901 1067 952 992 1224 1007 Females 11.5) 14.9 (50.0 (8.76.1 (16.6) 35.8.6 (33.4 (50. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.30-11.1 (11.7-69.5) 40.2-87.4) 21.9-51.3) 51. 319-85-7 gamma-Hexachlorocyclohexane CAS No.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.8) 52.4) 44.8 (23.8 (17.6) 653 758 589 1240 1533 1370 20 years and older 10. 2005). In 2006.2) 13.Organochlorine Pesticides Hexachlorocyclohexane CAS No.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14. See the section “What’s New” at the beginning of this Report for details.3 (42.0 (<LOD-12.2 (29. respectively.4) < LOD 9.9-56.8 (9. particularly alpha and gamma have been detected widely in air.1 (27.70 (8.

521 (.140) .S.480 (.068-.080-.260) . 2008.410) .340) .220-. probably by blocking inhibitory neurotransmitters in the central nervous system.103-.450) .080) .220-.191-. Gunderson 1988). from 6% of samples in 1982-1984 to 2% in 1994 (FDA.290) .210 (. 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.01 (.360) . resulting in a half-life of about seven years.250) .910 (.089) .580-1.057-. tremors.103 (.700) .146-.098 (.170-.290 (.450-.390-..066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th . Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways.308-.Organochlorine Pesticides exposure to HCH is through the diet.070-.310) .191-.140) .250-.460) .230-.139 (.244-.501) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.442) Sample size 1893 2291 1959 Age group 12-19 years 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .100) . Workers who directly handled HCH have complained of headache.070 (.070) .281 (.051-. 1981).420-.690) .840) .080-. Rogan.110) . ataxia.210) .120 (.360 (..200-.050 (.150) .077) < LOD . and memory loss (Nigam et al.078 (.210-.124-.110) .240-.144 (.460 (.077) < LOD .140 (. 1977). paresthesias. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al. each result has been multiplied by 1.32) . 2002).103) 90th . **In survey period 2001-2002.410-. ingestion.081-.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.118 (.060) .190) .410) . 1996. The beta isomer accumulates in fatty tissues and is metabolized more slowly.294-.100 (. and nephropathy developed (IPCS.118-.170-.150-.056-.560 (. enlarged livers.073-.620) .057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 . interval) .096) .067 (.319) .040-.083) .. U.270 (.089-.130 (..190-1.222 (.350 (.190-.250 (.370-. Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.680) .057-.080-.064 (.210 (.200 (.100-.057 (<LOD-. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.069) .083 (.280-.070-.062 (.234 (. Distribution is mainly to fatty tissues.340-. 1986).050 (<LOD-.400) .064) .091) .560) .5528.090-.330-.050-.280-.160 (.067) .174) .480 (.254) 95th .050-.058 (<LOD-.350) .173-.125) < LOD < LOD < LOD .120-.167 (.090 (. When animals were chronically fed lindane at high doses.287 (.37) 1. respectively.710) . FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.070 (.510) .570 (.100 (.470 (.580 (. for lindane.065 (.390 (.260-.305) . population from the National Health and Nutrition Examination Survey.442 (.130-.086) < LOD < LOD < LOD < LOD < LOD < LOD .072 (.250 (..051 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 105 .814) .062 (.216 (.150 (. HCH isomers are absorbed after inhalation.250-.100-.250 (.410 (.120 (.S.120 (.404) .092 (. The U. HCH crosses the placenta and is also excreted in breast milk (Radomski et al.050) .090 (.290) .587) 653 758 589 1240 1533 1370 20 years and older . which may vary for some chemicals by year and by individual sample. hepatic enzyme induction.090 (. Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.056-.120) .214) .S.190) .372 (. the serum half-life was about 20 hours among children (Ginsburg et al.661) 901 1067 952 992 1224 1007 Females .480) .180-.290 (. EPA has established a drinking water standard.110-.119) .331 (.065 (.412 (.220 (.310 (.140) . See the section “What’s New” at the beginning of this Report for details.047-.130) .050-.360-.620-1. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD . and FDA has established a bottled water standard and food residue tolerances for lindane.150) .160) . Saxena et al.290 (. 1983). 1971.080 (. OSHA and ACGIH have established workplace standards and guidelines.450 (.175 (. After dermal application of lindane 1% lotion.221-.600) .059-.330 (.048 (<LOD-.080 (.110) .380 (.120) .470) .120-.100) .400) .220) .050-.050 (.300-.160-.070-.310) .05) . or dermal exposure.320 (.100-.382-.131-. and seizures.260) .240 (.297-.050 (<LOD-.120-.080) * * * * * * .200-.

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

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

Needham LL. August 2005. Patterson DG Jr.58:1185-1201. Placental transfer of pesticides in humans.106(5):279-289. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Organochlorines in Swedish women: determinants of serum concentrations. India. Falk C. Bates MN.htm. Bull Environ Contam Toxicol 2004. The Great Lakes Consortium.96:34-4Food and Drug Administration (FDA).54:1431-1443. Environ Health Perspect 1998. Schulz C. 4/21/09 Ginsburg CM. 4/21/09 Anderson HA. Raju GS.cdc. Angerer J.48:127-134. April 1982 to 1984.html. Heinrich R. International Programme on Chemical Safety (IPCS). Krause C. J Assoc Off Anal Chem 1988. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. Piechotowski I. J Pediatr 1977. Sturgeon SR.cfsan. Olson J. Lepom P. selected elements.fda. Bai KM.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Bottimore DP. Stehr-Green. PA. Kutty D. Darnerud PO. Cancer Causes and Control 1998. Paepke O. Reisch JS. Zoellner I. Metabolism of gammahexachlorocyclohexane in man. Int Arch Occup Environ Health 1986. Atuma S. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. and other chemicals.150:981-990. Available at URL: http://www. Needham LL. Majumder SK. et al. Bhatnagar VK.27:405-421. et al. Brock JW. Bhargava AK. Needham LL. Chemosphere 2004.205:297-308. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Potischman N. Visweswariah K. Pollutants in breast milk. Aune M. Biomonitoring of persistent organochlorine pesticides. 2002. dietary intakes of pesticides. Rivas A. and HCB residues in human blood in Ahmedabad. Rev Environ Contam Toxicol 1991. Burse VW. Environ Res 2004. August 2008. Rey AA.inchem.120:1-82. Kaus S. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Olea N. Becker K. Lindane. Wood PH. 4/21/09 Kutz FW. Bjerselius R. et al. Radomski JL. Buckland SJ. 108 Fourth National Report on Human Exposure to Environmental Chemicals . Absorption of lindane (g benzene hexachloride) in infants and children. Environ Health Perspect 2003.html. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Int Arch Occup Environ Health 1983. Toxicol Appl Pharmacol 1971. Kulkarni PK. Kashyap R. Karnik AB.20(2):186-193. Link B. Krishna Murti CR. children and newborn infants.111:349355. gov/toxprofiles/tp43. Chemosphere 2005. Zaidi SS. Hanrahan L. Gabrio T. Garrett N. Rogan WJ. Occupational exposure to hexachlorocyclohexane. et al.atsdr. org/documents/jmpr/jmpmono/2002pr08. et al. Nigam SK. FDA total diet study. Herrman T. Ellis H. Lowry W. Cerrillo I.71(6):1200-1209. Deichmann WB. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Saxena MC. Olea-Serrano MF.72:261265. available at URL: http://www. J Toxicol Environ Health 1989.gov/~dms/pesrpts. Brinton LA.57(4):315-320. Arch Toxicol 1981. Available at URL: http://www.91:998-1000. Gunderson EL. Saiyed HN. VI. Crespo J. Int J Hyg Environ Health 2002.9(4):417-424. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Arch Pediatr Adolesc Med 1996. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). Toxicological profile for hexachlorocyclohexanes update [online]. Botella B. HCH. Rothman N. Levels of DDT. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Exposure of women to organochlorine pesticides in Southern Spain. Granath F. Demographic and seasonal influences on human serum pesticide residue levels. Seiwert M. Siddiqui MKJ. Glynn AW. et al. Astolfi E.52(1):59-67. Maass R. et al.

6.6 (<LOD-108) 9.3-225) 15.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.S.70 (<LOD-15.6 (<LOD-23. 1995). water.3 (15. 1985.70-40. and 7. it is a highly persistent chemical in the environment.6-305) 15. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8.6) 9.7) < LOD 66.7) 8. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR. after which it is widely distributed in the body and stored in fat.4) < LOD 15.0 (12.8 (12.S. respectively.4) < LOD 63.70-24.2 (7.5 (9. The most likely sources of human exposure to mirex are eating fish from contaminated water or living in areas with soil contaminated by historic mirex manufacturing.6) < LOD < LOD < LOD < LOD 71.4-230) 18.S.5 (<LOD-115) 153 (30. mirex was detected in human adipose samples. see Data Analysis section) for Survey years 99-00..4 (8. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours.1 (8. since 1977. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. aquatic organisms. disposal. 01-02. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57. < LOD means less than the limit of detection. Some states and the U.10 (<LOD-15.1 (<LOD-65.0) * * * 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. which may vary for some chemicals by year and by individual sample. Human health effects from mirex at low environmental doses or at biomonitored levels from low environmental Serum Mirex (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.7 (<LOD-47. or pesticide application.10-37.5-82. 1991).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. 10.5. Mirex binds strongly to soil.0 (14. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U.0-374) 11. where it was applied directly to soil and by aerial spraying.0 (<LOD-108) < LOD < LOD 50.1 (13.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15. Occupational exposure is limited to workers at sites where mirex contamination is present.8) < LOD 15. and 03-04 are 14. Fourth National Report on Human Exposure to Environmental Chemicals 109 .8 (<LOD-73.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2-230) 13.6 (<LOD-31.5-291) 11. In studies conducted in the 1970’s and 1980’s. population from the National Health and Nutrition Examination Survey..1 (<LOD-104) < LOD < LOD < LOD < LOD 39.5-425) 40.1) 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.S.40 (<LOD-13. 2385-85-5 General Information Mirex has not been produced or used in the U. resulting in exposure to newborns and nursing infants. and foods.Organochlorine Pesticides Mirex CAS No.7 (12. soil.2) 51.3 (15. Mirex can cross the placenta and be excreted in breast milk.5 (<LOD-42. Formerly.90-29. Survey Geometric mean (95% conf. sediments.S. Mirex is absorbed through the skin and from the gastrointestinal tract. where it has a half-life of 12 years. especially those from persons living in the southeastern U. animals. Mirex has been detected in air. Mirex is not metabolized in the body. (Kutz et al.

Biomonitoring Information In the NHANES 1999-2000. 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.090-1.470) . More information about external exposure (i.077 (<LOD-. as well as in a subsample of NHANES II (1976-1980) participants. The U.080-1.8.140 (<LOD-.02) .410 (.089-.268) < LOD .635) < LOD .070-1.79) .108 (.052-.470) . 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. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.610) < LOD < LOD < LOD < LOD .73) .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 .256 (. 110 Fourth National Report on Human Exposure to Environmental Chemicals . environmental levels) and health effects is available from the ATSDR at: http://www.37) .054 (<LOD-. Laboratory animals fed high doses developed liver enlargement and liver tumors.215) 659 728 592 1194 1529 1359 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .090-1. 2005). Smith.430 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .170) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .090 (<LOD-.090 (<LOD-.106 (.html. and NTP classifies mirex as reasonably anticipated to be a human carcinogen.S.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and 4. 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.gov/toxpro2.112 (.170) < LOD .690) .92) . and 2003-2004 subsamples.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. 7.090-1.. In addition.055-.090 (<LOD-. 2004). 1995. 2001-2002.062-.059 (<LOD-.080-1.170-3. 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. The geometric mean mirex levels of the Inuit mothers were 8. serum mirex levels were generally below the limits of detection (Stehr-Green.053-.220) .470 (.Organochlorine Pesticides exposures are unknown.079 (<LOD-. EPA has established environmental standards for mirex.450) 1.220 (<LOD-.106) < LOD ...510) < LOD < LOD .S.100 (<LOD-. reproductive toxicity included decreased fertility and testicular damage.41) .450 (. which may vary for some chemicals by year and by individual sample.370 (. IARC classifies mirex as possibly carcinogenic to humans.atsdr.cdc.093 (. In samples obtained between 1994 and 1997.08 (.102) < LOD < LOD < LOD < LOD .170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .7 ng/g of lipid.110 (<LOD-.064 (<LOD-. 1989). * Not calculated: proportion of results below limit of detection was too high to provide a valid result.100 (<LOD-. Survey Geometric mean (95% conf. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR. 1991).e.310 (. population from the National Health and Nutrition Examination Survey.79) .

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

20) < LOD 90th 5.S. and sediments.50 (1.30-27. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR.6-TCP in any of the samples (U.30-11. 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.4.6-trichlorophenol (2.30-27.20) < LOD 5. Occupational exposures.60 (2.0) < LOD 21.80 (2.30 (. which may vary for some chemicals by year and by individual sample.4.00-8.50-63. soils.4.0) < LOD 11.0) < LOD 5. surface water.50) < LOD 1.00-3. Both chemicals have been detected in air.40 (2.7.00 (2. Exposure to trichlorophenols also may result from metabolism of lindane.60 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.0 (5.30-3. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.8) 21.40 (1.6-TCP).S.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.40 (1.71 (<LOD-8.4.0) 2. < LOD means less than the limit of detection.80) < LOD 1.30-27.980-3.40-11. other organochlorines.40 (. 95-95-4 2.9.0) 5.9 (<LOD-121) 9.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.40) < LOD 4.60-18.71 (<LOD-8.10-3.57 (<LOD-15.950 (<LOD-1.0 (4. EPA.4.4.80 (1. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds. 1999).0) 2.50 (2. hexachlorobenzene. Such workers would probably Urinary 2.980-3.0 (8.19 (<LOD-6. and polychlorinated benzenes (Kohil et al.20-36.S.50 (.4.0 (4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols. Survey Geometric mean (95% conf.27) 696 661 521 696 603 939 Limit of detection (LOD.940-3. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites. Trichlorophenols are no longer manufactured commercially.20 (4. recent sampling of U. 2.3.Organochlorine Pesticides 2.60 (4.0 (4.80-41. 2006).4.00-3. 1999).27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.0) 2.4.6-Trichlorophenol CAS No. 1976).920-3.0 (3.40 (2.42 (<LOD-8.0 (3. 2.20) < LOD 1. 112 Fourth National Report on Human Exposure to Environmental Chemicals .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 1.63) 18.5-trichlorophenol (2.40) < LOD 6.5TCP and 2. usually at herbicide production or waste incineration facilities.50-25.00 (3.30) < LOD < LOD < LOD < LOD < LOD 1.5-Trichlorophenol CAS No.4.40 (2.900-2. public drinking water systems did not detect 2.0) 2.40) < LOD 1. are metabolites of several organochlorine chemicals.4. Historically.6-TCP were used as intermediates in the production of certain pesticides..0) 14. interval) Selected percentiles ( 95% confidence interval) Sample 95th 16.50-16. however.03) 9.40 (2.60) < LOD 8.9 and 0.0) < LOD 5.5-trichlorophenol.40-18.7) 24.30-44.40 (. may occur by inhalation or dermal routes.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.0) 2.42 (<LOD-12.20-71.31 (<LOD-9.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR.30-40. 2.90-33.0) 2.0) < LOD 11.30) < LOD 4. Formation of 2.4.60-8.72) < LOD 1.0) < LOD 5.5-TCP) and 2. including hexachlorobenzene and hexachlorocyclohexanes.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . population from the National Health and Nutrition Examination Survey.

62-20.cdc.8 (5.69-18. in addition to dioxins.6-TCP as reasonably anticipated to be a human carcinogen. 1995) were similar.4. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2.6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. leukemias. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.24-11.11) 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..6-TCP levels at the 95th percentile were up to eight times higher than 3.74) 11.73 (<LOD-8..67 (1. In the same 2-6 year old children.9) 12.69 (2.9 (5. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.2) < LOD 5.6-TCP.00) < LOD 4.83-12.4.4.4.46 (1.43) < LOD 12.33) < LOD < LOD < LOD < LOD < LOD 2.82 (<LOD-32.4.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). Fourth National Report on Human Exposure to Environmental Chemicals 113 .68 (<LOD-8. Radon et al.90 (4. which includes trichlorophenols.19-12.02) < LOD 7.43 (2.75 (<LOD-6..47-8.Organochlorine Pesticides be exposed to mixtures of chlorophenols. and other chlorinated compounds.3 (5.4. animals showed hepatocellular abnormalities.980 (<LOD-1.57 (<LOD-7.27-17.7 (4.78 (3.95 (3.88-16.17) 9.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2. Laboratory animals chronically fed high doses of 2.93-11.5) 11. NTP classifies 2.78-19.53-3.0) 7..6-TCP had increased rates of hepatic tumors. The 95th percentiles for 2.78) < LOD 1.5-TCP. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.4.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.gov/toxpro2.5) < LOD 12.5-TCP nor 2. Neither 2.e.50) < LOD 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.13-13.4) < LOD 3.8) 4.4) < LOD 3..55 (4.1 (<LOD-58.2 (2. the 95th percentile urinary 2.32) < LOD 4.4.4 (6.. the 95th percentile urinary 2.2) 2. and lymphomas. Urinary 2. environmental levels) and health effects is available from ATSDR at: http://www. 7. IARC classifies combined exposures to polychlorophenols. population from the National Health and Nutrition Examination Survey.atsdr. However.6) 4.16) < LOD 90th 5.24 (3. Survey Geometric mean (95% conf. as being possibly carcinogenic to humans.36 (1.24) < LOD 6.4.64 (4.3 mg/L reported in German adults aged 18-69 years (Becker et al.75 (3. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al.. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.44 (.00-19.3 mg/L in a nonrandom subsample from NHANES III (Hill et al.05-8.68-4. Among 6-11 year old children in NHANES 1999-2000.79-4..6) 4.37-11. 2004).28-25.57 (3.4) 5. urinary 2.0 mg/L.57 (<LOD-7.37) 16.80 (1.16 (.4.02-3.86 (3. Human health effects from 2.49 (1. At lower doses.31) < LOD 2.05-17.S.8) < LOD 9.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .920-2.5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.15) < LOD 2.00-29.60-3. 2003).37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.24) < LOD 1.1) 2.5-TCP or 2. More information about external exposure (i.53-3.html.44 (1.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.4.6) 4.. 2003).5-TCP and limited for 2.19-4.67 (1.29 (1.20-6.4. 2003. furans.24) < LOD 5. 1995) and up to 19 times higher than the 95th percentile value of 1.820-2.4.6-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. 1989).81 (<LOD-9. 1989).

20 (3.70 (2.25-11.12) 2. Biomonitoring studies on levels of 2. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.10-2.4.6-TCP exposure and health effects. 2004).99) 6..50 (2.20-3.30) 4.0) 19.1-25.00-21.0) 11.7-16.4 (10. for males in NHANES 19992002 (Agramunt et al.3-26.5-TCP or 2.73-9.4.47 (3.4.40) 2.9 (13.2) 25.4. interval) 2.3) 37.0) 12.0-50.0) 10.09) 15.0) 11.4..2) 12.4.5-TCP or 2..5-TCP and 2. Biomonitoring data will also help scientists plan and conduct research about 2.9) 13.32) 3.3.53) 2.40 (2.70-6.30-11.90-8.50-5.67-12.80-20.70) 1.1 (10. Urinary 2.5-TCP and 2.10-3.70 (2.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.75 (8.0 (4.4.98-11.7) 33.6-TCP (0.02) 2.90) 2.40) 4.4.6 (12.54) 6.20) 4.5-TCP and to the median 2.0 (12.74-3.00 (2. Mean values of 2.0 (11.7 (13.0 (16.4 (9.4.95-6.36 mg/g creatinine.0) 17.8-24.7 (9.0) 7.4. Finding a measurable amount of 2.9) size 1989 2503 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 2.40-2.4.4-17.3) 20.00 (4.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.52-3.6) 21.4 (17.06) * 2. 1998).0) 6.95 (4.0-38.3-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60) 6.4.0-44.80 (2.0) 13.60-3. 114 Fourth National Report on Human Exposure to Environmental Chemicals .74 (2.45 (2. < LOD means less than the limit of detection.80 (3.6-TCP level.4. Urinary 2.45) < LOD 11.9 (11.0 (7.2-0.4. population from the National Health and Nutrition Examination Survey.9) 694 677 519 696 602 931 Limit of detection (LOD.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.70) 3. was about six times lower than the median urinary levels for males in this Report (Radon et al.69 (3.10) 2.5-TCP or 2.0 (9.6-22.49 (6. Survey Geometric mean (95% conf.66 (8. 1991).60 (3.0) 9.31 (3.4.6 (11. the median urinary 2.55-3.26 (2.40 (2.5-TCP or 2.6-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.6TCP values.6-TCP in urine does not mean that the level of 2.20-6.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.95) 3.0 (15.90 (4.28) 24.80-7.78 (2.10 (5.65 (5.87-14.0 (8.0 and 1.85) * 3.40-14. respectively.23) 2.98-7.0-68.20-23. 0.60-21.0) 13.1) 16.S.33-4.32) * 3.89 (3.7) 21.04) 2.0 (14.0 (8.6-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. 2003).90 (3.4.89-6. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.4.0-37.30-2.70-3.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 2.3 (11.45 (5.85 (2.08 (2.65) 15.7-3.23-2.92 (2.5 mg/g creatinine) were similar to the limit of detection for 2.58-3.51-12.8 (9.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002.40) 3.40-4.80-25.63) 90th 15.30-33.91-4.0) 13.60-37.58 (1.5-TCP level of 0.6TCP causes an adverse health effect.80-6.0) 15.23) 3.0-54.40-32.57 (<LOD-2.6 mg/g creatinine) and 2.31) * 2.32-4.0) 14.0 (6.80) 1.3) 23.46-3.44) 75th 4.79 (5.72-10.0-41.6-TCP than are found in the general population.0) 7.70-6.59) 4.36-5..30-2.2 (14.0) 13.24 (2.0 (14.52 (2.1 (8.67) 4.20 (3.8) 32.78 (2.0) 9.56 (3.8) 18.35-3.6-17.0 (20.10-3.3 (11.68 (<LOD-2.5-TCP (0.28) * 2.8-13.70) 5.84) 2.6-19.01-6.09-7. In harbor workers exposed to chlorophenol-contaminated river silt.53) 4.00-4.40) 2.0) 17.00 (1.6) 26.60 (2.4.4 (8.14 (2. which may vary for some chemicals by year and by individual sample.0 (6.45-9.0 (15.7 mg/L.0) 10.80 (2.40-7.0 (20.0-38.0) 14.76) 3.8-15. similar to the limit of detection for this Report (Anderson et al.4.4.07 (<LOD-3.10) 6.0 (13.0 (6.18-3.70) 5.60) < LOD 5.40-2.0-18.60 (3.0) 19.0 (14.59-6.36 (1.0-43.48-26.5-46.

88-7.40 (2.24 (1.30-2.63 (<LOD-2.25-2.71 (3.19-5.32 (2.73-22.6 (5.90 (1.8) 11.0 (6.28-4.29-4.41 (3.18-2.33 (1.53 (3.5) 8. Fourth National Report on Human Exposure to Environmental Chemicals 115 .87) 2.51) 18.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.1 (13.33 (7.81) 2.9-64.43-7.1-32.58 (4. population from the National Health and Nutrition Examination Survey.2 (8.06) 4.47-5.29-4.52 (5.7) 6.60-2.75) 75th 4.3) 8.1) 14.04-16.2 (12.00) 4.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.7) 25.6) 8.4) 9.25 (3.82 (8.22-2.8) 21.26-13.05 (6.43 (<LOD-2.Organochlorine Pesticides Urinary 2.9 (9.6 (10.4) 8.6-31.25 (3.56) < LOD 11.65-2.92) 4.83-5.82 (3.8 (7.22 (3.6) 12.77) 2.14-13.72-16.02) 3.6 (12.87 (3.6-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5) 11.9-34.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.40 (7. interval) 2.5-28.46-14.4 (12.88) 1.17-4.17) 13.78) 90th 12.83-6.51-21.91 (3.9) 19.13-6.87-7.48-2.21-11.11) 10.38 (2.82) 2.76) 2.50 (2.06) 11.5 (7.49-3.06-2.94-13.09-3.70-9.6 (6.23) 4.32-19.73) 5.33) * 2.52) 2.1) 11.01 (3.53) 4.0) 10.10 (6.3-23.41-6.53) * 2.00 (3.5) 11.72) 32.62-15.3 (9.65-21.52 (3.42 (2.5 (8.S.96) < LOD 4.91 (7.6) 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 2.49) 4.63 (2.18-4.15 (6.56 (7.4 (11.78) 2.7-36.99-2.59 (2.9) 8.33-2.2) 19.89) 10.9) 8.02 (1.51 (2.9-29.9) 7.65) 18.8) 19.00) 4.0) 8.1 (8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.81-9.04-2.2 (13.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.7 (14.22 (<LOD-2.38 (4.22 (1.90) 2.82-2.77-4.63) 4.38) 22.98 (1.91-2.6) 13.05 (3.27-9.42) 2.56-5.66-4.26 (6.88) * 2.76) 4.67-17.38-5.79-17.5 (10.65) 2.83-6.08-2.20-2.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.60 (4.29 (6.63-13.22-9.0 (11.35 (3.8 (8.5) 9.68) 2.9 (9.88 (2.6 (9.13 (1.10-9.6 (22.44 (3.6 (9.3-37.76) 1.95-2.23 (1.88) 5.25-17.2 (7.53-11.50-8.87-6.88) 4.17) 2.54 (2.8) 12.89-2.63-15.16-10.0 (9.15 (1.98) 10.87) * 2.00 (2.4) 4.43 (2. Survey Geometric mean (95% conf.25-15.83 (3.5) 12.76-8.52) 2.9-32.1-21.10) 4.78 (2.55-2.88) 4.68) 2.63) * 4.4.14-2.

Poschadel B. Int Arch Occup Environ Health 1991. Anderson HA.54(3):203-208. Radon K. The analysis of occurrence data from the first unregulated contaminant monitoring regulation (UCMR 1) in support of regulatory determinations for the second drinking water contaminant candidate list [online]. Aitio A. Pekari K.gov/toxprofiles/tp107.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport.epa. Toxicological profile for chlorophenols [online]. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Holler JS. U. Jones D. Arch Environ Contam Toxicol 1989.EPA). Fast DM. Environmental Protection Agency (U. html. Bailey SL. Am J Ind Med 2004. Environ Health Perspect 1998. Hill RH Jr. Corbella J. Urinary excretion of chlorinated phenols in saw-mill workers. Seifert B. Hill RH Jr. Baur X. The Great Lakes Consortium. Available at URL: http://www. Available at URL: http://www. Becker K. Baker S. Gregg M. Szadkowski D. Kohli J. Heinrich-Ramm R. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. Luotamo M.106(5):279-289. Jarvisalo J. Smith SJ. S. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children.146:83-91. Safe A. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Domingo A. Shealy DB.71:99108. Int J Hyg Environ Health 2003. et al. To T.cdc.45:440-445. Needham LL. Wegner R. Environ Res 1995. et al.pdf. July 1999. December 2006 Draft. 4/21/09 Agramunt MC. Pesticide residues in urine of adults living in the United States: reference range concentrations. Schulz C. Hanrahan L. Head SL. The metabolism of higher chlorinated benzene isomers. Needham LL. Lindroos L. Seiwert M.63:57-62.atsdr. Falk C.18(4):469-474. et al. Burse VW. Chlorophenol exposure in harbor workers exposed to river silt aerosols.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Domingo JL. Can J Biochem 1976. Olson J. Toxicol Lett 2003. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation.S. 206:15-24. Kaus S.

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

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

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

60) < LOD < LOD 4.40-16.0 (8.19) 9.08-15.76 (2.40-19.35-16.2) 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. 120 Fourth National Report on Human Exposure to Environmental Chemicals .0) 5.0 (7.30 (4.0) 5.71-9.70) < LOD < LOD 75th 3.95) 5.42-3.9) 8.00-27.38-5.830 (<LOD-3.14) * * .1 (10.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.00-12.600 (<LOD-1.80-24.860-2.74 (8.970-2.16 (2.55-6.2.42) .30 (2.8 (14.4) 18.90 (1.15) 14.35-11.5) 15.0-28.8) 7.43-12.82) 10.5-17.40-5.60) .2.80 (2. < LOD means less than the limit of detection.46) 10.80) 2.20 (.810-1.08-2.39 (8.1) 10.60-25.08 (<LOD-2.85 (3. 0.50) 2.97) 8.5) 20.0) 12.56 (6.81) 11.48-7.37 (3.58 (3.86-15.0) 11.67) 3.54 (3.00) 3.0) 10.32) 1.02-5. 01-02.0) 11.50 (4.80) .0) 7.66) * * 1.10 (.01) * * 1.7 (14.0) 10.16) 4.47) 5.27-15.0 (8.623-1. respectively.13-2.33 (5.12) 4.2) 16.2 (7. population from the National Health and Nutrition Examination Survey.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 1.30-6.80) 11.2-20.2) 16.94) * * .3) 14.26 (5.32 (.0) 11. interval) 1.0 (7.58 (5.599-1.6) 7.02) 4.10 (2.10) < LOD .7) 11.4 (7.579-1.0) 6.50-36.34-7.45 (2.26-8.840-1.20-30.07-10.0 (5.11 (.0 (12.10 (.0 (9.0 (7.4 (9.3) 16.8 (12.30-4.03 (.758-1.1-23. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.22 (.99 (5.0 (6.90-5.8) 19.0) 6.290 (<LOD-1.80) 2.12-19.21 (.0) 10. which may vary for some chemicals by year and by individual sample.21) 9.50 (.30 (2.0 (7.52) 6.34-3.61 (3.70-23.90) 2.70) .44-38.7 (12.82-12.20 (.717-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.53) 4.96-3.0) 10.780) < LOD 3.2 (11.00-12.9) 952 1187 928 997 1333 1003 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.8) 11.1-17.26-6.61) 4.29) * * 1.3-15.70 (4.52) * * 1.70) < LOD < LOD 1.20 (2.44-3.2 (9.39 (3.40-14.70-14.2) 14.47) * * 1.8-32.757-2.86 (1.4 (7.20 (.71 (2.40-11.58 (2.981 (.15-12.13 (2.6) 18.00 (1.52-11.00-7.60 (1.750-1.9 (8.98-12.93-24.81) 11.9) 14.60-18.890 (<LOD-2.740-2.13 (2.0) 6.20 (.60-11.S.90-4.80-4.70 (2.35-12.10) < LOD < LOD 4.490-2.4 (9.56 (1.80-22.8 (9.93 (4.20-7.9-18.33-18.0) 20.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.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.5 (11.620-1.72) 5.83 (5.80) 2.8 (8.80 (4.8) 7.1.40 (.79-7.10 (2.0) 15.51) 2.5-16.27-3.0) 11.56-13.2 (7.97) 90th 7.0 (9.00-27.89) 9. and 0.05-7.1) 13.1) 95th 13.17-3.79 (5.74 (8.81) 1.00) 3.36-4.63) 1.00-19.2 (9.0) 9.0-27.73) * * .0 (8.70-19. and 03-04 are 0.3) 17.44 (2.2 (14.90) 3.00 (5.98-5.5 (8.70-11.0 (4.0) 10.55-8.80) 4.2 (7. see Data Analysis section) for Survey years 99-00.04) < LOD 1.1 (9.57-7.0) 5.955 (.80) .60 (5.4) 20.56 (4.50 (2.954 (.0 (6.40-1.670-1.94) 3.91) 4.68-7.2 (14.20-4.80) 3.700-1.23-5.4) 17.10-7.00 (4.50-5.530 (<LOD-2.28) 1.290 (<LOD-.

608-1.98) 9.57) 4.56) 4.02-14.38) .5-32.790 (.03 (2.37 (5.650-1.75 (7.69-10.8) 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 1.20-8.54-15.00) 8.83) 8.2 (6.75) 2.45-5.94-23.25) < LOD .87 (1.430-1.633-1.38 (1.8) 16.03) 2.3) 15.85 (6.4) 4.76) < LOD .6 (9.61 (1.85) 2.54-4.94 (2.95) 2.883 (.40-28.66 (1.6) 9.81-5.68) < LOD < LOD 3.56) .29 (2. Fourth National Report on Human Exposure to Environmental Chemicals 121 .40-12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.88 (5.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.89) * * 1.39 (2.47) 2.1) 4.5) 7.0 (8.41) .40) < LOD < LOD 75th 2.05) .53 (6.54-11.94-9.92-2.21-23.90-8.9 (5.2 (10.62) .28 (2.74) 4.67-19.29) * * .79-9.02 (2.4 (4.66 (5.2) 9.92-5.10 (3.80 (6.5) 8.43 (3.40-3.02 (7.00-13.61-29.31 (3.5-20.04-6.94-10.78 (2.62-5.34) < LOD < LOD .1 (10.3) 5.82-14.80 (7.53) 9.47 (3.960 (<LOD-2.46-5.56) 7.98) .540-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50) 7.71-2.11-6.66-15.47 (1.03) 2.8) 7.37) 9.03-6.82-26.9) 12.5) 7.31-14.54) .35 (1.67) 1.75-7.47 (3.510-1.23) 4.43 (.830-1.09-11.37-5.7) 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.710 (<LOD-1.932 (.9 (9.90-5.7 (9.34 (6.47) * * .60) * * .2) 8.45-5.1 (9.42 (3.960 (.8 (10.890 (<LOD-1.82-14.69) 2.54-2.45-11.860 (.60-9.7) 12.69) 4.93) 9.28) 10.98) .36) * * 1.67) 4.71) 10.66-34.40 (3.03 (7.46) 2.09 (.4 (9.00-17.924 (.566-1.34) * * .40-14.574-1.27) < LOD 2.1 (11.35) < LOD < LOD 3.15-10.28 (4.780 (<LOD-1.73 (1.87 (3.13) 4.25) 6.14 (3.2) 95th 12.88-10.855 (.2) 7.2 (8.60) 2.26) * * .6) 13.74) 90th 7.7 (8.5-16.750 (<LOD-1.80 (2.76-4.68-4.52) 4.04 (1.84) 7. interval) .9 (9.18 (.06-2.9-28.900 (.818 (.57-10.0) 7.93-9.00 (4.30 (1.09) 2.6 (10.3) 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 1.84 (5.43) 2.64-5.440 (<LOD-2.88) 2.00-19.1 (8.41-12.10-13.996 (.6) 8.05 (.93-5.2) 5.820 (.41) Selected percentiles ( 95% confidence interval) Total * * 50th .57 (6. population from the National Health and Nutrition Examination Survey.5 (4.37-3.56-13.28 (5.920 (.01-2.94-22.79-3.75 (3.1) 4.72) 11.28-9.500-1.1-15.98-5.51-5.7) 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 .05 (1.32-12.6) 11.69 (4.8) 6.87-5.40-5.02-2.24-3.42) 12.61 (1.75) 14.07 (.66 (2.1 (6.1 (7.560-1.2) 5.870-2.S.549-1.8) 12.0) 6.9) 16.61-13.81 (1.620-1.3) 12.30) 2.83 (7.7 (10.80) 9.55-20.3) 16.23 (4.5) 11.533-1.2) 13.9) 11.4) 4.44 (2.94 (4.98 (3.57 (4.77 (6.37 (4.7) 5.53-11.89-3.7) 18.58) * * 1.95 (3.98-22.773-1.19 (4.890 (<LOD-1.34 (6.40) 4.88-15.5-13.4) 13.82-6.5) 12.570-1.00 (4.

95-9.80-12.0) 13.580-2.8 (12. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .33-11.90-9.00) 7.3 (12.8) 8.22 (6.34-10.0-33.00-9.6) 14.3 (9.90 (6.81-6.51) < LOD 1.28 (7.20) .80) .90 (2.10 (.0 (8. respectively.3) 20.50-4.70 (1.5 (8.82) 8.6-19.80 (5.70-9.0) 13.00) 8.88) 10.00-18.42 (1.90-15.27 (3.670 (<LOD-1.63-14.53 (3.00) 3.00-4.6) 952 1187 946 997 1332 1019 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * 1.27) 9.31-7.04 (3.60) < LOD < LOD 2.0) 9.4 (10.75 (3.96) 3.9-14.00) 3.80) .46-4. and 03-04 are 0.5-26.S.8 (12.50-5.24 (2.5 (8.52 (6.0) 11.8) 9.66) 4.00 (.66-13.7) 10.11-6.2 (9.27 (7.01 (2.7 (10.60 (5.3 (9.59-3.95 (2.80-3.8-21.90 (2.96) 90th 7.9-15.0) 7.3) 14.34 (6.74) * * * * * 1.0-29.4-17.0) 23.46-28.1 (10.90 (6.58 (1.0-24.5.0 (9.70-8.8-20.0 (10.12 (4.90-31.25 (2.62-17.67) 4.58.7) 15. population from the National Health and Nutrition Examination Survey.4 (14.92) 9.1) 11.15-6.77-3.22-12.5) 21. and 0.9 (12.89 (2. < LOD means less than the limit of detection.20-18.14 (6.84-4.78) 5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80-14.8) Sample size 1949 2519 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.80-8.50) 3.6 (10. see Data Analysis section) for Survey years 99-00.16-1.35-3.41) 3.40 (2. 0.6) 14.24-5.20-4.30) < LOD < LOD 4.90 (6.740 (<LOD-1.70-9.30) 3.790 (<LOD-1.90 (2.15-2.10 (<LOD-1.70) 2.35) 4.6-41.90 (5.88) 3.60 (6. which may vary for some chemicals by year and by individual sample. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0 (13.27) 4.970 (<LOD-2.40) < LOD < LOD 75th 2.7-21.0) 19.10-15.910 (<LOD-2.40 (2.29) < LOD < LOD < LOD < LOD 3.0 (7.00-18.20-8.80) 5.9-17.89) 2.00-16.41-5.31-12.7) 16.6 (10.80-4.34-5.5.8-20.34-3.67) 3.2) 14.0) 18.6) 18.90) 8.06 (2.670 (<LOD-1.0 (10.0) 14.90 (6.80-21.6) 11.2 (7.1-23.18) * * * * * * * * 1.0) 6.0) 12.1 (10.86-10.39-13.35 (6.50) . 01-02.0-24.22) 8.60 (2.10-4.17 (7.99 (3.75 (2.0) 14.80 (2.20 (<LOD-2.0) 12.47-6.20) 3.27) .7) 22.9 (7.90) 4.80 (2.0) 11.70 (8.3 (6.9) 95th 14.64) 10. 122 Fourth National Report on Human Exposure to Environmental Chemicals .8-17.67-10.0 (9.0) 9.3 (11.90-15.7 (11.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.4 (10.4) 7.80-6.49-4.77-14.7) 14.45 (3.0 (15.680 (<LOD-1.3 (7.9) 9.3) 10.39 (5.3) 22.22 (6.73) 7.92-17.670 (<LOD-1.4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (5.37) 2.31) 1.9) 16.37 (3.4) 11.0-19.00-4.670 (<LOD-1.95 (5.70-5.3) 8.72) 2.0 (14.5) 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 * * * * * * .10-10.30) 8.97-4.50) 5.30) 3.650-1.7-19.98-9.5 (9.20) 3.61 (3.0) 12.61-32.10) 6.18 (3.00) < LOD .90 (1.29-4.9) 10.30) < LOD < LOD .

79-9.4) 7.0 (13.6 (11. population from the National Health and Nutrition Examination Survey.00 (<LOD-1.94 (5.7) 9.14 (2.3-21.95 (2.12 (7.68-19.7-23.30) 8.30-5.34-18.2) 12.25 (4.93 (<LOD-2.89-13.4) 15.93-10.3) 6.5 (10.86 (3.88 (1.28 (1.25-9.0-21.0 (8.89-10.42-19.03) 3.5-17.54) 9.64-11.28) 6.9) 16.11 (5.590 (<LOD-.23-3.1 (19. Fourth National Report on Human Exposure to Environmental Chemicals 123 .72-4.6 (11.810 (<LOD-1.06 (<LOD-1.18) 2.760 (<LOD-1.00 (7.61 (2.5) 8.50-17.920 (<LOD-1.0) 14.9 (9.93 (6.78 (6.6) 12.42) 7.0 (10.09-11.77) 3.91) 3.16-14.2) 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.29) 3.78-10.89-3.19) 3.88-7.82-8.1) 20.27) * * * * * * * * 1.03 (6.80) 3.940) < LOD < LOD 1.38 (2.45) 6.4 (11.79-6.95) 3.51-7.52-3.6) 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 * * * * * * .27) < LOD .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.27) 5.68-4.33) 3.3-15.6 (13.29 (5.81 (7.68-10.37-5.3) 9.4) 16.54-5.83 (7.92) 3.97-4.2) 8.2) 10.30) 7.6) 7.63 (2.07-3.07 (5.7 (10.41 (7.00 (5.9-17.15) < LOD < LOD 75th 2.620 (<LOD-.74-4.00 (3.21-21.32) 2.78 (4.07) 2.45) 3.63 (6.0 (11.4) 7.5) 10.74-19.910 (<LOD-1.2 (9.53-8.4-15.86) 9.43 (2.4-16.2) 19.86-3.95) 90th 8.72) 4.850 (<LOD-1.94-14.3) 8.2) 15.1) 13.530-1.71 (1.6) 14.89-3.6 (10.6) 952 1187 945 997 1331 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * .99) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.12) < LOD < LOD 4.83 (6.16 (3.7) 14.7) 15.9 (9.69-11.37) 3.59-3.05-3.5 (11.11-3.9 (9.77 (2.28-12.73 (5.4) 9.973 (.5 (15.34) < LOD < LOD < LOD < LOD 3.89 (2.8) 11.00 (2.27-13.3-17.55) .67 (1.950) .9-25.38 (.00 (<LOD-1.30) 2.75-3.32-8.04) 9.87 (3.71) < LOD < LOD 2.890-2.44-6.27) 1.7) 12.6) 13.1) 10.5) 22.70-35.39-17.7) 14.51-10.02-4.6) 95th 16.1 (8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2) 12.96-11.6) 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 1.38 (1.01-5.4-16.91-9.8) 14.42) 8.21) * * * * * 1.93 (2.8) 16.5) 13.03 (2.09-11.78) 4.89) 5.15 (1.20-3.8 (8.38) 1.6 (13.7-19.77 (2.68) .00) 8.7 (11. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .3-34.5 (8.2) 12.85-17.1 (13.67 (7.97) < LOD .4-18.3-17.29-2.29 (2.82-11.9) 19.6) 6.07) 2.96-10.4) 7.00) 2.36 (2.7 (10.89 (3.0-19.5 (9.85-8.33-10.4) 6.75-3.3 (7.2 (9.99 (4.2-15.690 (.3) 12.06) .50 (6.7 (8.6-19.2) 16.8 (10.47-9.92 (5.6 (12.55) 16.55 (2.S.780-1.54 (7.48 (2.70-2.38-13.58 (4.2-30.

20 (2.79) .550 (.590-.04) .59-2.47 (1.850) < LOD .89) 471 575 296 664 822 690 814 1122 919 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .749 (.80) 3.59-6.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.47) 2.490 (<LOD-.54) .90) 2.19-1.49) 2.90-4.57 (2.96-5.710 (.390-. population from the National Health and Nutrition Examination Survey.30) 1.60) 2.08 (2.75-2.74) 3.160 (<LOD-.597) * .95-5.70-7.910-1.17) 1.83) .570 (.31) 95th 2.14 (1.960) .600-1.78) . < LOD means less than the limit of detection.949) .20 (1.353-.540 (.61 (1.10) 1.30-3.20) 2.98) .460-.20 (1.880) < LOD .970) 1.740 (.382-.75 (2.10) 1.303-.570 (<LOD-.720-1.657) * * .04) 1.34) 2.87-3.80) 2.30) 4.34) 2.930 (.500 (<LOD-.31-3.94 (2.42-2.80) 2.33-2.592) * .00-2.11-3.29-2.77-2.76 (1. 0.16) 1.22-8.60 (2.20) 2.22-2.587) * * .359-.720 (.46-3.40 (1.31) 2.425 (.54 (2.343 (.210 (<LOD-.00) 2.750-1.570) * .90) 2.90) 3.31-3.10) 3.18 (.970) .15) 2.710 (.467 (.730) .505 (.840 (. see Data Analysis section) for Survey years 99-00.10-1.940) < LOD .449 (.41 (2.77 (1.70-2.830 (.20) 1.960 (. and 03-04 are 0.32) 3.13) .930-1.580-.740 (.73 (1.810) . respectively.820 (.45-4.83 (2.26 (2.22-3.880 (.740-.584) .09.00 (1.83) 1.980) 1.570 (<LOD-.70 (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 * .13) 2.340-.570 (.388-.95 (2.69-4.S. interval) Selected percentiles ( 95% confidence interval) Total * .201-.390-.30 (1.14-1.440-.20-2.37-2.41-5.48 (1.780 (.50 (1.78) Sample size 1949 2519 1905 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.46) 1.380-.780) .10-1.70 (1.560-.26) .65 (2.750) 1.930) 1.48 (2.910) 1.36-4.49) .01-3.00) 1.80 (2.50 (1.20-2.760 (.510 (<LOD-.45 (2.70 (1.240 (<LOD-.20-1.68-5.46 (2.32-1.39) 2.680-1.32 (1.690-.79) .55 (3.80) 3.27 (3.960-1.86) 3.398-.17-4.23-3.336-.00-4.2.83) 2.89) .455 (.95) 2.96-3. 01-02.510 (.58 (1.97 (2.21) 3.960) 1.860) < LOD < LOD .740-1.450 (<LOD-.64 (1.600 (<LOD-. 124 Fourth National Report on Human Exposure to Environmental Chemicals .457 (.50 (1.11-3.98 (2.960) .820 (.30-1.280-.50 (1.50-2.18 (1.30 (.90 (1.720-1.600-.700) .16) 2.54-2.40 (1.20-3.350-.30 (.592) * 50th .50) 1.549 (.20) 3.98-3.16-3.80) 5.990-1.22-3.570-1.38) 1.690) .618) * .80 (1.690 (.03) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.620-1.780 (.76-6.57 (1.60-4.710) .20 (1.260 (<LOD-.680-1.01-1.25-1.880) < LOD 75th .01) .10) 1.22 (1.94) .30) 2.89-6.800 (.585) * * .550 (.45 (1. and 0.94 (3.380-.592-.46 (1.30) 4. which may vary for some chemicals by year and by individual sample.73-5.45 (1.790 (.400) .86 (1.20) 3.690-1.89) 1.30-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.20) 1.650-.05-3.05-2.700) .60) 3.63 (1.30 (.380) .50-2.50 (1.950) 90th 1.91) 2.930) < LOD .910 (.17) 1.80) 3.670) .35) 1.453 (.83 (2.1.350-.88) 1.27 (2.580-1.74-5.73 (2.29) 1.08 (2.759) * .459 (.15) 2.09 (.

23) 3.38 (2.32 (.00 (3.64 (2.17) 2.69 (3.310-.380-.67-3.06) 4.49 (1.510 (.690) < LOD < LOD .57 (3.08-2.55 (1.92-8.72) 1.67) .07-2.180 (<LOD-.84 (2.700 (.73-3.64 (2.80) 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 * .310 (<LOD-.42) .81) 2.820) 1.61-3.04-1.14 (2.49-4.23 (.11) 1.80) 2.79) 1.38 (1.47 (1.33 (1.136-.820) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.69 (1.393 (.08-2.71) .97) 2.63 (1.32) 2.640 (.880) 1.08 (2.390-1.02-3.460) .38-3.67) 1.510-.72 (1.00-1.08-3.30) 3.67 (1.580-.440-1.490 (.520 (.720-1.45 (1.380-1.45 (2.710 (.16) 1.73 (2.330-.742) * * .447 (.99) 2.61 (3.06-2.230 (<LOD-.05-2.22-3.62 (2.09) .88 (1.330 (<LOD-.05) 1.05) < LOD .82 (2.940-1.97 (1.08 (.460 (.08-3.590-1.403) .58) 3.840) 1.790) .800) < LOD .29-4.57 (1.670 (.560-.660-.60) 1.310 (<LOD-.07-3.280 (<LOD-.590) * 50th .980-1.530 (.08-3.630) * .75) 6.02-3.67 (1.28 (1.870) .550-.88) .550-.320-.597) * .500-.89-3.550) .70 (3.16-2.760) < LOD 75th .33) .10) 2.285-.66) .22) 4.75 (1.39 (1.08) 1.448 (.58-6.510 (.62 (1.60) .91 (1.390) .270-.36) 3.460-1. Fourth National Report on Human Exposure to Environmental Chemicals 125 .04-5.688) * .43) 1.509 (.77-3.08-2.850) 1.591 (.22) 1.60 (2.900) 1.95) 1.07) 5.17) 2.11-2.43) 2.02-6.92) 3.32) 1.800-1.520-.47 (1.19 (1.79 (1.07) 1.08-3.318-.350) .930-1.253-.750 (.05-4.00-3.47-4.700 (.97) 1.34 (1.234 (.08) 2.470 (<LOD-.72 (2.830) 90th 1.412-.645) .44-2.700 (.20-7.42 (.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 * .32) 5.70 (2.97) 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.75 (2. interval) Selected percentiles ( 95% confidence interval) Total * .370-.471-.680 (. population from the National Health and Nutrition Examination Survey.39) 2.710 (.42-6.444-.22) .400-1.17-2.04) 95th 2.335-.84-6.830 (.305 (.270 (<LOD-.77-4.372 (.25-3.43 (1.400) .97 (1.740) .23) 2.75-3.07) 1.250 (<LOD-.61-3.31-1.740) < LOD 1.470) .05 (1.550-1.480) .S.92 (1.250 (<LOD-.65) 2.920) .560 (.61) 2.52 (1.739) * .55-3.57-4.590 (.22-3.72-4.99) 1.552 (.57-2.89 (1.76) 1.640 (.300-.760) .20) 1.720 (.78) 3.07 (.840) .368) * .13 (1.52) 3.24) 4.950-2.23) 2.480-1.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.58 (1.18-2.270-.11 (.66 (2.53) .380) .580) .560-.535 (.377-.22-2.910) < LOD .750 (.07) 1.540-.640 (.990-1.60 (1.790 (.82) 2.580 (.44) 2.16-1.41 (.50) 1.71) 2.710 (.94) .23) 1.30-2.22 (2.453 (.32-1.72) Sample size 1949 2518 1903 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * .50 (1.348-.71 (1.42-8.20-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.515) * * .98) 1.300 (<LOD-.730) .320-.90) 2.03-1.77 (3.03-2.485) * * .870 (.43) 2.840) 1.87 (2.

0) 28.9-21.5) 30.0) 32.2 (12.2-80.60 (2.6-22.40) < LOD 2.0-41.0-58.0-110) 42.6 (26.0-110) 34.610 (<LOD-1.43-7.0) 4.2) 16.S.75-14.81-3.10 (1.10-4.60) < LOD 1.8) 32.53) 40.4-22.0 (24.0) 16.0-69.29-9.0) 18.7 (12.14) 5.0-260) 34.77 (1.1-20.2-27.0-52.50-5.48-2.6 (15.40-16.1 (25. 01-02.92-5.9) 17.61-2.50-7.65 (4.4.9) 38.530-4.41 (1.9 (10.21 (3.98) * 2.0) 30.45) 2.67 (1.57-2.4) 19.64-8.1-40.20) 1.0) 17.99 (2.10 (1.58-2.26) 75th 11.0-29.3) 31.0 (38.10-13.79-2.41) 1.40) < LOD 1.4) 38.9 (19.70-17.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.8-21.5 (24.0 (40.2 (19.3 (23.41-4. 0.7-41.5-27.45) 2.0-50.8 (12.42) 1.6-27.20-4.1-47.1 (22.79 (1.29) 2.06) * 2.70) 5.9 (23.3 (14.0-230) 35.7) 20.0 (8.8-24.54 (3.63-6.6-45.16) * 1.0 (38.70 (.9) 18.0 (38.0 (38.2-33.2) 31.1) 18. population from the National Health and Nutrition Examination Survey.83-2. which may vary for some chemicals by year and by individual sample.0-41.8) 39.5-20.4 (10.2-62.0) 31.83-2.0) 33.53) 1.0-39.70) 1.76 (2.71) 5.83 (1.86 (1.10 (7.12 (3.05) 1.83 (3.21 (1.0-43.90 (1.7 (12.10 (1.0 (33.70 (7.9-51. and 0.40) 50th 2.78 (1.11 (4.600-2.78) 9.32 (2.8 (22.7-22.0) 6.09 (4.0 (20.0 (38.4 (15.04) 3.30 (.18.30-14.0 (6.0 (13.98 (1.8 (12.1 (26.05) * 2.1 (25.35-6.0) 17.10 (1.41) 1.0 (8.46-6.40-4.10) 39.0 (11.48) 5.19) 2.46-2.0 (20.13 (1.2-26.02 (2.5.0) 3. < LOD means less than the limit of detection.90 (1.830-3.7 (28.0-53. respectively.0) 20.1-19.04 (<LOD-2.9 (19.0) 16.20 (2.18) 6.0) 5.0 (8.3) 38.44) 2.0 (19.97) 6.8 (26.0) 15.36-2.9 (27.48-2.58) 16.50 (2.0) 45.59 (1.0 (38.16) 2.80) .0) 42.1-25.0) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3 (12.88) 3.07-5.1) 140 (46.0-41.77) 38.88) 1.0) 3.00-24.80-18.26 (.81-2.690-3.80) < LOD 1.8) 41.17-2.54 (1.8) 62.0) 4.94 (1.1 (11.30) 11.0-47.2-39. 126 Fourth National Report on Human Exposure to Environmental Chemicals .0 (26.6-54.1 (10.0) 8.96) 5.18) 20. interval) 1.53 (1.93-3.80) 1.44) Selected percentiles ( 95% confidence interval) Total * 2.18) 14.91 (4.85) * 2.2-47.90) 11.0) 3.3 (12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4 (19.3 (24.0 (17.0-53.29-4.95 (5.11) 2.0-58.0) 3.04-8.69) 2.86-3.92) * 2.21 (4.66-5.70 (1.59 (1.0-31.6 (9.3) 28.1-46.5-45.0) 19. see Data Analysis section) for Survey years 99-00.50-20.00 (.0-49.0-62.44-7.44) 3.71 (4.70) 1.52 (4.33 (5.27-6.1) 38. and 03-04 are 0.5) 69.3 (10.5-74.50-2.3) 33.6) 52.80-2.0 (37.19-2.7) 47.5-40.1) 95th 48.23) 9.6 (11.80) 90th 38.830-4.71-2.470 (<LOD-1.23-2.0) 28.61 (1.64-3.72 (1.74-2.4-76.49-2.79 (2.53) * 2.1) 38.3) 26.13) 12.8) 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 1.31-6.41) 5.25-3.0) 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 2.0) 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 2.10) .85 (1.0 (32.05-3.87-7.0 (25.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.70 (1.0) 13.46 (.0) 15.23-2.0 (38.0) 20.0-92.9) 48.2-27.0-62.0 (21.00 (.0-39.76 (2.70-6.12) 1.06 (1.90-8.57-2.13 (1.50-17.660-2.0 (7.30) 4.82 (1.

8) 15.2) 41.2 (8.0 (39.0 (32.1) 25.95 (2.67-16.7) 34.8-43.70 (1.38-5.2) 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 1.8) 31.23) < LOD 2.899-2.46-5.750 (<LOD-1.9-18.3-42.07-2.06) 1.870-3.4-67.0) 25.6) 7.22-3.66 (1.1) 25.9) 24.0 (19.19-14.17) 2.19) 5.18) 3.34) * 1.6) 11.5 (6.870-3.860 (<LOD-1.4 (25.17-3.24 (1.55 (2.2 (15.6-38.0-118) 29.11) < LOD 1.2) 4.02) * 1.51) < LOD 1.6) 3.16 (1.0 (23.67-3.43-12.4-39.61 (1.7 (18.7-19.82) 1.56) 1.16 (1.4 (12.09 (5.6-51.1 (50.16 (1.7 (10.79-17.5 (34.9) 12.20-5.7) 95th 51.60) 4.84-13.61-2.5-36.06) 75th 9.6 (11.18) * 2.2-47.07-2.6 (24.00) 6.5-97.6) 3.4 (5.95-16.0-70.54-2.38-1.6) 23.54-15.8) 23.5 (8.1 (33.1-63.0-40.3 (9.83) .48) 1.44) 9.870-3.69-5.0-71.82 (2.62) 4.2) Sample size 1948 2517 1962 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.4-34.0) 3.59-15.7 (18.4 (19.02 (.670-1.37 (1.S.46) 1.1-60.4) 3.2) 33.26-4.02) 1.8-45.27) 50th 2.80 (1.68) 47.6) 19. interval) 1.07) 9.22 (2.38 (3.3) 28.2 (16.1) 27.52 (1.7) 61.28) 1.4) 12.27 (6.35 (2.16-2.00 (4.18-1.5-190) 30.6 (27.7) 15.27-3.7) 30.63-5.0) 48.33-5.3 (10.3-27.80-8.19) 5.3 (10.03) 1.4 (9.40 (5.8) 3.9-52.9) 24.0) 10.5) 27.48 (4.7-109) 22.33) 2.8) 11.08 (1.88 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.94) 1.9) 54.19-6.29-5.57 (6.0 (14.86) * 3.12 (1.1 (39.71-2.4) 12.68 (1.22-2.53) 1.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylthiophosphate (DMTP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00) 1.22 (.43-2.35) 1.27) 10.45-1.9-95.890-4.86) * 2.76-2.95-16.28 (1.9 (10.39 (1.35) .36-13.1 (34.56 (2.8-26.11-2.2-70.58-17.21 (4.96) 2.7-43.1) 15.888-1.50 (2.3) 13.2-38. population from the National Health and Nutrition Examination Survey.0) 13.1) 36.7-38.2) 13.32-3.9-41.4 (21.5 (15.23-1.33) < LOD 1.41 (2.5 (17.9-36.1) 13.75 (1.30) 28.06) 1.0 (6.4-71.0) 30.62 (2.03-2.40-7.2 (22.59-2.64 (1.83 (.14-8.01 (.47 (3.1 (25.32 (3.26-2.69-18.9 (39.0 (17.6) 112 (40.36 (4.94) 19.91 (6.4 (25.6-49.7) 23.45 (1.14 (. Fourth National Report on Human Exposure to Environmental Chemicals 127 .3 (20.2) 36.91-2.71) 8.8) 32.4-21.5-43.75) * 1.0 (23.66 (1.46-22.1) 13.06-1.3-19.930 (<LOD-1.4 (11.60 (.37-2.88 (4.51) .75 (1.58-2.6-32.7-47.2 (21.94-20.9 (13.3 (8.0 (25.2) 13.96-16.2 (9.3-22.2) 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.57) 4.31) 2.9) 3.1) 17. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.79 (2.59-2.25-3.88 (4.95) 90th 32.61-22.5 (13.40-4.1-22.70-4.99-4.0) 952 1187 945 996 1330 1017 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.15 (.12) 3.9) 3.8-34.19 (1.8 (7.67 (1.50-5.1 (12.0) 47.08) 1.88 (1.52-4.7 (24.33) 1.7) 26.4) 14.9 (19.7-37.66) 8.7 (11.6 (7.71 (1.93) 5.00-16.43) * 2.9 (26.7-20.67 (1.680-4.5 (41.9-37.40 (2.75-6.2-34.23) 37.9 (7.47 (1.72) 2.1) 52.47-17.20) Selected percentiles ( 95% confidence interval) Total * 1.2-28.97 (1.46-6.38) 5.7) 66.1) 27.5 (15.5) 70.90 (.36) 10.8-37.

162) * * * * * .850) < LOD .460-.130-.180) .700-1.550) .610-1.650 (.540) .290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.050-.410-.200) < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700-1.310) < LOD < LOD < LOD < LOD .870 (.990) .830 (.650) .100 (. and 0.440-1.090 (<LOD-.630 (.610-.090 (<LOD-.160-.320-.170-.080 (<LOD-.410) < LOD < LOD < LOD < LOD .740) < LOD .120-.870 (.530-.770) < LOD 95th .32) .640) .30) .230) .490 (.850 (.470 (.410-.610 (.700-1.130-.40) .940 (. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .640 (.990 (.290) < LOD < LOD < LOD < LOD .30) . see Data Analysis section) for Survey years 99-00.42) .140-.171) * * .650-1. population from the National Health and Nutrition Examination Survey.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 * * * * * * * * * .15) .05. 01-02.600 (.260 (.220 (.090 (<LOD-.830 (.690-1.650-1.820 (.360-.300-.720 (.900 (.350) .080 (<LOD-.680-1.680) .540 (<LOD-.730) .190 (.30) .380-.380-.310-.610 (.110-.10) .720) .370-. and 03-04 are 0.640) .10 (.310 (.870 (.150) .160) .870 (.270 (.58) .320 (.150 (<LOD-.540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .630 (.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 * * * * * * .410-1.120-.130 (.840) .870) < LOD .390) < LOD < LOD .510-1.10) .720-1.S.820 (. respectively.290) < LOD < LOD < LOD < LOD 90th .140-.780) < LOD 1.860) .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 .430-.420-.870 (.680-1.12 (.310 (.660 (.140) .640-1.090 (<LOD-.680 (.560 (.090 (<LOD-. 128 Fourth National Report on Human Exposure to Environmental Chemicals .840) .117 (.130) .850 (.42) .770 (.090 (<LOD-.10) .13) .140-.280) < LOD < LOD < LOD < LOD .230-.560 (.450 (. < LOD means less than the limit of detection.370-.130) .650) .460 (.390 (.930 (.130-. 0.084-.60) 1. which may vary for some chemicals by year and by individual sample.700-1.190 (.00) .1.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.470-1.290 (<LOD-.160) .310) < LOD < LOD < LOD < LOD .330-.1.400-.20) .450 (.210 (.990) .380-.03) .300-1.350) < LOD < LOD < LOD < LOD .240 (<LOD-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.210 (.760) < LOD .430 (.570) .540) .120 (<LOD-.450 (.860-1.36) .220 (<LOD-.730-.190 (.830) < LOD .620 (.360-.830) .099-.

58) 1.300-.110) .060-.520-.390-.700 (.860-2.86) .100-.02-1.700) .240-.660-1.24) .320 (<LOD-.19 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.01 (.410) .36 (1.070 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.450) .170 (.150-.29 (.070 (<LOD-.810 (.700-1.540 (.38) 1.200 (.03 (.120) .780) < LOD 1.700 (.330 (.380-.090 (<LOD-.940) .740) < LOD 1.300-.230 (<LOD-.400) .190 (.110) .560 (.24 (.310) < LOD < LOD < LOD < LOD .570-1.170) < LOD < LOD .62) 1.970) .14) 1.110-.380-1.540) 471 576 310 664 821 715 814 1118 937 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .360-.270 (.640-1.050 (<LOD-.09) .860 (.300 (.500-1.470 (<LOD-.400 (<LOD-.670-1.090 (.750) < LOD 95th .490-1.380 (.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .800-1.12) < LOD .02) .230-.340-.510-.550 (.180-.360) < LOD < LOD < LOD < LOD .86) .084-.780 (.250-.670 (.190 (.570-.760) .66) 1.070 (<LOD-.850 (.390-.00) < LOD .410 (.280) < LOD < LOD < LOD < LOD .360-.43) .161) * * .330-.330-.070 (<LOD-.210 (.440 (.330-.140-.580) < LOD .990) .600) .190-.260) .580 (.670 (.67) .03 (.580-1.710-1.540) .140-.600-1.03) .450 (.360 (.057-.03 (.080) .500) .260-. population from the National Health and Nutrition Examination Survey.380-.730 (.410 (.550 (.650-1.730) .080 (<LOD-.140-.940) .310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.960) .410-.410-.460 (.410) < LOD < LOD .111) * * * * * .610-1.640) 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 .60) .230) < LOD < LOD < LOD < LOD .140-.860 (.730) .20) 1. Fourth National Report on Human Exposure to Environmental Chemicals 129 .380-.870) .720 (.140) .440-1.370 (<LOD-.220) < LOD < LOD < LOD < LOD .730) .78) .100 (<LOD-.080 (.110) .990) .580 (.570 (.880 (.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.270) < LOD < LOD < LOD < LOD .880-1.200 (.220 (.110) .650) < LOD .S.140-.740 (.116 (.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 * * * * * * * * * .170 (.720 (.580) .500 (<LOD-.330 (.120) .890 (.290) < LOD < LOD < LOD < LOD 90th .540 (.

610 (.770 (<LOD-1.11 (1.900 (.90) .170-1.260-.0 (5.40 (1.29-10.880) 5.15) 14.35) 5.20 (1.0 (17.12-1.330 (<LOD-1.90-37.30 (2.3) 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 * * * * * * * * * .90-28.24-7. respectively.70-30.210-1.51 (2.40 (1.0) 4.65) 1.48 (2.350-.11) . which may vary for some chemicals by year and by individual sample.55-8.750-1.0) 4.40-20.49 (1.01) 5.53 (2.63 (3.82-4.00 (.730 (.36-3.52) 5.720) 2.47 (3.38-3.52 (1. see Data Analysis section) for Survey years 99-00.800) 90th 13.0 (5.61 (1.35-10.0-38.0 (17.40-8.46 (1.690 (.0 (13.590 (.15) 19.90 (1.350-.28) 1.07-3.12) * * * * * * * * .28) .80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.910) 2.85-3. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.66) 4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.07 (3.14) .960 (.53-7.640 (.0) 4.97) 20.99) 11.70-17. population from the National Health and Nutrition Examination Survey.00 (1.40-4.30-6.0 (17.S.21-3.32 (1.510-.30 (.890 (.48) 13.10 (3.94-3.480-.07-3.74 (3.67 (2.960 (<LOD-1.49) 17.05-3.90 (2. and 03-04 are 0.6) 5.20-4.380-.07) 1.10-3.49 (1.250 (<LOD-.50) .13 (3.07 (3.74) 5.32-9.70) 2.90) .20 (1.0) 5.0) 2.35) 11.90) .00-17.30-7.0 (16.0 (17.190-1.30-3.20-4.59-5.86) 4.87) 5.94 (1.425-1.750-2.83) 2.90-9.580 (.0 (4.83-3.52 (1.0 (17.620-1.840-3.0) 2.70-7.640 (.03 (.70-3.60) 1.51-8.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.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 .26 (2.42) 2.80 (4.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. < LOD means less than the limit of detection.0-38.30) 95th 19.10 (3.87) 12.00) .840 (.691 (.90-20.99) 19.28-9.610) < LOD < LOD < LOD < LOD < LOD 2.770) 2.0-39.42) .97) 20.870) < LOD < LOD .45 (2.20) < LOD < LOD < LOD < LOD < LOD 1.00-17.60) .40) 2.0) 4.0) 7.31) .0-40.50) 2.08.23-6.850) 16.39 (2.740 (.76 (1.62) 471 575 306 664 821 699 814 1122 925 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .0 (4.0 (6.21) 3.96 (1.0) 3.20-17.600 (.370-.53) 20.67 (1.1.94-8.110 (<LOD-. 0.14) 2. 01-02. 130 Fourth National Report on Human Exposure to Environmental Chemicals .0 (3.0 (5.11) 13.0) 2.10-3.800) 17.40-7.30) .88-3.07 (1.0) 5.830 (.1.05 (3.70-50.0 (5.62-8.00) 1.10 (.0 (5.0-40.83-3.40) 1.99 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.43-4.0) 2.0) 5.0) 5.080-1.30 (1.63) 32.68) 2.0) 2.840 (<LOD-1.0) 2.55-4.30 (1.33 (4.18) 1.31-10.800-4.10-9.39) .30 (1.00) .400-1.360-1.36-3.37) . and 0.0 (7.67) .0) 2.0-44.14-5.0-38.05 (2.

Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40-2.790 (.04-16.40 (.630-1.7) 4.02) .500 (.5-40.6) 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 * * * * * * * * * .43) .96) 2.15) 9.67) 1.8) 2.91-4.69) 2.81-17.06 (.08) .47) 5.474-1.11-5.56 (1.8) 4.75) 5.7) 5.71 (2.41) 18.31-7.40) 1.970-3.7 (6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.03) 2.1) 2.02 (.32) 9.580 (.45 (1.59 (1.88-3.14 (1.7) 6.33-4.33 (1.2 (8.150 (<LOD-.31) .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 * * * * * * .62 (1.00) .88 (.57-40.340 (.25-38.48 (4.9) 6.47-10.85 (1.748 (.730-3.8) 2.90-6.31-18.540-1.780-4.50 (2.340-.10) 2.80) 3.51-4.9) 5.620-3.56) 2.74 (2.700) < LOD < LOD < LOD < LOD < LOD 1.92 (2.01 (1.28-6.270-.49-2.96-8.07-21.82-11.660) < LOD < LOD .84) 9.10 (2.37) 4.21-3.370 (.09-3.7 (12.0 (4.8) 1.470 (.5 (8.370-1.22-27.430) 1.85-3.83 (4.86) .83-11.1 (7.04 (1.61) 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 .60 (1.580-1.360 (.67-6.33-5.1) 672 678 497 509 694 551 595 947 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.88) 17.250 (<LOD-.12 (4.65 (2.830-3.64-4.4) 2.840-3.02-4.340-.1 (5. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.830 (.53) .25 (1.40-12.450 (.33-3.18) * * * * * * * * .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.55 (3.35 (.8-33. population from the National Health and Nutrition Examination Survey.670 (.30 (4.02 (1.25-9.55) 21.5) 2.0 (9.22) 2.820) .79 (.56) .18) 1.51-44.850-3.540 (.8 (20.930) .71 (.39) 20.14-6.44-11.580) 16.260-.50) .53) 27.5) 7.64) 30.650) 90th 10.57) 8.55) 21.18) 95th 21.17) 5.00-19.17 (1.12-4.10-3.11) .860-2.29-4.48-42.36 (.66-47.690-5.340-.88 (2.940-4.44) .270 (<LOD-.700) 6.69-7.960 (.29 (4.770) .590) 2.430 (<LOD-.67) 2.2-38.0) 4.240-.80 (.740-1.50) 11.07 (2.5 (9.57) 1.73 (4.190-1.800-2.31) .48-7.03) 16.260-.67 (2. Fourth National Report on Human Exposure to Environmental Chemicals 131 .790) 11.890 (.710 (<LOD-1.600 (<LOD-1.23-7.13 (2.77 (.S.91) 2.32-6.41 (4.62-17.5 (11.3) 3.27 (2.7) 3.24) 3.320-1.4 (4.33 (3.86 (3.96-25.5) 2.47-10.8) 7.89 (2.52 (.370) < LOD < LOD < LOD < LOD < LOD 1.330-1.05) .97) .47) .560 (.4-34.820 (.38 (2.50 (4.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.8) 7.310-.580) 1.57 (.9 (11.98 (4.3) 2.390-.650 (.

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low-level exposure to the organophosphate diazinon. National Academy of Sciences. Levy LS. Int J Occup Environ Health 2006. Washington (DC). Effects of chronic. Rohlman D. Berry H. and spatial learning in monkeys and rats. Pesticides in the Diets of Infants and Children. Pilkington A. Environ Health Perspect 2005.332(1-3):71-80. Steenland K. Malathion deposition.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Jamal GA. Heaton RK.12(2):153-172.pdf. and cholinesterase status of date dusters and harvesters in California. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. metabolite clearance.30(2):98-103. Jenkins B. Eskenazi B. Lambert WE. et al. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. Keifer M. Rosenstock L. Lasarev M. Office of Prevention Pesticides and Toxic Substances. Occup Environ Med 2001. Terry AV Jr.S. Rothlein J. Savage EP. The Pesticide Health Effects Study Group. McCauley L. et al. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Robson MG. Lu C.epa. O’Malley M.68(3):209-227 Maizlish N. Takamiya K. Irish RM. May. London L. Ruberu DK. Vitayavirasak B. Lancet 1995.43(1):38-45. Arch Environ Health 1975. Available at URL: http://www. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Salvini S. J Toxicol Environ Health A 2005. Tumino R. Thompson ML.52(10):648-653. Aprea C. A behavioral evaluation of pest control workers with short-term. 1991.114(5):691-696. Hore P. van der Hoek W. Neurotoxicology 2005. 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. Stokes L. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Arch Environ Contam Toxicol 2000. EPA. Wickremasinghe AR. Environmental Protection Agency (U. Prendergast MA. vibration sense and tremor among South African farm workers. Russo J. Lewis JA. Stark A. Barr DB.338(8761):223-227. Spurgeon A. Daniell WE. Santana J. Environ Health Perspect 2006. Chrislip D. Mounce LM.2000 and 2001 market estimates. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Frasca G. Phillips J. Bradman A. Lasarev M. Weisskopf C.84(5):731-736. Petchuay C. Kidd M. Am J Public Health 1994. S. J Occup Environ Med 2002. Scherer J. low-level organophosphate exposure on delayed recall.12(2):134-141. Pesticide industry sales and usage . Weerasekera G.52(2):190-195. et al. EPA). Buccafusco JJ. et al. Arch Environ Health 1988. Caltabiano LM. Muniz J. Nell V. et al. Seiber J. Rodnitzky RL. Occup Environ Med 1995. Calvert IA. Gillham R. Burcar PJ. 1993 [online].44(4):352-357. Sci Total Environ 2004. Rothlein J.S. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand.php?record_id=2126&page=1. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. McConnell R. Scand J Work Environ Health 1998. Buchanan D. Johnson C.26(2):199-209. Visuthismajarn P.nap. Marshall E. Smit LA.345(8958):11351139. Neurotoxicol Teratol 1998. 4/7/09 Young JG. Am J Ind Med 1987. Available at URL: http://books.24(1):18-29.58(11):702710. National Research Council (NRC).38(4):546-563. Neurotoxicity among pesticide applicators exposed to organophosphates. Beach J. Claypoole K. Schenker M. Bull Environ Contam Toxicol 1994. Narang A. Dinoff TM. Masala G. Pedersen L. Stephens R. Effects of long-term organophosphate exposures on neurological symptoms. discrimination. Gladstone EA. Ames RG. Washington (DC): U. Myers JE. Hansen S. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers. U. Lancet. Keefe TJ. 2004. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. Bravo R. Samuels S. Fourth National Report on Human Exposure to Environmental Chemicals 133 .113(4):504-508. 1/12/09 Peiris-John RJ. Chronic neurological sequelae to organophosphate pesticide poisoning.20(2):115-22.edu/ openbook. Muniz J. gov/oppbead1/pestsales/01pestsales/market_estimates2001. Saieva C.

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

71 (1.80 (7.40-26. and dust.47-11.0 (7.0-28.0) 6.0) 12.0) 12.30 (2.77 (1.40 (6.60-3.71 (6.13 (1.05-5. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators. pre.0) 8.92 (1.74 (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.0 (7.72-4.63 (2.30-9.20-16.63 (1.S.70-5.50-4..9 (10.5.36 (4.20) 2. Approximately 80.97) 7.5) 7.51 (1.57 (2.24-1.32) 2. chlorpyrifos was no longer registered for indoor residential uses in the United States. applied to structures to kill termites.60-2.90 (6.00-24.20-2.7) 8.17 (1.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.61-7. interval) 1.90-7.70-15.52-12.9-18.00) 1.38 (3.0) 10.39) 4.84) 1.44 (3. It also has been applied directly on animals to kill mites.61) 75th 3.0) 12. Chlorpyrifos is Urinary 3.90) 3.44-5.24-3.37 (4.44-2.30) 4.46-2.03) 1.79-2. 2005).5 (8.72) 2.50-8.4-15.10 (5.50 (2.50-4.21) 3.02) 1.00) 3.22) 2.80) 1.77) 1.30) 4.0) 10.30 (4.10 (1.50-5. dermal.70 (1.40-13.25) 3.43-2.76 (1. Exposure can also result from contact with contaminated surfaces.95) 7.47-9.3 (11.60 (5. but can be detected in streams receiving runoff from application sites.51) 1.10 (3.9 (9.60) 5.77-15.8-15.90-2.31-2.39-2.20 (2.96) 3.50-14. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.55-5. 2002).7) 9.15 (1.28-3.28) 2.3) size 1994 2509 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th 1.50 (1. air.47-13.50-2.40-10.2 (10. It has low leachability. Survey Geometric mean (95% conf.90-8. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.5-24.3 (10. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.70-16.0 (10.4.25) 1.30-5. For instance.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.0) 11.10 (4.000 pounds are used per year.87-6.66-4.40) 9.8) 9.50-2.7-23.40) 2.and post-construction structural applications for termite control were to be phased out by 2005 (U.97) 4.90 (2.4 (10.98-15.40 (5.86) 4.0) 18.EPA. staying bound to soil particles.20) 2.89 (2.70-17.0) 9. population from the National Health and Nutrition Examination Survey.52-2.90 (1.61 (1. 2007).60-4. The general population may be exposed to chlorpyrifos via oral.50 (2.3) 8.20-14.90-4.0 (9.04-10.3 (8.26) 7.0 (7.10) 2.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.04-10.09 (3.97) 2.30) 5.0) 10.80) 2.9) 11.45 (1.0) 12. although some tolerances for specific food crops have been reduced in the past to avoid exceeding recommended intake limits for total dietary intake in special groups (U. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.31-2.80-8.05) 1.77-6.20) 10.20 (4.59-2.67 (2.10) 6. 1999.0 (7.60 (2.90 (3.66-15.20-4.02 (1.43-2.40 (5. After 2001. 2002).71 (2.19 (1. 2921-88-2 Chlorpyrifos-methyl CAS No.30-11.0) 8.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1.50 (1.0) 12. and on plants for days to several weeks.0) 15.80 (1.13-3.29) 90th 7.4 (8.67 (2.20-11.37 (1.60 (4. Approximately 21-24 million pounds per year were used domestically from 1987-1998. and inhalation routes.59) 2.EPA.0 (13. and sprayed to kill mosquitoes.09 (2.27 (7. USGS.78 (7.35) 2.4 and 0.51-2.90) 7.50 (2.1-16.9) 697 660 521 701 602 947 Limit of detection (LOD. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use.95 (4.67 (1.89-2.6) 7.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.19-3. in 142 urban homes and preschools in North Carolina.02 (7.20) 4.5.60-3.30 (2. and is infrequently detected in ground water (IPCS.91) 16.83) 1.53 (1.94 (4.0) 14.01) 1.47 (4.30-1.90 (1.4 (9.10-17. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.74-9. 5598-13-0 General Information The chemical 3. Estimated intakes from diet and water have not exceeded recommended intake limits.99-4.64) 3.7) 13.47) 1.9 (7.97-7.37) 5. Fourth National Report on Human Exposure to Environmental Chemicals 135 .32-1.S.22 (1.0) 7.81-2.30-12.40-2.80-10.1) 5.68 (7.70) 1.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl.97) 2.88 (1.62-2.00) 2.80) 12.00-8.8) 10.70 (1. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.63 (8.0 (7.29-1.70-11.34) 1.16) 2.91 (1.76 (1.20-3.68-2.30-2.80) 4.35) 1.S.

1984).24-5.75 (1.71) 3.91) 10.4) 4.91-4. vomiting. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.44-6.49 (1. and producing acute symptoms such as nausea.3) 8.88 (1.33) 2.20-1.07) 5.91 (3.58-5.58 (1.66-11.05-4.35) 2.72-2.63 (5.23-1. 2002).00-8.68) 1. 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.15 (4.94-14. neurotransmission.83-11. Based on animal data and human cholinesterase monitoring during occupational exposure.05-8.21-1.47-2. 2005.43 (4. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.45 (1.21-6.91) 1.0) 10.0) 12.3 (7. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates.80-4.17-4. resulting in excess acetylcholine at nerve terminals.30-1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).33 (1.47 (1.64-7.8) 9.22 (4. 2006.01) 3.48 (2.24 (1.09 (1.57) 9.03) 1.EPA.97 (3.14-8.5 (6.56) 5.56-2.36) 1.81) 2.S.1 (7.49-2.07) 1.06-4.82) 8.44 (5.01) 3.48 (1.92 (1.59) 3.6) 9.58) 5.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.33 (5. Survey Geometric mean (95% conf.51 (1.39) 6.12-3.97-3.62) 1.14) 1.09-3.46 (1.31) 1.76 (3. weakness.85 (3.41 (1. Once absorbed.88) 6.85) 1.45-1.79-13.93) 2.2) 6.9 (12.24-4.19) 6. Urinary 3. 2005.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.98 (7.16 (4.93) 5.00-13..91 (4.. 2006b).62-7.94-12. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.82-4.S.90-9.37 (1. and other metabolites.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 1.89) 4.35-1. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.93 (4.20 (2.00 (7.93 (1.74) 1.88-8.85-4.02 (5.88-8.39-1.95 (1.97) 3.97) 3.91-13.33 (.1 (10.54) 5. TCPy can also occur in the environment from the breakdown of the parent compounds.55 (1.24-24.27-1.6-Trichloro-2-pyridinol (creatinine corrected) Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.56 (1.65-15. population from the National Health and Nutrition Examination Survey.02) 7.28) 2.88-10.97 (2.80-11.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .88-9.47 (5. 2000). 2006a.58) 1.38) 3.73 (1. paralysis.63-2.99) 1.0) 6.11-9.42-2. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al. In pesticide applicators.. TCPy is more persistent in the environment than chlorpyrifos itself (U.53-5.83) 1. Thus.84-6.1-38.55) 1.59-2. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.0) 16.92-2.55 (4.86 (3. Roy et al.72) 2.940-1.56) 2.17-4.19) 3.54 (2.34-1.24) 75th 2. 2006. Ricceri et al.46 (2.71 (1.75) 6.64-2.11 (2. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.23) 14. 2005.29 (3.42 (6.30-4.58 (4.19-1.05) 3.53 (2.70-4.50 (4.57-2.5) 5.66) 1.77) 1. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis..72) 1.40) 1.87-3.85) 4.12) 1.1-21. interval) 1.16) 6. cholinergic effects.56 (4.83-2.25-12.22-6.12-1.44 (5.80-6. Slotkin et al.31-4.22) 1.68) 6.58 (1. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.39 (2.3) 8.76 (2.93 (2.05-1.47 (1.00) 1. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.01) 1.09-2.05-3.49-2.62) 90th 5..22 (6.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1. and seizures.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.11) 7..5.63 (4.60-3.80) 3.98 (6.08) 6.91) 1.39 (4.06 (5..31-1.33-7.7) 7.44 (1.96) 3.19-2.2 (7.82 (2.24-1.35) 1. Howard et al.25-11.3) 9.66 (1.42 (5.91) 2..27-7.11 (2.57-2.81 (3.88 (1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.69 (1.25-1.44 (1.43-10.49-2.26-14.92) 3.64 (1.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.82 (3.57) 2.95 (3..99-8.44 (6. Metabolic hydrolysis leads to the formation of TCPy.85 (2.52 (5. Betancourt et al.24) 5.09-1.06 (1.60 (1.86 (1.78 (1.28) 2.65-11.32) 1.86 (1.6) 10.

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

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Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats. Toxicol Sci 2006. Weltzien E. Mandel JS.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Available at URL: http://www. Sanderson WT. Levin ED. Environmental Protection Agency (U. Tsai WY. Striley C.111(2):201-205. Environ Res 1995. Hein MJ. Lein PJ.112(10):1116-1124. Cometa MF. 2921-882. Bucelli R. Saunders JH. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . et al. Environmental Health Criteria 198. A longitudinal investigation of selected pesticide metabolites in urine. Hammerstrom KA. Edwards RD. Executive summary of safety and toxicity information. Seidler FJ. Ryde IT. Bennett DH. J Expo Anal Environ Epidemiol 2005. Baker S. Lorenzini P. Barr DB. Kromhout H. Kinney P. Bravo R. Gurunathan S. Reid TM.113(2):211-219. Barr DB. Jones PA. Yang D. et al.5. Harley K. Nolan RJ. Environ Health Perspect 2005. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population. Available at URL: http://ntp.15(3):271-281. Capone F.207(2):112-124. chlorpyrifos. Gregg M. et al. Environ Health Perspect 2006.114(2):260-263.S. Fortuna S. et al. Environ Health Perspect 2006a.71:99108. Jewell NP. Bravo R. Freeman N. National Toxicology Program (NTP). Ozkaynak H. et al. Exposures of preschool children to chlorpyrifos and its degradation product 3.niehs. Steenland K. Bailey SL. Head SL. Environ Health Perspect 2003. Freshour NL. Scand J Work Environ Health 2005. Chapman P. Hines CJ. Venerosi A. Chlorpyrifos: pharmacokinetics in human volunteers. Ricceri L. Dick RB. Alexander BH.10(4):327-340. Pellizzari E.9(5):494-501. Interim registration eligibility decision for chlorpyrifos.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC).73:8-15. Chrislip DW. J Expo Anal Environ Epidemiol 2005. 1999. Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition. Hore P. Baker BA. Adgate JL. Ryan PB.93(1):105-113. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Toepel K. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. J Expo Anal Environ Epidemiol 2000. Int J Hyg Environ Health 2001. Hardt J. February 5. Biomonitoring for farm families in the farm family exposure study.114(5):746-751. Zhang J. Howell RJ. 4/7/09 Perera FP. Lu C. Temporal variability of urinary levels of nonpersistent insecticides in adult men.org/documents/jmpr/jmpmono/ v99pr03. 2005. Slotkin TA. Toxicol Appl Pharmacol 2005. Herrick RF. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity.108(4):293-300. Slotkin TA.S. Ryan L.51(1):53-65. et al. Seidler FJ. 1992. Acquavella JF. Heederik D. Morgan MK. Slotkin TA. Urinary pesticide concentrations among children.htm.inchem. Sharma V. Howard AS. U. Tate CA. 4/7/09 Koch HM. Toxicol Appl Pharmacol 1984. Pesticide residues in urine of adults living in the United States: reference range concentrations. Fenske RA. Environ Health Perspect 2004. et al. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Curwin BD. Barr D. Brain Res Dev Brain Res 2005. et al. Croghan CW. gov/ntpweb/index. Robson M. Lioy PJ. et al. Chuang JC. Rick DL. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application.6-trichloro 2-pyridinol in their everyday environments.155(1):71-80. Environ Health Perspect 2006b. Neurologic function among termiticide applicators exposed to chlorpyrifos. Jett DA. Irish R. Angerer J.nih. Bruun D. Third National Report on Human Exposure to Environmental Chemicals. Atlanta (GA).15(4):297-309. EPA).

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

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

270) < LOD 659 701 920 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 141 .27) < LOD < LOD 567 814 1099 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1169 1311 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2480 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf.S.670 (<LOD-1. < LOD means less than the limit of detection. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 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 . Survey Geometric mean (95% conf.Organophosphorus Insecticides: Specific Metabolites Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2. see Data Analysis section) for Survey year 01-02 is 0.200 (<LOD-. population from the National Health and Nutrition Examination Survey.380 (<LOD-. Urinary 3-Chloro-7-hydroxy-4-methyl-2H-chromen-2-one/ol (creatinine corrected) Metabolite of Coumaphos Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.200 (<LOD-.S.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 .

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

Before these restrictions. 2004). It is also used for cattle ear tag applications to control flies and ticks and.S. as inferred Urinary 2-Isopropyl-4-methyl-6-hydroxypyrimidine Metabolite of Diazinon Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 1998). and particularly when it was ingested in granular form.Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No. fruits. but these uses have been phased out. Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. Fourth National Report on Human Exposure to Environmental Chemicals 143 .2 and 0. 2004). 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. diazinon cannot be sold for residential use. and other metabolites. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. diazinon was widely used in residential and garden application. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. vegetable. seed and foliar applications are planned to be phased out (U. Survey Geometric mean (95% conf.7. Inhalational and dermal routes of exposure can be significant for pesticide applicators. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).S.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 1.49 (<LOD-2. in some pest strips. USGS. aerial. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. which may vary for some chemicals by year and by individual sample.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. Prior to 2000. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. < LOD means less than the limit of detection. 1998. in the past. but is rapidly absorbed orally (IPCS. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.EPA. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks. Estimated intakes from diet and water do not exceed recommended intake limits (U. population from the National Health and Nutrition Examination Survey. Most granular formulations. and forage crops. since 2004. 2007). Once absorbed.EPA. It is toxic to birds. Diazinon is not well-absorbed through the skin. diazinon produced wild bird kills before use restrictions were in place.45 (<LOD-3.S. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. an organophosphorus insecticide that is used to control insects on nuts. 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.

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.. In the U... The U. 2-isopropyl-4-methyl-6-hydroxypyrimidine can also occur in the environment from the breakdown of the parent compound. teratogen. and producing acute symptoms such as nausea. subsamples of NHANES 1999-2000 and 20012002. diazinon and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. vomiting. In addition to being a human metabolite of diazinon. Survey Geometric mean (95% conf. 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.html and from U.gov/pesticides/. and indoor applications have been documented. Olsson et al. 2003)..72 (<LOD-4.EPA considers diazinon unlikely to be carcinogenic in humans.gov/toxpro2. Seifert and Pewnim. Biomonitoring Information Urinary levels of 2-isopropyl-4-methyl-6hydroxypyrimidine reflect recent exposure. 2000. 144 Fourth National Report on Human Exposure to Environmental Chemicals .Organophosphorus Insecticides: Specific Metabolites from dialkyl phosphate metabolite excretion (Garfitt et al. Additional information about external exposure (i. weakness. There has been only limited study of diazinon at systemically non-toxic doses that do not result in cholinergic signs (Anthony et al. the detection of 2-isopropyl4-methyl-6-hydroxypyrimidine in a person’s urine may reflect exposure to the environmental degradate. resulting in excess acetylcholine at nerve terminals.e. 2002). agricultural.epa. population from the National Health and Nutrition Examination Survey.S. Urinary 2-Isopropyl-4-methyl-6-hydroxypyrimidine (creatinine corrected) Metabolite of Diazinon Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.76 (<LOD-3.S. At high doses. 1986. 1998).48) < LOD < LOD 644 678 484 699 554 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.atsdr. Diazinon is not considered to be a mutagen. Intoxications in humans from intentional overdose. animal carcinogen. EPA at: http://www. cholinergic effects.S. in the 2001-2002 subsample (CDC. environmental levels) and health effects is available from ATSDR at: http://www. and seizures. 1986 Rajendra et al. respectively. most of the measurements of 2-isopropyl-4-methyl6-hydroxypyrimidine in urine were below the limit of detection. Human health effects from diazinon at low environmental doses or at biomonitored levels from low environmental exposures are unknown. paralysis. diazinon does not accumulate in tissues (IPCS. Diazinon has moderate acute toxicity in animal studies. respectively (Baker et al.S. 1998). In animals. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. although the 95th percentiles for children 6-11 years old and for non-Hispanic blacks were 1. 1992).45 and 1..cdc. or reproductive toxicant (IPCS. 2-isopropyl-4-methyl-6-hydroxypyrimidine was detectable in 57% and 43% of the 130 and 140 participants.. Thus.49 μg/L. In two nonrandom samples of United States adults and children.

9(2):117-131. 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. Driskell WJ. Available at URL: http://www. J Expo Anal Environ Epidemiol 2000. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. 2007 [online]. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers.50(5):505-515. Bouchard M. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses.37(4):501-507. March 2006. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. Ann Occup Hyg 2006. 4/7/09 Lu C. The Quality of Our Nation’s Waters. Diazinon. Mason HJ. Swan SH. et al. 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . EPA 738-R-04-006. Bull Environ Contam Toxicol 1986. Pesticides in the Nation’s Streams and Ground Water.gov/circ/2005/1291/.111(12):1478-1484. Available at URL: http://www. In 54 Canadian greenhouse workers. Seifert J.Organophosphorus Insecticides: Specific Metabolites 2005). Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon.10(6 Pt 2):789-798.. U. Biochem Pharmacol 1992. Needham LL. Environmental Health Criteria 198. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Noisel N. May 2004. Olsson AO. Brunet RC. 1998. Sadowski MA. Carrier G. Rajendra W. Available at URL: http://pubs. Semen quality in relation to biomarkers of pesticide exposure.inchem. Fenske RA. Effects of chronic intake of diazinon on blood and brain monoamines and amino acids.S. 2005. Toxicol Lett 2002. Nguyen JV. Barr DB. Bravo R. Oloffs PC. Cocker J. Barr DB. Geological Survey (USGS). Baker SE. Banister EW. EPA). International Programme on Chemical Safety-INCHEM (IPCS). 2006).usgs. In 23 children.114(2):260-263.gov/ oppsrrd1/REDs/diazinon_ired. Study for Future Families Research Group. Dumas P.org/documents/ehc/ehc/ehc198. Atlanta (GA).pdf. Beeson MD.44(11):2243-2250.htm..376(6):808-815. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.S. In a small number of men visiting fertility clinics in Missouri and Minnesota. revised February 15. Drug Chem Toxicol 1986. Garfitt SJ. Interim reregistration eligibility decision (IRED.134(1-3):105-113.S. Third National Report on Human Exposure to Environmental Chemicals. Drobnis EZ. Effect of sublethal levels of diazinon: histopathology of liver. Diazinon. Oloffs PC. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al. Liu F. Barr DB. References Anthony J. Irish R. Swan et al. Pewnim T. Environ Health Perspect 2003. Anal Bioanal Chem 2003. 2006). Barr DB. Jones K. Redmon JB. Environ Health Perspect 2006.epa. 1992-2001. Centers for Disease Control and Prevention (CDC). 1/14/09 U. Banister E. Kruse RL. Toepel K. Environmental Protection Agency (U.

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

S. Lu et al.. Thomas et al... EPA at: http://www. 1999. environmental levels) and health effects is available from ATSDR at: http://www.atsdr. 2005).. Biomonitoring Information Levels of urinary malathion dicarboxylic acid reflect recent exposure. Urinary Malathion dicarboxylic acid (creatinine corrected) Metabolite of Malathion Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.. A study of 13 children from an agricultural region of Washington State reported median levels that were below the detection limit in the NHANES 1999-2000 subsample (Kissel et al. Additional information about external exposure (i. some of the postshift urine levels in duster-applicators were thousandsfold higher than the detection limits in the NHANES 1999-2000 subsample. 1996. 2005.gov/pesticides/. 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. Replacing conventional diets with organic diets in 23 children led to a tenfold decrease in urinary levels of malathion dicarboxylic acid. and it is not considered an animal teratogen or a reproductive toxicant. Malathion itself has not been considered genotoxic (U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Human studies of single oral doses between 0. Fourth National Report on Human Exposure to Environmental Chemicals 147 . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects..html and from U.Organophosphorus Insecticides: Specific Metabolites direct ingestion of agricultural strength solutions.S..gov/toxpro2. Malathion dicarboxylic acid was infrequently detected in multiple samples from 80 Maryland residents in 1995-96 (MacIntosh et al. 2000). CDC.. 2006).cdc. Pluth et al. Giri et al. median urinary levels on the conventional diet were similar to the detection limit in the NHANES 1999-2000 subsample (CDC.EPA. 2006).S. 2003).e. representative subsample from NHANES 19992000 (Adgate.. 2006). but cholinesterase activity was not affected.EPA. The 95th percentile urinary levels of malathion dicarboxylic acid in both urban and nonurban Minnesota children aged 3-13 years (adjusted for sociodemographic variables) in 1997 were several-fold higher than the analytical detection limits reported for children aged 6-11 years in the U. a malaoxon metabolite and a technical grade impurity tested positive in some chromosomal tests (Blasiak et al. 2002. 2001.. Of 382 pregnant women living in an agricultural community.S. but isomalathion. 1993.epa. Survey Geometric mean (95% conf. Toxicity from unprotected bystander exposure during applications is rare (U. Flessel et al.74 (<LOD-5. 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. 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. Finding a measurable amount of malathion dicarboxylic acid in urine does not mean that the level will result in an adverse health effect. IARC considers malathion not classifiable as a human carcinogen. Malathion does not appear to produce human reproductive or teratogenic effects at environmental levels of exposure (Grether et al. 2004).S. 1987. 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. population from the National Health and Nutrition Examination Survey.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.5 and 5.. 1990).0 mg/kg/day have shown no acetylcholinesterase inhibition or other short term effects (IPCS. 2005). 1999).

Malathion (addendum). Mutat Res 1999. Irish R. Clayton CA. Jewell NP. Griffith W.445(2):275-283. and cholinesterase status of date dusters and harvesters in California. Trzeciak A. Arch Environ Contam Toxicol 2000. Gosselin NH.114(2):260-263. Sharma GD. Bouchard M. Lu C. July 2006. Grether JK. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. 4/7/09 Kissel JC. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Pesticides in the Nation’s Streams and Ground Water. Eberly LE. Prasad SB. O’Neill JP. Third National Report on Human Exposure to Environmental Chemicals. U. Available at URL: http://www.109(6):583-590. Toepel K.56(10):2393-2399. March 2006. Lioy PJ. EPA 738-R06-030. Atlanta (GA).132(4):794-795.22(1):7-17. Neutra R. Geological Survey (USGS). Genetic toxicity of malathion: a review. Hertz-Picciotto I. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. Barr DB. Barr DB. 2007 [online].pdf. Kedan G. Rappaport E.org/documents/jmpr/jmpmono/v2003pr06. Goldhaber M. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.S. International Programme on Chemical Safety-INCHEM (IPCS). Cancer Res 1996. Samuel O. Lu C. Krieger RI. Petitti D. Dumoulin MJ. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. htm. Albertini RJ. Harley K. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Barr DB. Dinoff TM.S. Available at URL: http://www. Environ Health Perspect 2006. Blasiak J. Reproductive outcome in women exposed to malathion.gov/oppsrrd1/REDs/ malathion_red. Bradman A. J Expo Anal Environ Epidemiol 2005. Available at URL: http://pubs. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Mutat Res 2002. Centers for Disease Control and Prevention (CDC). Environ Mol Mutagen 1993. et al. Szyfter K. Am J Public Health 1987.15(2):164-171. Eskenazi B.77:1009-1010. Ryan PB.S.112(10):1116-1124.74(2):following table of contents.usgs. Harris JA. revised February 15.inchem. EPA).514(1-2):223231. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. et al. Weltzien E. Toxicol Sci 2003 May.9(5):494-501. Quintana PJ. A longitudinal investigation of selected pesticide metabolites in urine. Environmental Protection Agency (U. Reregistration eligibility decision (RED) Malathion.73(1):182-94. Pluth JM. Barr DB. Curl CL. metabolite clearance. Am J Epidemiol 1990. Erratum in: Toxicol Sci 2003 Aug. Malathion deposition. Needham LL. Swan SH. The Quality of Our Nation’s Waters. Flessel P. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals . 1992-2001. Carrier G. Thomas D. Hooper K. Environ Health Perspect 2004. Nicklas JA. Giri S. Jaloszynski P.38(4):546-553. Brunet RC. MacIntosh DL. 2005. Giri A.gov/circ/2005/1291/. et al.epa. Environ Health Perspect 2001. Fenske RA. 6/1/09 U. Freeman NC. Hammerstrom KA. Bravo R. J Expo Anal Environ Epidemiol 1999.

50 (1.0) 4.50 (1. Fourth National Report on Human Exposure to Environmental Chemicals 149 ..50) 3.60) 1.50 (1.50) 2. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.50) 3.32-1.18-3. and oral routes can occur in pesticide and agricultural workers (Muttray et al.27) 2.71 (2. < LOD means less than the limit of detection.49 (1.50 (1.89 (2.EPA.70 (<LOD-3. pulmonary. all registered uses were voluntarily cancelled (U.46 (3.57-4.60 (4. was once a restricted-use insecticide with limited applications on certain agricultural crops.41-4.80 (1. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. methyl parathion was rapidly absorbed after ingestion. 1977).67) < LOD 1.60-19.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No. 2000). 2007).37-4. Survey Geometric mean (95% conf. Increased risk of exposure via dermal.70-6.0 (3.70-3. Methyl Parathion. but by 2003.860 (<LOD-1.28 (1.61) < LOD 1.80) 2.01) 695 660 518 679 603 941 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.00 (2. In animal studies. Estimated intakes from diet and drinking water have been below recommended limits. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion.32-3.79) 4.70-3.09-1.15-3.33) 2. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. first registered in 1948.02-6.32 (1.33 (1.37) 2.70) 2. and eliminated rapidly from the body after absorption (Kramer et al.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .10) 22.66 (2.71 (3.30 (1.01-4.11-4. Many previous registered agricultural uses of methyl parathion have been cancelled (U.45 (1.37-2.22-3. 2003). which may vary for some chemicals by year and by individual sample.60-5.44) 2. 2002.58) 3.70) 2. and aquatic invertebrates. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .50-9. on cereal grains.10-11.80 (2. and to a lesser extent.0) 3.770 (.74) 5.69) 4.47) 2.50) 1.00 (2.28 (1.21 (2. Both are toxic to birds.40) 2.10 (<LOD-6.910) < LOD .70 (2. Methyl parathion is not registered for residential use in the United States.70-6.60-24. binds tightly to soils resulting in low leachability.50 (2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.8 and 0.30-5.36-1. and of the chemical nitrobenzene..45) 5.16) < LOD 1.0) 3.80 (2.05) 4.90-11.0) 2.910) < LOD < LOD .90 (1. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.70 (3.0) 3.40) 1.69 (2.00) 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 1.92) 5.298-00-0 Ethyl Parathion CAS No.21-1. It had been applied to cotton. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion.92-2.. Methyl parathion use is highly restricted.0) 3.20 (<LOD-2.11) 2.90-9.50 (2.70 (2. fish. In the 1990s. Once absorbed.57) 1.48) 90th 2.1.300-. Morgan et al. population from the National Health and Nutrition Examination Survey.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .EPA. peak domestic use was as high as 5-6 million pounds per year.67 (1.19 (. Given its limited use.37-4.20 (2.30-3.700 (<LOD-. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS. and has a short half-life in soils and on plants.62 (1.10 (3.32-1.S.730 (<LOD-.790 (<LOD-.40-4.850) < LOD . with limited applications in agriculture.70-6.20) 5. ethyl parathion.40 (1.28-4.910) < LOD < LOD < LOD 1.10) 4.10 (3.0) 3.40) 4.85 (2. 2006). more slowly absorbed through the skin.30 (2.61) < LOD 1.91-3.60-36.26 (1.70 (2.70) 2. Ethyl parathion.S.20-5.40-3.34 (3.72 (3.10-1. Methyl parathion has low water solubility.990-1.01) 4.12) < LOD < LOD 1.40-4.S.940 (<LOD-2.13-1. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.30-16.00) 3.50-14.

cdc. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS.980 (. Karanth and Pope et al.39 (1.55) 2.08 (1.96 (1.86 (2.33-6. 1991)..77-7. 2006.84) 3.840 (. ethyl parathion.690-1.83 (1. gov/pesticides/. Jaga and Dharmani.33-3. 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.00 (1.720 (<LOD-.07 (1.880 (.530) < LOD < LOD < LOD . Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.00 (1.97-10.30-1. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion.440 (<LOD-.7) 3.S.57) 6. Additional information about external exposure (i.94-4. 2003.04 (2.2) 2. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene.05) 4.88 (1. and unintentional acute or chronic high-level occupational exposure (Hill et al.96 (1.Organophosphorus Insecticides: Specific Metabolites Metabolites”).48-4. but lists ethyl parathion as a possible human carcinogen.01 (.09) 2.35-3.. cholinergic effects. WHO.23) 1.93 (2.370 (<LOD-.78 (2.67 (3.14-3.20) 3. paranitrophenol.82) < LOD . In addition to being a metabolite of methyl and ethyl parathion. methyl parathion.56-2.20) .atsdr.1) 2.. Methyl parathion is not considered genotoxic.08) < LOD .21) 1.17) .720-1. weakness.70) 3. and other metabolites.400 (<LOD-. environmental levels) and health effects is available from ATSDR at: http://www.44-3.33-3.25) 1.. 1995. 1990.10) 90th 2.S.78) 2.430 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.790-1. 2005.30) 3.01 (2.500) < LOD < LOD .310-. 2004).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 .. vomiting. Methyl Parathion.830-1. At high animal doses of methyl parathion. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.89 (2.970 (.11) 1.26 (1.43) 4. In large doses.25 (2.57-7. IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.11-4.13-12.82 (2.15-10. EPA at: http://www.970 (.87 (1.870) < LOD .850-1. teratogenic. and producing acute symptoms such as nausea.92 (2. Lores et al.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. Orsorio et al.60-2.04) 1.94-47.2) 2. gov/toxpro2.57-2.26) 17.73 (1.88) 1..31) < LOD .03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .61) 4. does not inhibit acetylcholinesterase enzymes.html and from U.EPA considers methyl parathion unlikely to be carcinogenic to humans.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.39) 1. 1995).97 (<LOD-4.91 (1. Survey Geometric mean (95% conf.76-14.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .59 (1. accidental exposure.29) 1. 1978.790-.930 (.950) < LOD .98-7.800-1. Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 150 Fourth National Report on Human Exposure to Environmental Chemicals ..78-2. Slotkin et al.07) 2.60 (1.97 (2.20 (3. Zurich et al. Thus.3) 2.29) 2. The metabolite.4 (3.44-3.680 (<LOD-1.. 2006.00) 2.80 (1.940 (<LOD-1. paralysis. and seizures.71) 1.95) 1.17-4.91) 1. Parathion and methyl parathion have high acute toxicity in animal testing.80 (1. resulting in excess acetylcholine at nerve terminals.71 (1.S.89 (2.15) 3.35-3. 2004).55 (<LOD-3. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.10 (1.21-21.90 (1.01-3.38-3.67-2.79 (1.31-3. population from the National Health and Nutrition Examination Survey.60) 2.540) < LOD .79) 1.730-1.9) 1.13) 4.41-2.72-2.640) < LOD < LOD 1. U.08-3.e.37-1.16-4.epa.78-2.930 (. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.29 (2.

Karanth S. Pharmacokinetics of methyl parathion: a comparison following single intravenous.S. 4/7/09 Jaga K. Head SL. J Biomed Sci 2002. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Bradman A. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.110 Suppl 6:1085-1091. Lin LI. Gregg M. Rockhold RW. Atlanta (GA). Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Chicago area methyl parathion response.215(3):182-190. Barr JR.71:99108. Bailey SL. Pope C. 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. Hetzler HL. Environ Res 1995. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Hryhorczuk DO. Rubin et al. International Programme on Chemical Safety-INCHEM (IPCS).21(1):5767. 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. Lewalter J. CDC. et al. 2002). Griffith W.org/documents/jmpr/jmpmono/v95pr14. 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. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. 2005). DiPietro E.inchem. Kramer RE..14(4):213-216. and levels were similar or slightly lower that those in a small convenience sample of the U. a range of values several hundred times higher than levels found in the U. Hill RH Jr. et al. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Clark JM. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1999). et al.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Kissel JC. 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. McClure PC. Head SL. Hill et al. 2002. Leng G. Baker S.56(7):449553. Weltzien E. Jewell NP. 2005. Cline RE. Pesticide residues in urine of adults living in the United States: reference range concentrations. J Expo Anal Environ Epidemiol 2005. Ashley DL. Environ Health Perspect 2004.htm. Lu C. Giordano G. and many residents were symptomatic (Barr et al. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter.9:311-320. Morgan DP. References Barr DB. Neurotoxicol Teratol 2003. Pesticide workers may have much higher levels following pesticide applications. 1995). Kedan G..5 mg (500 µg)/g creatinine for workers at the end of shift. Guizzetti M. Turner WE. Baker RC. population (Olsson et al. Alley CC. Needham LL. general population (CDC. Costa LG. Barr DB.6(2-3):159-173. McCann et al. Hill RH Jr.33(5):270-276. 1995. Wellman SE. Lores EM. Eskenazi B. J Anal Toxicol 1990. 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. Centers for Disease Control and Prevention (CDC). Available at URL: http:// www..25(5):599-606. Methyl parathion: an organophosphate insecticide not quite forgotten. Harley K. Parathion-Methyl (addendum). Bradway DE. Curl CL. Environ Health Perspect 2002. 2005. Dharmani C. Moomey CM.. Environ Health Perspect 2002. Arch Environ Health 1978. Rev Environ Health 2006.. et al. 2005). Arch Environ Contam Toxicol 1977. Occup Environ Med 1999. Barr DB. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine. Pathak S. Barr DB. McCann KG. Slach EF. Role of individual susceptibility in risk assessment of pesticides.110 Suppl 6:1075-1078. Laboratory investigation of a poisoning epidemic in Sierra Leone.15(2):164-171. Runkle KD. Shealy DB. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. 2005..112(10):1116-1124. Baker SE. Third National Report on Human Exposure to Environmental Chemicals. 2004). Toxicology 2005. Moseman RF. ACGIH recommends a BEI of 0. et al.S. In a study of workers who handle parathion. oral or dermal administration. 2002..

epa. Available at URL: http://www. 1/12/07 U.20(4):533-546. 5/19/09 Zurich MG.162(2-3):219-224. Anal Bioanal Chem 2003.S. Toxicol Lett 2006. EPA).gov/circ/2005/1291/. Honegger P. Ethyl parathion. Seidler FJ. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County. Case No. Olsson AO. Nguyen JV. Jung D. Backer G.S. Osorio AM. Geological Survey (USGS). Environ Health Perspect 2006.04/106. revised February 15. Investigation of a fatality among parathion applicators in California.pdf. Ryde IT. Methyl parathion in drinking water. Hill RH Jr.110 Suppl 6:1047-1051.S.gov/oppsrrd1/REDs/factsheets/0155fct. 6/1/09 World Health Organization (WHO). March 2006.pdf.114(10):1542-1546. May 2003. 1992-2001. Rosenberg J. U. Pesticides in the Nation’s Streams and Ground Water. Schilter B. September 2000. Facts.Organophosphorus Insecticides: Specific Metabolites Muttray A. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Kieszak S. Environ Health Perspect 2002. Slotkin TA. Dunlop B. Levin ED.int/water_sanitation_health/dwq/chemicals/ methylparathion. 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.epa. Sadowski MA. gov/oppsrrd1/REDs/methylparathion_ired. Costa LG. Ames RG. Ohio.usgs. Barr DB. EPA-738-FOO-009. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. 1995-1996. pdf. 0153. 2007 [online]. Environmental Protection Agency (U. WHO/SDE/WSH/03.D. The Quality of Our Nation’s Waters. Available at URL: http://pubs.376(6):808-815. Environmental Protection Agency (U.201(2):97-104. Tate CA. EPA). Esteban E. 152 Fourth National Report on Human Exposure to Environmental Chemicals . Toxicol Appl Pharmacol 2004. Mengle DC. et al. Yacovac R. Letzel S. Monnet-Tschudi F.who. 2004. Available at URL: http://www. Interim reregistration eligibility decision (IRED) for Methyl Parathion.S.E. Am J Ind Med 1991. 1/14/09 U. Hill G. Available at URL: http://www. R.S. Rubin C. External and internal exposure of wine growers spraying methyl parathion.

subsample of NHANES 2001-2002. At high doses. Metabolic hydrolysis leads to the formation of 2-(diethylamino)-6methylpyrimidin-4-ol/one. It easily hydrolyzes in the environment to 2-(diethylamino)-6-methylpyrimidine and other breakdown products.47 μg/L for the total population (CDC. Olsson et al. and producing acute symptoms such as nausea. Pirimiphos-methyl is not considered mutagenic. Toxic effects below doses that cause inhibition of acetylcholinesterase are unknown. weevils. 1992). and seizures. 2006). and other metabolites. In addition to being a human metabolite of pirimiphos-methyl in the body. phosphorothioates such as pirimiphos-methyl are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.S. most of the urinary measurements of 2-(diethylamino)-6-methylpyrimidin-4-ol/one were below the limit of detection. cholinergic effects. which are mainly excreted in the urine (IPCS. which has limited applications for control of beetles.S. It has a lesser use as a cattle ear tag application to control flies. fish. Pirimiphos-methyl is not registered for residential use in the United States. the detection of 2-(diethylamino)-6-methylpyrimidin-4-ol/one may also reflect exposure to the environmental degradate. Biomonitoring Information Urinary levels of 2-(diethylamino)-6-methylpyrimidin-4ol/one reflect recent exposure. Pirimiphosmethyl has low acute toxicity in animal studies. In animal studies. EPA at: http://www. Thus. resulting in excess acetylcholine at nerve terminals. 2003). or known to cause delayed neurotoxicity. vomiting. The metabolite 2-(diethylamino)-6-methylpyrimidin-4-ol/one does not inhibit acetylcholinesterase enzymes.S.epa. sorghum. or reproductive toxicity (IPCS. 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. U. pirimiphos-methyl is rapidly absorbed and metabolized to 12 metabolites. 1992.S. and it is not considered persistent. In the U. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). pirimiphos-methyl and other organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. Though considered moderately-to-highly toxic in birds.EPA.gov/pesticides/. weakness. Finding a measurable amount of 2-(diethylamino)-6methylpyrimidin-4-ol/one in urine does not mean that the level will result in an adverse health effect. Biomonitoring studies of 2-(diethylamino)-6-methylpyrimidin-4-ol/ one provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of pirimiphos-methyl than are found in the general population. 2006). teratogenic.Organophosphorus Insecticides: Specific Metabolites Pirimiphos-methyl CAS No. although the 95th percentile was characterized at 0. In the general population. In a nonrandom sample of 140 urine specimens obtained from adults and children in the United States. 29232-93-7 General Information The chemical 2-(diethylamino)-6-methylpyrimidin-4-ol/ one is a metabolite of the organophosphorus insecticide pirimiphos-methyl. Estimated intakes from diet and water have not exceeded recommended intake limits (U. Once absorbed. paralysis. and moths on stored grain products such as corn. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.EPA. (2003) detected 2-(diethylamino)6-methylpyrimidin-4-ol/one in 7.1% of the sampled population. and seed. Fourth National Report on Human Exposure to Environmental Chemicals 153 . and aquatic invertebrates. occurrence of such toxicity is mitigated by its rapid degradation and its use in closed storage systems. 2-(diethylamino)-6-methylpyrimidin-4-ol/one can also occur in the environment. 2005). Additional information about pesticides is available from U.

610 (<LOD-1.200-.770) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .820) < LOD < LOD .670 (<LOD-1.07) .210-.500 (.950) < LOD < LOD 1.680 (<LOD-. which may vary for some chemicals by year and by individual sample.27) .250 (<LOD-.840) 669 687 929 Limit of detection (LOD.700-.17 (.670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .55) .210-1.840 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.15) < LOD .740-1.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.21) < LOD .31) .94) . interval) Selected percentiles ( 95% confidence interval) Sample 95th .760 (<LOD-.00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .210 (<LOD-.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .700-1. see Data Analysis section) for Survey year 01-02 is 0. 154 Fourth National Report on Human Exposure to Environmental Chemicals . interval) Selected percentiles ( 95% confidence interval) Sample 95th .780 (<LOD-1.580-1. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .2.64) .850 (.780 (<LOD-1. Survey Geometric mean (95% conf.780 (.410 (<LOD-1.S.470 (.430 (<LOD-.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 . population from the National Health and Nutrition Examination Survey. population from the National Health and Nutrition Examination Survey. Urinary 2-(Diethylamino)-6-methylpyrimidin-4-ol/one (creatinine corrected) Metabolite of Pirimiphos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.740 (.780 (.300-1.

2535.inchem. Available at URL: http://www. 4/7/09 International Programme on Chemical Safety-INCHEM (IPCS).gov/~acrobat/tds1byps. Anal Bioanal Chem 2003.epa.fda. Available at URL: http://www. Atlanta (GA). Third National Report on Human Exposure to Environmental Chemicals. cfsan. EPA).S. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. gov/oppsrrd1/REDs/pirimiphos-methyl_ired. Nguyen JV. 2005. 1/14/09 Fourth National Report on Human Exposure to Environmental Chemicals 155 .htm. org/documents/jmpr/jmpmono/v92pr16. Pirimiphos-methyl.pdf. Food and Drug Administration (FDA). Available at URL: http://www. Pesticides residues in food: 1992 evaluations Part II Toxicology. Sadowski MA.pdf. Case No. Environmental Protection Agency (U. Finalization of interim registration eligibility decision for pirimiphos-methyl.S. July 2006. U. 850. Total Diet Study: Summary of Residues Found Ordered by Pesticide. Market Baskets 91-3-01-4. June 2003.376(6):808-815.Organophosphorus Insecticides: Specific Metabolites References Centers for Disease Control and Prevention (CDC). 4/7/09 Olsson AO. Barr DB.

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

choreoathetosis. cdc. Garey J. Kim et al. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley... Regul Toxicol Pharmacol 2002. Generally. 2002). In California... Elwan MA. 2006. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. 2005). Lewalter J. Bernardi MM. and seizures (ATSDR. EPA at: http://www. Moniz AC. dopaminergic. Sunami O. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002. et al. Leng G. Toxicol Appl Pharmacol 1991. J Reprod Dev 2004. Bernardi MM. 2003. Wieseler B.1/15/09 Aziz MH. 2005). et al. Kunimatsu T. 2001. Xenobiotica 1997.211(3):188-197. McCarthy AR. Leng A. epa. Spinosa HS. bioallethrin and deltamethrin. WHO. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Effects of prenatal exposure to deltamethrin on forced swimming behavior. neurochemical changes in cholinergic. Elwan et al. and permethrin) in the Hershberger and uterotrophic assays. Ose K. 2005). Florio JC. 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. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Garey J.8(1):18-21. Okuno Y.35(2 Pt 1):227-237.62:101-108. Biochem Biophys Res Commun 1998. Leng G. Miller GW. Go V. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Cruz-Casallas PE. salivation. 2002.. References Agency for Toxic Substances and Disease Registry (ATSDR). though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. Eriksson and Fredriksson. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats.gov/toxprofiles/ tp155. Abell AD. Shukla Y. 2004. Yamada T. motor activity. Shafer.html. Kunimatsu et al. Neurotoxicol Teratol 2005. Richardson JR.300(3):161-165.. 2003.205(6):459-472. Lee SJ. Shin JH. 2002). Moniz et al. Chen JH. Additional information about pesticides is available from U. 1991. Yang J. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. Neurotoxic effects of two different pyrethroids. Kuhn K.. Berger-Preiss E. Lazarini et al. 2003. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. Fredriksson A. Wolff MS. Zhao RC. Song L. J Environ Monit 2006. hypersensitivity. Kim HS. Idel H. Idel H. 2006. Pauluhn J. 2003. et al. 2000. tremor.23(6):665-673. Leng G.cdc. Environ Health Perspect 1999. Fourth National Report on Human Exposure to Environmental Chemicals 157 .html. 1999. Kuhn KH. Seth PK.27(12):1273-1283. Int J Hyg Environ Health 2002. and striatal dopamine levels in male and female rats..8(1):197-202. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Thomson BM. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. Neurosci Lett 2001. Pogo BG. McCarthy et al. Soderlund et al. Go et al. Pyrethroid pesticide-induced alterations in dopamine transporter function. Kim TS. Estrogenic and antiprogestagenic activities of pyrethroid insecticides. Caudle WM. Salzgeber SA. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Toxicol Appl Pharmacol 2006.gov/toxpro2. Kim IY. In developing rodents.. Kamita Y. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Varoli FM. fenvalerate. 2006).108(1):78-85. Wang SL.107(3):173-177. Eriksson P. Ranft U. Toxicological profile for pyrethrins and pyrethroids. Hu et al. 2005). Ray et al.50(2):245-255...Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. Garey and Wolff. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. 1998. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. Levsen K.gov/pesticides/ and from ATSDR at: http://www. Available from URL: http://www.atsdr. et al. Adhami VM.S.. Agrawal AK. Hu JY.atsdr. Sugiri D. Lemonica IP.251(3):855-859. Estrogenicity of pyrethroid insecticide metabolites. Lazarini CA. 2001. Shaw IC. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Neurotoxicol Teratol 2001. Bull Environ Contam Toxicol 1999. Guillot TS. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Kang IH.. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Wolff MS. September 2003.27(4):609-614.

synergies.gov/pesticides/ health/mosquitoes/pyrethroids4mosquitoes. Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs. O’Malley M. 19962002. pdf. Available at URL: http://pubs. 5/26/09 Woollen BH. Safety of pyrethroids for public health use. resmethrin. Available at URL: http://www. June 2006a.usgs. Xenobiotica 1992.epa. Mullin LS. Pyrethroid insecticides: poisoning syndromes.htm. Marsh JR. Environmental Protection Agency (U. Sargent D. sumithrin synthetic pyrethroids for mosquito control.171:3-59. EPA). 5/26/09 U. Revised February 25. June 2006b. Spencer J. Available at URL: http://whqlibdoc. Lesser JE. Pesticide and Evaluation Scheme. Environmental Protection Agency (U. Mechanisms of pyrethroid neurotoxicity: implications for cumulative risk assessment.10. U. 5/26/09 U. EPA).S. March 2006. 5/26/09 158 Fourth National Report on Human Exposure to Environmental Chemicals . J Toxicol Clin Toxicol 2000.gov/ circ/2005/1291/.S. Available at URL: http://www.htm. 2007.epa. Soderlund DM.Pyrethroid Pesticides Ray DE. Shafer TJ.S.gov/oppsrrd1/REDs/ factsheets/permethrin_fs.113(2):123-136. Forshaw PJ.epa. Rev Environ Contam Toxicol 2006. EPA).pdf. Sheets LP. 2005.22(8):983-991. Pesticides in the Nation’s Streams and Ground Water. Pyrethroid illnesses in California. April 2002. Permethrin. World Health Organization (WHO). Toxicology 2002.int/hq/2005/WHO_ CDS_WHOPES_GCDPP_2005. Piccirillo VJ. Environ Health Perspect 2005.S. 1992–2001. Crofton KM. et al.38:95-101.S. Laird WJ.S. Permethrin Facts (Reregistration Eligibility Decision Fact Sheet). 5/26/09 U. Environmental Protection Agency (U. Meyer DA.S. Geological Survey (USGS). and therapy. Available at URL: http://www.who.gov/oppsrrd1/REDs/cypermethrin_red. The metabolism of cypermethrin in man: differences in urinary metabolite profiles following oral and dermal administration.186:57-72. Clark JM. Reregistration Eligibility Decision for Cypermethrin.

Following an indoor application exposure.2 μg/L) in the U. In an analysis of 217 urine specimens from a nonrandom sample of United States residents. most of which were dermal and respiratory irritations (Spencer and O’Malley. 2001. 2004). Seven individuals participating in floor exercises on cyfluthrin treated carpet demonstrated a rise in the urinary excretion of 4-fluoro-3-phenoxybenzoic acid in the 72 hours following the activity (Williams et al.. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. Cyfluthrin is rapidly metabolized and eliminated from the body.95 µg/L.. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. representative subsample in NHANES 2001-2002 (CDC. 2006). Fourth National Report on Human Exposure to Environmental Chemicals 159 . but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment.. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. 2001) showed that urinary levels of 4-fluoro-3-phenoxybenzoic acid at the 95th percentile ranged from either slightly higher or lower than the detection limit in the U.S. 2005. 2005). Thus. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0. 2005). (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0.68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin. 2003). Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). Leng et al... Finding a measurable amount of 4-fluoro-3-phenoxybenzoic acid in urine does not mean that the level will result in an adverse health effect. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. Studies in Germany of 396 children and adolescents (Becker et al.Pyrethroid Pesticides Cyfluthrin CAS No..S. Urinary levels for adults and children in these studies were similar (Heudorf et al. 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. Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate. 2003). Baker et al.. 2003). 2006) and 1177 urban adults and children (Heudorf et al. representative 2001-2002 NHANES subsample (CDC.

see Data Analysis section) for Survey years 99-00 and 01-02 are 0.Pyrethroid Pesticides Urinary 4-Fluoro-3-phenoxybenzoic acid Metabolite of Cyfluthrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1949 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 473 580 662 831 814 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 950 1193 999 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 666 680 517 701 594 957 Limit of detection (LOD.2. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. 160 Fourth National Report on Human Exposure to Environmental Chemicals .2 and 0. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

Krieger RI. Arch Environ Contam Toxicol 2004. Hoppe HW. Sugiri D. 2005. Ranft U. Rev Environ Contam Toxicol 2006. Hadnagy W. Environ Health Perspect 2001. Williams RL.46(3):281-288.209(3):293-299. Centers for Disease Control and Prevention (CDC). Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.186:57-72. Int Arch Occup Environ Health 2004. Heudorf U. Berger-Preiss E. Atlanta (GA).77(1):67-72. Heudorf U.209(3):221-233. O’Malley M. Heudorf U. Third National Report on Human Exposure to Environmental Chemicals. Angerer J. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Becker K.109(3):213-217. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. 162 Fourth National Report on Human Exposure to Environmental Chemicals . Bernard CE. Int J Hyg Environ Health 2006. Barr DB. 19962002. J Expo Anal Environ Epidemiol 2003. Int J Hyg Environ Health 2006. Seiwert M. Leng G. Kolossa-Gehring M.13(2):112-119.Pyrethroid Pesticides References Baker SE. Angerer J. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Idel H. Butte W. Angerer J. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Pyrethroid illnesses in California. Drexler H. Schulz C. Angerer J. et al. Olsson AO.206(2):85-92. Ball M. Spencer J. Int J Hyg Environ Health 2003.

54) .400-.890 (.200-. cis-cypermethrin.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.740 (.160 (<LOD-.1.07 (.510 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.155-.200-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.110-.530 (.240) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.210) 90th .110-.230) . cis-permethrin.490-.790 (.580) 1.300 (.and trans-isomers.180) .160 (.380-.270-.670-1.630-.330) .210-.2-Dichlorovinyl)-2.250 (. and trans-cyfluthrin.410) .490-1.28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . the presence of trans-3-(2.15) .47 (.510 (.330 (.600 (. Kuhn et al. Cyfluthrin. but it can also reflect exposure to cis-3-(2. 1999).670 (.260 (.850 (. 52315-07-8 CAS No.740-2. The presence of cis-3-(2.500 (. trans-cypermethrin. population from the National Health and Nutrition Examination Survey.2-dichlorovinyl)-2.200-..420-.32) .470 (.500 (.2-dichlorovinyl)-2.50) .780) .350) .380-.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.900 (.220-.630 (. < LOD means less than the limit of detection.460 (.790-1.690) .640 (.770) . Survey Geometric mean (95% conf. ciscypermethrin and cis-cyfluthrin.920) 1..570 (.300-. which may vary for some chemicals by year and by individual sample.410) .710) .35) .68 (.80) .68) .340-. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.220-.2-dichlorovinyl)- CAS No.150 (.340) .670-1.13 (.53) .120-.380) .730 (.21) .68359-37-5 Cypermethrin Permethrin CAS No.160 (.280 (.430-.680 (.2dichlorovinyl)-2.77 (.340) .44 (.730 (. The chemical trans-3(2.11) .240) .140 (<LOD-.08) .460-.490-.440 (.120-.370 (.510 (.200) < LOD < LOD < LOD .180 (.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.960 (.220-.310) . transcypermethrin and trans-cyfluthrin.300-.110-.120-.680-3.24) 1.28) 671 680 518 701 591 957 Limit of detection (LOD.880 (.740) 1. Fourth National Report on Human Exposure to Environmental Chemicals 163 .270 (.710-1.220) .S.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .12 (.280-.820 (.2-dichlorovinyl)2.380 (.740-1.2-dichlorovinyl)-2.890 (.730 (.520) .43) .550) .2dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.700) . and ciscyfluthrin. Similarly.200 (. Generally. 1985. 1999).250-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.68) .220-.630) .170 (.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .380-. Biomonitoring Information Urinary levels of cis.650-1.200) .210) .950-2. but can also reflect exposure to trans-3(2.270 (.110 (<LOD-.140 (.200) .202 (.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 .460-1.370-.610) .120-. more of the trans-metabolite than Urinary cis-3-(2.790-1. In the body.600) .790) . 1985.870) 1.670-2.270 (.910-5.770-1.262) * * * < LOD < LOD .300 (. Kuhn et al. cis-3-(2.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.600-1.490-1.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.35) 1.or trans-3-(2.570-.470-1.610) . trans-permethrin.580-1.1 and 0.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.630) .

In these volunteers.450-.2-dichlorovinyl)-2.430 (.640-. urinary levels of cis-3-(2. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.320-.540) ..190 (. population from the National Health and Nutrition Examination Survey.710 (. 2002).220) .170 (. In the same residents.03) 1..350) .138 (.550-1.690-1..390 (.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.430-1.430-.540 (.640-1.150-.550 (.120 (.640-1.550-1.400 (.750-1.290 (.640 (. 2006.S.. 2001. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. representative NHANES 2001-2002 subsample (CDC.320) .11) .270-. 2006) and 1177 urban adults and children (Heudorf et al.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.33) .2-dichlorovinyl)-2.340) .440-.250 (<LOD-.24) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.470-1.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . Studies in Germany of 396 children and adolescents (Becker et al. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.250) 90th .190) .2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.250-.31) .11) 1.150-.230-.880) .160 (<LOD-. 2003).590) .260 (. Other studies have provided evidence that urinary levels of cis.780 (.270) .290-. 2005).700-2.390-.440-. the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.340-.280-.12-2. 2001) showed urinary levels of cis. 164 Fourth National Report on Human Exposure to Environmental Chemicals ..11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .49) . 2005). the median and 95th percentile of urinary levels of cis-3-(2.300) .67 (.2-dichlorovinyl)-2.250) ..370-.680-1. median urinary levels of trans-3-(2.340) .200 (.440 (.550) .180 (.700) .580) .280 (.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.170 (.250-. In a study of urban residents in Germany (Berger-Preiss et al.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.570) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-.2-dimethylcyclopropane carboxylic acid did not increase.260 (.S. 2005). 2006).08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .59) .380 (.182) * * * < LOD < LOD .130-.240 (<LOD-.400-1.180-. urinary trans-3-(2.560) .260-.12 (.890) . Lu et al.and trans-3(2.2dichlorovinyl)-2.and trans-3-(2.11 (.59) .900 (. Survey Geometric mean (95% conf.220 (.540 (.230-.104-.510-1.2dichlorovinyl)-2.230-.270 (.890 (.800 (.370-.840 (. 2005) In a small group of indoor pest-control operators.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates.2-dichlorovinyl)-2.420 (..21) .Pyrethroid Pesticides 2. Cyfluthrin.250) .260) .750 (.59 (1.300) .140-.2-Dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.500 (.230 (. Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.550) .370-. 2004.350 (. Schettgen et al.360-1.600 (.200-.450 (.410) .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 .2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al..37) .710-3.200-.380-.380) .830) .700) .210-. 2004).840 (. 2006).530 (.590 (.80) .29 (.450-1.810 (. 2002). post- Urinary cis-3-(2.11) . 2005).390-.780) 1. 2003).290) .680 (.530 (. In a study of volunteers.270) .560) 1.250-..680-1.300 (.260 (.920 (.33 (.640) 1.150-.220 (.080-.580-1.290) . 2006.67) .190) .200) .170) < LOD < LOD < LOD .440 (..300 (.

91 (1.89 (2.10) 2.20 (.750) .41 (1.520-.25 (1.23) 2.56 (1.920-1.28 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.49-3.56) 2.63) 1.780 (. < LOD means less than the limit of detection.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .490 (<LOD-.60-4.860) .4.940 (.63) 1.22 (1.90) 1.64-4.23 (. 2005). and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.84 (1.54 (1.2-dichlorovinyl)-2.970 (.840-1.14-2.03-1.68) 1.710 (.12-6.410-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.19) 1.820) .85) 4.37 (1.55-5.55-3.460-.530) .810-1.60) 1.95) 2.66) .14) 1.19 (2.420 (<LOD-.17 (.550 (.400 (<LOD-.13) .910-1.410-.69 (1.2dichlorovinyl)-2. which may vary for some chemicals by year and by individual sample.62 (1.16) 1.520) .560 (.76-4.S.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.94 (1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .43) 2.20 (. Urinary trans-3-(2.500-.440 (<LOD-.and trans-3-(2.2-dichlorovinyl)-2.670) .68) 2.49-5.41-14.400-.620) < LOD 2.76-3. however. Biomonitoring studies on urinary levels of cisor trans-3-(2.48) 4. 2005).55-4.95) 3.11-2.14-6.2-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.28 (2.81) 2.20 (.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.7) 2.69) 1.25-3.49-3.42 (2.660) 1.59 (1.or trans-3-(2.07-3.07 (1.01 (1. Survey Geometric mean (95% conf.35) 1.800-1.68-2.50 (1.560 (.08) 1.68-3.11-1.830-1.560 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.97-11. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC.4 and 0.680-1.470 (<LOD-.580 (.850-1.490-1.09 (. The maximum post-application urinary levels.77) 1.08-6. trans-Cypermethrin.19 (3.77) 2.01) 4.66) 691 680 518 690 595 954 Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 165 .910-1.60) .54) 4.40 (1.56 (1.42) 1.2-Dichlorovinyl)-2.700-1.27 (1. Finding a measurable amount of cis.Pyrethroid Pesticides application median urinary levels of summed cis. population from the National Health and Nutrition Examination Survey.470 (.460-.670) .77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .5) 2.610) 1. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.760) .410 (<LOD-.56) 2.500 (.480-.03-1.17 (.700) .410 (<LOD-.730) .500) .26 (.68) 1.70) size 1976 2525 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD 75th .08-4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.77 (1.87 (1.39-5.570) 90th 1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.17-1.39 (1.

33-2.42) 1.47 (1.80) 1.36 (1.970 (. population from the National Health and Nutrition Examination Survey.40-2.770) < LOD 2.15-3.580) .15) 3.640) .530 (<LOD-.31 (2.700-.74) 2.16 (1.37 (1.56-2.98 (1.410-.800-1.87 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.800-1.00) 1.10) 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 .45-2.61) 1.570-.480-.57 (1.28) 2.81 (2.720 (<LOD-.850-3.520 (<LOD-.11) .33 (1.36) 2.26 (1.11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .13) 1.610-.500-.31 (.440-.540) .900 (<LOD-1.730) .60) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.530 (.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . 166 Fourth National Report on Human Exposure to Environmental Chemicals .30-3.60) 2.89) 2.22) 1.13) .31) 1.15-3.570 (.35 (1.08 (.27-2.660) .87-3.27-2.07) 2.22-2.57) 3.07-3.87-8.780 (<LOD-.07-2.760 (. Survey Geometric mean (95% conf.02-1.86 (2.44) 2.64 (1.880 (<LOD-1.39) 1.47-2.87) 1.08 (.29) 1.700 (.91-11.19) .12 (.70 (.41) 1.Pyrethroid Pesticides Urinary trans-3-(2.91) 1.880 (.91 (1.68) 3.55 (2. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.67 (2.34-3.39 (1.880-1. trans-Cypermethrin.00 (1.780) .850) .780) 90th 1.48-2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.560 (.720-1.60 (1.65 (2.00) 1.3) 2.22-1.00) 5.930-1.12-1.20 (1.42 (.720-1.15-3.75 (1.74) .34-4.2-Dichlorovinyl)-2.470-.570 (<LOD-.580 (.65) 1.740) .87) 1.15) 2.56-5.15 (1.19 (1.30-6.07) 2.47-2.56 (1.850) 1.45 (1.35) 1.700 (.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.S.670) .48 (1.00-5.33-1.750) .20-2.55 (2.470 (.55 (2.820-2.07-1.

Permethrin and its two metabolite residues in seven agricultural crops. Hadnagy W. Schulz C. Seiwert M. Leng G. Bravo R. George DA. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Butte W. Sugiri D. Atlanta (GA). Angerer J. J AOAC 1985. Leng G. Levsen K. 2005. Barr DB.76(7):492-498.209(3):221-233. Drexler H. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring.206(2):85-92. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Berger-Preiss E. Heudorf U. Int J Hyg Environ Health 2003. Int Arch Occup Environ Health 2004. et al. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Idel H. Ranft U. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Schettgen T. Angerer J.109(3):213-217. Heudorf U. Ranft U.62:101-108. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Int Arch Occup Environ Health 2003.77(1):67-72. Kuhn K. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Int J Hyg Environ Health 2002. Environ Health Perspect 2001. Drexler H.209(3):293-299. Angerer J. Environ Health Perspect 2006. Hoppe HW. Centers for Disease Control and Prevention (CDC). Kolossa-Gehring M. Bull Environ Contam Toxicol 1999. Int J Hyg Environ Health 2006. Biological monitoring of workers after the application of insecticidal pyrethroids.68(6):1160-1163.134(1-3):141-145. Pearson M. Lu C. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Angerer J. Idel H.114(9):14191423. Heudorf U.205(6):459-472. Heudorf U. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Angerer J. Hardt J. Int J Hyg Environ Health 2006. Wieseler B. Ball M. Leng G. Angerer J. Sugiri D.Pyrethroid Pesticides References Becker K. Third National Report on Human Exposure to Environmental Chemicals. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Idel H. Berger-Preiss E. Bartell S.

in some situations replacing the use of DDT.. 2006) and 1177 urban adults and children (Heudorf et al.2-dibromovinyl)-2.2-dibromovinyl)-2.2-dibromovinyl)-2. 2005).2-dibromovinyl)-2. 52918-63-5 General Information Cis-3-(2.2-dibromovinyl)2. 168 Fourth National Report on Human Exposure to Environmental Chemicals . The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample. in detection of cis-3-(2. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. 1990).5 μg/L) than the detection limit (0. 2001) showed that urinary levels of cis-3-(2. mean peak urinary levels of cis-3-(2. Biomonitoring studies provide physicians and public health officials with reference values so that they can determine whether other people have been exposed to higher levels of deltamethrin than levels found in the general population. Following residential spraying with deltamethrin for malaria protection in Mexico. urinary levels of cis-3-(2. (2004) reported a geometric mean concentration of cis-3(2. Finding a measurable amount of cis-3-(2. Thus. Outside the U..Pyrethroid Pesticides Deltamethrin CAS No.. In an analysis of 217 urine specimens from a nonrandom sample of United States residents..1 μg/L) for the NHANES 2001-2002 subsample (CDC.2-dibromovinyl)-2.2-dibromovinyl)-2. 2001. 2005)..2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin. Biomonitoring Information Urinary levels of cis-3-(2. 2005). deltamethrin has been used against mosquitoes that carry malaria. Deltamethrin can degrade to cis-3(2.2dimethylcyclopropane carboxylic acid formed in the environment.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. Urinary levels for adults and children in these studies were similar (Heudorf et al.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid of 0.3-0.39 µg/L.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. Baker et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.2-dibromovinyl)-2. In the NHANES 2001-2002 subsample.2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in the environment (IPCS.. Studies in Germany of 396 children and adolescents (Becker et al.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.S. 2004).2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.

see Data Analysis section) for Survey years 99-00 and 01-02 are 0.2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD. Survey Geometric mean (95% conf. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 169 . < LOD means less than the limit of detection.2-Dibromovinyl)-2.1 and 0.1. * 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.S.Pyrethroid Pesticides Urinary cis-3-(2.

2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 170 Fourth National Report on Human Exposure to Environmental Chemicals . 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.Pyrethroid Pesticides Urinary cis-3-(2. population from the National Health and Nutrition Examination Survey.2-Dibromovinyl)-2.

Heudorf U. Torres-Dosal A. Batres LE. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Fourth National Report on Human Exposure to Environmental Chemicals 171 .inchem. Angerer J. Seiwert M. Available at URL: http://www. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Deltamethrin. toxicokinetics. Heudorf U. 5/26/09 Ortiz-Perez MD. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. [online] 1990.109(3):213-217. et al. Ball M. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Carranza C. Heudorf U. Atlanta (GA). 2005. International Programme On Chemical Safety (IPCS). Grimaldo M.113(6):782-786.org/documents/ehc/ehc/ ehc97. Lopez-Guzman OD. Int J Hyg Environ Health 2006.Pyrethroid Pesticides References Becker K. Hoppe HW.209(3):221-233. et al. Kolossa-Gehring M. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. and genotoxicity in exposed children. Int J Hyg Environ Health 2006. Centers for Disease Control and Prevention (CDC). Environ Health Perspect 2001. Environmental Health Criteria 97. Int Arch Occup Environ Health 2004. Angerer J. Schulz C.209(3):293-299. Angerer J. Third National Report on Human Exposure to Environmental Chemicals. Butte W. Angerer J.77(1):67-72.htm. Drexler H. Environ Health Perspect 2005.

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

670 (.35 (2.200-.48-2.384) .81 (1.33 (1.230-.38 (2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.52-4.05) 1.45-5.260 (.32 (1.417 (.04-5.30) 3.78) 6.34 (2.570-.02-6.510-.311 (.292-.49 (1.41) 3.960 (.49-2.51-6.700 (.86 (1.27-11.730 (.353 (.340) 75th .65 (1.320) .266-.315 (.320) .325 (.210-.295) .42-2.470-.69 (1.32 (2.290 (.710 (.780) 4. Deltamethrin.740 (.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .38 (2.280 (.41-2.454 (.62-8.740 (.21 (2.267 (.300 (.362) .25 (2.530-.820) .600 (.90) 1.360) .72 (1.230 (.800) 1.610) .35) 2.65-2.73) 1.710 (.49-2.650 (.190-.S.12 (.34) 8.800 (.51-3.226-.440) .352-.220-.590-.530-.78 (1.300 (.320) .990) .23 (2.260 (.29-1.560-.340) . population from the National Health and Nutrition Examination Survey.92-3.30 (.41 (1.200-.50 (2.640 (.05) .14-6.240 (. Survey Geometric mean (95% conf.53-3.247-.180-.233-.355) .330) .28) 1.76 (1.364) .300 (.390) .760 (.276-.850) .750) .63-3.250 (.297 (.32-21.277-.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 .210-.53) 1.270) .62-6.369) .Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.253-.69) 3.63 (3.490) .75 (1.373) .830) 90th 1.428-.680 (.12) 4.430-.04) .33 (2.560-1.387) .507 (.41-3.18 (2.246-.260-.450 (.230-.16-1.230-.250-.25 (2.26) 2.430-. interval) .630) .35 (1.30 (1.12) .370) .8) 3.160-.427) .260 (.35) 1.273 (.490-.240 (.1) 3.46) .55 (1.49 (1.560-.350-.374) 99-00 01-02 99-00 01-02 99-00 01-02 .271-.25-4.71 (1.26) 2.298 (.840-1.406) .78) 1.292 (.33) .300) .270 (.78) 1.820) .26-2.700-1.601) .03 (3.160-.89-71.336 (.340) 1.25-7.570-1.550-.590 (.520 (.64) 697 680 524 701 603 957 Limit of detection (LOD.27-2.330) .320 (.265-.434) .18 (1.79) 3.34-6.810) 1.227-.45 (2.420) .940) 1.39) 2.13) .288-.750) .1) 3.27-2.48-2.190-.328 (.60) .13 (.44) 5.83-11.250 (.16) 1.1. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.93 (1.36) 1.25-1. Fourth National Report on Human Exposure to Environmental Chemicals 173 .46) 2.238-.62) 5.595) .750-1.35) 2.1 and 0.321 (.01 (1.43) 3.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.54) 1.190-.320) .620-1.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .1) 3.200-.56-5.314) .190-.52-5.586) .830-2.870 (.250 (.314 (.288 (.230 (.850) .510-.

39) 1.216-.37 (1.240 (.02 (2.750-1.530-.440-.677) .437) .13 (.378 (.84 (1.580 (.300-.357) .330) .11 (.390-.60-4.440-.278) .55) 3.460-.72 (1.630) .490 (.230) .200-.41-4.730) .43 (2.280) .13-1.43) 1.88-5.270 (.229-.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 .460-.365) 99-00 01-02 99-00 01-02 99-00 01-02 .320) .234 (.190-.83) 1.49-2.272) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.670) .240-.400) .10 (2.311 (.74) 3.67 (1.610 (.04 (3.150-.91) 9.238-.00) 1.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.35) 1.550 (.670) 3.210 (.270) .41) 1.530-.13-1.52 (1.570) . Survey Geometric mean (95% conf.64-5.19) 2.224-.17 (.860-1.43-64.840-1.270-.328) .330 (.19 (2.21-4.264 (.178-.299-.300-.250) .160-.36-6.37) 1.540 (.700-1.09) 3.290) .02-1.03-1.48 (1.590) .81 (1.53 (1.80) 4.261-.490-.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.67 (1.51-7.07-5.19-6.930) 1.510 (.350) .15-2.63-3.329) .25-2.362 (.21 (1.590-1.200-.253) .94 (1.316 (.740) .210 (.52) 2.480 (.280) .550 (.225-.190-.49 (1.63) 1.240-.590) .720) 90th 1.03 (.500) .04 (.91 (2.650) .83 (1.07) 2.860 (.200-.274-.49) 3.280 (.16-4.275 (.272 (.720 (.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .446) .210-.73) 1.35-3.730) .321-.270) .35) .261 (.550 (.96 (1.370 (.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .44) 2.401) .323 (.387) .760) .640 (.640 (.590) .220 (.55 (1.480-.202-.36 (1.27) 1.25-5.240 (.280 (.290-.310) .00) 1.410-.61-2.329) .534) .380 (.00) 5.330) .25) 2.580) .250 (.400-.73-4.290) .240-.240-.246 (.410) .226-.271-.173-.06-3.0) 3.86 (1.510 (.227 (.200-.510 (.380-.440-.309 (.560 (.490 (. Deltamethrin.230-.62) .09-2.280 (.32 (2. interval) .230-.62) 1.75-8.330) 75th .44 (1.240 (.60) 1.270 (.350 (.312 (.40 (1.09-2.423 (.54 (1.40) 2.420-.250 (.860-1.810) 1.330) 1.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .370-.450 (.335-.35 (1. population from the National Health and Nutrition Examination Survey.S.49) 1.240 (.91-4.22 (1.91) .372) .220-.930) .730-1.11 (.309) .274 (.67) 1.95) 1.960-1.400-.17-1.05-3.280-.43 (1.90) 3.190 (.09 (.

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

280) .140) .190 (.270) .150-.310) . and 0.098-.07.140) . The absorption. or other substances containing antimony is another means of exposure.250-.300) .370) .230-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.350) .120-.210) .140) .120 (.330) .190 (.04.100) .220) .132 (.180-.390) .200) .230) .180-.160) . castings.090 (<LOD-.430 (.300) .340 (.350-.330 (.460 (.220) 95th .320) Total .180 (.150) .460 (.079-.170-.600) .131-.175 (.470) .340 (.200-.120 (.164-.130) < LOD .126 (.080-.220-.105 (.190) . storage batteries.126-.169 (.160 (.270 (.145 (.125 (.440) .230-.140) .Metals Antimony CAS No. distribution.200) .176 (.270 (. sheet and pipe metal.260 (.280-.330) .350) .230) .130-.120) .290-.148-.115-.220) .095 (. see Data Analysis section) for Survey years 99-00.470) .280-.170-.280 (.180 (.180) .240 (.470 (.220-.320) .110) .250-.04.117-. Antimony can exist in one of four valences in its various chemical and physical forms: -3.310) .350 (.140) .080) .120-.200-.150 (.290 (. enamels.170-.310 (.320-.230 (.110 (.230 (. and 03-04 are 0.114) .137) .400 (.460) .230-.130-. 01-02.320-.220-.190-.410) .088-.130-.350 (.130 (. fireworks. Stibine is a metal hydride form of antimony used in the semiconductor industry.390-.136) * .710) .160-. People are exposed to antimony primarily through food and.160) .099 (.320 (.190) .220-.360 (.230-.200) .128 (.150-.280-.260-.390-.122 (.136-.320-.160) .190-.400) .240-.270-.100 (.430 (.100-.340) . It is also used in paints.134 (.141-. from air and drinking water.330) .200 (.260-.410) . interval) .180) .210) .280) .390) .230 (. solder.190-.108 (.112-. 176 Fourth National Report on Human Exposure to Environmental Chemicals .120-.280) .390) .160-.220-.160 (.080) . 7440-36-0 General Information Antimony is found in ores or other minerals.130 (. water.390 (.150 (.120 (.310 (.250) .180 (.100-.150) 90th .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.170 (.260 (. 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.240 (.510) . 0.130-.250 (.087-. ammunition.140 (.440) .120) .S.220) .490) .350) .150-.280-. ceramics.280-.570) .180 (.500) . and +5.130 (.157) .240-.400 (. and glass.161) .123 (.390) .103) .320-.170) . Workplace exposures can occur at smelters.560) .240 (.310 (. Dermal contact with soil.154-.180 (.110-.410-.120-.190 (.330) 1132 1335 1281 1144 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .145) Selected percentiles ( 95% confidence interval) 50th . often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.200 (.350) . and as a fire-retardant in textiles and plastics.154) .180-.090-.109-. +3.140 (.330-.100 (.140) .156-.120 (.142 (. 0.200 (.370-.300-.210) . respectively.260) .200 (.400 (.250 (.120-.360) . and excretion of antimony vary depending on its oxidation state.150-.180 (.300 (.420) .120-. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications.350-.207) .190) .130 (.180-.120) .130-.360-.400) .220 (.220-.530) .260) .130-.070 (<LOD-.350-.260 (.500) .200) .143 (.137) .190) .134-.250-.200-.300-.150) .170-.310 (.270 (. < LOD means less than the limit of detection.240 (.119-. which may vary for some chemicals by year and by individual sample.117-.350 (.130 (.119) .130-.184) . to a lesser extent.200 (.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 .128 (.240) .197) .140 (.490 (.130 (.160) .170-.360 (.110-.330-.350 (.130) .190-.135) * .210 (. coal-fired plants.120) .120-.460 (. and refuse incinerators that process or release antimony.230-.210-.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 .390-.200 (.160) .160 (.140-.290-.270) .250-.210 (. and pewter.150-.190 (.330 (.144) .093 (.154) .110-.095-.090-.310-.200-.210) .070 (<LOD-.140 (.132 (.250 (.133) * .280 (.330) . metal bearings.210) .190) .160) .130 (.220 (.160-.360) .260) .300-.090) 75th .130 (.190-.190 (. It is used in metal alloys.230) .330 (. population from the National Health and Nutrition Examination Survey.210-.440 (.070-.115) .240 (.400-.270 (.120-.080 (<LOD-. Antimony enters the environment from natural sources and from its use in industry.150) .310-.108-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.090 (.178) .150 (.350 (.170 (.120 (.180-.430 (.160-.120-.300) .130) .130) .320 (.400) .280) .146 (.110-.300 (.158 (.

skin.217 (.080 (.181) .095-.124-.333 (.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 .179-.129) * .109 (.097-.121 (. The toxicity of stibine after acute inhalational exposure is similar to that of arsine.228 (.152) .102-.125 (. and ulcers (Werrin. population from the National Health and Nutrition Examination Survey.125-.233) .102-. 1954).164-. diarrhea.176 (.075 (.130 (.098) .444) .187) .159-.280 (.257) .250 (.129 (.127) .371 (.171) .084) .269 (. 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.250) .087) .127 (.131) .500) .156 (.333-.128-.061-. Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.295 (.227-.199-.149) .333-.195 (.112 (.417) .200-.417) .213 (. 1953).115-. liver.139 (.248) .357) .318-.317) .078 (.320-.206-.132) .109-.188-.236 (.178 (.242-.208 (.253 (.143) .209-.167 (.317) .152) .131-.135) .373) .108-.471) .298 (.115 (.120 (.338 (.267 (.153-.068 (.189 (.308) .191 (. 1986).092) . Histopathologic inflammatory and degenerative changes in the lung.194-..124-.148-.204-.132 (..120 (.205-.081) .263-.116-.176-.144-.225 (.181) .276 (.209) . Ming-Hsin et al.266 (.320 (.113-.106-. and gastrointestinal symptoms such as vomiting.391) .149-.200) .Metals than for trivalent compounds (Elinder and Friberg.225) .333 (.119-.318-.250-.265 (.124) .079 (<LOD-.333-1.430) .086 (.192-. 1958) and occupational exposures (Briegner et al.173-.207) .134) . abdominal pain.075 (.265-.129) .209 (.245) .115-.146-.300) .082) .111 (.278) .195-.256 (.140) .173 (. 1988. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.317) . and route of exposure (Elinder and Friberg.127) .126-.357-.222 (.124 (.277 (.082) . interval) .136) .200-.255-.147-.310 (.241-.081 (<LOD-.400 (.271-.235-.263 (.338) . Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.112 (.156-.250-.167 (.120 (. species..220) .135 (.192 (.146-.118 (. Acute antimony poisoning may cause a metallic taste.320) .196 (.192) .069-.153 (.228-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.126 (.195-.127) .116 (.250-.099-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.099-.429) .727) .288 (.107-.280-.108-.119-.161) .109 (.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 .113) .170 (. Fourth National Report on Human Exposure to Environmental Chemicals 177 .143) 90th .104-.414) .485) .178-.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.135 (.244-.164 (.250-.300 (.133) .247) .138) * .429 (.226 (.268) .121) .076-.320 (.069-.115 (.313-.159-.248-.135) .238 (.741 (.151) .127) .159-.230) 95th .122 (.096-.229-. and eyes.175 (.150-.238) .185 (.138-..130) .208-.200-.438) .137 (.471 (.121 (.123) .071-.160 (.103-.233 (.278 (.364 (.405) .117-. 1973).122 (.421) .103-.089) .300) .112-.214) .193) .425) .281-.193 (.186) .167-.320-.118 (.164) .211) .161) .310) .135) .107-.230-.315) .239-.074 (.310) .076-.308-.143) . 1986).321) .120 (.113-.117-.095-.130) .146) .294) Total .238) . and kidney have been demonstrated in high dose animal studies depending on the dose.250 (.129 (. Inorganic antimony salts irritate the mucous membranes.333) .176 (.261) .104-.385 (.111-.100 (.077) .30) .148) * .255) .480) .143 (.162-.163 (.224 (.150-.233-.259 (.139 (.108 (.138-.333 (.098-.138 (.183) .267-.267) .286 (.343 (.115 (.228 (.172-.444) ..130) .198) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.114 (.181) .126) .185 (.085) .338 (. 1944).106-.241-.352 (.117-.173) .741) .352) .272) .364 (.154-.131 (.447 (.148-.253-.115) .173 (.209) .119 (.082 (<LOD-.203) .092-. 1962).188) .114 (.S.143) Selected percentiles ( 95% confidence interval) 50th .107-. 1995).108-.391) .380 (.105-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.167 (.203) .147) .333-.114 (.185-.145) . myocardium.068-.098-.086) 75th .140) < LOD . resulting in hemolysis with abdominal and back pain (Dernehl et al.163 (.146-.123 (.182 (.080 (<LOD-.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 .

Chia-Yu H.html. Dunkelberg.. Ludersdorf et al. and hydrogen sulfide. Review of elements in blood. Dernehl CU. gallium. 1990. Lauwerys R. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Shao-Chi C. Kiberd B. Yu H-S. Cullen A. Chemotherapy for leishmaniasis: Biochemical mechanisms. Lenert G. et al. Iavicoli I. 1995. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Atlanta (GA). Nordberg GF. stibine. Biological monitoring of exposures to aluminum. Element reference values in tissues from inhabitants of the European community. Antimony trioxide is rated by IARC as a possible human carcinogen. 1994) have reported values slightly higher than those in this Report. Kentner M. Earlier measurements in general populations (Minoia et al. 2002. Int Arch Occup Environ Health 1987. Carelli G.13:361-362. Sabbioni E. Industrial Medicine and Surgery (Dec. Apostoli P. Konings J. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000.e. Elinder CG. Iavicoli et al. Hamilton EI. Weltle D. Briegner H. Paschal et al.. Dezateux et al. 2004.. Third National Report on Human Exposure to Environmental Chemicals.106:33-39. Centers for Disease Control and Prevention (CDC).16: 33-39. Delves HT. Petrucci F. arsenic.59:469-474. 1998) or compiled reference ranges (Hamilton et al. O’Regan M. 20012002. 1987). gov/toxpro2.S. Cheng-Wei L. Gebel TW. Ho C-K. Stocks J. Stone FD. population.. Pietra R. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals .cdc. Minoia C. Int Arch Occup Environ Health 1995.64(2):182-185. Schaller KH. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.51:238-240. Semisch CW. and antimony in optoelectronic industry workers. Pozzoli L. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Antimony. pp. Cordasco EM. Suchenwirth R. Matthews T. Yang C-Y. Stasney J.Metals to antimony have been established by OSHA and ACGIH. Biomonitoring of a worker population exposed to low antimony trioxide levels. Leinemann M. 1998. Urinary antimony in infancy.. Piatnek DA. Handbook on the toxicology of metals.. Mayne P. environmental levels) and health effects is available from ATSDR at: http://www. Liao Y-H et al. 1998). Industrial Medicine 1944. and a drinking water standard has been established by the U. Kentner et al. Luedersdorf R.46:931-936. Br J Ind Med 1991. Kuo-Juie Y. Pilgrim L. eds. even when exposure levels were below workplace air standards (Bailly et al. Wade A. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Mahieu P. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure. Environ Health Perspect 1998.)1954. VI. Arsine. J Occup Environ Med 2004.atsdr. New York: Elsevier. et al. Chen J-R.. Buchet JP. J Clin Pathol 1998. In: Friberg L. Information about external exposure (i. 1997). Delves HT. EPA. Ming-Hsin H. indium. respectively. 2005.76(2):103-115. References Berman JD. Sci Total Environ 1994.. Van der Venne MT. Mayer P. Ju-Sun P. Bolten C.67:119-123. Sabbioni E.. Arch Dis Child 1997.48:93-97. Biological assessment of exposure to antimony and lead in the glass-producing industry.10(3):560-586. Roland H. Biomonitoring Information Levels of urinary antimony reflect recent exposure. Fuchs A. Friberg L. External and internal antimony exposure in starter battery production.158:165-190. Alimonti A. Chin Med J 1958. Trace element reference values in tissues from inhabitants of the European community I. and future strategies. and 2003-2004. 2nd ed. Pulmonary edema of environmental origin. Dezateux C. Bailly R. Chest 1973. Gallorini M. Caroli S.521-523. or exposure differences. 1986.. Costeloe K. 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. Schacke G. 26-42. HH..76:432436. J Trace Elem Med Biol 2002. Wu M-T. Nau CA. Liao Y-H. Rev Infect Dis 1988. Vouk VB. et al.. which may be due to methodologic. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony. 1991. Antimony in blood and urine of infants. Stead FM. clinical efficacy. Skulsukai G. Industrial antimony poisoning.

Quarterly Bulletin of the Association of Food and Drug Officials 1962. and serum of Italian subjects.Metals in urine. Morrow JC. 27:38-45.76(1):53-59. et al. Jackson RJ. blood. Fourth National Report on Human Exposure to Environmental Chemicals 179 . Werrin M. Pirkle JL. Industrial Hygiene and Occupational Medicine 1953. Sci Total Environ 1990. Sampson EJ. Chemical food poisoning. Paschal DC. Ting BG. Trace metals in urine of United States residents: reference range concentrations. Renes LE.95:89-105. Antimony poisoning in industry.99-108. Environ Res 1998.

Also.90-14.7-95. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.6 (15.8 (48.57) Selected percentiles ( 95% confidence interval) 50th 7.90 (7.9) 21.3-15.8) 17. were used as treatments for syphilis.2 (13.4 (31.84) 8.4) 13.5) 41. see Data Analysis section) for Survey year 03-04 is 0.27) 9. it is found in over 200 crystalline or mineral forms.30 (6.4 (7. such as arsenopyrite (FeAsS) and realgar (As4S4).80) 6. and play sets. meats.70-9.4 (48.5) 43.5 (34. arsenic compounds.2 (12.7) 65. copper arsenates.6 (32.80 (5. In the last century. Since the 1940s.0 (43.6 (13.02-8. pesticides.90 (7.1 (38. 2005).25-9.6) 618 722 1074 Limit of detection (LOD. The United States no longer produces arsenic from mining but imports about 22.9-62.5 (36. lead. and as homicidal poisons. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot. interval) 8.10-10.66-8.8) 30. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted. Various arsenic compounds were used in paint pigments and for tanning animal hides. and.10 (6. retaining walls.5-41.8-77. Survey years 03-04 Geometric mean (95% conf. particularly arsenic trioxide. lead hydrogen arsenate. semiconductors.2-20.2-61.70 (6.00-9.2) 15. 180 Fourth National Report on Human Exposure to Environmental Chemicals .1) 7.34-9. mental disorders.50-14. and arsenosugars. arsenocholine.6 (9. and in lead-acid storage battery grids. Before the 20th century.5) 66.0 (14.84) 8.3) 10.50 (8.29 (8.6-35.74.2-93. grain.S. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.1 (32.8) 34.90-8.12 (6. Arsenic and its compounds have had many uses in the past and present as medicines.2 (51. arsenic as elemental metalloids may be used in some ammunition. the smelting of copper.1) 15. cancers.70) 8.40) 7.90) 16.9 (8.8) 7.80-9.7) 90th 37. trimethylarsine oxide.7) 24. and produce.5 (23.19-9.30 (7.97) 8.90) 75th 16.3-19.5 (14.5 (40.Metals Arsenic CAS No.9-34.4 (26. gaseous hydride manufactured in small quantities for use in the semiconductor industry. mostly for use in wood preservation (ATSDR. referred to as inorganic arsenic compounds.9-46.5-52.08 (5. solders.3) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2557 03-04 03-04 03-04 7.2 (41. and arsenates (oxidation states of -3.7-83. Arsine (AsH3) is a reactive.10) 10.9) 68. aluminum. black.0-60.0 (15.4) 40. sodium arsenite.1) 290 725 1542 03-04 03-04 9.7 (11. as alloy in metal bearings. and as a cosmetic to lighten complexion. to a lesser extent. alloys. and indium arsenides are used in the semiconductor industry. ocean and fresh waters.30) 17.34-10.0 (22. Gallium. Water sources contain mostly inorganic arsenate. to a lesser extent.6) 11.1) 1281 1276 03-04 03-04 03-04 9.2) 46.9 (17.4 (24. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks. cacodylic acid.1-18.20 (8.0-19.000 metric tons annually.4) 60.12-10. or rarely as elemental metalloids (yellow.6-141) 53.6-43. Arsenic trioxide (As2O3.2-17. Arsenic trioxide is approved to treat acute promyelocytic leukemia.5) 95th 65. though in some locations arsenite may be prevalent (WHO.90 (5.3-111) 78. and foods.00 (6. arsenites.5-178) 46. +3 and +5).8) 7. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action. from coal burning. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.90-7.90-11. and other metals.10-7. psoriasis.4-65.8-61. and gray forms).55 (7.8) 29.1-40. Although it is still widely used in the United States. 2001). Arsenic is measurable in most soils. population from the National Health and Nutrition Examination Survey.13-8.5-19. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.90-8.0 (11. 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts.41 (7. General population exposure to inorganic arsenic can occur through consumption of drinking water and.77) 6. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.8) 33. In nature.

and folate status (Chen et al.8 (20. kelp.1) 7.0 (17.50 (6.24 (7.7) 95th 50.33 (6.31 (6. are used in enclosed ultraclean operations within the semiconductor industry.8 (27.4) 54.7 (11.3-53.3-64.6-17. 2001).0) 33. Gamble et al. age. dust. EPA.8-32. In aquatic sediments.5 (9.88) 7. arsenic does not show biomagnification in the food chain (WHO.0-26.7 (9. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.7-18. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO.6 (10.13) 8.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.1 (14.0) 1281 1276 03-04 03-04 03-04 8. 2001).8-75.0 (31. shellfish. organic arsenic can be converted back to methylated and inorganic arsenic.2) 90th 30. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals.04 (5.8 (12.44) 6.01) 11. 1988).9-56. population from the National Health and Nutrition Examination Survey.47 (6.7 (25.3-41.99-9.2-46.S.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 . Arsenate is reduced in the body to arsenite (oxidation state +3).3) 6.1 (11. 2003..4-64. 2001).7-188) 27.51) 75th 14. though some reduction may occur in the gut prior to absorption.96) 12. interval) 8.93-9. 2001). and some other seafood can contain organic forms of arsenic including arsenobetaine.9) 13.32 (5.47 (7.88 (5.0-18.7-35. 2001).S. Smoking tobacco is also a source of inorganic arsenic.4 (24.75 (5.07-9. selenium.3-62.28-7.75) 13. EPA’s maximum contaminant level (Hughes.18 (5. U.3 (27.5) 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 8.66-8.58-10. dose level.5) 290 725 1542 03-04 03-04 8.0) 42.S. have caused clinical arsenic poisoning. trimethylarsine oxide (TMAO). 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. 2006. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation. Tseng. Inorganic forms of arsenic demonstrate high acute toxicity. Fish. as observed in Bangladesh where millions of people have been exposed.64 (7.76 (6.41) 6.4 (11. 2007. NRC. inorganic arsenic is widely distributed within the body. WHO..8) 22.9 (45.2 (12.6 (17.8 (11. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA.66 (7.38-10. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC.2) 15. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al. 2001.2) 40.6) 45.2-15. Chowdhury et al.06 (4. but is poorly absorbed dermally (WHO.8-62. 2007.61 (7..7-17.20-9.7) 28. Survey years 03-04 Geometric mean (95% conf.4 (42.3) 9. so exposure to the general population is extremely limited.5) 17.81-9.04) 7.0-69. Steinmaus et al. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established. 2001.25 (6.0) 26. WHO. mine tailings).g.0-38. After absorption.25-9. In aquatic organisms.11 (5.23-7...1) 58.4 (40.33-10. and arsenosugars.8) 27.1-36.1) 24. The reduced form of MMA (oxidation state Urinary Total Arsenic (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9) 53. cacodylic acid and monosodium methyl arsenate. 2001). The semiconductor dopants. gallium arsenide and indium arsenide.86-17. 2006. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet..00 (6. Though modest bioconcentration occurs in some aquatic life. arsenocholine. Direct exposure to DMA and MMA may result from use of the two pesticides. Children may have additional exposures from ingestion of contaminated soils (e.59) Selected percentiles ( 95% confidence interval) 50th 7.4) 32.0) 12.3 (24.10-16.4 (26.10-8.35) 7.1) 6.12-10.93-8. and contact with CCA-preserved wood structures.40) 8.7-34.8 (21.66-8. 2007.5-17.47-6.6 (35.44-11.0) 14.30-9. 2001). Extremely high groundwater arsenic levels. 2001).45) 5.5-120) 40.01) 7.1) 8.4 (12.

2007.. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. Arsenic has many actions demonstrated in cellular studies. 1998. and DNA repair inhibition (Cohen et al. increased oxidative stress. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. Chronic human intake of arsenic at less than acutely toxic doses. 2004). Such actions may lead to decreased energy production.60) 1. vomiting. WHO. and diarrhea. Cohen et al. including inhibition of numerous enzymes. respectively. WHO.30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.S. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al.. substitution in phosphate metabolism.. 2004.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1. noncirrhotic portal hypertension. 182 Fourth National Report on Human Exposure to Environmental Chemicals . 2001). hypertension. food residue. With chronic exposure. WHO.. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose.. gluconeogenesis. Taiwan.20 (<LOD-1. Chronic arsenic exposure in humans is considered to be a cause of skin. Bangladesh. Cellular glucose uptake. cell transformations. and altered gene expression. 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. some of these effects may take years to develop.10 (<LOD-1. 2006. hepatotoxicity.20 (<LOD-1.. 2001). renal failure.10 (<LOD-1. and childhood neurodevelopmental effects in observational human studies. which may vary for some chemicals by year and by individual sample. Bredfeldt et al. < LOD means less than the limit of detection.50) 621 725 1078 Limit of detection (LOD. 2006.S.10 (<LOD-1. apoptosis. Although arsenate is reduced in the body to arsenite.50) 1. see Data Analysis section) for Survey year 03-04 is 1. Raml et al.. Survey years 03-04 Geometric mean (95% conf.80) 1. arsenic trioxide) includes hemorrhagic gastritis with nausea. U. The U. hematocytopenias. NRC. and hyperpigmentation of the skin (NRC. population from the National Health and Nutrition Examination Survey. which can lead to dehydration and shock.g. leading to a decrease in adenosine triphosphate energy production. drinking water have not been associated with increased cancer rates (Schoen et al. NRC. 2001..EPA. Cardiac arrhythmias. fatty acid oxidation. The organic forms of arsenic occurring in seafood have little known toxicity. but additional or confirmatory research is needed (Kapaj et al. 2007. Chile). and production of glutathione may be affected as well.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al... 2006) or when exposure occurs in smokers (Chen et al. and by uncoupling oxidative phosphorylation (NRC.S. peripheral vascular disease. 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.0. Laboratory studies using inorganic arsenic have shown chromosomal aberrations..g.S. can cause peripheral sensorimotor neuropathies. 2004). WHO. including drinking water sources with elevated arsenic levels (e. and it also will inhibit succinate dehydrogenase. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.30) 1.10 (<LOD-1. Studies of arsenic at levels typical of U. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide..60) 1. 2007). 2001). 2001). it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. lung. interference in signal transduction pathways.20 (<LOD-1.EPA has established drinking water. and bladder cancer (IARC. 2000.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1.10 (<LOD-1. and endothelial injury (Kumagai and Sumi. cytotoxicity. hyperkeratosis. Chronic elevated arsenic intakes have been associated with diabetes. Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. 2001).20 (<LOD-1. 2006. Acutely. 2001. 2001).

html. Caldwell et al. had decreased since the prior 1990– 1992 survey. 2006.. 2006..S.69 (<LOD-3. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U.00) 1. Survey years 03-04 Geometric mean (95% conf. Caldwell et al. In a Nevada town where groundwater levels were naturally elevated. 2007. population in NHANES 2003–2004 (Schulz et al. population from the National Health and Nutrition Examination Survey.. 2004. 2007. 2000. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Consequently. 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.95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2003. Additional information about external exposure (i.. 1992. Vahter et al. Calderon et al.33 (<LOD-3. 2001).18) 3. Several studies have shown that urinary arsenic levels are not correlated with low levels of arsenic measured in house dust or in washings taken from hands (Hysong et al. Meza et al. environmental levels) and health effects is available from ATSDR at: http://www. Though CCA-treated wood contains several thousand times more arsenic than untreated wood.cdc.e.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.. 1986). 2008. In the German Environmental Survey III of 1998. population (Rubin et al. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al. 1999).. WHO.. and the FDA has established a bottled drinking water standard. 1999.. 2006.Metals compounds... but generally only at maternally toxic doses (WHO..70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2.19) 3. Valenzuela et al. 2006). 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. population in the National Health and Nutrition Examination Survey (NHANES) 2003–2004 were similar to levels reported in the National Human Exposure Assessment Survey (NHEXAS) 1995–1996 for about 80 children residing in the Great Lakes region (Caldwell et al. IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens. Fourth National Report on Human Exposure to Environmental Chemicals 183 . and were about two-fold lower than those for the U.89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. median urinary total arsenic levels in 4052 adults varied with seafood intake. 1998. 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 3.75 (<LOD-2. Pellizzari and Clayton. 1999. 2006). 2006).41) 3. Pellizzari and Clayton 2006).61 (<LOD-3.50) 1. Levels of total urinary arsenic in the U. Shalat et al.. Josyula et al..75 (<LOD-2. 2008). 2001).. DMA produced bladder cancer in some chronic rat studies (Cohen et al.. 2006). Pellizzari and Clayton. Compared with this Report. although urinary arsenic levels were not associated with CCA contact (Shalat et al. Offergelt et al. 2008).. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al...33 (<LOD-3.04 (<LOD-3.80 (<LOD-4.. In animal studies. 2001). 2004..atsdr. 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. 2000). Shalat et al.S.. gov/toxpro2.18 (<LOD-3.. arsenic has been fetotoxic and teratogenic.S..S.

4-35.1) 45.6.. When seafood intake is avoided. 2001).5) 29.6) 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. and other factors such as nutrition.800) 1. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.. population from the National Health and Nutrition Examination Survey..66 (1. MMA. geometric mean levels were about 70-fold higher than for the U. 2000.7 (13.80 (. population showed a higher contribution of arsenobetaine (Caldwell et al.40) 5. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al.3-39.2-38.00-12.5 (26.62) 2. In the residents of a Chilean town who consumed water with high levels of arsenic. when seafood organic arsenic is subtracted).400-.2 (6.40) 75th 5. arsenite. 2000.90-7.0) 29..55 (1. 2007) with higher levels of arsenic in the drinking water. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al. respectively. In the late 1980s.20-3.4 (16.60-3.900 (.8. which may vary for some chemicals by year and by individual sample.2-35. and TMAO.8) 35.S. with DMA.20) 7.1-94.70-21.700-1. vasospasm.20 (.20) 3.3) 35.31-1. 1996. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH. in NHEXAS 1995–1996.30) 2. 2003).500-1.50) 90th 16.e.3) 95th 35.800-4.900-1.17-1.45 (1.6.50) ..37 (1.0 (27. 2008).. Median and mean total urinary arsenic levels for residents in some districts in Bangladesh were reported to be about 50-fold higher than respective levels in the U. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2008)..40-6. Aposhian et al.20-190) 31..11-1.600 (. 2008). In most human studies. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i.20-25. WHO. Tseng et al. see Data Analysis section) for Survey year 03-04 is 0. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.800 (. Measurable organic arsenic species in this Report are three biologically generated environmental forms. Some noncancer effects of arsenic (e.00 (1. 2000. 2008.00) 3.70 (5.70-21.00-1.19 (. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.20 (4.40-7..68) ..7) 13. 1990.00-6. 2005. 1..700-1.5) 621 725 1078 Limit of detection (LOD.0-23.50-6. 2005.80) 1. 184 Fourth National Report on Human Exposure to Environmental Chemicals . 1985. Caldwell et al. Total arsenic measured in the urine includes all species of inorganic and organic arsenic.4) 23.871-1. interval) 1. The higher percentiles of total urinary arsenic levels in the U.20 (1.1-25. 2008).70 (3.74 (1.29 (1.20 (2.S. and 0. Blom et al. 2001.800 (.S.. These associations are stronger at higher urinary levels.9-23.80 (4. and duration of exposure are also considered important.800-1.6 (25.00-4.4) 31.10) 4.9) 13.8-40.3) 1284 1284 03-04 03-04 03-04 1. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. and two methylated metabolic products.4... < LOD means less than the limit of detection. population (Sun et al.9 (7.9 (6.00 (.6-44. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level..30 (1.20) 18. methylation capacity.30) 10..30 (2. China. Chowdhury et al.5) 32. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine.S.5) 292 728 1548 03-04 03-04 1. and TMAO were detected in only 7. 2005.8-50.3% of a representative sample of the U.Metals other areas of the world (Ahsan et al.80 (3. Valenzuela et al.60) 1. Sun et al. arsenocholine. arsenite. 2008.50) ..43-1.28) 1.48-2.6 (13.80-5.0 (26. 2006). arsenocholine. 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. After recent seafood ingestion. 2007).S. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.83) Selected percentiles ( 95% confidence interval) 50th 1. population in the NHANES 2003–2004 subsample.10) 8.7) 15. Caceres et al. Individually measurable species resulting from inorganic arsenic exposure are arsenate. arsenobetaine. Pellizzari and Clayton. Survey years 03-04 Geometric mean (95% conf.7 (21. DMA and MMA. Caldwell et al.3 (21.1) 18.0) 4.70) 6.. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al. dermal keratosis.7-22.05) < LOD .8 (12. Also.5 (14.1-51. population (Ahsan et al...10 (4. Arsenate.g.90-29.93) 1. Caldwell et al. For residents of Inner Mongolia.3 (9.8 (17.6 (11.

45) 1.91) 90th 16.6) 19.43) 75th 5.5-20. Survey years 03-04 Geometric mean (95% conf.67) 1.36) 2.80) .909-1.6 (6.4-28.61-6. 2006.16 (..05 (.4-21.72) 12.0 (9.2 (12. population from the National Health and Nutrition Examination Survey..70) 5.612-1.05) 1.2 (12.58 (3. 2001).83) 2.9-18. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.80-153) 17. 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. which is below the ACGIH BEI (Caldwell et al.79 (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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.12) < LOD .6 (9. interval) 1.40) 1. population for the sum of inorganic related species was 18. 2003.4 (24.0-36.78-5..91 (4.53 (.50-7. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.44 (1.6-29. Information about the biological exposure indices is provided here for comparison.65 (1. In recent years.9) 32.43) 14.13-39.4) 13.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.67) 4. Vahter et al.3) 1284 1284 03-04 03-04 03-04 1. 1998.Metals as with DMA.9 (25.88 (5..3 (10.29 (4.29-14.64-29.25-7.7) 17. 2001).10 (.938-1.50-15. Sun et al.37-2.51-2. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.3-24.00 (1.786-1.4-82.19-2. 2008).7) 9.15-4.93 (1.40 (1.S.S.83) 8.11 (. WHO.82) Selected percentiles ( 95% confidence interval) 50th 1. The 95th percentile of the U.47 (2. 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.3 (10.15-1.4) 32. Offergelt et al.8) 29.5) 17.47 (1.5 (18.54 (1.5) 26.14 (1. 2008).21) 5.1-36.2 (13.5 (18. not to imply a safety level for general population exposure.39-3.18-1..88) 2.25 (.638) 1.4 (11.2 (4.3) 95th 29.1 (26. Fourth National Report on Human Exposure to Environmental Chemicals 185 .15-1. 2007).833-1.9) 14. 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.68 (1.1) 26.901-2.4) 292 728 1548 03-04 03-04 1. 1992.400-..73-6. Caldwell et al.7) 30. 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. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.62-6.76-27.30) 1.32-7..81 (4.959-1.00 (3.30-1.55) 1..6-32.1-18.4) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1.9 μg/L.9 (13.51) 5.78 (3.82) 4.28) 1.531 (. 1986.6-46.877 (.

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.6. Survey years 03-04 Geometric mean (95% conf. Survey years 03-04 Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. 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. 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.S. Urinary Arsenocholine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. < LOD means less than the limit of detection. 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. population from the National Health and Nutrition Examination Survey. 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 1. which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 187 . population from the National Health and Nutrition Examination Survey. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.2.20 (<LOD-1.Metals Urinary Arsenous (III) Acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (<LOD-2.S. Survey years 03-04 Geometric mean (95% conf.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. Survey years 03-04 Geometric mean (95% conf.08 (<LOD-4.40 (<LOD-1. < LOD means less than the limit of detection.80) < LOD 621 725 1078 Limit of detection (LOD.00 (<LOD-3. Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.44) 2.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.95 (<LOD-2.70) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. see Data Analysis section) for Survey year 03-04 is 1.00) 1. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

74 (2. Survey years 03-04 Geometric mean (95% conf.69-3.48 (3.00-11.37 (2. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.82-9.69 (3.00-22.00) 5.73 (3.30 (7.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.05) 5.90 (3.62) 4.00 (3.49) 10.22) 4.0-17.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .00-12.50-15.00 (3.1-15.00-4.1-18.0) 9.45) 3.71-4.00-15.00-8.00 (7.78) 4.97-3.61-16.0-16.6) 1284 1284 03-04 03-04 03-04 4.6-18.00 (6.91) 75th 5.0) 292 728 1548 03-04 03-04 4.90) 2.28) 2.0) 13.0) 13.86 (2.00 (3.98) 4.00-4.00) 75th 6.00) 7.03-6.9) 12.16 (4.0 (14.9 (11.31-4.05) 10.0-17.70-4.81 (5.7) 1284 1284 03-04 03-04 03-04 4.52) 3.46 (4.70 (3.60-7.00) 90th 11.9) 5.92) 3.9 (7.61-11.13-4.00 (5.82) 3.00-5. see Data Analysis section) for Survey year 03-04 is 1.0 (10.0 (10.00 (6.80) 7.49-4.11) 4.57 (3.00 (3.0 (9.30) 3.0-18.33-4.00-7.27-2.44) 5.0) 11.00-4.86-7.50-5.0 (12.69 (3.94) 3.00) 12.24-4.69-6.00-4.6 (9.34 (3.10) 6.95-3.00-15.20-4.7) 13.0) 9.85 (3.2) 10.00) 3.44 (2.18 (6.45) 8.1-22.7-16.00 (4.8) 7.0 (13.78 (4.90) 5.00-3.32 (4.0) 95th 16.00 (5.0) 16.0) 11.5 (11.32-10.34 (3.48 (2.0 (8.S.9) 13.84-8.3 (8.00 (5.09 (7.29-4.5) 12.7 (10. interval) 3.70-3. interval) 3.17-6.70-12.73) 6.59 (6.95 (4.80-5.0 (8.06) 5.94-3.0) 17.0) 14.0-25.14) 3.00-13.S.00-12.80-3.16-11.34) 3.0) 17.0-16.1 (8.14) Selected percentiles ( 95% confidence interval) 50th 3.00 (3.12 (3.10) 3.25 (4.7) 12.33) 3.00-4.65-6.37 (3.00 (3.00 (5.27-5.45 (8.8) 7.77 (3.57-5.00-3.17-4.82-5.80) 2.60-6. population from the National Health and Nutrition Examination Survey.0 (9.0) 9.00-10.67) 8.0) 12.00) 6.88 (4.00 (5.0-12.50 (4.00) 6.00-9.6) 292 728 1548 03-04 03-04 3.0-19.39-3.03 (3.20) 11.7.42) 3.86-21.3 (8.84-18.60-4.67) 9.00-7.00 (6.65-8.24) 3.00) 9.95-6.74) 90th 9.08 (2.34-4.80-6.79 (3.00-7.20-12.3 (7.00-11.0) 16.89 (3.71) 3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.0 (10.00-7.27 (2. Survey years 03-04 Geometric mean (95% conf.32 (8.0 (10.0 (9.12-4.0 (12.55 (2.00) 6.27 (3.00) 4.70) 5.00-15.0) 621 725 1078 Limit of detection (LOD.72 (4.38 (3.0 (13.31) 4.00) 4.00-4. population from the National Health and Nutrition Examination Survey.9) 11.00) 3.19) Selected percentiles ( 95% confidence interval) 50th 3.8) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 3.15) 4.92-12.34-4.0) 10.5) 95th 13.71 (3.80 (4.4 (7.16 (2.60-3.95-4.71 (4.00 (7.11 (3.05) 3.00) 6.0 (11.00-11.17 (2.

58) 2.20) 2.10 (.50 (1.900-1.40-2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.11-1.816 (<LOD-.52 (2.80 (1.88-2.79) 2.50 (<LOD-1.86) 3.33 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.88 (1.60-2.90 (1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .43-3.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.34) 2.30) 1.00) 1.40 (1.10-3.71-2.00) 2.40-3.20 (1.28 (1.86 (2.70) 2.07-3.00-2.40) 1.15-1.80-2.20 (1.50) 621 725 1077 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey.00) 1.60) 2.20 (1. population from the National Health and Nutrition Examination Survey.73-2.00 (<LOD-1.86 (2.10 (1.20 (1.57) 95th 2.80 (1.46 (1.70-2.63 (<LOD-1.70-2.23) 1.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.10-1.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00) 2.62) 2.30 (1.70-2.70-2.20-1.18-1.10-1.36 (1.30 (2.00) 1.00-1.07 (1.853-1.85) 1.20-3.18-1.20 (1.00-2.00 (2.30-1.30 (1.16 (2.61-3.S.50 (2.37 (1.05-1.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.10 (.85) 2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.53 (1.60) 1.985) 1.82-2.9.20 (1.36) 1.80 (2.40-3.30-2.40-2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.53-2.31-3.50 (1.96-2.22) 3. Survey years 03-04 Geometric mean (95% conf.70-3.45) 3.30 (1.00 (1.10 (<LOD-1.17) 2.90 (2. Survey years 03-04 Geometric mean (95% conf.82-2.14-1.84-3.31 (1.30) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.80) 1.90) 1.60 (2.80 (1.80) 1.60) 2.00 (2.81) 1.00-1.40) 2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.10) 2.80-2.10) 95th 2.77) 1.93) . which may vary for some chemicals by year and by individual sample. 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) 2.88 (1.28 (1.86) 2.90) 2.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.10 (1.46-2.60 (1.22 (1.61) 2.50-2.30-1. see Data Analysis section) for Survey year 03-04 is 0.30) 90th 1.07) 2.50) 1.40 (2.33 (1.35-3. < LOD means less than the limit of detection.40) 1.00 (<LOD-1.54) 90th 2.S.30) 2.80 (1.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.00-4.

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

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12 (2.20) 2.49) 11.60-3.46) 1.30 (5.85) 1. Some barium salts are freely soluble in water.62) 1.54-1.15-1.38 (1. The general population can be exposed to low amounts of barium in air.51 (1.35) 5. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.47) 4.61-8.92) 2.66 (4. Fourth National Report on Human Exposure to Environmental Chemicals 193 .65 (5.10) 5.70-3.53) 1.70-5.54 (6.60-2.20-1. Barium compounds are used by the oil and gas industries to make drilling muds.48) 1.10-4.1) 9.41-1.31. such as barium chloride.86) 6.37) 1.15) 5.88) 4.2) 6.71) 2.31 (2.66) Selected percentiles ( 95% confidence interval) 50th 1.56 (2.40 (5.80) 1. and ceramics.40 (1.54) 2.53-5.29-5. depilatories.27) 2.11-1.48-4.05-2.93 (4.30 (1.51) 7. interval) 1.75) 2.50 (1.78) 1.15 (2.50) 2.44 (1.30-1.60) 4.16 (1. soluble forms of barium.44-5.78-3.25 (1.57-7.37) 5.14-6.36-1.20-8. 7440-39-3 Medically.70-8.87) 7.80-7.43) 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 1.87-14.31-2.12 (2. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).50) 4.76-2.99-5.70) 5.51) 1.80 (2.10) 3.41-3.34 (1.47-1.34 (2.03 (1.06-2.20 (3.91 (2.90-9.26) 2.50-6.02 (7.96-2.43 (5.49) 8.00-3.80 (1.50) 1.50-6.91) 6.76) 1.61 (2.34 (1.40) 7.74) 3.65-5.01 (4.86 (4.29-1.04-2.18-1.56 (1.61 (3.50 (4.75-3.54-8.88 (5.38 (1.80 (5.10 (4.82) 2.9) 5.26) 5.60 (1.36 (4.21 (1.86-5.77-3. glass.48-4.49-1.60-10.35-4.39) 1.72) 1.43 (1.40-13.50 (1.62) 1.65) 1.10 (2.20-6.25-11.50 (1.44-2.90 (6.37-8.30) 3.24-1.21-8.50) 2.50 (1.63 (8.00 (2.76-3. water.80 (2.8) 9. respectively.28) 90th 5. whereas others are practically insoluble (e.08-8.12.50 (6.50 (4.39) 4.30) 5. tiles.45) 7.73) 1. such as brazil nuts.70-2.Metals Barium CAS No.60) 3.00-8.30-5.56 (1.27 (1.91) 2.12-1.4) 7.26-1.43 (1.30 (2.00) 1.09 (1.47-1. fireworks.11 (2.64-3.35 (1.57 (5.00-76.56 (6.40 (1.87-3.30) 5.12.77 (3.01-7.20-5.20-1.49) 2.59) 3.60) 1.97 (1.71) 1.18) 3.52 (1.53) 2.63 (2. Certain foods.74-3.63) Total 1. In single dose animal studies.54) 1.81-2.73-5.12) 6.90) 4.49-9. population from the National Health and Nutrition Examination Survey.11 (3.49) 4. bricks. Barium compounds are also used commercially in paint.20 (4.30-2.24-1.30) 8.70-2.05% of the earth’s crust.40 (5.12) 7.88) 1.36) 5.35 (3.8 (6.14-1.90) 2.22-1.87-9.07 (2.90) 1.35-1. Barium salts have also been available as rodenticides.40) 3.78-2.48) 1.20-8.90) 2. rubber.86 (4.70) 4.61 (1.82-6.21-2.76 (3.14 (6.09 (2.64 (1.54 (2. are high in barium (Genter.49 (1.16) 5.73) 3.72) 75th 3.46) 1.73 (6.60) 1.11 (3.8) 5.55-3.63 (1.68 (1.74-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.93-8.65) 3.51) 2.33 (1.70 (1.43) 2.80 (1. 01-02.87-7.36 (1.38) 2.73 (5.37-1. Small amounts of barium can be released into the air during mining and other industrial processes.56) 4.00) 4.85 (2.82) 1. 0. 2001).90-2.80-2.20-1.69 (1. and 0.95 (4.40 (4.39 (1.15 (6.70) 3.41) 1.30 (5.15-11.10) 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 1.55-7.17-1.80) 7.45 (1.65) 1.70) 1.71 (2.30) 5.81-3.65-8.80-3. barium sulfate and barium carbonate).71-9.24 (4.34) 2.50-1.20-1.. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.32-7.62 (1.70) 1.72) 4.50 (2. Workers employed by industries that make or use barium compounds can be exposed to barium dust.04-6.40 (5.29) 5.61 (1.50 (1.62 (1.g.52 (4.15 (1.50-1.18 (6.30-1.S.54-1.38) 8.28-1.00 (1.30-3.70-6.77) 1.98) 1.21 (1.67) 6.00) 6.63 (5.19-1.80 (1.57) 3. and 03-04 are 0.93-2.22) 6.63) 1.10 (3.90 (1. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60-6.60-6.06-1.42 (1.61 (5.60 (2.46-1.4) 6.4) 9.40 (1.27 (1.85) 1.10-5.20-8.25-1.78) 1.65-1.50 (5.08 (6.99 (4. see Data Analysis section) for Survey years 99-00.70 (5.50 (4.39-1.94-6.30) 4.54) 1.15-1.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.90-13.36-1.50 (3.64) Sample size 2180 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.43) 6.88) 7.87 (6.40) 7.32) 8.30-2.30 (3.86-4.81-2. In nature.35 (2.76-7.84) 5.63) 1.80) 6.90 (4.59-11.26-7.20 (1.39 (1.37 (4.32-1.80-5. and food.30) 2.87 (5. it combines with other chemicals such as sulfur or carbon and oxygen.48 (6.70) 7.00) 1.95-6.71) 95th 6.56) 1.35-1.19) 2.22-1.

49-1.881 (.02-5.37-1.51 (1.55-6.55 (1.88 (2.43-6.19-1.75) 2.47) 1.16 (1.39-10.46) 3.20 (1.27) 7.11) .19-1.832-1. Chronic high doses in animals resulted in kidney damage (McCauley et al.76) 2.703-1.26-1.75) 2.59 (1.58 (4.35-1..57-5.80-6.38) 4.54 (1. hypertension.37 (1.46) 2..29-3.8) 4.891 (.13-2.22-1.74) 1.84-5.58) 1.91 (3.38 (1.00 (3.20-8.29-4.33 (1.84 (3.56-3.33) 1.04) 5.73-2.25 (1.42) 1.2) 5.24-1.58-6.68) 3.85-5.90-2.10) 3.41 (1. 2001).29-1.11-2.44-2.50) 1.44 (1.12) 2.25-11.00) 4.47 (2.49 (1. such as those used in medical radiographic procedures.30) 2.33-1.3 (6.777-1.68 (2.60 (5.47) 4.04 (2.72) 6. and route of exposure.60 (2. The health effects of exposure to barium compounds depend on the dose.28) 5.57 (6.16-1.65 (5.46-22.24-1.59 (1.57) 2.44-2.41) 4.52) 2.S.76 (3.31 (1.0) 7.87) 1.31-1.92) 2.83) 2.77-5.24-3.21 (1.11) .38 (4.36-1.81-7.00-7.45-1.60 (2.45) 95th 6.32) 2.29) 1.96) 4.63) 1. 1986).905 (.18 (1.26-1.45-6.51-3.45) 1.49-1.38-7.40 (1.2 (3.35-3.89) 90th 4.50) 2.00) 4.84) 2.27-1.45-1.48-5.64 (1.27 (2.14-2.38-1.10) 6.01) 1.55 (4.54) 2.67-6. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.76-3.75) 1.2) 6.58) 4.24 (3. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.56 (1.74 (5.76) 2.99) 1. 1984.08-1.91) 2.62 (4.97-3.99 (2.33) 6.61) 2.97) 1.36 (3.16) 11.24 (5.23-2.45 (1.26) 4.64) 7.50) 1.03-1.47 (5.28 (1. interval) 1.81-6.68-3.76 (2.55) .39) 4. chemical form.30 (1.24-6.34 (1. in urine.71 (5.82) 1.19-2.00) 1.963 (.19-1.59) 2.39 (2.61 (4.48-3.89 (2.40-1.29 (1.3) 6. 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.48 (1.26-1.37) 2.46 (2.02 (3.64) 7.10-1.98 (2.32 (1.22-1.57-10. Following intravenous injection in animals.32 (2.96) 7.38 (4.73-4.75-22.77) 1.36-2.51 (3.37 (1.91-2.79-5.01 (4. Insoluble barium salts.36 (3.75) 1.69-9.64 (1.26-1.32 (1.40 (1.80) 3.42) 1.52) 7.62 (1. 1989).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. and cardiac dysrhythmias.39-5. population from the National Health and Nutrition Examination Survey.880-1.46) 1.51) 4.0) 5.51) 6.02) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.52 (3.48) 2.96-6.34-1.84-2.10-2.70) 1.68-3.92 (4.58 (2.754-1.69 (5.97-4.20) 4.63-4.31-1.53 (2.18 (1.56) 4.59) 1.710-1.24-11.31) 5.4) 5.38-5. Barium is not rated for human carcinogenicity.99 (4.59-7.65 (2.20-2.38) 1.49 (1.39 (2.53-21.48 (1.86) 5.22-2.24) 3.27) 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 .41 (1.5) 1083 1334 1281 1097 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.31-1. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.75-3.60 (1.77) 5.01 (5.83) 3.00-1.59) 1.72) 4.39-1.70) 4.13-3.54) 1. 1994.36-1.97 (4.30 (1.38) 1.81-6.03) 1.76) 1.55-5.37-2.03-1. Wones et al.38 (1.05-1.68 (3. diarrhea.80) 4.34-5.36 (1.921 (. weakness.45 (3. NTP.49-1.06) 2.33 (5.60) 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 2.31 (4.74) 1.41) 5.56) Selected percentiles ( 95% confidence interval) 50th 1.29-7.88 (6.27-3.96) 4.00 (2.35-1.52-10.96) 4.96 (4.55 (1.36 (1.24-6.4 (5. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.72 (2. paralysis.77) Total 1.40 (1.23-5.62) 2.34-3.03) 3.62 (2.73) 2.00 (5. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U..28-11.66 (1.56 (1.52) 1.77) 1. Toxicity from soluble barium salts is rare. are not absorbed when administered.48-1.96 (4.43) 1.77) 1.36 (5.57-7.02) 4.91 (3. vomiting.39 (3.45-8.64 (1.48 (1.00) 6.04) 1.76 (4.64 (1.23-1.25) 4.78 (2.29-4.39-1.00 (3.53) .28-7.Metals was eliminated primarily in feces and to a lesser extent.22-4.42 (4.50 (4.47) 1.58) 75th 2.47) 10.33 (1.28-1.51) 4.55 (5.09) 6.32) 2.79) 1.06) .20-1.39 (2.86-7.10 (6.51 (1.03) 2.97 (5.52-4.41 (2. 1990). about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.08-2.0) 6.54 (2. 1985. Symptoms following acute high dose include perioral paresthesias. water solubility.28-6. Perry et al.47-8.34) 1.82) 1.60 (1.33-4.915 (.70) 10.68 (3.26-4.68) 1. a benign condition that may occur among barite ore miners.15-4.29 (3.86 (2.

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

In medicine.13. and can be found in mineral rocks. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. 7440-41-7 General Information Pure beryllium is a hard gray metal. respectively. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and 03-04 are 0. are mined for commercial recovery of beryllium. and 0.130 (<LOD-. Beryllium compounds are commercially mined. population from the National Health and Nutrition Examination Survey.13. near some hazardous waste sites. which may vary for some chemicals by year and by individual sample. x-ray machines. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes.130 (<LOD-. the lightest of all metals. eating food. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 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 . Two types of minerals. aircraft. beryllium is used in instruments.13. nuclear. Exposure to beryllium occurs mostly in the workplace. see Data Analysis section) for Survey years 99-00. 0. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and refined beryllium is used in mirrors and special metal alloys for the automobile. In studies of laboratory animals. bertrandite and beryl. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air. coal. electrical. < LOD means less than the limit of detection. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. and from breathing tobacco smoke. Low-level beryllium exposure in the general population can occur through breathing air. computer. and dental bridges. and machine-parts industries.Metals Beryllium CAS No.150) < LOD < LOD < LOD < LOD 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 01-02. or drinking water containing the metal.S.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 . 196 Fourth National Report on Human Exposure to Environmental Chemicals . soil.140 (<LOD-. and volcanic dust.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.

Chronic beryllium disease. IARC has classified beryllium as a human carcinogen.281 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Air levels greater than 100 µg/m3 can result in erythema and edema of the lung mucosa.231 (<LOD-. More information about external exposure Urinary Beryllium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. respectively. Fourth National Report on Human Exposure to Environmental Chemicals 197 .346 (<LOD-. is a granulomatous interstitial lung disease that is caused by chronic beryllium inhalation and the resultant immunologic response. including contact dermatitis and subcutaneous nodules. The effects of occupational exposure to beryllium depend on the concentration of beryllium in the inhaled air and the duration of air exposure. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . which produces pneumonitis.S. Maier. population from the National Health and Nutrition Examination Survey. NTP considers beryllium to be a known human carcinogen.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 . based upon excess lung and central nervous system cancers in studies of workers. and drinking water and environmental standards have been established by U. Skin exposure can result in delayed hypersensitivity reactions. 2003. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.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. Workplace air standards and guidelines for external exposure have been established by OSHA and ACGIH. or berylliosis. Genetic factors modify individual sensitivity to beryllium and susceptibility to developing chronic beryllium disease (McCanlies et al. Human health effects from beryllium at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1990).Metals days has been calculated for beryllium elimination from the human skeleton (IPCS.. S. 2002).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 . EPA.

gov/toxpro2. which approximate this Report’s limit of detection.1 μg/L).76(1):53-59.cdc. Levels of beryllium in urine for the U. Given these results. McCanlies EC. and serum of Italian subjects. Minoia C. Ash KO.. Apostoli P. Morrow JC. Howerton K. population are lower than levels in workers. Schaller KH. and 2003-2004. Maier L. Minoia et al.e. 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. Sabbioni E. Ting BG. Sabbioni E.Metals (i. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Van der Venne MT. Beryllium [online]. and the 95th percentile for males in NHANES 2001-2002. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. Jackson RJ. Sci Total Environ 1990. 2001).atsdr. Atlanta (GA) 2005.23:827-839. et al.74:162-166.. Sci Total Environ 1994.org/documents/ehc/ehc/ ehc106. Comparison of representative ranges based on U. Weston A. Genetic and exposure risks for chronic beryllium disease. Pozzoli L. Pirkle JL. VI. Clin Chim Acta 2000.. Clin Chest Med 2002. Am J Epidemiol 2003. blood.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller. They reported urinary beryllium levels ranging from 0. Andrew M. Gallorini M. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure.S. environmental levels) and health effects is available from ATSDR at: http://www. In other studies. Element reference values in tissues from inhabitants of the European community.S. 1998).158:165-190. Centers for Disease Control and Prevention (CDC).htm..296(1-2):71-90. Costa R. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. References Apostoli P. Kriess K. 106. it is likely that urinary beryllium levels in the U. patient population and literature reference intervals for urinary trace elements.12 to 0. Paschal et al. 1990. Paschal DC. Available at URL: http://www. Sampson EJ.13 μg/L.inchem. Hamilton EI. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. Review of elements in blood. 20012002.95:89-105. Trace element reference values in tissues from inhabitants of the European community I.157:388-398. population were generally undetectable in NHANES 1999-2000. Trace metals in urine of United States residents: reference range concentrations. A study of 46 elements in urine. Environmental Health Criteria.. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Pietra R. 3/27/08 Komaromy-Hiller G. 0. Third National Report on Human Exposure to Environmental Chemicals. Environ Res 1998. Int Arch Occup Environ Health 2001. and the fact that most NHANES participant levels were undetectable. less than 0.e.S. Hamilton et al. International Programme on Chemical Safety (IPCS).html. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures. HLA-DPB1 and chronic beryllium disease: a HuGE review. 198 Fourth National Report on Human Exposure to Environmental Chemicals . 1990. 2000.

700) .600-.400 (.500-.200 (.300-.00 (.00-1.300 (.500) .500 (. Other uses include pigment production.S.800) .50) 1. as zinc sulfide) and to a lesser extent.600) 90th 1.00 (.50 (1.300) 1.300-.00-1.3.300) .400-.400) .10 (1.300 (.200 (.300 (<LOD-.00-1.70) 1.20-1.400 (.300-.40 (1.376-.20) .500 (.300) .gov/minerals/pubs/commodity/cadmium).70) 1.80) 1.50-1.300) .304-.600 (.400) < LOD .400 (. and 03-04 are 0. malleable.513) .400) .600) .400) .400-.600) .400 (.900-1.20-1.400 (. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.900 (.362-.300-.50-1.300-.600 (.40) 1.30) 1.500 (.10 (1.20) 1.300) .400) .20) 95th 1.403) .S.500 (.900-1.400 (.60 (1. and 0. plastic stabilizers.200-. Cadmium also may be emitted into the air from zinc.50) 1.300 (.344) .300-. population from the National Health and Nutrition Examination Survey.20) 1.441) * .40 (1.20-1.3.900-1.30-1.296-.600) .500-.403 (.300-.00 (.20 (1.300-.326 (.309-.378-.300-.500 (.40) 1. during refining of lead and copper from sulfide ore.10 (.400 (. < LOD means less than the limit of detection.500) .700-1.40-1.50 (1.266-.400 (. 0. which may vary for some chemicals by year and by individual sample.500-.300 (.275-.304 (.500-.300) .320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .500 (.600 (.900-1.382 (.500-.40 (1.300-.30-1.30) .400-.283 (. lead.300) .420 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.331) .14.400 (.700) .300 (.400) .Metals Cadmium CAS No.300-.368-. U.600 (. respectively.60) 1.600) .300) .400 (.20-1.500-.200-.300) 75th .200-.800-1.60 (1.20) 1.400 (. or copper smelters (U.300) .10 (1. Fourth National Report on Human Exposure to Environmental Chemicals 199 .400 (.600-.200 (.500) .366) * * .10) 1.400-.500-.00 (.700) .10) 1.600 (.600 (.500 (.300-. cadmium use has declined in response to environmental concerns (http:// minerals.600 (.300) .40 (1.900-1.00 (.900-1.400) .400) < LOD .367-.300 (.30-1.400-.800 (.30 (1.400-.600 (.300-.500 (.300 (<LOD-.800) .216-. EPA.10) 1.400-.30-1.424) * . see Data Analysis section) for Survey years 99-00.20) 1.300 (.800) 1.usgs.50-1.300 (.00 (.300-.300-.468 (.300-.20) .00-1.400) .10) 1.10) 1.300 (.20) 1.300-.600) .300 (. 01-02. and nonferrous alloys.300-.427) * .500-.S.300-.470) * .386-.500-.40 (1. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.200-.80) 1.378 (.600 (.600 (.10) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.400-.10) 1.300) .400 (.700) 1.70) 1.500-.289-.700-1.300 (<LOD-.400) < LOD < LOD < LOD .304 (.398) < LOD < LOD < LOD < LOD < LOD < LOD . and incineration of municipal waste materials.393 (.700) .700) .50-1.50) 1.20-1.300 (.700) .400) .60) 1.500-.600) .400) .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 .500 (. interval) .300-.200 (<LOD-.10 (1.235 (.900-1. coatings and plating.500) .00) .500-.359-.421 (.600) .40-1.500-.700 (.00 (.500) .400 (.30) 1.800 (.900-1.00-1.449) Selected percentiles ( 95% confidence interval) 50th .20-1.200-.500-. Since 2001.500-.900 (.300) .313 (.500-.333 (.60) Total * .395 (.20) 1.400-.20) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.20) 1.400) .30) 1.300-.400-.400 (.00 (.10 (1.500) .60 (1.200) .400) .50 (1.600 (.500-.20 (.00 (.600) .300-.600 (.600 (.700) .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 .00-1.500) . 7440-43-9 General Information Cadmium is a soft.200 (<LOD-.452) .400) < LOD .50 (1.60-1.10 (1.60 (1.700) .300 (<LOD-.600-. The predominant commercial use of cadmium is in battery manufacturing.200) .400) .300) .00) .80 (1.425 (.255) .500-.10) 1.337) .30-1.600-1.300 (.600 (.60 (1.600) .00 (1.400 (.300) .600) 1.20-1.400) .400-.800-1.412 (.40 (1.400) .10 (1.70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.60) 1.90) 1.40 (1.900-1.00-1.70) 1.361-.300 (.00-1.426-.700-1.00-1.400 (.460) .300 (.900-1.00 (1.00 (.

20 (1.57) 1.109 (.03) . see Data Analysis section) for Survey years 99-00.160) .836-1.191 (.251) .260-.800-.890-1.109-.479) .480) .157) .989-1.316 (.167-.09-1.090) .462 (.20 (1.262) .198) .229) . respectively.17) .25) 1.381-.195-.17 (.445 (.960 (.980-1. Horiguchi et al.36) 1.339) .450 (.390-.790 (.190-.28-1.219 (.Metals 2000).445 (.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 .272-.20) 1. With chronic exposure.519) .150) .17 (.48 (1.545 (.860) 1.210 (.227 (.498-.211-.238) .234 (..221 (.06.237-.13-1.190-.230) .519) .41 (.705-.135 (.310 (. 2003).130 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .980-1.589 (.230 (.559 (. zinc.220-. 1994).452 (.366-. 2003).189-.170 (.43) 1.210) .813 (.19) 1.322 (.203) .255) .890 (.22 (1.500) .199 (.134) .763-.210 (.150-.858 (.980 (.** Survey Geometric mean (95% conf. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.232 (.202-.257) .476-.700-.121 (.180 (.818 (.101) .633-1.115-.211 (.07-1.06.26) 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.436-.880) .82) 1.817 (. whose body burdens of cadmium can be approximately twice that of nonsmokers.206) .875) .194-. calcium.34) 1.229-. rice. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.918-1.192-.492 (.741-1. copper) and protein. an inducible metal binding protein.963-1.270 (.223 (.067-.12-1. 01-02.440-.210) .171-.450 (.806) .209 (.820-1.412) .387) .730-.265 (.717-. including many food crops such as cereal grains.596) .260-.810-1. 2003).980) .32 (1.169-.458 (.233) .078 (.493-.214-.20 (1.299) .456-. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al. Cadmium is absorbed via inhalation and ingestion.360) . About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.285-.141 (.202 (.160-.28) 1.295) .839 (.193 (.551 (.362) .231) .47) 1.107-.28 (1.10 (1.192-.04 (.204 (.148-.277 (.110-.092 (..350 (.800 (.221) .400-. and 03-04 are 0.112-.135-.148) . cadmium accumulates in the liver and kidneys where it is bound to metallothionein.848 (.190-. Diamond et al. 0.177-..196-.077 (.193-.282 (.273 (. 2001).308) .220 (.01) .235) .52 (1.203 (.875 (.892-1.733) .550 (.120 (. Renal tubular and glomerular damage.714-1.700-.329 (.870) .400-.320) .980) .265) .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 . and various seeds.230) 75th .247) .433-.977) .283 (.222) . 200 Fourth National Report on Human Exposure to Environmental Chemicals .302 (.289-. Cadmium absorption may be increased with iron deficiency (Berglund et al.820 (. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.290-..260 (.153-.187 (. Inhalation of cigarette smoke is a predominant source of exposure in smokers. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.233) .191-.200 (.490) .530) .72) 1.366) .249) .390 (.175 (.51 (1.607) .15) 1.281 (. ingestion through food is the largest source of exposure.065-.481) .30-1.270 (.960) 1.455 (.733-.20-1.892 (.179-.160 (.126) ..181 (.640) .633 (.886-1.327 (.080 (.700-.26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.510) .173) .238-.38) .257-.229) .067-.393-.219 (.175 (.326) .243-.240) .081) .610) .219 (.790 (.855-1.200-.160) .061 (<LOD-.220) .336) .210 (.06.200-.430) .354) .092) .447 (.01 (.38) .165-.13) .06-1.100-.990) .232) .02-1.077 (.200 (.191-.430-.38) 1.136) .886) .183-.390-.351-.24) 1.820) 1.249-. 1999.580) .061-.261-.372) .466 (.686-.284) .713) .06) . The kidney is a critical target and shows the earliest sign of cadmium toxicity.440 (.170-.38) 1.280 (.157-.128 (.972 (.330-. Kikuchi et al.178-.551) .510-.388-.241) .226) . potatoes.255) .817 (.S.240-.087-.206 (.210 (.140 (.500) 90th .184-. **All results are corrected for molybdenum oxide interference in the ICP-MS method.06-1.210 (.255) .520-.919) .748-1.239 (.253-.540) . and 0. To a lesser extent. population from the National Health and Nutrition Examination Survey.940-1. however.753-.470-.843-1.060-.22 (.189) .151-.208-.680 (. For nonsmokers who are not exposed to cadmium in the workplace.310) .12 (.279 (.15) .313) .530 (.440 (.366-.490) 1.83) 1.04 (.207-.475 (.114-.170-. interval) .263) .300) . 2004a.246) .090) .189-.01-1.17 (.507) . 2003.482) .423-.306 (.426 (.300 (.766 (.216 (.220) Selected percentiles ( 95% confidence interval) Sample 95th 1.623) .. drinking water is a source for cadmium intake.394-.539) .13 (. Cadmium in soil is absorbed by plants.74) 1.25 (1.15 (.201 (.220-.261-. wheat.

757) .122 (.242) .253 (.219 (.418) .338 (.211 (.434 (.227-.412 (.491-.168-.300-.270 (.476) .830-1. 1996..278) .247-.850) .308 (.865 (. 2003.182) .178-.209) Selected percentiles ( 95% confidence interval) Sample 95th .666-.063-.216-.177) .335 (.181-.207) .769 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.199-.154-.289) .113-.415) .181 (.158-.226) 75th .917) .350) .252 (. 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.438-.690-.05) 1.674-1.173-.919 (.210) .247-.364) ..137-.197-.979 (.156 (.441-.147-.091 (.418-.191 (.135) .940 (.219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .232) .470) .191) ..156) .716-.404 (.131-.382-.818) .143-.289) .288-.668-.507-. At lower environmental exposures.516-.293-. 2004).754) ..090 (. Noonan et al.187) .545) .404) .202 (.826-1.398-.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.078 (.168 (.693 (.196 (.431) .181) .985 (.210 (.174-.085 (. Fourth National Report on Human Exposure to Environmental Chemicals 201 .387 (.223) .205 (.304-.449) .100 (.729 (.691-.178) .470) .137 (.268 (.190 (.13) .678 (.712 (.175-.130-.645-.850) .184) .233 (.686 (. 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. During the 1950’s and 1960’s.198) .161-.813-1.500-.106) . Jarup et al.238-. interval) .725-1.238) .340) .784) .07) .084 (.175 (.140-.292) .074-.647-.931 (.168-.650-.667) .184-.501 (.150-.630-.423 (.806-1.07 (.215 (.156-.631) .607) . two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.282 (.182) .538) .159 (.622 (.757 (.206-.183 (.783 (.962) .170-.718 (.094) .126 (.856) .708-1.228-.941 (.** Survey Geometric mean (95% conf.440) .16) 1.209) .101) ..727-.377-.111-.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 . 2000.147 (.263-.856 (.182) .187-.617 (.162 (.303) .325 (.336-.239-.311) .175 (.779 (.16) .884) .051-.329 (.185) .719 (.426-.189-.722-.343-. most often a result of occupational exposure (Roels et al.487 (.147-.222-.071 (.078-.12) 1.261) .833-1.818) .283 (.433-.256-.381-.533) .591 (.536 (.136-.199 (.083-. 1999). 2002.144-.107) .690 (.194-.143) .795) 1.839) .212 (.075 (<LOD-.234-.909-1.444-.828) .273 (.653) . 2004b).423-.253) .562-.38) .789 (.929) .091) .551) .267 (.085-..321) .123-. 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.740 (. Olsson et al.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 .077-.446) .873 (.479 (.084-.224 (.075-.191-.490 (.181 (.518) . 1999).783) .274) 1.00 (.266-.232) .614) .472) .225) . Staessen et al.17) .700) . 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.481 (.207-.157-.10) 1.235) .663 (.06 (.267 (.123-.192) .112) .201-.391-.08) .432 (.296 (.104) .096) .414-.220 (.247-.171-.927-1.140-.250) .281) .Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.767) .091 (.240) .146-.414 (.318 (.261 (.200 (.208-.208 (. 2002.792 (.159 (.093 (. 1999).245 (.166 (..170 (.830) .143-.173 (. 2002. Horiguchi et al.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .998) .387-.331 (.097) .241) .352) .00 (. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.281) .086 (.229) .263 (.484 (.163 (.221-.906) .221 (.537-.876-1.176 (.388-.176 (.802 (.690-.154 (.. However.204-.210 (.687-.234 (.421 (.531 (.225) .316) .297) .440) .09 (.767 (.950) .240) .261-.813-.148 (.308) .716) .104) .288) .874-1.163) .218) .266) . 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.559-.304) .541) .136-.185 (.234) .280 (. can result from high dose chronic exposure.438) 90th .473 (. population from the National Health and Nutrition Examination Survey.687 (.560-.288 (.688-.827) ..382) .190 (.02 (.236-.184-.S.157-.183) .917 (.219 (.700 (.316 (.826-1.255-.696-.678-..940-1.098) .067-.

2003. 2002). 2002. 2006). Animal studies have demonstrated reproductive and teratogenic effects.S. People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. 2000. Occupational standards are provided here for comparison only. as may occur from welding cadmium-alloyed metals. However..atsdr.. 2003. Horiguchi et al. 1999). has resulted in severe. 2005. pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies.... the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1... Acute and heavy exposure to airborne dusts and fumes. 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. In adults aged 60 years and older. respectively. Becker et al. Blood and urine cadmium levels are typically higher 202 in cigarette smokers. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. Horiguchi et al. Becker et al. Both IARC and NTP consider cadmium a human carcinogen. Wennberg et al.. Becker et al. For NHANES 19992000. Information about external exposure (i. with peak values observed in the fifth to sixth decades (CDC. potentially fatal pneumonitis (Fernandez et al.. 2000. Moriguchi et al. 2006.. 2004). 2005. data (CDC. Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity. 2002. 2004b. 2002.. 1996).. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al.html. Salpietro et al. 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. 2002.S... Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood.. Women had higher blood and urine cadmium levels compared to men of similar ages.. 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. Friedman et al.. Wilhelm et al. 2002). Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures.gov/ toxpro2. 1999.. 1988). CDC.... respectively. approached these values associated with subclinical changes in renal function and bone mineral density. 2004. 2005). Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. Cadmium can produce lung. 2005. Jarup et al. In postmenopausal women. 2000. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals .. 2004. 2006).. Creatinine-corrected urine cadmium values in U. 2002). Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect.. 2005. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. 2002.. 2003. Komaromy-Hiller et al. 2002) and length at birth (Nishijo et al... 2003. Noonan et al. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH. The 95th percentiles for cadmium levels in this Report were less than the OSHA standards for both blood cadmium (5 mg/L) and urine cadmium (3 mg/gram of creatinine).. Staessen et al.46 mg/gram of creatinine) (Ezaki 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. 2002). 2002). Ezaki et al. Olsson et al. 2000).1 mg/L (Alfven et al. Staessen et al.26 and 3.S. Suwazono et al.e. Wennberg et al.cdc. 2003. 2002. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles.. 1999). EPA. 2006. and drinking water and environmental standards have been established by U... urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney.. Olsson et al. 2004. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al..... Olsson et al. Further research is needed to address the public health consequences of such exposure in the United States. Staessen et al. not to imply a safety level for general population exposure.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. Jin et al. 2003). maternal blood or maternal urine and birth weight (Nishijo et al. Zhang et al. Mannino et al. Ezaki et al. environmental levels) and health effects is available from ATSDR at: http://www. In the typical environmental exposure. 1996. 2004b). Jarup et al.. intermediate in former smokers and lower in never-smokers (Becker et al..... 2004. 2003.

96:353-359. Tsukahara T.gov/toxprofiles/tp5. Int J Hyg Environ Health 2002. Holguin F. Becker K. Lauwerys R. Fourth National Report on Human Exposure to Environmental Chemicals 203 . et al. et al. Fernandez MA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. et al. Nermell B. Kikuchi Y. a1-Microglobulin as a promising marker of cadmium-induced tubular dysfunction. et al. Mascagni P. Bregante G. Lundh T. Anthropometric. Consonni D. Jarup L. Kumagai N. Sasaki S. Berglund M. Seifert B. Schulz C. Miyamoto K. Fayers PM.59:497]. Chislovska NV.76:186-196. Third National Report on Human Exposure to Environmental Chemicals. Furuki K. Takebayashi T. Ye T.13(11):1627-1631. Pharmacokinetic/ pharmacodynamics (PK/PD) modeling of risks of kidney toxicity from exposure to cadmium: estimates of dietary risks in the U. Environ Health Perspect 1994. Fukui Y. Nordberg G.cdc. et al.66(Pt A):2141-2164. Environ Res 2004. Darbyshire J. Krause C. and dietary predictors of elevated blood cadmium levels in Ukranian children: Ukraine ELSPAC group. Miyamoto K. Taylor AJ. 196:114-123. Nerbrand C. Friedman LS. ShkiryakNizhnyk AZ. Wang H.296(1-2):71-90. Hellstrom L. Cadmium and lead in blood in relation to low bone mineral density and tubular proteinuria. Comprehensive study of the effects of age.46:372-374. Pickering CA. Alfven T. et al. Okamoto S. Dietary exposure to cadmium at close to the current provisional tolerable weekly intake does not affect renal function among female Japanese farmers. Int Arch Occup Environ Health 2003. Mucha A. Kaus S. Ezaki T. Jarup L. Buchet JP. Thorax 2004. Savage-Brown A. 2005. 4/8/09 Alfven T. Sanz P. Clin Chim Acta 2000. Gadea E. Ezaki T.110:699-702. Lukyanova EM. Jin T. Persson B.95:20–31. et al.59:194-8. Becker K. Uemura T. Centers for Disease Control and Prevention (CDC). Atlanta (GA).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. Lison D. No clear-cut evidence for cadmium-induced renal tubular dysfunction among over 10. Lancet 1999.102:83-89.S. iron deficiency. possibly better than b2microglobulin. Moriguchi J. Serra J. Carlsson MD. Environ Health Perspect 2005. Hotz P. J Toxicol Environ Health 2003. 1999 [online]. Toxicological profile for cadmium update. Komaromy-Hiller G. Grubb A. Toffoletto F. Int J Hyg Environ Health 2003. Seiwert M. Kundiev YT. et al. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. J Occup Health 2003. Howerton K. Urinary cadmium levels predict lower lung function in current and former smokers: data from the Third National Health and Nutrition Examination Survey. Ash KO. Olfactory function in workers exposed to moderate airborne cadmium levels. Agency for Toxic Substances and Disease Registry (ATSDR). Environ Health Perspect 2002. Fatal chemical pneumonitis due to cadmium fumes.atsdr. diabetes mellitus. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. References Akesson A. Available at URL: http://www. Renal effects of low-level environmental cadmium exposure: 5-year follow-up of a subcohort from the Cadmibel study. Cadmium fume inhalation and emphysema. Osteoporosis and renal dysfunction in a general population exposed to cadmium in China. Vahter M. Palomar M. patient population and literature reference intervals for urinary trace elements. Lepom P. Toxicol Appl Pharmacol 2004a. Neurotoxicology 2003. Stock AL. Seiwert M.1(8587):663-667. Nomiyama T. Dekio F. et al. Lidfeldt J.354:1508– 1513. Toxicol Lett 2004. Choudhury H. Environ Res 2004b. Horiguchi H. Occup Med 1996. Environ Res 2006. Vahter M. Lancet 1988. Bellerup P. Greves HM. Ukai H.24:717-724. Low level exposure to cadmium and early kidney damage: the OSCAR study [published erratum appears in Occup Environ Med 2002. Machida M. Tsukahara T. 102:10581066. Diamond GL. Horiguchi H. Davison AG. Comparison of representative ranges based on U. et al.html. Bernard A.000 women in the Japanese general population: a nationwide large-scale survey. Bo M. Furuki K. and cadmium burden on dietary cadmium absorption in cadmium-exposed female Japanese farmers. population. 206:15-24. Oguma E.148(1-2):11-20. Costa R. Kaus S. Jones RL. Moriguchi J. Occup Environ Med 2000. Thayer WC.205:297-308. environmental. Tubular and glomerular kidney effects in Swedish women with low environmental cadmium exposure. Venables KM. Oguma E. Schulz C. et al. Fukui Y.57:668-672. Uptake of cadmium in meals from the digestive tract of young non-smoking Japanese female volunteers. Intestinal absorption of dietary cadmium in women depends on body iron stores and fiber intake. Sasaki S. Chiappino G. Ikeda Y. Ikeda Y.S. Akesson A. Mannino DM.45:43-52. Elinder CG. Machida M. Zhu G.

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04 (4.5) 10.49) 4.93 (4.09-5.10-5.10-8.13 (5.80) 7.00-8.90-10.97) 4.94 (4. respectively.05) 5.4) 10.1) 11.15-8. the body half-life is estimated to be 70-109 days based on 137Cs exposures.7 (9.90 (6.7) 11.64-5.20-7.8) 9.21 (4.57-5.86 (7.00 (7.8-13.16-6.3 (8.60-7.9 (11.81) 4.20) 7.59-5.77 (4.02 (4.80 (8.4) 12. Fourth National Report on Human Exposure to Environmental Chemicals 205 .05-5.10-9.36 (6.25 (3.32 (3.7 (9.9) 8.53-11.42) 7.23-4.70 (6.7 (9.30 (6.13 (8.1 (10.22 (4.12-11.77-8.68 (7.64) 5.83-4.40 (4.80 (8. and high-power gas-ion devices.84) 5.50 (6.60-6.26 (3.43-8.9) 11.55 (4.33 (5.1) 9.45-8.01-6.32) 4.59) 7.39-4.40) 5.49 (5.97-7.07-11.5 (10.3) 10.1 (11.87-7.56) 5.3-13.95) 5.5-13.4 (9.9 (11.10-7.09) 5.89) 4.83) 6.6 (9.76-6.4 (10.8) 9.64-10.1-12.80-13.33 (6.42-7.90) 5.9) Total 4. 0.62 (5.29) 4.77 (9.00-4.9 (10. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.14.25) 4.12) 5.4) 9.1) 9.7-14.08-5.81 (4.87 (4.8) 12.5 (8.80 (4.74-5.08 (6.8) 12.42) 6.40-5.90) 5.60) 5. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.55 (7. semiconductors.10 (6.90) 4.20-5. However.70 (6.50 (4.6) 11.99) 7. 01-02.20 (4.90-12.03 (4.69-6.9 (11.77 (9.98 (7.90 (4.3) 10.34) 9.7 (10.63 (4.0) 9.59-5. and clay.82-4.4) 10.81) 4.63-4.30-10.25-5.33-5.3) 9. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. photographic emulsions.56-11.27 (7.84-5.74 (4.0) 10.90) 7.20-8.79 (4.80-11.37) 7.91 (7.86-11.70-8.05-5. although cesium was generally of low toxicity when given to animals. For absorbed cesium salts.0) 12.30-5.55-11.20) 4.98 (7.00) 4.0 (10.00) 7.7) 10.50 (4.71) 4.46) 7.44 (8.7 (11.2-13.54-11.7) 11.50) 9.1) 11.13-8.40-7.49 (4.2-13.71 (8.08-5.70 (9.61) 7.40-5.70 (8.00-9.50) 5.80-10.53 (6.70 (4.4) 11.8) 11.07) 4.1) 10.3-15.29 (4.34 (4.3 (8.89-5.0-15. interval) 4.00) 6.64 (4.50 (4.39) 7.3) 10.6 (9.2-13.81-14.2-14.50 (7.5) 12.70-5.5-14.01) 7. population from the National Health and Nutrition Examination Survey.97 (7.89) 5. cesium hydroxide is corrosive and irritating at high concentrations. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.2 (9.60) 7.63) 6. infrared lamps. see Data Analysis section) for Survey years 99-00. and 0.95 (3.56 (4.7 (10.0) 12.20 (6.8 (10.49) 75th 7.40-11.20-4. and cardiac arrhythmia (ATSDR.50-7.30) 5.99-11.70) 7.90-10.70 (5.80 (8.08 (7.9 (10. diarrhea.6 (11.4 (9.7) 10.71-5.9) 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.S. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.1-13.27-5. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.70 (8.40-11.16-6.17 (6.21) 90th 9.4-13. Whether cesium compounds are carcinogenic is unknown.62 (5.59-5.70) 5.00-10.82) 5.87 (4.80-6.40-5.87) 5.45-5.87 (4.35-5.32-5.20) 8.5-14.84 (4.03-4.8) 12.04) 7.26-11.23) 9.52-9.3-13.5-16.7 (10.12-5.36 (3.22-4.30 (6.91-8.92-13.5) 9.12 (4.36) 3.60-12.0) 11.47-8.17) 4.6 (11.31-8.54) 4.8 (10.60-5.2.6 (9.2) 12.13 (7. nausea. Most human exposure to cesium occurs through the diet.10 (6.27) 4. and 03-04 are 0.47-4.38) 5.99-11.90) 9.60 (8.0) 12.4) 12. Little is known about the health effects of this metal.84-9.64) 5.60-6.66 (7.60) 7.56 (4.1-12.20) 5.6) 10. Radioactive 137Cs has been used medically to treat cancer.35 (4.40) 5.88 (8.0) 11.10 (8.59 (5.68) 9.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.24) 4.95-4.30) 7.61-6.96 (6.72-7.2-12.80 (4.43 (5.94 (4.26) 7.17-6.10 (8.2 (9.97) 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 4.52) 7.05) 5.14.2) 11.26) 4.4) 95th 11.64) 4.3) 12.62) 4.Metals Cesium CAS No.80-10.3) 10.40) 7.99-6.80 (4.1 (9.8) 11.73-11. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.01-8.94-4.8 (11.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. soil.9) 12.71-8.71-9.90-8.35 (4.0-13.00-8. scintillation counters.73-5.86-12.7 (8.37) 5.6 (9.74) Selected percentiles ( 95% confidence interval) 50th 4.90-10. and as polymerization catalysts.84) 8.40-5.9 (11.71 (4.60-7.81) 9.14 (4.99) 9.80-10.90-12.0 (9.94) 4.67 (4.60 (7.70) 5. 2004).03 (4.72) 4.08) 7.

17) 4.49) 3.35 (3.6) 6.66-6.53 (6.48) 7.06 (5.16-8.67 (5.82-4.47) 4.47 (7.65 (6.97-5.26 (3.47) 6.38) 10.31-6.43-11.44 (4.83) 8.02 (5.21-4.36-10.50-5. (2000) found urinary cesium levels that were slightly lower than those reported for the U.30 (3.16) 5.39) 8.56) 4.54 (4.15-4. Using clinically submitted specimens.40) 7.08 (6.02-4.50) 4.62-8.99-4.95-12.48) 90th 7.50 (6.07-4.79 (5.53 (4.90-3.43 (3.87-4.13) 7.31-4.81 (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 3.41) 9.S.65-3.56) 4.46 (8..52-5.56) 3.3-15.91) 5.84-9.5) 9..75 (6. Two small studies of European populations reported urinary cesium levels similar to U.30-4.08) 3.80) 6.64 (4.56 (4.53) 3.25) 4.39 (5.33-3.41-7.17 (6.45 (4. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.21-3.56-10.95 (3. population results shown in this Report (Alimonti et al.91) 4.38 (3.57) 3.46-8.21 (2.3) 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 3.3 (9.51 (4.64) 4.87) 5.96 (4.2 (8.59) 4.00-10.11 (5.87 (5.37-3.53) 6.84-11.95-6.70 (7.54 (3.42 (4.60) 3.90-8.27 (8.86 (4.68) 4.63-6.5) 9.08 (3.41) 4.06) 5.00-8. Minoia et al.8 (9.03) 5.95) 4.31 (4.20-4.00) 6.05-4.03) 6.96-4.42-4.9 (9.04) 5.63) 6.58) 8.60 (3.55-5.46) 6.96) 4.18-6.99-9.67) 5.88-10.20-4.54 (4.27) 4.97) 8.85-4.09) 4.08) 4.76-9.68) 3.08 (5.95 (5.05) 6.14-6. population from the National Health and Nutrition Examination Survey.58-5.89-4.16-8.65-4.7) 10.00-5.26-6.0) Total 4.50) 4.35 (4.43 (8.85) 5.92) 3.30-4.20) 5.01-8.1) 11.74) 3.47) 7.44) 3.16-5.35-7. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.17) 9.91) 5.68) 6.99) 4.70) 6.00-9.51 (3.24-4.13-9.71 (7.9) 10.66 (6.78) 4.05 (4.84-7.46-4.91 (5.68-11.43 (4.97-4.75-11.83-7.50 (5.24-10.77 (7.04-5.35) 3.72 (4.9 (10.0 (7.66 (5.12) 3.43) 8.14-7.40-5.72-5.74 (4.50) 8.41 (4.77-5.05) 3.84-7.36-6.04-11..44-5.98) 5.93-9.14 (6.03-6.30) 10. 2005.74 (5.90-8.74) 75th 5.77 (4.30 (7. population. 1990).83-6.43-6.62) 5.29) 4.63 (7.96) 4.73 (3.42-4.3) 9.30 (4.2 (8.10-4.29-3.41-4.46 (7.35-11. and were also roughly similar to those in this Report.33 (5.71) 6.98 (6.79) 6.76-6.29-3.18 (7.77 (6. 2004).27-4.84-9.63 (4.90 (7.94) 7.21-5.04) 6.38 (3.34 (5.10 (5.78) 4. interval) 4.67 (6.07) 8.08-3.72) 4.7-12.08-7. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.22-11.07 (5.41 (5.78 (3.24 (3.15 (7.43 (4.42 (5.14) 4.7) 10.28 (5.0) 7.20-4.13-9.58 (4.06 (3.28) 7.06) 4.31 (4.92 (5.50 (7.48-6.63 (6.29) 5.20-8.42-6.64) 9.18) 8.22 (3.44-9.11 (5.96-4.51 (3.61 (7.29) 4.51) 4.45-6.51 (7.51 (4.27-6.64 (8.03-5.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.09 (4.00 (8.78 (3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.66 (5.S.8) 5.3) 11.5 (9.77) 4.47 (4.10 (3.58 (6.55 (3.00-5.70) 7.28) 8.12-6.26 (4.30) 10.79-5. Komaromy-Hiller et al.55) 4.8) 6.60-20.23 (7.93-7.68 (4.33-8.64-6.79) 9.25) Selected percentiles ( 95% confidence interval) 50th 4.08) 4.54 (5.91 (5.6 (9.37) 4.10 (3.18-7.19-3.39) 5.22) 6.6 (9.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .63-6.58) 3.12 (3.75 (7.95) 8.41 (8.38-7.05-3.15-11.95) 10.98 (7.38-12.3 (10.2) 11.91-7.44 (8.27 (6.74-11.61-3.87) 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 5.05-3.50) 4.33 (5.09) 8.13 (3.40) 6.91-6.27 (6.14-4.98) 5.15) 95th 8.59-8.17-4. Biomonitoring studies on levels of cesium can provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cesium than are found in the general population.14) 4.S.07) 8.3 (8.64) 5.00-4.60 (5.60-10.10) 7.99-9.8) 10.47) 6.94 (5.19-6.91-9.4) 10.36-3.99 (3.81 (4.88-4.73-4.28 (4.5) 7.82) 7.79) 4.85) 4. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

Toxicological profile for cesium. J Expo Anal Environ Epidemiol 2004. Sci Total Environ 1990. blood. Apostoli P. Komaromy-Hiller G. Gallorini M. Ronchi P.atsdr. Wolfe MI. Mincione G. 2000. 4/8/09 Alimonti A. Clin Chim Acta 2000. New Mexico. Gatti A. Pietra R. Uncertainty of inductively coupled plasma mass spectrometry based measurements: An application to the analysis of urinary barium. antimony and tungsten.95:89-105. Trace element reference values in tissues from inhabitants of the European community I. et al. Ash KO. Fourth National Report on Human Exposure to Environmental Chemicals 207 . patient population and literature reference intervals for urinary trace elements.S. Assessment of urinary metals following exposure to a large vegetative fire. Sewell CM. Forte G. Costa R.html. Comparison of representative ranges based on U. Mott JA. Wood CM. Atlanta (GA) 2005. cesium.19:3131-3138. Sabbioni E. et al. Rapid Commun Mass Spectrom 2005. Spezia S. Pozzoli L. Paschal D. Third National Report on Human Exposure to Environmental Chemicals. et al.Metals References Agency for Toxic Substances and Disease Registry (ATSDR).gov/toxprofiles/tp157.296(1-2):71-90.14:120-128. Voorhees RE. Minoia C. Centers for Disease Control and Prevention (CDC). A study of 46 elements in urine.cdc. and serum of Italian subjects. Howerton K. Available at URL: http://www.2004 [online].

660) .820 (.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 .950 (.316 (.710) .372) .620-.640) .56) 1.68 (1.770) .543) .29 (1.04-1.369 (.950-1.950-1.410 (.820 (.690-.60 (1.590-.750 (.600 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. large appliances.360-.285 (.04 (.461 (.64) 1.45 (1.980-1.23) .760 (.359 (. industry is imported or obtained by recycling scrap metal that contains cobalt.660) .330) .500 (.05) 1.515 (.920) 1.800) .540-.870-1.440-.380-.410-.428-.19) .99) 1.50 (1.46 (1.28 (1.16) 1.47) 1.331-.583) .360-.880-1.530 (.313) .388-. Cobalt may be released into the systemic circulation of patients who receive joint prostheses that are Urinary Cobalt Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.610 (. seawater.581) .670-.420) .06 (.410-.07-1.12) 1.487) . hard metal (alloys of cobalt and tungsten carbide). blue-colored pigments.373-.17 (1.330 (.670 (.47 (1.22-1.450) .338-. 208 Fourth National Report on Human Exposure to Environmental Chemicals .650 (.540) 1.710 (.740 (.15 (1.860 (.810) .800-.33-1.14-1.580 (.340-.410) .810-. and magnetic recording media.379 (.320 (.270-.450-.03-1.371 (.900) .300-.630 (.350 (.590-.690-.490-.370 (.360-.460) .16) 1.333-.570-.480-.650 (.47 (1.05 (.640) .32 (1.44) 1.377-.600) .405-.465) .470 (.890-1.24 (.730) 1.760) .33 (1.270-.520) .370-.410 (.330-.24 (1.450) .399) .08-1.410 (.560 (. hard metal or in combination with other elements. Cobalt is used as a drying agent in paints.520 (.340 (.410 (. Usual human exposure is from food sources.469-.840) .367 (.398 (.424) .39) 1.36) 1.650-.540-.400-.28-2.430 (.16 (.81) 1.590 (.280-.09 (.680 (.14) .03) 1.890-1.270-. and fertilizers.950) .670-.490-.520 (.680 (. see Data Analysis section) for Survey years 99-00.65) 1.570-.16 (1.334) .900) .580 (.374 (.520-.01 (.430) .21) 1.550 (.520) .17 (1. and in synthesizing polyester and other materials.07. Cobalt compounds are also used in manufacturing battery electrodes.435 (.530-.520 (.73) 1.410-.310 (.620-. It is emitted into the environment from burning coal and oil and car and truck exhaust.430 (.390 (.390-.930) .430) .17 (.355-.690 (.340) .540-.375 (.520 (. and 03-04 are 0.980) .630 (.740-.373) .630-.564) .26-1.380 (.52 (1.414) . population from the National Health and Nutrition Examination Survey.500) .610) .26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.520-.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 . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.32 (1.431) .910-1.410) .350-.850-1.900-1.28 (1.460-.32-2.01 (.59 (1.680) .450-.291-.710) 1.520-.420) .670 (.336-.03) . diamond-polishing wheels.502) .07 (.850-1. Cobalt compounds are used as catalysts in producing oil and gas.370-.960-1.430 (.04-1.380 (.520-.09) .550-. varnishes.393-.390 (.480 (.430-.386) . interval) .03) 1. and soil. 01-02.890) 95th 1.480 (. and inks.26-2.53) 1.350-.01-2.940-1.343) 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 .416) .75 (1.750-. shiny.92) 1.352 (.570 (.950 (.370-.340) .431) .519 (.26) Total .379 (.450) .01-1.26) 1.308-.450) .800-.348-.305-.900-1.370) .16-1.08.316-.327-.06-1.02-1.427-.04-1.28 (1.48) 1.600-.20 (1.398) . automobile airbags.81) 1.348-.460) .417) .00) .570) .850) 1.510) 1.390) .452 (. The cobalt used in U.42) 1.740-.460 (.47) 1.12) 1.496) . 0.700) .67) 1.810) .640) .300 (.790-.15-1.06 (.350) 75th .07-1.670 (.319) . It is also a component of porcelain enamel applied to steel bathroom fixtures.340-. respectively.463-.660-.900) .07.930 (.48) 1.830-1.343 (.03 (.540-.23-2.530) .17-1.25-1.50) 1.419) Selected percentiles ( 95% confidence interval) 50th .04) 1. Cobalt occurs naturally in airborne dust. steel-belted radial tires.394) .22) 1.364-.418 (.620) .750 (.03 (.590) . 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.850) .32) 1.390 (. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.460) .870 (.930-1.750 (.09 (.380-.499 (.610) .790) .404) .333-.700) .37-1.22 (1. and kitchenware.380 (.S.610-.680) .580 (.470) .434 (.13) 1.290-.870 (.350-.940-1.259-.460 (.570) .301 (.420 (.294 (.410 (.454 (.820 (.05 (.790 (.550) 90th . and 0.16-1.16 (1.620-.310-.890) .920-1.523) .Metals Cobalt CAS No.08) .880 (.32) 1.339 (.940 (.890-1.S.

337 (.73) 1.328 (.468) .281) .505) .830 (.500-.297) .317 (.744) 1.760-1.537 (.16 (1.895-1.523 (. Exposure in the workplace may come from electroplating.560-.290 (.821-3.301) .990-1.365) .750) .298 (.02 (.990) .310) .861 (.689 (.428-.11-1.251-. cobalt is excreted predominantly in the urine.660-.781-1.215-.344-.272-.296-.777-.463-.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 . 1994).976 (.700 (.599) . and to a lesser extent.595) ..503-.334) .457) .328) .844 (.369 (.301-.273 (.00 (.Metals fabricated from cobalt alloys (Lhotka et al.368) .333-.608 (.929) .872 (.792-1.378 (.12 (.469-. Once absorbed and distributed in the body.481) 90th .393 (.. Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.29 (1.333-.35) 1.563-.548 (.842) .593) .964 (.425-.667-1.669) .259 (.237-.388 (.16 (.829-1.352) .15) 1.561) .523 (.444 (.335 (. population from the National Health and Nutrition Examination Survey.14 (.271 (.404-.407 (.667-1. 1979).785) .247 (.291 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.362) .683-.353-.384) .513-.419) .57) 1.00) .304-.278-.396) .372) .328 (.333-.960 (.402 (.19) .304) .594) .543) .727 (.626-. in the feces.293 (.591 (.280-.361 (.408 (.36) 1.04-1.282 (..513 (.00) .824 (.306) 75th .850 (.911-1.279) .513) .00 (.282-.786-.268 (.611) .609) .851 (.10 (.327-.879-1.33) 1.04 (.952 (.50) 1.574-.376 (.495 (.353 (.55) .533 (.302-.600-.319-.488) .833-1.562) .547 (.421) .27) 1.297-.10) .289) .457 (.467-.554 (.471-.382-.349) . Cobalt is absorbed by oral and pulmonary routes.861-1.363) .700 (.694) .10) Total .290 (.616-.29) 1.963-1.313-.257-.542 (. 1994.391 (.343-.691 (.857-1.417 (.900-1.429) 1.28) 1.248-.36) 1. respectively.00 (.955) .29 (1.256-.381) .529 (..774 (.500-.955) .303-.562) .342-.29) .248-.487-.632-.25 (.937 (.03-1.29 (1.400 (.239-.343 (.314 (.16 (. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.333 (.290 (. Smith et al.581) .757-1.50) 1.10-1.585) .277-.16) .738 (.352 (.83) 1.644 (.457-.361 (.337) .24) .361-.728 (.829) .438) .S.708) .339-.703-.361-.850-1.365-. interval) .917) ..449) .471-.635 (.409) .50 (1.368) .358 (.425) .324) .11-1.821 (.316 (.30 (1. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.294-.296) .259-.938) .243-.35) .435-.306 (.433) .522) .15 (.479-.434-.06 (.250) .313-.479) .753-.905) .426 (.582-.12-1.476-.848 (.461) .630-.630-. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.309) .963-1.737 (.386 (. or using diamond-polishing wheels that contain cobalt metal.275-.259) .327 (.17) .313-. 1972).487-.452-.279 (.534-.378-.606 (.792 (.781) 95th 1.393-. with pulmonary clearance half-lives of from one to two years (Hedge et al. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.378-.275-.360) ..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 .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 .00-1.975 (. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).449-.25 (.838 (.355) .380-.313 (.471 (.392 (.442-.278 (.407) .274-.44 (.740-1.326-.60) 1.662) .300) .09) 1.348) .515 (.313-.455 (.368 (.673-.753) 1.898 (.257 (.826-1.387) .03 (.932-1.23 (1.963) .550-.949) .391) Selected percentiles ( 95% confidence interval) 50th .647) .331-.313-.417) .638-1.388 (. using hard metal cutting tools.435 (.640) . an essential human nutrient.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 .804) 1.346 (.60) 1. A portion of cobalt retained for long periods is concentrated in the liver.615) .534 (.679-. refining or processing alloys.323) .54) 1.611) .362-.49) 1. 1972). Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.286) .728) .895-1.352 (. 2003).963) .736-.500 (.329-.634-.439) .394) .733-1.475 (.329 (.508-.234 (.462) .33) . Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.983-1.362 (.552 (.750-.704-.324-.554 (.27) 1.00 (.983) .598 (.847) .396) .707) .756 (.738 (.938-1.723 (.378-.

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

Jarvis JQ. Long-term clearance of inhaled 60Co. et al. Epidemiological survey of workers exposed to cobalt oxides.50(9):835-842. Iavicoli I. Blunn G. Kuska Y.150.48:172-173. Leghissa P.44:124-132.242:1412-1415.36:732-734. The release of metals from metal-onmetal surface arthroplasty of the hip. and cobalt metals. Uitti J. et al.95:29-37. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Sanghrajka AP. Ziaee H. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Alessandrelli M. Int Arch Occup Environ Health. Ichikawa Y. Kusaka Y. Moulin JJ. Buchet JP. Dunstan E. Laippala P. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Arch Intern Med 1990. Br J Ind Med 1993.204:147-160. et al. Chess DG.Metals effects of cobalt. Thabe H. Health Phys 1979. Sci Total Environ 1994. Kiilunen M. Bunn HF. White MA. 1985. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Falcone G.148:241-248.20(1):25-31. Bourne RB. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium. Kristiansen J. Linna A. J Bone Joint Surg Br 2005. Hoher T. Lauwerys R.51(7):447450.87(5):628-631. Boca Raton (FL): Lewis Publishers. Buchet JP.216:253-270. Mosconi G. J Bone Joint Surg Br 2006. Salvatori S.58(10):631-634. Am J Ind Med 2003. Peltier A. Cresti R. Lasfargues G. Occup Environ Med 1994.22:359367. Contact Dermatitis 2003. Kirsch-Volders M. Salama A.(1-3):133-139. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Bacis M. Daniel J. Lauwerys R. Pisati G. Weber A. MacDonald SJ. Edmonds CJ. Trace element reference values in tissues from inhabitants of the European Union. et al.150(1-3):167-171. Zhuber K. Co-sensitivity between cobalt and other transition metals. McCalden RW. Hedge AG. Dickel H. et al. Mutat Res 2003. Kriss JP. Schaller KH. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. DeSantis V. Sabbioni E. Lison D. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Outcome of occupational asthma due to cobalt hypersensitivity. Respiratory health of cobalt production workers. Fourth National Report on Human Exposure to Environmental Chemicals 211 .28(5):1121-1128. Stanescu D. Occupationallyinduced “isolated cobalt sensitization. Shirakawa T. Lhotka C. Roto P. Int Arch Occup Environ Health 1997. Biological monitoring of workers exposed to cobalt metal. Sci Total Environ 1994. Schank M. Lisi P. Absorption and retention of cobalt in man by whole-body counting. Cobalt and antimony: genotoxicity and carcinogenicity. Science 1988. Gross RT. Sabbioni E. a study of 13 elements in blood and urine of a United Kingdom population. Weyher I. Radulescu M. Thakker DM.21(2):189-195.45:246-247. Sabbioni E. Goldberg MA. Sci Total Environ 1997. cobalt salts. Kato M. Unwin P.533:135-152. Kraus T. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. oxides.34:620-626. Cannon SR. Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Zobelein P. Lung cancer risk in hard-metal workers. Tilley S. Angerer J. Linnainmaa M. J Occup Med 1992. Smith T. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Hoet P. Lison D. J Rheumatol 2001.150:177-183. Zedda S. Wild P. Dunning SP. Romazini S. De Boeck M. Goto S. Chest 1989. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. X. Iversen BS.” Contact Dermatitis 2001. Lauwerys RB. Pradhan C.406:282-296. Meier R. Steffan I. Am J Epidemiol 1998.157:117121. Zweymuller K. Hammon E. Heki S. Christensen JM. Swennen B. Sci Total Environ 1998. HoffmannB. Clin Orthop Relat Res 2003. Thomassen H. Barnaby CF. Lison D. 2001. Cobalt cardiomyopathy. Oksa P. A report of two cases from mineral assay laboratories and a review of the literature. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust. Cleland D. salt. Szekeres T. J Orthop Res 2003. Bozec C. Health Phys 1972.69(3):193-200. et al.55(4):269-276. and hard metal dust. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Carnes WH. Swennen B. Diepgen TL. Molders J. Schramel P. Fujimura N. Rorabeck CH. Vitali MT. J Trace Elem Med Biol 2006. Occup Environ Med 2001.88(4):443448. Robinson C. McMinn DJ. Goto S. Meyer zum Buschenfelde K-H. Palmroos P. 3rd ed. Ghat IS.

90) 1.30-1.43-1.20 (2.00 (3.50 (1.00-4.10-4.50-5.30-1.45 (1.90) 3.00-2.20 (1.900 (.51 (1.70 (3.50-3.80 (2.30) 95th 5. leaded glass.40) Total 1.60-1. respectively.75-2.40) 2.30 (2.60 (2.60-6.50) 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 2.10 (3.43) 1.60 (1.50-1.30 (1.90-4.80 (1.70-2. 7439-92-1 General Information Elemental lead is a soft.60 (3.00 (2.40-1. antique-molded or cast ornaments.00) 4.36-1.40-3.00) 3. 0.60 (2.20 (1.10 (4.25 (1.80 (1.10) 4.00-4.40 (3.70) 1.50 (4.14-1.70-4.10) 1.00 (1.50-1.10-3.30 (4.50 (1.89) 1.00) 2.69) 1.00 (6.53) 1.31) 1.878-1.50-2.90) 2.60 (1.20-1. adult lead exposures tend to be limited to Blood Lead Geometric mean and selected percentiles of blood concentrations (in µg/dL) for the U.10-1.60-4.36-1.60-4.30-2.69) 1.60) 3.30) 1.60) 723 898 911 905 1044 856 2135 2231 2081 4207 4772 4525 6-11 years 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 2.80 (5.32-1.70 (2.60) 4.30-1.90) 2.900-1.00) 1.80) 2.80-2.60 (3.60) 5.69 (1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.10-3.50-4.40 (5. see Data Analysis section) for Survey years 99-00.50 (1.00) 2.50 (4.62-1.28.37 (1.00) 1.04-1.80 (1.g.80) 1.90) 5.60) 2.40) 2.70) 1. population from the National Health and Nutrition Examination Survey.55-1.51) 1.70-3.10-2.50 (1.80-4.90 (3.00) 3.70) 3.66) 1.20) 3.93-2.10-8.10-2.70) 4.70-2.70) 4.3.00-1.30 (2.30) 5.30 (2.70) 1.60-3.00) .40 (2.10-6.30 (1.65 (1.71-1.90 (3.60 (2.40-3.40 (1.30) 2.50 (3.50) 1.60) 5.30) 2.60) 3.86) 1.20 (1.10) 1.40) 1.01 (1.90-4. the main source of lead exposure for the general U.30-5.20) 3.60) 1.36) 1.30 (4.60) 3.3.55 (1.60-2.90 (1.40) 1.60-1.10 (2.68-1.10) 5.20) 3.20-2.55-1.60-1.90 (3.49-1.10) 3. metal alloys (e.10 (2.80) 1.20-3.40-1.39-1.10 (1.10 (1.00) 1.60) 1.10 (1.20 (3.50) 5.00 (4.90-6.10-2.30-4.70) 1.50-4.70) 4.30-2.30-1.25) 1.46 (1.80 (1.40-1.10) 3.60) 2.00-6.60 (2.S.20 (1.20) 4.90-2.20 (3.899-.80-5.10-4.40-1.20) 5.Metals Lead CAS No.20-2.80-3.800-1.80 (2.50) 3.70 (1. and 0.60 (4.20 (1. Elemental lead can be combined with other elements to form inorganic and organic compounds. blue-gray metal that occurs naturally in soils and rocks.10) 1.69 (1.10 (2. Since lead has been eliminated from gasoline.70 (2.90-3.80 (4. ceramic glazes.40 (2.30 (2.20 (3.48) 1.20) 90th 3.60 (1.72) Selected percentiles ( 95% confidence interval) 50th 1.30 (1.19 (1.81) 1.00) 1.00 (4.40) 2.20 (3.50-5.20 (3.83 (1.50 (2.78 (1.00 (5.00) 2.50 (2.00-5.50) 4.40-2.60-2.60) 1.23 (1.60 (1.87) 1.60) 2.40 (1.80) 3.80-3.62) 1.942 (.60) 1.90) 2.87 (1. plastics.37 (1.70) 2.70 (1.70) 3.37-1. Lead was used in plumbing for centuries and may still be present.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.14-1.50-3.90 (4.80) 2. brass.40) 3.90 (3.30 (2. Lead is most often mined from ores or recycled from scrap metal or batteries.60) 2.32-1. ammunition. malleable.43 (1.70-1. such as lead phosphate and tetraethyl lead.25 (1.90-4.10-3.30 (2.17) .12-1.50) 1.75 (1.60) 4.00) 1.20) .30-2.50 (2.60 (3.45-1.50) 2. Lead has a variety of uses in manufacturing: storage batteries.70-1.70-2.40-1.60 (2.70-1.20) 3.90-2.90) 1.60) 1.22 (1.52 (1.80) 1.60 (1.80-4.80 (3.14-1.09) 1.52-1.60 (1. 01-02.40-5.00-4.66 (1.90) 2.30-2.70 (5.95) 1.70 (1.80 (5.50-2. solders. bronze).60 (2.10-3.40-6.50) 5.50 (2.50) 1.70) 3.70-5.50) 4.90-4. population was aerosolized lead emitted from combustion engines that used leaded gasoline.60 (1.80 (4.40) 5.50) 75th 2.20) 1.60) 2. interval) 1.90) 2.91) 1.96-2.56 (1.00-1.02) 1.30-6.80-3.60) 4.50-2.90-2.20-3.30-1.20-3.20 (2.30-1.40) 2.30 (3.90 (2.50-1.40 (1.20-3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.50-6.60) 3.40-2.70 (1.00) 6.60-1.00) 5.43) 1.10-1.20-1.10-6.39) 1.30 (2. and 03-04 are 0. dense.40 (4.20 (3.50 (3.90 (1.80) 2.00 (1.52-1.00) 4.70-6. Before the 1980’s.43 (1.10-2.40 (1.20 (3.20-6.10-1.70 (2.900 (.40-3.10) 2.50-2.50-1.80) 2.40-1.30) 2.70) 1.20-4.60 (3.80) 1.40-2.10) 2.50 (2. and for radiation shielding.20) 4.946 (.50) 1.70) 4.50) 7.90) 1.62 (1.20 (4.90) 3.90-2.20) 2.80 (1.80) 1.60) 4. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.90 (3.30 (1.70 (3. In the past.50) 2.S.80 (1.40) 1.80-4.75-1.75) 1.00) 2.10-2.10) 3.40-6.80 (2.40) 4.10-2.90 (2.80) 3913 4339 4132 4057 4606 4241 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.77 (1.34-1.80-3.50-1.40-4.30 (4.986) . 212 Fourth National Report on Human Exposure to Environmental Chemicals .

27) 1.03 (1.10-3.70-3. Approximately half of the absorbed lead may be incorporated into bone.20) . Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.800-.10) .00 (2.00-2.785) .636 (.30 (2. population from the National Health and Nutrition Examination Survey.40) 1.14 (1.20 (1.04 (.580-..31-3.620 (.20) .40 (2.10) .00) .700-1.40 (2.20-2.66 (2.900) .44-2.540 (.10-1.674) 1.59) 1.23) .09) 1. stained glass framing.91) 2.50-2.11 (1.00 (1.90-2.30-1.923 (.50 (2.30) 2.33-2.70) 1.70-2.82 (1.10) 2.595-.506-.02) 1. or water contaminated by mining or smelting operations.10 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) 2.00) .40-1.00) 1.986) .78-2.700-.862) .600-.20 (1.553-.800) .80-3.613) .17 (1.900 (.940 (.40-3.610 (.70) 2.04) .10-1. imported children’s trinkets and toys.10-3.00 (.00) 2. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone. battery and radiator manufacturing) and recreational sources.628) 1.20-1.60-3.651) .04-2.604 (.40) 1. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.540-.07-1.29 (2.640 (.840 (.20) 1.00-1.708-.848 (. 2007.00-1.572-.40 (1.900 (.941) .766 (.Metals occupational (e.900) . In the blood.50) 1.00 (1.590 (.90-2.620) 1.80) 1.90) 1.02 (.800 (. Fourth National Report on Human Exposure to Environmental Chemicals 213 .90 (2.700 (.535-.82 (2.700 (.642 (.690) 75th 1.90) 2. and 03-04 are 0.33.60-1.33 (2.30) 1.900-1.560-.40 (2.700) .800) .40) 1.g.30 (3.970-1.800 (.90 (2. 01-02.20 (3. 0.660) .40 (1.89) 2.640-.695 (.00) .70 (2. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.20 (1.60 (1.591 (.10 (1.80 (1.573 (.680) .808 (.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 1.12) 90th 2.650) 1.80-2.10-1.80-2.30-1.960-1.11) 2.41) 2.815 (.50) 1.70 (2.62) Total . However.80) 1.27 (1.14-1.10 (1.671-.60 (2.790 (.50-2.30-1.40) 1.680-.600-.900) .60-2.60-2.40) 2.90) 2.800 (.13) .738) .80) 3.72) 1.40 (1.680-. older plumbing systems with leaded pipes or lead soldered connections.00 (1.20-1.S.03-2.60-3.800) .20 (2.857) . or after soluble lead compounds are ingested.50 (2.749) . Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.900 (. dust.700 (. CDC.900-1.21 (2.00) . pewter utensils and drinking vessels.86) 1.78-2.700 (.40-1.20-2.1.990) 1. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.960 (.641-. respectively.04 (.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 .50-2.800) . and contact with soil.90) 2.600) .688 (.579-.18-1.600 (.990) 2.40-1.40-2.625-.30) 2.60 (1.35 (.10) 1.50) 1.564 (.700-.50 (1.800-1.30) 1.50 (2. lead-based painted surfaces undergoing renovation or demolition.659 (.86 (1.833 (.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.730 (.579-.80 (2.73 (1.30-5.745-.600 (.800-. bullet fragments retained in human tissue. 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.70) 3.661-.32 (1.757-..40-1.818) .915-1.605) .60 (1.90 (1.630 (.700-.773) .920 (.20 (2.52-1.70) 1.80) 1.86) 95th 2.556-.40-5.931) .752 (.30) 1.70 (2.52 (1.700) 1.07 (.49 (1.00 (1.66 (2.680) Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.900-1.800-1.900-1.80) 2.729-.00-2.70 (1.80) 2.558 (.00) 2.10 (1.20) .80) 2.820-1.960-1.70 (2.701) .90 (1.86-2.828) Selected percentiles ( 95% confidence interval) 50th .50) 3.78-2.80 (1.10 (.40 (1.920 (.10-5.60 (1.20 (1.20 (1.20 (2.97) 4.800) .30) 2.637-.60) 2.480-. lead-containing folk remedies and cosmetics.50 (1.50-3.910-.800 (.30-3.29) 2.80) 2.40) 2.62-4.30) 1.31 (1.570-.00-2.589-.10-1.731 (.753 (.625 (.52-1.30) 1.718) .691-.80) 3.616) .700 (.700-.14 (1.50) 2.600-.40) 1.10) 2.24-1.710-1.70) 3.70) 1.30-1.04) 2. 2000).00-1.710-.850 (.10 (.10-1.810-1.06) .20) 1.90-3.526-.1. lead-contaminated dust in indoor firing ranges. Lead is absorbed into the body after fine lead particulates or fumes are inhaled.90 (1.900) .20) 1.75) 4.13-3.500-.90-2.19 (1.10 (.40) 2.90-2.80) 2.700-.900) .50) 2.822-1.75) 3.90-4.64) 2.955-1.600-.677 (.50-1.40 (1.22) 1.59-2.700 (.30) .900) . 1991).20-1.10-3.20 (1.30 (1.30-2.795 (.40 (2.20) .40) 3.600) .23-4. and 0.935) 1.90-3.600-. see Data Analysis section) for Survey years 99-00. interval) .833-1.90 (2.

676) .655) 75th 1.933) .44) 1.618 (.03) 90th 1.09) 1.594-.06 (.06) .828) .15-2. 1995).722 (.701) .763) .933-1.59-3.87) 1.593 (.11) 1.61) 1.720 (.14) 1.671 (.03) .682) .26) Total .50-2.383-.88-2.400) .918 (.914-1.00) .55 (1.18) . scant amounts are lost through sweat.603-.33) 2.721 (.37-1.645-.730) 1. with lesser amounts eliminated via the feces.92) 2.10) 1.638 (.586-.15-3.33 (1.88) 1.587-. Staessen et al.17-1.62-1.38 (2.51 (1.S.22) 1.693 (.41 (1.08) ..71-2.36-2.37-1.917-1.79 (1.10 (1.97 (1.853-1.957-1.41-1.436) .94-2.86 (1.17 (.588-.601-.46 (1.469 (.10 (.622 (.635 (.75 (2.66) 2.08) .603 (. For instance.541-.45 (1.742) .43) 2. In 1991.55 (1.40-1.62-3.609 (.79) 2.753) .88) 2. and iron.625 (.18) 2. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.00 (1.707 (.27 (1.35) 2.61) 1.56-3.702) .00 (1.68 (1.07) .61) 3.64-2.632 (.43 (1.31 (1.496 (.608 (. and through binding to ion channels and regulatory proteins.0) 3.85-2.96 (1.979 (.74 (1.828-1. Nash et al.810 (.03) 2.812-1..677 (.702-.981-1.06 (1.28-1.50) 1.876-1.29 (1. BLLs and associated toxic effects differ in children and adults.38 (2.24 (1.03) 2.52 (1.649 (.644) .18) 1.64 (1..03) 1. Schwartz.97-18.677) .11) .47 (2.47) 1.977) 1. The toxic effects of lead result from its interference with the physiologic actions of calcium.655) .23 (1.688) .00 (.20) . 1995.535) .793-1.667-.98) 2. The skeleton acts as a storage depot.644 (.31) 1.662) Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.946-1.08-2.612-.988 (. 1993.712 (.679) 1.623 (.62) 2.20-3.997-1.26) 2. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.755 (. and paralysis.657) 1.22) .708 (.05-1.623 (.19-5.926 (.28) 2.604-.11 (.62-2.79) 1.01 (.05 (.20) .592-.938-1.559-.731-. abdominal pain.703) .77) 2.583-.58) 1.725) .98 (1.72-2.03) .Metals 90% of the body lead burden in most adults.971 (.52) 1.774 (.605-. 1996).31) 1.65 (1.71 (1.648 (.746) .408-.66 (1.796-1.39-1.83 (2.621 (.652 (. seizures.781-1. Lead can cross the placenta and enter the developing fetal brain. 2004.05 (1.98-2.31 (2.588-.571-.14 (1.25-1.69 (1.645-.667-.508) .97) 1.681-.698) .375 (. 2003.83) 1.709 (.696 (.698) .510-.73) 2.03) 1.00 (1.06) 1.53) 1.988-1.920-1.11 (.48 (1.606-. 2007).758) .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 .15-2.460-.18 (1.667) .870 (.15) 1.56) 3.03 (.962 (. 1991.01) .654) .734) .11 (1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.404 (.608-.88) 2.11-1.12-1.677-.603-.862-.97) 1.722 (. O’Flaherty.94 (1.25-1.404-.686) .64) 2. 1993).681-.09-1.683-.73-2. with a half-life of years to decades.72) .900 (.09-1.02) 1.673) .739) .561-.03 (1.975-1.615 (. based on prospective population studies. interval) .89-2.12) 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 .89-5.78-4.33) 1.841-1.679-.43) 1. kidney injury.710) .61) 1.03-2.790) .46 (2. CDC.75-2. encephalopathy.85) 1.633 (.639 (.56 (1.22-2. and nails (Leggett. 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.44 (1.718) .992-1.02-1.914 (.18) 1. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.428) .569 (.639 (. population from the National Health and Nutrition Examination Survey.50-2.742) Selected percentiles ( 95% confidence interval) 50th .82) 1. Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.72-2.22) 1. zinc.05-1.43-1.658 (.607-.594-.38 (2.718) 1.404 (.551-.56-2.990 (.938 (.03 (. BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.380-.668-.50-1.342-.659-.701 (.838) .31 (1.940 (.49 (1.63) 4.639) .66 (1.15) 1.11 (1. Large amounts of lead in the body can cause anemia.461) .670) 1.898) .50 (1.918-1.03 (.529-.28) .579-.85-2.893) .53-1.702) .882-1.34-1.09-1.07-1. through the inhibition of certain enzymes.78 (2.50-2.43 (2.720 (.33-1.51) 1.67-4.65-2.571-.800-.887 (.639 (.22-1.85 (1.88 (1.64) 95th 2.10) 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites 214 Fourth National Report on Human Exposure to Environmental Chemicals .07 (.765) .04-3.41) .617-.655-.641 (.70 (1. hair.725) .432 (.492-. Approximately 70% of lead excretion occurs via the urine.700-.63) 1.61) 1.44 (1.992-1.851) .47 (1.963-1.19) 1.04) 2.914 (.615 (.

2003). environmental levels) and health effects is available from ATSDR at: http://www. 2002a). A general population survey of adults in Italy tested in 2000 found BLLs slightly more than double those reported for U. Workplace standards and guidelines for lead exposure and monitoring have been established by OSHA and ACGIH. 2007). Jones et al. At low environmental exposures.e. lead in women may be associated with hypertension during pregnancy..6%) were lower than those from NHANES 1991-1994. 1987. Muntner et al. Korrick et al. Lanphear et al.S. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. residing in housing built before the 1950’s.xls). and low family income (CDC. 2000). 2003. premature delivery.. 1991...gov/toxpro2. 2001). In occupationally exposed adults.S. 1996.. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR.2 µg/dL in males and 3.3 million children tested had BLLs of 10 mg/dL or higher (http://www. Payton et al. adults in the 1999-2000 NHANES sample.4% in NHANES 1999-2004. 2002).. High dose occupational lead exposure. Information about external exposure (i. both the geometric mean (1. may alter sperm morphology. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. 2000). A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3.atsdr. 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. Urine levels may reflect recently absorbed lead. when the geometric mean BLL was 2..000 adults. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.6% in NHANES 1988-1991 to 1.4% of children had BLLs of 10µg/dL or higher (CDC. Pirkle et al.. though there is greater individual variation in urine lead than in blood and greater potential for contamination. Surveillance data reported by U. Bellinger 2005.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1..g. the geometric mean BLL was 3. For example.. Schwartz et al.Metals µg/dL or higher as the level of concern in children. 2003.21% of approximately 3. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. The U..gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006.. including minority race or ethnicity.cdc.. Data submitted through state public health programs from 2006 showed that 1. 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.. 1999).5 per 100. and organic lead compounds not classifiable with respect to human carcinogenicity. and spontaneous abortion (Baghurst et al. which is an 84% decline..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. 2009). More recently. Staessen et al.75 µg/dL in U. and peripheral neuropathy generally occurring at much higher levels (e. adults in the 19992000 NHANES sample (Apostoli et al... 2006). approximately 11. 2005b). Overall.7 µg/dL and 4. 2002. adult residents. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. CDC. 1994). 2005b. respectively..07 µg/dL (Becker et al. BLLs higher than 40 mg/dL can result in proximal tubular dysfunction and decreased glomerular filtration rate leading to interstitial and peritubular fibrosis when high body burdens persist. seizures. and decrease fertility (Alexander et al. BLLs reflect both recent intake and equilibration with stored lead in other tissues. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors..S.. EPA.0 µg/dL in females (Soldin et al. Fourth National Report on Human Exposure to Environmental Chemicals 215 . urban residence. 1996. 2003. with overt encephalopathy. higher than 100-200 µg/dL). subtle or nonspecific neurocognitive effects have been reported at BLLs as low as 20-30 µg/dL (Mantere et al. In NHANES 1999-2002 in children 1-5 years old..html. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.. particularly in the skeleton. Schwartz. 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.. 1999). 2005a). 1995. Telisman et al. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al.S. 1984. 1998). 1996. However. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. reduce sperm count. almost double the geometric mean of 1. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8.S.S. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. Borja-Aburto et al. IARC considers inorganic lead compounds probable human carcinogens. the prevalence rate has declined annually since 1994 (CDC. Both drinking water and ambient air standards for lead have been established by the U. 2006).cdc. usually with BLLs greater than 40 mg/dL.

Blood lead reference values: the results of an Italian polycentric study. 1999-2002. Jusko TA.26:359-371. Kuehnemann TJ. Rios C. Baghurst PA. Wager C. Managing Elevated Blood Lead Levels Among Young Children.cdc. Bellinger D. Canfield RL.150(6):590-597. Lanphear BP. Hu H. Semen quality of men employed at a lead smelter.gov/nceh/lead/publications/ books/plpyc/contents.287:1-11. Centers for Disease Control and Prevention (CDC). Chiodo LM. Atlanta (GA). Weiss ST. Rotnitzky A. Vimpani FB. The relationship of bone and blood lead to hypertension. Brody DJ. Muller CH. McMichael AJ.gov/nceh/lead/ CaseManagement/caseManage_main. Neurotoxicol 1987. Hernberg S.cdc. Lead and hypertension in a sample of middle-aged women. Cox C. Available from URL: http://www. Sparrow D. Manton WI. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Speizer FE. Blanco J. Age-specific kinetic model of lead metal in humans.atsdr. MMWR Morb Mortal Wkly Rep 2005a. gov/mmwr/preview/mmwrhtml/mm5420a5.348:15171526. Neurodevelopmental effects of postnatal lead exposure at very low levels. Payton M.55(32):876-879. Available at URL: http://www.53:411-416.html. Environ Res 2000. Blood lead levels—United States. MMWR Morb Mortal Wkly Rep 2006.htm.123:e376-e385. Rotnitzky A. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas.cdc. Homa DM. JAMA 1996. IARC Monogr Eval Carcinog Risks Hum 2006.275(15):1171-1176. References Agency for Toxic Substances and Disease Registry (ATSDR). Krause C. Cory-Slechta DA. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals .73:409-420. Jacobson SW. Third National Report on Human Exposure to Environmental Chemicals.54(20):513-516. Ga. Adult blood lead epidemiology and surveillance—United States. Checkoway H. Occup Environ Med 1996. Mantere P. Kaus S. Pirkle JL. 4/14/09 Centers for Disease Control and Prevention (CDC). Leggett RW. Bellinger D. Sparrow D.gov/mmwr/preview/mmwrhtml/ mm5532a2. Ganzi A. Lead.gov/toxprofiles/tp13. Public Health Rep 2000.87:1-471. doi:10. Caldwell KL. et al. Farias P. Kim R. 2005b. Cox C. Angle CR. Auinger P. 4/14/09 Centers for Disease Control and Prevention (CDC). Atlanta (GA).10:43-50.115:521-529. N Engl J Med 2003. 1991 [online]. Weiss ST. et al. Sci Total Environ 2002.htm. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. 2002 [online]. Acquisition and retention of lead by young children.htm. Coresh J. Hänninen H. Am J Epidemiol 1999. van Netten C. Luukkonen R. Becker K. Preventing Lead Poisoning in Young Children. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. et al. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents.82:60-80. Muntner P. Vupputyuri S. Lepom P.89:330-335. Available at URL: http://www. JAMA 1996. Ronchi L. Available at URL: http://www.htm.8(3):395-401. Aug 2007 [online]. 4/14/09 Centers for Disease Control and Prevention (CDC). 1988-2004. Schulz C. Jones RL. 2005.1542/peds:2007-3608. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Aro A. Seiwert M. Reese YR. Teratogen update: lead and pregnancy. Available at URL: http://www. Hu H. Birth Defects Research (Part A).275:1177-1181. Neurotoxicol Teratol 2004. Korrick SA. Apostoli P. Borja-Aburto VH. CDC. Lanphear BP. 4/14/09 Alexander BH. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Henderson CR.101(7):598-616.205:297-308. Wigg NR.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. Am J Public Health 1999.113(4):1016-1022. Jacobson JL. Pediatrics 2004. Hertz-Picciotto I. Inorganic and Organic Lead Compounds. Baj A. Scand J Work Environ Health 1984. Int J Hyg Environ Health 2002. Meyer PA. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Rojas LM. Toxicological profile for lead. Robertson EF. Hunter DJ. Ewers TG. Kaufman JD. Atlanta. Hu H. Pediatrics 2009. Korrick S. Dietrich K. 2003-2004. 4/14/09 Centers for Disease Control and Prevention (CDC). Neri A. et al. et al. Environ Health Perspect 1993. Batuman V.cdc. Stanek KL. Bavazzano P. Roberts RR. Blood lead levels measured prospectively and risk of spontaneous abortion.cdc.

JAMA 2003. Kidney Int 2003. Schwartz J. Arch Environ Health 1995. Exposure of the U. Int J Hyg Environ Health 2006. Weiss ST. et al. Gunter EW. Hickman T.209:301305. O’Flaherty EJ. Lustberg M. 50:31-37. Lee BK.104(1):60-66. Jurasovic J. Toxicol Appl Pharmacol 1993. Gavella M.9:303-327. Association of blood lead. Kinetics of lead disposition in humans.153(5):453464. Low-level lead exposure and blood pressure. Kaufmann RB. J Hum Hypertens 1995. Smith DR.S. Pizent A. Stewar WF. Hwang KY. Lee GS. and copper in men. population to lead: 1991-1994.106:745-750. zinc. Cvitkovic P. Amery A. Sparrow D. Use of endogenous.289(12):1523-1531. Clin Chim Acta 2003. Revised and new reference values for arsenic. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. Roels H. and hypertension in perimenopausal and postmenopausal women. Am J Epidemiol 1994. Rocic B. Payton M. Semen quality and reproductive endocrine function in relation to biomarkers of lead.140:821-829. Blood lead. Kaufmann R. et al. Telisman S. Schwenk M. IV. Lee SS. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Blood lead concentrations in children: new ranges. Hanak B. Brody DJ. Schwartz BS. blood pressure. cadmium. Soldin OP. stable lead isotopes to determine release of lead from the skeleton. Lauwerys RR.327:109-113. Paschal DC. Environ Health Perspect 1998. Lead. and tibia lead with neurobehavioral test scores in South Korean lead workers. dimercaptosuccinic acidchelatable lead. Schulz D. Osterloh JD. cadmium. Rubin R. Nash D. Wilhelm M. Sherwin R.Metals results from NHANES III. Am J Epidemiol 2001. Hu H. blood pressure and cardiovascular disease in men. lead. Low-level lead exposure and renal function in the Normative Aging Study. Staessen JA. Soldin SJ.118:16-29.63:1044-1050. Magder L.108(1):45-53. Pirkle JL. Environ Health Perspect 1996. Environ Health Perspect 2000. Flegal AR. Physiologically based models for bone-seeking elements.

90-3.00 (2.30) 1.979 (. sulfur.60) 1.700 (.30) 5. such as chlorine (e. mercuric chloride).50) 2.00) 3. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach. and dental amalgam.80 (3.800 (.700-.50-3.30-5.30) 4132 4241 03-04 03-04 03-04 .10-3.30 (2..900) 75th 1.2.700-. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore. population from the National Health and Nutrition Examination Survey.400-.S.60) 1.40) 1.40 (3.90 (1.80) 4.30 (1.30) 3.00 (1. to form inorganic mercury compounds or salts.00-5. 1999 . phenylmercuric acetate) or topical antiseptics (e. electrical lamps. synthetic organomercury compounds were once used in pharmaceutical applications.60) 2085 2293 3478 Limit of detection (LOD.797 (.00 (.500 (. have often required public health intervention (Zeitz et al. predominantly from fish and other seafood.40-3.500 (.700-.700) .50) 4.40 (3.20-4..60-2.12) . thermostats and switches).20 (2.400 (.. Apart from methyl mercury.00-1.80 (1.800 (.40) 3.500-. Atmospheric elemental mercury can be deposited on land and water.877 (. constitutes the main source of dietary mercury exposure in the general population.80) 1.. Poorly absorbed from the gastrointestinal tract.50-1.50) 5.g. Some cosmetic skin creams from countries other than the U.Metals Mercury CAS No.900) 1.. an organic form of mercury.50) 1.800-1.S.70 (1.90 (4..800-1.814 (. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. thermometers. The ingestion of methyl mercury. 218 Fourth National Report on Human Exposure to Environmental Chemicals .40 (4. which can bioaccumulate in aquatic and terrestrial food chains.400-.776 (.60-5.500) .363-.781 (.30-2.563 (.60 (2. inorganic.00 (. see Data Analysis section) for Survey year 03-04 is 0.20-3. and mining and smelting.50-2.753-1.00) 1.300 (. Also.00 (2.00) 1.300) . elemental mercury is absorbed mainly by inhaling volatilized vapor. and mercury compounds are still used as preservatives (e. it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury.919) .20-4..70-2.900) 1.90) 90th 3.60 (1.50) Total Age group 1-5 years 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 8373 03-04 03-04 03-04 03-04 .600) 1..800 (.30-4. Elemental mercury is a shiny.372) .419 (. Accidental spills of elemental mercury.60-6. thimerosal.00) 4.00) .00 (.900) 1.80 (1.30) 1.600 (. merbromin). Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).655-. sphygmomanometers and barometers.886) . and is distributed to most tissues.70) 911 856 2081 4525 03-04 03-04 .70 (4. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges. may contain inorganic mercury.60-3.700-.90) 3.903) Selected percentiles ( 95% confidence interval) 50th .30-6.472-. Woods et al. After elemental mercury is absorbed.30) 3.500-.g.714-. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities. 1980.40-2.800 (.574) .927) . or oxygen. Hursh et al.00 (2.326 (. Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements.70 (3. and organic forms. The kinetics of the different forms of mercury vary considerably.703-. Kingman et al.60 (1. IARC.g.800-1. Survey years 03-04 Geometric mean (95% conf. with the highest concentrations occurring in the kidneys (Barregard et al.900) .40-1. interval) . In addition. 1994.70 (1.00 (.418-. 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic). which create an episodic potential for volatization and inhalation of mercury vapor.672) ..60-6. 1998.285-. solid-waste incineration. 1993).80 (1.484) . 2007).20) 2.10) .g. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.900 (.90) 95th 4.490 (.700-.300-.800-1. Other major uses include electrical equipment (e.800-1.40-1.860-1. 2002).40-2.80) 3. Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.40 (4.700) .02) .90 (1.689-.

Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.20) .300 (.06-1..70) 4.10-1.. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola.700 (.265-.500-.600) ...00 (2.40-2.300 (.70 (1.541-.00) 1.60 (3.90 (4.35 (1.871-1. 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.27) .00) 6. 1991.700-1.40) 2.800 (.7) 4. McDowell et al. a measure of accumulated dose (Cernichiari et al.50) 1.343 (. 1999-2002. Geometric mean Survey years (95% conf. Excretion occurs by renal and fecal routes.200-. National Health and Nutrition Examination Survey.10 (1.50) 3.700 (..00-1.20 (2.500-1.825-1. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.919) .90 (4.800) 1.200-.300) .00 (2.800 (. 1996)..30-4.40) 1.297-.30-11.40) 5.00 (2.60) 1.10) . 1994).30-2.20) 1.30 (.90 (1. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.30-3.. urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al.90) 5.377) .. 2003).00-6.30) 1. 1990). Methyl mercury enters the brain and other tissues (Vahter et al. Jonsson et al.300) .800-1..30-6.800-1.700-.60 (1.10 (3.70-3.50-12. 1992 and 1999. with most elimination occurring through in the feces (Sherlock et al.73) 1. 1971).00-2. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al.269-. Myers et al.10) 1.20-2.60 (2.10) .900-1.06 (.60) 2.500-.80) 1.80 (3.200 (.90) Sample size 705 872 318 432 387 440 1709 1928 Age Group 1-5 years (females and males) Females Males 16-49 years (females only) 99-00 01-02 99-00 01-02 99-00 01-02 99-00 01-02 .60 (3.697-. Suzuki et al. 1984.407) .50 (2..00) 1.500 (.70-5.10 (1.20-11.00) .70-3. 1992). 1995.00) 4.700 (.30 (1.10 (. for both acute and chronic exposures.800-1.475) ...90 (1.40-2.30) 3. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.329 (.00) 2.369) 1.726-1.200 (.50) 95th 2. 1992.50) 2.268-.307 (.00-2.00-2.200-.. Methyl mercury is incorporated into growing hair.40 (1.300 (. Vimy et al. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .200-.90 (3.318 (. 1998).824) 1.30) 1.700-.50-2. population.300) .20-3.50 (1.400-.70) 1.Metals the tissues to mercurous and mercuric inorganic forms. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days.. 1996.90) 2.738-. and a useful marker of exposure in epidemiologic studies (Grandjean et al.80 (1.90) 90th 1. Smith et al.500-.300 (.299-.900 (.14 and 0..70) 4..70-6.90) 2.20 (. 1994.300) .800) . thereafter.01) . 1993).664-1.30-6.30-5. Sandborgh-Englund et al.200-..00) 7.. 1993).800) . 2004.80) 579 527 370 436 588 806 Limit of detection (LOD. After exposure to elemental mercury.700 (. Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.20) .20-3.300) .90) 3.820 (.940) Race/ethnicity (females.667 (. 1994) and then undergoes slow dealkylation to inorganic mercury.70-5. 1975.3) 4. Vahter et al. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.600) ..14.10-3.60 (1.70 (1.700-1.02 (.30 (1.60) 1.20-3. Miettinen et al.500-.30-4.900 (. 2005).. 1973).800 (.40-1. Smith and Farris.S.00-3.00 (1.29) .70 (1.30 (1.900-1.833 (. 1969.0) 4.395) . excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al.10 (.600 (.800) 75th . 2003).374) .40 (1.500-.10 (1.23) .256-.900 (. 1998).50-3.377 (.60) 3.300) . interval) Selected percentiles (95% confidence interval) 50th . Fourth National Report on Human Exposure to Environmental Chemicals 219 .30-6.00 (3.80-3.50) 1.60 (1..200-.500 (.700) 2. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.944 (. 1999). Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara 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.10 (5.317 (.800) 1.

500 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .. hearing impairment..500 (..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. and sleep disturbance (Bidstrup et al. limb deformities.. 2003).500-.500-. 2004).600 (. the existence of a causal relation is unresolved (Chan and Egeland. 2004).500-. Salonen et al. Smith et al. At levels below those that cause acute lung injury.700) .600) .800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .600) . 1983).500-. Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al.600-.500-.. dysarthria. high-dose exposure to elemental mercury vapor may cause severe pneumonitis.. The constellation of findings may include anorexia. 2006.600-.700 (. 1996).700 (. and pinkish discoloration of the hands and feet (Tunnessen et al. and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.600) .600 (.600) .600 (.500-. 2000. Sakamoto et al. 1963). Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al.800) .600) . 220 Fourth National Report on Human Exposure to Environmental Chemicals . overt signs and symptoms of chronic inhalation may include tremor. 1951.500-.42.600) .600-. Drexler and Schaller.. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.600 (. cerebellar ataxia. Acute. and cerebral palsy (NRC..600 (. which may vary for some chemicals by year and by individual sample.. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. fatigue. gingivitis. and progressive constriction of the visual fields.600) . 2005). Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. depression.600 (.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0.700-. Once absorbed. Smith et al.600) .700 (. ataxia. short-term memory loss. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al. In recent epidemiologic studies. Stern 2005.500-. 2004. maculopapular rash.600 (. < LOD means less than the limit of detection.500) .600-.. 2000). 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. DeRouen et al.600) . population from the National Health and Nutrition Examination Survey.. Factor-Litvak et al. 2006. causing parasthesias.Metals may be more efficient for inorganic mercury (Grandjean et al. typically after a latent period of weeks to months.. Oskarsson et al.700) 2007 2240 3406 Limit of detection (LOD.. pain in the extremities. Rissanen 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 .700-. insomnia. 1998. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. 2000. Overt poisoning from methyl mercury primarily affects the central nervous system. 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. hypertension.. 1987). Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. Vupputuri et al. altered physical growth. irritability. 1970. Rice. dysarthria. and neurocognitive and behavioral disturbances.600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .800) ..500 (<LOD-. the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis. sensory impairments.700 (. anorexia. Bellinger et al.700-..700 (. 1995. Inorganic mercury exposure usually occurs by ingestion. 2004. 1995.500-.700 (.S. particularly irritability.. 2002.. 1993). Sakamoto et al.600 (. 2005.

460 (.20 (1.520) .430 (.76-3. 2006).360-.304) . In Germany the geometric mean for blood mercury was 0.63-2.290-.14) 90th 2.330-. adult women in several ethnic subgroups (Hightower et al.408) .440 (. Among the three racial/ethnic groups.93 (1.430 (. These distinctions can help interpret mercury blood levels in people.890 (. Mahaffey et al.160-. Schober et al.. et al. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.430) .gov/mercury and from ATSDR at: http:// www. and the age-related changes differed across the groups (Caldwell et al.88 (1.05) 3..570) .78-2.200 (. see Data Analysis section) for Survey year 03-04 is 0.13-2.480) 75th 1. 2000).420 (.441 (. Survey years 03-04 Geometric mean (95% conf. These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.23) .88) 287 722 1529 03-04 03-04 .23) 2..S.. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity.S.cdc.280-.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 . Grandjean et al. Over the NHANES 1999-2006 survey periods. In NHANES 19992002.30) 3.330-.55 µg/L. Fourth National Report on Human Exposure to Environmental Chemicals 221 .340-.495 (.05) 1.447 (.atsdr. who participated in a 1998 representative population survey (Becker et al.29) 1. 2009).60) 619 713 1066 Limit of detection (LOD.09 (2.509) .700-1.08 (1. 1998).610-1.16 (1.463) .78 µg/L for adults and 0.870-1.77-2. 2004.254 (. 2001.61) 1.76-3. EPA at: http://www. particularly methyl mercury. 2003).58 µg/L for 4645 adults. 2003). aged 18 to 69 years.358 (.33 (2.350-.42) 95th 3.00) 1.66) 3. population from the National Health and Nutrition Examination Survey.700 (. 758 children. the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC.e.840-1.313-.89) 3.555) ..442-.epa.46) 3.433 (..54 (2. Kingman et al.370) . although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females..940 (. Urinary mercury consists mostly of inorganic mercury (Cianciola et al.530) . From 1996 through 1998. and increased slightly in non-Hispanic white children (Caldwell. EPA.870-1.530-.405-. During the same survey periods.24 (2.Metals standard for inorganic mercury has been established by U. However.. the total blood mercury concentration is due mostly to the dietary intake of organic forms.19 (1.S.07 (. total blood mercury geometric mean levels in females aged 16-49 years did not change.67-3.770-1.9 years).410-.12 (.. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women. interval) .18) 2.68 (2.31) 2.330 (.360 (.420 (.. range 40 years to 78 years) had an average total blood mercury concentration of 2.52) 2.24) 1.60 (1. environmental levels) and health effects is available from the U.476 (.39-3.26 (1.400 (.gov/toxprofiles.480 (.250) ..330-.85-2.60-2.88-3. slightly higher total blood mercury levels were found in U.28) 1.19 (2. Total blood mercury levels increase with greater fish consumption (Dewailly et al.549) .840) 1.31) 1266 1272 03-04 03-04 03-04 . 2001.396-. average age 9.492) Selected percentiles ( 95% confidence interval) 50th .S.460) .530) . 1997. Information about external exposure (i. Biomonitoring Information In the general population. military veterans (mean age 52. 2009).46 µg/L for children.413-.14.580) .97) 2. Sanzo et al. 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..213-.. A cohort of 1127 U.534) .8 years.930-1.360-.. 2002). 1998).03-4.509) .99-6. Benes et al.01 (.S. total blood mercury increased with age.90) 2. the median concentration of blood mercury was 0. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al.406-.65) 1.96 (1. average age 33 years.416 (.960 (. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.67-2.34-3. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.16 (.00 (.08 (1.382-. 1995.96 (1.76-4.14-2.840-1.

population from the National Health and Nutrition Examination Survey.566) . representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.265-.486) Selected percentiles ( 95% confidence interval) 50th .06 (. DeRouen et al.714-1.362 (.67 (1..343 (.964-1.535) 1.54 (2.64-2.480) .S.447-.619-. 1998). 1992).532 (.88-2.87) 2. An expert-panel report recently prepared for the U. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine. ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L.79) 1.970 (.464 (.. interval) . a biomarker of perturbation in renal tubular function.30) 1..255 (. Urinary mercury levels in recent German (Becker et al.599) .11) 2. mean urinary mercury was 3.S.13-2.508 (.62 (1.800-1. and on average.652) .S.225-. 2009). 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.307-.09) 1.40-1.537) .11) 1.12-3.392-.990) .28 (. Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.25 (.476 (.S. 1988.545 (.309-.365 (.16) 1. not to imply a safety level for general population exposure..51-2.41-2. 2003).455-.417) . reversible increase in urinary N-acetyl-glucosaminidase.S.620-.40 (1.498) 75th .32 (1.44) 1.00 (..875-1.969-1. 2006.Metals 2000)..384 (..00) 286 722 1529 03-04 03-04 . the urine mercury increased by approximately 0. 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.365 (..11-2.31 (1.1 µg/L.196-.65 (1.404-. 2002) adult population surveys were similar to those in a U.88-2.588) .07) 1.03) 2.79 (1.1 µg/L for each surface with a dental amalgam (Kingman et al..391-. et al.333-.87 (1.297 (.400) .455) . 2002).616) .246-.909 (.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 .78-4.280-.76 (1.61) 1. Czech (Benes et al.687) . among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al. 2009)..485 (. Information about the biological exposure indices is provided here for comparison.525 (.391) .522-.35 (1. Langworth et al.18-1.39) 1.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals .01) 2. In the study of U. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.32-2. Levels in U.217 (.376-.289) . 2005). Survey years 03-04 Geometric mean (95% conf.208-.385-.06 (.77 (2.88 (1.455-.00) 90th 1.276 (.784) 1. 2006).630) .443 (. and Italian (Apostoli et al.358) . women of childbearing age have generally been much lower than these levels (CDC. et al.306 (. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.785-1.696 (.347) .46-2.667-1.56) 1266 1271 03-04 03-04 03-04 .21) 1.472-. Urine mercury and the number of dental amalgams were correlated.587 (. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect.30) 2.275) .13 (1.400-.67 (1. military veterans with dental amalgams.23-2.768 (.04-3.463 (.368) .301-.63) 1.86) 95th 2. Department of Health and Human Services noted that several studies have observed a modest.447 (.

92) 3.35 (1.68) 3.806) .99 (3.909-1.27-1.3) 5.13 (2.631-.710) 1.65) 1.28 (1.16) 5.50 (2. Geometric mean (95% conf.84 (2.43-1.610-.665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .799) .05 (3.24-1.624-.27 (1.639 (.632 (.61) 1.91-7.579-.59-5.37) 1.56) 3.709) .22-3.22 (.00 (3.637) .30 (2.77) 2.540-.99) 1.77) 1.62 (3.04-10.32) 2.Metals Urinary Mercury−Females Aged 16-49 Years Old.07-2.95 (2.569-.57-4.68 (3.48 (2.45) 2.744) 1.32 (1.62 (1.79) 3.52) 3.606 (.774) .664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .31-1.21 (1.09-1.657 (.557-.30 (1.910) . 1999-2002.68-3.14 and 0.691) .656-.79) 1.32-3.18 (3.47) 1.87-4.62 (4.596 (.719 (.85-3.14-2.475-.30 (2.18) 3.616-.76-5.07) 1.85) 4.426-.501-.565 (.520-.615 (.37 (1.516 (.930) .526-.42) 90th 2.97) 2. National Health and Nutrition Examination Survey.46-4.850-1.03-2.89 (2.50 (1. 1999-2002.622-.97) 2.14) 3.10-4.03 (.15-1. Geometric mean Survey years (95% conf.07-5.832-1.65-4.97 (1.650) 1.46) 3.41 (1.846) .420-.636-.15 (2.824) .91 (2.520-.09-1.41-6.61-6.83-3.522 (.709) 75th 1.723 (. 16-49 years) 99-00 01-02 .742-1.790) .35) .578-. 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.724 (.41 (2.31 (1.S.03) 1.51 (3.560 (.53-3.760 (.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.06 (.686) . 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.410-.24) 6.92) 2.45) 2.600 (.810) .706 (.41 (1.831) .97) 2.27 (2.30-2.45) 95th 3.04-1.76) 2.42) 2.710 (.540 (.81-6.76 (1.45-3.23-1.502-. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.13-4.56 (1.94) 1.605-.69-3.84 (2.664) .14.580-.45 (1.55-3.655 (. population.17) 95th 5.670) 75th 1.833) .23-1.772 (.500-.831) .70 (2.710 (.553-.665) .508-.55) 90th 3.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.47) 1.42-3.10-2.51) .45-2. 16-49 years) 99-00 01-02 .21-3.98 (5.39-3.S.44) 3.50-4.620 (.46 (1.69 (1.25) 2.721 (.699) 1.92) 4.387-.966) .450-.03 (.00) 2.592 (. National Health and Nutrition Examination Survey.99 (2.582-. interval) Selected percentiles (95% confidence interval) Survey years 50th .685 (.870) .809) .580 (.56) 4.14-1.05 (2.740 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.54) 595 531 381 442 594 826 Limit of detection (LOD. population.72) 1.16-5.81 (3.99-2.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .00 (2.21 (2.560-.38) 4.650 (.892) .658 (.650 (. interval) Selected percentiles (95% confidence interval) 50th .

German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Trachtenberg F. Schulz C. Cent Eur J Public Health 2000. Benes B. Mangili A. Dewailly E. Brewer R. Schaller KH. Factor-Litvak P. Conradi N. Harvey DG. Tavares M. Pb. Markers of early renal changes induced by industrial pollutants. Krause C. Clarkson T. Methylmercury exposure biomarkers as indicators of neurotoxicity in children aged 7 years. Begg M. 52:19-33. Br J Ind Med 1993. Kaus S.212:588-598. Hultberg B.2:856-861. JAMA 2006.205:297-308. Weihe P. ACGIH. Barregard L. Skerfving S. Drexler H. Enzymuria in workers exposed to inorganic mercury. Total blood mercury concentrations in the U. Kjellstrom T. Debes F. Hg. Seiwert M. Int Arch Occup Environ Health 1988. Mortensen ME. Leitão J. Cernichiari E. Buchet JP. Martin MD. Jorgensen PJ. Sallsten G.56(4):350-357.S. Barregard L. The concentration levels of Cd. Int J Hyg Environ Health 2003. Ayotte P. Bates MN. Apostoli P. Budtz-Jorgensen E. Int Arch Occup Environ Health 1999. Kinetics of mercury in blood and urine after brief occupational exposure. Snihs JO. Environ Health Perspect 2005. Based on the Documentation of the Threshold Limit Values for Chemical Substances and Physical Agents and Biological Exposure Indices. Seifert B. Attewell R. Environ Health Perspect 2003. 2005. McKinlay S. Gagliardi T. Hasselgren G. Third National Report on Human Exposure to Environmental Chemicals. Daniel D. Rosenbaum G. Castro-Caldas A. Arch Environ Health 2001. Vahter M. Woods JS. Exposure of the Inuit population of Nunavik (Arctic Quebec) to lead and mercury. Luis H. Niklasson B. Lancet 1951. Metabolism of methyl mercury (203Hg) compounds in man. Barregard L. Jorgensen PJ. Zn.149:301-305. Environ Res 1998. Schulz C. DeRouen TA. Grandjean P. Cortesi I. Becker K. Neuropsychological and renal effects of dental amalgam in children: a randomized clinical trial. Woods JS. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Arch Environ Health 1969. Cox C.61:65-69. Roels H. Grandjean P. Sandborgh-englund B. Impact of maternal seafood diet on fetal exposure to mercury. Becker K. Ekman L. Caldwell KL. Health effects of dental amalgam exposure: a retrospective cohort study. Bruneau S. Int JHyg Environ Health 2002. Cernichiari E. Tissue levels of mercury determined in a deceased worker after occupational exposure. 2007 TLVs and BEIs. Am J Epidemiol 1999. Transport of methylmercury and inorganic mercury to the fetus and breast-fed infant. Jarvholm B. Cerna M. Kline J. Osterloh JD. mercury exposure. Sci Total Environ 2002. Barbon R. Lebel G. selenium. Caudill SP. Videro T. Kaus S. Egeland FM. et al. Cutress T.47(3):185-195. et al. Jones RL. Assessment of reference values for mercury in urine: the results of an Italian polycentric study. Weihe P. et al.77(2):124-129. Neurotoxicology 1995. Drago I. Biennow M. et al. et al. Centers for Disease Control and Prevention (CDC).Metals References Aberg B. Garrett N. Bjornberg KA. Fish consumption. Smid J. Levallois P. J Toxicol Environ Health 1997. and heart diseases. Persson G. Marsh DO. Schutz A. Nutr Rev 2004. The mercury concentration in breast milk resulting from amalgam fillings and dietary habits. Jacobs D. Int J Hyg Environ Health 2009. Geier J.7(3):176-184.289:1324.16(4):705-710. Cianciola ME. and lead. 224 Fourth National Report on Human Exposure to Environmental Chemicals . Int J Epidemiol 2004. Townes BD.295(15):17841792. Barregard L. Echeverria D.19:478-484. JAMA 2006.8(2):117-119. Bonnell JA. Lepom P.111:719-723. Chronic mercury poisoning in men repairing direct-current meters. Greitz U. Cu. Application to workers exposed to mercury vapour. 206:15-24. Seiwert M.. and Se in blood of the population in the Czech Republic. Leroux BG.33:1-9. Elia G. Mercury derived from dental amalgams and neuropsychologic function. I. Bernard AM. Martin MD. Arch Environ Health 1992. population: 19992006. Cernichiari E. Locket S. Neurobehavioral effects of dental amalgam in children: a randomized clinical trial. Cejchanova M. White RF. Lauwerys RR. Martins IP. Lapham LW. Falk R. Epidemiologic assessment of measures used to indicate lowlevel exposure to mercury vapor (Hgo). Bernardo M. Berglund B. Cincinnati (OH): Signature Publications. Weber JP. Arch Environ Health 1992. Spevackova V. Cardenas A. Myers GJ.295(15):1775-1783. Fawcett J.50:17-27. Schuzt A.113(10):1381-1385. Chan JM. Monitoring methylmercury during pregnancy: maternal hari predicts fetal brain exposure. et al. Sallsten G. Bidstrup PL. et al.72:169-173. Sallsten G. Aposian HV. Subrt P. Bellinger DC. Atlanta (GA).62(2):68-72.

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Sinks TH. et al. Blood mercury levels in US children and women of childbearing age. 1999-2000.258(4 Pt 2):R939-945. Am J Physiol 1990. Friberg L. Vupputuri S. Leitao JG.2:117-131. et al. Acrodynia: exposure to mercury from fluorescent light bulbs. Vorwald AJ. Shen DD. Daniels JL. JAMA 2003. The hair-organ relationship in mercury concentration in contemporary Japanese. Baser M.97(2):195-200. Sherlock J. Smith JC.31:687-700. Turner MD. Am Ind Hyg Assoc J 1970. Hongo T. Takahashi Y. Smith AE. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Environ Health Perspect 2003. Whittle K. Environ Health Perspect 2002. Stern AH. Most B. Lorscheider FL. 1993-1998. Sandler DP. Amurrio A. Aguinagalde FX. Patil LS. Amiano P. Burbacher T. Environ Res 2005.37:245-252. Martin MD. Pediatrics 1987. Toxicol Appl Pharmacol 1996. Toxicol Appl Pharmacol 1994. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain.128(2):25125-25126. Kaye WE. Allen PV. Jones RL. Toxicol Appl Pharmacol 1994.79:786789.111(12):1465-1470. et al.Metals Sanzo JM. Br J Ind Med 1983. Goldberg J. Mottet NK. Fisher HL. Azpiri MA.124:221-229. Longnecker MP. Environ Health Perspect 2007. Zeitz P.98(1):133-142. Lind B. McDowell M. Bolger PM. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Hum Toxicol 1984. Yoshinaga J. Stern AH. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Mooney TF. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Newton G. Environ Res 2005. Suzuki T. Smith RG. Tunnessen WW.115(10):1527-1531. Farris FF. Public Health Nutr 2001. Leroux BG. Imai H. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Vimy MJ. Bernardo MF. Nakazawa M. Osterloh J. Topping G. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Effects of occupational exposure to elemental mercury on short term memory. Guo S. Woods JS. Vahter M. McMahon KJ.110:129-132. Methyl mercury pharmacokinetics in man: a reevaluation. The kinetics of intravenously administered methyl mercury in man.4(5):981-988.48(4):221229. The contribution of dental amalgam to urinary mercury excretion in children. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. DeRouen TA. Schober SE. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Smith JC. Orr MF. Matsuo N. Hall LL. Effects of exposure to mercury in the manufacture of chlorine. Langolf GD. Hislop D. Dorronsoro M. Smith PJ. Arch Environ Health 1993.289(13):1667-1674.40:413-419.

9 (32.1) 59.3-115) 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. lubricants.2-59.2 (61.0) 39.6 (40.5-66.7) 46.0-77.3 (38.8) 75.3 (53.3 (47.5-46.7-92.9-109) 97.3) 83.5-52. hydrogenation catalysts.3-47.0 (46.7) 57.3) 65.6-46.3 (64.1-88.2) 40.9 (37.5 (43.7 (44.3 (79.6) 71.7-60.2-42.5) 47..8-106) 88.5-68. 0.S.7) 51.6) 53. respectively. and 03-04 are 0. Fourth National Report on Human Exposure to Environmental Chemicals 227 .4 (72.7 (58. urinary excretion over six days CAS No.2 (49.3) 85.2) 52. 1997).2 (83.5 (41.9 (73.3) 41.6 (52.2) 48.9 (40.5 (41. aldehyde dehydrogenase.0-65.7-105) 69.1-44.5) 80.1-55.4) 56.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.9-55.7-50. 2001.9) 67.0 (42.4) 45.1 (91.2) 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 (41.7-84.9 (78. and in pigments for ceramics. WHO.8-49.6-58.4 (80.3-44.2-37.0 (48.0) 97. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM. 01-02.6 (40.6-111) 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 52.4) 49. see Data Analysis section) for survey years 99-00.7 (50.1) 126 (106-147) 109 (94.1) 60.9 (33.5 (81. The recommended dietary allowance for adult men and women is 45 µg/day (IOM.7 (45.7) 77.0-62.7) 45.5 (49.3) 54.0) 62.6-82. At a daily oral molybdenum dose of 24 µg.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 (99.0) 55.6-62.0-38. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.7-51.9 (44.8-94.8 (42.4 (48.2 (69.9-56.9 (52.6 (43.8.2-79.7 (51.3 (55.7-96.2 (49.7) 78.1) 35.2-59.5.1 (34.5-91. population from the National Health and Nutrition Examination survey.1) 82.2) 37.5-41.1-63.1-52.0 (76.4 (48.7) 78.7 (37. 7439-98-7 General Information Elemental molybdenum is a silver-white.0 (81.0 (43.0 (42.2) 41.Metals Molybdenum or ore deposits.5 (37.9-55.7-41.1-48.3 (71. and paints.2) 79.6-72.7-68.2-53.0-56.7) 75th 84.0-100) 63. More recently.0) 54.8 (67.7-39.0-85.1 (38.2-70.0-101) 82.8) 44.8.7 (36.8) 39.6) 51. 1996).1-59.7-47.8-46.6 (73.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.1) 57.6) 71.7-122) 93.4) 52. 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.4 (79.8) 48.5-65. 2001).9-85.1 (71.3) 37.7 (73.7) 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. Compounds of molybdenum are also used as corrosion inhibitors.8 (85.3 (84.0) 84.2 (38. and 1.0) 60.7) 86.8) 40.2) 53.4) 76.9 (34.4-82.2 (63.3 (73.6 (55. In humans.6-96.5) 44.0-71.7-91.3-75.3-108) 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 47.8 (82.7-73.6) 93. chemical reagents in hospital laboratories.7 (71. inks.9) 34.3) 47.5) 85.2 (56.0-53. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8-108) 87.5 (48.4-61.0-110) 90.5 (67.6-55.2 (55.3-91.8-90.3 (55. which exert homeostatic regulation over molybdenum balance.4-52.9-82.6-42. interval) 45.5-124) 108 (92.4 (34. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.4) 41. Excretion occurs predominantly via the kidneys. semiconductor and battery industries have begun to use molybdenum.5) 80.5 (74.6) Selected percentiles ( 95% confidence interval) 50th 50.5-52.3 (37.6 (55.1-51.9) 62.2 (40.1) 46.4-75.9-83. and xanthine oxidase (Kisker et al.5) 60.2-91.0) 45. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.3 (46. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.8) 46.1-52.4) 42.

7-62.2) 39.6 (71.5 (38.9 (73.6-61.2 (57.3-68.5 (83. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.8) 38.1-79.6-88.6 (38.0-41.0 (74.7) 112 (95.6) 48.5 (35.9-117) 57.5 (39. population from the National Health and Nutrition Examination survey.6-63.2 (40.1 (54.2) 38.0) 72.2-80.5-70.1 (44.1-41.5-35. 2001).0) 39.3 (36.1-81.8-52.2 (69.8 (37.4) 44.5 (37. Based on studies finding adverse reproductive effects in rats and mice.5) 63.S.0) 39.0) 44.4-41.5 (65.1-112) 78.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.2-65.2 (43.7) 75th 63.3 (58.2) 42.1 (38.7 (66.6) 39.5-119) 90.4 (44.7) 53.2) 39.9-87.7) 62.8) 71.4-42.2 (73.2 (40.9-41.6) 39.4-39.5 (40.3 (36.1 (30.2-49.8) 79. U.3-115) 98.5-44.2-96.6-45.9) 41.9-45.9 (49.3 (37.4-106) 85.0-133) 119 (88. of the ingested dose (Turnlund et al.2) 43.1-39.8-42.6) Selected percentiles ( 95% confidence interval) 50th 41.1 (39.6 (59.6-61.4 (56.5-92.9-61.3 (71.6-41.7-137) 129 (109-155) 112 (97.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al. 1999).7) 45.5 (59. 1997).3-43.3) 64.3-141) 109 (81.4) 61.7 (75.5-45.0-38.3) 41.6-78.0-46.8-47.8-67.1) 101 (83.4) 122 (107-133) 109 (99.9-68.9) 31.9-40. and urinary levels reflect intake from all sources.4) 47.7) 115 (93.6 (36.1-127) 90.2) 58.9-71.5-97.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.5 (34. respectively.7) 57.5-69.6) 43.5-60.5-50.3 (53.3 (83.9) 44.5 (78.0 (58.3) 57. In industry.9-118) 91.0) 62.9 mg/kg/day and established a tolerable upper intake level of 0.7) 42.4 (37.0-120) 85.1) 37.2 (33. but available epidemiologic data are scant.4-107) 85.1) 37.9 (39.3-102) 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 40.9-45.3) 43.2 (37.3) 56.2 (52.5 (41.1-43..3-59.9 (39.5) 90th 108 (97.8 (36.8-84.2) 55.7 (30.1-34.1-100) 86. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.6 (36.1 (33. Biomonitoring Information Molybdenum is an essential element for health.2 (40.2-47.2-121) 107 (92.4 (55.0) 53.3-52.6) 36.4) 77.1 (40.9 (40.2-96. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.5 (79.4) 89.8 (75.8) 39.8) 62.7-38..5 (50.5 (41.0) 88. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.1-39.0) 33.3-56.2-40.9-96.7) 41.9) 92.S.6-76.3 (55.1-43.8-118) 81.1) 40. interval) 43.5) 72.5 (39.8) 37.8 (57.7-100) 77.3) 61.8-66.5-62.5 (36.5) 60.4 (78.5 (37. at daily oral doses of 95 µg and 428 µg. urinary excretion over six days rose to 50% and 67%.4) 40.1-40.2) 42.0 (35.5 (80.0) 38.7-120) 87.5) 71.9 (79.2-41.8) 38.8-65.8 (56.5 (65.1-67.4-118) 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 .Metals was 18% of the ingested dose.0-103) 103 (90.8 (90.9 (35.1) 43.1 (38.2 (36.4-66.3-46. 1961.3 (37.4) 48.9 (64.3) 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) 56.0-46.5-48.3-44.4) 60. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Molybdenum is generally considered to be of low human toxicity. 1995).8) 61.3) 37.4-76.3 (71.5 (54.6 (57.4 (40. and clinical or epidemiologic evidence of adverse effects is limited.5-46.5) 73. EPA.6 (42. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.7-43.1 (42.3) 44.9) 40.7 (77.8-46.4 (67.9) 79.3) 40.1-38.8) 45.4-120) 101 (84.3 (51.3-45.8-47.2) 37.9-42.0) 36.7-44.7-52. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.5 (40.9 (36.1 (49.2 (50.1) 65.1 (82.4) 58.1 (37.9 (64.2-46..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. 1993).1-109) 89.0 (80.5-99.0-56.2) 37.4 (53.1-45.7-40.03 mg/kg/day in humans (IOM.5 (35.4-185) 106 (94.4) 116 (101-126) 104 (88.4 (59. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.7-93.6-63.

Am J Clin Nutr 1995. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Kisker C. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No.htm. pp.Metals in urine for the U. Molybdenum 1993 [online]. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al.S. Occup Environ Med 1999. Menne C. Environmental Protection Agency (U.epa. White and Sabbioni. References Centers for Disease Control and Prevention (CDC). Available at URL: http://www.S. Christensen JM. J Trace Elem Med Biol 2001. Dietary reference intakes for vitamin A. Yarovaya GA. vanadium. copper. Available at URL: http://books. Keyes WR. Droste JHJ. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. Standing Committee on the Scientific Evaluation of Dietary Reference Intakes.. World Health Organization (WHO). 1996. molybdenum. manganese. Schaub J. edu/openbook. X. 1998. (DC): National Academy Press. Molybdenum-cofactorcontaining enzymes: structure and mechanism. pp. Turci R. 4/14/09 Sievers E. Minoia C. nickel.216:253-270. arsenic. Zhurnal Obshchey Biologii 1961. Weyler JJ. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Schleyerbach U.66:233-267. boron. 16:1313-1319. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. Food and Nutrition Board.gov/index. Molybdenum.gov/iris/ subst/0425. excretion.62(4):790-796. Koval’skiy GA. 1998). A study of 13 elements in blood and urine of a United Kingdom population. Available at URL: http://ntp. Trace element reference values in tissues from inhabitants of the European Union. Rapid Comm Mass Spectrom 2002. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. 4/14/09 Iversen BS. Peiffer GL. Shmavonyan DM. Fourth National Report on Human Exposure to Environmental Chemicals 229 . 2001). et al.nih.nap. iodine. Ann Rev Biochem 1997. 420-441. TR-462.. EPA). Gatti A. Molybdenum in infancy: methodical investigation of urinary excretion. 2002. 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. Aprea C. Sci Total Environ 1998. Sciarra G. Institute of Medicine (IOM). Washington. Turnlund JR. Molybdenum absorption. Atlanta (GA). 4/14/09 White MA. vitamin K.niehs.php?record_id=10026&page=420. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Schindelin H. chromium. iron.123(1):81-85. National Toxicology Program (NTP). Minoia et al. silicon. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. Occupational risk factors of lung cancer: a hospital based case-control study. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. and zinc: a report of the Panel on Micronutrients. Sabbioni E. Sabbioni E. 56:322-327. U.22(3):179-191.. Third National Report on Human Exposure to Environmental Chemicals. Geneva: WHO. 2005.15(2-3):149-154. In: Trace elements in human nutrition and health. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Vermeire PA. White MA. 2001. Rees DC. Ronchi A. Kristiansen J. Van Meerbeeck JP.S. 2005). Analyst 1998. van Sprundel MP. 144-154.

which may vary for some chemicals by year and by individual sample. and high catalytic activity. however. thick-film circuits printed on ceramic substrates. respectively.g. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. copper. and 03-04 are 0.. jewelry. 7440-06-4 General Information Platinum is a silver-gray. as oxidation catalysts in chemical manufacturing. 01-02.07. and 0. dental alloys. and as drugs (e. Platinum compounds are used in electrodes.04. carboplatin) in the treatment of cancer. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. strength at high temperatures.. 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. 1998).S. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 230 Fourth National Report on Human Exposure to Environmental Chemicals . 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.04. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. cisplatin. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. see Data Analysis section) for Survey years 99-00. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 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. 0.Metals Platinum CAS No. and iron. Important properties of platinum are resistance to corrosion. < LOD means less than the limit of detection.

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

Gieler U. Nowak D. Grimm CH. Begerow J. Kaus S. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Available at URL: http://www. Schierl R. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. 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. Int Arch Occup Environ Health 1997.04 µg/L) in this Report. Environ Res 1975a. 232 Fourth National Report on Human Exposure to Environmental Chemicals . Kuster W. and in blood and urine in the United Kingdom.. Bocca B. Pethran A.org/documents/ehc/ehc/ ehc125. Parrot JL. population were below the limit of detection (0. Occup Environ Med 2004. 3/31/08 Moore W Jr. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Raab W. Thornton I. which elevate urinary platinum by five to twelve-fold (Begerow et al. Schierl. Pethran A. Herr CE.9:152-158. Saindelle A. Urinary platinum levels associated with dental gold alloys..S. Fruhmann G. Hall L.. Influences on human internal exposure to environmental platinum. 1999. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Turfeld M. Int J Hyg Environ Health 2004.org/documents/ehc/ehc/ehc125. Hauff K. 2004). Platinum. Platinum concentrations in urban road dust and soil.01 µg/L (Becker et al. Senofonte O.htm. International Programme on Chemical Safety (IPCS). Br J Pharmacol 1969. 1991 [online]. et al. Part 1: monitoring of urinary concentrations. 2003. Ewers U. Schulz C.207(1):69-73. Moore W Jr. Herr et al.. 2003. Petrucci F.htm. 2004. Levels of platinum in urine for the U. Int Arch Occup Environ Health 2003. Kavanagh P. Wilhelm M. Biomarkers 1999. 2004) or less than 0. Hysell D. pp. van de Weyer C. Ensslin AS.13(1):24-30. Pethran et al. Huber R. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Biomonitoring Information Urinary platinum levels reflect recent exposure. Environ Health Perspect 1975b. et al. Analyst 1998. Schierl R. Uptake of antineoplastic agents in pharmacy and hospital personnel.4(1):27-36. Arch Environ Health:1969. Campbell K. J Expo Anal Environ Epidemiol 2003. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Carelli G. 206:15-24. Seifert B. Rommelt H. eds..55(2):138-140. Schierl et al. 2003. Hysell D. 2003). et al. In: Bingham E. New York: John Wiley & Sons. et al.10:63-71. Neuendorf J.70(3):205-208. Stilianakis NI.. Blanks R. Jankofsky M. 1998). Urinary excretion of platinum from platinum-industry workers. ruthenium. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al. 2001).76(1):5-10. 289-380. 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.123(3):451-454.Metals the International Programme on Chemical Safety at http:// www.61(7):636-9. Saindelle A.inchem. Czerczak S. palladium. Farago ME. Boos KS. Patty’s Toxicology. Hebert R. Iavicoli I. Arch Environ Health 2001. Schierl R. 5th ed.19:685-691.. Angerer J. 1997. 1998). rhodium. Gromiec JP. Several studies have shown that background concentrations in general populations were usually less than 0. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Nickel. 2000. Kulka U. and gold excretion of patients after insertion of noble-metal dental alloys. Biomonitoring of traffic police officers exposed to airborne platinum. Duneman L:Long-term urinary platinum. osmium. Ruff F: Histamine release by sodium cholorplatinate.56(3):283-286. Ruff F: Platinum and platinosis. Herr et al. Crocker W. Seiwert M. International Journal of Hygiene and Environmental Health 2003.. Powell CH. References Becker K.35:313-321. Cohrssen B. Kazantzis G. Schierl R. palladium. Wilhelm et al. Environmental Health Criteria 125.005 µg/L (Iavicoli et al. Schulz C.. Alimonti A. Occup Environ Med 1998.. Allergy and histamine release due to some platinum salts.inchem.. Fries HG. and platinum. Kelly J.

280) .215) .02.330-.156-.160 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.450 (.400) 95th .170 (. Fourth National Report on Human Exposure to Environmental Chemicals 233 .167-.201 (.330) .360 (.200) .220 (.420) .380-.180-.400-.217) .Metals Thallium depilatory cosmetics.250-.270 (.470) .280 (.310-.160-.390-.147-.201 (.202 (.200-.137-.02.430) .220 (.156) .190 (.153-.200-.370 (.197 (.190 (.450 (.165 (.400 (.550 (.159 (. 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.202) .440 (.260-.180-.148-.350-.240-.170-. 0.290 (.150-.370 (.S. however.134-.163) .260 (.250) .640) .240) .390-.300 (.160-.350-. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.320) .500) .410-.170-.200-.370-.133-.260-.220 (.270 (.250-.210-.145 (.167-.210 (.450 (.360 (.250 (.218) .170-.410-.230 (.590) .150-.410 (.480) .400 (.480) .330) .162-.440) .360 (.430-.290-.410-.182-. thallium readily crosses the placenta and also distributes into breast milk.320) .300) .250-.420) .250-.370-.400 (.420) .191 (.220 (.185 (.340-. interval) .420 (. see Data Analysis section) for Survey years 99-00.360) .410-.440) .159 (.230) .210 (. it has not been specifically mined or refined in the United States since 1984.181-.145-. Human health effects from thallium at low environmental CAS No.330-.173) .480) .290 (. 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.370 (.220) .360 (.200) .300) .360-.390) .360-.460) .350) . Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.187-.320-.172 (.400) .180 (.300) .510 (.280 (.220-.310 (.500) .460 (.510) .440 (.200-.440) .380-.147-.410 (.160-.230-.180-.290 (. and 03-04 are 0.410 (.150-.370-.350-.290-.420) .240-.400-.250-.200 (.630) .330) .280) . In the United States.260-.243) .390) .149 (.290) 90th .410) .390 (.220) .440-.330) .176 (.150-.180 (.280) .160 (.290) .230-.480) .590) .360-.430-.450) .270-.220 (.160-.200) .430 (.196) .260-.320 (.340-.370-.171 (.420-.410 (.350-.218) .400) .147-.154-.270 (.170-.300 (.370 (.160 (.150-.460-.350) .200 (.160 (.450 (.156) .200 (.420-.340-.170 (.240) .220) .170 (.280-.179-.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 .270 (.240) .192) Selected percentiles ( 95% confidence interval) 50th .200 (.183) . 01-02.420) .290 (.173) .420) .250-.280 (.340) .400 (.430-.239) .450 (.178) .330-.520) .190-.430) .172 (.340 (.260-.330-.370 (. and 0. From these and other sources.520) . In the past.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 .520) .400) .410 (.440 (.225) .400-.450 (.410 (.185-.210) .270-.177) .172) .500) .560) .188) .146 (.350-.400 (.02.420) .330-.450 (.155 (.390-.145-.157-.290) .184 (.300 (.197-.340-.320) .180) 75th .370) .183) .230-.170) .200) .370 (.480) .500 (.270) .350 (.350 (.400-.180) .180 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.420-. thallium was obtained as a by-product of smelting other metals.410-.330-.470) .160 (.220) .470) .360-.290 (.430 (.490) . representing distribution into other tissues.260 (.196) .200 (..490) .200 (. the latter being the current major industrial consumer of thallium in this country.220) . respectively.490) .250-.220) .400-.300-.360-.390 (.380 (.290) .410-.160-.520 (.340) .390) .250 (.230) .450 (.280-.190 (.135-.170) .400) .390-.310 (.170-.370 (.470 (. In addition. Thallium disappears from the blood with a half-life of several days.430 (.158) .190 (.170-.430 (.270-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.206) .490 (.290) .230) .290 (.300) .380 (.350-.173-.310 (.159 (.270 (.260) .310) .202 (.440 (.175) . population from the National Health and Nutrition Examination Survey.150-.470 (.420-.390) .167 (.380) .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 .460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.170) .370) .330-.690) .240-.230) .180-.270) .217 (.140-.250-.450 (.200) .190 (.260 (.490) Total .170-.200) . 2005).190 (.144 (.

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

Sci Total Environ 1990.gov/toxprofiles/tp54.76(1):53-59. et al. 7/15/09 Blanchardon E. Toxicological profile for thallium. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. blood. 2005.atsdr. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. Buhlmeyer G. White and Sabbioni.. Schmidt M. Sci Total Environ 1998. A study of 13 elements in blood and urine of a United Kingdom population. White MA. Investigation of a working population exposed to thallium.47(3):223-231. 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. Trace element reference values in tissues from inhabitants of the European Union. Pozzoli L. Martin J-C. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. Radiat Prot Dosim. Dolger R. Marcus RL. Challeton-de Vathaire C. Raithel HJ. 1990. Minoia et al. Kramer U.cdc. References Agency for Toxic Substances and Disease Registry (ATSDR). Ting BG. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging.5 μg/L.S. Brockhaus et al.113(1):47-53. 1992 [online]. Pirkle JL.. Centers for Disease Control and Prevention. 1998. Available at URL: http://www. Apostoli P. 1985). Paschal DC. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Schaller et al. Brockhaus A. Boisson P. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. J Soc Occup Med 1985. et al. (1981) studied 1. Soddemann H. Fourth National Report on Human Exposure to Environmental Chemicals 235 .95:89-105.Metals (CDC. Cassot G. Manke G. Environ Res 1998. Third National Report on Human Exposure to Environmental Chemicals. population) are thought to correspond to workplace exposures at the threshold limit value of 0. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. Schaller KH.. 1980.. Sabbioni E. Pietra R. and serum of Italian subjects.216:253-270. Valentin H. with concentrations ranging up to 76. A study of 46 elements in urine. et al. 1981. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L. Morrow JC. Sabbioni E. Jackson RJ. Paschal et al.html. Int Arch Occup Environ Health 1981. Trace element reference values in tissues from inhabitants of the European community I.48(4):375-389. Sampson EJ. Atlanta (GA).265 people living near a thallium-emitting cement plant in Germany. Minoia C. 1998). Gallorini M. 2005. 2005) and are shown with results from NHANES 2003-2004 in this Report. Ewers U.1 mg/m3 (Marcus. X. Investigations of thallium-exposed workers in cement factories.35(1):4-9. Int Arch Occup Environ Health 1980. Trace metals in urine of United States residents: reference range concentrations. Celier D. Wiegand H. 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.

190-.360 (.140 (. Little information is available on the toxicity of tungsten.060-.130-.160 (.210-.340-.092 (.180 (.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 .076 (.130) .070) .095-.400 (.530 (.077-.100-.060-.100 (.062 (.360) .490) .140 (.092 (.100-.137 (.310-.230-.240 (.350) .Metals Tungsten CAS No. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.270 (.170-.150-.105) .510 (.160-.210 (.460) .320 (.158 (.069-.380-.170) .088 (.100) .090 (.110-.310-.101 (.290) .340-.073 (.550) .090-.220-.190) .082-.100) .180) .210) .170 (.430-.080 (.070-.140-.116) .800) .082) .090-.460 (.160-.290-.470-.160) .260 (.410-.04.380 (.800) .090) .950) .330-.270-.123-.100) .120) .470 (.056-.084 (.290-.160) .560 (.062 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .350) .071-.060 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.350 (.101-.110 (.126) .204) .360-.090-.530 (.170) .560) .110-.420-.370 (.250) .150) .380) . see Data Analysis section) for Survey years 99-00.074-.210 (.060 (.300 (.070 (.300) .100 (.570 (.070-.170) .081 (.430) .360-.460) .090-.140 (.068) .340) .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 .140 (.073) .250-.130-.250) .130) .080) .300 (.113 (.490 (. which are used in rock drills and metal-cutting tools.190-.090-.090) .110 (.560) .090-.400-.073-.260-.270 (.380 (.250-.580) .04.130) .092) .270-.111-.210 (.240-.550) .310-.500) .110 (.410 (.060-.650) .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 .210 (.400 (.150 (.160-. their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone.160 (.470) .590) . Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).140-. filaments for incandescent lamps.110 (.480) Total .130) . mainly as scheelite (CaWO4).260-.190 (.330) .096 (.050-.350) . Tungsten is used mainly for producing hard metals.250) .300) 95th .120-.180-.640 (. Evidence is lacking for the carcinogenicity of tungsten.050-.080 (.250) . Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.160 (.380-.090-.093) .080) . Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.270-.080 (.620 (.370-.082 (.360 (.630) .310-.200) .151) .200-.050-.230 (.550 (.110) .100-.120 (.260 (.087) .S.390 (.093-.113 (.070-.370 (.065-.090) . and for producing ferrotungsten.550) .091) .060-.270-.320-.190-. and 0.056-.120-.080 (.130 (. Occupational exposure is from dusts released during grinding or drilling of hard metals.160-.310) .070) .300 (.070) .100) .190-.230) .160 (. and 03-04 are 0.170) .670) .107 (.130 (.570 (.120-.290 (.290) .087-.113 (.069) .160 (.280 (.080-.100 (. and as catalysts in the petroleum industry.060-.180-.130-.230) .520) .120) . respectively.133) .260-. Tungsten compounds are used as lubricating agents. Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.070-.100) Selected percentiles ( 95% confidence interval) 50th .230-.210 (. bronzes in pigments.170 (.520) .380-.430 (.105 (.080-.370-.180) .080) .080-.400 (.110 (.500 (.070) .300-.400) .430 (.310-.084) .510-.110-.096-.520) .53) .060 (.180-.180 (.070 (.113 (.270 (.084-.450-.470 (. which is used in the steel industry.320) .260) . interval) .050-.090 (.086 (.130-.330-.135) .220) .180) .076 (.060-.510-1.04. 0.073-.390) . population from the National Health and Nutrition Examination Survey.530 (.066-.360 (.560) .080) 75th .420-.450 (.180-.082 (.690) .060 (.180) .120-.460 (.093 (.097-.060 (.120) .00) .620) .104) .310 (.120) .230-. 01-02.500 (.330 (.430 (.095-.140) 90th .380-.058-.070-.150 (.132) .470) .220) .290-.340-.109) .770 (.220 (.120) .350-1.560) .430-.120-.280 (.100 (.120) .070 (.090 (.330) .200 (.620) .830) .078-.150 (.122) .090-.320 (.460 (.120-.080 (.250) . Survey years 99-00 01-02 03-04 Geometric mean (95% conf.250) .060 (.110) .790) .100) .220) .230-.130) .190 (.090) .064-.088) .065 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.400 (.071 (.370 (.280-.370) .320-.810) .440) .

124-.130-.267-.267) .169) .084) .078-.167-.S.555 (.354-.060-.315-.200-. 2001-2002. population from the National Health and Nutrition Examination Survey.188-.237) .439 (.079) .250 (.077) . Patients with medically-inserted tungsten found at increased levels in drinking water.205-.107-.197) .333 (.059-.453) .279 (.216-.344-.181 (.S.067 (.088) .667) .085) . A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.091) .063-.065-.071) .136-.306) .209-. Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U.063 (.122-.214-.083) .164 (.287) .077-.111 (.201) .074) 75th .089) .144 (.145 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.329-.078 (.465) . measure urinary tungsten. Nicolaou et al.071) .165) .074-.233-.075) .300) .294 (.077) .075-.224) .255 (.143 (.080-.138 (.081 (.108) .073 (.258-.105 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.071-.090-.078 (.300-.190) .061-.066 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.284) .333 (.065-.279 (.079 (.096) .073 (.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 .880) .080 (.083 (.155-.179-.061-.090-.086) .065-.203-.138) .084) .197) .120) .237-.060-.216-.347 (.091 (.317) ...138 (..358) .119-.28) .075-.067 (.098-.582) .108-. 1997).237) .066 (.117 (.339 (.436-1.554) .150-.060 (.120) .064-.217-.064-.(Kraus et al.054-. similar to those in this Report (Schramel et al.117) .074 (.072-.484) .124 (. 2001).091) .095) Selected percentiles ( 95% confidence interval) 50th .083-.081) .379 (.360 (.069-.231 (.222-.093) .079) .078) Sample size 2338 2651 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .167) .109-.158) .199 (.634 (.179-.094) .167-.431) .098 (.077-.739) .293 (.285) .082 (.255 (.136-.146 (.098-.250-.286-.088) .452-.091 (.152-.116 (.121 (.119 (.058-.087) .139 (.067-.089 (.079) .065 (.331-.049-.353 (.326) .381) .797) .158) .308) .333 (.186 (.059-.150 (.093-.139) .317-.278-.153-.431) .059-.359 (.174 (. interval) .133) 90th .353 (.130 (.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 .072 (.359 (.426) .211 (.084 (.333 (.056-.265 (.215 (.071) .143-.275 (.329 (.302-.364 (.074-.082) .074) .301) .133) .216 (. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.081-.100) .063-.465) .061-.198) .125) .100 (.073 (.062 (.199 (.198-.436) .098) .106 (.121-.126-.167) . (1987) found possibly due to methodologic.068-.154) .333) .075) .161) . In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.073 (.063 (.136-.146) .667 (.065 (.197 (.341 (.197-.116) .497 (.080-.055-. 2003.158 (.222) .283) . 1998). and 2003-2004 (Paschal et al.168 (.080 (.109 (.065) .333) .414) .333-.605) .253-.258 (.339 (.412 (.174) .072-.122-.094) .075 (.150-.459) .084 (.083) . population.S.231-.063-.354) .340 (.091) .386) .823) . population (CDC.462) .245-.053-.094-.439 (.086) .301) .100) .484 (.253) 95th .301) .086) .054-.250 (. 2005).431) .104-.253 (.214) .105 (.082) .270 (.087 (.125 (.148) .146 (. Using neutron activation analysis to 2000.217-.071 (.122 (.151 (.410-.078) .056-.170-.139-.272-.133) .057-.Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.187) .169 (.068 (.426) .085-.300-.063-. 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.086-.218 (.439) Total .216-.085 (.180-.727) .070 (.092) .098-.383 (.070 (.333-.184 (.482 (.176-.103-.095-.500) .091) .079 (.057-.075 (.081 (.279 (.078) .083 (. or exposure that a control group of non-metal workers had mean levels differences.317 (.302-.255-.116-.099-.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 .069 (.299 (.131-.136-.216 (.240-.158) .300 (.200-.148 (.392) .375) .176-.059 (.385 (.144-.215) .261-.071 (.208-.071 (.538) .154) .206-.079) .308) .153) .157) .201 (.136 (.069 (.

Paschal DC. Wendler I. National Center for Environmental Health. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load.Metals blood. Seghizzi P.(2):73-77. Lenhart M. platinum. Cancer Clusters.62:380-384.76(1):53-59. Angerer J. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. 2005.cdc.. The determination of metals (antimony. Third National Report on Human Exposure to Environmental Chemicals. et al. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Ting BG. mercury. Churchill County (Fallon). Schramel P.gov/nceh/clusters/Fallon/study. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis.58(10):631-634. Sampson EJ. Zobelein P. Catheter Cardiovasc Interv 2004. Nevada Exposure Asssessment. J Trace Elem Electrolytes Health Dis 1987. Cassina G. Morrow JC. Kraus T. bismuth. Pietra R. References Bachthaler M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Environ Res 1998. 238 Fourth National Report on Human Exposure to Environmental Chemicals . Int Arch Occup Environ Health 1997. 2004). Pirkle JL. Nicolaou G. Feuerbach S. Mosconi G. 4/15/09 Centers for Disease Control and Prevention. Occup Environ Med 2001. thallium. Atlanta (GA). Schaller KH.htm. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. Sabioni E. palladium. Available at URL: http://www. Centers for Disease Control and Prevention. Trace metals in urine of United States residents: reference range concentrations. Angerer J. tellurium. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report. Paetzel C. Manke C. Schramel P. cadmium. urine. 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.69(3):219-223. lead. [online] 2003. Link J. and hair (Bachthaler et al. Weber A. Jackson RJ.

007 (.014 (. Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).020-.028-.039-.009-.021 (.029-.023) .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 .009) .010-.007-.008 (.026-.022-. 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.017) .007 (.033 (.018 (.011-.007-.007-.031 (.031-.017-.011-.009 (.027) .013) .037 (.042 (.006-.028-.046 (.033 (.015 (.016) . Thus.024-.009 (. including nuclear weapons.029 (.011) .009) .007-.016) .017 (.047 (.013 (.020) .018) .035) .046 (.046 (.009-.030) .013-.020-.020-.006 (.031 (.005-.032 (.279) .027-.010-.008 (.021-.009-.008-.010) .049) .009 (.039) .010) * .008 (.011) .021) .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 . Fourth National Report on Human Exposure to Environmental Chemicals 239 .008 (.038 (.060 (.011) .052 (.014 (.024-.017-.015-.007 (.009) * .007-.037) .007-.006-.017) .008) .025-.017-. and 0.007) .008-.065) .040) .027) .040) .063) .040-.S.009-. or processing. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.023-.010) .023-.017) .048) .067) . nuclear fuel.011) .028 (.006-.010-.008 (.062) .050) .027) .008-.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.010) .008) .046-.014 (.007 (.010) * .007-.040 (.010) .017 (. in some ceramics.013 (.009) .018) .011) .043) .034) . 01-02.015 (.023 (.017) .024-.035) .008 (.016) .009) .008-.009) Selected percentiles ( 95% confidence interval) 50th .007 (.008 (.036) . 235U (about 0.015) . and 03-04 are 0.007-.005-.014 (.044 (.022 (.051) .007) .012-.042) .010 (.009) .026-.006-.013-.005-.010-.008-.007-.041 (.034-.007 (.010) .017-.031 (.056) .007-.039) 1227 1335 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .008) .006-.030 (.012) .010 (.027-.023) . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks. and as an aid in electron microscopy and photography.019-.030 (.011-.067) .039) .012 (.007 (.065) .005.020-.045) .013 (.013 (.020) .011 (.009) .007) 75th .088) .021) .023-.007-.015 (.012-.036) .009) .026) 95th .036-.016) .007-.046) .036 (.012) .012 (.027 (. Uranium has many commercial uses.008 (.005-.037-.037) .041 (.054) .012-.006-.009) .016-.013-.007) .009) .013 (.011 (.021) . milling.012 (.007 (.027 (.158) .013) 90th .006-.027 (.028 (.010) .006-.007-.008) . In workplaces that involve uranium mining.038) .023-.007-. Since the 1990’s.010 (.127) .012) .043 (.020-.012-.035-.021 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.008 (.016) .053 (.009 (. and 234U.012 (.006-.007-.066) .006 (.011-.Metals Uranium CAS No.018) .008 (.040 (. interval) .021 (. 0.010) .007 (.053) .027 (.011-.009) .033-. respectively.012 (.009-.011-.011-.016-.048 (.008 (.009-. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.030 (.034-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.009 (.050) .031 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.026 (.015) .009 (.021-.010-.023 (.049) .004.037) Total .008-.005-.006 (.008 (.018) .008-. Variable concentrations of uranium occur naturally in drinking water sources.019-.009-.046 (.031 (.026 (.018 (.017-.040-.009) . see Data Analysis section) for Survey years 99-00.009) .054) .018-.012-.006 (.015 (.114 (.026) .019-.012-. human exposure occurs primarily by inhaling dust and other small particles.072) .013 (.008 (.028 (.064 (.006-.012) .030-.029-.026 (.056) .037) .009 (.027-.009) .036-.008 (.073) . 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.010-.009 (.006-.008 (.008) .045) .016-.016 (.010 (.009-.017-.019 (.006-.019-.016) .006-.012 (.024 (.007-.009 (.008-.055 (.010) .011) .027) .007-.004.023 (.011) .023) .022-.017) .008 (.009-.009 (.009-.054-.72%). population from the National Health and Nutrition Examination Survey.007) .033) .022) .036 (.007-.026) .007 (.013 (.022-.010 (.007) .020 (.014 (.069) .008 (.007 (.014 (.

029 (.010) .024) .010 (.005-.009 (.026 (.007-.011-.009) * .008) .035 (.007 (.006) .013 (.028) .010-.030-.016) . Health effects from uranium exposure result from chemical toxicity to the kidney.017-.028 (.013-.007-.019 (.024) .030-.051) . low level exposure. After exposure to soluble uranium salts.023-.037 (.008 (.041) .074) .010) .007-. 240 Fourth National Report on Human Exposure to Environmental Chemicals .010 (. Depending upon the specific compound and solubility.014-.006 (.009-.030 (.011-.025-.008) .053) .034 (.019-.008 (.034-.033 (.013 (.010) * . about 50% of the absorbed dose is eliminated in the urine within the first 24 hours. After long term or repeated exposure.028-.009) Selected percentiles ( 95% confidence interval) 50th .013 (.006) .013 (.009) .039) .006-.020 (.028 (.016) .008-.009) .008 (. liver.008) . Studies of persons with chronic exposure to soluble uranium salts in drinking water have not shown kidney Urinary Uranium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.021-.056) .012 (.014 (.005-.009) .016) .012) .006-.042) .021 (. Uranium is eliminated in feces and urine.080) .042) .019-.013 (.016) .009) .008) 75th .029 (.007 (.014) .010 (.009-.018 (.020 (.019) .015-.011-.015) .100 (.010 (.006 (.033 (.024) .005-.007-.027) .010) . 1992).015 (.026 (.017) . where limited absorption occurs (less than 5%).015 (.013 (.014-.029) .061) .015-.010-.011 (.033 (.022-.018-.029) .027-.010-.024) . 2005).005 (.006-.005 (.018-.008 (.051) .025-.006-.008 (.006) .013 (.009) .012) .018) .028) .006-.005-.029) .008 (.007 (.012 (.007-.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 .007) .024 (.007 (.146) .025 (.030 (.008 (.006-. interval) .015) .007 (.044) .011) . Human health effects from uranium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.025-.008-.016) .007) .006 (.026) .027-. Inhaled uranium-containing particles are retained in the lungs.015-.010 (.020-.016) .024-.011-.1%-6% of an ingested dose may be absorbed.034 (.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.008) .029 (.006-.030) .008-.058) .008) . kidneys.007 (.008) .007 (.006-. and bones can accumulate uranium with the largest amounts being stored in bones (Li et al.027-.016-.050) .004-.014) .009) .017) .031-.014) .007 (.270) .024 (.016) .006-.012 (.. with much slower elimination from bone.024-.010) .006 (.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 .007-.006-. the shrapnel acts as a source of chronic.014 (.008) .019) .042-.007 (.034) .025 (.019 (.012-.015 (.011) * .008) .039) Total .006-.005-.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) .017-.005 (.014-.022-.054) .019-.010-.011-.017-.010-.022 (.007) .040 (. Soluble forms of uranium salts are poorly absorbed in the gastrointestinal tract.011-.024 (.012-.011-.034 (.032) .013) .029) .007-.077) .007 (.007-.025) 95th .006-.006-.010-.067) .039) .034-.013 (.006-.018-.005-.008) .059 (..033 (.008-.021 (.009 (.007 (.S.024) .019 (.017 (.009) .011-.030) .012 (.017) .014) 90th .020) .009-.027 (.010) .053) .017 (.007 (.016) .019-.048) .012) .009) .015 (.010-.006-.021 (.011) .009-.033) .020-.008 (.030 (.007 (.018-. population from the National Health and Nutrition Examination Survey.034 (.013 (.007 (.027) .013 (.010-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.006) . After inhalation.006 (.007 (.032) .050) .006-. the initial half-life of uranium is about 15 days (Bhattacharyya et al.011 (.009 (.006-.007 (.013) .034 (.008-.007-.005 (.012 (.028) .009-. which represents distribution and excretion.012 (.016-.026-.051) . 0.051 (.025-.007 (.006-.027 (.013) .008 (.012 (.011) . 2003).018-.047) .007 (.009-.027-.009 (.021 (.045 (.028) .004-.021) .015) .022) .008 (.007 (.026 (.Metals impact.022 (.027 (.006-.006-.007 (.006-.031 (.010-.010-.010) . Radiation risks from exposure to natural uranium are very low.008) .022 (.008) .035 (.017-. In cases of retained DU shrapnel.024-. the half-life of insoluble uranium in the lungs is several years (Durakovic et al.015-.022-.050 (.006-.016-.016 (.020-.009) .010-.048) .016-.007-.020 (.015-.020-.005-.007 (.006) .006 (.009 (.009) .008-. which can occur occasionally from high occupational exposure.043 (.006-.039) .011-..058) .019-.063) .015) .

. 1994. Ejnik JW. Tolmachev et al. Galletti. In 17 U. with emphasis on quality control. pp.gov/ toxpro2. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. Durakovic A. Byrne AR.. 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000. ingestion.cdc.. Stradling GN. Vol. 2002. Zimmerman I. 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.1992. Guidebook for the treatment of accidental internal radionuclide contamination of workers. Drinking water and other environmental standards have been established by U. 1992.S.. In two studies of a Finnish population with high natural uranium concentrations in their drinking water.65 μg/L). Hamilton MM. et al. Benedik L. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry.. soldiers evaluated before.. EPA. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Karpas et al.. Dang HS. Kent (England): Nuclear Technology Publishing. respectively. Atlanta (GA). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Health Phys 2000. Pullat VR. Centers for Disease Control and Prevention (CDC).. or wound contamination. the geometric mean urinary uranium concentration was 0. In: Gerber GB.1996. 2003.e. 2004). McDiarmid M.011 μg/L (McDiarmid et al.. Komaromy-Hiller et al.. Breitenstein BD. and 2003-2004 (Dang et al.162 μg/L) (Orloff et al. Pillai KC.55 μg/L (median 0. 41 (1). McDiarmid et al. 28 soldiers who may have been exposed to DU by inhalation. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U.atsdr. 2006.61 μg/g creatinine.S. Uranium content of blood. soldiers who had been injured and had embedded DU shrapnel for as long as eight years. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. 2006). Fourth National Report on Human Exposure to Environmental Chemicals 241 . 2006). Carmichael AJ. Information about external exposure (i. Muggenburg BA.168(8):600-605. the median urinary concentration was 0.078 μg/L (ranging up to 5. In the same study.. 2000).78:143-146.110 to 45 μg/L (Ejnik et al.S. Dietz LA. in that the levels were below their respective detection limits (Byrne et al. Boyd P. Horan P. 2005. 2002). but in whom no shrapnel was embedded.. population. had a mean urinary uranium concentration of 0. Determining the normal concentration of uranium in urine and application of the data to its biokinetics. during. Volf V. Sci Total Environ 1991.html. Radiation protection dosimetry. although slightly increased during and after deployment. Mil Med 2003.107:143-157. 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. and no consistent effects on multiple endpoints of kidney function were found.. 2004). 1978). IARC and NTP have no ratings for uranium human carcinogenicity.. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population.Metals injury associated with elevated urinary uranium levels (Kurttio et al. A cohort of 46 U. Hamilton et al. Third National Report on Human Exposure to Environmental Chemicals. (May et al... eds. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. (Kurttio et al. Thomas RG. urinary levels of uranium were as high as 9. NRC. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.066 μg/g creatinine (Gwiazda et al. 2004). 2000). 2006). The U. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. Follow up of 32 veterans with embedded shrapnel showed that increased urinary uranium levels persisted more than 12 years after the first exposure (McDiarmid et al. Health Phys 1992.S. In a study of 105 persons exposed to natural uranium in well water. environmental levels) and health effects is available from ATSDR at: http://www. 1991. Metivier H.62:562-566. 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. Squibb K. 2001-2002. the median urinary uranium concentration was 2. 2004). Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. Six workers in a depleted uranium program showed concentrations of 0. 2006). 1-49.S. References Bhattacharyya MH...S. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts.

242 Fourth National Report on Human Exposure to Environmental Chemicals . Hollriegl V. Cordero S. Kurttio P. Health Phys 2004. Katorza E. Auvinen A. Marino R. McDiarmid MA. Karpas Z. Nuclear Regulatory Commission (NRC) Guide 8. Oeh U. Metcalf S. Lorber A.71(6):879-85. Mistry K. Human exposure to uranium in groundwater. Lewis BM.82(4): 527-532. Hancock RG. Engelhardt SM. J Toxicol Environ Health A 2004. Kane R.296(1-2):71-90. Sabbioni E. Cremisini C. Komaromy-Hiller G. Squibb K. U. Uranium and thorium in urine of United States residents: reference range concentrations. Heller J. Andrews WS. Biokinetic modeling of uranium in man after injection and ingestion.87:51-56.S.110(4):337-342. Wilson PD.85:228-235. Pirkle JL. Int Arch Occup Environ Health 2006. patient population and literature reference intervals for urinary trace elements. McDiarmid MA. et al. Auvinen A. et al. Pinto V. May LM. Saha H. Ejnik J. Health Phys 2002. Pekkanen J. Halicz L. Howerton K. Shelly T. Noguchi H.158:165-190. McDiarmid M. et al. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Orloff KG. Saha H. Gucer P. Sampson EJ. Clin Chim Acta 2000. Roth P. U. concentration and daily excretion of uranium in urine of Japanese. Oberbroekling KJ. Makelainen I. et al. Element reference values in tissues from inhabitants of the European community.22–Bioassay at uranium mills. Am J Kidney Dis 2006. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Charp P.81:45-51. Komulainen H. Jarrett JM. Oliver M. Wahl W. Smith D. Kuwabara J. Health Phys 2004. Health Phys 1996. Uranium daily intake and urinary excretion: a preliminary study in Italy.S. Sci Total Environ 1994. Kalinsky V. Jackson RJ. Salonen L. Environ Health Perspect 2002. Comparison of representative ranges based on U.44:29-40.47(6):972-982. Biologic monitoring for urinary uranium in Gulf War I veterans. Health Phys 2006. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. Renal effects of uranium in drinking water. NRC). Roiz J. rapid. Harmionen A. Scott K. Inductively coupled plasma mass spectrometry as a simple. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Ash KO. VI. Van der Venne MT.67(8-10):697-714. Gwiazda RH. Kidney toxicity of ingested uranium from drinking water. Ough EA. Costa R. Kurttio P. Washington (DC): NRC. Environ Res 1999. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Nuclear Regulatory Commission (U. Li WB.Metals Galletti M. Englehardt SA. Paretzke HG. Marko R. Radiat Environ Biophys 2005. Bennett LG. et al. Environ Res 2004. Tolmachev S. Squibb K. Salonen L. July 1978.S.79(1):11-21. D’Annibale L.91(2):144-153. Paschal DC. et al. Karpas Z.86:12-18. Health Phys 2003. Hamilton EI.S. Review of elements in blood. Ting BG.94:319-326.

0) 9.0-18.0 (11.20) 3.19 (3.0 (9.80-4.74-3.0 (12.90 (3.65) 3.22-5.30 (5.0 (12.76 (3.0 (9.0-17.20 (2.0) 19. and limited applications in pharmaceutics.80 (6. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms.01 (2.50-7.0) 11. lettuce) can be the main sources of intake for humans (FDA.68) 4.50 (5.75-3.70-7.0) 14.51 (3.50-3.0-18.0-14.0) 14.0-18.80-6.11) 4.0 (10. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.10) 3.40) 3.30 (2.20 (6.0) 13.40-4.80 (3.90 (5.00) 4.10) 5.90-6.40 (4.0-15.10) 12.0) 13.70-9.0-19.80 (7.81) Selected percentiles ( 95% confidence interval) 50th 3.20-4.93 (4.0 (9. Other manufactured uses include fireworks.10-12.45-4.40-4.21 (2.66) 3.81-16.00-6.40-13.20 (4.89-3.0 (11.05 (2.0) 13.30-7.0) 11.40) 6.10 (6.50-11.0 (11.35 (3.60 (4.30-19.90 (2.50-4.20 (5.90-10.0 (11.0-17.30-17.20 (4.80-15.54 (3.0 (11.20-11. milk.67-5.0) 11. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.30-6.0) 16.0-17.90-12.0 (11. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.93-3.50 (8.76) 4.40) 2.20) 4.60 (7.10) 5. and reducing agents.0) 10.18-3.0) 13.10 (6.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.40) 4. but has strong oxidant properties in the presence of concentrated acids.40 (5.40-7.19-4.0 (11.0 (8.93-4.20 (8.51 (3.0) 13.20-12.38) 5.10-11.90-3.30 (5.70 (3.0) 9.0-20.0 (12.0 (13.30-7.40 (5. leather tanning.70-3.50) 3.10 (7. In addition.16) 3.08-3.50) 6.0) 15. certain catalytic metals. Drinking water.0) 10. laboratory analysis. potassium.0) 95th 14.0-17.00-5.40) 3.50) 5. 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.20) 7.70-5.62 (3.0) 14.75 (3. Perchlorate is stable under most environmental and physiological conditions.90-11.79 (2.00) 3.80 (3.44-4.0) 15.60-7.40 (3.80-12.11) 3.0) 12.70-6.80) 3.02 (3.40-11. EPA’s Contaminant Candidate List (CCL) for drinking water in 1998 following discoveries of its presence in drinking water supplies throughout the southwestern United States (U.0) 708 617 681 652 1228 1092 Limit of detection (LOD. Perchlorate was added to the U.84) 14.0-17.46) 3.0 (11.0 (8.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.03) 3.0 (11. matches.5 hours and has a small estimated volume of distribution (Crump and Gibbs.70) 3.S.30) 6. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.20 (7. 2002).40 (5.49-3. see Data Analysis section) for Survey years 01-02 and 03-04 are 0. It is normally found and produced as the anion of a sodium.S. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 . 1998).0 (9.20-3.10-4.0-15.70-12.56) 3.09) 3.40 (3.90-9.60) 5. 2005).60) 3..0 (9.05 and 0.50 (3.70-11. interval) 3.90-3.40-5.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.70-3.87-3.80-4.0) 13.26 (2. population from the National Health and Nutrition Examination Survey.80) 75th 6. or ammonium salt.0 (12.31) 2.0 (8.80-8. 2007).29-3.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0) 13.88) 3.60-6.40) 90th 10. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7.00) 7.90 (4..60 (4.90) 6.EPA. Inhibition of iodine uptake by competition for the sodium/iodide symporter in the thyroid can be estimated in humans by measuring radioiodine uptake CAS No.0) 8.40-6. fabric dyeing.32 (3.40 (8.10 (2.90-9.0) 8.90 (5.0-29.0) 9.30 (2.22 (2.0 (11. and certain plants with high water content (e.80) 7.70 (3. 2005).10-7.30) 6.0) 10.20 (2.07-4.0 (8.0) 9.0) 9. Survey years 01-02 03-04 Geometric mean (95% conf. and electroplating.0 (8.0) 13.10) 3.96 (3.Perchlorate Perchlorate (Urbansky.0-23.g.12) 3.60) 8.39-4.0) 9.0-17.00-6.40 (4.20-4.80) 12.90 (5.50) 5.10-11.47-4.90-11.0 (9.00) 3.50-4.05.50) 11.90) 5.0 (9.S.10 (5. 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.70 (3.00) 5.40) 3.

.3) 11.0) 14.6-17. Steinmaus et al.33 (7.50 (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.20 (2.61 (5..21 (2.0 (11.70 (4.80 (7. levels and sufficient in most participants (Tellez et al. NAS.60-5.0) 11.0) 6.93) 3.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3.S.0 (9.56 (3. menopausal status.20-4.S.1-14. interval) 3.10) 6.90-11.52 (8.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.42 (3. although iodine intake was higher than U.40 (4.22 (2.0) 12.04-3.4 (10.g.10) 4.43) 6. Lawrence et al.29-6.08) 3. 2000). 2002. 2005.1-16.95 (2.3-14. population from the National Health and Nutrition Examination Survey.50) 6.00) 4.5 (13. Greer et al.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 .80-3.30) 75th 5.20-9.35) 3.20-3.09) 3.25 (3. 2006.90-15.0-14.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.20) 3. 2002).37 (4.7 (11.00-11.00-3.10) 13.47) 2.80 (4.0 (11.58) 2. Follicular cell thyroid tumors would Urinary Perchlorate (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.50 (6.10-3.70-15.90 (4. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.4) 8.74) 7.1) 8.70) 2. nitrate.20-10. 2005).33-12.87-3. 2005).02) 3. dietary iodine intake. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability. 2001.34-3. gender.89-3.70 (2.40) 5.10 (4.1-13.26) 4.05 (4.32) 5.3) 8.90 (2.86) 4.3 (10.20) 8.89 (2.87 (5..45) 3.12-2.. However.51 (3. thiocyanate.90 (2.0) 4.87) 7.0) 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 3.60-15.0) 12.. in a representative sample of U.0-17.80) Selected percentiles ( 95% confidence interval) 50th 3.6) 12.60-11.64-3.60 (3.0) 9.53 (2.00) 3.93-5.0-19.54 (3.02-4.46 (3.50-3.14 (2.67) 5.10 (4.4 (11.04-3.35 (2.08 (3.39-4.50) 2.70-5.50) 9.83 (5.40 (3.61-10.4) 13.29) 2. medications). 2003.70) 10.90 (7.30 (3.52-9.46-13.30) 5.1 (11.1 (8..25) 5.5) 8.35 (4.60) 3.60-5. 2002.EPA. 2005.40) 3. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.1-22.99-3.0) 13. Lamm and Doemland. In the U.81-3.33-6.0 (8.93-7. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses.44-6. chronicity of exposure.40 (3.30 (6.41-9.93-5.19-6.93-8.90-9.00) 9.66) 3.80 (7.10 (1. Many factors may be important in consideration of perchlorate action on the thyroid: dose. perchlorate is negative in most genotoxic assays (U. 2005).0 (9.10-7.0) 7.56-3.51-4..90-3.26 (3.80-3.0) 9.60-11.4 (8.22-4. Also.22-4.25) 5.S.09 (7.S.2) 8.45-2.64) 5.0) 10. U.30-5. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.00-2.40-10.60-8. age. Survey years 01-02 03-04 Geometric mean (95% conf.25) 5.96) 2.12 (6.19-10.70-3.10 (6.20 (6.60-6.36 (8.87) 2.60-8.00 (4.. 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..03 (2.00 (6.15-12.90-2.0-44. 2007).73) 3.0 (8.72 (3.0) 13.46-4.54 (2.40) 17.3) 12.40 (7.2) 8.99 (5.50-9.50) 5.61-5.07 (2.20 (3.91) 4.24-2.8 (11.30-10.S.39 (3.97-5.98) 3.0 (11.60) 8.0) 12.4 (11.24 (4.76-3.18-3.90-20.EPA.30) 90th 9.30 (5.22-6.10) 3. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.30-5. up to 68% RUI has been demonstrated.39) 2..4-16.71 (5.0) 12.77 (3.00 (2.87 (7.16-3.6) 20.Perchlorate inhibition (RUI).90) 5.S. levels.37-13.76 (3.0 (9. women with urinary levels of iodine less than 100 micrograms per day.0-14.0 (10. and the presence of other substances known to affect thyroid function (e.10 (2.50) 2.60) 10.20 (7.S.75) 3.84) 2.44) 3. Li et al.82 (5. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.70-4. 1999.30) 3.20-3. altered thyroid function was not found in Chilean pregnant women or their newborns with mean urinary perchlorate levels about 40-fold higher than average U.50-5.70 (2.20 (4.59) 3.60-3. During gestation and infancy.50) 95th 12.

Lamm SH. Steinmaus C.S. 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. Pirkle JL.115(9):1333-1338. EPA reference dose (Blount et al. Perchlorate Exposure of the US Population. 2005. Skeels MR. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans. 2005). J Expo Sci Environ Epidemiol 2007. and nitrate on thyroid function in workers exposed to perchlorate long-term. 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. Lamm S. Tellez RT. Miller MD. Low dose perchlorate (3 mg daily) and thyroid function.. Gibbs JP.gov/safewater/ccl/perchlorate/perchlorate.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Lawrence JE.10(8):659-663. May 2007. population. Lamm SH. Magnani B. Blount et al. Erratum in: J Occup Environ Med 2004. 2001-2002.40(21):6608-6614. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.17(4):400-407. Deyhle GM. Osterloh JD. Cross M. Kelsh MA. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Abarca CR. Perchlorate in the United States. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Kirk AB. 2007).html.11(3):295. Health Implications of Perchlorate Ingestion. Chacon PM. Crump KS. Analysis of relative source contributions to the food chain.113(11):A732. Primary congenital hypothyroidism. Pino S. Dasgupta PK. Landingham CB. Greer SE. The levels seen in NHANES 20032004 show a similar pattern to NHANES 2001-2002. The effect of short-term low-dose perchlorate on various aspects of thyroid function.. Richman K.fda. Sesser DE. J Occup Environ Med 2003. Available at URL: http://www. Also. (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. Braverman LE. Doemland M. Blount BC. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Valentin-Blasini L.. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey.46(5):509.atsdr. Valentin-Blasini L.gov/toxpro2. newborn thyroid function. National Research Council of the National Academies. 6/2/09 Greer MA.S. Biomonitoring Information Urinary perchlorate levels reflect recent exposure. Lau EC. Braverman LE. 2005). Thyroid 2000. Food and Drug Administration (FDA). References Blount BC. Lawrence J. Pino S. The effect of perchlorate. Washington (DC): National Academy Press. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Caldwell KL. Thyroid 2001. Buffler PA. and environmental perchlorate exposure among residents of a Southern California community. Jackson WA.EPA at: http://www. Byrd D.cdc. J Occup Environ Med 2000. Braverman LE. National Academy of Sciences (NAS).45(10):1116-1127. J Clin Endocrinol Metab 2005. Howd R. Li Z. He X. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. et al.113(8):10011008. CFSAN/Office of Plant & Dairy Foods. Pirkle JL. Environ Health Perspect 2005. Environ Health Perspect 2002. Barnard JC. et al.114(12):1865-1871. Goodman G. Environ Health Perspect 2006. Osterloh JD. Erratum in: Environ Health Perspect 2005. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Page Last Updated: 05/28/2009. most of the population is considered to be below the U. Li FX. Rutherford GW.110(9):927-937. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Environ Sci Technol 2006. et al. Mauldin JP. Additional information about exposure and health effects is available from the U. Neonatal thyroxine level and perchlorate in drinking water. Blount BC. Pleus RC.42(2):200-205.41(5):409-411. 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. Lamm SH. Benchmark calculations for perchlorate from three human cohorts.S. Crump KS. Environ Health Perspect 2007. Daaboul JJ.htm.90(2):700-706. thiocyanate.html and from ATSDR at: http://www. epa. Dyke JV.

Perchlorate pregnancy and the neonatal period. Perchlorate. Integrated Risk Information System (IRIS). 246 Fourth National Report on Human Exposure to Environmental Chemicals . Revised 2/11/05.S. cfm?substance_nmbr=1007. No.gov/iris/quickview.S. U.epa. Available from URL: http://cfpub. Drinking Water Contaminant Candidate List. EPA).S. Environ Sci Pollut Res Int 2002. 1988. EPA).1/15/06 U. Doc. Environmental Protection Agency (U.15(9):963-975.9(3):187-192. Environmental Protection Agency (U. Thyroid 2005. Urbansky TF. EPA/600/F-98/002 Washington (DC). Perchlorate as an environmental contaminant.S.

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

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

500) .50) . 2004. 2004.500) .400) .. see Data Analysis section) for Survey year 03-04 is 0... Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. PFOS.S.300-1. 2007b.. population from the National Health and Nutrition Examination Survey.300 (<LOD-. 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.700 (. 2003a.500-1.500-.108 times higher than background serum levels in humans (Butenoff et al.3. hepatotoxicity. 2003..900 (. development in offspring was stunted and hypothyroxinemia was observed.600 (.800 (. 2003a. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats.00) .. 2004). In comparing three separate reports on adults.. thyroidal). perfluorohexanesulfonate (PFHxS). EPA. and no substantial age trends were seen within adults ages 20-69 (Olsen et al.. and there was no clear evidence of excess all-cause or diseasespecific mortality.. 2001.10) . animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11.800 (.40) .600 (.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. Harada et al.800 (. elderly and children. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. PFOA.900 (. 2003a).900 (. monkeys.500-1. 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.400-1. Fei et al. which may vary for some chemicals by year and by individual sample. Thibodeaux et al. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. At doses causing maternal toxicity. Kennedy et al. and changes in thyroid hormone concentrations (Grasty et al.600 (.800) 1.80) 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 . 2005).400-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500) . < LOD means less than the limit of detection. 2007a.800) 1.10 (.400-1. 2003. developmental and teratogenic effects were demonstrated in offspring. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal. the potential to estimate risks to humans from animal doses is uncertain. PFOA.. Animal studies of PFOS have demonstrated weight loss.00) . 2003..400 (<LOD-. possibly related to lung immaturity (Lau et al.400 (<LOD-.S.00 (. Survey Geometric mean (95% conf.500 (<LOD-1.400-.300 (<LOD-. Cook et al.. U. 2003). Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. However.. Olsen et al. Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.10) . 2003)..10) * 03-04 03-04 * * < LOD < LOD < LOD . 2007. or increased cancer rates (Alexander et al. 2004a.500) 90th .. population.800 (. Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants. 1999.S. 2003). 2003a).400-1. Analysis of the NHANES 20032004 subsample demonstrated higher levels of PFOA and PFOS in males and a slight increase in levels of PFOS with age (Calafat et al. Olsen et al.300 (<LOD-.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. interval) Selected percentiles ( 95% confidence interval) Sample 95th . reproductive. 1992. In such studies.700) .. 2007a.. At high but non-toxic maternal doses of PFOS..20) .400-1.500) ..500 (.500-1. EPA.80) 485 538 962 Limit of detection (LOD.500-3.400 (<LOD-. U. 2004). 2007).80) 640 1454 03-04 03-04 * * < LOD < LOD .. PFOS.S.600-2. 2003a.500 (.00) .. Olsen et al.400-1. Lau et al. the median PFCs values tend to be roughly similar in these age categories (Olsen et al. 2004b). 2005). and humans. 2007b).500-1. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al.

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

Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.600 (.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. see Data Analysis section) for Survey year 03-04 is 0.900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD .3. population from the National Health and Nutrition Examination Survey. Fourth National Report on Human Exposure to Environmental Chemicals 251 . population from the National Health and Nutrition Examination Survey.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 .400 (<LOD-.S. which may vary for some chemicals by year and by individual sample. < LOD means less than the limit of detection.500) 485 538 962 Limit of detection (LOD. see Data Analysis section) for Survey year 03-04 is 1.900) < LOD .400) . Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample. Survey Geometric mean (95% conf.500 (<LOD-.400 (<LOD-.S.300-.500-. < 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.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 .400 (.300 (<LOD-.300 (<LOD-.600) < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD.0.

72) 1.10) 4.60-3.0) 8.90) 8.30 (7.900-1.30) 03-04 03-04 .10) 8.60) 2.91) 2.10-5.30 (1.30) .16) Selected percentiles ( 95% confidence interval) Sample 95th 8.56-1.77-2.800-1.00-6.80 (4.50-3.00 (1.50 (2.50 (1.80-8.30) 3.20) 1.30) 3.60) 1.70-2.60 (6.70-7.60) 9.00-1.54) .40) 1.40) 1.20) 03-04 03-04 2.20-1.6) 7.586-.60-7.60 (1. interval) .00 (2.20-1.40) 640 1454 03-04 03-04 1.700 (.800 (.60-2.50 (4.80-7.40-3.93 (1.30 (1.10) 75th 1.10 (4.12) .50 (1.00 (1.809) 1.70-10.90 (2.30-2.14) Selected percentiles ( 95% confidence interval) Sample 95th 3.42 (1.900) 1.900 (.10 (.17 (1.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.40) .5) 8.40) 640 1454 03-04 03-04 2.20 (1.80-8.30 (3.10) 5.90) 1.00 (5.70) 1.3.900-1.00 (.50 (1.40) 2.08) 2.80-4.00-8.50 (1. see Data Analysis section) for Survey year 03-04 is 0.90) 1.05-2. 252 Fourth National Report on Human Exposure to Environmental Chemicals .40 (1.S.816-1.60 (1.20) 2.60-4. population from the National Health and Nutrition Examination Survey.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.70 (1.00 (.80-4.10-9.00-7.80-3.70-6.80) 4.90-2.17-1.912-1.10) 1.40 (1.80-4.40 (2.80) 5.70) 2.900-1.3 (9.20 (6.30 (1.80-7.963 (.10 (1.10 (4.50-10.852 (.700-1.80) 3.70) 1.50) 6.10) 1053 1041 03-04 03-04 03-04 .721-1.00) 2.30-12.16) .01 (1.90-10.10) 6.826-1.600-.40 (1.70) 13.900-1.70 (2.86 (1.00 (1.00) 1.40 (1.87-2.10) 75th 3.90 (4.900-1.20) 485 538 962 Limit of detection (LOD.90) 3.90 (1.40) 4.1) 485 538 962 Limit of detection (LOD.90 (1.10 (.20-1. Survey Geometric mean (95% conf.S.50) 2.20) 1.60-3.04) .50-6.80) 90th 2.40-1.20-3.60-2.10) 4. see Data Analysis section) for Survey year 03-04 is 0.30-9.60-2. Survey Geometric mean (95% conf.70-2.10-9.80-12.00) 1.40-1.60 (1.900-1.20 (6.835-1.80-6.03) 1.90) 1.20) .72 (1. interval) 1.70) 3.30) 3.70-5. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.20 (1.09 (. population from the National Health and Nutrition Examination Survey.62-2.30 (6.20-1.689 (.27) 1.966 (.50 (6.60) 3.26) 2.51) 1.861 (.50 (6.73-2.984 (.92 (1.80 (1.90) 90th 5.70) 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 1.30-6.90 (4.90 (1.67-2.00 (1.80-2.90 (1.30 (2.60-8.80-3.00-1.5) 5.14 (.70) 2.50) 2.50 (4.834-1.10) 1.20 (1.20-2.80 (1.1.697-1.10 (.30 (2.30 (1.20 (1.00) 3.50-6.90-19.44 (2.0) 1053 1041 03-04 03-04 03-04 1.900 (.10) 6.80) 1.60-4.

2-57.20) 5.20 (4.90) 6.9 (17.4) 75th 30.70) 6.21-3.35) 3.0 (20. see Data Analysis section) for Survey year 03-04 is 0. population from the National Health and Nutrition Examination Survey.2 (27.0) 21.5) 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 21.50) 4.2) 45.4 (28.9) 22.6) 18.47 (4.60-9.90 (7.79) 4.2) 30.20-9.9-23.6) 21.60 (3.80-12.6-45.8-35.8 (45.8 (37.3 (35.0 (27.8-30.9) 27.70 (5.20-4.00 (5.0) 36.3) 42.80) 8.40 (6.40) 75th 5.6) 7.1-25.8) 32.0) 21.60 (4.40-6.7 (35.30 (3.53) 3.9-19.30) 7.30-5.00 (3.1 (24.6 (35.70) 4.5 (28.4) 21.95 (3.1 (19.1) 57.3) 41.50) 7.6-24.80-4.5) 9.96 (3.7-30.8) 46.6) 9.65-4.10 (6.2 (18.40) 90th 7.0) 43.47-4.4) 56.50 (3.60 (7.7-23.37 (2.10 (3.2 (19.70-10.50-6.5) 1053 1041 03-04 03-04 03-04 14.4-42.4 (19.80 (6.9 (22. interval) 3.2 (21.3 (17.8-22. interval) 20.7 (43. Fourth National Report on Human Exposure to Environmental Chemicals 253 .S.70-7.1-24.7 (19.5 (28.90-4.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.0) 90th 41.70 (3.60 (5.8-81.10) 5.5) 8.60-14.4 (23.S.2) 30.7 (7.84-3.20 (4.91) 3.70) 3.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.3-61.80 (7.20) 7.80 (6.1 (23.4 (19.2-22.3) 28.70-9.40-6.7-49. Survey Geometric mean (95% conf.10-3.10 (3.5-21.60-6.8) 27.1-52.20) 10.6 (42.27) 4.89 (3.80-9.30-6.7-53.70-5.99-3.5) 32.30 (3.67-4.60 (6.5-62.90-12.70 (5.3 (44.6) 1053 1041 03-04 03-04 03-04 3.3 (35.80 (5.6) 42. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.8-22.0) 23.7 (35.85-4.60) 03-04 03-04 3.70-7.90 (7.6) 62.1-36.8 (34.2) 640 1454 03-04 03-04 4.6-50.20) 4.5-33.20) 5.0) 485 538 962 Limit of detection (LOD.8-78.3) 485 538 962 Limit of detection (LOD.0) 03-04 03-04 19.2 (16.60 (6.7 (43.40) 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 4.0-66. see Data Analysis section) for Survey year 03-04 is 0.6 (44.1) 15.07-4.0-20. population from the National Health and Nutrition Examination Survey.9) 9.82) 4.1.4.30 (5.0-70.7-69.50-13.40-10.60-13.4-17.50 (4.1-33.40) 3.4 (17.4) 20.5) 7.90-4.00) 3.90 (7.5) 19.90 (5.20) 7.0-16.9 (13.30-8.5) 57.4-25.3 (28.6 (19.60) 8.4) 640 1454 03-04 03-04 23.5-23.2 (28.7-33.40 (4.50-4.40-14.30-11.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.18 (3.00 (5.9 (19.7) 39.11 (2.9-38.40-17.8-22.30) 6. Survey Geometric mean (95% conf.7 (13.5) 18.30-3.6) 35.1-35.3-22.9) 22.20-5.

500) .300 (.400 (<LOD-.300 (.400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .200-.300 (.300-.4. 254 Fourth National Report on Human Exposure to Environmental Chemicals .300 (.500) < LOD 485 538 962 Limit of detection (LOD.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .200-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . < LOD means less than the limit of detection.200 (<LOD-. < LOD means less than the limit of detection.300) . Serum 2-(N-Ethyl-perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.300) .300 (. Survey Geometric mean (95% conf.200-.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300-. population from the National Health and Nutrition Examination Survey. 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 . which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 0.300) .300) .300 (.300 (.200-.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.200-. see Data Analysis section) for Survey year 03-04 is 0.300) .300) .Perfluorochemicals Serum Perfluorooctane sulfonamide (PFOSA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. population from the National Health and Nutrition Examination Survey.500) 485 538 962 Limit of detection (LOD.300-.S. Survey Geometric mean (95% conf.2.300) .300 (.200-.300 (.300 (.300 (.300 (.200-.400) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th 90th .500) . which may vary for some chemicals by year and by individual sample.300 (.200-.S.500) .200-.200-.300-.

70) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th .700) 1.700 (<LOD-.50) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD 75th . which may vary for some chemicals by year and by individual sample.900-1.00) < LOD .50 (1.80) 1.3.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD .10) 1.10) * 03-04 03-04 * * < LOD < LOD .20 (1. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.00 (.10) .10 (1. population from the National Health and Nutrition Examination Survey.S.900-1. which may vary for some chemicals by year and by individual sample.900-1.800) .10) .30 (1.700) 1.700 (<LOD-.10-1.500 (<LOD-.600 (<LOD-1.700 (<LOD-.400 (<LOD-.400 (<LOD-1.6.700) .900-1.10 (. * 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 1. < LOD means less than the limit of detection.600 (<LOD-.00-1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .30 (1. population from the National Health and Nutrition Examination Survey.600 (<LOD-1.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .10-1.S. see Data Analysis section) for Survey year 03-04 is 0.00 (.900) 1.20-1.00 (. see Data Analysis section) for Survey year 03-04 is 0.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.80) 1.10) 1.300 (<LOD-.900) 485 538 962 Limit of detection (LOD.900-1.30) .60) 640 1454 03-04 03-04 * * < LOD < LOD .700 (<LOD-.30) 1.600) .900 (<LOD-1.10 (.40) 1.700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .700) 90th 1.700 (<LOD-2.600 (<LOD-1.900-1.10-1.900) .900 (.10 (.10-1.900-1.300 (<LOD-1.300-2. Survey Geometric mean (95% conf. < LOD means less than the limit of detection.700 (<LOD-.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 .800) . Survey Geometric mean (95% conf.50 (1.00 (.40) < LOD < LOD .700 (<LOD-.30) 1.800 (<LOD-.20) 1.30 (1.60) 485 538 962 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-1.90) .

Katakura M.113(2):209-217. Toxicol Appl Pharmacol 1990. Tully JS. Gaylor DW.7(4):371-377. Environ Sci Technol 2004.63:490496. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. Inoue K. Kawashima Y. Reidy JA. Cook JC. Hurtt ME. Rev Environ Contam Toxicol 2003. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002.179:99-121. Needham LL. McLaughlin JK.115(11):1596-1602. Laane RW. Jarnberg U. Androgenic deficiency in male rats treated with perfluorodecanoic acid.38(17):4489-4495. Kudo N. Kumar KS. Ingall GB. Environ Sci Technol 2004. et al.40:21282134. Kannan K. and perfluorinated contaminants in livers of polar bears from Alaska.99(2):253-261. Wong LY. Yun SH. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Taniyasu S. Yamashita N. Toxicol Appl Pharmacol 1995. Frame SR. O’Connor JC. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats. Wijeratna S. Needham LL. Mandel JH. de Voogt P. Burris JM. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States.and perfluorinated acids. et al. Liu RC. Fillmann G. Ye Y. et al. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Chem Biol Interact 2000. Mandel JH. Needham LL. Dinglasan MJ. Grasty RC. Sasaki S. Keller JM. Aguilar-Villalobos M. Calafat AM. Grey BE. Harada K. Occup Environ Med 2003.Perfluorochemicals References Alexander BH. Environ Health Perspect 2007. Watanabe T. Calafat AM. Environ Health Perspect. The influence of time. Apelberg BJ. Butenhoff JL. Tully JS. The toxicology of perfluorooctanoate. Chlorinated.39(23):9057-9063. Polyfluoroalkyl chemicals in the U. Kuklenyik Z. Birth Defects Res B Dev Reprod Toxicol 2003. brominated. Murray SM. Mabury SA. Guruge KS. Reidy JA. Holmstrom KE.46(2):141-147. Environ Sci Technol 2005. Characterization of risk for general population exposure to perfluorooctanoate. Needham LL. Harada K. Yoshinaga T. Reidy JA. Bookstaff RC. et al. Calafat AM. Biegel LB. Kuklenyik Z. O’Connor JC. Arendt MD. Crit Rev Toxicol 2004. Caudill SP. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Seacat AM.68(6):465-471. Butenhoff JL. Reidy JA. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Fluorotelomer alcohol biodegradation yields poly. Moore JA. Calafat AM. in vivo. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat.104(2):322-333. Rodricks J.115(11):1670-1676. Saito N. Perfluorinated chemicals in selected residents of the American continent. Corsolini S. Tarone RE. Bandai N. Environmental and toxicity effects of perfluoroalkylated substances. Yamashita N. Lau CS. et al. Environ Sci Technol 2007a. Halden RU. Olsen GW. Day RD. Toxicol Sci 2001. Herbstman JB. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Calafat AM. Hurtt ME. Environ Sci Technol 2005. Kuklenyik Z. Hekster FM. Bignert A. Taniyasu S.38(10):2857-2864. Peterson RE. Fei C. Seneviratne HR. Koizumi A. Frame SR. Environ Health Perspect 2007.60(1):44-55.39(1):80-84.60(10):722729. Chemosphere 2006b. Evans TJ.39(23):9101-9108. Kennedy GL Jr.1968--2003.Koizumi A. Hurtt ME.124(2):119-132. Rogers JM. Olsen GW. Mohotti KM. Olsen J.39(3):363-380. et al. J Occup Health 2004. 256 Fourth National Report on Human Exposure to Environmental Chemicals .134(1):18-25. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Environ Res 2005. Environ Sci Technol 2005. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Kannan K. Morikawa A. Cook JC. Kamiyama S. Cook JC. Falandysz J. Saito N. Mandel JS. Witter FR. Moore RW. Environ Sci Technol 2006a.34(4):351-384. Caudill SP.41:2237-2242. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Perkins RG. Kannan K. Toxicol Appl Pharmacol 1992. Kuklenyik Z. Olsen GW. 2007b. and ex vivo studies. Yoshinaga T. et al. Suzuki E. Biegel LB.S. Regul Toxicol Pharmacol 2004. Inoue K. Loganathan BG.S. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Edwards EA. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats. J Environ Monit 2005.115(11):1677-1682.

van Belle G. Burris JM. Butenhoff JL.111(16):1892-1901. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Nesbit DJ. Cao XL et al.epa. Half-life of serum elimination of perfluoroo ctanesulfonate. I: maternal and prenatal evaluations. Richards JH. Korzeniowski SH.) Tittlemier SA. Burlew MM.. fate and transport of perfluorocarboxylates. Seacat AM. J Children’s Health 2004b. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Lundberg JK. Butenhoff JL. Yamashita N. Environ Health Perspect 2005. Sterchele PF. Hansen KJ. Mandel JH. Yamashita N.68(1):249-264.41(9):799-806. Miller JP. Burris JM. Horii Y. Lundberg JK. Horii Y. Lau C. Lau C. Toxicol Sci 2003. Toxicol Appl Pharmacol 2004.40(1):32-44. 2003a. Grey BE. Olsen GW. Church TR. Olsen GW. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water.45(3):260-270. Reagen WK. Hansen KJ. Seacat AM. Hanson RG. Ellefson ME. Kannan K. Environ Health Perspect. fish. Olsen GW. Butenhoff JL.54(11):1599-1611. Moisey J. Seymour C. birds. Burris JM.1177(2):183-190. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Hansen KJ. et al.113(5):539-545. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. Taniyasu S. Mandel JH. Grey BE. Rogers JM. Biochim Biophys Acta 1993.perfluorohexanesulfonate.55:3203-3210. Environmental Protection Agency (U. et al. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Environ Sci Technol 2003. J Occup Environ Med 2003b. Cousins IT. A global survey of perfluorinated acids in oceans. The developmental toxicity of perfluoroalkyl acids and their derivatives. Huang HY.51(8-12):658-668. Bronson R. et al. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Olsen GW. et al. Petrick G. Toxicol Sci 2003. Coordinate induction of acyl-CoA binding protein. and food items prepared in their packaging. htm. Burris JM. Pepper K. Thibodeaux JR. (Erratum in: Environ Health Perspect.111(16):1900) Olsen GW. Kawashima Y. Environ Health Perspect 2003a. Washington.74(2):382-392. U. Hansen KJ.S. Ehresman DJ. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. Available from URL: http://www. Larson EB.68:105–111.Perfluorochemicals Kudo N. Mair DC. Butenhoff JL. Prevedouros K. Mandel JH. Burris JM. Case MT.37(12):2634-2639. et al. and perfluorooctanoate in retired fluorochemical production workers. Sources. Froehlich JW. perfluorooctanoate andother fluorochemicals in human blood. 2007a. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Rogers JM.198(2):231-241. J Occup Environ Med 1999. Environ Sci Technol 2006.74(2):369-381.gov/opptintr/pfoa/pfoara. Olsen GW. 2003. and humans from Japan. Barbee BD. Church TR. Hanari N. Thibodeaux JR. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Helzlsouer KJ.S. Historical comparison of perfluorooctanesulfonate. fast foods. Kannan K. Chemosphere 2004a.115(9):1298-1305. Butenhoff JL. Olsen GW. Church TR. Olsen GW. Thomford PJ. Gamo T. 1/15/06 Vanden Heuvel JP. Olsen GW. II: postnatal evaluation. J Ag Food Chem 2007. Chemosphere 2007b. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat. Peterson RE. Ehresman DJ. Hansen KJ.2(1):53-76. Zobel LR. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Mar Pollut Bull 2005. Taniyasu S. et al. fish. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Mandel JH. Buck RC.26(1):47-51. Hanson RG. Butenhoff JL. Rogers JM. Toxicol Sci 2002. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Stanton ME. EPA).82(1):359. (Erratum in: Toxicol Sci 2004. Biol Pharm Bull 2003.

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

Corbett JT. Slakman AR.gov/ reports/index. NTP-CERHR. Silva MJ. Scotter MJ. 2007. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . Calafat AM. 2000a. reducing estrogen production. 2002. 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. Toxicological profile for di-n-butyl phthalate update [online].cdc. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al.. 2003. and Sertoli cell abnormalities in the male animals and.html. Population estimates of concentrations of specific phthalate metabolites may differ by age. The Handbook of Environmental Chemistry. 2000b. 2004). Jordan S. 4/20/09 Albro PW..atsdr. Pharmacokinetics. Environ Health Perspect 1997. 2004. and race/ethnicity (Silva et al. 2004.gov/ toxprofiles/tp9. Schroeder JL. 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. In animals. 1985. 2000c. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.21:13-34. McDonnell DP. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. 2004.html. Sauer MJ. but there are known species-related differences in the hydrolysis of diester phthalates. Herbert AR... Part Q: Phthalate Esters. efficiency of intestinal absorption. van der Broek PH. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. Matthews HB. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. The monoester metabolites are thought to mediate toxic effects for some of the phthalates.atsdr. A biomarker approach to measuring human dietary exposure to certain phthalate diesters.niehs. 2007). Needham LL.gov/toxpro2. Food Addit Contam 2001. Information about external exposure (i. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. In Staples CA (ed). Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. ovarian abnormalities in the female animals (Jarfelt et al. Vol. interactions with macromolecules and species differences in metabolism of DEHP. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al. Drug Metab Rev 1989. Hoppin et al. Hauser et al. 2001..cdc. Massey RC.805:49-56.e.cdc... 1982).. which may be a pathway to the development of liver toxicity and cancers in these animals. Connor C. 2006). 1982. phthalates have been shown to induce peroxisomal proliferation in rodents. 2004.3.18(12):10681074. Silvapathasundaram S. 1986). McKee et al. gender.html. 227-262.New York. Metabolism of di(2-ethylhexyl) phthalate. Available at URL: http://www. However.. 105:734-742. 2003.. phthalates produced anti-androgenic effects by reducing testosterone production and. Evaluation of a recombinant yeast cell estrogen screening assay. Cousins IT. 2001. Albro PW and Lavenhar SR. Kessler et al.html). References Agency for Toxic Substances and Disease Registry (ATSDR). 2002). Available at URL: http://www..gov/toxprofiles/ tp135. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. Lovekamp-Swan and Davis. pp.. testicular atrophy. Dave M. 2005. Dirven HA. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). Also. Hauser et al... Springer. These differences may contribute to species-specific differences in toxicity (ATSDR. Jongeneelen FJ..45:19-25. 2006). Anderson WA. 2005). Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. 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. Clark K. J Chromatogr B 2004.Phthalates and metabolites have been tested. Toxicological profile for di(2-ethylhexyl)phthalate update [online]. Peck and Albro. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. Environ Health Perspect 1982. Springall C.nih. Assessment of critical exposure pathways. variation also occurs in the same person during repetitive monitoring (Fromme et al. Coldham NG. at very high levels. High doses of di2-ethylhexyl phthalate (DEHP). Rhodes et al. and extent of metabolite conjugation to glucuronide (Albro et al. atsdr. Mackay D.. 2002). at higher doses. Castle L. 2001). dibutyl phthalate (DBP).

National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Int J Hyg Environ Health 2007. Reynolds T. Tsukino H. Davis BJ. Environ Health Perspect 2004.html. Main KM. J Androl 2004. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Silva MJ. David RM. Park S. Filser J.26(8):1219-24. Meeker JD. Research Triangle Park (NC).niehs.16(4):487-493.nih.110(5):515-518. Environ Health Perspect 2002. gov/chemicals/dehp/dehp-eval.106(1):23-26. et al. 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 . 6/2/09 Okubo T.html. 2006 [online]. Hartle RW. Calafat AM. NTP-CERHR. Am Ind Hyg Assoc J 1985. Research Triangle Park (NC). Biol Pharm Bull 2003. Brock JW. Milligan SR. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).111(2):139-145. et al. Davis BJ. 2000b [online].Phthalates in human urine samples. Henttu P. Leffers H. Environ Health Perspect 1998. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Parker MG. Silva MJ. Hoppin JA. Yoshimura M.19(4):505-515. Meeker JD. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004.nih. Research Triangle Park (NC). Csanády G. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate. White R.112(17):1734-1740. Liss GM. Singh NP.html. 2000a [online].18(1):122.195:142-153. Available at URL: http://cerhr. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay. Mechanisms of phthalate ester toxicity in the female reproductive system. Silva MJ. Hanaoka T.niehs. Giwercman A. Jonsson BAG. 6/2/09 NTP-CERHR. and infant formula by tandem mass spectrometry (LC-MS-MS).382:10841092. Sumpter JP. Borch J. Butala JH. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Grote K.html. consumer milk. Environ Health Perspect 2003. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Baird DD. Duty S. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Available at URL: http://cerhr. Park MG. Environ Health Perspect 1995. Rylander L. Koch HM. Research Triangle Park (NC). Hum Reprod 2007. Angerer J. 6/2/09 NTP-CERHR. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Hagmar L. Brock JW. Andersson A-M. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Reprod Toxicol 2004.gov/chemicals/dehp/dehp-eval. Suzuki T.11(5):381-387. 6/2/09 NTP-CERHR. Determination of phthalate monoesters in human milk.103:582-587. Epidemiol 2005.niehs. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). Reproducibility of urinary phthalate metabolites in first morning urine samples. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate.nih. Albro PW.niehs. Skerfving S. Richthoff J. Lovekamp-Swan T. Available at URL: http://cerhr.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. McKee RH. Environ Health Perspect 1997. Occurrence and daily variation of phthalate metabolites in the urine of an adult population.210:21-33. et al. Yokoyama Y. Mortensen GK.112(17):1740]. Chen Z. Kessler W. Toxicol Appl Pharmacol 2004. Nielsen J. Harris CA.22(3):688-695.25(2):293-302. Kano I. Zhang S. Boehmer S. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Jacobsen H. Reprod Toxicol 2005. Kalita JC. Bolte G. Chahoud I.64(8):555-560. Gans G. Balasubramanian AV. Scand J Work Environ Health 1985. Wang P. Ryan L. Jobling S. Hass U.46(11):643-647. The estrogenic activity of phthalate esters in vitro. Stringer WT. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Calafat AM. 2000c [online]. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Skakkebaek NE. Duty SM.105:802-811. Dalgaard M. Numtip W. Hauser R.gov/chemicals/ phthalates/dbp/dbp-eval. Drexler H. et al. 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Clemons JH.112(3):331-338. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Zacharewski TR. Orton TC.58:339349. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man.114(11):1643-1648. Bratt H. Crit Rev Toxicol 2006. Fourth National Report on Human Exposure to Environmental Chemicals 261 . Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Rusyn I.45:11-17.S. et al. et al. Matthews JB. Rhodes C. Environ Health Perspect 1986. Cunningham ML. Jackson SJ.Phthalates phthalate (DEHP): a cross-sectional study in China. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. Klinefelter GR. Batten PL. Pratt IA. 112(5):A270]. Environ Health Perspect 2006. Abbott BD. Fielden MR. Hodge CC. Wu ZF. Silva MJ.65:299-308. Caudill SP. Toxicol Sci 2000. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Environ Health Perspect 1982. Lambright CR. Albro PW. Toxicol Sci 1998. Ostby JS. Peck CC. Parks LG. Peters JM. et al.36:459-479. Urinary levels of seven phthalate metabolites in the U. Barlow NJ.46:282-293. Malek NA. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Environ Health Perspect 2004. Reidy JA. Barr DB. Meek MD.

.7-14.6) 13.6) 37.2) 32.0 (12.5-40.8-98. vinyl tile.0-26.1) 13.3-82.1 (14. it can be released into the ambient air during use or disposal of the products.7 (51.5 (76.3) 63.1 (14.2) 17.7 (80.7) 40.1) 14.3-21.3.9 (21.8-133) 89. particularly male animals (McKee et al.8-16.2) 33.9) 18.6 (66.3) 13.S.9) 49.5-36.7) 23.2 (43.6-79.4) 108 (96.7-16.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16. 2004.0 (23.2-17.4 (53.2) 66.6-39.9) 11.5) 65.2) 14.0 (11.6) 29.7-58. residents (Blount et al.8-16.3-18.4) 35.6-38.9-27.2-183) 101 (78.9 (70.6-116) 122 (102-142) 101 (85.1) 76.1-120) 52.9) 14.3 (13.1) 32.6-132) 103 (84.8 (50.9-30.2) 12.2-16.9-14.6) 50.1-35.9-87. NTPCERHR.4-15.0) 32.6 (13.2 (47.9) 12.1-43.4) 129 (98.3 (12.9) 14.2 (11.7 (53.4) 33.5 (67.0) 23.5-36. 2001-2002.0-106) 58.4 (59.5-94.4 (13.9 (28.0-55.3 (22.6) 16.8.6-43.0-85.8) 24.0-130) 101 (86.8) 14.2-155) 91. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.3-18. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.3) 15.9) 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 (20.0 (55.2) 69.4) 98.3-130) 122 (88.3 (30.1) Selected percentiles ( 95% confidence interval) 50th 17.2-19.8-14.9) 13.8 (28.8-72.8-13.8 (71.2) 14.8 (38. 01-02.3-34.7 (13.4) 65.8 (10.6-29.0 (30.5 (66.3 (12. interval) 15.9 (22.2-20.9 (16.5-35.1 (58.4 (31.3-91.3 (54.4-92.6-92.0) 34.6) 35.7 (11.2-116) 122 (102-143) 101 (84.3-161) 99.2 (14.1) 68.0) 20.8 (21.7 (12.3) 94.5) 30.5) 27.9-28.0 (14.6) 25.6) 35. 262 Fourth National Report on Human Exposure to Environmental Chemicals . because it is not bound to products in which it is incorporated.8 (53.5-41.1-90.3 (29.0) 70.7 (15. sealants.6) 67.8-14.4) 80.3-75.9-47. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.4) 71.4-25.2) 13.9 (11.8-76.1) 67.5 (61.0) 24. and diet is the major source for general population exposure. 2000). respectively.1-214) 166 (116-191) 145 (110-213) 88.5-14.2-39.8-121) 79.4 (68.4 (10.6 (21. 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.4) 14. see Data Analysis section) for Survey years 99-00.4-24.5) 82.2-16.9 (12.1 (55.5 (26.6-92.8) 33.1) 29.0 (15.0) 90th 67.2) 15.1-15.7-25.6 (12.3-88.6) 13.3) 13.7-119) 99.4) 12.1) 31.5-25.4 (27.1-38.9-49.9 (13.1-16. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.7-82. and 0.4-16.9-16.8-64.5 (47.3 (29. and to a lesser extent.9) 15.3-74.4-127) 80.3 (12.5 (55.2-38.2-115) 113 (91.8) 28.5-84.4-62.2 (25.6) 63.6-18.7-16. High dose BzBP and its monoester metabolites.6) 14.5-62.3 (33.0 (30.4) 51. can produce developmental and reproductive toxicity in rodents.3 (44.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93.5) 15..5-145) 138 (106-241) 143 (127-179) 120 (99.6 (13.2-31.8 (86. 0.9-190) 86.6-150) 94.4) 81.8-35.2 (10.0 (33.1-61.7) 38.6 (53.8 (12.1 (20.5 (13.0 (43.8 (80. car care products.2-33.5 (27.4 (32.7 (82. BzBP can be released into the environment during its production and.8-48.3) 54.5-18.1-15.7-13. and 03-04 are 0.1 (19.4 (63.4) 35.2 (19.8 (14.4 (53.6 (13.4 (48.2-40.6) 24.3-12.1.0 (26.8 (71.6) 95th 103 (94.7-15.2 (19.3-43.8-17.0) 33.6 (13.5) 55. 2000).9-62.7-172) 103 (74.1-116) 122 (93. Food crops take up BzBP.2) 22.8 (30.5 (57.4) 49.1 (13.3) 23.8-41.4 (29.5) 23. some personal care products.4 (32.5-33.4-120) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 13.1-18.1 (10.0) 16.6 (32.5-97.5) 15.1 (32.1) 12.0 (27.7-35.6 (41.1-16.6-72.3-27.9 (39.6) 14.9 (12.Phthalates Benzylbutyl Phthalate CAS No.6-17.3) 37. population from the National Health and Nutrition Examination Survey.7-17.7-16.8-18.1 (13.S. IARC considers BzBP not classifiable with respect to human carcinogenicity.8) 63.4) 38.5) 16.6) 15.7-170) 169 (134-198) 152 (99.1-39.4) 75th 35.3-125) Total 15.0 (15.8-17.7 (70.0 (34. including MBzP.2) 78.4 (10.9) 43. and 2003-2004 were generally similar those reported in U.

9 (55.8) 33.0 (41.7-19.9 (12.1 (23.0 (10.1) 39.9-104) 62.0 (49.6 (30.S.8 (69.2-78.0-15.8 (10.69-11.8 (64.5) 10.8-85..4 (46.4-19.7-12.5-42.1-12.5-79. and females compared to males (Silva et al.5-26.7-20..9 (43.6) 13. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.3 (39.3-64.8) 108 (75.7) 25.4 (60. 2003)..6 (24.6 (30.0 (11. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.0 (38.8-16.95-14..3 (24.8-14.3) 13.6) 53.9-13.7-90.5-31. Hauser et al.7 (11.3 (12.4) 21.1 (34.5 (48.6-47.1-12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.8-42.3) 18.8) 80.Phthalates York City (Adibi et al.6 (11.1) 27. Urinary Mono-benzyl phthalate (MBzP) (creatinine corrected) Metabolite of Benzylbutyl phthalate (BzBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.5) 46.1 (9.9 (24.4-23.6-26.1-27. Hoppin et al.8) 46.4 (13.7 (13.7-15.4-102) 70.3-11.1 (13.9) 12.9 (24.0) 60.0-90.5-23.7-397) 70.9 (29.4-42.6 (11.5 (35. population from the National Health and Nutrition Examination Survey.8-27.9 (10.7) 11.1 (14.2-26.5 (42.4-18.4) 15.7 (19.6 (19.8-14.6-116) 74.8-34.5-13.0) 49.4 (21.6-86.4) 60.8-13. in men attending a Boston infertility clinic (Duty et al.3) 36.4-99.3-38. 2002.2-12.9) 64.3) 29.1-35.4 (26.8 (13.4) 50.9) 12.4-79. In NHANES 1999-2000.7-14. 2003).2-57.1-120) 77.1-58.0) Selected percentiles ( 95% confidence interval) 50th 13.0-51.7-61.5 (56.5) 41.8 (49. 2005).5-16.. 2004.1) 35.1 (25.2 (27.4-90.8) 11.3-16.1) 17.2) 11.3) 55.8-13.5-99.1 (21.3-34.0) 24.4-142) 134 (116-176) 136 (85. 2006).2) 26.9) 100 (80.8-69.3 (35.3 (23..9) 11.7 (55.2-13.2) 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) 11. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.5-38.4 (11.8-60. and in a small sample of German residents (Koch et al.9) 42.5-76.9-13.9) 24.5 (12.1-125) 86. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.4-14.0-48. 2007).4) 17.8) 33. 2004).2-15.3) 13. 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) 12.4-17.3) 67.8-13.8) 54.5 (11.8-64.6 (15.7 (21.0-109) 65.4-60.7 (23.0) 24.2) 15.3) 89.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .5-213) 49.2 (69.8-39.9-69.4 (10.3) 14.1-14.4 (12.3 (38.3) 73.1-29.9-28.0) 13.4 (11.7) 46.7 (38.6) 12.8-15.4) 51.3 (13.4) 90th 50.5 (49. 2005.9 (39.9 (10.1 (15.4 (69.9-115) 57.3 (15.1 (46.6 (57.9 (12.1) 142 (99. A small study of African-American women in Washington.2) 12.5-26.8-80.2-51.1 (13.1 (53.3) 12.6 (51.8) 53.6) 25.3) 90.1-79.3) 13.8) 56.7-31.2 (40.8) 24.9) 11.0-27.5) 78. In an annual sample of German university students.4 (11.4-14.9 (51.1) 12.5-58.7-56.4 (25.6 (14.4 (63.2-21.7) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 40.8 (11.2) 67.2 (56.9 (15.5) 16.5) 13.4 (34.9-83..9-16.5 (10.7 (13.0 (41.0-26.2-15.7 (59.1) 24.5 (9.1) 23.6 (34.8 (30.7) 38.0 (12.5-58.73-12.8) 53.8 (57.1) 24.7 (11.7-14.8) 34.7-19.4) 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 12.1 (21.3) 16.6) 75th 25.1 (21.2 (41.6-81.1 (43..1 (11.7-123) 77.9-14.6 (11.8 (46.2) 32.6 (36.4) 13.9 (22.6) 58.5 (10.9) 52.2-49.5) 23.0 (12.6) 30.8 (12.0 (67.3 (60.5-29.6) 38.4) 28.8) 16.0) 12.3) 21.8) 15.4) 13. interval) 14.4-93.5) 20.7) 19.9 (9.7-29.8) 13.8) 68.6-20.6-99. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.1 (41..7-69.0 (33. 2007).5) 17.1 (19.7 (54.0 (13.2-13.7) 56.6-15. adolescents compared with adults.7-20.6) 12..5) 95th 77.3) 14. Limited studies in children younger than 2 years old have found median and geometric mean urine MBzP that were similar to children aged 6-11 years in the NHANES subsamples (Brock et al.5-61.8-48.6-40.4) 104 (89.0) 15.7 (11.9-40.3-73.4 (33.6 (22.4) 44.3) 37.0-53.8-173) 195 (121-305) 229 (99.7 (12.9 (54.8-15.4-15.5-57.9-62.1 (18.7 (18.8) 26.9) 12.8 (50. in young Swedish men (Jonsson et al.9 (15.6) 73.2) 11.2) 11.1 (21. Weuve et al. 2002).1) 80.0 (62.5) 14.7-15.4) 25.2-117) 95.9) Total 14.4-27.6-12.8) 71.2-17.4-116) 73.6-13.7 (14.4) 14.9-23.4 (74.

et al. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. et al. Reidy JA. Rylander L. Reproducibility of urinary phthalate metabolites in first morning urine samples. Barr D. Chen Z. Hodge CC. Epidemiol 2005. Jonsson BAG. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Koch HM. Caudill SP.111(14):1719-1722.68:309-314. Eckard R.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. 2005. Jedrychowski W. Research Triangle Park (NC). Environ Health Perspect 2003. Giwercman A. Environ Health Perspect 2004.html. David RM. Ryan L.108(10):979-982. et al. Wittassek M.Phthalates References Adibi JJ. Calafat AM. Singh NP. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters.93:177-185. Helm D. Silva MJ. 4/20/09 Silva MJ. Green RA. Int J Hyg Environ Health 2007. Hum Reprod 2007. Schettler T. Centers for Disease Control and Prevention (CDC). Koch HM. J Androl 2004.22(3):688-695. Camann DE. Wiesmuller GA. Poland.16(4):487-493.18(1):122. Environ Health Perspect 2002. Barr DB. Sanchez GN. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Phthalate monoesters levels in the urine of young children. Caudill SP. Butala JH. Ryan L. Environ Health Perspect 2000. Angerer J. McKee RH. Perera FP. et al. Sampson EJ.112(3):331-338. Needham LL. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Brock JW. Hoppin JA. Caudill SP. Duty S. Available at URL: http://cerhr.210(3-4):319-333. NTP-CERHR. Davis BJ. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Blount BC.niehs. Third National Report on Human Exposure to Environmental Chemicals. 264 Fourth National Report on Human Exposure to Environmental Chemicals . Gans G. Levels of seven urinary phthalate metabolites in a human reference population. Rossbach B. Silva MJ. Prenatal exposures to phthalates among women in New York City and Krakow. Hagmar L. Drexler H.25(2):293-302. Reprod Toxicol 2004. Weuve J. Needham LL. et al.110(5):515-518.nih. Hauser R. Bull Environ Contam Toxicol 2002. Environ Res 2003. Brock JW. 2000 [online]. et al. Dobler L.S. Richthoff J. Atlanta (GA). 112(5):A270]. Urinary levels of seven phthalate metabolites in the U. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Silva MJ. et al. Hilborn ED. Malek NA. Jacek R. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Duty SM. Hu H. Calafat AM.114(9):1424-1431. Silva MJ. Pirkle JL. Baird DD. Environ Health Perspect 2006. Brock JW. Meeker JD.

00-11.90 (3.80) 75th 5. residents (Blount et al. and insecticides.59) 3.0) 13.46-5. Following oral administration of DBP to humans.5 (20.84) 4. 2005)..3 (16.4 (20. In addition.90-2.80-5. Survey Geometric mean (95% conf.70-4.40-17.6 (14.30) 10. 2004.17) 4.40 (2. and in a small sample of Japanese adults (Itoh et al. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.30) 5.0-38.30) 6. 2005)..4) 5.6) 17. mostly as MnBP (Anderson et al.S.5 (17.50) 8. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.7) 15.20-12.0) 24. Studies of children found age-related differences in urine MBP levels.70) 3.40-3.90 (4. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.8 (9.4) 22.5) 23.56 (5.90-7.6 (10.5-16.20-12.20) 7.28-5.80 (3.7-31.40 (6.7 (17.97-7.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.6 (13. about 65% to 80% of a dose is eliminated in urine within 24 hours.6-34.30 (1.1-25.30) 10.50-10.0) 9.20-2.30-11.5-24.6) 10. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.40 (2. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.66) 2.2 (12.0 (13.5) 19.9 (16.91) 4.0 and 0.50-2.8) 40.70-4.1) 25.5) 25.10) 3.44-2.10) 9.70 (2.00) 10.6) 16.3-43.97) 2.30-7.10-9.90-4.07 (3.50-6.3 (16..3.7) 14..40-3.81 (3.80 (5.5) 12.72-3.2-22. they have been referred to as monobutyl phthalate (MBP).20) 4. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.40 (7.3 (19.40-4.6) 26.1-20.7-31.7) 7.5) 22.3-19.40-9.3 (13.50) 5. 2001).9-23.2 (8.6) 12.40) 5.9) 10.00-6.48 (2..0-25.00 (7.56-4.60 (4.6) 16.90 (4.6 (14.30-2.6 (9. in men attending a Boston infertility clinic (Duty et al.50 (6.30-3.46 (3.0) size 2782 2605 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th 2. Koch et al.20 (6.00-4. 2005.50) 2.22 (3.7-20.00-9.55) 2. Fourth National Report on Human Exposure to Environmental Chemicals 265 . DBP can produce reproductive toxicity in male rodents (McKee et al.00) 6.6-26.1-12.10) 2.60 (8.2-33.Phthalates Di-n-butyl Phthalate CAS No.2-14.30) 2. population from the National Health and Nutrition Examination Survey. 84-74-2 Di-isobutyl Phthalate CAS No.02) 4.60 (5..10-9.3) 3.3) 33.S.30-6.49-2.30 (3.96) 3.5 (11. 2005).0) 12.4-12. When total DBP metabolites have been measured. OSHA has established a workplace air standard for external exposure to DBP.00 (5.2 (11. NTP-CERHR.80 (5.3-24.00-6. interval) 2.22) 3.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.40 (3.70) 5.30-6.90) 12.0 (11.10) 8.20-6.30 (4.00) 7.6 (10.50) 7.20 (3. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity.94) Selected percentiles ( 95% confidence interval) Sample 95th 17.55 (3.67 (5.7 (17.3-30. 2004.6-14. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates.3 (13.10 (3.7) 4.50-4.10 (4.70 (5.80-5.7 (16.0-14.56 (3.1 (13.2) 5.0) 20.5 (10.. 2003). 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. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.19-3.5) 18.97) 4.7 (7.7) 18.5) 14.3) 18.40-12. 2003). 2007).17 (2.60) 3.82-3.9-14.11-3.40-4.68 (2.1 (8.80 (2.0 (19.7-18.7 (18.73 (2. Hauser et al.46 (2.7 (9.8) 21.40-5.26 (2.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.10) 11.4) 12.90-4.6 (29.3-48.6) 17.5) 18.50 (3. 2000).30-13. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.9) 15.5-16.6-18.6-20.50) 18.60-6.20 (7.24-8.6 (13.10 (4.9 (16.00) 4.71 (2.20-9.5 (27. pharmaceutical coatings. 2000.8) 677 652 703 699 1216 1088 Limit of detection (LOD.80 (2.1-17.4-27.0 (13. and also in some printing inks. Biomonitoring Information Median concentrations reported in the NHANES 19992000.90 (6.0-18.5-29.3-18.56) 3.3 (18..46) 2. CDC.33 (2.00) 4. in a small sample of pregnant women in New York City (Adibi et al.60 (2.73-5.63) 3..50) 90th 12.3-20. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.85-6.4 (14.1) 16.10-2.37) 6.43) 6.3 (11.70-8.6 (11.1) 22.

08) 75th 4.69-7.74 (4. Survey Geometric mean (95% conf.39) 5.43) 3.3) 16.8) 10.52 (2.17 (2.72-7.7 (9.03 (5.46 (2.1-24.78) 8.13 (2.58-3.82 (4. up to four and 13 fold.0 (10.68) 3.89 (3.6 (12.00-7.81 (3.04) 7.09-2.22 (2.28 (4.18 (4.0-18.68) 5.83 (2.33-9.64-10. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.1) 13.84 (8.44 (3.6 (9.21) 10.51) 2.6-19.46-11.94-12.53-3.91-6.69 (2.18-4.79-8.33 (3.8 (9.66) 10.76 (3.19 (2.4-16.93-6.81 (6.3) 13.4) 15.20-2.1-25.2 (10.32 (7.52-20.4 (12.7) 11.9) 12.53-4.and gender.92 (7.0 (8. population from the National Health and Nutrition Examination Survey.5 (9. 2007).0) 15.5 (11.11) 5.95-3.8 (8.29-8.28-13.80 (3.65 (4.31) 2.79-6.00-3. samples from German university students had consistently higher median urine levels of MnBP and MiBP.57-4.04) 3.. 2005). An analysis of NHANES 2001-2002 showed similar age.2 (11.14 (4.2) 24.79 (4.38-10.67-5.89-5.42) 2.95) 10.88 (2.41 (2.52) 3.7) 10.69) 6.58-4.54) 2.3 (17. 2002.3) 28.0 (12. 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) 3..S. 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.2-15.80-3.20 (7. to about two to fourfold higher (Fromme et al.13-6.73) Selected percentiles ( 95% confidence interval) Sample 95th 12. 2006).6) 13.80) 7.78-8.89) 6. respectively.18-10.56) 5.31 (7.62-12. the students’ median values for MiBP levels remained relatively unchanged.99) 7.1-12.07 (2.57 (3.05) 2.52-3.47-5..Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.9 (15.31) 2.56-15.03-7.66) 4.11-2.35) 3.66 (8.7 (21.20 (2.11 (5.7) 3.5) 15.3 (13.47-12.64-7.7 (13.74-3.76-3.86-4. 2004).54 (2.36-2.2) 9.00 (3.36-7. Differences in urinary MBP population estimates by gender have also been shown (Silva et al..57 (3.76-15.6) 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 2.07-5.33) 3.32 (3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.64-7.9-16.84 (4.85 (2.02 (7.5) 13.25) 5.6 (15.34 (3.1 (10.56-4.32) 7.20-3.37) 3.97-2.6 (8.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.7 (11.30) 2.46) 3.24) 3.30 (6.45) 3..17-12.1 (11.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.73 (5.20-4.51) 15.43) 3.75 (6. than adults in NHANES subsamples during the same time period.3) 13.82) 4.65-4.33 (2.18 (1.1-15.99-4.0) 11.20 (2.2-13..53-5. 2004).6 (10.75 (4.1) 4.9-40.59 (4.86) 6.0) 7.55-6.9-26.26 (2. Between 1998 and 2003.81) 4.3) 18.8-36.94) 6.4) 23. In an analysis of NHANES 1999-2000.04-5. interval) 2.62 (6.98 (2.1) 11.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.65-11.8 (10.56) 2.15-4.7) 19.6) 11.5-19.29-3.2) 8.31 (2.10-5.18) 3.21 (5.8-18.1) 15. while MnBP declined (Wittassek et al.9 (11.72) 5. Over this time.43) 3.27-12.61-3.03-11.08-2.18) 4.69) 4. 2005). Urinary Mono-isobutyl phthalate (MiBP) (creatinine corrected) Metabolite of Di-isobutyl phthalate (DBP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.17) 90th 8. ranging from more than one-tenth the NHANES median (Itoh et al.39-3. 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.01-2.6-19.95) 2.9 (9.6 (8.1) 7.4) 7.68 (2.38 (6.1) 10.66) 2.7-28.54 (4.47 (3.76-3.8-13.8-18..1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .26-2.81) 9.02-10.78) 9. 2007).96 (3.94 (5.00-3.15) 3.51) 5. Weuve et al.

6-29.2 (74.1 (18.6 (22.4-42.9 (17.2-56.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.1) 19.1) 25.4-44.9-79.1 (58.5) 37.2) 90th 98.1) 31.2-33. Survey Geometric mean (95% conf.9 (79.6-20.9.3 (56.7-92.7-124) 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.6) 80.3-24.1) 20.6-69.1) 17.4 (35.8-29.0 (15.1 (36.3-21.6) 46.2) 42.6-44.5 (74.0) 20.1 (16.6) 38.1) 30.1) 36.8 (19.9 (79.1 (17.1 (34.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.2) 68.6 (44.5) 31.0) 30.5) 95.5) 19.1 (19.7) 28.3) 23.6) 17.6-29.9) 46.4 (19.9-87.2) 20.5) 17.8) 23.4 (35.5 (59.3) 19.2-159) 92.2-23.0 (78.4 (35.5-27.7) 92.1-82.6-33.0) 27.4 (23.4 (25.6-36.1.8) 19.5) 24.7 (22. and 03-04 are 0.3) 26.7 (64.1) 23.6-49.5) 26.2-87.3 (36. respectively.0-73.1) 46.6-37.5) 65.4) 22.6 (55.3) 21.6 (90.5-47.6-31.5) 36.7-116) 95.5 (30.4) 20.0 (72.3 (23.2 (59.1 (31.2-24.1-22.0 (25.3 (30.8-132) 95.3 (17.3-67.2 (19.9 (20.5-117) 95.9) 29.6-48.4 (84.2-21.5-47.2) 32.2 (25.1 (19.7-53.9) 36.1) 47.7-42.5-53.8-22.7-117) 118 (108-143) 93.9-114) 116 (97.8) 75th 51.0 (36.4) 59. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.7-34.2-93.0) 31. referred to as monobutyl phthalate (MBP).5) 21.1-20.8) 48.6) 20.4 (38.7) 124 (98.5) 20.9-42.7 (18.1-29.1) 23.5) 36.9-22.4-60.7 (19.2 (21.2-32.2 (17.2 (78.0) 117 (104-131) 112 (84.0) 21.5) 40.6 (48.0-19.7 (51.6 (26.0) 84.3) 24.0) 38.5 (29.0 (20.2-22.0 (18. *In the 1999-2000 survey period.6 (16.8 (57. 01-02.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.5-44.7-121) 97.4-18.7-42.4) 52.2 (58.3) 18.9-33.1-24.3-60.5) 34.4.7 (16.0 (45.7 (38.1 (54.3 (37.0 (30.6 (61.3 (42.3-79.3-76.4) 64.6 (65.1) 23.6) 39. interval) 24.0-24.7-24.8-123) 101 (90.1 (41.1 (62.2 (21.2-114) 73.6) 35.4-159) 107 (84.7-26.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.9-53.4 (35.4 (71.7 (18.5) 78.8-119) 90.3-136) 137 (107-162) 119 (90.3 (60.4 (72.9) 75.8-111) 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 23.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.7-34.3 (30.2-63.3 (51. Fourth National Report on Human Exposure to Environmental Chemicals 267 .4-20.7 (24.7-111) 64.2) 26.1 (26.0) 120 (98.6) 71.6 (19. see Data Analysis section) for survey years 99-00.9-92.0-24.1 (21.7 (43.0-21.0-58.0 (17.8) 58.1 (28.7 (28.9) 71.1-27.7) 42.0 (23.8) 43.1 (19.2 (75.3-145) 85.7) 74.S.1-51.6-40.3 (23.0-26.7-106) 69.5 (28.9-101) 77.4 (36.6-113) 108 (90.6) 21.5-42. population from the National Health and Nutrition Examination Survey.3) 40.4-25.9-28.4-31.4-26.2 (20.3-85.8-25.9) 18.3-96.5-43.3-40.2-49.7 (33.5 (59.7-127) 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 22.1 (19.6-24.2 (18.0-19.1 (51.7-91.9) 21.0-32.8) 62.9-22.7 (70.5) 85.9 (17.5) 47. and 0.9) 26.4 (21.7) 52.5-121) 106 (94.1-92.2) 38.7-20.3) 36.6 (32.2 (79.1-80.0 (31.2) 62.1-75. 1.6-143) 127 (99.5-60.0-51.8-42.

1-99.7-28.1-128) 97.0 (15. population from the National Health and Nutrition Examination Survey.1) 17.4 (68.9) 19.4-164) 96.9 (30.9) 49.0 (61.2-85.4 (31.3) 18.2) 16.7 (60.7 (81.8) 75th 38.4 (33.6) 65.2 (19.0) 29.0) 53.7 (12.7-20.0) 81.3-81.8) 34.9 (37.0) 28.9 (21.0 (71.0-19.6) 37.2-73.6-22.9 (30.8) 19.1-99.1 (34.3 (16.9) 20.2-22.0) 26.2) 31.6) 24.1-32.1-62.6) 39.4) 51.3 (52.8 (16.9-38.1) 61.3 (17.3-106) 74.8 (18.2) 74.4 (37.3) 19.0) 25.4 (17.1-23.5 (81.9 (20.6-24.0) 108 (71.6-26.4) 15.6-32.7-19.8-24.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.3) 20.9 (73.0 (26.6) 25.9 (64.4) 19.6) 34.3 (42.5-23.5 (30.8 (17.3-49.5-41.3-71.2-106) 64.7 (28.6 (74.9-105) 85.1 (29.6) 64.8) 22.3) 17.6) 14.5 (18.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.2-28.3 (71.6-42.3-78.1-21.4-61.3 (55.7 (60.8-24.6 (17.1 (56.3) 52.8 (25.2-22.0) 19.4-131) 81.4-47.4 (53.8 (13.4-34.9-84.6-43.0 (43.7 (54.0) 59.0) 35.2) 159 (102-263) 147 (93.3) 35.5-70.1) 21.4 (47.0-60.7) 19.4 (31.9) 14.0-75.S.6) 31.7) 42.3-21.4) 20.1-18.9-68.4-76.8) 17.1) 20.0 (19.7 (16.8) 30.3) 19.4 (45.0 (70.9) 52.5 (15.0-92.1) 50.4-24.5 (18.9 (35.2-179) 84.0 (27.6-74.7 (19.9) 30.8) 34.2-108) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 *In the 1999-2000 survey period.4-103) 117 (83.3-40.9-49.9 (35.0) 55.4 (16.4 (31.3-23.5-30.8) 28.8 (50.5-37.2-22.3) 33.9-100) 86.3 (21.7-39.5-21.6) 38.7-51.6 (57.5) 17.9-14.7-26.5) 82.5 (14.4 (56.4 (16.6-128) 96.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.5) 60.4-72.5) 134 (93.2 (83.0-38.6-119) 63.3-17.8 (22.9-26.3-18.4) 53.3) 59.9 (16.6-27.1) 20.1) 44.5) 90th 68.7-19.2) 65.3 (24.3) 21.9 (56.5-142) 89.0-113) 104 (83.1) 53.2 (38.0) 70.1) 22.8) 13.8) 63.3-20.5-15.8-32.6 (19.4-65.6 (41.0 (52.9-68.8) 23.3 (48.4-135) 71.1-83.2) 21.7) 36.6-23.5) 39.3 (17.6-44.8) 40.4 (20.7-37.5-16.2-21.4 (13.9) 28.9-56.3 (28.6-53.6 (25.9 (39.0-41.7 (14.5-22.0-17.5 (64.3-32.4 (50.9) 24.9 (19.8-235) 137 (108-198) 88.9-34.4) 62.8 (18.1) 42. Survey Geometric mean (95% conf.6-92.7-21.6-16.3 (76.4) 15.3-39.5) 21.2 (35.6 (25.6) 83.8) 17.0 (16.3) 33.0 (50.5-142) 81.2-61.6 (61.9) 91.7-78.6 (29.9-36.6-50. interval) 22. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.5) 84.7-42.4) 21.4 (50.6-28.1) 37.3-21.3-114) 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 17.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.9 (30.9-70.6-155) 91.3 (69.8) 20.8) 20.3 (60.2-86.0 (18.9) 62.5) 91.2 (19.9) 39.6-19.8) 17.3) 67.0-90.2-48.6-24.7-23. 268 Fourth National Report on Human Exposure to Environmental Chemicals .0 (34.3 (46.7 (27.7 (57.4 (18.1 (46.3-26.7 (43.3-38.7-80.6) 23.2-16.0) 41.8-43.6) 24.3 (17.8) 35.6-23.8 (33.6 (27.0) 94.3 (19.1 (21.8-23.2-27.5-64.0) 75.7) 20.5-76.1) 35.8 (65.0-47.0 (69.4 (19.6 (31.5-18.0 (18.1 (15.4 (17.2-18.8 (18.6-44.6 (72.3 (52.1 (61.4) 16.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.2) 59.7 (73.0 (20.4 (23.7 (20.6) 18.9 (58.1 (32.2 (16.

Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Rossbach B. Chen Z. Blount BC. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. Itoh H. Silva MJ. Bull Environ Contam Toxicol 2002. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Fourth National Report on Human Exposure to Environmental Chemicals 269 . Urinary phthalate metabolites and biomarkers of reproductive function in young men. Sampson EJ. Ryan L. Barr D. Food Addit Contam 2001. Camann DE. Brock JW.68:309-314. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Rylander L. Masunaga S. Int J Hyg Environ Health 2005. Angerer J. Caudill SP. Centers for Disease Control and Prevention (CDC). Needham LL.114(9):1424-1431. Scotter MJ. Hu H. et al. Caudill SP. et al. 112(5):A270]. Available at URL: http://cerhr.111(14):1719-1722. Drexler H.gov/chemicals/ phthalates/dbp/dbp-eval. 4/20/09 Silva MJ. Massey RC. Meeker JD. 2000 [online]. Sanchez GN. Calafat AM. Levels of seven urinary phthalate metabolites in a human reference population. Epidemiol 2005. Helm D. Malek NA.18(12):10681074. McKee RH.210:21-33. Hum Reprod 2007. Third National Report on Human Exposure to Environmental Chemicals. Occurrence and daily variation of phthalate metabolites in the urine of an adult population.108(10)979-982.210(3-4):319-33. Eckard R. Gans G. Reprod Toxicol 2004. Brock JW.niehs. Hagmar L. Research Triangle Park (NC). Singh NP. Jonsson BAG.S. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Castle L. Environ Health Perspect 2003.112(3):331-338. David RM.208:237-245. Richthoff J. Ryan L. Atlanta (GA). Silva MJ. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Barr DB. Schettler T.html. Environ Res 2003. J Androl 2004. Koch HM. et al. Environ Health Perspect 2006. Springall C.22(3):688-695. Phthalate monoesters levels in the urine of young children. Hauser R. Hilborn ED. Bolte G. et al. Koch HM. Silva MJ. Boehmer S.16(4):487-493. Perera FP. Anderson WA.18(1):122. Yoshida K. Caudill SP.93:177-185. Int J Hyg Environ Health 2007. Weuve J. Hodge CC. Environ Health Perspect 2000. Reidy JA. Butala JH.25(2):293-302. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. 2005. Drexler H. Angerer J. Jacek R. et al. et al. NTP-CERHR. Jedrychowski W. Giwercman A. Wittassek M. Wiesmuller GA. Prenatal exposures to phthalates among women in New York City and Krakow. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Silva MJ. Duty S. Needham LL. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). et al. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach.Phthalates References Adibi JJ. Int J Hyg Environ Health 2007. Pirkle JL. Green RA. Urinary levels of seven phthalate metabolites in the U. Fromme H. Koch HM. Environ Health Perspect 2004.nih. Dobler L. Duty SM. Calafat AM. Poland. et al.

400-.400 (.500) < LOD 1. In this Report.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 .500 (.200-.300 (.2.300-.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.600) .300 (.600) . including nitrocellulose.600) . Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) 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.500-.300 (<LOD-.200-.70 (1.10 (<LOD-1.500 (. and polymers.400 (. which may vary for some chemicals by year and by individual sample.00-3.10 (.00 (<LOD-1. 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.300-. and polyvinyl chloride.S.Phthalates Dicyclohexyl Phthalate CAS No. 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-.50) .400 (.400-.500) 1.300 (.300 (.70 (1.50) .600) .400) < LOD 1.500) < LOD < LOD .700) .600) < LOD .600 (.400-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300) < LOD . People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.10) .600) .300-.300 (.700) .80) .400 (<LOD-.400-.300-.500) .300-.300-.400) < LOD < LOD .500) .500) . only levels at or above the 90th percentile could be characterized.9.400 (<LOD-.300-. and 0.10 (<LOD-1. resins. respectively.10 (<LOD-2.500) 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 . population from the National Health and Nutrition Examination Survey.300 (.300 (.00 (<LOD-1. see Data Analysis section) for Survey years 99-00.500) 1.200-. and 03-04 are 0. 01-02.3. Survey Geometric mean (95% conf.400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .400 (.400) 1.400 (<LOD-.500) < LOD < LOD .00-2. 270 Fourth National Report on Human Exposure to Environmental Chemicals .400 (<LOD-.500 (.90) .300) < LOD .500) .700) .500 (. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.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 1.70) .200-. polyvinyl acetate.500) 1.200 (<LOD-.400-. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity.200-.500 (. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.900-1. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection.300-.20) . < LOD means less than the limit of detection.00) .500 (.300-.400-.400 (.500 (.70) .400 (. 0.400) 1.200-.500 (.400 (.500 (.300-.00 (<LOD-1.

53) .450 (.910 (.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .590 (<LOD-. population from the National Health and Nutrition Examination Survey.560) 1.54) .710) .390 (.500) 3.670 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.470 (.82 (1.510 (.590 (.350-.36-1.770 (.530-1.400-.490) .12-1.10) .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 .770-1.690) < LOD 2.330 (.370 (<LOD-.740) < LOD < LOD .480 (.220 (<LOD-.54-6.770-1.44) .14 (<LOD-3.630 (<LOD-.33) .310-.170-.830) 1.67 (1.630 (<LOD-.00 (<LOD-3.06) .06) .310) < LOD . Survey Geometric mean (95% conf.660) .360-.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.910 (.410 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.530-.270) < LOD .530) 1.950 (.690) < LOD < LOD .16) .530 (.800-1.910 (.290-.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 .380-.S.18) .82) .660) < LOD < LOD .11) .00) .74) .34) .330 (.420-.420-.54 (<LOD-2.380 (.500 (.510-.53) .770-1.690-1.470) 3.420-.880 (.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.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.790-1.240-.670-1.22 (<LOD-1.770) < LOD 2.17) .260-.05) .940 (.43 (1.610 (.450 (.620) < LOD .33 (<LOD-3.400-.500-.16 (<LOD-3. Fourth National Report on Human Exposure to Environmental Chemicals 271 .250 (.740) .910 (.690 (.

3 (82.Phthalates Diethyl Phthalate CAS No.1 (71. 2001-2002. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity. DC (Hoppin et al. soaps. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. 2002).3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. shampoos.S. 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. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples.8-111) 85. 2007).4. 01-02. and 03-04 are 1.7) 71.3 (74. and also in men attending a Boston infertility clinic (Hauser et al. particularly those containing fragrances.4 (62.. respectively.9-92..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. Biomonitoring Information MEP levels in the NHANES 1999-2000.7 (70. 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.1-93. deodorants.9. population from the National Health and Nutrition Examination Survey.9 (61.. In contrast. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. colognes. and 0. 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.2-102) 95. 272 Fourth National Report on Human Exposure to Environmental Chemicals . and hand lotions. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products. 0.2. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. Products that may contain DEP include perfumes.5) 81. 2003) and African-American women in Washington. see Data Analysis section) for Survey years 99-00.

Other population estimates also differed by sex and race ethnicity (Silva et al..3-105) 87. 2003) were slightly lower than levels found in NHANES 2001-2002.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. 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 92.0-156) 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 . 2002).9 (82.9-110) 96.Phthalates 2002 (Brock et al.7-110) 81. the adjusted geometric mean levels of urinary MEP were lower in the group aged 6-11 years than in either of the other age groups.2 (66. population from the National Health and Nutrition Examination Survey. This age-related trend is opposite the direction seen for other phthalates. 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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.6 (77.0 (66.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. 2005). 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. Median MEP levels found in a small sample of German residents (Koch et al.5-113) 122 (93. In an analysis of NHANES 1999-2000. 2004). Analysis of NHANES 2001-2002 showed similar findings.5-114) 101 (87. 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.6 (65.

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

5 (11.6) 14.1) 19.5-36.1-17.70-8.2-35.8 (17.82) 3.27) 2.9-55. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood. population from the National Health and Nutrition Examination Survey.80 (8.40-8.85) 4.60) 9.10 (3.50-14.10-5.1) 29.6-130) 31.2) 4.2 (11.10-11.39) 3.70-4.00) 2.61 (3.92-2.5) 40.0) 39.10-5. which is used for many consumer products.00) 1.50-3.0-19.9) 27.70 (1.07-4.90 (3.40-8.91-3.7) 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 3.9-57.3-64.1) 25. and 0. respectively.20 (1. Fourth National Report on Human Exposure to Environmental Chemicals 275 .82 (3.50-5. and in humans.70-5.92-5.24-4.20 (3.27 (3.60 (5.15 (1.1-17.70 (8.00 (5. 01-02.9-26.10-5.6 (16.89-3.80-4.9 (16.80-27.9) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.0 (14.00-3.00) 9.25-3.6) 9.70-3.40 (6.4) 22.5-41.30-6.00 (7.43 (3.51) 4.10) 3.90) 4.7) 35.10-3.4) 20.10) 3.6-60.23 (2.87-2.90) 4.79) 2.60) 3.0) 23.5-28.9) 13.2) 42.10-11.20 (4.90-3.5) 23.10) 2.50-20.8 (19.77 (2.70 (1.1-48.4-40.42-5.10-4.70-6.0 (17.3 (11.1-29.80) 13.40) 9.3-26.70-2.8) 15.7-18.9-19.4-27.5-27.93) 6.10-3.80-3.5 (18.7) 27.6) 95th 23.50) 4.42) 3. Albro and Lavenhar. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).60) 7.5-40.4-20. DEHP has been removed from or replaced in most toys and food packaging in the United States. MEHP is primarily formed by the hydrolysis of DEHP in the gastrointestinal tract and then absorbed.1 (11.3) 28.40-12.4-53.5 (31.23) 3.7) 8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.40) 4.90 (1.40-11.0) 31.70) 2. see Data Analysis section) for Survey years 99-00.50 (7.3-25.40 (4.3-49.35) 4.50-3.30-8.67-4.85 (3.50-6.8-36.6-38.1 (10.80 (4.80) 6. Peck and Albro.1 (8.80-4.0-18.80 (1.40 (4.60) 8. toys. DEHP is metabolized to more than 30 metabol