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.

Fourth National Report on Human Exposure to Environmental Chemicals

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Paradichlorobenzene) 1.5'-Tetrachlorobiphenyl (PCB 44) 2.4-Dichlorobenzene (p-Dichlorobenzene.2'.4-Tribromodiphenyl ether (BDE 17) 2.3’.3'.5.2'4.4'.3-Dichlorobenzene (m-Dichlorobenzene) 1.4.gov/exposurereport/chemical_selection.2-Dichloroethane (Ethylene dichloride) 1.6'-Decachlorobiphenyl (PCB 209) Perchlorate Perfluorinated Compounds Perfluorobutane sulfonic acid (PFBuS) Perfluorodecanoic acid (PFDeA) Perfluorododecanoic acid (PFDoA) Perfluoroheptanoic acid (PFHpA) Perfluorohexane sulfonic acid (PFHxS) Perfluorononanoic acid (PFNA) Perfluorooctane sulfonamide (PFOSA) Perfluorooctane sulfonic acid (PFOS) 2-(N-Ethyl-Perfluorooctane sulfonamido) acetic acid (Et-PFOSA-AcOH) 2-(N-Methyl-perfluorooctane sulfonamido) acetic acid (Me-PFOSA-AcOH) Perfluorooctanoic acid (PFOA) Perfluoroundecanoic acid (PFUA) Phthalate Metabolite Mono-(2-ethyl-5-carboxypentyl) phthalate (MECPP) Polybrominated Diphenyl Ethers (PBDE) and Polybrominated Biphenyl 2.4'-Tribromodiphenyl ether (BDE 28) 2.2-bis[4-Hydroxyphenyl] propane) 4-tert-Octyl phenol (4-[1.5'.4.2'.6-Heptabromodiphenyl ether (BDE 183) 2.2-Dichloroethene Dichloromethane (Methylene chloride) 1.4'-Pentabromodiphenyl ether (BDE 85) 2.2'.3-Tetramethylbutyl] phenol) Triclosan (2.4.4.2-Dichloropropane 2. Total Arsenic (V) acid Arsenobetaine Arsenocholine Arsenous (III) acid Dimethylarsinic acid Monomethylarsonic acid Trimethylarsine oxide Disinfection By-Products (Trihalomethanes) Bromodichloromethane Dibromochloromethane (Chlorodibromomethane) Bromoform (Tribromomethane) Chloroform (Trichloromethane) Environmental Phenols Benzophenone-3 (2-Hydroxy-4-methoxybenzophenone) Bisphenol A (2.2-Dichlorobenzene (o-Dichlorobenzene) 1.4.4.4'.5'-Hexabromobiphenyl (BB 153) Volatile Organic Compounds (VOCs) Benzene Chlorobenzene (Monochlorobenzene) 1.2'3.and p-Xylene o-Xylene 2 Fourth National Report on Human Exposure to Environmental Chemicals .What’s New in this Report What’s New in this Report In this Fourth Report.4. 75 new chemicals are added for the 2003-2004 survey period and are listed in Table 1.4’-Trichloro-2’-hydroxyphenyl ether) Non-dioxin-like Polychlorinated Biphenyls 2.4.2'.2-Trichloroethane Trichloroethene (Trichloroethylene) m.2-Tetrachloroethane Tetrachloroethene Tetrachloromethane (Carbon tetrachloride) Toluene 1.4.2'.5.2'.1.1. The process for selection is described at http://www.3.5'-Hexabromodiphenyl ether (BDE 153) 2.4.1-Dichloroethene (Vinylidene chloride) cis-1.3.4.4’.4'. 2009 Acrylamide Adducts Acrylamide Glycidamide Total and Speciated Arsenic Arsenic.2'.3.2-Dichloroethene trans-1.html.5'-Tetrachlorobiphenyl (PCB 49) 2.5’.1-Dichloroethane 1.4'-Tetrabromodiphenyl ether (BDE 47) 2.5-Dimethylfuran Ethylbenzene Hexachloroethane Methyl-tert-butyl ether (MTBE) Nitrobenzene Styrene 1.6-Pentabromodiphenyl ether (BDE 100) 2.4.1.5.6.4'.2’.1.1-Trichloroethane (Methyl chloroform) 1.6'-Hexabromodiphenyl ether (BDE 154) 2.2. Chemicals reported for the first time in the Fourth National Report on Human Exposure to Environmental Chemicals.5-Pentabromodiphenyl ether (BDE 99) 2.4'.cdc.4'-Tetrabromodiphenyl ether (BDE 66) 2.2'.2'.4’. Table 1.3.2-Dibromo-3-chloropropane (DBCP) Dibromomethane 1.5.

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

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

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

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

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

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

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

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

4 (51.1-61.. pulp and paper production. 2005).6) 71.9-52.1) 101 (95.7 (65.2 (58. 217 million pounds of acrylamide were produced commercially in the U.2-59. In humans.2-114) 163 (147-191) 96. Commercially. FAO/WHO. 2005.7) 96.0 (67. (NTP-CERHR. see Data Analysis section) for Survey year 03-04 is 3. 2002). and from dermal contact with products that contain residual acrylamide. Estimated intakes in children are about twice that of adults (DiNovi and Howard.2) 57. 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. glycidamide.6) 90th 141 (124-155) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 59. 2005).0 (53. ocular and dermal irritation from direct contact with acrylamide containing materials.5-85.S.7-64.9 (60.4-83. 2005). mineral processing.S. acrylamide is synthesized and used in the production of polyacrylamide polymer. Smaller scale applications of polyacrylamides include additives to paperboard used for food packaging. Elimination occurs mainly in the urine as mercapturic acid conjugates. such as potatoes and some grains.3) 70. 79-06-1 General Information Acrylamide is a small organic molecule existing as a white crystalline powder in its pure state. and is either metabolized to the reactive epoxide.7) 54.1) 53. and binding agents. and cosmetics (NTP-CERHR.4) 57.6-104) 82.9 (54.9) 75.9-61. 2004.4 (54.7-60.0) 85.8-55.9) 58. In 1997. EPA reference dose of 0. 2004).6-108) 61.9) 57. drinking water.6) 73. gels.4 (53.8 (81. widely distributed in tissues. In the general population. Acrylamide is not thought to accumulate in the body at environmental doses.7 (58. EPA.4 (54. in some sealing grouts. Survey Geometric mean (95% conf.1) 46.S. 2005).4) 57.7) 75th 79.7 (63.1 (47. and well below doses known to cause nerve damage or carcinogenicity in animals. soil conditioners.0-115) 156 (120-203) 146 (129-163) 149 (125-179) 218 (172-271) 197 (172-223) 1792 1874 2994 Limit of detection (LOD.5-80.6 (51. but are generally above the U. Fennell et al.0.2-91.1 (73. EPA.8 (91. These estimated intakes are hundreds of times lower than occupational exposures.0-49.9-105) 86.3) 63.8 (57. Recently.5 (52..8 (52. and in some cosmetics. smoking.1) 55. 1990. but can covalently bind to form adducts with proteins.4-76.0 (57. the main source of exposure is from the diet.0 (69.Acrylamide Acrylamide CAS No. environmental releases of acrylamide can enter aquatic systems and soils where it degrades within days and does not bioaccumulate (U..7 (55. 2006).3) 86.5 (44.5 (74. and in the synthesis or compounding of dye materials.1) 62.7-64.3 (53. and an average daily intake is estimated as 0.4-60. are heated at temperatures used for frying and baking.2-70. it was discovered that acrylamide is formed when starch-rich foods. Polyacrylamides are useful water-compatible polymers used in water treatment.2-67.2 (62. as an absorbent in disposable diapers.6 (81.2-93.3-71.0-104) 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 (69. Animal studies indicate that acrylamide is well absorbed. FDA.6-75. 2005). 1994). in permanent press fabrics. interval) 61.4) 100 (89. Tareke et al.0-66.7) 73. acrylamide has produced upper airway irritation following inhalation of high levels.S.6-65. 2006.5 (79.9) 63.4) 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. Fourth National Report on Human Exposure to Environmental Chemicals 11 .0-58. population from the National Health and Nutrition Examination Survey.5) 58.S.0) 57.7) 58.6) 90.2-77.6-66. although additional exposures from cosmetic products could add a similar amount (NTP-CERHR. or to glutathione conjugates (Calleman et al.3-2.5) 66.2) 57. and peripheral neuropathy following chronic Acrylamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.4-89.6) 50.1 (88.2-118) 98.2 μg/kg/day (U.4 (59.4-60. People may be exposed to acrylamide from foods.1 (52.1-64.6 (56.2 (75.8-57.1 (83.0-108) 152 (139-175) 126 (111-142) 108 (86.6-61.1-57. Since acrylamide has limited volatility and high water solubility. Natural substances in the food are converted to acrylamide.1-64.0 μg/kg for adults (FAO/ WHO.3 (55.

2008). 2005. Glycidamide has been shown to react with DNA (Doerge et al. 1997..5-92. Several of these studies have shown that smokers have adduct levels that are three to fourfold higher than non-smokers.4-65.9-62. 2005.2 (63. Maniere et al.S.epa.5-66. 2001). 2005. 1997. and neuronal DNA reactivity (Doerge et al. Klaunig et al.4) 46.5) 87.9) 75. EPA.9-77.6-64.4) 53..3) 85. glycidamide (NTP-CERHR.3) 59.9-138) 143 (130-159) 96. 2006).. Mucci et al.2) 87.9 (57.4) 83.2-91.6-90. 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.8 (44.1-62. Rice. scrotal.S.1-56. see Data Analysis section) for Survey year 03-04 is 4..Acrylamide occupational exposures.5) 90th 130 (120-141) 03-04 03-04 03-04 03-04 03-04 03-04 03-04 71.5) 71. Vesper 2005) and smoking (Bergmark. 2004).8) 60. 2005)..0-62.5 (59. Biomonitoring Information Acrylamide and glycidamide hemoglobin adducts (AHA and GHA. EPA. 2005. Schettgen et al. male germinal cell injury.. 2005.. 2004.1-70.4 (51.8 (51. levels of AHA adducts decline but may remain detectable for several months (Hagmar et al.0) 118 (103-126) 121 (112-134) 113 (94. 2002.5 (83. 2005.S.0 (75.7) 74. population from the National Health and Nutrition Examination Survey.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..4 (90. Adducts are formed when either acrylamide or glycidamide react to form a permanent covalent bond with hemoglobin in the blood. 2003.1) 60. 2005) and sperm DNA adducts (Xie et al. Axonal degeneration.1 (70.. Hagmar et al.7 (61.4 (56. 2008).9) 65.1 (57. NTP-CERHR.5 (42..2) 65...2 (72.9-64.7 (57. IARC classifies acrylamide as probably carcinogenic to humans.6 (66. U.9 (58..8-61. to increase the unscheduled synthesis of DNA in tumor susceptible tissues (Klaunig et al. 12 Fourth National Report on Human Exposure to Environmental Chemicals .7) 61. gov/iris/ and from the Food and Agriculture Organization of the United Nations and WHO at: http://www.3) 59..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.pdf. Additional information is available from U.4-59.3) 59.3-101) 95.4-103) 79. uterine.S.0-93..5-64. adrenal.4 (61. After exposure ceases.4 (57. 2005.1 (66. 2009). 2005.who.0.9-76.5) 75th 85. and other sites) (FAO/WHO. dominant lethality).5-94. 2005). Puppel et al..7 (84.9) 87.5) 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. 2006).7-64.2-68. 2005. Schettgen et al.5 (56. and cancer (mammary. Vesper et al..2-90.. interval) 59.1-60.0 (80..1 (56. 2005.9 (81. presynaptic nerve terminal binding (LoPachin.3-78. Glycidamide Geometric mean and selected percentiles of hemoglobin adduct concentrations (in pmol/g hemoglobin) for the U.8-48. and to increase DNA reactivity when glutathione availability is reduced (Klaunig et al.3 (56. In addition.2 (56. although different analytic methods can affect results.int/ ipcs/food/jecfa/summaries/summary_report_64_final. 2005) have been demonstrated in animals. 2005).4-98. 2006) have been demonstrated after acrylamide dosing.6-62.0) 94. most non-smokers had levels less than about 100 pmol/gram hemoglobin.7 (87.8-49. probably through its epoxide metabolite.. thyroid. reproductive effects (reduced litter size.2) 55.7) 60.9) 59.6 (90.9-78.1 (82.4 (81. Acrylamide is clastogenic and can produce dominant lethal mutations. respectively) are markers of integrated acrylamide exposure over the preceding few months. 2006. Animal studies have shown that acrylamide can cause nerve damage (neuropathy). 2005). Survey Geometric mean (95% conf. Younger children may have slightly higher levels possibly due to increased intake of acrylamide-containing foods relative to body size (Dybing et al.0 (70. fetal death.1) 56.1) 62.7) 90.8) 45. Puppel et al. altered gene expression in testicular tissues (Yang et al.7-86. 2005.7-62. U. 2002. EPA at: http://www. AHA levels have been shown to increase with dietary intake (Hagmar et al. Levels of AHA and GHA reported the NHANES 20032004 sample are generally similar to those seen in several previous studies of non-occupationally exposed subjects (Bergmark et al.0 (52.

DNA adducts derived from administration of acrylamide and glycidamide to mice and rats.580(1-2):131-141.fda. smokers and nonsmokers. Andersen M. He F.. Tian G. Bergmark E. 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. Zhang S. symptoms of numbness or tingling in the extremities did not occur in exposed workers whose AHA levels were below 510 pmol/gram hemoglobin. Mechanisms of acrylamide induced rodent carcinogenesis. 2004. Food Chem. Mutat Res 2005. Chem Res Toxicol 1997 Jan. Axmon A. Snyder RW. Italy. Adv Exp Med Biol 2005. Survey data on acrylamide in food: individual food products. Tornqvist M. 64th Meeting: Summary and Conclusions (FAO/WHO). Toxicol 2005. 2/3/09 Perez HL. Acrylamide intake through diet and human cancer risk. Costa LG. Calleman CJ. et al.126(2):361-371. Paulsson B. April 13-15.3:406-412. 2009 Jan 8.561:49-62. July.10(1):78-84. Joint FAO/WHO Expert Committee on Food Additives. Rome. Food and Drug Administration (FDA). References Bergmark E. Farmer PB. McDaniel LP. et al.. Human exposure and internal dose assessments of acrylamide in food. and 39% of workers with levels above 1000 pmol/gram hemoglobin had these symptoms (Hagmar et al. 8-17 February 2005.27(4):219-226.561:21-37. Available at URL: http://www. et al. Bergmark E. Spicer R. 1999). 2/3/09 Hagmar L. Churchwell MI. 2004 Acrylamide in Food Workshop: Update Scientific Issues. 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. and Research Strategies. Malmberg B. DNA damage and DNA adduct formation in rat tissues following oral administration of acrylamide. Wilson KM. Relationships between biomarkers of exposure and neurological effects in a group of workers exposed to acrylamide. Adv Exp Med Biol 2005. Perez et al.43:365–410. Uncertainties.pdf. Health effects of occupational exposure to acrylamide using hemoglobin adducts as biomarkers of internal dose. CFSAN/Office of Plant and Dairy Foods. Metabolism and hemoglobin adduct formation of acrylamide in humans. Monograph on the Potential Human Reproductive and Developmental Effects of Acrylamide. Granath F. Determination of hemoglobin adducts in humans occupationally exposed to acrylamide. Godard T. Calleman CJ.who. 054472. Twaddle NC. Paulsen JE. National Toxicology Program. et al. 6013-6019. Laurentie M. 2001). In another study. Tornqvist M. Becher G. NIH Publication No.int/ipcs/ food/jecfa/summaries/summary_report_64_final. Biomarkers of human exposure to acrylamide and relation to polymorphisms in metabolizing genes. Nordander C. Cheong HK.580(1-2):157-165. Fennell TR. J Agric Food Chem 2008. Wirfalt E. Wu Y. Toxicol Sci 2005. Fennell TR.html#u1004. Osterman-Golkar S. smoking habits and gender. Simultaneous analysis of hemoglobin adducts of acrylamide and Fourth National Report on Human Exposure to Environmental Chemicals 13 . Kamendulis LM. Kautiainen A. Doerge DR. Hagmar et al. Bridson WE. Available at URL: http://cerhr. Churchwell MI. Bergmark E. He F.. Alexander J. Magnusson AL. Illinois. Available at URL: http://www.56. Guffroy M. da Costa GG. gov/~dms/acrydata. Toxicol Sci. Aprea P.pdf.85:447-459. et al. 2005. Calleman CJ. Acrylamide neurotoxicity: neurological.Acrylamide In occupational settings.120(1):45-54. Toxicol Appl Pharmacol 1993. February. Bruze M. Differences in hemoglobin adduct levels of acrylamide in the general population with respect to dietary intake.Toxicol Appl Pharmacol 1994.. Costa LG. LoPachin RM. The Updated Exposure Assessment for Acrylamide. Bjellaas T.580(1-2):119-129. Mutat Res 2005. Center for the Evaluation of Risks to Human Reproduction (NTP-CERHR). morphological and molecular endpoints in animal models. Acrylamide is metabolized to glycidamide in the rat: evidence from hemoglobin adduct formation.cfsan. Chicago. Mutat Res 2005. Burgess J. Mucci LA.niehs. Haugen M. Chem Res Toxicol 1990.gov/chemicals/ acrylamide/Acrylamide_Monograph. 1993.nih. Hagmar L. [Epub ahead of print] Dybing E. Maniere I. AHA levels were several fold to several hundredfold higher than levels in non-exposed non-smokers (Bergmark et al. Doerge DR.. Yang JS. Rosen I. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Scand J Work Environ Health 2001. 2001. Hemoglobin adducts of acrylamide and acrylonitrile in laboratory workers. 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. Beland FA. Duale N. 2/3/09 Klaunig JE. DiNovi M and Howard D. 1994). 2006. Summer SCJ.

134(1-3):65-70. Adduction of biomacromolecules with acrylamide (AA) in mice at environmental dose levels studied by accelerator mass spectrometry. Schettgen T. acrylonitrile and acrylamide-biomarkers in occupational and environmental medicine. Ospina M. Sun H. Fu D. Automated method for measuring globin adducts of acrylamide and glycidamide at optimized Edman reaction conditions. Available at URL: http://www. Weiss T.S. Angerer J. Environmental Protection Agency (U.580(1-2):3-20. Mutat Res 2005. Kutting B.163(2):101-8. Schettgen T. Angerer J. Meyers T. Myers GL. et al. Yang HJ. Licea-Perez H. J Agric Food Chem 2008. et al. Liu Y. Integrated Risk Information System (IRIS). Rossbach B.txt. Han DU. Rydberg P. Tjønneland A.gov/iris/subst/0286. Chemical Summary for Acrylamide.19(4):527-34. 14 Fourth National Report on Human Exposure to Environmental Chemicals . Hallmans G. Available at URL: http://www.gov/chemfact/s_acryla. 1994.207(6):531-9. Lee SH. Toxicol Lett 2006. Int J Hyg Environ Health 2003. Karlsson P. Meyers T. Pilot study on the impact of potato chips consumption on biomarkers of acrylamide exposure.580(1-2):71-80. Reprod Toxicol 2005. Drexler H. Liu K. Adv Exp Med Biol 2005. Acrylamide. A first approach to estimate the internal exposure to acrylamide in smoking and non-smoking adults from Germany. Jin Y. Drexler H. 2/3/09 Vesper HW. U. Ingham L. J Agric Food Chem 2002.epa. Cross-sectional study on acrylamide hemoglobin adducts in subpopulations from the European Prospective Investigation into Cancer and Nutrition (EPIC) Study. Tareke E. Anal Biochem 1999. Angerer J. Han CH. propylene oxide. Lee MH. Letzel S. Vesper HW. a carcinogen formed in heated foodstuffs. Tjaden Z.206(1):9-14. September. Agudo A. Washington (DC). Int J Hyg Environ Health 2004. The carcinogenicity of acrylamide. Choi JH. Marko D.50(17):4998-5006. Fueller F. Eriksson S. 2/3/09. Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population. Rapid Commun Mass Spectrom 2006.S. Rice JM. Puppel N.561:89-96. Xie Q. Mutat Res 2005 Feb 7. Broding HC. Ospina M. revised 1/3/06. Toxicological effects of acrylamide on rat testicular gene expression profile. Drexler H. Environmental Protection Agency (U. EPA). DNA strand breaking capacity of acrylamide and glycidamide in mammalian cells.20(6):959-64.S. Office of Pollution Prevention and Toxics.htm. EPA).epa. Gray JG. Vesper HW. Schettgen T. Benetou V.Acrylamide glycidamide by gas chromatography-mass spectrometry. Analysis of acrylamide. Ding X. Chae C. U.S. Smith A. Tornqvist M.274(1):59-68. Slimani N.56(15):6046-53. Toxicol Lett 2002. Hemoglobin adducts of ethylene oxide.

93) .95) 1.23 (.216 (.180 (.30) * .175 (.110) .234) .030-.310-1.059-.180) .22) 2. and more than 50 compounds present in ETS are known or reasonably anticipated to be human carcinogens (NTP. stroke.17 (1.96) 2.030-. emphysema.84-3.50) 3. 2004).580-1.120-.193) .17) .054 (.052 (<LOD-.19) .094) .040-.137-.480-1.20) .126) .145) .302) .02) 1.620 (.052 (<LOD-.110) . 2006).12) 1.120) .730 (.22) 2789 3152 2937 3210 3667 3383 Females Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 * .148-.32) 1. and 0.62 (2. maternal exposure during pregnancy can result in lower birth weight.14-1.110 (.49) 2241 1878 1707 1333 1602 1704 1950 2847 2500 Non-Hispanic blacks Non-Hispanic whites 99-00 01-02** 03-04 Limit of detection (LOD.050 (.770) .360) .14) .120 (.S.080) < LOD .66-3.690 (.17 (.77 (1.860 (.Cotinine Cotinine CAS No.68) .060-.110-.726) .15) 2.68) 2.187) .130 (.20-2.030-.197) .55 (1.500 (.073) < LOD .320) .21-1.090-.142-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.180) .54) size 5999 6819 6320 Total years 99-00 01-02** 03-04 50th .111-.89) 1.230 (.44) 2.053 (<LOD-.087) < LOD < LOD .630 (.01 (1.070) .63 (2.140 (.080-. DHHS.630 (.047-.057-.080) < LOD < LOD .160) .144 (.120 (.505 (.163 (.92 (1.040 (.44 (2.201) .120 (.077) .23 (1.087 (. and various other disorders (U. acute respiratory infections.85 (1.34 (1.930 (.115-.410) . ear problems.20 (1. Serum Cotinine Metabolite of nicotine (component of tobacco smoke) Geometric mean and selected percentiles of serum concentrations (in ng/mL) for the non-smoking U.100-.60-2.080-.540-.76 (1.65 (1.450-.625) .370-.770) .167 (.015 ng/mL.910-1.99) 2.15 (2.312) .120 (. and exacerbated asthma (U.81-2.32-2.70-2.14) .280 (.02) 1.131 (.01) 3.015.63-2.059-.058 (.090-.990 (. 1998).308 (.50-4.05 ng/mL.580) .104-. Cigarettes contain about 1.213) . Persons exposed to secondhand tobacco smoke (environmental tobacco smoke [ETS]) may have adverse health effects that include lung cancer and coronary heart disease.066-.49) 1.230) .070 (<LOD-.060-. DHHS.050 (<LOD-.140-.83-2.S.79) 3.78) 2.087-.140 (.350-.45) 1.300) .38-2.200) 1.070) 75th .050) .26-1.55-2.080 (.060 (. The smoke produced by burning tobacco contains at least 250 chemicals that are toxic or carcinogenic.124 (.086 (.110 (.11) .88 (.30) 2.05) 1.108) * .33-2.18-3.160-.088-.75) 1.220) .21 (.150) . population from the National Health and Nutrition Examination Survey.080-.160) .190-.21-1.790) .630 (.12 (2. producing roughly 1–2 mg of bioavailable nicotine per cigarette (Benowitz and Jacob.050 (<LOD-. Children exposed to ETS are at increased risk for sudden infant death syndrome.20 (.310) 90th 1.05.110-.00) .043-.260-1.050-.061) < LOD .02 (.19) 1.68 (1.180 (.080 (.950 (.950-1.160 (.42-4.99) 2.430-1.820) .54 (1. 83% of measurements had an LOD of 0.09-3.840) 3.198) * . Survey Geometric mean (95% conf.050-.120-.040 (.350 (.180) .140-.19-2.50 (1.188) . cardiovascular disease.57) 2. Fourth National Report on Human Exposure to Environmental Chemicals 15 .96 (1.900-1.080-.020-.740-1.66) 1.106-.20) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.040 (. and 17% had an LOD of 0.533-.089) Age group 3-11 years 99-00 01-02** 03-04 .S.154-.070-. which may vary for some chemicals by year and by individual sample.660) .050 (<LOD-.620-1.800 (.139) * .400-.540 (.30) 2.160 (.163) .44) 2.150) .12-4.060 (<LOD-.075 (.084) .70) 2.510 (.310-1.600-1. and 03-04 are 0.62) 2.990) .77 (2.92) 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 .062 (.53-4.44 (1.997-3.090-. The consequences of smoking and of using smokeless tobacco products are well known and include an increased risk for several types of cancer.137 (. see Data Analysis section) for Survey years 99-00.071 (.23-2.120 (. acute respiratory illness.240 (.16) .54) 1.670) .060 (<LOD-.5% nicotine by weight (Kozlowski et al.030 (.071) .770-1.12 (1.480-.060-.060) .48-3.068) .520 (.110 (.110 (.070) .42 (1.32-2.040-.35 (2.850 (.88 (1. < LOD means less than the limit of detection.164 (. 2004).220-.920 (.66 (1.39) 3.260) 1.39 (1.54 (1.190-.066) .96-4.350-.53 (1.28) .050 (<LOD-.428-. 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.470-.28-1.47-3.580 (.621-1. respectively.110-.160 (.077) .190-.310) .506 (.49) 1.063) .164 (.94) 1. ** In the 2001-2002 survey period.23 (2.110 (.180) .48-2.220) .04 (1.87-3.076-.570-1.047-.50-1.130) .00) 1.050) .068) .09-3.570 (.180) .210 (.740-1.09-2.77 (1.060 (.153-.710 (.43 (1.40) .066 (.960-1..

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

Hukkanen J. Exposure of the U. Available at URL: http://ntp.S Department of Health and Human Services (U. Vol 83. Fong I. Benowitz NL. Pharmacol Rev 2005. Jacob III P. Nicotine metabolism and intake in black and white smokers. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.S. [online]. iarc.S. Warner K. 4/13/09 National Cancer Institute (NCI). Sosnoff CS.280:152-156.114(6):853-858. Curtin LR. population to environmental tobacco smoke: the Third National Health and Nutrition Examination Survey. Turner DM. Department of Heath and Human Services. BMJ 1975. 4/13/09 Centers for Disease Control and Prevention (CDC).nih. Etzel RA. DHHS).fr/ENG/Monographs/ allmonos90. Mowery PD. Maurer KR. Department of Heath and Human Services. Strauss WJ. Absorption and metabolism of nicotine from cigarettes. 11th ed. Benowitz NL. Metabolism and disposition kinetics of nicotine.18:188-204. JAMA 1998. In Report on Carcinogens. Giovino G. Tobacco Smoke. Herrera B.niehs. Third National Report on Human Exposure to Environmental Chemicals. cigarette smokers: the Third National Health and Nutrition Examination Survey. Centers for Disease Control and Prevention. National Center for Fourth National Report on Human Exposure to Environmental Chemicals 17 . DHHS). Environ Health Perspect 2006.94(2):314-320. Vogler GP.php. Vol 38. Tobacco related exposures.gov/library/ secondhandsmoke/.15:302-307. Tob Control 2006. Aiba M. Tob Control 1998. June. Available at URL: http://monographs. J Pharmacol Exp Ther 1999. Schwartz SS. Schober SE. IARC Monogr Eval Carcinog Risks Hum. Health Effects of Exposure to Environmental Tobacco Smoke: The Report of the California Environmental Protection Agency.275:1233-1240. 4/13/09 International Agency for Research on Cancer. population to secondhand smoke: 1988-2002. and the United States. References Armitage AK.Cotinine and public health officials determine whether people have been exposed to higher levels of ETS than are found in the general population. Pechacek TF.S.56:483-493.pdf. Dollery CT. Filter ventilation and nicotine content of tobacco in cigarettes from Canada. Summary of Data Reported and Evaluation [online] 1986. 1988-1991. available at URL: http://mtn. National Toxicology Program (NTP). Bernert JT.280:135-140.S. Centers for Disease Control and Prevention. Pirkle JL.niosh.php. Sweeney CT. Jarvis MJ. Biomonitoring data can also help scientists plan and conduct research about exposure to ETS and about its health effects. U.pdf. Coordinating Center for Health Promotion. Benowitz NL.291(3):1196-1203.surgeongeneral. Clin Pharmacol Ther 1994. Brody DJ. Summary of Data Reported and Evaluation [online] 2004. the United Kingdom. Atlanta (GA): 2005. Benowitz NL. Respiratory nicotine absorption in non-smoking females during passive smoking. Kira S. Available at URL: http://monographs. Benowitz NL. Available at URL: http:// cancercontrol. Pechacek TF. 4/13/09 U. 1991. JAMA 1998.S. Richter PA. Pickett MA. Jacob P III. Soliman S. Pollack HA.cdc. Caraballo R. Flegal KM. The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General — Executive Summary. Office on Smoking and Health [online] 2006. Racial/ethnic differences in serum cotinine levels among adult U.gov/ntp/roc/eleventh/profiles/ s176toba.7:369-375. The Health Consequences of Smoking: The Surgeon General’s Report—Executive Summary.63:139-43.gov/eid/rmca/critdocs/ criteriadoc/33. et al.iarc. Smoke-free laws and secondhand smoke exposure in US nonsmoking adults. Jacob P.S. Perez-Stable EJ. Herrera B. Mehta NY.S. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Kozlowski LT.fr/ENG/Monographs/allmonos90. International Agency for Research on Cancer. Trends in the exposure of nonsmokers in the U.4:313-316. Decrease in the prevalence of environmental tobacco smoke exposure in the home during the 1990s in families with children.S Department of Health and Human Services (U. National Center for Chronic Disease Prevention and Health Promotion. 4/13/09 Perez-Stable EJ. 1999-2002. Int Arch Occup Environ Health 1991. U. Cotinine as a biomarker of environmental tobacco smoke exposure. Available at URL: http://www. Metabolism of nicotine to cotinine studied by a dual stable isotope method.57(1):79115. Tobacco Smoke and Involuntary Smoking. et al. 2004. Houseman TH. Ethnic differences in N-glucuronidation of nicotine and cotinine. Giovino GA. Smoking and Tobacco Control Monograph 10 [online]. IARC Monogr Eval Carcinog Risks Hum. 1988-1991. Jacob P III. U. Current Intelligence Bulletin 54: Environmental tobacco smoke in the workplace. Am J Public Health 2004. JAMA 1996. Bernert JT. National Institute for Occupational Safety and Hygiene (NIOSH). Centers for Disease Control.gov/tcrb/monographs/10/. Pirkle JL. Modin G. Coordinating Center for Health Promotion. Epidemiol Rev 1996. Caudill SP.cancer. Brody DJ. George CF. 1999. 4/13/09 Iwase A. Lewis PJ.

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

130-.110 (. 2003).S.S.210 (.S. Survey Geometric mean (95% conf.110 (. There are over 225 insect repellents brands containing DEET. and they range in concentration from 4% to 100%.240) < LOD .180 (.epa.140) < LOD . 2003). which may vary for some chemicals by year and by individual sample. Human health effects from DEET at low environmental doses or at biomonitored levels from low environmental exposures are unknown.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 . and it has not been rated by IARC or NTP with respect to human carcinogenicity. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.210) 480 580 672 829 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .130-. DEET can be applied to clothing and the skin to repel biting insects.220) size 1977 2535 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD 90th .130-.100-. have been reported as result of self-poisoning by ingestion or excessive dermal application.520) < LOD .270) 688 678 518 700 598 956 Limit of detection (LOD. Additional information is available from U. DEET has low acute toxicity.N. including seizures and encephalopathy.N-Diethyl-meta-toluamide (DEET) CAS No.100-.S.S.180) < LOD .130 (. DEET is also used in combination with dermal sun screens (U.140) < LOD .110-.100 (<LOD-. Neurological effects in humans.1. but higher DEET concentrations and different formulations may result in greater absorption (Sudakin and Trevathan.120-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.130) < LOD . DEET is metabolized via hydroxylation and dealkylation pathways and eliminated in the urine within approximately 24 hours (Selim et al.110-. DEET is not registered for use on agricultural commodities. < LOD means less than the limit of detection. People in outdoor occupations may apply DEET more frequently or use higher concentration formulations resulting in higher levels of exposure..120-.140) < LOD . 2002).100-. Most reports of adverse effects from overexposure to DEET involve skin reactions (Bell et al.100-.110 (<LOD-.100-. 2005).140 (.110 (.220 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .EPA. One survey detected DEET in 74% of sampled streams in the U.130) < LOD .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 . Its use is recommended for prevention of several vector-borne diseases.130 (.N-Diethyl-meta-toluamide (DEET) N. DEET is not genotoxic. Sudakin and Trevathan.N-Diethyl-meta-toluamide (DEET) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U..130 (. Urinary N. 1998).110 (. Fourth National Report on Human Exposure to Environmental Chemicals 19 .190) < LOD .140-.gov/pesticides/. About 3-8% of dermally applied DEET is absorbed.180 (.100-. (U.150) < LOD .560) < LOD .130-.250) < LOD . (Kolpin et al. 1998). After absorption. EPA.110 (<LOD-.160) < LOD .S.N-diethyl-meta-toluamide (DEET) is an insect repellent that was first marketed in 1957. DEET is not a developmental or reproductive toxicant in animals (U. General population exposure to DEET occurs from skin application and from inhalation of aerosol formulations.170 (.180 (. 1995.170 (. Exposure can also occur from consuming food contaminated by DEET on hands or that was sprayed nearby.449 and 0.EPA at: http://www. population from the National Health and Nutrition Examination Survey. 2002). 134-62-3 General Information N..

410 (. population from the National Health and Nutrition Examination Survey.370) < LOD .350) < LOD .500 (.270 (<LOD-. representative subsamples from NHANES 2001-2002.580) 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 .230-.500) 480 580 672 828 825 1126 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .190-.410 (.270) < LOD .N-Diethyl-meta-toluamide (DEET) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.320) < LOD .N-Diethyl-meta-toluamide (DEET) Biomonitoring Information Urinary levels of DEET reflect recent exposure.170-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result..640 (.250 (.S. Urinary N. 20 Fourth National Report on Human Exposure to Environmental Chemicals .93) < LOD .190 (.280 (.240-.S. the limit of detection was lower than for the NHANES 1999-2000 survey period (CDC.690 µg/L were measured in eight park employees who applied 71% DEET once a day (Smallwood et al.250-. DEET was detected in 10% of 60 Latino children in eastern North Carolina farm worker households (Arcury et al.280-1.230-.630) < LOD . In this survey period.N.190 (<LOD-.350) < LOD .290-.480 (.190 (. 2007).440) < LOD . Urinary DEET levels as high as 5.240) < LOD .270 (. 2005).130 (<LOD-.230) < LOD . Biomonitoring studies on levels of DEET provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of DEET than are found in the general population. Urinary levels of DEET were characterized only at the 90th and 95th percentiles of the U..270-.330 (.140-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD .300) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . Finding a measurable amount of DEET in urine does not mean that the level of DEET causes an adverse health effect.370-.150-.150) < LOD .350-.300 (.320 (.550) 688 678 518 699 598 956 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.390-. Survey Geometric mean (95% conf.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 .490) < LOD .410-.200 (.250) < LOD . 1992).330 (.

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

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

gov/chemicals/bisphenol/bisphenol. Reidy JA. McConnell EE. Koh WS. Gray GM. Furukawa M.14(2):149-157. 2007.it/DOCUMENTS/ Existing-Chemicals/RISK_ASSESSMENT/SUMMARY/ bisphenolasum325.10:875-921. Kim JC. Doull J. 2/4/09 Fujimaki K. Cunha G. Hlywka JJ. Available at URL: http://cerhr.pdf .312(2):441-448. N. vom Saal FS. Chung MK.pdf. 2/4/09 European Commission. Han SS. Kuklenyik Z. Imai H. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A.nih. Chem Res Toxicol 2001. Regul Toxicol Pharmacol 2002. 1999-2000: a national reconnaissance. 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. Italy. Furlong ET. Yang M. Calafat AM. Matthews JB. Serizawa S.. National Institute of Environmental Health Sciences. National Institutes of Health. Barton L. Endocrinology 2008.Environmental Phenols References Akingbemi BT..pdf . Reidy JA. Joskow R. Three-generation reproductive toxicity study of dietary bisphenol A in CD Sprague-Dawley rats. September. Kawamura N. Wong LY. Marr MC. Rubin C. Kim CS.eu/ health/ph_risk/committees/sct/documents/out156_en.69(22):2611-2625. Watanabe C. Hum Ecol Risk Assess 2004. Klinefelter GR. streams. Gender differences in the levels of bisphenol A metabolites in urine. et al. Hanaoka T.jrc. Environ Health Perspect 2008.gov/chemicals/bisphenol/BPAFinalEPVF112607.102(19):7014-7019. Hara K. Available at URL: http://ec. Yoshinaga J. et al. Bradley S. Cha SW.149:988-994.113(4):391-395. Joint Research Centre Institute of Health and Consumer Protection. Calafat AM.nih. and Hajszan. Pyo MY. Barber LB. Ekong J. J Am Dent Assoc 2006. Kolpin DW.S. Measurement of bisphenol A in human urine using liquid chromatography with multi-channel coulometric electrochemical detection. 2/4/09 National Toxicology Program’s Report of the Endocrine Disruptors Low-Dose Peer Review (NTP). Estrogenic chemicals in plastic and oral contraceptives disrupt development of the fetal mouse prostate and urethra. et al. Toxicol Sci 2002. August 2001. Bisphenol A. Rhomberg et al.Scientific Committee on Toxicity. Occup Environ Med 2002. In vitro and in vivo interactions of bisphenol A and its metabolite. Watanabe S. Twomey K.nih. 2002. Nippon Eiseigaku Zasshi 2004.niehs. Reprod Toxicol 2001. Tyl RW. 2/4/09 National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Proc Natl Acad Sci USA 2005.. Lynch BS. Ecotoxicity and the Environment (CSTEE). Urinary bisphenol A and plasma hormone concentrations in male workers exposed to bisphenol A diglycidyl ether and mixed organic solvents. Exposure of the U. Fujii S. 2/4/09 Ouchi K. Endocrinology 2004. Kiguchi M. Howdeshell KL. Cohen JT. European Commission.pdf. MacLusky.780(2):365-370. DirectorateGeneral Health and Consumer Protection. Kim YH. with estrogen receptors alpha and beta. Tsugane S. Needham LL.gov/ntp/htdocs/liason/ LowDosePeerFinalRpt. National Toxicology Program. Richter CA.59(9):625-628. Zacharewski TR. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004.116(1):39-44. Zaugg SD. Available at URL: http://ntp. Environ Health Perspect 2005. National Toxicology Program Center for the Evaluation of Risks to Human Production (NTP-CERHR). Thomas BF. Evaluation of developmental toxicity in rats exposed to the environmental estrogen bisphenol A during pregnancy. U. 4. Myers CB. Available at URL: http://cerhr.59(4):403-408. May 22. and other organic wastewater contaminants in U.4’-Isopropylidenediphenol (Bisphenol-A) Summary Assessment Report. Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite. hormones. Hughes C. Life Sci 2001. 2008. Han SY. Barr JR. Szigeti-Buck. Bisphenol A prevents the synaptogenic response to testosterone in the brain of adult male rats. Caudill SP. 32 Fourth National Report on Human Exposure to Environmental Chemicals .J. Ikka T.europa. NTP-CERHR Panel Report on Reproductive and Developmental Toxicity of Bisphenol A. Arakawa C. T. Brine DR. Environ Sci Technol 2002. and Hardy MP. C. Rat two-generation reproductive toxicity study of bisphenol A.S. Urinary concentrations of bisphenol A and 4-nonylphenol in a human reference population. niehs. Barr DB. Harazono A. 5: 505-523. Biochem Biophys Res Commun 2003. Ema M. Kroes R. Pharmaceuticals. Park S. Timms BG. Available at URL: http://ecb. Needham LL. Department of Health and Human Services. Shin HC. Weight of the evidence evaluation of low-dose reproductive and developmental effects of bisphenol A.145:592-603. NC.68(1):121-146. Calafat AM. An evaluation of the possible carcinogenicity of bisphenol A to humans. Brussels. Human Health.pdf. niehs. Sottas CM. Ispra. Haighton LA. Research Triangle Park. Koulova AI. bisphenol A glucuronide. Needham LL. Leranth. Exposure to bisphenol A from bis-glycidyl dimethacrylatebased dental sealants. Meyer MT. Keimowitz AR.35(2 Pt 1):238-254. 2003. November 26.S.36(6):1202-1211.137(3):353-362. K. Belgium. J Chromatogr B Analyt Technol Biomed Life Sci 2002. Thurman EM. Munro IC. Ye X.

Fourth National Report on Human Exposure to Environmental Chemicals 33 . Kim SY. Endocrinology 2006.15:12811287. Welshons WV.147(6 Suppl):S56-69. Lordo RA.Environmental Phenols Volkel W. and nonylphenol at home and daycare. Chuang JC. An observational study of the potential exposures of preschool children to pentachlorophenol. Large effects from small exposures. Nagel SC. Dekant W. Low-dose in utero effects of xenoestrogens in mice and their relevance to humans: an analytical review of the literature. III. vom Saal FS.44(4):546-51. Hughes C. Biological monitoring of bisphenol a in a Korean population.113(8):926-33. Lee SM. Endocrine mechanisms mediating effects of bisphenol A at levels of human exposure.40(7):905-12. Csanady GA. bisphenol-A. Environ Health Perspect 2005. Yang M. et al. Metabolism and kinetics of bisphenol A in humans at low doses following oral administration. Environ Res 2007. Food Chem Toxicol 2002. Chem Res Toxicol 2002. Wilson NK. Morgan MK. An extensive new literature concerning low-dose effects of bisphenol A shows the need for a new risk assessment. Sheldon LS. Arch Environ Contam Toxicol 2003. Filser JG. Witorsch RJ. Colnot T. Chang SS. Kawamoto T. Jang JY.103(1):9-20. Vom Saal FS.

Disposition in humans has not been studied sufficiently. to shorter chain alkylphenol ethoxylates.200-. over 500.30-2.00 (. Indoor and to a lesser extent.50 (1.3.400 (...30 (1. 2000. see Data Analysis section) for Survey year 03-04 is 0.20-2. have demonstrated estrogenic effects particularly when injected at high doses in animals.600-1..40) * 03-04 03-04 03-04 .80 (1. pesticides. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.10) 1.200-.300 (<LOD-. fish) and drinking water. Commercial formulations of alkylphenol ethoxylates usually contain a mixture of oligomers and isomers.60-3.400 (.800-1.10 (1. the various alkylphenols have also been used as emulsifiers and modifiers in paints.10-2.10 (. altered estrus cycles and reproductive outcomes.40) 1. These high dose parenteral effects of 4-tert-octylphenol have included altered sex hormone levels and hypothalamicpituitary suppression. In the 1990s..900 (. In rats..30 (1. through sewage.60) .S.300-.40 (1. The alkylphenol ethoxylates enter the environment through human use of products containing them.20-2.00 (1. Bian et al.10) 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 .70 (1. and from contact with some personal care products and detergents.60-3.60-3. and to alkylphenoxycarboxylates.500 (.000 tons of alkylphenol ethoxylates were produced annually worldwide.369 (.60-3.300 (<LOD-. Urinary 4-tert-Octylphenol (4-[1.500-1. and through manufacturing waste streams (Warhurst.50) .600) 1. 2002).900 (..268-.600-1.500) . streams in 30 states (Kolpin et al.40) 2. 1997. population from the National Health and Nutrition Examination Survey.3-Tetramethylbutyl] phenol) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. altered neonatal sexual development. and was quickly eliminated from the blood (Certa et al.900 (. 1995.70 (1. several European nations banned the use of alkylphenol ethoxylates in domestic detergents and other uses.300 (<LOD-. 2006.40) 2. Survey Geometric mean (95% conf. an alkylphenol.389 (.50-3. Saito et al. leading to inhalation as another potential exposure route (Rudel et al.60) 1. During the 1980s and 1990s. including 4-tert-octylphenol..30) 1.g.40) 1. which may vary for some chemicals by year and by individual sample. 2003. orally administered 4-tert-octylphenol was well absorbed. Several alkylphenols. and some of their degradation products are toxic to aquatic life.50) 1. Laws et al.00 (. which are anionic surfactants used in detergents. 4-octylphenol monoethoxylate was detected in 43.80 (1. 140-66-9 General Information 4-tert-Octyphenol.20) 2.S.600-1.50-2. 34 Fourth National Report on Human Exposure to Environmental Chemicals . 2000. textiles.600) .90) 2. Human health effects from 4-tert-octylphenol or the corresponding octylphenol ethoxylates at low environmental doses or at biomonitored levels from low environmental exposures are unknown. The alkylphenols can bioaccumulate in some fish.Environmental Phenols 4-tert-Octylphenol CAS No.400 (.400) 1.50) 1.600) .20-2.500) 75th .600) . Blake and Boockfor.1..50) 1.30) 2.507) * < LOD . and some personal care products.20-2.300 (<LOD-. < LOD means less than the limit of detection.600-1. Ying et al.2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and impaired spermatogenesis (e.80) 2.500) . Octylphenols and nonylphenols can also enter the environment directly from manufacturing waste streams.500-1. Less frequently.300-.70 (1. Nonylphenol ethoxylates are more commonly used than octylphenol ethoxylates.60-3.900 (.30) 90th 1.. industrial cleaners.00) 1229 1288 03-04 03-04 03-04 * . and the polyethoxy chain may consist of up to 50 ethoxy units. and emulsifiers. In 1999-2000. Katsuda et al.300 (<LOD-. did not bioaccumulate.. impaired steroidogenesis.20) 314 715 1488 03-04 03-04 * * . 1996). Human exposure to alkylphenols and alkylphenol ethoxylates may occur through ingestion of contaminated foods (e.5% of 139 U.600-1.500) .299-. Alkylphenols also have been used as plasticizers and antioxidants in plastics and resins. 2002). testicular atrophy.90) 2.30 (1.10 (. 2004).900 (.477) .20-2.60) 613 652 1092 Limit of detection (LOD.20-2.357 (.60-3.70 (1.80 (1. outdoor air may have detectable levels of 4-tert-octylphenol and 4-tert-octylphenol monoethoxylates. They are biodegraded to the corresponding alkylphenol (octylphenol or nonylphenol).497) * .600-1.30 (.g.20 (1.50) . is used to manufacture alkylphenol ethoxylates.20) 1.30 (1.700-1.274-.

Tyl et al.630-1. (2008) showed that urinary levels of 4-tertoctyphenol were detectable in slightly greater than half of the participants of the U.349) * < LOD .68) 2.850 (. Finding measurable amounts of 4-tert-octylphenol in the urine does not mean that the levels of 4-tert-octylphenol cause an adverse health effect.570) . Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.02-4.33) 3.S.470) 75th .337-.11) 1. at lower or environmentally relevant doses (Blake et al.Environmental Phenols Myllymaki et al.435 (.410 (. population from the National Health and Nutrition Examination Survey.78) 1228 1286 03-04 03-04 03-04 * .73) 2.05-2. 2001). Nagao et al.78 (1. Sweeney et al.76 (2.18-4. 1999).11) 2. IARC and NTP have not rated octylphenol.420) .740 (.20 (1.500-1.03-6.620) .160-.67-2.300 (<LOD-.96-4.270 (.00) 1.550-1.24) 612 651 1091 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.S.62 (1.53-3. 2005. 4-tert-Octylphenol is not considered directly genotoxic.15) 1.400) .31 (1.33 (2..43) 1.276 (..450) . 2001.320 (<LOD-. Urinary 4-tert-Octylphenol (4-[1. In a small number of adult Japanese volunteers.65-3.. Survey Geometric mean (95% conf.280-.81 (1.910 (.620-1.450) 1.17 (.540-1. * 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 35 .890-2.41) . Biomonitoring Information Urinary levels of 4-tert-octyphenol reflect recent exposure. the urinary concentrations of 4-tert-octyphenol were near or below the detection limit (Inoue et al.610) .11-2.00) size 2514 Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th .43) 1.00 (.36-3.3-Tetramethylbutyl] phenol) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.730-1.170-.640-1.43-3.00) 2.25) 90th 1.860 (. 2004). interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.270-. or their corresponding ethoxylates with respect to human carcinogenicity. 2003.62 (1.207-.10-2.770 (.06 (2.03 (1.40-4.64 (.71) 2.22) .50 (2.460 (.40 (1. representative subsample of NHANES 2003-2004.62) .29) 2.470-1.470-1.384) * . nonylphenol.370 (<LOD-.78) 3. It is unclear if estrogenic or other effects occur in animals through oral dosing.25-2.31-2.269 (.260 (<LOD-. 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..00 (.00) 2.25) 2.199-. Kawaguchi et al.08) 1. Calafat et al.03 (1...270 (. Yoshida et al.14) 314 713 1487 03-04 03-04 * * .530) .85 (1. 2004.560) . 2000.68-2.60 (1.740 (.54) * 03-04 03-04 03-04 .59 (1.1.59) 1.3.380 (<LOD-.

Ferrell JM. Makino T. Bodman GJ. Maternal exposure to octylphenol suppresses ovine fetal follicle-stimulating hormone secretion.Environmental Phenols References Bian Q. Exposure of the U. and other organic wastewater contaminants in U. 1995. Endocrinology 2000. Two-generation reproduction study with para-tert-octylphenol in rats. Blake CA. Maekawa A. Yoshida M. Horie M. Chen J. Qian J. Toxicokinetics of p-tert-octylphenol in male Wistar rats. Maekawa A. Reproductive effects in male and female rats from neonatal exposure to p-octylphenol. Katsuda S. Katsuda S. Arch Toxicol 1996. Indoor Air 2004. Carey SA. Food Chem Toxicol 2006.S. Taya K. Raychoudhury SS. Takenaka A. Sakui N. Environ Int 2002. Kawaguchi M. Watanabe G. polybrominated diphenyl ethers. Ye X. Cooper RL. Seto H.207(1):59-68. Fail PA. Barber LB. Song L. Ito R. Inoue K. Warhurst AM. pesticides. Muller AM. Karjalainen M.14(5):325-332. et al. Onuki A. Williams B. Tyl RW. Takai N. Toppari J. Sweeney T. J Chromatogr B Analyt Technol Biomed Life Sci 2004. Yoshimura S. Saito I. Marr MC. Yoshida M. Phthalates. hormones. Chronic administration of the environmental pollutant 4-tert-octylphenol to adult male rats interferes with the secretion of luteinizing hormone.165(3):217-226. Certa H. Yoshimura Y.foe. Wong LY. Nicol L. Environ Sci Technol 2003. Taya K. Indoor air pollution by alkylphenols in Tokyo.S.pdf. Thurman EM. Toxicol Sci 2000.799(1):119-125. Needham LL. Izumi S. Brooks AN. Regul Toxicol Pharmacol 1999. Environ Sci Technol 2002. Anal Chim Acta 486:41-50. 1999-2000: a national reconnaissance.141(7):2667-2673. testis size. Watanabe G. Okada F. Paranko J. Nair-Menon JU. Environ Health Perspect 2008. et al. Available at URL: http:// www. Boockfor FR. McCoy GL. and testosterone. Kolpin DW. 2003. Zaugg SD. Toxicol Appl Pharmacol 2005. Estrogenic activity of octylphenol. prolactin. Nagao T. Rudel RA. Roche JF. Wiegand HJ. Meyer MT. Irreversible effects of neonatal exposure to p-tert-octylphenol on the reproductive tract in female rats.28(3):215-226. bisphenol A and methoxychlor in rats. and other endocrine-disrupting compounds in indoor air and dust. Kawaguchi M. Furlong ET. Seely JC.71(1-2):112-122. Toxicol Lett 2001. Saito Y. Reprod Toxicol 2004. Millette CF. Environmental fate of alkylphenols and alkylphenol ethoxylates--a review. Biol Reprod 1997. Ono H.44(8):1355-1361.36(6):1202-1211. Pharmaceuticals. Fedtke N.18(1):43-51. An environmental assessment of alkylphenol ethoxylates and alkylphenols. Xu L.121(1):21-33.folliclestimulating hormone. Effects of neonatal exposure to a high-dose p-tertoctylphenol on the male reproductive tract in rats. et al. Usumi K. 2/4/09 Ying GG. Wang X.uk/resource/reports/ethoxylates_alkylphenols. Boockfor FR. Brine DR.37(20):4543-53. Reprod Toxicol 2001. Bolt HM. nonylphenol. 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. et al. Measurement of 4-nonylphenol and 4-tert-octylphenol in human urine by column-switching liquid chromatography-mass spectrometry. Camann DE. Inoue K. Nakagomi M. population to bisphenol A and 4-tertiary-octylphenol: 2003-2004. Korn LR. Spengler JD.116(1):39-44. Myers CB. Kookana R.57(2):255-266.54(1):154-167. and sertoli cell number.15(6):683-692. Infantile 4-tert-octylphenol exposure transiently inhibits rat ovarian steroidogenesis and steroidogenic acute regulatory protein (StAR) expression.co. streams. Effects of 4-tert-octylphenol given in drinking water for 4 months on the male reproductive system of Fischer 344 rats. Myllymaki SA. The toxic effects of 4-tert-octylphenol on the reproductive system of male rats. Blake CA. 36 Fourth National Report on Human Exposure to Environmental Chemicals . Brody JG. Laws SC. Toxicol Appl Pharmacol 2000. Calafat AM. alkylphenols. Reidy JA.30(2 Pt 1):81-95. Haavisto TE.

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

9) 32.7 (28.3 (11.1-39.6 (12.0-213) 213 (160-272) 453 (263-1150) 260 (127-513) 358 (276-480) 612 651 1091 38 Fourth National Report on Human Exposure to Environmental Chemicals .4) 357 (225-456) 203 (87.4 (38.2) 9.2 (27.1) 9.3 (26.9) 75th 47.2) 12.1) 7.4’-Trichloro-2’-hydroxyphenyl ether) (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. interval) 13.6-37.4) 7.0-15.6-111) 33.4 (12. interval) 12.70-16.16 (6.4.4-19.21 (6.48-10.3 (8.94 (7.8-60. see Data Analysis section) for Survey year 03-04 is 2.3-67.20 (7.20-13.2-58.0-73.6) 10.9 (33.8 (21.1) 11.0 (8.1 (8.S.6 (30.6-14.2-14.4.6-65.0 (36. population from the National Health and Nutrition Examination Survey.60 (8.7 (9.3-15.9 (50.22-10.6 (10.8) 116 (39.6) 31.4’-Trichloro-2’-hydroxyphenyl ether) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.4) 90th 249 (188-304) 03-04 03-04 03-04 8.00-8.54 (8.6) 237 (175-294) 182 (138-217) 384 (294-506) 336 (225-480) 1228 1286 03-04 03-04 03-04 13.2) 13.2 (11.7 (14. Urinary Triclosan (2.9-61.1) 9. Survey Geometric mean (95% conf.5) 13.40-17.S.3) 47.40-11.45 (5.8-63.32-14.4) 75th 43.6-14.5) 20.8) 9.9) 8.29-12.30-14.11-11.1 (15.4-18.7) 123 (36.7 (11.1) 13.1 (45.38-18.6) 12.3-35.5) 11.1) 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 9.80 (5. population from the National Health and Nutrition Examination Survey.7-318) 224 (186-272) 236 (115-336) 356 (169-580) 385 (308-506) 314 713 1487 03-04 03-04 13.3-31.0-19.4 (32.Environmental Phenols Urinary Triclosan (2.4) 73.6) 90th 212 (172-241) 03-04 03-04 03-04 9.5) 66.4) 317 (231-433) 144 (96.45-10.60 (6.0-15.1) 50.48 (8.4) 25.5 (11.74 (5.92-12.82 (8.0) 65.0 (26.93 (7.20-10.20-11.7 (39.18 (5.5-86.10) 84.3.8) 7.2 (10.0) 49.4-163) 304 (134-566) 261 (198-317) 157 (113-380) 655 (310-890) 472 (406-522) 314 715 1488 03-04 03-04 16.2 (13.4) 51.1) 9.5-341) 245 (163-334) 597 (372-992) 450 (254-750) 461 (383-527) 613 652 1092 Limit of detection (LOD.8-112) 30.45-13.7) 10.4 (11.50-10.3) 10.6) 39.8) 14.8-85.0 (34.2-58.2 (37.8-127) 37.1) 9.0) 9.6-15.86-12.9) 7.1) 14.55 (4.3) 6.5-250) 574 (461-716) 380 (258-430) 1229 1288 03-04 03-04 03-04 14.9-236) 193 (90.90-10.50) 10.72-13. Survey Geometric mean (95% conf.9 (8.7) 292 (151-432) 132 (78.6 (9.2 (25.89-11.2-46.3 (9.00 (4.20 (7.43-13.9 (11.0 (11.10-9.5-14.6-20.6) 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.

Lyman FL. Am J Infect Control 1996. The oral retention and antiplaque efficacy of triclosan in human volunteers.69(20):1861-1873. Bhargava HN. 4. Disposition and excretion of Irgasan DP300 and its chlorinated derivatives in mice. Sandborgh-Englund G.524:241-247. Ishibashi H. Effects of nonylphenol and triclosan on production of plasma vitellogenin and testosterone in male South African clawed frogs (Xenopus laevis). Needham LL. Kaneshima H. Triclosan: applications and safety. Shiratsuchi H. Arch Environ Contam Toxicol 1988. Clapson DJ. Larson EL. Reidy JA. Urinary concentrations of triclosan in the U. et al.38(4):361370. Benson WH. Kolpin DW. Readman JW. Hirano M.28(9):1748-1751. Randomized trial of a hexachlorophene preparation and P-300 bacteriostatic soaps. Osachoff H. Food Chem Toxicol 2000. Williams PE. Watanabe N.38(2):64-71. Pilot study of urinary biomarkers of phytoestrogens. Pharmaceuticals. Anal Chim Acta 1004. Matsumura N. population: 2003-2004. Britton JA. Leonard PA. Environ Sci Technol 2002. Meyer MT. Teitelbaum SL.4’-trichloro-2’hydroxydiphenyl ether). Zaugg SD. Hong HC. Environ Health Perspect 2008. Williams FM. Developmental evaluation of a potential non-steroidal estrogen: triclosan. Wigmore H. Skirrow RC. Aranami K.116(3):303-307. Ye X. Foran CM. Levy SB. Consumer antibacterial soaps: effective or just risky? Clin Infect Dis 2007.80(3):217-227. Chemosphere 2007.66:1052-1056. et al. Pharmacokinetics of triclosan following oral ingestion in humans. Moss T. Calafat AM.83(1):84. Fourth National Report on Human Exposure to Environmental Chemicals 39 . Thurman EM. J Invest Dermatol 1976.S.S. The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development. streams. hormones. Okui T.4. Pinney SM. et al. Adolfsson-Erici M. Ebersole R. Wong LY.Environmental Phenols References Aiello AE. 1999-2000: a national reconnaissance. Odham G. et al. Gunderson MP.24(3):209-218. Aquat Toxicol 2006. Toxicology of 2. Biol Pharm Bull 2005. Ogawa H. Evidence of 2.23(5):579-583. Hernando MD.. Erratum in: Aquat Toxicol 2007. Windham G.7/2. Gomez MJ.45 Suppl 2:S137-S147. Environ Health Perspect 2007. Ekstrand J. Veldhoen N. Barber LB. Furia T. Aguera A. Fernandez-Alba AR. Bodey GP. Chelimo C. and phenols in girls.50(1-5):153-156. phthalates.67(4):532-537. Br J Clin Pharmacol 1987. Ferrer I. Katsura E. Nagao Y. Bennett ER. J Toxicol Environ Health A 2006. Mezcua M. Wolff MS.17(5):637-644. Percutaneous penetration and dermal metabolism of triclosan (2. Mar Environ Res 2000.8-dibenzodichloro-pdioxin as a photodegradation product of triclosan in water and wastewater samples. and other organic wastewater contaminants in U. Gilbert RJ. Kanetoshi A. Howes D. 4’-trichloro-2’-hydroxydiphenyl ether. Furlong ET. Photolytic degradation of triclosan in freshwater and seawater. IMS Ind Med Surg 1969.36(6):1202-1211.115:116-121.

60) 1.350) < LOD .91 (1.350 (.350-.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. bactericide.650) 1.30 (1.25 and 0.04) 1.53) 482 577 681 826 831 1125 99-00 01-02 99-00 01-02 * * * * .890-1.350 (.10 (<LOD-1.. 1997). Human exposure to PCP has become less common.350-. ingestion of contaminated food or water.350 (.76) . After absorption.00) 1.350-.350 (.350-.350 (.90 (1. After a single dose. the elimination half-life may be a week or more (Uhl et al. and it is used primarily as a preservative for wood to be used outdoors (e.350-.30) .350 (. hypertension. high dose exposure to PCP can induce a hypermetabolic state and excessive heat production as a result of uncoupling mitochondrial oxidative phosphorylation.45-2.58-2. which may vary for some chemicals by year and by individual sample.Fungicides Pentachlorophenol inhale it or absorb it through exposed skin.60) 1.350) 90th .350-2.01 (<LOD-1.350) < LOD .78) 1.30) 1.350) . To-Figueras et al.530) 1. PCP also may be eliminated in urine as a metabolite of hexachlorobenzene.590-1.350 (. 1986). 1979).350-.350) < LOD .350) < LOD . Human health effects from PCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. air.73 (1.350-.350 (. mollusicide.30) 1..40 (.70) 2. other polychlorinated benzenes.23 (.00 (. population from the National Health and Nutrition Examination Survey.58-2.33) .350) < LOD .980 (. utility poles and fence posts). and dermal contact with PCP-treated products.65 (.80) . water and sediments because of the large amounts that were produced and used historically.350-1.94 (1. Since 1984.53) 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 . are eliminated in the urine.67) 1.70) .860-2.350 (. 2002. herbicide.350) < LOD . 1976.350-. so it is relatively non-persistent.350 (.37) .990-2.890 (.83 (2. The parent compound and conjugates. PCP is distributed to most tissues and is not extensively metabolized.510-5.350) < LOD .500-2.18 (<LOD-1.680-1..350) < LOD .98 (1.47-5.350 (.32 (.510-3.350 (.65 (.30 (.5.350) < LOD .350-1.94 (1.650 (. Acute. < LOD means less than the limit of detection. Survey Geometric mean (95% conf.350-.350-.350-2.350) < LOD . PCP is degraded by sunlight and metabolized rapidly by microorganisms.350) < LOD .g. In the environment.390 (.48-2.350) < 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.10 (. and animals.770 (..10) 1. General population exposure to PCP may occur by inhalation of contaminated air. 40 Fourth National Report on Human Exposure to Environmental Chemicals .350-.350-1.76) 1. with repeated or chronic exposure.10) 1.350-. algaecide and insecticide.S.48 (.350 (.350-.350-.S.850-2. PCP use in the U.350) < LOD . along with small amounts of tetrachlorohydroquinone and conjugates.350) < LOD .350) < LOD .42) 973 1190 1021 1338 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .. PCP cannot be used on wood in residential or agricultural buildings.350-2.51) 1.350 (. has been restricted.350-.90) 1.08-3.350 (.350 (.00) 1.390 (.350 (.09) .350-.660 (.76) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * . PCP is absorbed rapidly and well by all exposure routes.33-2.350-2. and metabolic acidosis were observed in CAS No.350-.350-.90) 2.350-.00) 2. Kohli et al.42) 696 680 521 696 603 951 Limit of detection (LOD.350-.62 (.350 (.75) 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.37 (.50) 1.64) 1. Effects including hyperthermia.350) < LOD < LOD 75th .350) < LOD .30 (. PCP is eliminated over a few days (Braun et al.350 (.10 (1. PCP has been detected in soils. plants.960) 1.350 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.350-.990 (<LOD-2.630 (.350-.480-2. and possibly of lindane (IPCS.54-2.350-1.47-3.350-2. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.

children in the 1980’s.82 (1.06) 1.34 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. IARC has determined that pentachlorophenol is possibly carcinogenic to humans.35) 1.78) 1. and adversely affected thyroid function (U.590) < LOD .99) 482 577 681 825 831 1125 99-00 01-02 99-00 01-02 * * * * .67-3.560) < LOD .220-.35-2.06-3.360-.atsdr.320) < LOD ...67-2.40) 1.830) < LOD .08) 696 680 521 695 603 951 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.560-.510-.21 (.300 (.40) 1.09 (<LOD-2.710-1.90) 1. Death can result from seizures and cardiovascular collapse.30) 1.83 (1.06 (.78) 1.25) 1.S.S.260 (.00-1.6 and 14.25 (1. inhalation.290-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.490) < LOD .320) < LOD .75 (<LOD-2.950-1.25-2.Fungicides adults and children severely exposed to PCP through ingestion. 2000).25 (1.08 and 5. 1989).350) < LOD .67 (1. 1991).9 mg/L.340-. the median and 95th percentile urinary PCP levels were approximately three times lower than comparable values in German adults (2.36) .500-.67 (1.400 (.30-2.e. or skin absorption. 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.900-1. OSHA has established an occupational standard.800-1.69 (1.52 (<LOD-1..16 (.800) < LOD 1.94 (1.310) < LOD . and the FDA has established a standard for bottled water. 2004.780) < LOD .73 (1.75) 1.13 (.760 (. EPA has developed standards for PCP in drinking water and the environment.67 (1.25-2.67 (1.67 (1.11) 2.95) 3.590-1.52 (<LOD-1..84 (1.48-2. In animals.330-.82) 1.570 (.920 (.650 (.300 (.630 (.epa.gov/ toxpro2.250 (.850 (.S.29-3.610 (.950-1.57 (1.18) . 1995). 2003).16-1.30) 1.84) 1.780-1.990 (.40) 1. Among adults in the NHANES 1999-2000 subsample.560) < LOD ..370 (.10 (1.18 (1.55) 1.360 (. 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.380-.19) 2.300 (. respectively) (Seifert et al. The U. 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.S.94-3.94 (1. urinary PCP levels at the 95th percentile were approximately fivefold lower than 95th percentile values measured in a nonrandom subsample from NHANES III (1988-1994) participants (Hill et al.92) 1.40-2.35-2..430-.EPA.09-1. In NHANES 2001-2002 subsamples.57 (. In a small sample of U. 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.280) < LOD . population from the National Health and Nutrition Examination Survey.0 mg/L.30 (. 2003). respectively) (Becker et al. Urinary PCP levels at the 95th percentile in this Report are approximately half the corresponding 95th percentile values found in German adults evaluated in 1998 (Becker et al.500 (.290-.75) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .21-2.310-. carcinogenic.40) 1.S.26 (1.00-1.320 (.700-2.240-.84-4.220-.19) 2. Pentachlorophenol is not mutagenic or teratogenic.320) < LOD < LOD 75th .00) 1. Fourth National Report on Human Exposure to Environmental Chemicals 41 .650) 90th 1.56) 1. More information about external exposure (i.52 (1.430) < LOD .19) 2.290) < LOD .580-. environmental levels) and health effects is available from the U..40) 1.26 (1.55) 973 1190 1021 1337 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .cdc.270-. chronically administered high doses of PCP were hepatotoxic.html.52) 1.25-1.470 (.420) < LOD .51) 1. EPA at: http://www.gov/ pesticides/ and from ATSDR at: http://www.650 (.730) < LOD . van Raaij et al.510-.35) 1.270-. 1989).10-2.950-1.910-1.09) 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 .250 (..79) 1.19 (1.500-1.440 (.67-3. Survey Geometric mean (95% conf.

Phillips DL. Pesticide residues in urine of adults living in the United States: reference range concentrations.71:99108. Barrot C. International Programme on Chemical Safety (IPCS). Toxicology 1991: 67(1):107-16. Can J Biochem 1976. drinking water and indoor air. J Expo Anal Environ Epidemiol 2000. Rodamilans M. Braun WH. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. Environ Health Perspect 1997. Seiwert M. Fast DM. van den Berg KJ. Sala M. Needham LL. Needham LL. Helm D. Biomonitoring data can also help scientists plan and conduct research about PCP exposure and health effects. urine. Hill RH Jr.4:289296. Lindane. Kaus S. available at URL: http://www. Seiwert M. 2002. Metabolism of hexachlorobenzene in humans: association between serum levels and urinary metabolites in a highly exposed population. Seifert B. 4/21/09 Kohli J. Available at URL: h t t p : / / w w w.105(1):78-83. Arch Toxicol 1986. Environmental Protection Agency (U.58:182-186.18:475-481. U. Chenoweth MB. 11/30/2004. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. et al. Gregg M. Hill RH. hair. Cline RE. Head SL. References Becker K. The metabolism of higher chlorinated benzene isomers. Int J Hyg Environ Health 2003. Becker K. htm. Bragt PC. Notten WR.18(4):469-474. Arch Environ Contam Toxicol 1989. Otero R. 206:15-24.org/documents/jmpr/jmpmono/2002pr08. Krause C. et al. 4/21/09 van Raaij JA. Smith SJ. Safe A. Arch Environ Contam Toxicol 1989.S. Dev Toxicol Environ Sci 1979. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Blau GE. Shealy DB. Uhl S. house dust. Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats. Hill RH Jr. Holler JS.10:552-65. Engel R. To T. 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. Schulz C. Jones D. Santiago-Silva M. Pentachlorophenol measurements in body fluids of people in log homes and workplaces.54(3):203-208.S. The German Environmental Survey 1990/1992 (GerES II): reference concentrations of selected environmental pollutants in blood. Baker S. Seifert B. r e g u l a t i o n s . EPA). Schlatter C. PCP: Human Risk Characterization [online]. 42 Fourth National Report on Human Exposure to Environmental Chemicals . Pharmacokinetics of pentachlorophenol in man. Schulz C.Fungicides Finding a measurable amount of PCP in urine does not mean that the level of PCP causes an adverse health effect. Bailey SL. To-Figueras J. et al. The metabolism/ pharmacokinetics of pentachlorophenol in man and a comparison with the rat and monkey. Environ Res 1995.inchem. Schmid P. 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.

500-2. inhalational.496 (.00 (1.610-1. and sanitizers.450 (<LOD-.90) .00-2.390-.836) * .60-2.490 (<LOD-.20) 2.710) 3. OPP is efficiently absorbed from the gastrointestinal tract and through the skin. whereas SOPP is not volatile and is more water soluble.560-8.370-.480-1.88) 1.S.50) .00) < LOD .508 (.60 (1. 1998).02) 1. and it has limited water solubility.690) < LOD .402-.742) * .3 and 0.570-2.470 (<LOD-.S.770 (.490 (<LOD-.580-1. OPP is volatile. Fourth National Report on Human Exposure to Environmental Chemicals 43 .30 (1.696) * . OPP is still used as a disinfectant fungicide for industrial applications..600) < LOD 1.19 (.90) 1.509 (.14 (<LOD-3. are antimicrobial agents used as bacteriostats.40-2.33 (.570 (.76) 1. but OPP and SOPP are still used on pears and citrus (U.60 (1. EPA.28 (.40-5. fungicides.30-7.10 (1.850 (.600-1.490 (<LOD-.350-1.632) Selected percentiles ( 95% confidence interval) Sample 95th 2.610 (. which may vary for some chemicals by year and by individual sample.770 (. leaving the chemical residue OPP.890 (. SOPP is applied topically to the crop and then rinsed off.600) < LOD .10) 1.30) < LOD . in paints.552 (.34) 1.638) * .10 (1.570 (. 1989).Fungicides ortho-Phenylphenol CAS No.30-2.90 (1.50) 1.760-2. Survey Geometric mean (95% conf.17 (.389-.860) * 99-00 01-02 99-00 01-02 99-00 01-02 .600) < LOD 75th .590-2.40 (.00 (1.3. < LOD means less than the limit of detection.60-3.10) 2. 2002. 1998.498 (.80 (2. or 2-phenylphenol) and its water-soluble salt.386-. Both have been used in agriculture to control fungal and bacterial growth on stored crops.22) 2. Available evidence suggests that OPP does not accumulate in the body.90) .91) 973 1190 1018 1339 99-00 01-02 99-00 01-02 99-00 01-02 . and as a wood preservative.540-2.50 (1.880-2.420 (<LOD-.490 (<LOD-.10-2. Most agricultural food applications have been revoked.10) 1.23) 695 680 520 695 603 953 Limit of detection (LOD. formulate. OPP is considered to be moderately toxic after acute oral doses in animal studies.20 (1.85) 2.790) 2. or apply these chemicals may be more highly exposed than the general population. population from the National Health and Nutrition Examination Survey.630) < LOD .621) * .50) < LOD .00 (1.92 (. or oral routes from residential use and by ingesting treated food or food that was in contact with treated surfaces or equipment.450 (<LOD-. it was used in home sanitizers for surfaces.10) .950) < LOD .20) < LOD 1.50) < LOD .90) 2.497 (.370-.740 (. Timchalk et al.600) < LOD . Workers who manufacture.520 (. OPP was detected in 40 of 60 different canned beers at concentrations in the low parts per billion (Coelhan et al.00 (1.10) .EPA.970 (.433-.780) < LOD .493 (. 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. 2006).10-1.S.09) 2.20) < LOD 2.690-1.820 (. 2006).860 (. interval) .349-.50-2. however.567 (.30) < LOD 90th 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 .50 (1. 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.466 (.600-1.50-4.22 (.30) < LOD 1.389-. such as fruits and vegetables.890 (.60 (1.80-3.50 (1.750-2.364-..370-.410-. 90-43-7 General Information Ortho-phenylphenol (OPP. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Both chemicals degrade within hours to weeks in the environment (U.EPA.710-2.90 (1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. on ornamental plants and turfs.20-2.670) 2.640) < LOD . 2006).624) * .840-1. small amounts of OPP have been measured in human adipose tissue (Onstot and Stanley.30) 1.570-1.636) * . In the past.800-3.20-3.600-1.645) * . Estimated human intakes have been below recommended intake limits (U.07 (.23) 480 577 681 827 830 1125 99-00 01-02 99-00 01-02 .61) 2.80) 1.03) 1. General population exposure can occur via dermal.27 (.490 (<LOD-.40-7.50) < LOD . sodium ortho-phenylphenate (SOPP).450 (<LOD-.890) 1.40-5.830 (. Cnubben et al.00) .20 (1.10) .570-.80) 1.20 (.00) .930 (.28-3..550-1.50-3. 2006).

46) < LOD 1.02 (.0) 1.93) 1.550-. 2002.96) 1.75 (1.08-1. but no neurologic.38) 973 1190 1018 1338 99-00 01-02 99-00 01-02 99-00 01-02 . CDC..270-.86 (1.43-2.09-3.81) 1..650-1.33) 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 .38) 1.580) < LOD .410 (<LOD-.11 (.88-4.96 (1.69 (1. In high dose animal studies. U. Murata et al.91 (1.05-2.29) 1.750-2.38) 2.17) 2.791) * . 2000.75 (1.17) * 99-00 01-02 99-00 01-02 99-00 01-02 .320 (<LOD-. Volunteers exposed to 0.460-. IARC has classified SOPP as a possible human carcinogen.11 (. OPP or SOPP produced carcinomas of the bladder only after phase II detoxification pathways were saturated.27) < LOD .810) < LOD .380 (.560-2.343 (.09-6.558) Selected percentiles ( 95% confidence interval) Sample 95th 2. Bomhard et al.00 (.301-. 2005). or.51-3.62) .91) 695 680 520 694 603 953 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.508) * .61 (. less likely.93 (1.33) .403-.Fungicides anemia.61 (1.09 (1.970) 1.455-.440 (.580-1. reproductive..361-.810-1.291-.08-2.900-1.47) .980 (<LOD-1.12-2.00 (1.S.470 (<LOD-.480-.06-5.514 (.21 (.gov/pesticides/. Brusick.29) 1.59) .570) < LOD 1.. Biomonitoring studies on levels of OPP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of OPP than are found in the general population. population from the National Health and Nutrition Examination Survey.33-2.43 (1.64 (2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.311-. 2002. 1999.990) < LOD .93) . These metabolites may induce carcinogenicity via nongenotoxic regenerative hyperplasia of the bladder (Appel.24-2.43-2.58) 2.670 (.EPA at: http:// www.S.840 (.30) 480 577 681 826 830 1125 99-00 01-02 99-00 01-02 .28 (2.600-1. Ito et al.12) < LOD 1.910 (<LOD-1..59) 1.11-1.470) < LOD .860 (.89 (1. population in the subsamples from NHANES 1999-2000 and 2001-2002 (CDC.410 (<LOD-.750 (.473) * . leading to production of two metabolites.910 (.53) 1.780-14.78 (2. Detectable levels were seen in over half the U.910-1.07) 2.360 (<LOD-.. 1999. 2005).620-1.61 (2.780 (. 2002).11) 4. 44 Fourth National Report on Human Exposure to Environmental Chemicals .28 (<LOD-4. 1992.06-4.510-..01) 1.11) < LOD 90th 1. 1984. Zhao et al.40-13.568) * .38-3. Additional information is available from U.04-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. Pathak and Roy.496 (.770-2.17 (. OPP was not found to be mutagenic.96-4..74 (1.08) 1. 1993. interval) .550 (. Finding a measurable amount of OPP in urine does not mean that the level of OPP causes an adverse health effect.670) < LOD .666) * . Smith et al. or developmental toxicity was observed (Bomhard et al.97 (2.21-2.84 (1.382 (.S.EPA 2006).560) < LOD 75th .484) * .epa. 1997.06 (1.52 (.353-. 2005.32) 1.4) 3.248-..500) < LOD .656) * .13) 1.25-6.453 (.940-2.24-2. Urinary ortho-Phenylphenol (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.444 (.550) < LOD .20) < LOD 3.880-1.670 (. Biomonitoring Information Urinary OPP levels reflect recent exposure.S.96 (1.. 1984. and it has classified OPP as not classifiable with respect to human carcinogenicity.329-.420 (<LOD-.640-1.18) 2.26) 1.590) * .950) < LOD . 1986).690 (. Nakagawa et al. 1998.43) 3. Dermally applied OPP was not carcinogenic in a 2-year experimental study in animals (NTP.385 (.800-1.510 (<LOD-.610) < LOD 1.44 (1. ortho-phenylhydroquinone and ortho-phenylbenzoquinone. by possible genotoxic mechanisms (Hagiwara et al.17 (.900) < LOD .980 (.32) 3.31) < LOD .620-1.860 (.750 (. U.S.EPA 2006). Kwok et al.93) .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.21) 1.420 (<LOD-.

Cano M. Fourth National Report on Human Exposure to Environmental Chemicals 45 .epa. March 1986. 4/9/09. Shibata M.286(2):309-319. Buchholz BA. EPA). Sangha GK. rat and man. IARC Sci Publ 1984. Arch Toxicol 2000.35(2 Pt 1):198-208. Brusick D. food additives and natural products as promoters in rat urinary bladder carcinogenesis.. Ito N.54(16):5731-5735. Roberts AL. Available at URL: http://ntp. Crit Rev Toxicol 2002. Eadon G. Hakkert BC.703(12):97-104. The pharmacokinetics and metabolism of 14C/13C-labeled ortho-phenylphenol formation following dermal application to human volunteers. Environmental Protection Agency (U.pdf. U.EPA). J Chromatogr B Biomed Sci Appl 1997. Biochem Pharmacol 1992. 90-43-7) in Swiss CD-1 mice (dermal studies).43(7):14311437. Freyberger A. Urinary physiologic and chemical metabolic effects on the urothelial cytotoxicity and potential DNA adducts of o-phenylphenol in male rats. Selim S. Kawanishi S. Available at URL: http://www. Inoue S.gov/oppsrrd1/REDs/ phenylphenol_red. Comparative metabolism of orthophenylphenol in mouse.S. Hagiwara A. Nakagawa Y.pdf. Dose-dependent binding of ortho-phenylphenol to protein but not DNA in the urinary bladder of male F344 rats. Bartels MJ. J Agric Food Chem 2002. National Toxicology Program (NTP). Cnubben NH. Food Chem Toxicol 1984. Identification of SARA compounds in adipose tissue.niehs. Zhao S.45(5):460-481. Timchalk C. Timchalk C. Bomhard EM. 4/13/09 Onstot JD. Toxicol Appl Pharmacol 1999. Detection and characterization of DNA adducts formed from metabolites of the fungicide ortho-phenylphenol.32(6):551-625. Determination and levels of the biocide ortho-phenylphenol in canned beers from different countries. Narang A. Carcinogenesis 1999. Office of Toxic Substances. Hum Exp Toxicol 1998. Atlanta (GA). U. Hirose M.Fungicides References Appel KE. Vogel JS. 1989. Christenson WR. Meuling WJ. Comparative in vitro-in vivo percutaneous penetration of the fungicide ortho-phenylphenol. Analysis of genotoxicity and the carcinogenic mode of action for ortho-phenylphenol. Roy D.20(5):851-857. Bartels MJ. Coelhan M. Ito N. Bartels MJ. Fukushima S. J Agric Food Chem 2006. Tayama S. van de Sandt JJ.S. Environmental Protection Agency (U. Richter M. Brzak KA. St John MK. NTP Technical report on the toxicology and carcinogenesis studies of ortho-phenylphenol (CAS No. Stanley JS. Eastmond DA. Glas K. Christenson WR. Oxidative damage to cellular and isolated DNA by metabolites of a fungicide orthophenylphenol. Third National Report on Human Exposure to Environmental Chemicals. Mutat Res 1993. EPA-560/5-89-003. et al. Smith RA.gov/ntp/htdocs/LT_ rpts/tr301.150(2):402-413.22(10):809-814.nih. McNett DA. Hagiwara A.17(8):411-417. Sangha G. Gierthy J. Bromig KH.159(1):18-24.50(11):3351-3358. Pathak DN. 2005. Long-term toxicity and carcinogenicity study of sodium o-phenylphenate in B6C3F1 mice. Regul Toxicol Pharmacol 2002. Kwok ES. Brendler-Schwaab SY.28(6):579594. Leser KH. Moore GA. Bormett GA. Bartels MJ.S.(56):399-407. Turteltaub KW. Arnold LL. O-phenylphenol and its sodium and potassium salts: a toxicological assessment. Toxicol Appl Pharmacol 1998. Drugs. Xenobiotica 1998. Shirai T. Imaida K. Centers for Disease Control and Prevention (CDC). The carcinogenicity of the biocide ortho-phenylphenol.74(2):61-71. Fukushima S. In vivo genotoxicity of sodium orthophenylphenol: phenylbenzoquinone is one of the DNA-binding metabolite(s) of sodium ortho-phenylphenol. July 28. Determination of orthophenylphenol in human urine by gas chromatography-mass spectrometry. Environ Mol Mutagen 2005. Reregistration Eligibility Decision (RED) for 2-phenylphenol and salts (Orthophenylphenol or OPP). 2006. Elliott GR. Mendrala AL. Murata M.S. Moriya K. et al. Relationship between metabolism and cytotoxicity of ortho-phenylphenol in isolated rat hepatocytes. Moldeus P. Herbold BA. EPA 739 R-06004.

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

1998). 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. 2-hydroxyethyl-6-methylaniline. mainly corn.0 μg/L (Curwin et al. Additional information about external exposure (i. in some species and at doses above maximum tolerated doses. nasal epithelia. 2006). but it has produced testicular atrophy. the latter which may account for some observed effects (Coleman et al.EPA 2000.5 to 449 μg/L were measured in commercial applicators within 24 hours following its application (Barr et al. Acetochlor degrades in water to acetochlor sulfonic acid and acetochlor oxanilic acid.S. but other pathways occur. 2005).S. 1989.. Human health effects from acetochlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Jefferies et al.. and it is unlikely to be genotoxic at relevant doses (Ashby et al.EPA. and neurologic movement abnormalities (U. Acetochlor has low acute toxicity. Acetochlor is not mutagenic. NTP and IARC do not have ratings regarding human carcinogenicity. Kolpin et al... 2005).S. 2000. this metabolite is not a marker of exposure to most plant metabolites or environmental degradates. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. and hydroxymethyl ethyl aniline (U. remains in soils for up to 3 months. animals have demonstrated tumors of the lung. 2006). including one that produces 2-methyl-6ethylaniline and its reactive metabolite.S.. 2000).EPA. However. a major pathway for acetochlor metabolism involves mercapturate conjugation. and has been detected in watersheds of agricultural lands (Battaglin et al. U.S. 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. Acetochlor mercapturate was measured in the urine of farmers actively spraying the pesticide and the geometric mean was 8. Finding measurable amounts of acetochlor mercapturate in the urine does not mean that the levels of acetochlor mercapturate cause an adverse health effect.Herbicides Acetochlor Biomonitoring Information Urinary levels of acetochlor mercapturate reflect recent exposure. environmental levels) is available from U..EPA considers acetochlor likely to be carcinogenic in humans.e.EPA.gov/ pesticides/. Estimated human intakes of acetochlor have been below recommended limits (U. Hladik et al. Urinary levels of acetochlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample (CDC.epa... which are often more prevalent in the environment. and thyroid (U. It is absorbed by plants and inhibits plant protein synthesis.. 1996). General population exposure to acetochlor may occur through diet or drinking water.S. Acetochlor is moderately toxic to fish and honey bees. Acetochlor has not shown developmental or fetal toxicity in chronic animal studies. 2007). 2006). 2000. People exposed to acetochlor will excrete acetochlor mercapturate in their urine.. 2006). renal injury. Acetochlor is microbiologically degraded. Urinary acetochlor mercapturate levels of 0. 2005. Feng and Wratten. CAS No. 2000. however. Davison et al. Fourth National Report on Human Exposure to Environmental Chemicals 47 . 1994. In animals. Plants can degrade acetochlor to 2-ethyl-6-methylaniline. EPA at: http://www.

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

Deddens JA. Camann DE. Hsiao JJ. Rose RL. sulfonamide.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. Davison KL. and other herbicides in rivers. EPA 738-R-00-009.pdf.S. Barr JR. Hein MJ.248(2-3):123-133.EPA): http://pmep. Comparative metabolism and elimination of acetanilide compounds by rat. Available at URL: http://www. Linhart SM.html. Hodgson E. Environmental Protection Agency (U. Thurman EM.108(12):1151-1157. Larsen GL. Chem Res Toxicol 1998. Dialkylquinonimines validated as in vivo metabolites of alachlor. Burkhardt MR. Reynolds SJ. Ward EM. 5/30/06 U.edu/profiles/herbgrowthreg/24-d-butylate/acetochlor/acetochlor_pet_100. Barr DB. Xenobiotica 1994. Roberts AL. Kolpin DW.111(5):749-756. J Expo Anal Environ Epidemiol 2005.S. epa. Volume 65. Report of the Food Quality Protection Act (FQPA) Tolerance Reassessment Progress and Risk Management Decision (TRED) for Acetochlor. pages 3682-3690. Hines CJ. Peter CJ. EPA). Wilson AG. Coleman S. Centers for Disease Control and Prevention (CDC).S. Furlong ET.Herbicides References Ashby J. Barr DB. Curwin BD.37(4):10881093. Third National Report on Human Exposure to Environmental Chemicals. imidazolinone. Kinney PL.S. et al. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Atlanta (GA).15(6):500-508.15(9):702-735. et al.24(10):1003-1012. 5/30/06. Tinwell H. et al.cce. Sci Total Environ 2000. Hladik ML. Alavanja MC. Kier L. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Barr DB. 2005. Olsson AO.11(4):353359.17(6):559-566. Federal Register: January 24. Linderman R. Lefevre PA. Occurrence of sulfonylurea. Fourth National Report on Human Exposure to Environmental Chemicals 49 . Environ Sci Technol 2005. Wratten SJ. Andrews HF. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. EPA). Striley CA. Available at URL(non U. Heederik D. acetochlor. Acetochlor (Harness) Pesticide Petition Filing 1/00. J Expo Sci Environ Epidemiol 2007. Green T. Hum Exp Toxicol 1996. reservoirs and ground water in the Midwestern United States. March 2006. Sci Total Environ 2000. 2000.cornell. Bravo R. J Agri Food Chem 1989. 1998. U. Whyatt RM. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. Environ Health Perspect 2003. Evaluation of the potential carcinogenicity and genetic toxicity to humans of the herbicide acetochlor.39(17):6561-6574. Jefferies PR. Feng PCC.S. Feil VJ. Environ Health Perspect 2000. Battaglin WA. Quistad GB.gov/oppsrrd1/reregistration/REDs/acetochlor_tred. and metolachlor herbicides in rats. Sanderson WT. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Number 15. Identification of human urinary metabolites of acetochlor in exposed herbicide applicators by high performance liquid chromatography-tandem mass spectrometry. Environmental Protection Agency (U. Casida JE.

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

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

In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. Hum Exp Toxicol. An evaluation of the carcinogenic potential of the herbicide alachlor to man. who. Kinney PL. 2/27/09 U. Bull Environ Contam Toxicol 1996. Occurrence of sulfonylurea. Atlanta (GA). Chem Res Toxicol 1998. 86. Whyatt RM. sulfonamide. Available at URL: http://www. Available at URL: http://water. Barr DB.111(5):749-756. Background document for development of WHO Guidelines for Drinking-water Quality.11(4):353359. Shealy DB. Life Sci 1988. Identification of a major human urinary metabolite of alachlor by LC-MS/MS. 1998. 98-4245 (by Barbash JE. Feil VJ. Deddens JA. Wilson AG. Casida JE. Shoemaker DA. Sci Total Environ 2000. Sci Total Environ 2000. 1999. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water.56(9):883-889.usgs.epa. EPA 738R-98-020. Linhart SM.htm. Thake DC. and metolachlor herbicides in rats. Environ Sci Technol 2005. Jefferies PR. Andrews HF. Am Ind Hyg Assoc J 1995. Hladik ML. Brown MA.18(6):363-391.39(17):6561-6574. Gilliom RJ). Feng PCC.S.S. Geological Survey (USGS). Tolos W. No. Quantitative assessment of the mutagenic potential of environmental degradative products of alachlor. 1992-2001. Lau H.43(25):2087-94.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Martens MA. Larsen GL.S.S.inchem. 1997.gov/oppsrrd1/ REDs/0063. 2003. Kier LD. Hines CJ.php. revised February 15. Supplemental Technical Information (available on-line only). Camann DE. Sacramento. U. Erratum in: Life Sci 1989. Casida JE. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay. Thurman EM. 2007. Brown KK.24(10):1003-1012. 1996.248(2-3):123-133. WHO/ FAO Data Sheets on Pesticides. Barr JR. Biagini R. Striley CA. Third National Report on Human Exposure to Environmental Chemicals. Quistad GB. 2/27/00 52 Fourth National Report on Human Exposure to Environmental Chemicals .44(18):1325.395(2-3):159-171. Available at URL: http://www. Geneva. Casida JE. Geological Survey (USGS). Centers for Disease Control and Prevention (CDC). Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Hines CJ. Environ Health Perspect 2003. MacKenzie B. acetochlor. Tessier DM. Biagini RE. Circular 1291. 4/2/09 U. Henningsen G. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. World Health Organization. 2005.248(2-3):115-122. Dialkylquinonimines validated as in vivo metabolites of alachlor. Kolpin DW. et al. J Agri Food Chem 1989. Hull RD. Dialkylquinoneimine metabolites of chloroacetanilide herbicides induce sister chromatid exchanges in cultured human lymphocytes. Hill AB. Davison KL. DNA adduct formation by alachlor metabolites. et al. Hill RH Jr. Sanderson WT. 2/27/09 Jefferies PR. Clark JM. World Health Organization (WHO). Burkhardt MR. Finding minimal herbicide concentrations in ground water? Try looking for their degradates. J Ag Food Chem 1995. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Available at URL: http:// www.37(4):10881093. Furlong ET. International Programme on Chemical Safety (IPCS). Roberts AL. ALACHLOR.43(9):2504-2512.pdf.int/water_sanitation_health/dwq/chemicals/en/alachlor.47(6):503-517. Heydens WF. EPA). Mutat Res.org/documents/pds/pds/pest86_e. March 2006. Kolpin DW. imidazolinone.56(6):853-859.pdf. Peter CJ. Biological monitoring of commercial pesticide applicators for urine metabolites of the herbicide alachlor. Ann Occup Hyg 2003. Wratten SJ. December 1998. Reregistration Eligibility Decision (RED) Alachlor. Alachlor in Drinking-water. Thelin GP. California. and other herbicides in rivers. Quistad GB. Kimmel EC. Hsiao JJ. reservoirs and ground water in the Midwestern United States. Comparative metabolism and elimination of acetanilide compounds by rat.Herbicides References Battaglin WA. 1999. Driskell WJ. Xenobiotica 1994. Environmental Protection Agency (U.

metabolized. 1990). Catenacci et al. Atrazine does not bioaccumulate. Atrazine may alter the sexual development of frogs at environmental levels (Gammon et al.. 2003a). The dealkylated chloroatrazine metabolites.791 and 0. Survey Geometric mean (95% conf. 1982.EPA. 1996. Fourth National Report on Human Exposure to Environmental Chemicals 53 . 2005. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. resulting in atrazine mercapturate and N-dealkylation products (IPCS. U. Related chlorotriazine herbicides include simazine. Applicators of atrazine may be exposed dermally and by inhalation.Herbicides Atrazine CAS No. As a result. Atrazine has limited water solubility and is not tightly bound to soil. which may vary for some chemicals by year and by individual sample. 2003b). In regions where atrazine is used. More than 70 million pounds have been applied annually in recent years. all of which act by inhibiting plant photosynthesis. but estimates of seasonal intakes from drinking water in a small number of communities have exceeded the recommended limits (U. Hayes et al.S.. 1912-24-9 General Information Atrazine is a widely used chlorotriazine herbicide that acts against broadleaf and grassy weeds. and then eliminated in the urine over a few days (Bradway et al.S.S. atrazine use has progressively been restricted in an effort to reduce surface and ground water contamination... In soils. it is one of the more commonly detected pesticides in surface and ground waters (USGS. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.and post-emergence to agricultural land for crops such as corn and sorghum. Atrazine is well absorbed orally.S. population from the National Health and Nutrition Examination Survey. For the general population. 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. and cyanazine. glutathione conjugation appeared to be the major route of biotransformation. Atrazine was first registered as an herbicide in 1958.3. but it is leachable into ground and surface waters. propazine.. Bacteria and plants can metabolize atrazine to hydroxyatrazine.EPA. Atrazine mercapturate products accounted for a major proportion of human urinary metabolites (Lucas et al. In animals and humans. 2007). U. atrazine is slowly degraded to dealkylated products. 1993). Atrazine is applied pre. 2002. 1993. drinking water is an infrequent source of atrazine exposure. Urinary Atrazine mercapturate Metabolite of Atrazine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.. with about 75% of corn cropland receiving treatment. < LOD means less than the limit of detection. Timchalk et al. It has little toxicity in birds and moderate toxicity in some fish and aquatic invertebrates. 2003b). which have half-lives of several months.EPA. It is also used as a non-selective herbicide.

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

Cooper RL. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats.115(8):1254-1260. 3/11/09 Arcury TA.. No. In a study of 60 farm worker children. Pubertal development in female Wistar rats following exposure to propazine and atrazine biotransformation by-products. Extrom PC. Lioy PJ. Lucas AD.org/documents/pds/pds/pest82_e. McElroy WK. In a small number of field workers. Toxicol Sci 2000.html. Eldridge JC. et al. Sanborn JR. Determination of urinary residue levels of the N-dealkyl metabolites of triazine herbicides. J Toxicol Environ Health 1994. Gammon DW. Seiber JN. Schmid J. urinary concentrations ranged from 5-1756 μg/L (Lucas et al.. Chen H. Vonk A. Available at URL: http:// www. Bradway DE. 2007). Breckenridge CB. 2005). Eberly LE. Cooper RL. Short-term effects of chlorotriazines on estrus in female Sprague-Dawley and Fischer 344 rats. In small studies of Maryland residents in 19951996 (MacIntosh et al. Barr DB. Determination of atrazine metabolites in human urine: Fourth National Report on Human Exposure to Environmental Chemicals 55 . Reynolds SJ. 2001 [online]. Curwin BD. Stevens JT.. WHO/ FAO Data Sheets on Pesticides. Simpkins JW. Collins A.htm. 2005). Pfeifer KF. atrazine mercapturate was infrequently detected at the detection limit of < 1 μg/L. Environ Health Perspect 2007. Quandt SA. Deddens JA. Freeman NC. ATRAZINE. Atlanta (GA). Goodrow MH.47(6):503-517. Heederik D. Steroids 1999. Stoker TE. 1993).cdc. Ferrell JM. demasculinized frogs after exposure to the herbicide atrazine at low ecologically relevant doses. Barr DB. levels of atrazine mercapturate were generally not detectable (CDC. the urinary geometric mean levels for herbicide applicators in Ohio and Wisconsin were about 6 μg/L (Hines et al.2 μg/L in 15 farmers studied several days after spraying the pesticide (Curwin et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Third National Report on Human Exposure to Environmental Chemicals. diamino-S-chlorotriazine and hydroxyatrazine. Through immunoassay atrazine equivalents (detected mostly as atrazine mercapturate). Sanderson WT. Toxicol Lett 1993. J Toxicol Environ Health 1994. et al. Hermaphroditic. 82. Agency for Toxic Substances and Disease Registry (ATSDR). Shoemaker DA. 1996. Ann Occup Hyg 2003. Pest Manag Sci 2005.64(9):672-678. Tyrey L. Eldridge JC. Toxicol Sci 2000. Bersani M. 2001). Ferioli A. 2003. 2000). In the NHANES 2001-2002 subsample. Toxicological profile for atrazine.Herbicides Biomonitoring Information Urinary levels of atrazine mercapturate reflect recent exposure. J Expo Anal Environ Epidemiol 2005. International Programme on Chemical Safety (IPCS). Lee M. 3/11/09 Laws SC. Hines CJ. Finding measurable amounts of atrazine mercapturate in urine does not mean that the levels of atrazine mercapturate cause an adverse health effect.43(2):155-167. The mammary tumor response in triazine-treated female rats: a thresholdmediated interaction with strain and species-specific reproductive senescence. Moseman RF. Biagini RE.15(6):500-508.gov/toxprofiles/tp153. Clayton CA. The effects of atrazine on female wistar rats: an evaluation of the protocol for assessing pubertal development and thyroid function. et al. 2005. J Agric Food Chem 1982. Wetzel LT. et al. Maroni M. Aldous CN.inchem. A risk assessment of atrazine use in California: human health and ecological aspects. Stoker TE. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample..76(1):190-200. Cottica D. atrazine was detected in only four children (Arcury et al. Laws SC. Striley CA. Cooper RL. Jones AD.. Gillis JH.61(4):331-355. Blewett C. Mendoza M.109(6):583-590. Noriega N. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models.53(2):297-307. et al. Barbieri F. Brown KK. Atrazine disrupts the hypothalamic control of pituitary-ovarian function. Available at URL: http://www. Grzywacz JG. Proc Natl Acad Sci USA 2002. Fleenor-Heyser DG. Stoker TE. Geneva. Gillis JH. Tapia J. Catenacci G. World Health Organization.58(2):366-376. The geometric mean of urinary atrazine mercapturate was 1. Biological monitoring of human exposure to atrazine. Saiz SG. References Adgate JL. Ferrell JM.99(8):5476-5480. Centers for Disease Control and Prevention (CDC). Toxicol Sci 2003. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa. Carr WC Jr.. Goldman JM. Perry et al.43(2):155-167. Wetzel LT.atsdr.69(2):217-222. Hein MJ. Hayes TB. et al.30(2):244-247. 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.. Stuart AA. Pesticide urinary metabolite levels of children in eastern North Carolina farmworker households. Barr DB. 1999) and 83 Minnesota children with multiple urine collections during 1997 (Adgate et al. Environ Health Perspect 2001.

pdf. Hammerstrom KA. Toxicol Sci 2002. Osborne DW. Timchalk C. Toxicol Appl Pharmacol 2004. Urinary biomarkers of atrazine exposure among farm pesticide applicators.gov/nawqa/pnsp/pubs/ circ1291/supporting_info. The effect of atrazine on puberty in male Wistar rats: an evaluation in the protocol for the assessment of pubertal development and thyroid function. Toxicol Sci 2000. Tortorelli J. Perry M. EPA). Exposure parameters necessary for delayed puberty and mammary gland development in LongEvans rats exposed in utero to atrazine. Guidici DL. 0062.9(5):494-501.S. Ann Epidemiol 2000. Stoker TE.10(7):479. Pesticides and Toxic Substances. Cooper RL.Herbicides development of a biomarker of exposure. Chem Res Toxicol 1993.php.S. van den Berg M. MacIntosh DL.epa. J Toxicol Environ Health A 1999. May 2003a. revised February 15. Environmental Protection Agency (U. A longitudinal investigation of selected pesticide metabolites in urine. 6/1/09 U.27(6):599612. March 2006. Kastl PE. Washington (DC). Guidici DL.S.usgs. Dagenhart D. J Expo Anal Environ Epidemiol 1999. 3/11/09 U. Environmental Protection Agency (U. Determination of the effect of tridiphane on the pharmacokinetics of [14C]-atrazine following oral administration to male Fischer 344 rats. Fenton SE. Available at URL: http://water. The effects of atrazine metabolites on puberty and thyroid function in the male Wistar rat. Pesticides in the Nation’s Streams and Ground Water. Needham LL. Toxicology 1990. Singzoni B. Supplemental Technical Information (available on-line only). Sanderson JT. Wood C. U. Rayner JL.gov/scipoly/sap/meetings/2003/june/ finaljune2002telconfreport. EPA).61(1):27-40. Circular 1291.195(1):23-34. Stoker TE. Sathiakumar N. Geological Survey (USGS). Christiani D. 2007. Case No. Induction and inhibition of aromatase (CYP19) activity by various classes of pesticides in H295R human adrenocortical carcinoma cells. Cooper RL. Interim Reregistration Eligibility Decision For Atrazine. Langvardt PW. Available at URL: http://www. Ryan PB. Boerma J. 1992-2001. Laws SC. Delzell E. Crit Rev Toxicol 1997. White paper on potential developmental effects of atrazine on amphibians.gov/oppsrrd1/REDs/ atrazine_ired. Breckenridge CB. Dryzga MD.S. Office of Prevention.pdf. Environmental Fate and Effects Division. A risk characterization for atrazine: oncogenicity profile.S. Toxicol Appl Pharmacol 2002. EPA Office of Pesticide Programs. The Quality of Our Nation’s Waters. Available at URL: http://www. A review of epidemiologic studies of triazine herbicides and cancer. 4/2/09 56 Fourth National Report on Human Exposure to Environmental Chemicals .epa. Stevens JT. Wetzel L. Lansbergen GW. Laws SC. 2003b.56(2):69-109.67(2):198-206.182(1):44-54.58(1):50-59.6(1):107-116.

these herbicides can enhance plant growth.4-D can be applied either as an aqueous salt or as oil-soluble esters. It was first registered with U.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 . but at higher levels they are herbicidal. 1977).400) < LOD ..910) < LOD . see Data Analysis section) for Survey years 99-00 and 01-02 are 0.27 (1.20 (. myotonia.660) 1. 1974.930-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.210 (<LOD-.670-1.910) 1.690 (.43) 1. At low levels. General population exposure to 2.540-.760 (.4-Dichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. 2.210-. by direct contact with agricultural and residential areas after applications.680-1.S. agricultural.440-1.30 (<LOD-2.S. 2004).EPA.66) < LOD 1.4-D is eliminated mostly unchanged in the urine with an elimination half-life ranging from 10 to 33 hours (Arnold et al.260 (<LOD-. MCPA.420) < LOD .4-dichlorophenoxyacetic acid (2.4-D) controls broadleaf weeds in residential.610 (.32 (1.350) < LOD < LOD < LOD .930 (.80) 1.22) 962 1135 1015 1278 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD . 94-75-7 General Information Widely used throughout the United States. 4-D.S.420-. Fourth National Report on Human Exposure to Environmental Chemicals 57 . Human health effects from 2.EPA in 1948.60) 1. and aquatic environments. Recent estimates of chronic intakes of 2.560-1.03) 695 659 520 668 589 892 Limit of detection (LOD.370-.4-D were used in the U.740 (. the chlorophenoxy herbicide 2.EPA.2.410) < LOD . 2.24 (.10 (<LOD-1.952 and 0.690-1.4-D is rapidly absorbed via oral and inhalation routes. It is poorly bound in soils. 2.S.49) 477 546 677 797 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .00-2.10) < LOD 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.310) < LOD .4-D have been below recommended intake limits (U. 2007).330 (..20 (<LOD-1.27-2.960-1.16) < LOD . which may vary for some chemicals by year and by individual sample.4-Dichlorophenoxyacetic Acid CAS No.05-2.70) 1. in 2001 (U.610-. and it is often mixed with other chlorophenoxy acid herbicides (such as dicamba.890 (.13) < LOD . Survey Geometric mean (95% conf.250 (<LOD-.310 (. renal and hepatic injury. population from the National Health and Nutrition Examination Survey. hypotension. 1989. It is not well absorbed through the skin. Sauerhoff et al.910) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .55 (1.08) < LOD . Similar to other chlorophenoxy herbicides.320) 90th . it acts as a plant growth hormone.490 (.4-D or exposed for prolonged periods. with a half-life of several days to several weeks.48) < LOD 1.40) 1. Kohli et al.22) < LOD .21) 1.230 (<LOD-. It is rarely detected in ground waters (USGS. dizziness.730 (.51 (1.690 (. and by consuming food or drinking water contaminated with 2. Once absorbed. nausea..27 (.10 (<LOD-1. abdominal pain.250 (<LOD-. and mecoprop). < LOD means less than the limit of detection.S.810-1. headache.4-D has low acute toxicity. and delayed Urinary 2.07 (.490) < LOD < LOD < LOD .230-.4-D may occur during residential applications.890) < LOD .690 (. although dermal exposure may be significant for herbicide manufacturing plant workers exposed to high concentrations of 2.550-1. 2.4-D at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2005).560-. Intentional overdoses and unintentional high dose exposures to chlorophenoxy acid herbicides have resulted in weakness.02-1. Acid and salt forms are much less toxic to fish and aquatic invertebrates than the ester forms. As much as 62 million pounds of 2.Herbicides 2.

1995). 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. 1992)..470) < LOD . Hill et al. IPCS. population from the National Health and Nutrition Examination Survey.4-D was not found to be genotoxic or carcinogenic in animal studies (Garabrant and Philbert. or teratogenic effects in chronic rodent studies (Charles et al.670 (<LOD-1.380) < LOD . 2005. 1995.670 (.780) . Kutz et al. 1996. eyes. IOM. Average post-application urinary levels of 2.32 (<LOD-2.29) 477 546 677 796 823 1070 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD .780) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .340-.610-. with the exposure to chlorophenoxy herbicides as defoliants or contaminated herbicides. 2006.520-. 2004).560-.S.490 (. 2002.890) < LOD 1. It is unclear whether these associations are related to the chlorophenoxy herbicides. 2005).640 (. Pearce and McLean.Herbicides neuropathy (Bradberry et al.410 (<LOD-.24) 1. 1985. U. 2001. such as soft tissue sarcoma and non-Hodgkin’s lymphoma.480 (.EPA.S. 1989). 2003.4-D production plant workers and a few forestry workers spraying 2. other exposures.13 (.S.810-1.19) .440 (. or to contaminants in the herbicide formulations (specifically 2.790) < LOD .7. 58 Fourth National Report on Human Exposure to Environmental Chemicals . In previous samples of the U. CDC. 2005).550-. 2.EPA at: http://www. urinary 2..14 (. Survey Geometric mean (95% conf.780 (.330-..920) < LOD 1.27-1.410) < LOD 1..08 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Frank et al.720 (.40) 695 659 520 667 589 892 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.39) < LOD 1. Acute high doses administered to laboratory animals produced ataxia. 2005).4-Dichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.660) < LOD .08 (.16) 1.EPA.73) .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 .35) < LOD . liver. Kolmodin-Hedman and Erne. 2005.780-1. Post-application levels in farmers and home gardeners were dependent on Urinary 2.570) < LOD .660 (. 1996.560-.56) .680) < LOD .13 (.4-D reflect recent exposure. The acid and salt forms of 2.S. Knopp et al.4-D are eye irritants. 2.980) < LOD 1.EPA. developmental.S.4-D does not have significant reproductive.270-.S.890-1.17 (.390) < LOD < LOD < LOD .410) < LOD < LOD < LOD .26) 962 1135 1015 1277 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .620-. 1996.670 (. U.gov/pesticides/..790) 1.380-.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..270 (<LOD-. IPCS. IPCS. 2. Biomonitoring Information Urinary levels of 2.380 (<LOD-.610-. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. in small samples of children (Hill et al.3.850) < LOD . 2005). 2002.S.930-1..350 (<LOD-.820-1. 2000).740 (. and of adults and children (Baker et al.4-D had urinary levels several hundred to several thousand times higher than the 95th percentiles of the NHANES subsamples (CDC.590 (<LOD-1.990-1. Epidemiological studies have reported associations of several types of cancer.590 (<LOD-1. 1980.410) 90th . and evidence of histological injury to the kidneys. 2005.. adrenals and gonads (NTP. U. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 1.08 (.700 (.810-1.. 2005.41 (1.epa. 1994).8-tetrachlorodibenzo-pdioxin) (Garabrant and Philbert.380 (<LOD-. myotonia. population (Hill et al.05) .4-D levels were detectable in less than a quarter of the individuals studied.340 (.EPA 2005). U.580-.. Additional information is available from U. thyroid.

and the use of protective clothing or equipment (Arbuckle et al. TOX-63: TOXICITY REPORT CURVES. Veterans and Agent Orange: update 2002. Brody D. Board on Health Promotion and Disease Prevention. Gregg M. Tables. Ripley BD.inchem. Occup Environ Med 1994.. Solomon KR. Mandel et al. 3/17/09 Knopp D. Honeycutt R. TOX-63 Peroxisone Project (2. Beasley VR. Developmental toxicity studies in rats and rabbits on 2.60(1):121-131. Hein MJ. Garabrant DH. geometric mean urinary levels of 2.4-D). Arch Toxicol Suppl 1980. 2005 Charles JM. Available at URL: http://ntp. Finding a measurable amount of 2. Selected pesticide residues and metabolites in urine from a survey of the U. Kohli JD. Cook BT.4.4-D): exposure and urinary excretion.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. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Curwin BD.4-Dichlorophenoxyacetic Acid). International Programme on Chemical Safety-INCHEM (IPCS). Ritter L. Centers for Disease Control and Prevention (CDC). 2005). Biomonitoring studies of 2. Reynolds SJ.S.4-D.4-dichlorophenoxyacetic acid and its forms. the amount of pesticide applied. Murphy RS. Philbert MA.nih. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature. van Ravenzwaay B. Bus JS.php?record_id=10603. Kolmodin-Hedman B. Available at URL: http:// www. Review of 2. Forestry workers involved in aerial application of 2. Arch Environ Contam Toxicol 1985. Baker S. References Arbuckle TE.51(3):152-159. Sirons G J.4:97-100. Campbell RA. Atlanta (GA). Mandel JS. general population. Vet Hum Toxicol 1989. Baker SE. Xenobiotica 1974. To T. Scand J Work Environ Health 2005. Pesticides residues in food: 1996 evaluations Part II Toxicology. Wilson RD.4:427-435.edu/catalog. Hanley TR Jr. Frank R..4-dichlorophenoxyacetic acid in the chemical industry: results of a five year biological monitoring study. Khanna RN.4-D and 2.4-dichlorophenoxyacetic acid (2. Baker BA.4-dichlorophenoxyacetic acid in man. J Expo Anal Environ Epidemiol 2005 Nov. Scand J Work Environ Health 2005. other family members had levels ranging only slightly higher than the 95th percentile levels in NHANES 1999-2000 and 2001-2002 subsamples (CDC. Estimation of occupational exposure to phenoxy acids (2. Sircar KP. Erne K. J Expo Anal Environ Epidemiol 2000. Washington (DC): National Academies Press.18(4):469-474. 2006. Shealy DB. Carter-Pokras OD. Updated March 7. Fast DM. et al. Sanderson WT. Tandon JS.4-D in urine does not mean that the level of the 2. Third National Report on Human Exposure to Environmental Chemicals. J Toxicol Environ Health 1992.nap. cfm?objectid=06FF8DA6-E5A1-90CD-3F26562CEC5CDDE5.15(6):500-508. 3/17/09 Institute of Medicine (IOM). Chapman P. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry.htm. Environ Res 1995. Biomonitoring of herbicides in Ontario farm applicators. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Biomonitoring for farm families in the farm family exposure study.Herbicides the time since application. Needham LL. Driskell WJ. Bailey SL.4 dichlorophenoxyacetic acid (2. Smith SJ. Stephenson GR. Heederik D.71(2):99-108. Holler JS. Beeson MD. 2005).10(6 Pt 2):789-798. Pesticide residues in urine of adults living in the United States: reference range concentrations..27(1):23-38. 2003. Gupta BN. Cole DC. 914.gov/index. Head SL. Available at URL: http:// www.37(2):277-291. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.. the number of acres to which it was applied (Curwin et al. Exposure of homeowners and bystanders to 2. 3/17/09 Fourth National Report on Human Exposure to Environmental Chemicals 59 . Needham LL. et al.4-D than levels found in the general population. Dichlorophenoxyacetic acid. Barr DB. Barr DB. Absorption and excretion of 2.31(2):121-125.4-D will result in an adverse health effect.4-. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. Harris SA. 1992).31 Suppl 1:98-104.4-dichlorophenoxyacetic acid (2. Arnold EK.4:318-321. In farm families. et al.4-D were highest in the farmers who applied the 2.31 Suppl 1:90-97. National Toxicology Program (NTP). Assessment of exposure to 2. Survival and Growth Curves from NTP Toxicity Studies. 2005. Kutz FW. Harris et al. Hill RH Jr. Toxicol Sci 2001.4-D) epidemiology and toxicology. Arch Environ Contam Toxicol 1989. Alexander BH.5-T).niehs.32(4):233-257. Hill RH Jr. 2. Dhar MM. Acquavella JF. 2005. J Environ Sci Health B 1992. Crit Rev Toxicol 2002.org/documents/jmpr/jmpmono/v96pr04.

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

S. People exposed to metolachlor will excrete metolachlor mercapturate in their urine.EPA. 2000. 1995.epa. (2003) showed that 2. and field workers may have significant exposures via this route. 2005.7 μg/L in the urine of farmers after they had sprayed metolachlor (Curwin et al. 1989.2% of a small reference population had detectable metolachlor equivalents by immunoassay in their urine. formulators. and eliminated in urine and feces over two to three days (WHO. Hladik et al. General population exposure may occur through the consumption of contaminated food or drinking water. Metolachlor did not show developmental or reproductive toxicity in chronic animal studies.EPA. 2007. In animal studies. Urinary levels of metolachlor mercapturate were generally not detectable in the NHANES 2001-2002 subsample. Metolachlor is well absorbed dermally. 1995).. EPA at: http://www. 2003). soybeans. Salivation. Biomonitoring Information CAS No. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 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.. WHO. and convulsions were observed at lethal doses in animal studies. It is absorbed by plants and inhibits plant protein synthesis.EPA considers metolachlor to be a possible human carcinogen. 1998). Occasionally in the past.EPA.. Davison et al. Human health effects from metolachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown. metolachlor was quickly absorbed after dermal or oral doses. 1999. and on non-crop land for general weed control. EPA. WHO.S. 1995). Finding measurable amounts of metolachlor mercapturate in the urine does not mean that the levels of metolachlor mercapturate cause an adverse health effect. Metolachlor or its degradates can leach from soils and have been detected in watersheds of agricultural land. but another metabolic pathway can produce 2-methyl-6-ethylaniline and its reactive metabolite which may account for observed effects (Coleman et al. This metabolite is not a marker of exposure to either plant metabolites or environmental degradates of metolachlor which can be present in the environment. 2005). 1994. lacrimation. The geometric mean metolachlor mercapturate was 4. Feng and Wratten. sorghum and other crops. 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. Hines et al. 1995). Metolachlor shows little potential to bioaccumulate but is moderately toxic to fish. in both ground and surface waters (Battaglin et al. and it was not mutagenic in mammalian cells (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.. 2007. though the 95th percentile for males was 0. whereas 60% of applicators had detectable amounts.200 μg/L (CDC.S. NTP and IARC do not have ratings regarding human carcinogenicity. In animals. mercapturate conjugates were the predominant metabolites. Jefferies et al. Additional information is Urinary levels of metolachlor mercapturate reflect recent exposure. including corn.. Metolachlor has low potential for acute toxicity (U.Herbicides Metolachlor available from U.S.S. 2003). Kolpin et al.S. 2003). USGS. Fourth National Report on Human Exposure to Environmental Chemicals 61 . so applicators.. 2000. metolachlor levels in water have exceeded lifetime human health advisory levels (U.gov/pesticides/. Gilliom.. 2005). Estimated human intakes have been below recommended limits (U. U.

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

Comparative metabolism and elimination of acetanilide compounds by rat. U. R. Thelin GP. Background document for development of WHO Guidelines for Drinking-water Quality. Xenobiotica 1994. streams and groundwater. In vitro transformation of chloroacetanilide herbicides by rat liver enzymes: A comparative study of metolachlor and alachlor. revised February 15. Environmental Protection Agency (U. Brown KK. Burkhardt MR. Alavanja MC. Gillion. Atlanta (GA).15(6):500-508. EPA 738R-95-006. The Quality of Our Nation’s Waters Pesticides in the Nation’s Streams and Ground Water. Environ Sci Technol 2007. 1992-2001. Occurrence of sulfonylurea. Available at URL: http://water. Available at URL: http://www. Jefferies PR.who. Sacramento. Contemporary-use pesticides in personal air samples during pregnancy and blood samples at delivery among urban minority mothers and newborns. Circular 1291. Geological Survey (USGS). usgs.pdf.gov/nawqa/pnsp/pubs/circ1291/ supporting_info. Wratten SJ. J Agri Food Chem 1989. Dialkylquinonimines validated as in vivo metabolites of alachlor. EPA). Striley CA. 6/1/09 Whyatt RM. and other herbicides in rivers. Feng PCC. Hein MJ. March 2006. et al. Barr JR. 2003. Barr DB.248(2-3):123-133. 2005. 2007. Sanderson WT. Environ Health Perspect 2000. Camann DE. Linhart SM.41:3409-3414. Coleman S. Sci Total Environ 2000. Environ Health Perspect 2003. Thurman EM. Kolpin DW.S.47(6):503-517.24(10):1003-1012. and metolachlor herbicides in rats. Reregistration Eligibility Decision (RED) Metolachlor. Pesticides in U. 98-4245 (by Barbash JE.S. Rose RL. Furlong ET. Kinney PL. World Health Organization (WHO).248(2-3):115-122. Peter CJ. Reynolds SJ. Biagini RE. 3/27/09 Fourth National Report on Human Exposure to Environmental Chemicals 63 . April 1995.Herbicides References Battaglin WA. Barr DB.pdf. 1999. 4/2/09 U. Available at URL: http://water. et al.39(17):6561-6574. Metolachlor in Drinkingwater.S. 3/26/09 U. Quistad GB. Roberts AL.gov/nawqa/pnsp/pubs/files/051507. Third National Report on Human Exposure to Environmental Chemicals. Ann Occup Hyg 2003. sulfonamide. Larsen GL. Centers for Disease Control and Prevention (CDC).usgs. Water-Resources Investigations Report: Distribution of Major Herbicides in Ground Water of the United States Water Resource Investigations Report No. Feil VJ. Heederik D. Hodgson E. Urinary and hand wipe pesticide levels among farmers and nonfarmers in Iowa.html. 1998. Chem Res Toxicol 1998. Biological monitoring for selected herbicide biomarkers in the urine of exposed custom applicators: application of mixed-effect models. Finding minimal herbicide concentrations in ground water? Try looking for their degradates.php. Available at URL: http://water. Deddens JA.ESTfeature_gilliom.gov/nawqa/ pnsp/pubs/wrir984245/text. acetochlor.usgs. Linderman R. Sci Total Environ 2000. Casida JE. Shoemaker DA. J Expo Anal Environ Epidemiol 2005.S. Hladik ML.epa.S. Davison KL. Supplemental Technical Information (available on-line only).gov/oppsrrd1/ REDs/0001. Available at URL: http://www. imidazolinone. reservoirs and ground water in the Midwestern United States. Gilliom RJ). Environ Sci Technol 2005.pdf 3/30/09 Hines CJ. Comparative metabolism of chloroacetamide herbicides and selected metabolites in human and rat liver microsomes. Ward EM.int/water_sanitation_health/dwq/chemicals/ metolachlor. Geological Survey (USGS). California. Are neutral chloroacetamide herbicide degradates of potential environmental concern? Analysis and occurrence in the upper Chesapeake Bay.11(4):353359. Hsiao JJ.108(12):1151-1157. Andrews HF. Curwin BD. Kolpin DW.37(4):10881093.111(5):749-756.

. Although 2. 2004).4.4.5-T) is a chlorophenoxy acid herbicide that is no longer registered for use in the United States.5-T is eliminated mostly unchanged in the urine.5-Trichlorophenoxyacetic Acid CAS No.4..4.5-T in soil varies with conditions. Mohammad and St. such as soft tissue sarcoma and non-Hodgkin’s lymphoma. Human health effects from 2.4. < LOD means less than the limit of detection. dizziness..5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. At low levels. population from the National Health and Nutrition Examination Survey. 2007). but higher levels are herbicidal. Teratogenic and developmental effects have been reported in studies of multiple rodent strains treated with high doses of technical grade 2. with an elimination half-life of approximately 19 hours (Arnold et al. 93-76-5 General Information 2.4.g. myotonia. Kohli et al. Once absorbed into the body.5-Trichlorophenoxyacetic acid Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and delayed neuropathy (Bradberry et al. Omer. with the exposure to chlorophenoxy herbicides as defoliants Urinary 2. Ester forms of 2.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey Geometric mean (95% conf. Chlorophenoxy herbicides act as plant growth hormones. ranging from several weeks to many months.4. 64 Fourth National Report on Human Exposure to Environmental Chemicals .3.1. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2538 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 831 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 701 531 957 Limit of detection (LOD. 2.5-T was once applied as either an aqueous salt or as an oil-soluble ester. Given the commercial unavailability of 2. which may vary for some chemicals by year and by individual sample.8-tetrachlorodibenzo-p-dioxin (TCDD) led to the discontinuation of 2. see Data Analysis section) for Survey years 99-00 and 01-02 are 1. hypotension.5-T degrades to 2.5-trichlorophenol and other degradates.4. nausea. 2.4. abdominal pain. Agent Orange).4-D were used as defoliants in the Vietnam War (e.2 and 0. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness. Epidemiological studies have reported associations of several types of cancer.5T is rapidly absorbed via oral and inhalation routes. 1974).4. 1986.4.5-T and 2.5-T has been rarely detected in ground waters (USGS. Nelson et al.4.4.5-T use as a herbicide in 1985.5-T (Holson et al.4. it is not well absorbed through the skin. 2.4. 1992).4.. 1989. 2. and concern about contamination with 2.5-Trichlorophenoxyacetic acid (2.Herbicides 2. The half-life of 2. the general population is unlikely to be exposed to it. 1992.. headache. renal and hepatic injury.7. these herbicides can enhance plant growth.S.5-T.

IPCS.5-T were generally below the limit of detection.4.EPA at: http://www.5-T measured after a day of exposure in a few asymptomatic herbicide applicators were 35. Mean urinary levels of 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1814 2537 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 430 580 618 830 766 1127 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 891 1192 923 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 652 679 483 700 531 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. U.5-T also were below the limit of detection (Kutz et al. Additional information is available from U..4.4. Biomonitoring Information Urinary levels of 2. 1992). population from the National Health and Nutrition Examination Survey. 2.S.5-T itself is not mutagenic.4.4. Urinary 2. 2005. Pearce and McLean. similar to results of NHANES II (19761980). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.4. 1996. Fourth National Report on Human Exposure to Environmental Chemicals 65 . 2004).7. Finding a measurable amount of 2. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. urinary levels of 2.8-tetrachlorodibenzop-dioxin) (Garabrant and Philbert. IOM. In the NHANES 1999-2000 and 2001-2002 subsamples (CDC.S.5-T than levels found in the general population.4. It is unclear whether these associations are related to the chlorophenoxy herbicides.5-T reflect recent exposure.gov/pesticides/.000 times higher than the detection limit for the NHANES 2001-2002 data (Kolmodin-Hedman and Erne.4.epa. 1980). or to contaminants in the herbicide formulations (specifically 2.5-T does not mean that the level will result in an adverse health effect.5-Trichlorophenoxyacetic acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.S.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. Survey Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2005). Biomonitoring studies on 2. 2003.3.EPA.4. other exposures. 2002.Herbicides or contaminated herbicides. in which urinary levels of 2.

Scand J Work Environ Health 2005. Dhar MM. Holson JF. Centers for Disease Control and Prevention (CDC).4. Brody D. et al. Sircar KP.Herbicides References Arnold EK. Available at URL: http:// www. Fundam Appl Toxicol 1992.4. et al. Selected pesticide residues and metabolites in urine from a survey of the U. Proudfoot AT.4.5-T). 2003. The pharmacokinetics of chlorinated phenoxy acid herbicides: a literature.19(2):286-297. Philbert MA.php?record_id=10603.4.5-trichlorophenoxy acetic acid in man. Tandon JS.inchem. LaBorde JB. Khanna RN.S. Beasley VR. Nelson CJ. J Toxicol Environ Health 1992. Third National Report on Human Exposure to Environmental Chemicals. Arch Int Pharmacodyn Ther 1974.8(5):551-60.org/documents/jmpr/jmpmono/v96pr04. Developmental toxicity of 2. Pearce N.htm.4-D and 2. Pesticides residues in food: 1996 evaluations Part II Toxicology.19(2):298-306. Behavioral and developmental effects in rats following in utero exposure to 2. Veterans and Agent Orange: update 2002.31 Suppl 1:1825. Gaylor DW. Gupta BN. Murphy RS. Atlanta (GA). gov/oppbead1/pestsales/01pestsales/market_estimates2001.5-t mixture. Absorption and excretion of 2.4-D/2.epa. Sheehan DM. general population. Cook BT. Poisoning due to chlorophenoxy herbicides. Neurobehav Toxicol Teratol 1986. Bradberry SM. I. Toxicol Rev 2004.S. McLean D. 210:250-255.5-T). Board on Health Promotion and Disease Prevention. Available at URL: http://www.5-trichlorophenoxyacetic acid (2. Washington (DC): National Academies Press. Vet Hum Toxicol 1989. 2004. LaBorde JB. Arch Toxicol Suppl 1980.2000 and 2001 market estimates. Committee to Review the Health Effects in Vietnam Veterans of Exposure to Herbicides (Fourth Biennial Update. 914.nap.4. Crit Rev Toxicol 2002. Office of Prevention Pesticides and Toxic Substances.5-trichlorophenoxyacetic acid (2. Gaines TB. Environmental Protection Agency (U. Pesticide industry sales and usage .31(2):121-125. 3/17/09 Kohli JD. 3/17/09 66 Fourth National Report on Human Exposure to Environmental Chemicals .4. May. Dichlorophenoxyacetic acid. Garabrant DH.EPA).4:318-21. II. Kutz FW.23(2):65-73. Multireplicated dose-response studies in four inbred strains and one outbred stock of mice. Holson JF.S. Multireplicated dose-response studies with technical and analytical grades of 2. Washington (DC): U.32(4):233-257. McCallum WF. St Omer VE.4. Developmental toxicity of 2.4. Kolmodin-Hedman B. Available at URL: http:// www. Agricultural exposures and non-Hodgkin’s lymphoma.5-T). Erne K.pdf.4-D) epidemiology and toxicology.edu/catalog.4-. Vale JA. 2.EPA. Carter-Pokras OD. Gaines TB. Fundam Appl Toxicol 1992.5-T in four-way outcross mice. 2005. International Programme on Chemical Safety-INCHEM (IPCS). Mohammad FK. S. Estimation of occupational exposure to phenoxy acids (2. Wolff GL. Review of 2. U. 3/17/09 Institute of Medicine (IOM). Nelson CJ.37(2):277-91. discussion 5-7.4-dichlorophenoxyacetic acid (2.

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

Carbamate Insecticides

Carbofuran

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 827 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1340

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

* * * * * *

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

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

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

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

696 680 521 696 603 953

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

68

Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

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

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

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

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

Selected percentiles
( 95% confidence interval)

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

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

482 578 681 826 831 1125

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

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

973 1190 1021 1339

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

* * * * * *

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

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

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

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

696 680 521 695 603 953

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

Fourth National Report on Human Exposure to Environmental Chemicals

69

Carbamate Insecticides

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

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Carbamate Insecticides

Propoxur

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

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

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Carbamate Insecticides

Urinary 2-Isopropoxyphenol
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2503

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 820 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1325

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

* * * * * *

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

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

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

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

664 677 500 696 585 931

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Carbamate Insecticides

Urinary 2-Isopropoxyphenol (creatinine corrected)
Metabolite of Propoxur

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 1917 2502

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

years 99-00 01-02

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * * * *

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

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

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

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

456 574 655 819 806 1109

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

936 1178 981 1324

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

* * * * * *

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

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

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

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

664 677 500 695 585 931

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

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Carbamate Insecticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

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

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

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

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

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

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

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

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

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

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Organochlorine Pesticides

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

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Fourth National Report on Human Exposure to Environmental Chemicals

Organochlorine Pesticides

Aldrin

CAS No. 309-00-02

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

Dieldrin

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

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

Selected percentiles
( 95% confidence interval)

Sample 95th < LOD < LOD size 2275 1946

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

years 01-02 03-04

50th < LOD < LOD < LOD < LOD

75th < LOD < LOD

90th

* *

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

756 588 1519 1358

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

* * * *

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

< LOD < LOD < LOD < LOD

1057 946 1218 1000

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

* * * * * *

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

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

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

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

559 456 512 485 1045 881

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

Fourth National Report on Human Exposure to Environmental Chemicals

77

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

1) 15.100-.8-19.1 (13.147 (.086-.1-16.190) .112-.075) < LOD .069) < LOD < LOD .170) .8) 14. Survey years 01-02 03-04 Geometric mean (95% conf.089 (.124) .6) 9.058) < LOD .1-24.202) 539 456 484 487 980 885 < LOD means less than the limit of detection for the lipid adjusted serum level.090 (.055 (.1) 14.093) .7 (15.4 (12.0) 21.100) .054-. Fourth National Report on Human Exposure to Environmental Chemicals 79 .242) .80 (<LOD-10.7 (<LOD-15.190) .1) 10.4) 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 8.098 (.4) 539 456 484 487 980 885 Limits of detection (LOD.140 (.1-18.S.110) .7) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD 9.5 (<LOD-11.9 (12.150 (.080) .8.139 (.138) .090-.6) 16.9-23.180) .50 (8.053 (<LOD-.5-17. which may vary for some chemicals by year and by individual sample.070) .8-25.130) .7-22.070 (<LOD-.9 (14.077-.110-.120 (.4) 21.4) 95th 20.150 (.3 (18.2) 14.8) 15.088-.077 (.160) .4) 19.049-.30 (8.120 (. 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.139 (.064 (.109-. 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 .160 (.100 (.080-.060) .9-38.3 (14.2) 15.062-.6 (15.4) < LOD < LOD 16.8 (18.149) .090-.7 (14.056-. 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 9.147) 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 .102 (.130-.9 (13.4 (12. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.090 (<LOD-.8-17. < LOD means less than the limit of detection.120 (.2) 12.084-.130-.090-. population from the National Health and Nutrition Examination Survey.109 (.182) 716 587 1443 1365 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD .4-17.80-10.0 (10.059 (.100) .110 (.5) 21.8-24.096-.062 (.8) < LOD 8.40-9.120) .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.1) 15.110) .070-.158) .073-.108-.063-.113 (.109-.4-18.048 (<LOD-.90) 90th 15.10 (<LOD-16.5 and 7.100-.40-10.9 (13.138 (.7) 15.117) < LOD .50) 15.30 (8.9-22. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.101) .116) .8 (11.100-.062 (.140-.5-17.1) 20.3-21.080 (.180) .6 (14.7-19.S.120-.80-9.60-10.130 (. population from the National Health and Nutrition Examination Survey.0 (10.0-21. which may vary for some chemicals by year and by individual sample.6-24.1-19.5) 15.00-14.3 (19.083-.110 (. see Data Analysis section) for survey years 01-02 and 03-04 are 10.6-24.0-25.130) . Survey years 01-02 03-04 Geometric mean (95% conf.140) .5) 19.9 (12.3 (13.70 (7.2) 11.0 (15.0 (11.4) 20.6-33.112) 95th .103 (.110 (.1 (18.4) 14.3 (18.130-.6 (15.1) 13.177) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD .1) < LOD 9.2-15.5-15.160 (.00 (8.130) .5 (16.6) 19.2) Sample size 2159 1952 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD 10.064) 90th .8 (9.0) < LOD 9.8-17.054-.103 (.0) 19.054-.

15. Environ Health Perspect 1995. Fernandez MG. Toxicological profile for aldrin/dieldrin [online]. 80 Fourth National Report on Human Exposure to Environmental Chemicals .inchem. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. 6/1/09 Ward EM. Environmental Health Criteria 91. Academic Press. Anantharam V.usgs. Aldrin and Dieldrin [online]. Chemosphere 2004. In Hayes WJ. Teta MJ. Organochlorine exposure and risk of breast cancer.htm. 4/21/09 Jorgenson JL. International Programme on Chemical Safety (IPCS). Toxicol Lett 1992. Turner W.352:1816-1820.26:701-719.103(Suppl 7):113-122.Organochlorine Pesticides in the NHANES 2001-2002 and 2003-2004 subsamples (Edwards and Priestly 1994).fda. Part A 2000. Mann D.html. Roy ML. Priestly BG. Narahashi T. Daniel SE.org/documents/ehc/ ehc/ehc91. toxicology. Patterson DG Jr. Jr and Laws ER. 4/21/09 Bates MN. Vol. Handbook of Pesticide Toxicology. Cox. Reprod Toxicol 2000. September 2002. Available at URL: http://pubs. Ellis H. The E-SCREEN assay as a tool to identify estrogens: an update on estrogenic environmental pollutants. and lymphocyte sister chromatid exchange. Six high-priority organochlorine pesticides. Chung KL.54:1431-1443. Li AA. Basit A. Available at URL: http://www.9:1357-1367. Mumtaz MM. Environ Health Perspect 2001. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. Rosellini RA. Facca A. Mink PJ. VT. J Toxicol Environ Health 1989. et al. 4/21/09 Hoyer AP. Kanthasamy A. Kitzazwa M.91(1):122-126. United States Geological Survey (USGS). plasma dieldrin. 731-915. David VL. Sanchez-Ramos J. Buckland SJ. Pesticides in the Nation’s Stream and Ground Water. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Demographic and seasonal influences on human serum pesticide residue levels. either singly or in combination. Hartvig HB. McIntosh LJ.14:95-102. Sonnenschein C.59:229-234. et al. and epidemiology in the United States.cfsan. bioaccumulation. Evaluation of epidemiologic and animal data associating pesticides with Parkinson’s disease. Available at URL: http://www. Ginsburg KS.html.47:1059-1087. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Stehr-Green. Kanthasamy AG. 1989. Smith AG. Carlson JN. Finley B. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. No:429-436. Andersen A. J Toxicol Environ Health. J Occup Environ Med 2005. Exp Neurol 1998. Jr. References Agency for Toxic Substances and Disease Registry (ATSDR). Aldrin and dieldrin: A review of research on their production environmental deposition and fate.gov/toxprofiles/ tp1. Needham LL.cdc. Dieldrin-induced neurotoxicity: relevance to Parkinson’s disease pathogenesis.gov/ circ/2005/1291/. Edwards JW. Serrano FO. Soto AM. Revised Feb. August 2008. Chapin RE. 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. Patterson DG Jr. Organochlorine insecticides in substantia nigra in Parkinson’s disease. Garrett N. 1992-2001.150:263-271. Olea N. Schulte P. Eds. Available at URL: http://www. Frey JM. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Inc. Lancet 1998.64-65 Spec.gov/~dms/ pesrpts.atsdr. Chlorinated Hydrocarbon Insecticides. PA. Food and Drug Administration (FDA). Song S. 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. Grajewski B. Grandjean P. Effect of occupational exposure to aldrin on urinary D-glucaric acid. Cancer Epidemiol Biomarkers Prev 2000.109(Supp1):113-139. Neurotoxicol 2005. 2007 [online].66(4):229-234. 2 Classes of Pesticides. 1991.27:405-421. Jorgensen T. Tully DB. Exposure to low doses of the environmental chemical dieldrin causes behavioral deficits in animals prevented from coping with stress. New York. Psychopharmacology (Berl) 1987. Shore RF. Wienburg CL. Toxicity of dieldrin for dopaminergic neurons in mesencephalic cultures. pp. Brock JW. Corrigan FM. Int Arch Occup Environ Health 1994. are nonestrogenic in transfected HeLa cells.

5) < LOD < LOD 9.7 (32.. Survey Geometric mean (95% conf.9 (15.3 (28.7 (<LOD-13.6 (9.3 (<LOD-19.9) 39. 2007). chlordane was used to kill termites and other insects on agricultural crops.7 (43.5 (31.6-18.9) 13.4-21.7-39.5) 21.3 (9.2 (36.9) 36. respectively.0) 75th 20.3 (25.2-21. and dairy products are the usual sources of exposure to these chemicals in the general population.3-45.9) 11.1 (15.9) 23.9) 37.2) < LOD 11.6 (25.6-53.5) 10.6) 48.5-13.2-28.2 (41.5) 44.5. 57-74-9 Heptachlor CAS No. 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.8) 44.9) 17. fish.1) * 11.1-25.70 (<LOD-10.0-67.8 (10.5) 37.0 (37.4) 29. lawns.1) * 11.36-11.1) 90th 34. 10.2 (21.4-45.0) 41. Heptachlor and chlordane and their metabolites bioaccumulate in fatty animal tissues.1-51.0-33.20-11.3) 18.2 (39.8 (42.8 (18.6 (43.4 (30.1-19.6 (16.9 (21.6 (9.8-32.3-45.1 (11.2) 22.3 (27. interval) Selected percentiles ( 95% confidence interval) Sample 95th 44. Both of these chemicals and their metabolites can cross the placenta and are excreted into breast milk.10-18.4) < LOD < LOD < LOD 23.20 (<LOD-11.4) 22.2) < LOD 11.3) 10. see Data Analysis section) for Survey years 99-00.7 (19.1) 30.7) 19.Organochlorine Pesticides Chlordane CAS No. buildings.9 (36.9 (29. and 7.9-21.8-31.1-15.5-44.1) 16.8-43.7) 28.8 (17.0-13.8) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD 11.7 (34. and in soil.8 (40.1 (25.2) * 12.9-40.7-56.4) < LOD 11.1 (16.4 (22.4-40.1-25.S. 1994).2) 46.3) 37.0) 20.7) 9.6) 23.9 (17.6-24.30-11. Until 1988.0) 21.9-42.3 (21.7 (34.8-33.82-11.S.10 (8.1) 30.6) < LOD 11.2) 37.2 (37.9 (31.4 (10.8-20.4 (35.6) 39. 2007).5) < LOD < LOD < LOD < LOD 13.8) 52.20-10. Since 1992.1-65.8-33.8-42.0-18.9) 10.6) 8. heptachlor use has been limited to treatment of fire ants near power transformers. 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 (34.8) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * 11. 1994.0 (20.3) 41.9 (18.4-51.6-45.5-40.5) 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 * * * * 11.2-49.2 (28. Chlordane is not currently produced or used in the U.6) 9.9 (11.1 (<LOD-12.9 (26.7 (10.7 (17. which may vary for some chemicals by year and by individual sample.90 (8.4 (<LOD-12.6-12.69-10.9) 31. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and 03-04 are 14. in addition to trace amounts of numerous other related compounds (ATSDR.5) 9.0 (16.S.6) 11.89-10.8) 27. 76-44-8 General Information Chlordane and heptachlor are structurally related organochlorine pesticides and were used in the U.0) 31.1 (17.6) 49.5.5 (33. 01-02.3) 18.9 (15.5-65.7-25.7-14.8) 52.7) 19.3 (26.37 (8.8-23.9) 23.6) 20.5) 38.3-49.2-49. population from the National Health and Nutrition Examination Survey.63 (8.3 (11.3-43.1 (20.9-21.8) 53. As a result of the manufacturing process.9-38.7) 42.5 (41.0 (<LOD-12.7 (42.6) 9.2 (9.4) 18.9 (26.5 (8.8) 18.0 (26. the technical grade product of each chemical contains 10%-20% of the other chemical.5-42.1) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * 12.1 (27.6) 36. from the early 1950’s until the mid-1980’s.2) 34.7-12.1 (<LOD-12.1) 22.6-24.7) 35.7 (<LOD-32.3 (20. Heptachlor was used as a soil and seed treatment and for termite control in and around buildings until 1988.3-24.5) 56.7) 31.1 (44.2) 36.9 (11.2 (10.4 (30.2-56.5 (<LOD-12.0 (32.4) 37.1 (<LOD-12.8-73.1-50.5-41.4-14.5-32.5-38.2) 33.5) 628 557 462 350 501 493 559 1031 898 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6) 48.3-32.5-47.0) 27. Technical grade chlordane had contained 7% trans-nonachlor.5-43.8.2-26.4 (31.3) 10.0-61. Both pesticides are persistent in soils and sediments and have been detected in water from agricultural run-off and near production and disposal facilities (ATSDR.8-61.9) 47. foods high in fat such as meat.4) 12.8 (10.0) 37. Fourth National Report on Human Exposure to Environmental Chemicals 81 .9) 11.1 (40.10-11. Consequently.8 (17. < LOD means less than the limit of detection.0-25.74 (<LOD-10.4) 39.0-12.7-70.1) < LOD < LOD < LOD < LOD < LOD 8.

280-. 1986).070 (.290-.049 (<LOD-.230 (.220-.130) .130-. 2006).S.080) .120-.090-.100-.560) .207) .240) .108-.110 (<LOD-.070 (<LOD-. OSHA has established occupational exposure criteria.126) .057 (.242-.053-.300) .220 (.073) < LOD < LOD < LOD < LOD .230) .076) < LOD .180) .400) .140 (.440) .370 (.070-.310) .210-.300 (.063-.320 (.160) .260 (.260 (.260 (.200-. both chlordane and heptachlor induced hepatic cytochrome P450 enzymes and increased the incidence of liver tumors (NTP.207 (.130) . 2001. The U. In laboratory animal studies.280-. Epidemiologic studies have not demonstrated teratogenic or developmental effects (Baker et al.057-.140-. 1986).061-.310) .064) < LOD .140 (.258-.060 (<LOD-.077) .253-.270 (.290) .Organochlorine Pesticides (Dallaire et al.100 (.203-.160 (.180-.126 (.050 (<LOD-.430) .130-. 2007.320 (.119 (.213) * . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Subtle neurodevelopmental effects have been observed rodents after prenatal exposure to heptachlor (IPCS.120-.070-. Survey Geometric mean (95% conf.106-.070 (<LOD-. high doses of either chlordane or heptachlor block inhibitory neurotransmitters and result in central nervous system toxicity.140 (.290-.280-.240 (.340) .083) . dermal.400) . Smith.225 (. Takahashi et al.148) . characterized by seizures and paralysis.168-.220-.320) .250 (.200 (.140) .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.450) .290-.104) .063 (. Chlordane and heptachlor are absorbed after oral.270 (.063) * .190-.133) 90th .068) .140 (.130 (.150 (.130 (.091) .062) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * .260-.290 (. IARC considers chlordane and heptachlor as possibly carcinogenic to humans.302) .087-.070 (<LOD-.280) .250 (.170) . IARC.410) . and inhalation exposure.208 (.230 (.063 (.066-. and heptachlor epoxide in foods and bottled water. and alterations in immune function of offspring.077) .130 (.136) . Chronic feeding studies with either chlordane or heptachlor have demonstrated reduced fertility.110-.053-.120 (..130-.115 (.310-.069 (<LOD-.050-. Rogan.270 (.180) .160) .047 (<LOD-.258 (.104-.230-. and the U.227) < LOD .430) .083 (.115-.062) < LOD .170) . 1991).070) .066-.080 (. heptachlor.240-.170) .090) .199-.100 (<LOD-.150 (.246-.056 (.165-.250-.286 (..112 (.092) .070 (<LOD-. No clear evidence of excessive cancer rates was demonstrated in human epidemiologic studies (ATSDR.070) < LOD < LOD < LOD < LOD < LOD .082 (.223) . 1991.080) .370 (.067 (.320) .190-.070-.315 (.063 (.180-.210 (.130-. 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.170) .360) .216-.340) .146) .200-.063 (.286 (.100-.373) . 2007). The major metabolite of heptachlor is heptachlor epoxide.245-.510) .300) .280 (. Le Marchand et al.170) .080) . to heptachlor.310) .450) .189-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .066 (<LOD-.130-. Human health effects from either chlordane or heptachlor at low environmental doses or at biomonitored levels from low environmental exposures are unknown.075 (.058 (.074-.320 (.350) .150 (. Chlordane is metabolized primarily to oxychlordane and to a lesser extent.150-.280 (.204 (. Acute.230-.320 (.287) .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 * * * * . neonatal mortality.077) ..348) . 1996.068) 75th .063) .079) .146) < LOD < LOD .380) . which is also persistent in the body (ATSDR.090) .140-.200-.149 (.128 (.271 (.269 (.068-.079) < LOD < LOD < LOD . FDA established allowable residues of chlordane.S.058-. 1977a. 1981).230-.350 (. and breast milk is a major excretion route in lactating women..190-.189 (.065-. and NIOSH and ACGIH have recommended workplace exposure levels for each pesticide.330 (. 82 Fourth National Report on Human Exposure to Environmental Chemicals .240-.150) . EPA has established environmental criteria for chlordane and heptachlor.058-.077) .290) .300) .210 (. 2002.048-. population from the National Health and Nutrition Examination Survey.160) .080 (.291) size 1661 2249 1978 Total years 99-00 01-02 03-04 50th < LOD . Elimination of all these chemicals from the body occurs over months to years.310 (.120-. 1977b.055-.057) * . Shindell and Ulrich.073 (.300-. chronic doses of heptachlor have produced liver enlargement and injury.148-.S. which may vary for some chemicals by year and by individual sample.071 (.320) 663 752 595 998 1497 1383 20 years and older Gender Males 99-00 01-02 03-04 * .170-.370 (.066 (.350 (.231) .300) .

. mean serum heptachlor epoxide and oxychlordane levels were about sevenfold and threefold higher. 2000). In the Hawaii episode. 2002).atsdr.org/documents/cicads/cicads/cicad70. and 2003-2004 subsamples were comparable to levels measured in Swedish women from 1996-1997 (Glynn et al. transnonachlor. trans-nonachlor. inchem. than the 90th percentile values of NHANES 1999-2000 (Baker. 1988). 2004).cdc. Biomonitoring studies on levels of oxychlordane. from ATSDR at: http://www. or heptachlor epoxide causes an adverse health effect.gov/toxpro2. 2006).Organochlorine Pesticides about external exposure (i. In serum samples obtained in between 1994 and1997 from Inuit women in different Arctic countries. 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. Finding a measurable amount of oxychlordane. A recent assessment of heptachlor is available at: http://www. transnonachlor. 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 . A small sample of Polish women had mean levels of oxychlordane and trans-nonachlor that were about fivefold lower than in females in the NHANES 20012002 subsample (Jaraczweska et al. Levels of heptachlor epoxide among females in this Report were approximately one tenth of the corresponding 90th percentile for a cohort of pregnant women in California studied from 1963 to 1967 (James et al. For the exposed persons drinking milk in the Arkansas episode. than the 90th percentile values of NHANES 1999-2000 (Stehr-Green et al. and heptachlor epoxide provide physicians and public health officials with reference ranges so that they can determine whether people have been exposed to higher levels of heptachlor and chlordane than are found in the general population. 2003)...e. 1993). resulting in human exposure to heptachlor epoxide that was excreted into the milk...html.htm#ref. 2001-2002. Serum transnonachlor levels among females in the NHANES 19992001 subsample were about one half the levels obtained between 1994 and 1996 from women in New York (Wolff et al. Two episodes (one each in Arkansas and Hawaii) of inadvertent heptachlor contamination of dairy cattle feed occurred in the early-to-mid 1980’s. respectively. Biomonitoring Information Serum oxychlordane and trans-nonachlor levels in NHANES 1999-2000.. environmental levels) and scientists plan and conduct research on exposure and health health effects of chlordane and heptachlor is available effects.. or heptachlor epoxide in serum does not mean that the level of oxychlordane.

84 Fourth National Report on Human Exposure to Environmental Chemicals .8-24.8-23. interval) Selected percentiles ( 95% confidence interval) Sample 95th 24.5) 760 1047 956 829 1212 1007 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 7.8) 19. and 03-04 are 14.9-23.9) 15.0) 13.9-29.9 (12. Survey Geometric mean (95% conf.2-16.40) 15.3 (<LOD-25. population from the National Health and Nutrition Examination Survey.8) 16.0-17.2 (<LOD-16.6 (14.4 (<LOD-54.6 (8.6-17.0-54.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.8-24.8) 13.8) 19.1-16.2-27.3) 16.2-17.4) 18.5 (18.3) 18.1) 20.6 (<LOD-27.5 (11.8 (15.6) < LOD < LOD < LOD 27.6-21.6. 01-02.3) 10.1) 13.6 (13.3) 18.0) 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 13.2) 15.8.9-16.8) 20.3 (13.0-16. 10.8 (18.1-15.2) 26.0-17.90 (<LOD-9.5 (10.7-25.0 (15.8) 21.4) 21.8) 13.6 (16.5 (11.5) < LOD 14.2 (18.6 (12.7 (10.5) 19. see Data Analysis section) for Survey years 99-00. which may vary for some chemicals by year and by individual sample.2 (<LOD-62.2-27.1 (19.0-19.7 (16.2 (<LOD-25.4 (<LOD-19.3-18.S.9) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 8.0) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th 15.8-46.1-29. and 7.8 (13.4 (11.4 (15.8) 15.6 (11.1 (16.8) 14.8 (<LOD-23.2) 20.1) 23.8 (13.3) 23.6) 14. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.10-13. < LOD means less than the limit of detection.9-25.7-19.9-29.2) 13.20 (<LOD-9.8 (18.6 (16.7-18.0 (11.3) 18.3) 27.5.7 (13.3) 22.5) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.9 (15.6) 13.8) 14.6) 22.1-38. respectively.8-24.5 (<LOD-32.4 (11.5 (<LOD-21.50) < LOD < LOD < LOD 17.

094 (.170 (.111) .150 (.116) < LOD < LOD < LOD .107-.100 (.180) .180) .070-.104) .200) .310) .220) .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-.074-.190) .100 (.100-.170 (.130) .110-.170 (<LOD-.135 (.113) .170 (.130 (.097) < LOD .110) .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 . population from the National Health and Nutrition Examination Survey.082-. which may vary for some chemicals by year and by individual sample.130-.090-.130-.120 (<LOD-.180) .180) .071-.098 (.101 (.180) 598 553 460 336 503 490 539 1041 888 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.150 (.087 (.190) .140-.128 (.120 (.130) . Survey Geometric mean (95% conf.380) .100 (.100 (.270) .094 (.067-.113-.S.110 (<LOD-.180 (<LOD-.106-.090 (<LOD-.170) .090-.057 (<LOD-.100-.130-.200 (. Fourth National Report on Human Exposure to Environmental Chemicals 85 .090-.150 (<LOD-.090-.076-.111-.110 (<LOD-.055 (<LOD-.110 (.063) < LOD < LOD < LOD .090-.077-.120-.120 (<LOD-.170) .069 (.101 (.157) .140) .161) size 1589 2259 1963 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th 90th .063) .240) .130-.110 (.090-.200) .100 (<LOD-.130 (<LOD-.117) .126 (.108) * * * Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .190 (.108) .170) .053-.110) .149) .096 (.310) .108-.133 (.090 (.Organochlorine Pesticides Serum Heptachlor epoxide (whole weight) Metabolite of Heptachlor Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.110-.190) .120) .180 (.140) . * 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 .135 (.120) .

5-69.0-93.7) 28.3) 19.9 (15.8) 51.0-23.5) 19.6-20.5) 78.5-19.0) 33.0) 49.9 (16.9 (66.8 (30.0 (16.8-77.5 (15.2) 20.2-88.8 (26.8 (17.3-50.2) 59.9 (15.9-64.5 (44.3 (14.2-17.7-29.9 (28.7-17.0 (19.8-41.8 (12.0-113) 68.0-37.3) 18.3) 30.9-45.2 (14.9) 51.1) 17.9-58.7-160) 86.4-35.0-68.1) 16.1) 18.0) 75th 31.9-35.6) 13.0) 664 758 589 1269 1528 1366 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 17.3 (45.8 (28. respectively.1-34.1) 78.3) 25.7) 78.1-51.2-21.0-22.6) 10. 01-02.7 (35.1 (22.7 (30.8) 19.5-95.0 (42.1 (10.2 (25.4 (11.2 (19.9-40.5 (45.7-21.9-20.8-19.6) 54.6) 56.1) 17.5.5) 14.8 (26.10 (<LOD-11.8 (<LOD-20.1-22.S.8 (28.3) 15. 86 Fourth National Report on Human Exposure to Environmental Chemicals .8 (13.5) 36.1 (41.3 (49.7 (13.1 (48.7 (16.7-22.9-69.1) 17.0-20. and 03-04 are 14.8 (45.4-62.3) 16.5) 48.8-90.2 (26.3 (58.0 (15.8 (49.5-17. Survey Geometric mean (95% conf.5-111) 68.9) 14.2) 30.6-88.0 (60.8-129) 74.2 (64.0) 13.8-21.3-57.7-18.2-18.9-36.6 (<LOD-14.0) < LOD < LOD 8.2 (15.7) 73.0 (13.3 (14.6 (52.3) 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) 17.6) 84.6) 34.2) 17.8 (16.2 (7.0-93.7) 56.4-23.3) 36.1) 31. and 7. < LOD means less than the limit of detection.9) < LOD < LOD < LOD 20.3) 18.4 (67.0) Selected percentiles ( 95% confidence interval) Sample 95th 79.1 (17.8-19.4 (16.8 (28.3) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th 17. which may vary for some chemicals by year and by individual sample.4) 19.9) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * 11.2-37.8-67.2) 19.6-22.1 (65.1-34.1) 62.9-65.3-32.9 (51.3 (56.1-16.7) 14.3) 32.7-113) 68.6) 82.2-16.4-36.7) 52.1-18.5 (13.5) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * 20.5-36.7-23.6 (32.0-123) 74.8 (15.0-24.6 (15.0-23.1) 17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (62.3) 32.8) 47.6-19.3 (17.4-22.1) 32.8 (13.5 (15.9 (29.7 (11.8) 80.3 (16.8 (26.3-58.0) 19.9-89.1) 17.8.6) 25.7-32.2) 34.7-20.7) 15.2 (59.2 (36.6-54.5-20.0 (13.3-86.4 (12.1) 17.6) 56.0) 40.2 (60.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. population from the National Health and Nutrition Examination Survey.2) < LOD 10.9 (19.8 (71.4 (30.5) 30.5) 35.6 (16.6 (56.9-65.4) 16.1) 18.9) 14.8 (42.86-13.7 (59.9 (36.2-23.1-16.7-38.8-16.2-18.1) 78.0) 18.1) 30.0 (14.7 (28.8 (11.3) 30.1-20.0 (48.5) 20.6 (50.6-82.8-79.8-110) 59.0-59.0-143) 112 (68.5. interval) 18.7-77.1-28.7 (59.4) 59.6-66.8-16.4 (28.9 (<LOD-14.0-38.4 (45.7 (74.7-35.70 (<LOD-12.3-30.5 (25.5) 9.7) 78.2 (14.6 (12.7-34.5-87.5) 14.1-126) 67.5) 22.1-55.4-18.3-74.7) 59.0 (15.1) 14.3-21.9-22.4-67.8 (19.5) 26.4) 107 (84.5) 90th 55.0 (29.7) 35.9 (51.8-90.4) 55.7 (18.0 (42.4) 48.4-52.9) 51. see Data Analysis section) for Survey years 99-00.9 (47.1 (47.6 (57.6 (56.5) 77.0 (16.2) 39.2 (27.4) 20.3-39.7) 17.6) 60. 10.

580 (.460) .360-.680) .320-.080-.127) < LOD < LOD .094 (.131) .069) .106 (.310-.370 (.112 (.100-.190-.490 (.161-.090-.301-.096-.110 (.100 (.414 (.120) .070 (.420) .220) .240) .317 (.145-.417 (.190-.085-.367) .220 (.080) .830) .410-.350-.210) .090) .470 (.290-.220 (.120-.330 (.098 (.250) .470 (.100-.651) .510 (.109 (.068-.090-.470-.300) .130) .300-.117) .630) .186 (.310-.800) .330-.390 (.260) .130) .350 (.340-.100 (.397-.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.106 (.090-.110) .160 (.510-.470 (.380 (.171-.830) .540) .116 (.690) .111 (.220 (.240) .054-.327 (.120 (.116-.550 (.091) .320-.565) .130) .103 (.061-.395) .580 (.461 (.324 (.105 (.079-.580 (.085-.130) .288 (.055 (<LOD-.340-.100-.240-.079-.062 (.930) .109 (.630) .232) .594) .490) .080-.141) .250) .177-.191 (.440) .160-.565) 922 1062 955 1011 1224 1000 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 * .069-.590) .093) .130) .500) .210) .122) .041 (<LOD-.270-.400 (.124) .458 (.590 (.130) .099-.470-.090 (<LOD-.095-.242) .080 (.590 (.085-.430-.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.099-.20) .120 (.090-.684) .400) .173-.286-.140) .250) .170 (.240 (.081 (.114) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.640 (.130 (.060) .202 (.080-.220 (.310) .497-.080-.120) .310-.558) size 1933 2286 1955 Total years 99-00 01-02 03-04 50th .126) .360-.092 (.130 (.096-.190-.840) .120-.100) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * * .113) < LOD .084-.371) .409-.161) .285-.047-.090-. population from the National Health and Nutrition Examination Survey.310-.097) .220 (.125) .330-.093-.116) .089 (.158-.150) .210-.110 (.093-.103 (.087 (.108) .520 (.091-.186-.230 (.355 (.420 (.S.093-.410-1.112 (.120) .220 (.234) .098-.098 (.490 (.078 (.630) .082) .490-.280) .310 (.071 (<LOD-.104 (.960) . which may vary for some chemicals by year and by individual sample. Fourth National Report on Human Exposure to Environmental Chemicals 87 .183 (. Survey Geometric mean (95% conf.104-.150) .390-.190-.141) .108 (.400-.395-.110 (.060-.119) Selected percentiles ( 95% confidence interval) Sample 95th .210 (.390 (.100-.210-.430-.096) .573 (.125 (.520 (.760 (.122) .288-.190-.090 (.210 (.111-.205 (.130) .440-.119) < LOD < LOD < LOD .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 .120 (.211) 90th .400-.129) .390) .405) .210 (.081-.260) .370 (.110 (.120-.180-.390 (.430-.113) .460-.390) .128 (.343 (.520) .110-.134) .390 (.108) 75th .210) .190-.400 (.237) .220 (.090-.272-.060 (<LOD-.135 (.098) .106 (.480) .240) .120) .237) .559) .450) .600 (.180-.110 (.680 (.340) .078-.092 (.279-.460) . interval) .600) .110 (.220 (.180-.690) .

htm. Organochlorines in Swedish women: determinants of serum concentrations. Hansen JC. Estimation of Human Exposure to Heptachlor Epoxide and Related Pesticides in Hawaii. Takahashi W. Toxicological profile for heptachlor and heptachlor epoxide [online]. Eds. 1963-1967. Available at URL: http://ntp. Toxicological profile for chlordane [online]. 2006. In Hayes WJ.html. 88 Fourth National Report on Human Exposure to Environmental Chemicals . maternal serum and milk from Wielkopolska region. Covaci A. Granath F. Natl Cancer Inst Carcinog Tech Rep Ser 1977a.niehs. Vol.110(8):835-838. Drews K. Bjerselius R.41:145–148. Organochlorine exposures and breast cancer risk in New York City women. Distribution of polychlorinated biphenyls. International Agency for Research on Cancer (IARC) .pdf. Ayotte P. Trends in birth defects for a Hawaiian population exposed to heptachlor and for the United States.atsdr. Available at URL: http://www. Dendle WH.cdc. Shindell S and Ulrich S. Stehr-Green P. Mortality of workers employed in the manufacture of chlordane: an update.84:151-161. et al. Available at URL: http://www. Inc. 4/21/09 Dallaire F. Atuma S. Evaluation of human exposure to the heptachlor epoxide contamination of milk in Hawaii.inchem. Royce W. Natl Cancer Inst Carcinog Tech Rep Ser 1977b. 1979-1980.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). 4/21/09 Baker DB. et al. Academic Press. organochlorine pesticides and polybrominated diphenyl ethers in human umbilical cord serum. Wohlleb JC. 1994-1997 organochlorine compounds. Barker J. Available at URL: http://www. Vol. Arch Pediatr Adolesc Med 1996. Kolonel LN.111:349355. Determinants of serum polychlorinated biphenyls and organochlorine pesticides measured in women from the child health and development study cohort. Bleiweiss IJ. 6/1/09 National Toxicology Program (NTP). Senie R. 2 Classes of Pesticides. Bull Environ Contam Toxicol 1981:27:506-511. 9/25/07 International Programme in Chemical Safety (IPCS). Brower S.150:981-990. Lulek J. 731-915. Head SL. Chlordane and heptachlor [online]. Odland JO.259(3):374-377. Darnerud PO. KalubaSkotarczak A.org/site/foundation/ research/projects2. A Report to the Hawaii Heptachlor Research and Education Foundation. Pollutants in breast milk. Dewailly E. Concise International Chemical Assessment Document 70 Heptachlor [online]. Bioassay of chlordane for possible carcinogenicity. Muckle G.heptachlor. 2001. Charles MJ. Laliberte C. New York. Chlorinated Hydrocarbon Insecticides.inchem. Loo S. Gilman A. An evaluation of serum pesticide residue levels and liver function in persons exposed to dairy products contaminated with heptachlor.372:20-31. 1993. International Agency for Research on Cancer (IARC). 1991 pp.8:1-123. Available at URL: http://www. Glynn AW. J Occup Med 1986. Lawrence River (Quebec. Sci Tot Environ 2006. Environ Health Perspect 2003. Environ Health Perspect 2002. Hawaii Med J 1991. August 2007. Siegel BZ. Saidein D. Smith AG. Takei G.niehs.nih. Chashchin V.org/documents/iarc/ vol79/79-12. Dewailly E. 1986. Bioassay of heptachlor for possible carcinogenicity. Poland. Organochloride pesticide residues in human milk in Hawaii. LeMarchand L.html. Available at URL: http://ntp.330:55-70. 79. Jr and Laws ER. Wong L. Environ Res 2000. gov/toxprofiles/tp12. et al.50(3):108-118. May 1994. Van Oostdam JC. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St. Circumpolar maternal blood contaminant survey. Handbook of Pesticide Toxicology. Wolff MS.110:617-624.org/ documents/cicads/cicads/cicad70. Willman E.gov/ntp/ htdocs/LT_rpts/tr008.html. Keller JA. Sci Total Environ 2004.cdc.pdf. Voorspoels S. 4/21/09 Agency for Toxic Substances and Disease Registry (ATSDR). Baker DB. Aune M. et al. Available at URL: http://www.nih. Canada). 4/21/09 James RA. Environ Health Perspect 2002. Jaraczewska K.htm. Berkowitz GS. Tartter P.9:1-109. Jr. JAMA 1988.28:497501.gov/toxprofiles/tp31.gov/ntp/ htdocs/LT_rpts/tr009. 6/1/09 Rogan WJ. Hertz-Picciotto I.Summaries & Evaluations.atsdr. National Toxicology Program (NTP). Arch Environ Health.

1-71.0 (18. and trace amounts of several related compounds.1) 31.1 (33. DDT can be absorbed after ingestion.90 (<LOD-12. and 7.1-27.9 (<LOD-20.9) 17.7) < LOD 18.6) 635 566 461 356 514 490 564 1061 890 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.6 (<LOD-25.10-13.2-65.1’-dichloro-(2.5) 25.9 (10.Organochlorine Pesticides Dichlorodiphenyltrichloroethane (DDT) CAS No. after World War II until 1972. population.3-590) 293 (104-541) 48.8) 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. 17.0) 19.3) 21.4 (23.2-bis(p-chlorophenyl) ethane (DDD).2) 30. although DDT and DDE intakes have decreased over time (FDA.S.6 (25. DDT was used at one time as a treatment for head and body lice. It is still used in some countries. as well as in plant and animal tissues.5 (23.7 (15.7 (19.9-34.7. continues to be the primary source of DDT exposure. sediments. < LOD means less than the limit of detection.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 12.70 (8.2 (<LOD-40.8) 30.0-27.2-dichloroethenylidene)-bis[4-chlorobenzene] (DDE) and 1. DDT usually refers to the technical product.8-39. Survey Geometric mean (95% conf.7-16.4.3) 22. and dairy products. 1991).0) 20.8-23.3 (27.5 (14.0-35. or dermal exposure.0 (21.6 (31.8-26.0-53.9) < LOD < LOD 9.9 (21. The biodegradation half-life of DDT in soil varies from 2 to 15 years. Food imported from countries that still use DDT may contain the chemical or its residues.3) 28.1’-(2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. DDT is converted in the environment to other more stable chemical forms. These chemicals are highly persistent in soil.1 (<LOD-39.7) 12. respectively.6-33.5 (15. Only a small proportion of DDT is metabolized and excreted (Smith. Fourth National Report on Human Exposure to Environmental Chemicals 89 . which may vary for some chemicals by year and by individual sample. 2002.9 (10.9-28.0-155) 83. DDT and DDE are distributed to all body tissues with the highest concentrations found in adipose tissues (ATSDR.8) 36.3-236) 24.p’-DDD (4% or less). inhalation. and water.S.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. when virtually all use of it was banned.1 (23.00 (<LOD-10. including 1. p.8-17. It was produced and used in the U.2) 155 (59.3) 21. resulting in fetal exposure.p’-DDT (65%-80%).4) < LOD < LOD < LOD 61. 2008. depending on conditions. interval) Selected percentiles ( 95% confidence interval) Sample 95th 28. Smith.50-11. fish. Both Serum p.3 (<LOD-21. In the body.0 (10.p’-DDT (15%-21%).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. food.0 (18. particularly meat. DDT is converted to DDE and several other metabolites. Gunderson.10 (<LOD-12.2) < LOD < LOD 9. 1988).5) 23.3-16. o.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.5 (23.0-15.2 (11.9) 29. and 03-04 are 20. air. particularly for endemic vector and malaria control.2-95.9 (10. which is a mixture containing p. DDT and DDE can cross the placenta.3 (<LOD-31. 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) 15. population from the National Health and Nutrition Examination Survey.S. 01-02.5-54.8.5-36.6 (22. see Data Analysis section) for Survey years 99-00.4) < LOD 17. In the general U.0-37.5) < LOD < LOD 9.6 (9. 1991).0) 40.9) 14.0) 26.

Survey Geometric mean (95% conf.530 (. Jusko et al.142 (.075) 1.130 (<LOD-.260) . fertility. 2001). Reproductive effects in humans affecting birth weight.S. dioxins and furans).095) < LOD ..530) ..065-..064 (.250-1.130 (<LOD-.180) .400 (..130-. and o. 2004.180-.146 (.068-. Calle et al.150) . 2006. Epidemiologic studies of children with environmental exposure to DDT and DDE have not demonstrated neurologic or developmental abnormalities (Gladen et al.62 (. 2006.180 (.. Gray et al.190 (.240 (. Several reviews of cancer epidemiologic studies have concluded that a link between DDT and breast cancer is inconclusive (Beard.220) . 2001).084 (.240) .120-. 2006.220) . polychlorinated biphenyls.160-. 2000.105-. 2002.080-.059-.048 (<LOD-.086 (.150-. Mariussen and Fonnum. Human health effects from DDT at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 2006).230) . 2006).203) .054-.150 (<LOD-. overt signs of acute human toxicity include vomiting.170-. 1956). tremor.078 (. Gladen and Rogan.069) .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 . although the risk for preterm delivery may be related to maternal DDE levels (Longnecker et al.140-. and leukemia have also been inconclusive (ADSDR.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.. Hayes et al.400) . accidental exposures.071 (.061) < LOD < LOD < LOD .190 (.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 .26) 1.106) < LOD < LOD .128 (.201 (. lung cancer. 2001). and seizures. 2002.051 (<LOD-.189-.132-.120 (<LOD-.114-..098-. Beard.143) < LOD < LOD .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 . 2001). other organochlorines. resulting in exposure to nursing infants (Rogan. A workplace standard for DDT has been established by Serum p... both DDT and DDE may induce specific cytochrome P450 isozymes (Nims et al.00 (. reproductive organ abnormalities. 1995. 2002.343) < LOD . 2002.34) .087 (.106) .200 (.p’-DDE can produce anti-androgenic effects (Gray et al. Studies of DDT exposure and pancreatic cancer.570-4. 1996).150 (<LOD-.230) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Animal studies reported reduced fertility.290) .180 (. Experimental human dosing studies conducted over an 18 month period and during which doses well above environmental levels were given did not demonstrate overt clinical abnormalities (ATSDR.071-.g. and altered behavior after neonatal exposure (Eriksson and Talts.150-.627) . In high dose.112 (. 1998).. In laboratory animals.170) .. 2006).063 (<LOD-.078-.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. population from the National Health and Nutrition Examination Survey. Jusko et al. which may vary for some chemicals by year and by individual sample.167) size 1679 2305 1965 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * * .00) .Organochlorine Pesticides chemicals are excreted in breast milk.180) . Snedeker.170 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .079) < LOD < LOD . DDT may bind to estrogen receptors (Chen et al.140) . 90 Fourth National Report on Human Exposure to Environmental Chemicals .074-. 1997).106-. It is difficult to attribute outcomes in human studies solely to DDT because of potential co-exposure to other persistent organohalogen chemicals (e. and duration of lactation.313 (.p’-DDD and p. have not been consistently demonstrated (Beard.146 (.330-4.108 (.01) . premature delivery.190-1. Longnecker et al.420) .130 (<LOD-.250 (..

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

5) 22.25) 8. 1989).34 (7.80) 3.84-3.34) 6.80) 1.51-49.84 (3.39-1.36 (3.5) 10.04 (6.4) 9.p’-DDT.57 (3.18-4.36-1.860 ng/L) and DDE (about 14.25) 1.07) 1.72) 1.18-3.2 (9.57-3.3 (8.0 (12.37-16.68-4. In a subsample of NHANES II (19761980) participants.07) 1.39-2.02) 1.52 (1.13 (1.8) 686 758 588 1278 1540 1368 20 years and older Gender Males 99-00 01-02 03-04 1.62-6.64-2.46-2.4-19. 1971).5) 7.01-11.70) 1.26) 3.0 (9.8) 15.60-13.99) 1.1) 40.79) 4.66-17.75) 6.37-10.68) 2.69) 8.24) 1.85-4. o. 2001-2002 and 2003-2004 subsamples.71 (6.10) 2.66) 4.557) 1.58) 1.32 (1.11-1.75 (8. Finding a measurable amount of p.6) 13.48-4.6) 9.47 (1.41-12.90) 22.52-6.820-1.96) .S.38 (1.69 (1.50 (2.59 (4.92 (3.45 (1.7) 9.516 (.66) 1.75) 2.3 (9.66-4.58) 1.2 (19.31 (1.6 (7.7 (8.53) 7.36) 3.6 (8.9) 5. 2004).49 (1.18) 1.53) 1.500-.69 (2.19-14.63 (1.40-4. In the NHANES 1999-2000.43-4.40 (3.56-2.10-1.00 (6.52 (3.59) 6.12-1.88 (2.02-8.25-16.51) 1.72) 1.30 (1.57-13.49 (6.92 (3.6) 8.p’-DDT were below the limits of detection.54-7.635) 1.18 (6.10-5.65) 1.81) 11.51) 3.12 (6.61 (1.87 (5.46 (1.14 (1.3) 10.44) 1.490 ng/L) were found many years ago in a study of pesticide workers in Argentina (Radomski et al.17 (3.65 (1.46 (1.430-. 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.01-11..40-4. interval) 1.9) 7. Survey Geometric mean (95% conf.6 (17.03-1.01-15. Consumers of Great Lakes sport fish had mean serum DDE levels that were only slightly higher than nonconsumers.0) size 1964 2298 1956 Total years 99-00 01-02 03-04 50th 1.39) 1.76-3. Workers involved in production or application of DDT developed neurologic abnormalities associated with blood levels around 100-300 mg/L.37 (1.96) 1.69) 4.70-3.4 (8. 2004).56-6.p’-DDE in serum does not mean that the level of the chemical causes an adverse health effect.1) 12.30 (1.75) 1.68 (2.77 (1.680-1.54 (1.93 (7.75 (4.9-17.85 (1.32 (1.994-2.18-1.730) .59 (1.69 (.534-.64) 3.47) 3.24-17.05) 1.45 (1.88-35. less than one percent had detectable serum levels of o.6) 11.30-1.36-11.09-1.590 (. Serum p.4) 13.13) 4..02 (2. serum levels of o.78 (4.7-48.8 (13.91-3.13-2..57) 2.51-8.6) 9.22) .32-9.520 (.6) 9.419-.796 (.890-1.3) 16.01) 1.01) 1.43 (5.6 (9.34) 2.17-3.14) 2.28) 1.9-38.56-3.0) 657 566 457 416 515 487 732 1053 888 Non-Hispanic blacks 99-00 01-02 03-04 99-00 01-02 03-04 Non-Hispanic whites 92 Fourth National Report on Human Exposure to Environmental Chemicals .92) 1.03-4.21) 90th 7.2 (9.8 (13.15-4.16-1.81-5.646) .33-1.48 (6.79) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 .p’-DDT (Stehr-Green.58) 75th 3. 1991).39 (3.91 (6.01-1.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.43-8.79) Selected percentiles ( 95% confidence interval) Sample 95th 11.00 (.55 (2.9 (15.63-15.27) 3.7-19.18-1.31-12.76) 1.43-4.3) 13.32-1.97-4.76) 1.53-15.80) 1.87-16.4 (12.63 (1.34-11.57 (1.00) 7.6) 9.49 (1.2) 26.07 (5.8-90.27-1.8 (9.19) 4.36-2.51-15.29 (1.5) 5.06) 1.77 (1.91) 3.1) 7.40-8.80 (2.456 (.21) 3.1 (8.57-2.04-1.14-1.63 (6.05 (3.71) 32.30-1.32-1.385-.Organochlorine Pesticides nearby agriculture (Botella et al.561 (.1 (9.488-.3) 937 1069 955 1027 1229 1001 Females 99-00 01-02 03-04 Race/ethnicity Mexican Americans 99-00 01-02 03-04 3.22 (7.7-20.49) 8.97 (3.20 (. 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.66-2.37-1.726) . 2005). 309 versus 268 ng/g lipid.71) 12.00-1..3-43.55-9.14-9.2 (6.25 (.81 (7.6) 12.82) 1.66) 1.623 (.9 (26.01-1.51 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.81 (1.25-14.59) 3.76 (2.0) 2.34-3.82 (1.37-4.7) 16.59 (1.p’-DDT.14) 2.91-2.61-2.5) 16.01-5.16 (2.24 (1.81-18.10) .4) 14.32) 1. population from the National Health and Nutrition Examination Survey.26-10.54) 8.600) .965-1.8 (14.22-1.56) 2.7) 13.611-1.35) 1.26-2.90-8.06) 3.57 (1.25 (1.66) 3. considerably higher than levels in this Report (Smith.53 (2.23 (7.83 (1.963-1.2-32.85-10.11 (2.71 (5.26 (1.50-17.41 (1.2) 19. or p.12 (.870 (. High mean levels of whole blood DDT (about 3. which is similar to the overall geometric mean of 260 ng/g lipid in the NHANES 1999-2000 subsample (Bloom et al.38 (1.31-2.

respectively. population from the National Health and Nutrition Examination Survey.S.Organochlorine Pesticides Serum o. and 7. which may vary for some chemicals by year and by individual sample. and 03-04 are 20. 17.7.4. 01-02. Fourth National Report on Human Exposure to Environmental Chemicals 93 .8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. see Data Analysis section) for Survey years 99-00. Survey Geometric mean (95% conf. < LOD means less than the limit of detection. 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.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.

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

Frumkin H. Zhou H. Am J Public Health 1995. Talts U. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine. JAMA 1956.7(3):248-264..112(17):1761-1767. Gray KA.53(8):1161-1172. selected elements. and DDD [online]. Greenfield TA. Henley SJ. Saiyed HN. Burse VW. Darnerud PO. Jr.205:297-308. DDE. Bhatnagar VK. et al. Profiles of ortho-polychlorinated biphenyl congeners. Bjerselius R.gov/~dms/ pesrpts.17(6):692-700. April 1982 to 1984. Thun MJ. Bates MN. Brock JW.atsdr.1-dichloro2. Chemosphere 2005. Katz SH. CA Cancer J Clin 2002. DDE and shortened duration of lactation in a northern Mexican town. hypospadias. Rogan WJ. Bull Environ Contam Toxicol 2004. Drexler H. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Int J Hyg Environ Health 2003. Aune M. et al. Chemosphere 2004. dietary intakes of pesticides. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. September 2002. 4/21/09 Anderson HA. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Brock JW. Vena JE. Link B. Olea N. India. and HCB residues in human blood in Ahmedabad. Ellis H. Patterson DG Jr. Furr J. Olea-Serrano MF. FDA total diet study. Biomonitoring of persistent organochlorine pesticides. and Mirex among male Lake Ontario sportfish consumers: the New York State Angler cohort study. dichlorodiphenyldichloroethylene.155(4):313-322.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Davis MD. Longnecker MP. Hayes WJ. Biochem Pharmacol 1997.58:1185-1201.162:890-897. Piechotowski I. et al. Willman EJ. Neonatal exposure to neurotoxic pesticides increases adult susceptibility: a review of current findings. Lancet 2001. The Great Lakes Consortium. Angerer J. Levels of DDT. Savitz DA. Toxicological profile for DDT. Ostby J. Eriksson P. Becker K. et al. Needham LL. Food and Drug Administration (FDA). Garrett N. et al. Klebanoff MA. Epidemiology 2006. Moysich KB. Hurd C.fda.2-bi(p-chlorophenyl)ethylene and risk of cryptorchidism. and other chemicals. Buckland SJ. Am J Epidemiol 2002. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Sci Tot Environ 2006. Lepom P. DDT and human health. Available at URL: http://www. Organochlorines in Swedish women: determinants of serum concentrations. Falk C. Environ Health Perspect 2003. Seiwert M. Longnecker MP. Effects of environmental antiandrogens on reproductive development in experimental animals. Current internal exposure to pesticides in children and adolescents in Germany: blood plasma levels of pentachlorophenol (PCP). Crespo J. 4/21/09 Gladen BC.gov/ toxprofiles/tp35.72:261265. Barr DB. HCH. et al. Herrman T.85:504508. Hanrahan L. Schulz C. Zaidi SS. Kaus S. Baker RJ. Koepsell TD. Organochlorines and breast cancer risk. Prenatal DDT exposure in relation to anthropometric and pubertal measures in adolescent males. Environ Res 2004. Environ Res 2005. Zhou H. Klebanoff MA. Cerrillo I.111:349355. Environ Health Perspect 2004. a biostable metabolite of dichloro(diphenyl)trichloroethane (DDT). Needham LL. Durham WF. Paepke O. Environ Health Perspect 1998. Olson JR. Parks L. Chen CW. Gunderson EL. Neurotoxicol 2000.52:301-309. hexachlorobenzene. Kulkarni PK. Wolf CJ. Swanson MK. The effect of known repeated oral doses of chlorophenothane (DDT) in man. Heudorf U. Gladen BC. Association between maternal serum concentration of the DDT metabolite DDE and preterm and small-for-gestational-age babies at birth. Cueto C. Gabrio T.206:485-491. lindane (g-HCH). Calle EE. Available at URL: http://www. J Assoc Off Anal Chem 1988.html. Charles MJ.cdc.106(5):279-289.71(6):1200-1209. Klebanoff MA. Needham LL. Beard J. Hum Reprod Updat 2001. Bloom MS. Botella B. and dichloro(diphenyl)ethylene (DDE). Arnold SF. et al. Lambright C.355:7889. Maternal serum level of 1.cfsan. Jr. Maternal DDT exposures in relation to fetal and 5-year growth. Granath F. et al.96:34-40. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods.97(2):178192. Vorojeikina DP. Glynn AW.21(1-2)37-48. and polythelia among male offspring. August 2008. Notides AC. Krause C. Gray LE Jr.358:110-114. Fourth National Report on Human Exposure to Environmental Chemicals 95 . Transcriptional activation of the human estrogen receptor by DDT isomers and metabolites in yeast and MCF-7 cells. Zoellner I. Kashyap R. Exposure of women to organochlorine pesticides in Southern Spain. Atuma S.html. Olson J. Rivas A. Hediger ML.54:1431-1443. Int J Hyg Environ Health 2002. Jusko TA. et al.

54:1509-520. J Toxicol Environ Health 1989. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults.53:455-477. Chemosphere 2004. Jones CR. Thomas PE. Radomski JL. J Toxicol Environ Health Part A 1998. Pavuk M.27:405-421. Eds. Arch Pediatr Adolesc Med 1996. Academic Press. Chlorinated Hydrocarbon Insecticides. et al. Astolfi E. DDE. Demographic and seasonal influences on human serum pesticide residue levels. Lubet R. et al. Chovancova J. Petrik J. PA. Neurochemical targets and behavioral effects of organohalogen compounds: an update. 96 Fourth National Report on Human Exposure to Environmental Chemicals . Smith AG. Snedeker SM. Fonnum F. Toxicol Appl Pharmacol 1971. 1991 pp. Handbook of Pesticide Toxicology. New York. Rey AA. Vol.150:981-990. Environmental exposure to PCBs and cancer incidence in eastern Slovakia. Environ Health Perspect 2001. DDE.36:253-589.20(2):186-193. Stehr-Green. Nims R. 2 Classes of Pesticides. Jr and Laws ER. Cerhan JR. Comparative pharmacodynamics of CYP2B induction by DDT. Fox S. Schecter A. Rogan WJ. Deichmann WB. Reddy AB. and dieldrin.109:35-47. children and newborn infants. In Hayes WJ. Lynch CF. Jr. Inc. Pollutants in breast milk.Organochlorine Pesticides Mariussen E. Pesticides and breast cancer risk: a review of DDT. Crit Rev Toxicol 2006. 731-915. and DDD in male rat liver and cultured rat hepatocytes.

and occasionally at low levels in sediment and surface waters.. endrin has been detected with declining frequency in U. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S. Human health effects from endrin at low environmental doses or at biomonitored levels from low environmental exposures are unknown.S. Kavlock et al. Because it is metabolized so rapidly.. Endrin was not widely used as a termiticide. or from contact with contaminated soils and sediments in areas where endrin was applied. 1992). Skeletal abnormalities and cleft palate in the offspring were associated with endrin when it was fed to pregnant laboratory rodents (Chernoff et al.20 (<LOD-5. endrin can persist for years. EPA. An epidemic of acute endrin poisoning. Endrin was used as an insecticide.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 5.50) < LOD 5.60 (5. Serum Endrin (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U. Endrin does not accumulate in body tissues (IPCS. 2008). 1991). Survey Geometric mean (95% conf. anti-12hydroxyendrin.40) < LOD 547 433 487 446 1000 831 Limit of detection (LOD. rodenticide and avicide. 1979. 1987).40-5. Over time. endrin blocks inhibitory neurotransmitters in the central nervous system resulting in excitation and seizures (Narahashi et al. 1991). Ketoendrin is a major photodegradation product (IPCS.20 (<LOD-5. 1996.S. manufactured.S. Depending on soil conditions.40 (<LOD-6. characterized by generalized seizures in previously healthy persons occurred in Pakistan when sugar contaminated with endrin was ingested (Rowley et al. < LOD means less than the limit of detection. endrin usually is not detected in serum of exposed individuals.50) < LOD < LOD < LOD 5. inhalation or dermal exposure routes. a stereoisomer of dieldrin. total diet surveys (FDA. is no longer manufactured in the U. largely the result of historical agricultural application or run off from contaminated soils (ATSDR.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..09 and 7.30 (<LOD-6. 1992). 1981). In the body.S.8. 1992). unless the dose is high and the exposure is very recent. 1992.. Further conversion occurs to 12-ketoendrin and various conjugated metabolites which are excreted in urine and feces. General population exposure can occur after ingestion of endrin residues on food items imported from countries where endrin is still used.30) < LOD 5. Fourth National Report on Human Exposure to Environmental Chemicals 97 . see Data Analysis section) for Survey years 01-02 and 03-04 are 5.Organochlorine Pesticides Endrin CAS No. unlike aldrin and dieldrin. fatty infiltration. At high doses. IPCS. have been cancelled by the U. Hepatic effects of endrin exposure have included necrosis. Smith. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. Endrin has been detected in soils.40) < LOD size 2187 1825 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 03-04 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 5. and inflammation (Smith. or discarded. 72-20-8 General Information Endrin. High doses produced renal tubular necrosis and diffuse kidney degeneration in animals. endrin is converted rapidly to its major metabolite. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5. Endrin is absorbed rapidly after ingestion.10 (<LOD-5.10 (<LOD-5. All uses of the pesticide in the U.

.24 ng/g of serum) (Botella et al.020) < LOD .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 . Finding a measurable amount of endrin in serum does not mean that the level of endrin causes an adverse health effect.020) < LOD . Biomonitoring Information In the NHANES 2001-2002 and 2003-2004 subsamples. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.020 (<LOD-. IARC has determined that endrin is not classifiable with regard to human carcinogenicity. Workplace exposure standards for endrin have been established by OSHA.020 (<LOD-. 2004..020-. environmental levels) and health effects of endrin is available from ATSDR at: http://www. which may vary for some chemicals by year and by individual sample. serum levels of endrin were below the limit of detection.020 (<LOD-.. In a small study of Spanish women hospitalized for elective surgery. with the highest value 6. Biomonitoring studies on levels of endrin provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of endrin than are found in the general population.atsdr.html. 98 Fourth National Report on Human Exposure to Environmental Chemicals . endrin was detected in 9% of serum samples.S.gov/toxpro2.Organochlorine Pesticides The U.cdc.e. and the FDA monitors foods for pesticide residues. population from the National Health and Nutrition Examination Survey.020) < LOD < LOD < LOD . Ward et al. This finding is consistent with other general population studies (Bates et al. Information about external exposure (i.24 ng/mL (about 6.020 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2000). Serum Endrin (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U.020) < LOD < LOD < LOD 730 539 1457 1286 01-02 03-04 01-02 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .020) < LOD < 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 . 2004).020) < LOD 547 433 487 446 1000 831 < LOD means less than the limit of detection for the lipid adjusted serum level.020 (<LOD-.020 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th .020 (<LOD-.S. Survey Geometric mean (95% conf. EPA has established environmental standards for endrin..

I. pp. 1992. et al. Available at URL: http://www.96:34-40.79(6):928-934. Academic Press.fda. Narahashi T. Cerrillo I. August 2008. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. New York. Food and Drug Administration (FDA).cfsan. Toxicology 1981. Olea-Serrano MF. Gray LE. Endrin [online].13:155-165. Environ Res 2004.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Fourth National Report on Human Exposure to Environmental Chemicals 99 . Hanisch RC. Chlorinated Hydrocarbon Insecticides. Sokal D. Hardjotanojo W. Burse VW. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Convulsions caused by endrin poisoning in Pakistan. Rogers E. 4/21/09 Kavlock RJ. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Jr. Garrett N. Frey JM. II. Available at URL: http://www. Liddle J. Vol. Toxicol Lett 1992. Crespo J. Chemosphere 2004. Needham LL. Environmental Health Criteria 130. Inc. Smith AG. et al.54:1431-1443.gov/toxprofiles/tp89. Hanisch RC. Eds. 4/21/09 Bates MN. Grajewski B.htm. et al.atsdr.9:1357-136.inchem. Buckland SJ. Gray JA. Toxicological profile for endrin [online]. No:429-436. Available at URL: http://www. Ellis H. Chernoff N. Patterson DG Jr.64-65 Spec. Andersen A. Ward EM. Patterson DG Jr. Rivas A.gov/~dms/ pesrpts. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. 731-915. Cancer Epidemiol Biomarkers Prev 2000. 1991.21:141-150. Botella B. Pediatrics 1987.org/documents/ehc/ehc/ ehc130. Ginsburg KS. In Hayes WJ. Whitehouse DA. Perinatal toxicity of endrin in rodents. Schulte P. Rowley DL. Fetotoxic effects of prenatal exposure in hamsters. 2 Classes of Pesticides. Chernoff H. Rab MA. Sodium and GABA-activated channels as the targets of pyrethroids and cyclodienes. August 1996. Perinatal toxicity of endrin in rodents. Handbook of Pesticide Toxicology. et al. Turner W.html. Olea N. 4/21/09 International Programme on Chemical Safety (IPCS). Gray LE.cdc. Exposure of women to organochlorine pesticides in Southern Spain. Roy ML. Kavlock RJ. Saleem M. Fetotoxic effects of prenatal exposure in rats and mice. Gray J. Jr and Laws ER.html. Toxicology 1979.

8 (26.7) < LOD < LOD 75th < LOD < LOD 90th * * 15.8.6-trichlorophenol (2.3 (20.4) Age group 12-19 years 99-00 01-02 03-04 99-00 01-02 03-04 * * 13. HCB is well absorbed after oral administration.0.9-15. and accumulates in fatty tissues where it persists for years. wildfowl.6 (24.9) < LOD < LOD 15. Urinary metabolites include pentachlorophenol (PCP).6-19.1 (17. these metabolites can also be produced after exposure to other chlorinated compounds (Kohli et al.4 (18.8-15.5-14.4 (18.6-32.6) < LOD < LOD 26.4-15.. 2002).4. Hexachlorobenzene has entered the environment as a result of industrial activities and pesticide applications. air.S.9) < LOD < LOD 19.5-trichlorophenol (2.Organochlorine Pesticides Hexachlorobenzene CAS No.S.0) < LOD < LOD 15. 1997).6 (21.0 (18. and 03-04 are 118.7) * * 14. and 7.9) 19.4) < LOD < LOD 22.8) 583 554 460 350 511 488 636 1052 888 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.2-15.2-15.9 (25.5-33.6) < LOD < LOD 25.9-17.4) < LOD < LOD 33. Therefore. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.1 (14. which may vary for some chemicals by year and by individual sample.6-26. It is a persistent chemical and bioaccumulates in both aquatic and terrestrial food chains (ATSDR.3) 24.6-TCP) (To-Figueras et al.5-18. and sediment (Barber et al. see Data Analysis section) for Survey years 99-00.6) 591 747 588 1111 1530 1373 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * 14.1-20.6) < LOD < LOD 24.8) < LOD < LOD 27. HCB may be created as either a byproduct or an impurity in the manufacturing process for certain chemicals and pesticides. 2005).0) * * 15.0 (25.9) < LOD < LOD 28.2) < LOD < LOD 13.7-30.7 (27.5-TCP) and 2. and foods with a high fat content. < LOD means less than the limit of detection.3-22..7-21.4) < LOD < LOD 19.2 (14. respectively. or game taken from areas with HCB contamination.3 (14.9-24.8 (22.9-32. population from the National Health and Nutrition Examination Survey.3 (16. The FDA dietary surveys have shown that over time.S.7-22. particularly by consuming fish. 2008.7-16.1) * * 15.5 (13.9-30.4.1 (14.9 (14.6 (23.4) < LOD < LOD 23.4 (22.7-16.6-33.7-15. HCB is slowly metabolized.4) < LOD < LOD 14.0-16.9) < LOD < LOD 20.3 (22.8) size 1702 2277 1961 Total years 99-00 01-02 03-04 50th < LOD < LOD 14.1-16.9 (25. Survey Geometric mean (95% conf. 31. 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.5 (14.3-20.3) * * 15.0) < LOD < LOD 15. 2.3) < LOD < LOD 20.9-20.4-16. 118-74-1 General Information Hexachlorobenzene (HCB) was used from the 1930’s to the 1970’s in the U. 1976).9 (23.3-26.5-15.3) < LOD < LOD 29. 100 Fourth National Report on Human Exposure to Environmental Chemicals .2 (13.0) < LOD < LOD 24.5-15.7-26.4. and has been detected in soil.4 (11.8 (15.3 (12. water.2 (14. and elimination occurs by renal and fecal routes.7 (19.0-25.S.7-29. 01-02.5 (13.9) < LOD < LOD 20.2 (17. EPA cancelled its use in 1984.6) < LOD < LOD 26.7) 807 1058 957 895 1219 1004 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * 16.4..4) < LOD < LOD 18. 1988).0 (14.7 (15. primarily as a fungicide and seed treatment until the U.1) < LOD < LOD 15.6) < LOD < LOD 14.0-19.2 (24. Although it is not manufactured as an end-product in the U. breast milk is an additional route of elimination in nursing women.3 (22. distributes widely throughout the body. The general population may be exposed to HCB through diet.2) < LOD < LOD 29.2-31.4..0-28. Gunderson.5-14.0 (18.5) < LOD < LOD 18.7) < LOD < LOD 24. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD 28.6-44. Workers in chemical manufacturing industries may be exposed to HCB via inhalation or dermal pathways.9) < LOD < LOD 16. HCB has been detected in fewer foods since the 1980s (FDA.7 (15.1 (13.

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

4/21/09 Barber JL. Otero R. Int J Hyg Environ Health 2002. Food and Drug Administration (FDA). but approximately five times higher than the overall geometric mean level in 2003-2004 (Becker et al. Eskenazi B. than the limits of detection (on a whole weight basis) in NHANES 19992000 and 2001-2002 (Herrero et al. Ozalla D. Biomonitoring of persistent organochlorine pesticides. Fenster L. Becker K.17:388–399. factory workers chronically exposed to HCB and residents near the factory had serum HCB levels that were 150 to 50 times higher. Organochlorines in Swedish women: determinants of serum concentrations. Sala M. lower than the limit of detection (on a lipid adjusted basis) in NHANES 1999-2000 and 20012002. 2002. only 4. Herrero C. levels. 2006). 4/21/09 Glynn AW.. Link et al. Epidemiology of hexachlorobenzene-induced porphyria in Turkey: clinical and laboratory follow-up after 25 years. et al. April 1982 to 1984. Lackman. Seiwert M. Herrman T. 2003). IARC Sci Publ 1986. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Environ Health Perspect 2003. Kohli J. Gunderson EL. Glynn et al. Zoellner I. Safe A. HCB detection in serum also was proportional to age. FDA Pesticide Program Residue Monitoring 1993-2006 [online]. Granath F. In a representative sample of the 1998 German adult population. Urinary porphyrin excretion in a human population highly exposed to hexachlorobenzene. 2002. Schwartz JM. Biol Neonate 2002. van Wijk D. but overall. Kaus S. Dogramaci I. Available at URL: http://www. more HCB levels were quantified. Finding a measurable amount of hexachlorobenzene in serum does not mean that the level of the hexachlorobenzene causes an adverse health effect. 2002.cdc. Bertram et al. Lackmann.9% of participants had quantifiable levels (Stehr-Green. 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.135(4):400404. et al. Can J Biochem 1976.77:173182.81(2):82-85. et al. Barr DB. however. Polychlorinated biphenyls and hexachlorobenzene in full-term neonates. References Agency for Toxic Substances and Disease Registry (ATSDR). Agerelated increases of HCB in body fat and serum have been consistently noted in general population studies (Becker et al.. Cripps DJ.. dietary intakes of pesticides. Factors predicting organochlorine pesticide levels in pregnant Latina women living in a United States agricultural area. Temporal trends of organochlorine concentrations in umbilical cord blood of newborns from the lower north shore of the St.cfsan.54(3):203-208.. Residency near industrial or agricultural areas has been associated with higher serum HCB levels (Barber et al. Canada). Over the past two decades. Arch Dermatol 1999.205:297-308. Bjerselius R. Gabrio T. 1986.58:1185-1201. Bryan GT.. Bertram HP. 2002) and among children (Link et al. Holland NT. Jones D. Sweetman AJ. selected elements. Muller C. Gocmen A. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003..110(8):835-838. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. trends and processes.Organochlorine Pesticides in the NHANES 1999-2000 and 2001-2002 subsamples. J Assoc Off Anal Chem 1988. Muckle G. 102 Fourth National Report on Human Exposure to Environmental Chemicals . Lecha M.atsdr. declines in background HCB levels ranging from around 50%90% have been documented in studies using cord blood (Dallaire et al. Link B. Reference values updated. Environ Health Perspect 2002.. 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. Atuma S. Arch Neurol 1982. Lackmann GM. Aune M. and the geometric mean concentration of HCB in whole blood was 0. HCB levels were directly related to age. August 2008. Krause C.gov/~dms/ pesrpts.349:144. Dewailly E.71(6):1200-1209. Kemper FH. et al. 1989). distribution.html. Schulz C. 2002). Peters HA. In the 1976-1980 NHANES subsample. Santiago-Silva M.111:349355.. Darnerud PO. 2005).. Lawrence River (Quebec. Toxicological profile for hexachlorobenzene update [online]. Paepke O. The metabolism of higher chlorinated benzene isomers. September 2002. Jones KC. Chemosphere 2005. respectively. 2005).39(12):744-749. Bradman A.44 mg/L. Hexachlorobenzene in the global environment: emissions.. and other chemicals. Dallaire F. Ayotte P. 1999).gov/ toxprofiles/tp90. In Spain. Hexachlorobenzene content in human whole blood and adipose tissue: experiences in environmental specimen banking. Laliberte C. 2002. J Exp Sci Environ Epidemiol 2007. Available at URL: http://www.. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Piechotowski I. As a result of the lower limit of detection in NHANES 2003-2004. Lepom P. Sci Tot Environ 2005.fda. FDA total diet study. Bradman et al.html. 2005.

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

5-123) 49.5 (43.45) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 16.1 (18.0-70.3) 14.7) < LOD < LOD < LOD < LOD < LOD < LOD 37.2-67. 608-73-1 beta-Hexachlorocyclohexane CAS No.87 (9. General population Serum beta-Hexachlorocyclohexane (lipid adjusted) Geometric mean and selected percentiles of serum concentrations (in ng/g of lipid or parts per billion on a lipid-weight basis) for the U.8-68.80 (6. 6.2-55. **In survey period 2001-2002.5) 40.2) 13.9 (40.4) < LOD 9.5528.0) 35. 01-02.8 (17.8) * * * * * * 15.7) 18. interval) 9.50) 8.8-16.9-81. respectively. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf.1 (30.6) 653 758 589 1240 1533 1370 20 years and older 10.2 (34.5 (37.6 (33.6-47.9 (32.2-22.S.7) 32. Lindane (1%) lotion and shampoo are available by prescription for singleuse application to treat human scabies and head lice.2-42.7 (35. HCH does not bioaccumulate to an appreciable extent in plants (ATSDR.8 (33.1 (9.0-20.4) 21.7 (25.2) 62.S.36.3-85.6-37.7) 27.4 (50. EPA cancelled agricultural uses of lindane (ATSDR.6-14.9) 15.09) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD 14.1) 12.68 (<LOD-10.1) 31.6 (22.7) 23.9 (30.2-87.4-111) 84.6) 50. 2005). HCH isomers are lipophilic.20-16.0 (19.1-32.2-17.0 (<LOD-12.4) 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 21.0 (35.2-98.7) 10.1 (16.6 (40.76. beta.1-16. can be used as an insecticide and has been used to kill soil-dwelling and plant-eating insects.7-26. population from the National Health and Nutrition Examination Survey. formerly referred to as benzene hexachloride.4) 10. see Data Analysis section) for survey years 99-00.9 (26.8-199) 134 (85. containing about 64% alpha and 10%-15% gamma isomers.1-49.1-32.6) 36.2-52.4 (52.3 (42.1) 71. and delta. 319-85-7 gamma-Hexachlorocyclohexane CAS No.6-89.0 (14.60-13.7 (29.9) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th 19.0 (8.5 (24.6-18.9-14.6 (16. Lindane has a half-life of about two weeks in soils and water.9-178) 48.S.5 (11. It is no longer produced or sold in the U.80 (<LOD-14.9) 45.5) 29.46-11. Technical grade HCH is a mixture of all four isomers.0-111) 70.7) 97.6 (17.4) 44.8. 58-89-9 General Information Hexachlorocyclohexane (HCH).8 (64.7-69.90-8.2) 36.3) 34.1-27.9-21.7 (53.2 (31.70 (6.4 (16.0) 7.9-51.7 (30.3 (42.7 (62.1-36.2) 142 (99.9 (9.1) 12.6) 47.7-96.7 (<LOD-16.6) 16.9-24.2 (50. However.2 (18.7-166) 70.5) 14.0) 17.1 (27.6 (10.1 (12. HCH isomers.7) 10. 104 Fourth National Report on Human Exposure to Environmental Chemicals .5 (8.70 (8. and 7.8) 95th 68.7-96.0-23. exists in several isomeric forms.4 (11. water.1 (11.6-20.4-73.4 (12. and have been used either as fungicides or to synthesize other chemicals. gamma.4 (8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.66-12. environmental levels declined.6-42. the U.8) 52. The other isomers can be formed during the synthesis of lindane. including alpha. soil.2 (48. particularly alpha and gamma have been detected widely in air.5) 632 563 460 403 513 487 702 1051 887 Non-Hispanic blacks Non-Hispanic whites Limits of detection (LOD.1-15.5 (16.Organochlorine Pesticides Hexachlorocyclohexane CAS No. commonly known as lindane.70-12.0) 41.30-11.0) 71.9 (62.90) 7.8) 39.0-34.5) 11.04-10.2-46.8 (9.8) 12.7 (13.1 (9.5 (14.5) 22.5) 90th 42.2) 9.8-87.7-69.4) 27.90-8.5) 16. so they can accumulate in fatty tissues of animals.3) 37.2 (29.4) 51.9-56.9) 81.9 (50.8) < LOD 10.2 (9.8-19.8) 7. See the section “What’s New” at the beginning of this Report for details.6-135) 69.0-21. and sediment as a result of historic production and use.7) 73.2-20.89 (<LOD-9. < LOD means less than the limit of detection.5-29.8 (21. and 03-04 are 9. In 2006.6-62.4) 11.3-56.4) < LOD < LOD < LOD 46. The gamma isomer.6) 35.43 (<LOD-9. which may vary for some chemicals by year and by individual sample.8 (32.8 (23. each result has been multiplied by 1.8) 27.9 (11.3 (62.4-50.0) 8.4-45.61-12.3 (26.3-38.6) 18.3) 51.8-54.0 (37.1) 13.3 (13.0-70.0 (33. As pesticide applications of HCH were increasingly restricted or eliminated.7-20. 2005).1-37.9) 17.56-12.70-19.1 (21.3) 25.8 (10.7) 56.5) 67.4) 901 1067 952 992 1224 1007 Females 11.

244-.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.100-.460 (. enlarged livers.100 (.S.078 (.070) . which may vary for some chemicals by year and by individual sample.150) . and seizures.073-.350) .294-.281 (. for lindane.065 (.050 (<LOD-.410) . Pesticide applicators or agricultural workers could be exposed to HCH by inhalation and dermal pathways. 1971.412 (.240-.320 (.270 (.083 (..173-.120 (.216 (. The U.160-.210 (.250 (.067 (. paresthesias.118-.350 (.058) < LOD Gender Males 99-00 01-02** 03-04 99-00 01-02** 03-04 * * * < LOD < LOD < LOD .330 (.308-.103 (.096) .420-. HCH isomers are metabolized to chlorophenol metabolites that are excreted in the urine (Angerer et al.580 (.060) .047-.089-.064 (.080-.089) .146-.130) .404) .400) .661) 901 1067 952 992 1224 1007 Females . from 6% of samples in 1982-1984 to 2% in 1994 (FDA.390 (.067) . See the section “What’s New” at the beginning of this Report for details.380 (.400) .01 (.065 (.080 (.170-.130-.100-.620-1.330-.040-.144 (.090 (.260-.125) < LOD < LOD < LOD .360) .410 (.131-.280-.214) .210) . resulting in a half-life of about seven years.220) .120-.120) .110) .081-.5528.160) .091) .480) . or dermal exposure.058 (<LOD-. ingestion.167 (.150) .37) 1. 2002).139 (.221-.190-.560 (.310 (. IARC classifies Serum beta-Hexachlorocyclohexane (whole weight) Geometric mean and selected percentiles of serum concentrations (in ng/g of serum or parts per billion) for the U. 1983).. and memory loss (Nigam et al.080) .501) .170-.080-.057-.234 (. ataxia.250) .310) .600) .680) .051 (<LOD-.290 (. Rogan.521 (.340) . each result has been multiplied by 1.056-.620) .062 (.710) .064) . HCH crosses the placenta and is also excreted in breast milk (Radomski et al.Organochlorine Pesticides exposure to HCH is through the diet. After dermal application of lindane 1% lotion. Gunderson 1988).057 (<LOD-. Distribution is mainly to fatty tissues.200 (.250-.068-.560) .587) 653 758 589 1240 1533 1370 20 years and older .050-.310) .057-.840) .110-.910 (.056-.072 (.050-.450) . 1996.480 (.070 (.048 (<LOD-.057) < LOD Race/ethnicity Mexican Americans 99-00 01-02** 03-04 99-00 01-02** 03-04 99-00 01-02** 03-04 .100-.340-. tremors.120-.124-.331 (.140) .260) .290 (.050) .222 (.372 (.070-.190) . EPA has established a drinking water standard.050 (<LOD-..297-.120 (.191-.150 (. 1981). interval) .200-. The beta isomer accumulates in fatty tissues and is metabolized more slowly..05) .470 (.220 (. hepatic enzyme induction.062 (. **In survey period 2001-2002.220-. probably by blocking inhibitory neurotransmitters in the central nervous system.S.230-. Fourth National Report on Human Exposure to Environmental Chemicals 105 . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.050-.070-.200-.250 (.300-.050 (.174) .. Human health effects from HCH isomers at low environmental doses or at biomonitored levels from low environmental exposures are unknown.140) .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 .570 (.580-1. When animals were chronically fed lindane at high doses.410-.100 (.103) 90th .390-.382-.442 (.220-.086) < LOD < LOD < LOD < LOD < LOD < LOD .070-.069) .090 (.120) .120 (. and nephropathy developed (IPCS.050 (.191-. and FDA has established a bottled water standard and food residue tolerances for lindane. Saxena et al. the serum half-life was about 20 hours among children (Ginsburg et al.100) .700) .370-.140 (. U.077) < LOD .814) .050-. 2008.090-.080-.180-.290 (. FDA pesticide monitoring program has shown a temporal decline in the detection of lindane.051-.360-.110) .098 (.150-.118 (.290) .480 (.090 (.100) . population from the National Health and Nutrition Examination Survey.250 (. Survey years 99-00 01-02** 03-04 Geometric mean (95% conf. 1986).130 (.290) . Acute high doses of lindane after ingestion or excessive skin application of the 1% lotion have produced seizures in humans.119) .305) .077) < LOD .240 (. OSHA and ACGIH have established workplace standards and guidelines.059-.175 (.190) .120-.260) . 1977).210-.160 (.190-1.287 (.080) * * * * * * .450 (.S.470) .254) 95th .32) . respectively.110) .319) .510) .360 (.103-.066) Selected percentiles ( 95% confidence interval) Total * * 50th < LOD < LOD < LOD 75th .410) .280-.080 (. Workers who directly handled HCH have complained of headache.140) . HCH isomers are absorbed after inhalation.092 (.460) .690) .250-.070 (.083) . Acute high dose toxicity in rodents affects the central nervous system producing decreased activity.210 (.450-.

respectively. Link et al. were similar to the 95th percentiles in this Report. 2005. 106 Fourth National Report on Human Exposure to Environmental Chemicals . beta-HCH may be detected in a higher percentage of the general population than are the other HCH isomers. 1998. which were considerably lower (as much as twentyfold) than mean levels reported in small studies of adults in Spain (Botella et al.. Bates et al. Sturgeon et al. and 7. Stehr-Green. environmental levels) and health effects is available from the U. In NHANES 1999-2000. 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.atsdr. Additional factors associated with higher beta-HCH levels include rural residence. which may vary for some chemicals by year and by individual sample.html. In recent years. 2002. see Data Analysis section) for Survey years 99-00. older age. EPA at: http://www. Studies of general populations have shown declining beta-HCH levels since the 1970s (ATSDR. 1991. 2001-2002. and NTP classifies hexachlorocyclohexane isomers as reasonably anticipated to be human carcinogens. Kutz et al.epa.. aged 9-11 years. < LOD means less than the limit of detection. 1989). and 03-04 are 14. and 2003-2004.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. and a diet that includes meat (Becker et al. the maximum and 95th percentile beta-HCH values. 01-02. 1991.. Becker et al.. In an earlier (1996-1997) sample of German children. 2004).5. Radomski et al. 2004.. studies in populations with environmental exposure have reported lindane levels below the limit of detection in most persons (Anderson et al. respectively.gov/toxpro2. male sex. Survey Geometric mean (95% conf. serum levels of lindane were generally below the limits of detection. 2005..e. 1971.5.8... In populationbased studies of New Zealand adults and German adults and children. More information about external exposure (i..Organochlorine Pesticides hexachlorocyclohexane isomers as possibly carcinogenic to humans. Kutz et al.S. 1998). 1989... 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. 2002).S.gov/pesticides/ and from ATSDR at: http:// www.cdc. 2004) and India (Bhatnagar et al. population from the National Health and Nutrition Examination Survey. Stehr-Green. 10. Biomonitoring Information Because of its longer half-life.

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

Kaus S.106(5):279-289. Environ Health Perspect 1998. Rivas A. Int Arch Occup Environ Health 1983.cfsan. Atuma S. Radomski JL.27:405-421. Krishna Murti CR. Available at URL: http://www. et al.html.fda. Saxena MC. Ellis H. HCH. Saiyed HN. Kutty D. et al.72:261265. Absorption of lindane (g benzene hexachloride) in infants and children. Schulz C. Crespo J. Demographic and seasonal influences on human serum pesticide residue levels. Blood levels of organochlorine pesticides in Argentina: occupationally and nonoccupationally exposed adults. Arch Toxicol 1981. Bjerselius R. FDA Pesticide Program Residue Monitoring 1993-2006 [online].48:127-134. Heinrich R. Paepke O. Rev Environ Contam Toxicol 1991. Piechotowski I. VI. Bai KM. Angerer J. Placental transfer of pesticides in humans. Toxicol Appl Pharmacol 1971. Zoellner I. Olson J. Center for Food Safety and Applied Nutrition/Office of Plant and Dairy Foods. Krause C.gov/~dms/pesrpts. Needham LL.cdc. Toxicological profile for hexachlorocyclohexanes update [online]. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Zaidi SS.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Chemosphere 2004. Herrman T. Needham LL. Needham LL.111:349355. Nigam SK.150:981-990. Metabolism of gammahexachlorocyclohexane in man. Visweswariah K. Lepom P. org/documents/jmpr/jmpmono/2002pr08. Gabrio T. Lindane.205:297-308. Maass R. FDA total diet study. Darnerud PO. Becker K. Serum hexachlorocyclohexane residues in workers engaged at a HCH manufacturing plant. The Great Lakes Consortium.91:998-1000. et al. Burse VW.9(4):417-424. Hanrahan L.58:1185-1201. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.atsdr.52(1):59-67. Reisch JS. Seiwert M. Karnik AB. Rogan WJ. Stehr-Green. Deichmann WB. Rothman N. Exposure of women to organochlorine pesticides in Southern Spain. Available at URL: http://www. selected elements. Chemosphere 2005. Occupational exposure to hexachlorocyclohexane. Persistent organochlorines in the serum of the non-occupationally exposed New Zealand population. Glynn AW. et al. dietary intakes of pesticides. Majumder SK. Sturgeon SR. Bull Environ Contam Toxicol 2004. PCD/PCDFs and dioxin-like PCBs in blood of children from South West Germany (Baden-Wuerttemberg) from 1993-2003. 2002. Kulkarni PK. Cancer Causes and Control 1998. August 2008. Arch Pediatr Adolesc Med 1996. J Toxicol Environ Health 1989. Garrett N. Serum concentrations of organochlorine compounds and endometrial cancer risk (United States). and HCB residues in human blood in Ahmedabad. Environ Health Perspect 2003. Organochlorines in Swedish women: determinants of serum concentrations.html. Int J Hyg Environ Health 2002. Bhatnagar VK. International Programme on Chemical Safety (IPCS). Granath F. Bottimore DP. Aune M. Pesticide residues in food-2002-Joint FAO/WHO meeting on pesticide residues. et al. J Assoc Off Anal Chem 1988. Environ Res 2004. Patterson DG Jr. 4/21/09 Anderson HA. Organochlorine pesticides and polychlorinated biphenyls in human adipose tissue. Raju GS. Lowry W. Buckland SJ. Kashyap R. Gunderson EL. Olea N. children and newborn infants. 4/21/09 Ginsburg CM. et al. Brinton LA.htm. India. Falk C. Int Arch Occup Environ Health 1986. Bates MN.96:34-4Food and Drug Administration (FDA). Astolfi E. gov/toxprofiles/tp43. Wood PH. Levels of DDT. Bhargava AK. Olea-Serrano MF. Botella B. 4/21/09 Kutz FW.inchem. et al. and other chemicals. 108 Fourth National Report on Human Exposure to Environmental Chemicals . available at URL: http://www. Cerrillo I. August 2005.54:1431-1443.20(2):186-193. Potischman N.57(4):315-320. Brock JW. Biomonitoring of persistent organochlorine pesticides. Rey AA. Siddiqui MKJ. Link B. PA. J Pediatr 1977.120:1-82. Pollutants in breast milk. April 1982 to 1984.71(6):1200-1209.

2 (7.8 (<LOD-73. especially those from persons living in the southeastern U.10 (<LOD-15.5-291) 11.70-40. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD 57.0) * * * 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. Mirex binds strongly to soil. Mirex contamination of Lake Ontario and adjacent waterways has been well documented (ATSDR.4) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. Fourth National Report on Human Exposure to Environmental Chemicals 109 .. Mirex is absorbed through the skin and from the gastrointestinal tract. 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.1 (13.4) < LOD 15.7 (<LOD-47.3 (15. EPA have issued public health advisories or warnings that fish from contaminated lakes and rivers may contain mirex. 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. after which it is widely distributed in the body and stored in fat. and 7.6 (<LOD-23.6-305) 15.5 (<LOD-42. soil.0 (14.3 (15.5 (9. (Kutz et al.5 (<LOD-115) 153 (30.S.5.0-374) 11. or pesticide application. Survey Geometric mean (95% conf.Organochlorine Pesticides Mirex CAS No. sediments. Occupational exposure is limited to workers at sites where mirex contamination is present.S.40 (<LOD-13. its major uses were as a flame retardant additive and as a pesticide to kill fire ants and yellow jackets in the southeastern U. population from the National Health and Nutrition Examination Survey. respectively.2) 51.70 (<LOD-15. and 03-04 are 14. < LOD means less than the limit of detection.6) 9.4-230) 18.90-29.1 (8. 1985. which may vary for some chemicals by year and by individual sample.5-425) 40.8) < LOD 15.3) < LOD < LOD < LOD < LOD < LOD < LOD < LOD 15.S.3-225) 15.6 (<LOD-108) 9.2-230) 13. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.70-24.0 (12. aquatic organisms.1 (<LOD-65. 10. disposal. 1995).3) 887 1052 949 966 1205 1002 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 13. Mirex has been detected in air.7 (12. water.8 (12.6 (<LOD-31.10-37.7) 8. Some states and the U.6) < LOD < LOD < LOD < LOD 71. Mirex can cross the placenta and be excreted in breast milk. 01-02.0 (<LOD-108) < LOD < LOD 50.S. since 1977.1 (<LOD-104) < LOD < LOD < LOD < LOD 39.6. In studies conducted in the 1970’s and 1980’s..4 (8. Ingested mirex that is not absorbed is eliminated in the feces within about 48 hours. and foods.7) < LOD 66. resulting in exposure to newborns and nursing infants.8. where it has a half-life of 12 years.6) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th 15.4) < LOD 63. see Data Analysis section) for Survey years 99-00. Mirex is not metabolized in the body. it is a highly persistent chemical in the environment. Formerly. where it was applied directly to soil and by aerial spraying. 2385-85-5 General Information Mirex has not been produced or used in the U. mirex was detected in human adipose samples.5-82. 1991). animals.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.

S. as well as in a subsample of NHANES II (1976-1980) participants.690) .108 (. and the FDA monitors foods for pesticide residue and has established an action level for mirex in fish tissue.080-1.73) .090 (<LOD-.256 (.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 .054 (<LOD-. EPA has established environmental standards for mirex. population from the National Health and Nutrition Examination Survey.635) < LOD .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 . and 2003-2004 subsamples. Biomonitoring Information In the NHANES 1999-2000.052-. 110 Fourth National Report on Human Exposure to Environmental Chemicals . More information about external exposure (i. 1995.470) . reproductive toxicity included decreased fertility and testicular damage.450 (..7 ng/g of lipid.059 (<LOD-.S.02) .79) . Fishermen in New York who consumed Great Lakes sport fish had median levels of lipid-adjusted serum mirex that were lower than the 95th percentile value among males the NHANES 2001-2002 subsample (Bloom et al. IARC classifies mirex as possibly carcinogenic to humans. The geometric mean mirex levels of the Inuit mothers were 8. 1989).cdc. The U. 1991).220 (<LOD-.610) < LOD < LOD < LOD < LOD .41) .79) . and NTP classifies mirex as reasonably anticipated to be a human carcinogen. environmental levels) and health effects is available from the ATSDR at: http://www.450) 1.268) < LOD .470 (.430 (.089-. Survey Geometric mean (95% conf. In addition.92) .470) . 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 .064 (<LOD-.090 (<LOD-. and 4.079 (<LOD-.140 (<LOD-. 2005).106) < LOD .510) < LOD < LOD . which may vary for some chemicals by year and by individual sample.102) < LOD < LOD < LOD < LOD .080-1.220) .html. In samples obtained between 1994 and 1997.gov/toxpro2.053-.070-1.Organochlorine Pesticides exposures are unknown.106 (.37) .100 (<LOD-.174) 617 548 459 398 500 484 688 1049 884 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the lipid adjusted serum level.410 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2001-2002.170) < LOD . Smith. 7.090-1.e. developmental abnormalities including cataracts and edema in the offspring have been reported (ATSDR.atsdr..093 (.. Laboratory animals fed high doses developed liver enlargement and liver tumors.090-1. serum mirex levels were generally below the limits of detection (Stehr-Green.170-3.100 (<LOD-.062-.055-. 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.170) size 1853 2257 1951 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .090 (<LOD-. which is approximately twofold to threefold lower than the 90th percentile for females in the NHANES 20012002 subsample but similar to 95th percentile for females in the NHANES 2003-2004 subsample (Van Oostdam et al.240) < LOD < LOD < LOD < LOD < LOD < LOD < LOD .110 (<LOD-.077 (<LOD-.310 (. 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.8.112 (.090-1.08 (. 2004).370 (.

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

0) < LOD 11.63) 18.71 (<LOD-8.5TCP and 2.50 (1.40-18.0) < LOD 21.30) < LOD 4. hexachlorobenzene.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 1.60 (4.6-TCP was also used as a wood preservative and may still be used in production of some fungicides (ATSDR. recent sampling of U.0 (3.7.50 (.4.30) < LOD < LOD < LOD < LOD < LOD 1.42 (<LOD-8. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. EPA. which may vary for some chemicals by year and by individual sample. Environmental sources of these compounds include industrial discharges or run off from pesticide facilities or disposal sites.40 (.0 (4.20 (4. 1999). 88-06-2 Metabolites of Organochlorine Pesticides and Other Environmental Chemicals General Information The chlorophenols. 1976).9.5-trichlorophenol (2. General population exposure may occur by ingesting contaminated food or water and by inhaling contaminated air.30-27.27) 696 661 521 696 603 939 Limit of detection (LOD.4.80 (1.0 (3.4. 2.0) 2.27) 482 570 681 815 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.19 (<LOD-6.60-8.80-41. Small amounts of trichlorophenols also can be produced during combustion of natural materials and the chlorination of drinking water or waste water that contains phenols.50-63.3.40 (1.30-44.920-3. are metabolites of several organochlorine chemicals.40 (2.4.40) < LOD 6.6-trichlorophenol (2.0) 2.0) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.30 (.0) < LOD 5.50) < LOD 1.40 (2.40 (1. Formation of 2. other organochlorines. 2.S.0 (4.00 (3.20-71.4.00 (2.7) 24.4.57 (<LOD-15.20) < LOD 90th 5. Historically.5-TCP) and 2. Occupational exposures. Survey Geometric mean (95% conf.30-11.4. Such workers would probably Urinary 2.03) 9. population from the National Health and Nutrition Examination Survey.6-Trichlorophenol CAS No.40 (2.9 and 0.80) < LOD 1.0) 2.40) < LOD 1.5-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.10-3.4. 1999).80 (2.S. Trichlorophenols have been detected in fish taken from waters near waste water treatment and industrial discharges (ATSDR. 112 Fourth National Report on Human Exposure to Environmental Chemicals .0) 2.4. 2.40) < LOD 4.4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-Trichlorophenol CAS No.940-3.60-18.00-8.8) 21.8-tetrachlorodibenzo-p-dioxin occurs during the synthesis of 2.0) < LOD 973 1178 1021 1319 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .50-16.0) < LOD 5.6-TCP were used as intermediates in the production of certain pesticides.40 (. 95-95-4 2.30-27.0) 2. surface water.20) < LOD 1. public drinking water systems did not detect 2. Trichlorophenols are no longer manufactured commercially.50 (2.0 (5. including hexachlorobenzene and hexachlorocyclohexanes.4.900-2.4.60 (2.71 (<LOD-8.5-trichlorophenol.30-27. but they may be produced as by-products during manufacturing of other chlorinated aromatic compounds.90-33.0) 14.40 (2.72) < LOD 1.30-3. 2006).0) 2.980-3.0 (4. < LOD means less than the limit of detection.00-3. and sediments.0) < LOD 11. Exposure to trichlorophenols also may result from metabolism of lindane.6-TCP in any of the samples (U. may occur by inhalation or dermal routes.950 (<LOD-1. soils.S.0) 5.42 (<LOD-12.40-11. Both chemicals have been detected in air.00-3.20-36. however.60 (.0) < LOD 5..Organochlorine Pesticides 2.6-TCP). interval) Selected percentiles ( 95% confidence interval) Sample 95th 16. and polychlorinated benzenes (Kohil et al.980-3.20) < LOD 5.30-40. usually at herbicide production or waste incineration facilities.9 (<LOD-121) 9.31 (<LOD-9.0 (8.60) < LOD 8.50-25.

69 (2.5-TCP nor 2.50) < LOD 2. interval) Selected percentiles ( 95% confidence interval) Sample 95th 11.24-11.29 (1.53-3. but almost twenty times higher than 95th percentile values reported in German adults aged 18-69 years (Becker et al.02-3. recent small studies have not demonstrated increased exposure to trichlorophenols in workers who dredged contaminated soils or incinerated waste materials (Agramunt et al. urinary 2.4.57 (<LOD-7. the 95th percentile urinary 2. in addition to dioxins.33) < LOD < LOD < LOD < LOD < LOD 2.3 (5.27-17.74) 11.2) < LOD 5.24) < LOD 1.6-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.Organochlorine Pesticides be exposed to mixtures of chlorophenols.4.4.4.43) < LOD 12.4.79-4.4. However.html.57 (3.4) < LOD 3.4.. At lower doses.19-4.31) < LOD 2.4..6-TCP at low environmental doses or at biomonitored levels from low environmental exposures are unknown. 1995) were similar. was similar to the corresponding percentile for 6-11 year olds in NHANES 1999-2000 (Hill et al.37) 16.9 (5.68-4.4.00-19.6) 4.4..37-11.86 (3. 2003).9) 12.37) 696 661 521 695 603 939 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.15) < LOD 2. 1989).82 (<LOD-32.4..6) 4.44 (1.80 (1.980 (<LOD-1.2) 2.4 (6.43 (2. More information about external exposure (i. Neither 2. In the same 2-6 year old children.5) < LOD 12.11) 482 570 681 814 831 1112 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD 1.78-19.17) 9. as being possibly carcinogenic to humans.24) < LOD 5.60-3. 1995) and up to 19 times higher than the 95th percentile value of 1.1) 2.6-TCP had increased rates of hepatic tumors. Radon et al.24 (3.46 (1.28-25.36 (1.64 (4.6-TCP were developmental or reproductive toxicants in animals (ATSDR 1999). 1989).4) < LOD 3.0 mg/L.6-TCP as reasonably anticipated to be a human carcinogen. furans.32) < LOD 4.90 (4.00-29.3) < LOD 973 1178 1021 1318 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * .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 2.57 (<LOD-7.20-6.6) 4. which includes trichlorophenols. Urinary 2.73 (<LOD-8.68 (<LOD-8..e.8 (5.13-13..5-Trichlorophenol (creatinine corrected) Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.4.0) 7.8) < LOD 9. 2003.75 (<LOD-6.3 mg/L reported in German adults aged 18-69 years (Becker et al.19-12.83-12.4) 5. leukemias. 2003).44 (. animals showed hepatocellular abnormalities. Among 6-11 year old children in NHANES 1999-2000. Biomonitoring Information In the NHANES 1999-2000 and 2001-2002 subsamples.5-TCP and limited for 2. Human health effects from 2.69-18.8) 4.02) < LOD 7. Laboratory animals chronically fed high doses of 2.6-TCP levels at the 95th percentile were up to eight times higher than 3. IARC considers the experimental evidence for animal carcinogenicity inadequate for 2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67 (1.5-TCP. Survey Geometric mean (95% conf. and other chlorinated compounds.5) 11. and lymphomas.55 (4.75 (3.820-2.78 (3. population from the National Health and Nutrition Examination Survey.2 (2.88-16.05-17.05-8.5-TCP or 2.49 (1.47-8... the 95th percentile urinary 2.81 (<LOD-9.gov/toxpro2.93-11.62-20. environmental levels) and health effects is available from ATSDR at: http://www. The 95th percentiles for 2.1 (<LOD-58. 2004).cdc.2) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 2.5-TCP among adults in this Report and in a nonrandom subsample from NHANES III (Hill et al.95 (3.78) < LOD 1.920-2.00) < LOD 4.16 (. IARC classifies combined exposures to polychlorophenols.16) < LOD 90th 5.53-3.S.24) < LOD 6. NTP classifies 2.4.atsdr.6-TCP.7 (4.3 mg/L in a nonrandom subsample from NHANES III (Hill et al. 7. Fourth National Report on Human Exposure to Environmental Chemicals 113 .67 (1..

2) 25. which may vary for some chemicals by year and by individual sample.52 (2.6 mg/g creatinine) and 2. similar to the limit of detection for this Report (Anderson et al.0) 11.4.06) * 2.0 (16. In harbor workers exposed to chlorophenol-contaminated river silt.6-TCP were monitored in a group of hazardous waste incinerator workers from 19992002. Mean values of 2.80-6.90 (3.36 (1.65) 15.20) 4.09-7.10-3.0) 19.60) < LOD 5.4.48-26.23) 2.85 (2.0 (9.0 (4.3 (11. 1991).20 (3.2) 481 574 678 820 830 1109 99-00 01-02 99-00 01-02 2.58 (1.0) 14.70-3.70) 3.18-3.9 (13.0-50.0) 13.0 (15.0) 9.40-2.0 (6.0) 17.01-6.8-24.07 (<LOD-3.40-4.S.0-68.87-14..0) 13.00 (1.60-21. respectively. Biomonitoring studies on levels of 2.80) 1.99) 6.0) 10.32) 3.4. was about six times lower than the median urinary levels for males in this Report (Radon et al.00-21.0 (8.7) * 99-00 01-02 99-00 01-02 99-00 01-02 4.10-3.51-12.90-8.6-Trichlorophenol Metabolite of Several Organochlorine Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.26 (2.4 (10.45 (5.6 (12.23) 3.24 (2.2 (14.6-TCP exposure and health effects.1 (8.72-10.9) 694 677 519 696 602 931 Limit of detection (LOD.00-4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.7 (13. 2003).0 (7.40) 2.10-2.63) 90th 15.6-TCP provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of 2.5-46. Finding a measurable amount of 2.25-11.5-TCP or 2.4.6) 970 1178 1019 1325 99-00 01-02 99-00 01-02 99-00 01-02 2.95-6.0 (15.55-3.33-4.0-41.0 (11.0) 10.6TCP values.0) 9. Urinary 2.98-7.1-25.57 (<LOD-2. 0.0 (6. population from the National Health and Nutrition Examination Survey.8) 18.10) 2.40) 3. Survey Geometric mean (95% conf. for males in NHANES 19992002 (Agramunt et al.28) 24.58-3.60 (2.0) 13.36 mg/g creatinine.32-4.0-54.49 (6.9) 13.5-TCP or 2.91-4.35-3.0) 13.5-TCP level of 0. the median urinary 2.4.0 and 1.30-33.80-25.31 (3.0-43.4.4.0-38.69 (3.98-11.95) 3.4.1) 16.44) 75th 4.4.4.40 (2.60) 6.30-2.84) 2. 114 Fourth National Report on Human Exposure to Environmental Chemicals .0 (13.02) 2.4.2-0.20 (3.5-TCP and 2.7) 33.70) 1.65 (5.3-17. Urinary 2.23-2.4.4.7 mg/L.70) 5.45) < LOD 11.70) 5.0 (12.3-26.45 (2.4.7-16.8-15.6-TCP level.0) 17.70 (2.0) 12. interval) 2.4 (9.2) 12.9 (11.7 (9.0) 19. see Data Analysis section) for Survey years 99-00 and 01-02 are 1.74 (2.0) 7.8-13. Biomonitoring data will also help scientists plan and conduct research about 2.67) 4.0) 7.0 (6.50 (2.47 (3.4-17.50-5.10 (5.68 (<LOD-2.00 (2.5-TCP and 2.0-38.6TCP causes an adverse health effect.31) * 2.10) 6.5-TCP (0.3) 37.20-3.18) Selected percentiles ( 95% confidence interval) Sample 95th 25.4.0) 6.52-3.75 (8.4.5-TCP or 2.40-2.4.7-3.85) * 3.0 (14.70 (2.67-12.30-2.60-37.40-32.80 (2.78 (2.00 (4.3 (11..4.6-19.79 (5.14 (2.0-18.59) 4.4.12) 2.40-14.60-3.80-7.0-44.90 (4.74-3. 2004).0-37.9) 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. 1998)..60 (3.36-5. Sawmill workers exposed to chlorophenol wood preservatives had urinary 2.5-TCP or 2.89 (3.6 (11.30-11.09) 15.7) 21.45-9.59-6.80-20.76) 3.0 (20.3) 20.4 (8.5-TCP and to the median 2.08 (2.28) * 2..4.6) 26.70-6.60 (3.46-3.0) 11.80 (2.4 (17.53) 4.3.78 (2.20-23.95 (4.3) 23.6-TCP (0.54) 6.30) 4.0 (14.Organochlorine Pesticides A small study of adults who ate Great Lakes sport fish reported a mean urine 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.0 (20.32) * 3.8) 32.0 (14.6-22.6-TCP in urine does not mean that the level of 2.56 (3.73-9.04) 2.0) 15.80 (3.1 (10.0) 14.6-17.5 mg/g creatinine) were similar to the limit of detection for 2.40) 2.70-6.66 (8.40) 4.6) 21.92 (2.89-6.53) 2. < LOD means less than the limit of detection.20-6.40 (2.8 (9.40-7.0 (8.6-TCP than are found in the general population.90) 2.

23) 4.4) 4.09-3.41 (3.96) < LOD 4.56 (7.73-22.65-21.8) 12.1) 11.S.50 (2.83-5.53) * 2.82 (3.3) 8.65-2.87 (3.9) 8.6) 970 1178 1019 1324 99-00 01-02 99-00 01-02 99-00 01-02 2.68) 2.13-6.18-4.5) 12.4 (12.17-4.87) * 2.2) 19.27-9.87-7.87-6.13 (1.10 (6.71 (3.2 (13.90) 2.62-15.06) 4.01 (3.22 (<LOD-2.65) 18.10-9.00) 4.25-15.25-2.49) 4.9-64.66-4.23 (1.88 (2.95-2.54 (2.24 (1.83-6.1-32.33 (7.6) 12.33-2.Organochlorine Pesticides Urinary 2.0 (6.5) 11.4) 8.8) 21.6 (5.59 (2.6-31.91 (7.6 (10.60 (4.29 (6.5) 9.20-2.94-13.3-37.56-5.7-36.18-2.43 (<LOD-2.06-2.76-8.1) 694 677 519 695 602 931 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.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.32-19.4) 9.51 (2.99-2.5 (7.22-9.88) * 2.3-23.53-11.14-13.48-2.29-4.52) 2.72-16.38) 22.8 (7.38 (4.22-2.5) 11.5-28.0 (9.19-5.7) 6.77-4.9 (9.40 (7.6 (6.02) 3.89) 10.79-17.1 (13.82) 2.53 (3.87) 2.29-4.2 (7.88) 4.77) 2.2 (12.8) 11.8 (8.38 (2.81) Selected percentiles ( 95% confidence interval) Sample 95th 21.51-21.52 (5.75) 75th 4.76) 2.26) * 99-00 01-02 99-00 01-02 99-00 01-02 4.78 (2.1-21.83-6.05 (3.25-17.5 (8.5 (10.50-8.9 (9.4.72) 32.00) 4.05 (6.83 (3.63) * 4.26 (6.42 (2.1 (8.00 (2.70-9.17) 2.89-2.63-13.7) 25.33 (1.8) 19.88) 5.7 (14.58 (4.46-14. Fourth National Report on Human Exposure to Environmental Chemicals 115 .63 (<LOD-2.42) 2.9) 7.9-34.78) 2.43-7.10) 4.15 (1.3 (9.76) 4.44 (3.0) 10.22 (3.33) * 2.22 (1.52 (3.67-17.68) 2.76) 1.88) 1.02 (1.9-29.04-16.82 (8.52) 2.92) 4.6) 13.21-11.91-2.43 (2.63 (2.63-15.40 (2.0) 8. interval) 2.82-2.9) 19.32 (2.30-2.6 (22.90 (1.4 (11.98) 10.00 (3.41-6.5) 8.28-4.1) 14. Survey Geometric mean (95% conf.6 (9.81-9.38-5.11) 10.26-13.9) 481 574 678 819 830 1109 99-00 01-02 99-00 01-02 2.88) 4.65) 2.14-2.9) 8. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.25 (3.63) 4.6 (12.51) 18.56) < LOD 11.78) 90th 12. population from the National Health and Nutrition Examination Survey.49-3.2 (8.47-5.35 (3.55-2.53) 4.15 (6.25 (3.9-32.91 (3.06) 11.04-2.73) 5.60-2.6) 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 2.88-7.6) 8.08-2.81) 2.17) 13.0 (11.16-10.6 (9.98 (1.

epa. Holler JS.pdf. Arch Environ Contam Toxicol 1989. Lindroos L.Organochlorine Pesticides References Agency for Toxic Substances and Disease Registry (ATSDR). Gregg M. Fast DM.45:440-445. Wegner R. Int Arch Occup Environ Health 1991. Baker S. Anderson HA. Shealy DB. et al. Profiles of Great Lakes critical pollutants: a sentinel analysis of human blood and urine.gov/toxprofiles/tp107. Residues of chlorinated phenols and phenoxy acid herbicides in the urine of Arkansas children. Toxicol Lett 2003. Hanrahan L. Smith SJ. Environ Res 1995. Poschadel B. Domingo A.106(5):279-289.71:99108. Luotamo M. Heinrich-Ramm R. July 1999. 4/21/09 Agramunt MC. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Kohli J. Kaus S. Olson J. Environ Health Perspect 1998. 206:15-24. Needham LL. Needham LL.EPA). Am J Ind Med 2004. The Great Lakes Consortium. Seifert B. Baur X. Head SL.146:83-91. Bailey SL. Schulz C. Szadkowski D. December 2006 Draft. Environmental Protection Agency (U. Available at URL: http://www. et al.atsdr. Urinary excretion of chlorinated phenols in saw-mill workers. Seiwert M. S.54(3):203-208. Monitoring internal exposure to metals and organic substances in workers at a hazardous waste incinerator after 3 years of operation. 5/19/09 116 Fourth National Report on Human Exposure to Environmental Chemicals . Chlorophenol exposure in harbor workers exposed to river silt aerosols.cdc. Pesticide residues in urine of adults living in the United States: reference range concentrations. Aitio A. Hill RH Jr. Radon K. Becker K.S. Domingo JL. Safe A. Falk C. Pekari K. The analysis of occurrence data from the first unregulated contaminant monitoring regulation (UCMR 1) in support of regulatory determinations for the second drinking water contaminant candidate list [online]. Jones D. et al.gov/safewater/ccl/pdfs/reg_determine2/report_ ccl2-reg2_ucmr1_occurrencereport. Toxicological profile for chlorophenols [online]. Can J Biochem 1976. Jarvisalo J.63:57-62. Hill RH Jr.18(4):469-474. Int J Hyg Environ Health 2003. html. To T. Burse VW. Available at URL: http://www. The metabolism of higher chlorinated benzene isomers. U. Corbella J.

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

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

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

40-11.83 (5.66) * * 1.6) 7. which may vary for some chemicals by year and by individual sample.0) 5.54 (3.80) .10) < LOD .02-5.97) 90th 7.7) 11.00 (4.0 (12.2) 672 678 473 509 696 578 595 948 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.55-6.8 (8.0) 7.50 (.01) * * 1.40-14.58 (3.32) 1.0) 10.50) 2.48-7.9-18.3) 16.61 (3.0 (9.954 (.0) 10.0 (7.60) .0 (9.67) 3.2) 16.0) 11.5) 20.26-6.93 (4.50 (2.955 (.70) .60-25.91) 4.14) * * .0 (5.830 (<LOD-3.53) 4.39 (8.90) 3.52) * * 1.72) 5.0 (6.0 (6.0) 6.60 (1.51) 2.579-1.80) .90-4.0) 11.8) 7.20 (.27-15.860-2.9) 8.00 (5.2 (7.2.0) 11. and 03-04 are 0.93-24.0 (7.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. and 0.6) 18.0) 15.82) 10.19) 9.90 (1.73) * * .98-5.80) 3.30 (4.58 (2.71-9.8) 19.56 (6.80) 2.98-12.2.4 (7.80) 4.780) < LOD 3.22 (.0-28.1) 13.00-27.0) 10.21) 9.00-19.8 (14.2 (9.90) 2.10 (2.2-20.7 (14.02) 4.50 (4.74 (8.700-1.20 (2.2) 14.32 (.2 (9.3) 17.40-5.1 (10.57-7.33-18.27-3.50-36.52-11.42-3.70-19.0) 20.20-7.90-5.63) 1.0) 11. 0.3) 14.21 (.2 (14. interval) 1.00) 3.0) 5.530 (<LOD-2.43-12.4 (7.8-32.9 (8.00-27.81) 1.56 (1.79 (5.0 (7.757-2.600 (<LOD-1. population from the National Health and Nutrition Examination Survey.56-13.20 (.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 1.03 (.10) < LOD < LOD 4.40-1.86 (1.70 (4.0 (7. 120 Fourth National Report on Human Exposure to Environmental Chemicals .80 (4.10-7.10 (.70-23.5 (8.76 (2.70 (2.70) < LOD < LOD 1.56 (4.0) 10.981 (.10 (2.80) 2.05-7.0) 12. < LOD means less than the limit of detection.70-14.38-5.26 (5.840-1.490-2.50-5.95) 5.44 (2.45 (2.29) * * 1.35-11.623-1.30-6.68-7.33 (5.94) 3.5) 15.290 (<LOD-.40-19.52) 6.23-5.85 (3.30-4.0 (4.5-17.5 (11.00) 3.26-8.61) 4.1.34-7.4) 17.20 (.00 (1.00-7.80-4.12-19.2 (14.81) 11.08-15.15-12.20-30.8 (12.60-11. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00-12.1 (9.47) * * 1.34-3.47) 5.17-3.970-2.16 (2.15) 14.10 (.13 (2.2) 16.1) 95th 13.39 (3.9) 952 1187 928 997 1333 1003 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.71 (2.89) 9.07-10.12) 4.717-1.2) Sample size 1949 2520 1931 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.04) < LOD 1.08 (<LOD-2.60) < LOD < LOD 4.0 (8.8) 11.80-22. 01-02.58) Selected percentiles ( 95% confidence interval) Total * * 50th 1.13 (2.4 (9.44-3.94) * * .9) 14.35-16.0 (8.16) 4.S.0) 9.99 (5.0) 6.86-15.4) 18.0-27. see Data Analysis section) for Survey years 99-00.40 (.70-11.42) .30 (2.79-7.0) 6.0 (8.82-12.58 (5.4 (9.5-16.2 (7.620-1.890 (<LOD-2.81) 11.97) 8.1) 10.758-1.35-12.46) 10.0) 5.740-2.3-15.28) 1.40-16.2 (11.96-3.30 (2.2 (7.20-4.80 (2.55-8.1-23.70) < LOD < LOD 75th 3.44-38.11 (.13-2.36-4.37 (3.1-17.290 (<LOD-1.00-12.750-1.0) 10. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. respectively.60 (5.80) 11.8 (9.08-2.670-1.20 (.74 (8.810-1.80) 2.7 (12.4) 20.80-24.8) 7.599-1.60-18.

09) 2.84) 7.56) 4.15-10.42 (3.94-10.2) 95th 12.94 (2.500-1.570-1.47 (1.01-2.07 (.5 (4.7) 5.94-9.34 (6.9) 16.40) < LOD < LOD 75th 2.74) 90th 7.41) .54-2.57-10.82-14.02 (7.6) 9.62-5.26) * * .66 (1.20-8.31 (3.2) 7.90-8.3) 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 1.69) 4.92-5.21-23.6 (10.60) * * .64-5.69 (4.7) 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) .02 (2.80 (7.870-2.47) * * .45-5.566-1.75 (3.8) 16.93-9.883 (.860 (.8) 6.34) * * .1 (6.960 (.75 (7.900 (.00-17.633-1.83 (7.27) < LOD 2.7) 18.1) 4.9) 12.72) 11.44 (2.38) .84 (5.95 (3.440 (<LOD-2.88) 2.5) 7.98) .53 (6.43 (.76-4.1 (10.3) 5.75) 2.25) 6.43) 2.40) 4.0) 7.7 (10.53-11.09-11.5) 12.42) 12.79-3.5-20.60-9.81 (1.05 (1.28 (4.80 (6.68) < LOD < LOD 3.10 (3.75-7.98-22.40-14.40-28.2) 5.79-9.2) 13.76) < LOD .04 (1.3) 16.28-9.3) 12.71) 10.67) 4.1-15.8) 7.09 (.4) 4.780 (<LOD-1.8) 8.03 (2.57 (6.28 (5.30 (1.55-20.430-1.5) 11.02-14.37 (5.45-11.43 (3.6 (9.47 (3.30) 2.19 (4.1 (8.8 (10.8) 12.7) 672 678 472 509 695 577 595 948 751 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.98-5.35 (1.39 (2.85) 2.10-13.62) .54-4.37-3.14 (3.9-28.35) < LOD < LOD 3.88-15.818 (.620-1.05 (.82-26.02-2.61-29.32-12.75) 14.3) 15.67-19.7) 12.40-12.2 (8.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylphosphate (DEP) (creatinine corrected) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.03-6.88 (5.94 (4.90-5.56) .750 (<LOD-1.29) * * .00-19.574-1.533-1.69-10.40-5.24-3.74) 4.89) * * 1.1) 4.54) .77 (6.790 (.890 (<LOD-1.52) 4.56) 7.00) 8.924 (.2) 5.0 (8.2) 8.54-15.04-6.98) .06-2.80 (2.92-2.36) * * 1.03) 2.53) 9.37) 9.34) < LOD < LOD .03) 2.82-6.7 (8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.89-3.87 (1.1 (7.34 (6.93) 9.94-22.5-16.57 (4.2 (10.78 (2.4) 4.6) 13.40-3.560-1.0) 6.68-4.28 (2.37-5. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.67) 1.13) 4.5) 8.4 (9.66-15.98 (3.61 (1.5-13.58) * * 1.2) 9.6) 8.650-1.7 (9.46-5.47) 2.1 (11.38 (1.4) 13.61 (1.87-5.1 (9.5-32.608-1.66-34.40 (3.00-13.83) 8.S.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 1.11-6.25) < LOD .00 (4.9 (9.996 (.51-5.73 (1.66 (2.00 (4.60) 2.37 (4.4 (4. population from the National Health and Nutrition Examination Survey.03 (7.82-14.50) 7.29 (2.5) 7.855 (.98) 9.932 (.28) 10. Fourth National Report on Human Exposure to Environmental Chemicals 121 .830-1.710 (<LOD-1.71-2.540-1.57) 4.69) 2.23) 4.9) 11.61-13.95) 2.47 (3.960 (<LOD-2.46) 2.549-1.85 (6.6) 11.45-5.9 (5.890 (<LOD-1.9 (9.56-13.773-1.41) Selected percentiles ( 95% confidence interval) Total * * 50th .31-14.920 (.88-10.18 (.23 (4.66 (5.820 (.81-5.87 (3. interval) .41-12.2 (6.80) 9.54-11.93-5.510-1.94-23.

27 (3.88) 3.70-9.70 (8.4 (10.4 (14.46-28.40 (2.18) * * * * * * * * 1.70-5.90 (6.25 (2.80 (2.34 (6.70) 2.00-16.80-6.7 (10.0 (7.0) 13.0) 11.30) 8.04 (3.98-9.790 (<LOD-1.80-4.1 (10.30) 3.14 (6.6) 11.72) 2.6-41.58.9-15.39-13.0) 12.0 (9. 122 Fourth National Report on Human Exposure to Environmental Chemicals .0-33.0-19.00-18. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .4) 672 678 498 509 695 579 595 948 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.5) 21.10 (.8-17.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Dimethylphosphate (DMP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.00) 7.78) 5.20-8.37) 2.5 (8.9-14.82) 8.47-6.0) 14.0 (14.95-9.670 (<LOD-1.90-9.51) < LOD 1.3 (7.7-19.17 (7.740 (<LOD-1.50-4.7) 15.10 (<LOD-1.52 (6.0-24.2 (7.61-32. 01-02.88) 10.66) 4.24 (2.60 (5.1) 11.34-10.5) 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 * * * * * * .67-10.92-17.86-10.90-15.6 (10.58 (1.7) 14.2) 14.0) 11.95 (2.00-4.970 (<LOD-2.27) 4.8) 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 1.4) 11.0) 23.00-18.92) 9.8-20.8-20. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (10. and 0.0 (9.3) 14.3 (9.60) < LOD < LOD 2.0) 12.96) 3.8) 9.27) .0-29.90 (2.0) 6.77-14. which may vary for some chemicals by year and by individual sample.20-18.2 (9.20) 3.7) 22.97-4.12 (4.1-23.9) 10.01 (2.84-4.64) 10.0 (15. respectively.6-19.45 (3.29-4.4) 7.67) 4.31) 1.5 (8.67) 3.5-26.34-5.20 (<LOD-2.6) 18.90 (6.77-3.80-12.80) 5.59-3.15-2. and 03-04 are 0.00-9.20-4. population from the National Health and Nutrition Examination Survey.9) 16.80 (2.22 (6.8) 8.10) 6.8 (12.61 (3.0-24.4 (10. 0.3 (11.40) < LOD < LOD 75th 2.89 (2.27 (7.60 (6.35-3. < LOD means less than the limit of detection.40 (2.0) 18.7-21.75 (2.00-4.99 (3.0) 9.3) 10.90-15.00) 3.680 (<LOD-1.80) .50) .11-6.35) 4.06 (2.37 (3.34-3.30) 3.6) 14.0) 14.41-5.90-31.16-1.50) 5.75 (3.9 (7.95 (5.670 (<LOD-1.15-6.41) 3.650-1.5 (9.90 (2.96) 90th 7. see Data Analysis section) for Survey years 99-00.29) < LOD < LOD < LOD < LOD 3.70-9.70-8.80-21.6 (10.3) 22.5.00) < LOD .31-7.20) .00 (.53 (3.7) 10.70 (1.3 (12.7 (11.0) 13.S.27) 9.7) 16.8-21.10-4.90 (6.1 (10.63-14.42 (1.22) 8.60 (2.10-15.90 (5.66-13.0) 12.3) 20.80-14.89) 2.30) < LOD < LOD .3) 8.0) 9.0) 7.73) 7.0 (8.39 (5.0 (10.6) 14.35 (6.80) .9) 95th 14.46-4.50-5.90) 4.28 (7.6) 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 * * * 1.9-17.22 (6.9 (12.5.0) 19.49-4.580-2.910 (<LOD-2.3 (9.18 (3.0 (13.24-5.90 (6.31-12.90 (2.00) 8.90 (1.33-11.670 (<LOD-1.9) 9.80-3.90) 8. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.30) < LOD < LOD 4.62-17.74) * * * * * 1.81-6.3 (6.00) 3.80 (5.20) 3.0 (5.22-12.8 (12.10-10.80-8.4-17.670 (<LOD-1.50) 3.

18) 2.30) 8.85-8.02-4.86-3.82-8.01-5.82-11.63 (6.530-1.97) < LOD .0 (13.64-11.2) 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.37) 3.83 (6.55) .44-6.9 (9.9) 19.75-3.07 (5.55) 16.4-16.6 (11.80) 3.94-14.2 (9.0 (11.00 (2.33-10.6 (13.7) 15.3 (7.27) 1.29 (5.77 (2.32) 2.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.86) 9.9-25.27) 5.03 (6.1) 20.77) 3.1 (8.2) 16.72) 4.4) 6.16 (3.6) 95th 16.91-9.89 (3.29-2.920 (<LOD-1.6) 14.3-21.2) 12.70-35.4-18.34-18.7) 14.53-8.3-15.54 (7.85-17.6) 12.0) 14.5) 10.12 (7.87 (3.6 (13.96-11.4) 9.7) 9.88-7.0 (8. Fourth National Report on Human Exposure to Environmental Chemicals 123 .75-3.59-3.81 (7.5 (8.51-7.05-3.23-3.42) 7.6-19.7 (10.25-9.30) 7.3-34.3-17.2) 19.780-1.5 (15.950) .00 (7.34) < LOD < LOD < LOD < LOD 3.89-13.3) 6.68-10.38-13.2-30.09-11.42) 8.45) 6.3) 9.2 (9.4) 15.45) 3.21) * * * * * 1.973 (.5 (9.70-2.28 (1.6 (11.12) < LOD < LOD 4.9 (9.69-11. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th .7 (11.7-19.4) 7.4) 16.0-19.9 (9.27) * * * * * * * * 1.74-4.41 (7.6) 13.86 (3.06 (<LOD-1.4-15.7-23.99 (4.95 (2.78) 4.2) 12.89 (2.79-6.19) 3.3-17.39-17.54-5.5 (11.28) 6.78 (6.6 (12.58 (4.50-17.93 (<LOD-2.16-14.48 (2.83 (7.27) < LOD .71 (1.2-15.1 (13.07) 2.96-10.890-2.11-3.93 (6.63 (2.78 (4.89-10.93-10.6) 7.590 (<LOD-.68) .8 (8.95) 90th 8.38 (1.8 (10.810 (<LOD-1.61 (2.47-9.690 (.37-5.1) 13.09-11.940) < LOD < LOD 1.00) 2.74-19.28-12.88 (1.67 (1.3) 12.29) 3.2) 10.67 (7.1) 10.55 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.0-21.30) 2.36 (2.07) 2.3) 8.71) < LOD < LOD 2.5) 22.6) 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 * * * .92) 3.4 (11.15) < LOD < LOD 75th 2.620 (<LOD-.2) 8.27-13.73 (5.5 (10.7 (8.38) 1.52-3.8) 14.38 (2.5) 13.91) 3.910 (<LOD-1.93 (2.8) 11.89-3.6) 6.72-4.43 (2.54) 9.9-17.95) 3.06) .50 (6.29 (2.00) 8.5-17. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00 (3.00 (<LOD-1.7) 12.7 (10.11 (5.51-10.25 (4.15 (1.0 (10.42-19.77 (2.68-4.04) 9.33) 3. population from the National Health and Nutrition Examination Survey.9) 16.4) 7.8) 16.1 (19.2) 12.79-9.20-3.94 (5.89-3.14 (2.38 (.07-3.89) 5.850 (<LOD-1.S.7) 14.97-4.4-16.5) 8.4) 7.2) 15.760 (<LOD-1.00 (<LOD-1.68-19.30-5.6) 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 1.00 (5.32-8.78-10.99) 2.03 (2.6) 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 * * * * * * .92 (5.21-21.03) 3.6 (10.

740 (.880) < LOD 75th .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 * .16-3.80) 2.540 (.453 (.26) .440-.54-2.550 (.10) 1.79) .20) 1.95-5.31) 2.03) 1.750) 1.45 (2. and 03-04 are 0.960-1.65 (2.720-1.83 (2. population from the National Health and Nutrition Examination Survey.1.700) .45 (1.353-.580-.22 (1.27 (2.76-6.74-5. 124 Fourth National Report on Human Exposure to Environmental Chemicals .20 (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 * .560-.80) 2.46) 1.449 (.457 (.585) * * .670) .98) .00) 2.380-.40 (1.820 (.38) 1.00) 1.20-2.50 (1.46 (1.710 (.740-1.05-3.50-2.780 (.55 (3.340-.77-2.31-3.35) 1.64 (1.80) 3.50 (1.13) .30) 2.30 (.455 (.30 (.89) 672 678 478 509 695 553 595 948 745 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.80 (2.88) 1.54) .22-8.580-1.570 (<LOD-.620-1. interval) Selected percentiles ( 95% confidence interval) Total * .04) .720 (.50-2.94) .570 (<LOD-.80) 5.25-1.01) .70 (1.490 (<LOD-.990-1.17) 1.70 (1.48 (2.467 (.303-.597) * .05-2.22-3.89-6.96-3.880 (.29-2.17-4.31-3.86 (1.570 (.48 (1.08 (2.32-1.89) 1.201-.30-1.41 (2. see Data Analysis section) for Survey years 99-00.950) 90th 1.450 (<LOD-.20-1.930) 1.97 (2.810) .618) * .240 (<LOD-.13) 2.10) 3.910-1.880) < LOD .69-4.980) 1.20 (2.690-1.700) .10-1.20-3.95 (2.500 (<LOD-.73 (1.39) 2.20) 1.74) 3.34) 2.40 (1.350-.63 (1.70-2.49) .09 (.50 (1.61 (1.00-4.94 (2.30-3.54 (2.388-.590-. 0.30 (.20-2.86) 3.80 (1.20) 3.690) .20) 2.90 (1.790 (.26 (2.68-5.90) 3.17) 1.587) * * .740 (.749 (.94 (3.00-2.510 (<LOD-.30-3.91) 2.680-1.45-4.930) < LOD .46 (2.400) .37-2.59-6.46-3.19-1.98-3.570-1.20 (1.460-.570) * .18 (.425 (.459 (.15) 2.60 (2.657) * * .76 (1.260 (<LOD-.31) 95th 2.510 (.41-5.30 (1.730) .32 (1.949) .550 (.960) .22-2.382-.60-4.820 (.59-2.930-1.79) .75 (2.690 (.04) 1.970) .592-.34) 2.90) 2.83) 2.78) .359-.570 (.160 (<LOD-.96-5.650-.390-.75-2.690-.720-1.60) 3.860) < LOD < LOD .83) 1.710 (.940) < LOD .2.390-.87-3.970) 1.30) 1.505 (.30) 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.16) 1.910 (.710) .10-1.50 (1.45 (1.57 (2.47) 2.750-1.780) .20) 3.910) 1.49) 2.50) 1.20 (1.780 (.740-.50 (1. and 0.584) .27 (3.89) . 01-02.10) 1.S.21) 3.29) 1.57 (1.850) < LOD .800 (.83 (2.01-1.830 (.15) 2.70 (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 * .16) 2.23-3.960) .280-.11-3.77 (1.600 (<LOD-.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Urinary Diethylthiophosphate (DETP) Metabolite of Several Organophosphorus Insecticides Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.36-4.930 (.47 (1. which may vary for some chemicals by year and by individual sample.80) 3.759) * .09.73-5.95) 2.30) 4.73 (2.80) 3. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.380-.60) 2.18 (1.343 (.549 (.42-2. respectively.398-. < LOD means less than the limit of detection.350-.11-3.08 (2.20) 2.592) * .960 (.14-1.600-1.600-.592) * 50th .380) .760 (.680-1.960) 1.32) 3.01-3.10) 1.33-2.90-4.14 (1.90) 2.336-.98 (2.83) .210 (<LOD-.840 (.58 (1.70-7.00 (1.22-3.

20-2.39 (1.10) 2.515) * * .32 (.880) 1.510 (.05) < LOD .300-.47-4.23 (.490 (.22) .57-2.70 (2.720 (.471-.750 (.47 (1.560-.75 (2.480-1.560-.73 (2.00 (3.645) .07) 1.81) 2.350) .253-.480) .72 (2.64 (2.77-3.790 (.36) 3.61 (3.98) 1.17) 2.710 (.67) 1.77 (3.440-1.800) < LOD .390) .630) * .31-1.690) < LOD < LOD .550-.580 (.32) 2.230 (<LOD-.05) 1.470) .63 (1.700 (.69 (1.597) * .71) .32) 1.89-3.08-2.45 (1.07 (.08 (.75-3.760) < LOD 75th .60 (2.88 (1.33) .310-.69 (3.08 (2.70 (3.22-3.22-3.75 (1.64 (2.07-2.60 (1.41 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.44-2.380-.910) < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.95) 1.17) 2.590-1.520 (.270-.870) .23) 1.509 (.660-.739) * .57-4.02-3.67 (1.45 (2.04-5.740) < LOD 1.23) 2.800-1.88) .32-1.34 (1.550) .57 (3.50 (1.38 (2.18-2.180 (<LOD-.552 (.43) 2.65) 2.485) * * .73-3.55 (1.250 (<LOD-.820) 1.250 (<LOD-.82 (2.58) 3.16) 1.38 (1.02-6.08-3.320-.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 * .84 (2.11 (.535 (.335-.16-2.08-3.400) .08-3.09) . population from the National Health and Nutrition Examination Survey.79) 1.460) .710 (.460-1.380) .136-.22-2.60) 1.75) 6.66 (2.08-2.71 (1.52) 3.320-.448 (.500-.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 * .270 (<LOD-.62 (2.470 (<LOD-.760) .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.447 (.23) 3.377-.23) 2.97 (1.50) 1.42-6.680 (.372 (.13 (1.11) 1.790) .980-1.750 (.05-4.412-.870 (.97) 2.22) 4.590) * 50th .66) .52 (1.76) 1.234 (.43) 1.348-.30-2.840) 1.900) 1.580) .280 (<LOD-.453 (.330 (<LOD-.05-2.08) 1.540-.97 (1.78) 3.19 (1.368) * .72-4.688) * .61-3.460 (.92 (1.16-1.43) 2.670 (.24) 4.550-.49 (1.14 (2.530 (.840) .71) 2.990-1.80) 471 575 296 664 821 689 814 1122 918 12-19 years 20-59 years Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * .580-.820) .07) 5.30) 3.99) 1.28 (1.950-2.97) 1.720-1.90) 2.310 (<LOD-.830 (.38-3.60) .393 (.920) .67) .39) 2.730) . Fourth National Report on Human Exposure to Environmental Chemicals 125 .700 (.32) 5.42-8.42) .20-7.03-1.04) 95th 2.940-1.42 (.84-6.318-.61-3.61) 2.20) 1.29-4.07-3.49-4.33 (1.00-3.92-8.47 (1.840) 1.08-3.444-.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.285-.80) 2.17-2.640 (.640 (.07) 1.305 (.82) 2.370-.92) 3.89 (1.510-.390-1.830) 90th 1.06-2.25-3.520-.91 (1.44) 2.300 (<LOD-.72 (1.67-3.79 (1.99) 2.11-2.04-1.850) 1.08-2.58 (1.03-2.560 (.640 (.380-1.740) .591 (. interval) Selected percentiles ( 95% confidence interval) Total * .510 (.62 (1.330-.07) 1.02-3.57 (1.742) * * .67 (1.05 (1.43 (1.22 (2.22) 1.S.270-.930-1.55-3.550-1.06) 4.310 (<LOD-.400-1.58-6.403) .53) .94) .590 (.00-1.87 (2.77-4.700 (.08) 2.72) 1.710 (.

7 (12.6 (9.25-3.04 (<LOD-2.2-47.00-24.8 (12.1-40.1) 18.0-53.4 (19.96) 5.53) * 2.85 (1.92) * 2.4 (10.5-74.50-2.8) 41.7 (28.0-43.44-7.65 (4.98 (1.3) 26.0) 31.0-41.58) 16.06) * 2.95 (5.18) 6. which may vary for some chemicals by year and by individual sample.0) 28.S.8) 671 678 498 509 695 579 595 947 757 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.63-6.80) .67 (1.46 (.0 (33.05-3.0 (32.77 (1.90-8.71) 5.60 (2.50-5.66-5.0) 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 2.70) 1.0) 3.12 (3.71 (4.43-7.0 (8.87-7.10) 39.1-47.0) 6.0-49.42) 1.44) 3.0 (38.40) < LOD 1.690-3. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0 (20.4 (15.44) Selected percentiles ( 95% confidence interval) Total * 2.0-41.53) 40.6 (11.06 (1.79 (1.6 (15.61-2.1) 38.18) 20.80-2.2-33.17-2.5-20.92-5.36-2.82 (1.23-2.35-6.8 (22.57-2.0 (38.93-3.90 (1.30-14.0-230) 35. 0.97) 6.0) 32.0) 8.50 (2.4-22.0 (25.0) 28.0 (20.5.2) 31.78) 9.21 (3.57-2. respectively.470 (<LOD-1. 126 Fourth National Report on Human Exposure to Environmental Chemicals .50-17.59 (1.19-2.70 (1.14) 5.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.0 (11.19) 2.0) 16.2-80.9-51.0) 3.0-31.58-2.10 (1.530-4.00 (.9 (19.70-17.1 (10.5) 30.69) 2.2 (12.6-45.4) 38.0 (37.26) 75th 11. 01-02.7-41.1-25.71-2.79-2.3) 28.81-2.80-18. and 0.12) 1.9 (19.3) 33.0 (40.0) 3.0) 17.29) 2.83-2.1 (26.0 (26.0 (19.8 (12.1-20.30 (. see Data Analysis section) for Survey years 99-00.45) 2.5-27.0) 20.79 (2.10-13.75-14.13) 12.16) 2.4) 19.600-2.0) 15.0-110) 42.830-4.99 (2.0) 30.2) 16.80) 1.0 (8.72 (1.61 (1.40) 50th 2.1 (11.46-6.0-29.05) 1.3 (10.0 (38.1-46.0) 17.83-2.13 (1.8 (26.9 (27.3 (12.0) 13.10 (7.0) 19.0-110) 34.83 (1.94 (1.07-5.60) < LOD 1.6-22.2 (19.1) 38.0-41.0 (21.0 (13.0-92.2-26.0 (8.0) 4.41-4.2-27.3) 38.0) 42.16) * 1.5 (24.70-6.20 (2.8) 39.48-2.59 (1.23-2.610 (<LOD-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.3 (14.0-62.10) .9) 48.0 (7.0) 33.5-45.91 (4.98) * 2.80) < LOD 1.0) 20.48-2.45) 2.53 (1.40) < LOD 2.0-47.46-2.70) 1.50-20.0 (38.0-260) 34.10 (1.04) 3.0-58.3 (12.02 (2.29-4.10-4.6) 52.30) 4.0) 18.0 (38.7) 20.0-58.3 (24. population from the National Health and Nutrition Examination Survey.9 (10.33 (5.5) 69.0-50.0 (38.77) 38.0-39.1 (22.3) 31.29-9.10 (1.7-22.50-7.64-8.0-69.8-21.74-2.83 (3.76 (2.30) 11.18) 14.2-27.86-3.0) 16.78 (1.0) Sample size 1948 2518 1965 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 2.85) * 2.32 (2. interval) 1.40-4.48) 5.10 (1.0 (38.81-3.2-62. and 03-04 are 0.0-62.88) 1.70) 5.0) 4.54 (3.0) 45.7 (12.27-6.88) 3.6 (26.3 (23.41) 1.9) 18.41) 5.0 (17.5-40.11) 2.86 (1.2-39.0) 15.23) 9.7) 47.00 (.70 (1.6-27.90 (1.9) 17.1) 95th 48.4-76.660-2.21 (1.20) 1.49-2.0-52.76 (2.52 (4.8) 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 1.9) 38.830-3.1 (25.44) 2.0 (24.21 (4.0) 4.20-4.0) 3.18.41) 1.05) * 2.64-3.9-21.0 (6.11 (4.1) 140 (46.09 (4.6-54.41 (1.0-39.8) 32.80) 90th 38.26 (.70 (7.1 (25.0) 5.9 (23.13 (1.04-8.70 (.8) 62.40-16.1-19. < LOD means less than the limit of detection.54 (1.8-24.90) 11.0-53.53) 1.4.31-6.

17) 2.66 (1.6-51.60 (.95-16. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.5-97.1-22.62) 4.21 (4.9) 24.38-1.26-4.22 (2.7 (11.2 (15.7) 61.51) < LOD 1.5 (8.12) 3.67-16.0) 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 1.71-2.1) 13.4-71. Fourth National Report on Human Exposure to Environmental Chemicals 127 .2) 36.09 (5.19-14.6) 7.6) 3.8-37.1) 27.27) 10.0 (23.46) 1.4 (25.930 (<LOD-1.18-1.7 (10.94) 1.17-3.63-5.39 (1.6) 11.00) 6.0 (14.8-34.8) 23.33) 1.70-4.4 (21.80-8.4-21.9) 12.9 (7.2) 13.1) 27.08 (1.03) 1.6) 112 (40.8) 31.6 (7.60) 4.62 (2.9) 24.0) 25.8-26.7-109) 22. population from the National Health and Nutrition Examination Survey.38 (3.9-37.3-27.28 (1.7-38.40 (2.15 (.2-28.43) * 2.4 (19.3 (10.33) 2.19 (1.5 (17.68) 47.96) 2.56 (2.27 (6.0-71.5-36.0 (6.22-2.6-32.70 (1.8) 11.06-1.5 (15.23) < LOD 2.16 (1.88 (1.07) 9.7) 66.94-20.71) 8.870-3.1) 13.07-2.9 (26.1) 15.9-41.2) 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 1.11-2.9-18.66) 8.5) 70.8 (7.7-19.54-2.6 (27.7) 30.5 (13.7) 26.52-4.33) < LOD 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.6) 23.58-17.2 (22.2 (21.35) .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. interval) 1.9 (19.41 (2.59-2.1 (12.2-47.22-3.2 (8.50 (2.97 (1.4) 12.9-36.1 (50.870-3.5 (41.86) * 2.0) 10.69-18.38) 5.75) * 1.67 (1.06) 1.45 (1.24 (1.0) 47.54-15.32-3.08) 1.0 (39.29-5.899-2.3) 13.93) 5.64 (1.61-2.5) 27.3-22.51) .2) 4.3 (10.95) 90th 32.3) 28.14-8.680-4.30) 28.0) 48.1 (33.3 (8.5 (6.860 (<LOD-1.0-118) 29.57) 4.46-5.0-40.1 (34.36 (4.76-2.57 (6.40-7.14 (.79 (2.4) 12.52 (1.8) 3.7) 34.32 (3.46-22.7-37.68 (1.1) 25.36-13.7-20.6 (24.2) 41.20-5.40-4.5 (15.43-2.22 (.7 (18.2) 13.7-47.1-60.9) 3.1 (25.3 (9.82) 1.4) 14.1) 52.0 (32.19) 5.4-39.8) 15.55 (2.9-95.88 (4.2) 33.86) * 3.40 (5.4 (9.02) 1.37-2.9 (10.16 (1.8-45.83) .00) 1.69-5.25-3.02) * 1.4 (12.94) 19.9) 54.47 (1.8-43.67 (1.2) 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 2.61-22.870-3.47-17.18) * 2.6-38.4 (25.75-6.5 (34.2-34.00-16.50-5.9-52.58-2.03-2.96-16.88 (4.27-3.35) 1.1) 36.47 (3.3-19.36) 10.67-3.9) 3.16 (1.0 (19.27) 50th 2.750 (<LOD-1.59-15. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.48 (4.4-34.2-38.3 (20.0 (23.35 (2.00 (4.37 (1.75 (1.45-1.1) 25.19-6.7 (24.18) 3.7) 15.23) 37.670-1.01 (.S.99-4.7-43.84-13.71 (1.72) 2.88 (1.2-70.890-4.75 (1.19) 5.95-16.3-42.7) 23.02 (.6 (11.0) 30.6) 19.2 (16.91-2.6-49.1-63.95 (2.59-2.61 (1.06) 1.6) 3.34) * 1.5-43.44) 9.91 (6.23-1.12 (1.4) 3.28) 1.0) 3.7 (18.5-190) 30.66 (1.43-12.8) 32.38-5.1 (39.80 (1.26-2.06) 75th 9.4-67.11) < LOD 1.07-2.4 (5.0) 13.0 (25.0-70.48) 1.2 (9.16-2.33-5.9 (39.0 (17.7) 95th 51.53) 1.1) 17.83 (.31) 2.20) Selected percentiles ( 95% confidence interval) Total * 1.79-17.90 (.46-6.82 (2.888-1.9 (13.4 (11.56) 1.

300-.180) .450 (.870 (.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.170-.830) .310) < LOD < LOD < LOD < LOD .700-1.820 (.310-.990 (.870 (.S.680-1.530-.290) < LOD < LOD < LOD < LOD Non-Hispanic whites Limit of detection (LOD.140-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.850 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.540) .870 (.15) .240 (<LOD-.42) .200) < LOD < LOD .610 (.36) .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 * * * * * * * * * .430-.084-.870) < LOD .860) .310 (.00) .10) . and 0.730) .720 (.090 (<LOD-.310 (.360-. and 03-04 are 0.120-.150 (<LOD-.099-.510-1.280) < LOD < LOD < LOD < LOD .560 (.230) . respectively.870 (.700-1.360-.760) < LOD .720-1.870 (.410-.350) .100 (.130) .850) < LOD .600 (.05.730-.840) .120-.780) < LOD 1.430 (.840) .130) .640 (.10) . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .470-1.110-.220 (<LOD-.990) .160-.320 (.380-.940 (. < LOD means less than the limit of detection.30) .460 (.32) .850 (. which may vary for some chemicals by year and by individual sample.630 (.830) < LOD .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 .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 * * * * * * .117 (.680) .140) .080 (<LOD-.130-.13) .470 (.190 (.03) .610 (.650-1.150) .540 (<LOD-.390) < LOD < LOD .540) 672 678 498 509 694 579 595 947 757 Non-Hispanic blacks .490 (.60) 1.140-.640) .720) .10) . 128 Fourth National Report on Human Exposure to Environmental Chemicals .640) .370-.171) * * .380-.130 (.58) .190 (.930 (.1.770 (.130-.570) .270 (.610-.650) . 01-02.830 (.090 (<LOD-.630 (.460-.770) < LOD 95th . population from the National Health and Nutrition Examination Survey.160) .090 (<LOD-.660 (.450 (.190 (.090 (<LOD-.410-.380-.290) < LOD < LOD < LOD < LOD .700-1.310) < LOD < LOD < LOD < LOD .740) < LOD .330-.42) .30) .320-.830 (.410-1.160) .140-.080 (<LOD-.40) .290) < LOD < LOD < LOD < LOD 90th .700-1.1.650-1.300-1.120 (<LOD-.350) < LOD < LOD < LOD < LOD .450 (.090 (<LOD-.990) .540) .30) .680-1.130-.560 (.20) .680 (.650) .860-1.050-.610-1.650 (.620 (. see Data Analysis section) for Survey years 99-00.162) * * * * * .820 (.260 (.420-.230-.410) < LOD < LOD < LOD < LOD .440-1.290 (<LOD-.690-1. 0.220 (.210 (.550) .210 (.090 (<LOD-.370-.390 (.400-.12 (.900 (.10 (.640-1.

880 (.560 (.730 (.080) .570-.300 (.730) .170) < LOD < LOD .86) .170 (.01 (.070 (<LOD-.190 (.24) .380-.070 (<LOD-.870) .300-.86) .330-.450 (.580-1.12) < LOD .600) .190 (.570-1.070 (<LOD-.650-1.220 (.110-.310) < LOD < LOD < LOD < LOD .03 (.380 (.03) .800-1.640) 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 .20) 1.310) < LOD < LOD < LOD < LOD Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine.120) .600-1.810 (.940) .36 (1.500) .340-.S.330 (.700 (.580 (.03 (.360) < LOD < LOD < LOD < LOD .670-1.720 (.700) .084-.390-.860 (.330 (.550 (.070 (<LOD-.990) .380-.610-1.650) < LOD .760) .100 (<LOD-.140-.180-. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th 75th .250-.200 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.29 (.710-1.78) .140) .19 (.860-2.360 (.990) .540) .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 * * * * * * .100-.24 (.38) 1.520) 672 678 497 509 693 578 595 947 756 Non-Hispanic blacks .410-.730) .67) .400) .580 (.780) < LOD 1.500-1.410) .850 (.210 (.60) .03 (.140-.450) .300-.380-.220) < LOD < LOD < LOD < LOD .170 (.14) 1.58) 1.43) .161) * * .150-.230-.780 (.540 (.62) 1.720 (.580) < LOD .410-.080 (<LOD-.660-1.330-.540 (.140-.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.110) .09) .060-.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 * * * * * * * * * .970) .270) < LOD < LOD < LOD < LOD .120) .260-.200 (.500 (<LOD-.230 (<LOD-.140-. population from the National Health and Nutrition Examination Survey.00) < LOD .880-1.270 (.111) * * * * * .360-.460 (.440-1.400 (<LOD-.370 (<LOD-.080 (.090 (.110) .410 (.190-.700 (.410) < LOD < LOD .090 (<LOD-.940) .730) .410 (. Fourth National Report on Human Exposure to Environmental Chemicals 129 .116 (.700-1.360-.890 (.110) .470 (<LOD-.960) .320 (<LOD-.02-1.670 (.740 (.510-.140-.66) 1.230) < LOD < LOD < LOD < LOD .02) .390-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.740) < LOD 1.380-1.640-1.290) < LOD < LOD < LOD < LOD 90th .280) < LOD < LOD < LOD < LOD .550 (.860 (.110) .240-.750) < LOD 95th .050 (<LOD-.580) .490-1.260) .670 (.057-.330-.520-.570 (.440 (.

70-7.32 (1.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.770 (<LOD-1.60) 1. population from the National Health and Nutrition Examination Survey.62-8.05 (3.90) .880) 5.28-9.20-4.210-1.35) 5.480-.15) 19.63) 32.0 (16.840-3.360-1.0) 2.97) 20.14) 2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.42) .90 (1. 01-02. and 03-04 are 0.720) 2.190-1.90-37.080-1.0 (17.80 (4.43-4.0 (6.52) 5.30-3.28) 1.1.0) 5.23-6.76 (1.0 (17.250 (<LOD-.90-28.800) 90th 13.05 (2.70) 2.90 (2.0) 5.1.600 (.0 (4.10 (3.30 (1.20) < LOD < LOD < LOD < LOD < LOD 1.24-7.99 (1.10-9.50) .94-8.3) 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 * * * * * * * * * .28) .94 (1.0) 2.50) 2.97) 20.48 (2.31-10.40) 2. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 2.30-6.96 (1.0) 2.0-38.S.850) 16.00) 1.640 (.00) .40 (1.10 (3.0-40.690 (.42) 2.86) 4.350-.0-44.67 (2.11) 13.83-3.0) 4.66) 4.11 (1.6) 672 678 498 509 695 552 595 947 752 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.49) 17.0-38.12) * * * * * * * * .40) 1.30) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.74) 5.0) 2.0) 4.840 (.90-9.740 (.20 (1.10-3.0 (5.0 (3.40 (1.590 (.18) 1.610 (.40-8.36-3.0-38.88-3.30-7.01) 5.0) 2.67) .21-3. respectively.08.48) 13.45 (2.425-1.53) 20.0-39.910) 2.6) 5.11) .14-5.53-7.890 (.13 (3.510-.67 (1.00) .960 (<LOD-1.30 (2.70-50.30 (1.90) .10-3.63 (3.33 (4.36-3.51-8.610) < LOD < LOD < LOD < LOD < LOD 2.870) < LOD < LOD .29-10.51 (2.00 (1.00-17.07) 1.30 (1.40-4.10 (.380-.750-2.65) 1.15) 14.0 (17.03 (. < LOD means less than the limit of detection.900 (.70-17.0) 3.830 (.691 (.0) 2.330 (<LOD-1.26 (2.00 (.0 (17.94-3.39 (2.0) 4.07-3.00-17.0-40.260-.12-1.350-.110 (<LOD-. see Data Analysis section) for Survey years 99-00.20-17.52 (1.39) .770) 2.82-4.16) Sample size 1949 2518 1930 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .750-1.90-20.70-3.85-3.40-20.730 (.68) 2. which may vary for some chemicals by year and by individual sample.620-1.61 (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 * * * * * * .49 (1.55-8.59-5.20 (1.74 (3.0 (4.840 (<LOD-1.07-3.20-4.05-3.49 (1.32-9.53 (2.70-30.07 (3.0 (5.170-1.99) 19.37) .47 (3.0 (7. 0.52 (1.0 (5.0) 2.46 (1.55-4.40-7.07 (1.90) .800) 17. and 0.0) 4.30) 95th 19.800-4.80) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.21) 3.35) 11.960 (.400-1.14) .87) 12.83) 2.370-.0) 5.31) .87) 5.30 (.35-10.580 (.0 (5.38-3.0) 7.0 (17.0 (5. 130 Fourth National Report on Human Exposure to Environmental Chemicals .60) .07 (3.0) 5.0 (13.99) 11.640 (.83-3.

5 (8.270 (<LOD-.77 (.390-.57) 1.33-4.83 (4.90-6.02) .12-4.31-7.7) 6.450 (.4-34.820) .85 (1.53) 27.84) 9.61) 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 .40) 1.41 (4.71 (2.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.48-42.47-10. Fourth National Report on Human Exposure to Environmental Chemicals 131 .690-5.780-4.430) 1.07-21.800-2.25-9.240-.940-4.50) 11.25-38.27 (2.5) 7.35 (.57-40.40-2.710 (<LOD-1.01 (1.14 (1.48 (4.79 (.75) 5.06 (.43) .370-1.600 (<LOD-1.83-11.67 (2.820 (.39) 20.1) 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.7) 3.57) 8.18) * * * * * * * * .88 (.86) .840-3.470 (.474-1.28-6.7 (6.650) 90th 10.32) 9.48-7.430 (<LOD-.5) 2.580) 1.96-8.69) 2.670 (.5 (11.04 (1.33-3.6) 952 1187 934 997 1330 993 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * .9) 6.150 (<LOD-.850-3.1) 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 * * * * * * .580) 16.03) 16.340 (.340-.37) 4.44-11.62 (1.3) 2.69-7.15) 9.96-25.56) .5) 2.8 (20.7) 5.81-17.24) 3.65 (2.5-40.88 (2.73 (4.86 (3.50) .88) 17.730-3.29 (4.1) 2.67) 1.53) .4) 2.92 (2.8) 1.80 (.890 (.91) 2.5 (9.29-4.02-4.64-4.17 (1.00-19.55) 21.8) 4.04-16.700) < LOD < LOD < LOD < LOD < LOD 1.740-1.33 (1.660) < LOD < LOD .47) 5.51-44.18) 95th 21.07 (2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.82-11.0 (4.74 (2.960 (.41) 18.790 (.52 (.250 (<LOD-.02 (1.67) 2.7 (12.700) 6.310-.17) 5.36 (.7) 4.270-.540 (.930) .770) .8) 2.650 (.860-2.260-.09-3.9 (11.630-1.50 (4.31-18.S.91-4.47-10.340-.44) .9) 5.748 (.260-.13 (2.66-47.330-1. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th 1.14-6.59 (1.49-2.10) 2.33-5.31) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.0) 4.60 (1.03) 2.05) .55 (3.32-6.30 (4.0 (9.56 (1.790) 11.40 (.2-38.64) 30.190-1.12 (4.370) < LOD < LOD < LOD < LOD < LOD 1.60) < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 4.11) .31) .33 (3.370 (.4 (4.88-3.970-3.45 (1.580-1.89 (2.560 (.8) 2.3) 3.360 (.500 (.830-3. population from the National Health and Nutrition Examination Survey.22) 2.40-12.21-3.8) 7.1 (7.10-3.830 (.50 (2.23-7.2 (8.540-1.620-3.57 (.10 (2.97) .18) 1.47) .55) 21.340-.320-1.56) 2.98 (4.8-33.00) .25 (1.85-3.80) 3.1 (5.96) 2.8) 7.51-4.580 (.590) 2.22-27.71 (.38 (2.11-5.08) .62-17.02 (.67-6.

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Ruberu DK. Gillham R. Caltabiano LM. low-level exposure to the organophosphate diazinon.30(2):98-103. Daniell WE. Neuropsychological effects of long-term exposure to organophosphates in sheep dip. London L. Lambert WE. Office of Prevention Pesticides and Toxic Substances. Phillips J. McCauley L. Am J Public Health 1994. Frasca G. Keefe TJ. Arch Environ Health 1988. Burcar PJ. The Pesticide Health Effects Study Group. Johnson C. Savage EP. Mounce LM. Muniz J. Robson MG. et al. Ames RG.332(1-3):71-80. Hore P. Tumino R.12(2):153-172. Pesticide industry sales and usage . O’Malley M. Lu C. Scand J Work Environ Health 1998. Effects of occupational exposure to organophosphate pesticides on nerve and neuromuscular function. Washington (DC).S. Pedersen L. Bull Environ Contam Toxicol 1994. Stokes L. Hansen S. 2004. Takamiya K. Muniz J. Jenkins B. S. 1/12/09 Peiris-John RJ. Santana J.114(5):691-696. Association between in utero organophosphate pesticide exposure and abnormal reflexes in neonates. Fourth National Report on Human Exposure to Environmental Chemicals 133 . Levy LS. Steenland K. Irish RM. Dinoff TM.nap. Kidd M. Bravo R. Environmental Protection Agency (U.52(10):648-653. Aprea C. Twenty-four-hour urinary excretion of ten pesticide metabolites in healthy adults in two different areas of Italy (Florence and Ragusa). Arch Environ Health 1975. Neurotoxicity among pesticide applicators exposed to organophosphates.345(8958):11351139.68(3):209-227 Maizlish N.58(11):702710. and cholinesterase status of date dusters and harvesters in California. 1993 [online]. Rosenstock L.26(2):199-209. Petchuay C. Terry AV Jr. Saieva C. Barr DB. Schenker M. Lasarev M. Int J Occup Environ Health 2006. J Toxicol Environ Health A 2005. van der Hoek W. Gladstone EA. Prendergast MA. Buccafusco JJ.84(5):731-736. low-level organophosphate exposure on delayed recall. Am J Ind Med 1987. Rothlein J. Nell V. Jamal GA. vibration sense and tremor among South African farm workers. Pesticides in the Diets of Infants and Children. Monitoring of urinary alkyl phosphates in pestcontrol operators exposed to various organophosphorus insecticides. Weisskopf C. Chrislip D. Thompson ML.S.20(2):115-22. Scherer J. National Academy of Sciences. Occup Environ Med 1995. metabolite clearance. Chronic neurological sequelae of acute organophosphate pesticide poisoning. Available at URL: http://books. Effects of long-term organophosphate exposures on neurological symptoms. Weerasekera G. Sci Total Environ 2004.24(1):18-29.38(4):546-563. et al. Environ Health Perspect 2005. Spurgeon A.epa. Environ Health Perspect 2006. Visuthismajarn P. Claypoole K. Rodnitzky RL.Organophosphorus Insecticides: Dialkyl Phosphate Metabolites Krieger RI. Smit LA. Lancet. Buchanan D. Heaton RK.12(2):134-141.php?record_id=2126&page=1. Rohlman D. Wickremasinghe AR. Lewis JA.44(4):352-357. Narang A.52(2):190-195. U. Available at URL: http://www. Beach J. Berry H. and spatial learning in monkeys and rats. A behavioral evaluation of pest control workers with short-term. Calvert IA. Russo J. 4/7/09 Young JG. 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. et al. Occup Environ Med 2001.pdf. et al. Arch Environ Contam Toxicol 2000. gov/oppbead1/pestsales/01pestsales/market_estimates2001. 1991. Samuels S. McConnell R. May. Masala G. Bradman A. Seiber J. Occupational exposure to organophosphate pesticides: a neurobehavioral study. Chronic neurological sequelae to organophosphate pesticide poisoning. Washington (DC): U. Stark A. Marshall E. Salvini S.2000 and 2001 market estimates. Rothlein J. Chronic central nervous system effects of acute organophosphate pesticide intoxication. Keifer M. EPA). J Occup Environ Med 2002. Organophosphate pesticide exposure and neurobehavioral performance in agricultural and non-agricultural Hispanic workers.43(1):38-45. Vitayavirasak B. Myers JE. National Research Council (NRC). Variation in organophosphate pesticide metabolites in urine of children living in agricultural communities. EPA. Malathion deposition. Eskenazi B. Biological monitoring of organophosphate pesticides in preschool children in an agricultural community in Thailand.edu/ openbook. Stephens R. Effects of chronic. Lasarev M. et al. Neurotoxicol Teratol 1998. Lancet 1995.113(4):504-508. discrimination.338(8761):223-227. Neurotoxicology 2005. The presence of dialkylphosphates in fresh fruit juices: implication for organophosphorus pesticide exposure and risk assessments. Pilkington A.

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

0) 12.80-8.30-2.29) 90th 7.22) 2.74-9.32) 2.74 (1.70-17.62-2.0) 12.71 (1.00-8.0) 15.68-2.5.90) 7.30) 5.95) 7.0 (7.80) 2.81-2.01) 1.13-3.0 (7.04-10.36 (4.30-11. Approximately 80.1) 5.20-11.40 (5.91) 16.70) 1.10 (1.40) 9.4) 481 573 681 823 832 1113 99-00 01-02 99-00 01-02 1.09 (3.0) 18.09 (2.51-2.1-16.20-3.EPA.67 (2.37 (1.50-4.S.0) 11.50-2.04-10.6-trichloro-2-pyridinol (TCPy) is a metabolite of chlorpyrifos and chlorpyrifos-methyl. Fourth National Report on Human Exposure to Environmental Chemicals 135 .19-3.20-14. and on plants for days to several weeks.6) 7.72-4.30) 4.20) 4.98-15.28) 2.97) 2. dermal.40 (5.000 pounds are used per year.90-8.83) 1.24-3.55-5.50-2.90 (1.60 (5.50 (2.05-5. and dust.S.0) 10.79-2.40) 2.70 (1.20) 2.0) 7. Chlorpyrifos is not well absorbed through the skin but dermal exposure can be significant when other routes of exposure are low.90 (6.77 (1.10 (3. 2007).90-2.50 (2. Approximately 21-24 million pounds per year were used domestically from 1987-1998.3) 8.7) 13.0) 12. air.40-26.21) 3.10 (4.6-Trichloro-2-pyridinol Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0) 8.94 (4.50 (2.63 (8.30-1.43-2.8) 9.4-15.24-1.97) 2.14) Selected percentiles ( 95% confidence interval) Sample 95th 10.20) 2.0) 6.37) 5.50 (1.66-15.0 (7.0 (7.90-4.50-4.57 (2.0) 12. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.91 (1.4 (8. It also has been applied directly on animals to kill mites.63 (2. Chlorpyrifos-methyl is an organophosphorus insecticide also used in agriculture and not registered for residential use. Estimated intakes from diet and water have not exceeded recommended intake limits.39) 4.77-15.35) 1.50-8.9 (10.15 (1. Chlorpyrifos is Urinary 3. Chlorpyrifos is degraded in agricultural soils with a half-life of several months.44 (3.5) 7. The general population may be exposed to chlorpyrifos via oral.72) 2.9 (7.71 (6.4 (10.50-14.02) 1.3 (11. 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.61 (1.20-4.27 (7.60-3.70-16.90) 3. 2002).37 (4.31-2.25) 3.13 (1.80) 4. Survey Geometric mean (95% conf.51 (1.47-13.60-2.0 (9.5-24.16) 2.10-17.2 (10.47) 1.97) 7.30-5.30 (4. Exposure can also result from contact with contaminated surfaces.50-5.96) 3.88 (1.80 (1.77-6.63 (1.00) 3. USGS.38 (3.80 (7.0) 10. interval) 1. 2002).95 (4.0 (7.59) 2.9) 11.02 (1.9) 697 660 521 701 602 947 Limit of detection (LOD.32-1.97) 4.22 (1.26) 7. 5598-13-0 General Information The chemical 3.40-13.60 (4.0) 8.66-4.77) 1.44-5.30 (2.10 (5. population from the National Health and Nutrition Examination Survey.9 (9.51) 1.03) 99-00 01-02 99-00 01-02 99-00 01-02 2.89-2.3) 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 1.0-28.20-2. Chlorpyrifos is very toxic to fish and aquatic invertebrates and shows modest degrees of bioconcentration.4. in 142 urban homes and preschools in North Carolina.00) 2.8-15.30-12.0) 10. and sprayed to kill mosquitoes. and is infrequently detected in ground water (IPCS.10) 6.4 and 0.68 (7.76 (1.59-2. 1999.45 (1.25) 1.80) 12.80-10.8) 10.97-7.20-16. chlorpyrifos and TCPy were detected in all indoor air and dust samples (Morgan et al.86) 4.52-2.9-18.47-11.02 (7.S.60-4.28-3.44-2.05) 1.30) 4.7) 9.0 (13.61) 75th 3.43-2.99-4.70-15.90 (3.76 (1.78 (7.47-9.67 (2.40-10.60-3. 2921-88-2 Chlorpyrifos-methyl CAS No. chlorpyrifos was no longer registered for indoor residential uses in the United States.64) 3.0) 9.EPA.20 (2.3 (8.2) 972 1183 1022 1326 99-00 01-02 99-00 01-02 99-00 01-02 1. 2005).7) 8.5.19 (1.70 (1.90 (2. After 2001.0 (10. Chlorpyrifos is a broad spectrum organophosphorus insecticide that has been widely used to control insects on food crops such as corn.70-11.61-7.Organophosphorus Insecticides: Specific Metabolites Chlorpyrifos CAS No.53 (1. pre.3 (10.29-1.03) 1.0) 14. For instance.84) 1.35) 2.89 (2.17 (1.4 (9.50 (1.87-6.46-2.00) 1. applied to structures to kill termites.20 (4.0) 12.92 (1.10) 2. It has low leachability.40-2.60) 5.34) 1.39-2.60 (2.47 (4. Inhalational and dermal routes of exposure are important in pesticide formulators and applicators.80) 1. but can be detected in streams receiving runoff from application sites.31-2. staying bound to soil particles.00-24.40 (6.7-23.90-7.70-5.30 (2.and post-construction structural applications for termite control were to be phased out by 2005 (U.20) 10..30-9.90 (1. and inhalation routes.52-12.71 (2.5 (8.67 (1.

12-1. 2006a.97) 3.24-1.30-1.29 (3. resulting in excess acetylcholine at nerve terminals.75 (1.47 (1. Once absorbed.91-13.86 (1.45 (1.0) 10.8) 9.85-4. 2005.3) 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 1.95 (1.82 (2.31) 1.73 (1.60 (1.5.93) 2.58) 5.60-3.01) 99-00 01-02 99-00 01-02 99-00 01-02 3.82) 8.96) 3.91 (3.. Urinary 3.00) 1.65-11.24-4.86 (1.88) 6.940-1.82-4.98 (6.11) 7.12-3.99-8.22 (4. population from the National Health and Nutrition Examination Survey.55 (4.45-1.S.53-5.19-2.33) 2.57-2.81 (3.17-4.55 (1.64-7.41 (1.85) 1.75) 6.42 (6.97 (3.88-8.0) 6.01) 1.91-4.43 (4.2 (7.7) 7.89) 4.85 (2. Human health effects from chlorpyrifos or chlorpyrifosmethyl at low environmental doses or at biomonitored levels from low environmental exposures are unknown.23-1.71 (1.56 (1.63 (5.58) 1. Roy et al..97 (2.0) 481 573 681 822 832 1113 99-00 01-02 99-00 01-02 1.30-4.27-1.71) 3. Chlorpyrifos is eliminated from the body primarily in the urine with a half-life of approximately 27 hours (Nolan et al.37 (1.24) 5.53 (2..16) 6.46 (2.25-1.1-21.22-6.88 (1.22 (6.47 (5.82 (3.2) 6.59-2.1 (10.02 (5.83-2..95 (3.44 (5.54 (2.85 (3.59) 3.24-5.56) 5.5) 5.35-1.17-4.70-4.56) 2. 1984).80-6.58 (4.25-12. The metabolite TCPy does not inhibit acetylcholinesterase enzymes.76 (3.93 (2. Recent in vitro and in vivo animal studies suggest that effects on neuronal morphogenesis.S.62-7. 2006b).92-2.83-11.85) 4. Survey Geometric mean (95% conf.94-14.63 (4.72-2.EPA. vomiting.94-12..79-13.66-11.24) 75th 2.19) 3. 2002). and other metabolites.09 (1.49-2.6) 9.42-2.47-2.8) 972 1183 1022 1325 99-00 01-02 99-00 01-02 99-00 01-02 1.56 (4.57) 9.12) 1.78 (1.09-1. interval) 1.93) 5. TCPy can also occur in the environment from the breakdown of the parent compounds.1-38.39 (4.06-4.33 (5.49-2.57) 2. In pesticide applicators..24-24.66 (1. the detection of TCPy in a person’s urine may reflect exposure to the environmental degradates..72) 2.86 (3.01) 3.31-4.05) 3.85) Selected percentiles ( 95% confidence interval) Sample 95th 8.64 (1.62) 90th 5.52 (5.33 (.74) 1.19-1.02) 7.00-8.21-1.33 (1.28) 2.31-1.72) 1.68) 1.4) 4.62) 1.66) 1. Thus.5 (6.55) 1.42 (5.92) 3.77) 1.93 (1.48 (1.05-8.56-2.92 (1. Betancourt et al.3) 8.3) 8.05-1.11 (2.39 (2.88-10. 2005. 2006.84-6.49 (1.91) 1.16 (4.24 (1.43-10.44 (1.46 (1.22) 1.64-2.44 (6.58 (1.65-15.80-4.05-4.63-2.07) 1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”).44 (1.97) 3. These organophosphorus insecticides share a mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system. 2000).88 (1.25-11.27-7.32) 1. Metabolic hydrolysis leads to the formation of TCPy.15 (4.07) 5.9 (12.03) 1.0) 12.14-8. In addition to being a metabolite of chlorpyrifos and chlorpyrifos-methyl in the body.87-3.99) 1.47 (1. chronic exposure to chlorpyrifos may be associated with slight alterations in some components of neurophysiologic testing (Steenland et al.00 (7. weakness.91) 1.34-1.91 (4. Howard et al.81) 2.06 (1.3) 9.69 (1.50 (4. 2005.68) 6.06 (5.54) 5. neurotransmission. paralysis.35) 1.11 (2. and producing acute symptoms such as nausea.00-13.58 (1.44-6.0) 16. Slotkin et al.Organophosphorus Insecticides: Specific Metabolites rapidly absorbed following ingestion.93 (4.91) 10.88-9.39-1.20-1.08) 6.48 (2.09-2.. and behavior may occur at systemically nontoxic doses or at doses of chlorpyrifos that do not result in cholinergic signs (Aldridge et al.33-7.7) 697 660 521 700 602 947 136 Fourth National Report on Human Exposure to Environmental Chemicals .20 (2.01) 3. and seizures.51 (1. phosphorothioates such as chlorpyrifos are metabolically activated to the “oxon” form which has greater toxicity than the parent insecticide.36) 1.3 (7.05-3.35) 2.39) 6. Based on animal data and human cholinesterase monitoring during occupational exposure.97-3.38) 3.58-5..14) 1.09-3.90-9.21-6. TCPy is more persistent in the environment than chlorpyrifos itself (U.91) 2. ubiquitous lowlevel environmental exposures in humans would not be expected to result in inhibition of cholinesterase activity.26-14.80) 3.76 (2.80-11.11-9.23) 14. Chlorpyrifos and chlorpyrifos-methyl both demonstrate moderate acute toxicity in animal studies.88-8.98 (7.49-2. cholinergic effects.28) 2. 2006. Overt cholinergic toxicity from chlorpyrifos has been described following suicidal ingestion and unintentional high level occupational exposure.19) 6.6-Trichloro-2-pyridinol (creatinine corrected) Metabolite of Chlorpyrifos and Chlorpyrifos-methyl Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. Ricceri et al.44 (5. 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.40) 1.57-2.6) 10.83) 1.1 (7.

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

Shealy DB. Roy TS. Weltzien E. Lorenzini P. Chlorpyrifos: pharmacokinetics in human volunteers. February 5. Environ Health Perspect 2003.71:99108. Slotkin TA. gov/ntpweb/index. et al. Barr DB.114(10):1542-1546. Pesticide residues in urine of adults living in the United States: reference range concentrations. Gregg M. Effects of transplacental exposure to environmental pollution on birth outcomes in a multiethnic population.S.org/documents/jmpr/jmpmono/ v99pr03. Comparative developmental neurotoxicity of organophosphate insecticides: effects on brain development are separable from systemic toxicity. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.inchem. Ozkaynak H. Zhang J. Chlorpyrifos exerts opposing effects on axonal and dendritic growth in primary neuronal cultures. Hein MJ. Bradman A.73:8-15. Scand J Work Environ Health 2005. Angerer J. Lein PJ. Levin ED.5. Slotkin TA. Capone F. Rauh V. J Expo Anal Environ Epidemiol 2005.113(2):211-219.155(1):71-80. 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.htm. Morgan MK. Biological monitoring of exposure of the general population to the organophosphorus pesticides chlorpyrifos and chlorpyrifos-methyl by determination of their specific metabolite 3.114(2):260-263.15(4):297-309. Baker S. Dick RB. Howard AS. Bravo R. Striley C. Croghan CW. Sharma V. Venerosi A. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Acquavella JF.10(4):327-340. Saunders JH. Gurunathan S. Environ Health Perspect 2006. Hammerstrom KA. Environ Health Perspect 2004. Third National Report on Human Exposure to Environmental Chemicals. Barr DB. et al. et al. Exposures of preschool children to chlorpyrifos and its degradation product 3. mothers and fathers living in farm and non-farm households in Iowa. Toxicol Appl Pharmacol 2005. Lioy PJ. Ryan L. Environ Health Perspect 2000.cfm?objectid=6F5E95EB-F1F6-975E7C20F4211536F46F. Environ Health Perspect 2006b. Eskenazi B. 2921-882. Chlorpyrifos. 4/7/09 Koch HM. 4/7/09 Perera FP. Heederik D. MacIntosh DL. et al. Robertson GL. Tsai WY. J Expo Anal Environ Epidemiol 1999. Slotkin TA. Toepel K. Toxicol Sci 2006. et al. Hill RH Jr. Herrick RF. International Programme on Chemical Safety-INCHEM (IPCS). 2005. Harley K. Barr DB. et al. Chrislip DW. et al. Irish R. Bucelli R. Available at URL: http://www. Honeycutt R. Biomonitoring for farm families in the farm family exposure study. chlorpyrifos. Edwards RD. Interim registration eligibility decision for chlorpyrifos. Head SL. Bravo R. Sanderson WT. A longitudinal investigation of selected pesticide metabolites in urine. Howell RJ. 1999. J Expo Anal Environ Epidemiol 2005.108(4):293-300. Seidler FJ. Environ Res 1995. Freshour NL. et al. Urinary pesticide concentrations among children. Freeman N. EPA). Kinney P. Executive summary of safety and toxicity information.93(1):105-113. Int J Hyg Environ Health 2001. Barr D. Baker BA. Toxicol Appl Pharmacol 1984. Ricceri L. Chlorpyrifos accumulation patterns for child-accessible surfaces and objects and urinary metabolite excretion by children for 2 weeks after crack-and-crevice application.111(2):201-205. Available at URL: http://ntp.6-trichloro 2-pyridinol in their everyday environments. Rick DL. Bruun D. Wartenberg D. Fenske RA. Bailey SL. Fortuna S.112(10):1116-1124. Jewell NP. National Toxicology Program (NTP). 1992. Environ Health Perspect 2005. Bennett DH.6-trichloro-2-pyridinol. Needham LL. Mandel JS. U. Jones PA.15(3):271-281. Cometa MF.114(5):746-751. Levin ED. Adgate JL.51(1):53-65. Kromhout H. Quantitative morphological assessment reveals neuronal and glial deficits in hippocampus after a brief subtoxic exposure to chlorpyrifos in neonatal rats.5. Chapman P. Alexander BH. Meeker JD. Robson M.207(2):112-124. Ann Occup Hyg 2007. Hines CJ. Developmental neurotoxicity of organophosphorous pesticides: fetal and neonatal exposure to chlorpyrifos alters sex specific behaviors at adulthood in mice. Camann D.nih. Steenland K. J Expo Anal Environ Epidemiol 2000. Curwin BD.niehs. Neurologic function among termiticide applicators exposed to chlorpyrifos. Lu C. Environ Health Perspect 2006a. Pellizzari E. et al. Nolan RJ. Atlanta (GA). Environmental Protection Agency (U. House dust levels of selected insecticides and a herbicide measured by the EL and LWW samplers and comparisons to hand rinses and urine metabolites. Hore P. Jett DA. Hardt J. et al. Chuang JC. Temporal variability of urinary levels of nonpersistent insecticides in adult men. Seidler FJ. EPA 738-R- 138 Fourth National Report on Human Exposure to Environmental Chemicals . Sheldon LS.9(5):494-501. Yang D.S. Reid TM. Seidler FJ. Ryan PB.31 Suppl 1:98-104. Environmental Health Criteria 198. Ryde IT.204(2-3):175-180. Tate CA. Freeman N.Organophosphorus Insecticides: Specific Metabolites Centers for Disease Control and Prevention (CDC). Brain Res Dev Brain Res 2005.

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

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

2.200 (<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.380 (<LOD-.200 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.270) < LOD 659 701 920 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .670 (<LOD-1. population from the National Health and Nutrition Examination Survey. Survey Geometric mean (95% conf.S. which may vary for some chemicals by year and by individual sample.S. 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 .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 . 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 .560) < LOD 659 700 920 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. Fourth National Report on Human Exposure to Environmental Chemicals 141 . 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. < LOD means less than the limit of detection. see Data Analysis section) for Survey year 01-02 is 0.

2005.376(6):808-815.S. Third National Report on Human Exposure to Environmental Chemicals. Reregistration eligibility decision (RED) addendum and FPQA tolerance reassessment progress report: Coumaphos. EPA). Nguyen JV.gov/oppsrrd1/ REDs/0018tred. Atlanta (GA). Barr DB. Anal Bioanal Chem 2003. Environmental Protection Agency (U. September 2000. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Sadowski MA.12(6):619-645. Freshwater KJ. Available at URL: http://www.S. U. Eigenberg DA.Organophosphorus Insecticides: Specific Metabolites References Astroff AB. Reprod Toxicol 1998. Centers for Disease Control and Prevention (CDC). Olsson AO.pdf.epa. 1/14/09 142 Fourth National Report on Human Exposure to Environmental Chemicals . EPA 738-R-00-010. Comparative organophosphate-induced effects observed in adult and neonatal Sprague-Dawley rats during the conduct of multigeneration toxicity studies.

but is rapidly absorbed orally (IPCS. fruits.45 (<LOD-3.7. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Metabolites”). Prior to 2000. 2004). Before these restrictions. It is toxic to birds. 1998). Experimental diazinon exposure in people has demonstrated its rapid elimination into urine. Most granular formulations. in the past. and forage crops.49 (<LOD-2. Inhalational and dermal routes of exposure can be significant for pesticide applicators. < LOD means less than the limit of detection. Survey Geometric mean (95% conf. vegetable. 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 was widely used in residential and garden application.EPA. which may vary for some chemicals by year and by individual sample. population from the National Health and Nutrition Examination Survey. about 13 million pounds of diazinon were used annually on agricultural sites in the United States. Fourth National Report on Human Exposure to Environmental Chemicals 143 . Diazinon is not well-absorbed through the skin.05) < LOD < LOD 644 678 484 700 554 956 Limit of detection (LOD. and particularly when it was ingested in granular form. in some pest strips. USGS. 333-41-5 General Information The chemical 2-isopropyl-4-methyl-6-hydroxypyrimidine is a metabolite of diazinon. an organophosphorus insecticide that is used to control insects on nuts. but these uses have been phased out.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. 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. 2004).Organophosphorus Insecticides: Specific Metabolites Diazinon CAS No.S. diazinon produced wild bird kills before use restrictions were in place.S. and other metabolites. diazinon cannot be sold for residential use. Fish and aquatic invertebrates show modest degrees of bioconcentration and are very sensitive to toxic effects. see Data Analysis section) for Survey years 99-00 and 01-02 are 7. aerial. since 2004. 2007). Once absorbed. It has been infrequently detected in general groundwater sampling but has been detected in streams receiving runoff from application sites (IPCS. 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.S. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.2 and 0. 1998. phosphorothioates such as diazinon are metabolically activated to the “oxon” form which has greater toxicity. Estimated intakes from diet and water do not exceed recommended intake limits (U. Diazinon is biologically and chemically degraded in soils with a half-life of about a few weeks.EPA. Metabolic hydrolysis leads to the formation of 2-isopropyl4-methyl-6-hydroxypyrimidine. It is also used for cattle ear tag applications to control flies and ticks and. seed and foliar applications are planned to be phased out (U.

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

10(6 Pt 2):789-798. Rajendra W. 2005. J Expo Anal Environ Epidemiol 2000. Environmental Health Criteria 198. Third National Report on Human Exposure to Environmental Chemicals. Available at URL: http://pubs.134(1-3):105-113. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Beeson MD. 2007 [online]. Exposure to the organophosphate diazinon: data from a human volunteer study with oral and dermal doses.gov/circ/2005/1291/. Mason HJ. International Programme on Chemical Safety-INCHEM (IPCS). Irish R. Oloffs PC.usgs.50(5):505-515. 1992-2001. Semen quality in relation to biomarkers of pesticide exposure. March 2006.S. Toepel K. Driskell WJ. Kruse RL. Pewnim T. EPA). Swan et al. Environmental Protection Agency (U. Brunet RC. 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. Carrier G.gov/ oppsrrd1/REDs/diazinon_ired. Quantification of selected pesticide metabolites in human urine using isotope dilution high-performance liquid chromatography/ tandem mass spectrometry. Interim reregistration eligibility decision (IRED. Environ Health Perspect 2006. May 2004.9(2):117-131. Centers for Disease Control and Prevention (CDC).. Seifert J. Needham LL. In 23 children. et al. (2003) found that 2-isopropyl4-methyl-6-hydroxypyrimidine was detectable in 96% and 58% of the subjects. Redmon JB. Noisel N. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine. Olsson AO. 2006). 6/1/09 Fourth National Report on Human Exposure to Environmental Chemicals 145 . Effects of chronic intake of diazinon on blood and brain monoamines and amino acids. Dumas P.org/documents/ehc/ehc/ehc198.pdf. Bull Environ Contam Toxicol 1986.S.Organophosphorus Insecticides: Specific Metabolites 2005). Available at URL: http://www. Swan SH. 4/7/09 Lu C. Anal Bioanal Chem 2003.S. Alteration of mice L-tryptophan metabolism by the organophosphorous acid triester diazinon. Jones K. 1/14/09 U. Available at URL: http://www.37(4):501-507. Atlanta (GA). Sadowski MA.epa. Barr DB. Study for Future Families Research Group. revised February 15. Baker SE. Effect of sublethal levels of diazinon: histopathology of liver. Ann Occup Hyg 2006. Biological monitoring of exposure to organophosphorus insecticides in a group of horticultural greenhouse workers.114(2):260-263. Barr DB. 2006). The Quality of Our Nation’s Waters. Bouchard M. Barr DB. 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. References Anthony J. Drobnis EZ.inchem. Bravo R. Banister EW. Fenske RA. 1998. EPA 738-R-04-006. Drug Chem Toxicol 1986. Garfitt SJ. urinary 2-isopropyl-4-methyl-6-hydroxypyrimidine levels were below the limit of detection (Bouchard et al. In 54 Canadian greenhouse workers. Diazinon. U. Diazinon.376(6):808-815.htm. Liu F. Geological Survey (USGS). Biochem Pharmacol 1992. Nguyen JV.111(12):1478-1484. Oloffs PC. In a small number of men visiting fertility clinics in Missouri and Minnesota. Cocker J. urinary 2-isopropyl-4-methyl-6hydroxypyrimidine was detected in less than 14% of multiple samples collected during varied diets (Lu et al.. Barr DB. Pesticides in the Nation’s Streams and Ground Water. Toxicol Lett 2002. Environ Health Perspect 2003.44(11):2243-2250. Banister E. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides.

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

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

pdf. Thomas D. In vitro studies on the genotoxicity of the organophosphorus insecticide malathion and its two analogues. 6/1/09 148 Fourth National Report on Human Exposure to Environmental Chemicals .org/documents/jmpr/jmpmono/v2003pr06. EPA 738-R06-030.gov/oppsrrd1/REDs/ malathion_red. Environ Health Perspect 2004. and cholinesterase status of date dusters and harvesters in California. Harley K. Toepel K. Rappaport E. Petitti D. Szyfter K.38(4):546-553.S.22(1):7-17.56(10):2393-2399. Fenske RA. Jewell NP.gov/circ/2005/1291/. 6/1/09 U. Prasad SB.inchem.514(1-2):223231. Mutat Res 2002.epa. A longitudinal investigation of selected pesticide metabolites in urine. J Expo Anal Environ Epidemiol 2005.S. Eskenazi B. Giri S. Barr DB. Harris JA. Environ Health Perspect 2001. Environ Health Perspect 2006.Organophosphorus Insecticides: Specific Metabolites References Adgate JL. Bouchard M. Neutra R. Pluth JM. Available at URL: http://www. Giri A.74(2):following table of contents.77:1009-1010. Measurement of children’s exposure to pesticides: analysis of urinary metabolite levels in a probability-based sample.73(1):182-94. Gosselin NH. Bravo R. Lu C. Ryan PB. Hammerstrom KA. Dumoulin MJ. Erratum in: Toxicol Sci 2003 Aug. Malathion (addendum). Goldhaber M. Organic diets significantly lower children’s dietary exposure to organophosphorus pesticides. metabolite clearance. Centers for Disease Control and Prevention (CDC). O’Neill JP. Quintana PJ. et al.114(2):260-263. International Programme on Chemical Safety-INCHEM (IPCS). et al. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State. Dinoff TM. 2007 [online].S. Increased frequency of specific genomic deletions resulting from in vitro malathion exposure. Atlanta (GA). Freeman NC. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population. Needham LL. Reproductive outcome in women exposed to malathion. 1992-2001. 2005. EPA).usgs. Sharma GD. Griffith W. Hooper K. Am J Epidemiol 1990. Brunet RC. Cancer Res 1996. Third National Report on Human Exposure to Environmental Chemicals. Clayton CA.9(5):494-501. htm. Nicklas JA. Lioy PJ. Toxicol Sci 2003 May. Samuel O. Reregistration eligibility decision (RED) Malathion. Mutat Res 1999. Genetic toxicity of malathion: a review. Available at URL: http://www. et al. July 2006. Malathion deposition. U. 4/7/09 Kissel JC. Weltzien E. Blasiak J. Barr DB. Barr DB. Kedan G. Environmental Protection Agency (U. Barr DB. Kizer KW: Exposure to aerial malathion application and the occurrence of congenital anomalies and low birthweight. Grether JK. Albertini RJ. Jaloszynski P. A toxicokinetic model of malathion and its metabolites as a tool to assess human exposure and risk through measurements of urinary biomarkers. Hertz-Picciotto I. Arch Environ Contam Toxicol 2000. revised February 15.109(6):583-590. Available at URL: http://pubs.15(2):164-171.112(10):1116-1124. Krieger RI. Flessel P. Environ Mol Mutagen 1993. Am J Public Health 1987. Pesticides residues in food: 2003 FAO/WHO Meeting on Pesticide Residues. Genotoxic effects of malathion: an organophosphorus insecticide using three mammalian bioassays in vivo.445(2):275-283. Lu C. MacIntosh DL. Swan SH. Carrier G. Eberly LE.132(4):794-795. Pesticides in the Nation’s Streams and Ground Water. Trzeciak A. The Quality of Our Nation’s Waters. Geological Survey (USGS). J Expo Anal Environ Epidemiol 1999. Curl CL. Irish R. March 2006. Bradman A.

methyl parathion was rapidly absorbed after ingestion.0) 4.46 (3..10 (3.47) 2.70 (3.50 (1.20-5. Survey Geometric mean (95% conf. first registered in 1948.910) < LOD < LOD .18-3.27) 2.26 (1.0) 2.0) 3. Methyl parathion use is highly restricted. and aquatic invertebrates.91-3.0) 3.S.50) 2.32 (1.32-1. 2006).02-6.22-3.60-19.70-3..32-1.19 (.85 (2.66 (2.28-4.8 and 0. was once a restricted-use insecticide with limited applications on certain agricultural crops.57) 1.40 (1.0) 3.67 (1.40-4.990-1. In animal studies. the potential for human exposure to either ethyl or methyl parathion through the diet or drinking water is low. Ethyl and methyl parathion are infrequently detected in groundwater sampling (USGS.90-11.1.70-6. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.S.700 (<LOD-. and to a lesser extent. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.12) < LOD < LOD 1.60-36.940 (<LOD-2.74) 5.60-24.10 (3.13-1.61) < LOD 1.30-16.00) 3.92) 5.298-00-0 Ethyl Parathion CAS No..33 (1.00 (2.37-4.92-2. 2007).80 (1.70-3. < LOD means less than the limit of detection. Both are toxic to birds. population from the National Health and Nutrition Examination Survey. pulmonary.37-2.69 (2.34 (3. binds tightly to soils resulting in low leachability. interval) Selected percentiles ( 95% confidence interval) Sample 95th 5.58) 3.0 (3.60-5.70-6.EPA.71 (2.32-3.21 (2. and eliminated rapidly from the body after absorption (Kramer et al.37-4.15-3.70) 2.770 (. and oral routes can occur in pesticide and agricultural workers (Muttray et al.70) 2.860 (<LOD-1.10 (<LOD-6.Organophosphorus Insecticides: Specific Metabolites Methyl Parathion CAS No.60 (4.33) 2.50-9. Given its limited use.30-5.730 (<LOD-.50) 3.01) 695 660 518 679 603 941 Limit of detection (LOD.850) < LOD .79) 4.61) < LOD 1. all registered uses were voluntarily cancelled (U. phosphorothioates such as methyl and ethyl parathion are metabolically activated to the “oxon” forms which have greater toxicity than the parent insecticides.28 (1.50 (1. Fourth National Report on Human Exposure to Environmental Chemicals 149 . Methyl Parathion.67) < LOD 1.57-4.910) < LOD .EPA.71 (3.10-11.40-3.45 (1.0) 3. and has a short half-life in soils and on plants.44) 2.01) 4. Metabolism of ethyl or methyl parathion leads to the formation of paranitrophenol.90 (1. and of the chemical nitrobenzene. on cereal grains. Estimated intakes from diet and drinking water have been below recommended limits. Many previous registered agricultural uses of methyl parathion have been cancelled (U.80 (2.48) 90th 2.30-3.70 (2.S. O-ethyl-O-(4-nitrophenyl) phenylphosphonothioate.60) 1.72 (3.80 (2.62 (1.10) 22. It had been applied to cotton. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.11-4.70 (2.09-1.00 (2. In the 1990s. with limited applications in agriculture.910) < LOD < LOD < LOD 1.40) 4.70 (<LOD-3.01-4. more slowly absorbed through the skin.21-1. Morgan et al.49 (1. 2002.30 (1.790 (<LOD-. Methyl parathion has low water solubility.37) 2.50 (1.50 (2. ethyl parathion.50 (2.70 (2.20 (2.50 (1. dialkyl phosphate metabolites (see section titled “Organophosphorus Insecticides: Dialkyl Phosphate Urinary para-Nitrophenol Metabolite of Ethyl Parathion. but by 2003.16) < LOD 1. 2000). 2003).90-9.00) 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 1.10-1.70-6. Increased risk of exposure via dermal.41-4.300-.24) 479 565 680 813 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .40) 2.45) 5.50) 3. fish.20) 5.70) 2.50-14.69) 4.30 (2.36-1.89 (2.40-4.50) 1.40) 1.80) 2.71) 971 1164 1018 1313 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .28 (1.05) 4. Ethyl parathion. Methyl parathion is not registered for residential use in the United States.11) 2.02) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD . which may vary for some chemicals by year and by individual sample. 1977).10) 4.20 (<LOD-2. 56-38-2 General Information Para-nitrophenol is a metabolite of the insecticides methyl parathion. peak domestic use was as high as 5-6 million pounds per year. Once absorbed.0) 3.

35-3. Karanth and Pope et al. Survey Geometric mean (95% conf.96 (1.56-2. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.45) 695 660 518 678 603 941 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.20 (3.. and producing acute symptoms such as nausea.17-4.80 (1.880 (.60-2.03) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .88) 1.86 (2.09) 2.30-1. Slotkin et al.59 (1.2) 2.61) 4.4 (3.04 (2.88 (1.680 (<LOD-1.87 (1.55 (<LOD-3.06) 971 1164 1018 1312 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD .95) 1. EPA at: http://www.930 (.89 (2.21) 1.7) 3. retinal atrophy and sciatic nerve degeneration have also been observed (IPCS. and seizures.82 (2.91) 1.44-3..950) < LOD . Overt cholinergic toxicity and death from methyl and ethyl parathion have been described following suicidal ingestion.980 (.730-1.48-4. vomiting.15-10.90 (1. Recent in vitro and in vivo animal studies suggest that parathion may have additional neuronal and glial cell effects at lower doses (Guizzetti et al.970 (.08 (1.79 (1.60 (1.790-1.78 (2.57-7.07 (1.530) < LOD < LOD < LOD .500) < LOD < LOD .55) 2..25) 1. paralysis. or generally to have reproductive toxicity at doses below those causing acetylcholinesterase inhibition in most animal studies (IPCS.14-3.71 (1.440 (<LOD-. cholinergic effects.00) 2.72-2.38-3. In large doses. U. Lores et al.html and from U. Methyl Parathion.640) < LOD < LOD 1. and Nitrobenzene Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.41-2. WHO.S. methyl parathion.800-1.430 (.930 (. paranitrophenol. 1995. and unintentional acute or chronic high-level occupational exposure (Hill et al.11-4.67 (3.01 (2.71) 1. 2004).08) < LOD .96 (1. population from the National Health and Nutrition Examination Survey..20) ..84) 3.83 (1.17) .04) 1.11) 1. accidental exposure. Parathion and methyl parathion have high acute toxicity in animal testing.epa.33-6.33) 479 565 680 812 830 1099 99-00 01-02 99-00 01-02 * * * * < LOD .3) 2.2) 2..89 (2. 1995).80 (1. 1990.98-7. 2005.e.13-12.73 (1.830-1.05) 4.94-47.21-21.26) 17.31) < LOD .29) 2.720 (<LOD-. para-nitrophenol can also occur in the environment from the breakdown of the parent these organophosphorus pesticides and from nitrobenzene. 2006.57) 6.690-1.cdc.790-.9) 1.78-2.S.94-4. resulting in excess acetylcholine at nerve terminals.370 (<LOD-. 150 Fourth National Report on Human Exposure to Environmental Chemicals . 2003.540) < LOD . IARC does not consider ethyl parathion and methyl parathion classifiable as human carcinogens.310-.20) 3.93 (2. At high animal doses of methyl parathion. Jaga and Dharmani. and other metabolites.91 (1.720-1.30) 3.00 (1..10) 90th 2.79) 1.atsdr.60) 2.92 (2. The metabolite. Thus.39 (1.07) 2. 1991).850-1.78-2.33-3. weakness. 2004).. but lists ethyl parathion as a possible human carcinogen. Zurich et al.S.08-3.29) 1.70) 3.29 (2. ethyl parathion.97-10.97 (<LOD-4.25 (2. In addition to being a metabolite of methyl and ethyl parathion. gov/pesticides/.33-3.00 (1.82) < LOD .Organophosphorus Insecticides: Specific Metabolites Metabolites”).78) 2. Orsorio et al. Urinary para-Nitrophenol (creatinine corrected) Metabolite of Ethyl Parathion. interval) Selected percentiles ( 95% confidence interval) Sample 95th 4.01-3. gov/toxpro2. and other organophosphorus insecticides share a common mechanism of toxicity: inhibition of the activity of acetylcholinesterase enzymes in the nervous system.16-4.37-1. teratogenic.970 (. does not inhibit acetylcholinesterase enzymes.13) 4.57-2. 1978.840 (.35-3. Methyl parathion is not considered genotoxic.400 (<LOD-.EPA considers methyl parathion unlikely to be carcinogenic to humans.23) 1.31-3.77-7.44-3.26 (1.01 (.15) 3.940 (<LOD-1.23) size 1989 2476 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD 75th . Human health effects from parathion or ethyl parathion at low environmental doses or at biomonitored levels from low environmental exposures are unknown.67-2. the detection of para-nitrophenol in a person’s urine may also reflect exposure to the environmental degradate.1) 2.870) < LOD .39) 1.76-14. Additional information about external exposure (i. environmental levels) and health effects is available from ATSDR at: http://www.10 (1.97 (2. 2006.43) 4.

4/7/09 Jaga K. et al. Chicago area methyl parathion response. Bailey SL. Turner WE. Arch Environ Contam Toxicol 1977. Measurement of p-nitrophenol in the urine of residents whose homes were contaminated with methyl parathion. Shealy DB. Urinary excretion of paranitrophenol and alkyl phosphates following ingestion of methyl or ethyl parathion by human subjects. Needham LL. Age-related effects of chlorpyrifos and parathion on acetylcholine synthesis in rat striatum.. Clark JM... Moomey CM. 2005. Pesticide workers may have much higher levels following pesticide applications.6(2-3):159-173. J Expo Anal Environ Epidemiol 2005.15(2):164-171. Rockhold RW. CDC.. Third National Report on Human Exposure to Environmental Chemicals. 2004).5 mg (500 µg)/g creatinine for workers at the end of shift. 2002. Atlanta (GA). Environ Health Perspect 2002. Hryhorczuk DO. Organophosphorus pesticide poisonings in humans: determination of residues and metabolites in tissues and urine.S. a range of values several hundred times higher than levels found in the U. and levels were similar or slightly lower that those in a small convenience sample of the U. Baker RC.org/documents/jmpr/jmpmono/v95pr14. Lewalter J.inchem. Lin LI. Guizzetti M. Harley K. Comparison of organophosphorus pesticide metabolite levels in single and multiple daily urine samples collected from preschool children in Washington State.215(3):182-190. Environ Res 1995.71:99108.. Bradman A.. International Programme on Chemical Safety-INCHEM (IPCS).110 Suppl 6:1085-1091. 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.Organophosphorus Insecticides: Specific Metabolites Biomonitoring Information Urinary levels of para-nitrophenol reflect recent exposure. Ashley DL.htm. Eskenazi B.110 Suppl 6:1075-1078. Occup Environ Med 1999. Head SL. 1995). 2003) and in 482 pregnant females from an agricultural region of California (Eskenazi et al. Barr DB. Laboratory investigation of a poisoning epidemic in Sierra Leone. Levels of para-nitrophenol in the NHANES 1999-2000 and 2001-2002 subsamples were similar or slightly lower than those in a nonrandom subsample of NHANES III (19881994) participants (CDC. Weltzien E. Costa LG. Runkle KD. Head SL. Pope C. McCann KG.9:311-320.56(7):449553. Bradway DE. Neurotoxicol Teratol 2003. Barr DB. 1999). DiPietro E. Association of in utero organophosphate pesticide exposure and fetal growth and length of gestation in an agricultural population.25(5):599-606. Lores EM. 2005). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. general population (CDC. Available at URL: http:// www. Slach EF. oral or dermal administration. Barr JR. Barr DB. Leng G.14(4):213-216. Lu C. J Anal Toxicol 1990. Effect of organophosphorus insecticides and their metabolites on astroglial cell proliferation. Kissel JC. and many residents were symptomatic (Barr et al. Hetzler HL.. Alley CC. Fourth National Report on Human Exposure to Environmental Chemicals 151 . Centers for Disease Control and Prevention (CDC). Pathak S. 2002). Kramer RE. Environ Health Perspect 2004. 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. 2002. Curl CL.S. McClure PC.112(10):1116-1124. Finding a measurable amount of para-nitrophenol in urine does not mean that the level will result in an adverse health effect. Morgan DP. et al. Methyl parathion: an organophosphate insecticide not quite forgotten. et al. In a study of workers who handle parathion. 2005. References Barr DB. Arch Environ Health 1978. 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. Environ Health Perspect 2002. Toxicology 2005. Role of individual susceptibility in risk assessment of pesticides. Baker SE. Pharmacokinetics of methyl parathion: a comparison following single intravenous. J Biomed Sci 2002. Wellman SE. Dharmani C. et al. et al. 2005. Karanth S. Moseman RF. Griffith W. Rev Environ Health 2006.21(1):5767. Parathion-Methyl (addendum). Jewell NP. Pesticide residues in urine of adults living in the United States: reference range concentrations. 1995.33(5):270-276. end-of-shift urinary para-nitrophenol levels ranged from 190 to 410 µg/ gram of creatinine (Leng and Lewalter. Baker S. ACGIH recommends a BEI of 0. Hill et al. Cline RE. Rubin et al. population (Olsson et al. Hill RH Jr. McCann et al. Kedan G. 2005). Giordano G. Gregg M. Hill RH Jr.

pdf.S. Available at URL: http://pubs. revised February 15. External and internal exposure of wine growers spraying methyl parathion. 152 Fourth National Report on Human Exposure to Environmental Chemicals . 1/14/09 U. Schilter B. Methyl parathion in drinking water.162(2-3):219-224. EPA-738-FOO-009. 1995-1996. Barr DB. Hill RH Jr. A liquid chromatography/electrospray ionization tandem mass spectrometry method for quantification of specific organophosphorus pesticide biomarkers in human urine.epa.usgs. Rubin C. 0153. Investigation of a fatality among parathion applicators in California. Esteban E.S. 2007 [online]. Monnet-Tschudi F. Nguyen JV. et al. Interim reregistration eligibility decision (IRED) for Methyl Parathion. September 2000. 5/19/09 Zurich MG. WHO/SDE/WSH/03. Levin ED.376(6):808-815. Environ Health Perspect 2006. Am J Ind Med 1991. 6/1/09 World Health Organization (WHO). Environ Health Perspect 2002. Costa LG. R.int/water_sanitation_health/dwq/chemicals/ methylparathion. Seidler FJ. Slotkin TA.114(10):1542-1546. Honegger P. Hill G. Ohio.S.S.D.S.gov/circ/2005/1291/. Assessment of human exposure and human health effects after indoor application of methyl parathion in Lorain County.epa. 1992-2001. Case No. Rosenberg J.pdf. Kieszak S. Backer G. Involvement of glial cells in the neurotoxicity of parathion and chlorpyrifos. Ethyl parathion.who. Organophosphate insecticides target the serotonergic system in developing rat brain regions: disparate effects of diazinon and parathion at doses spanning the threshold for cholinesterase inhibition. The Quality of Our Nation’s Waters. Tate CA. Environmental Protection Agency (U. Sadowski MA. Pesticides in the Nation’s Streams and Ground Water. Jung D. Toxicol Appl Pharmacol 2004.04/106. Osorio AM.201(2):97-104.pdf. Letzel S. Dunlop B. gov/oppsrrd1/REDs/methylparathion_ired.110 Suppl 6:1047-1051. May 2003. 1/12/07 U. Facts. Mengle DC. Yacovac R. Olsson AO.Organophosphorus Insecticides: Specific Metabolites Muttray A. Anal Bioanal Chem 2003. Geological Survey (USGS). Available at URL: http://www. U. EPA).gov/oppsrrd1/REDs/factsheets/0155fct. Available at URL: http://www. Ryde IT. EPA).20(4):533-546. March 2006. Environmental Protection Agency (U. Toxicol Lett 2006. 2004. Available at URL: http://www. Ames RG.E.

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

27) .07) .470 (.S.780 (<LOD-1. population from the National Health and Nutrition Examination Survey.S. Survey Geometric mean (95% conf.31) . Survey Geometric mean (95% conf.55) .760 (<LOD-.880) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .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 .700-1.64) .00) 669 687 929 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. which may vary for some chemicals by year and by individual sample.610 (<LOD-1.08) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .850 (.17 (.740 (.580-1.840) 669 687 929 Limit of detection (LOD.410 (<LOD-1.200-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey.780 (<LOD-1.430 (<LOD-. < LOD means less than the limit of detection. 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.780 (.930) size 2481 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 01-02 50th < LOD < LOD 75th < LOD 90th * 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD .500 (.210-.250 (<LOD-.780 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.670 (<LOD-1.950) < LOD < LOD 1.820) < LOD < LOD .460) 1165 1316 01-02 01-02 01-02 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .700-. interval) Selected percentiles ( 95% confidence interval) Sample 95th .15) < LOD .740-1.770) 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 .670) 567 810 1104 01-02 01-02 * * < LOD < LOD < LOD < LOD < LOD < LOD .300-1.94) .680 (<LOD-.2. see Data Analysis section) for Survey year 01-02 is 0.210-1.840 (. 154 Fourth National Report on Human Exposure to Environmental Chemicals .210 (<LOD-.

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

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

Idel H. The pyrethroids in general use are not considered teratogenic or to have significant reproductive toxicity (ATSDR. et al. Toxicol Appl Pharmacol 2006.html. IARC considers deltamethrin and permethrin as not classifiable as to their human carcinogenicity. 2005)... Neurotoxic effects of two different pyrethroids.50(2):245-255. Transient dermal paresthesias have been reported among pesticide applicators after direct contact with certain types of pyrethroid pesticides. Wolff MS. on immature and adult mice: changes in behavioral and muscarinic receptor variables. Estrogenic and antiprogestagenic activities of pyrethroid insecticides...cdc. Elwan MA. Seth PK. 2005). 2001. Pyrethroid pesticide-induced alterations in dopamine transporter function.gov/toxprofiles/ tp155. Moniz AC. the pyrethroids are not considered genotoxic in in vitro testing or carcinogenic in animal testing (WHO. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Salzgeber SA. Ray et al.23(6):665-673.1/15/09 Aziz MH. Guillot TS. Additional information about pesticides is available from U. Kang IH.gov/pesticides/ and from ATSDR at: http://www. Hu JY. though a few pyrethroid pesticides and some metabolites have shown weak or inconsistent estrogenic effects on standardized assays (ATSDR. 2000. 2003. 2006. 2003. 2005).. EPA at: http://www. Shin JH. Kim IY.Pyrethroid Pesticides and other ion channels may also explain some pyrethroid effects. In California. Kunimatsu et al. Neurotoxicol Teratol 2001.107(3):173-177. Varoli FM. cdc. Lack of (anti-) androgenic or estrogenic effects of three pyrethroids (esfenvalerate. Garey J. Neurotoxicol Teratol 2005.8(1):197-202. McCarthy et al. Garey J. and permethrin) in the Hershberger and uterotrophic assays.62:101-108. 1991. Fourth National Report on Human Exposure to Environmental Chemicals 157 . Bernardi MM. Cruz-Casallas PE. and seizures (ATSDR.html. Pauluhn J. Wang SL. Human cases of systemic poisoning are rare and usually result from accidental exposure or intentional ingestion of pyrethroid insecticides. Garey and Wolff. Moniz et al. Lazarini et al. bioallethrin and deltamethrin. 2006)..108(1):78-85. Kuhn K. motor activity. Effects of prenatal exposure to deltamethrin on forced swimming behavior. Human doseexcretion studies with the pyrethroid insecticide cyfluthrin: urinary metabolite profile following inhalation. 2005). Wolff MS. paresthesias) reported in agricultural workers from 1996 to 2002 (Spencer and O’Malley. Spinosa HS. et al. Leng G.. Florio JC. WHO. Environ Health Perspect 1999.27(4):609-614. Signs and symptoms of acute pyrethroid poisoning after massive ingestions include agitation. Kamita Y. Go et al. Biochem Biophys Res Commun 1998. Go V. tremor. Abell AD. September 2003.S. fenvalerate. 2002). Okuno Y.205(6):459-472.atsdr. Shafer. Lee SJ. 2002. [Effects of fenvalerate on reproductive and endocrine systems of male rats] Zhonghua Nan Ke Xue 2002.300(3):161-165. Estrogenicity of pyrethroid insecticide metabolites. Toxicological profile for pyrethrins and pyrethroids.. Elwan et al. Neurodevelopmental consequences of gestational exposure (GD14-GD20) to low dose deltamethrin in rats. References Agency for Toxic Substances and Disease Registry (ATSDR). Kim HS. et al. Generally. Ose K. Int J Hyg Environ Health 2002. Zhao RC.35(2 Pt 1):227-237. In developing rodents. Lazarini CA. Shukla Y. Wieseler B. Pogo BG. choreoathetosis. Caudle WM. Leng G. Levsen K. Chen JH. Leng A. Leng G. Toxicol Appl Pharmacol 1991. Estrogenic potential of certain pyrethroid compounds in the MCF-7 human breast carcinoma cell line. dopaminergic. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Kim TS.atsdr. Fredriksson A. Regul Toxicol Pharmacol 2002. Bull Environ Contam Toxicol 1999. Ranft U. Berger-Preiss E. McCarthy AR. 2001. Richardson JR. Lemonica IP. Sunami O.251(3):855-859. Concomitant exposure to organophosphorus insecticides may increase pyrethroid toxicity by slowing metabolic clearance of the pyrethroid. and striatal dopamine levels in male and female rats. Assessing estrogenic activity of pyrethroid insecticides using in vitro combination assays. Xenobiotica 1997. Adhami VM. Kunimatsu T. Miller GW. J Environ Monit 2006. 1998.gov/toxpro2. Yamada T. 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. Sugiri D. Eriksson and Fredriksson. Song L. Thomson BM. Available from URL: http://www. epa. 2004. 2002). et al.. Kim et al. Idel H. Behavioral and endocrine changes induced by perinatal fenvalerate exposure in female rats..8(1):18-21. 1999. Eriksson P. neurochemical changes in cholinergic. hypersensitivity. and catecholaminergic pathways and behavioral changes have been demonstrated at subacute and subchronic doses for some pyrethroid pesticides (Aziz et al. Yang J. Lewalter J. Soderlund et al. Neurosci Lett 2001.211(3):188-197. J Reprod Dev 2004.. Hu et al. 2003. cyfluthrin was the most frequent pyrethroid associated with symptomatic effects (irritant respiratory and dermal effects. Shaw IC. salivation.. Bernardi MM. 2003. 2006.27(12):1273-1283.. Kuhn KH. Agrawal AK.

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

Biomonitoring Information Urinary levels of 4-fluoro-3-phenoxybenzoic acid reflect recent exposure to cyfluthrin or its environmental degradate.. 2005. Urinary levels for adults and children in these studies were similar (Heudorf et al.. Following an indoor application exposure. 2005). In an analysis of 217 urine specimens from a nonrandom sample of United States residents. representative 2001-2002 NHANES subsample (CDC. Baker et al.S. most of which were dermal and respiratory irritations (Spencer and O’Malley. the presence of 4-fluoro-3-phenoxybenzoic acid in urine not only reflects the metabolic transformation of cyfluthrin. 2005). 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. Fourth National Report on Human Exposure to Environmental Chemicals 159 .S. 2003).68359-37-5 General Information The chemical 4-fluoro-3-phenoxybenzoic acid is a specific metabolite of the pyrethroid insecticide cyfluthrin.. Leng et al. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al. Thus. 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.. Degradation of cyfluthrin to 4-fluoro-3-phenoxybenzoic acid occurs in the environment. 2006) and 1177 urban adults and children (Heudorf et al. (2004) reported a geometric mean concentration of 4-fluoro3-phenoxybenzoic acid of 0. Studies in Germany of 396 children and adolescents (Becker et al.. 2003). Cyfluthrin is rapidly metabolized and eliminated from the body. the mean elimination half-life of cyfluthrin from the plasma was 16 hours (Williams et al. 2006)..Pyrethroid Pesticides Cyfluthrin CAS No. but it can also reflect direct exposure to 4-fluoro-3-phenoxybenzoic acid formed in the environment. 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. In 57 volunteers entering areas previously spot-sprayed with various pyrethroid pesticides (including cyfluthrin). representative subsample in NHANES 2001-2002 (CDC.. Cyfluthrin accounted for one-third of pyrethroid-related worker illnesses reported in California from 1996-2002. 2004). 2001.2 μg/L) in the U. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Urinary levels of 4-fluoro-3-phenoxybenzoic acid were generally below the limit of detection (0.95 µg/L. median urinary levels of 4-fluoro-3-phenoxybenzoic acid were slightly less than the limit of detection in the NHANES 2001-2002 subsample (CDC. 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. 2003).

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

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

Heudorf U. Olsson AO.Pyrethroid Pesticides References Baker SE. Heudorf U. Int J Hyg Environ Health 2006. Int J Hyg Environ Health 2006. Butte W. Spencer J. Idel H. Bernard CE. Angerer J. Barr DB. Leng G. Arch Environ Contam Toxicol 2004. Environ Health Perspect 2001.186:57-72. Kolossa-Gehring M. Rev Environ Contam Toxicol 2006. Angerer J. Williams RL.206(2):85-92. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Ranft U. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Int Arch Occup Environ Health 2004.46(3):281-288. 162 Fourth National Report on Human Exposure to Environmental Chemicals .209(3):293-299. Human exposure to indoor residential cyfluthrin residues during a structured activity program. Sugiri D. et al. J Expo Anal Environ Epidemiol 2003.13(2):112-119. Hoppe HW. Atlanta (GA).209(3):221-233.77(1):67-72. Third National Report on Human Exposure to Environmental Chemicals. Seiwert M. Berger-Preiss E. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. 19962002. Angerer J. Becker K. Schulz C. Int J Hyg Environ Health 2003. Centers for Disease Control and Prevention (CDC). Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. 2005. Krieger RI. Heudorf U. Pyrethroid illnesses in California. O’Malley M. Ball M. Angerer J.109(3):213-217. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Hadnagy W. Drexler H.

200-.520) .500 (.180 (.790) .35) 1.68359-37-5 Cypermethrin Permethrin CAS No.850 (.140 (<LOD-.410) .340-.580-1.2-dichlorovinyl)-2. Survey Geometric mean (95% conf.32) .110-.580) 1. Fourth National Report on Human Exposure to Environmental Chemicals 163 .570-.550) .780) .200 (.280 (.160 (<LOD-. population from the National Health and Nutrition Examination Survey. trans-cypermethrin. Cyfluthrin.330) . Kuhn et al.430-.15) . transcypermethrin and trans-cyfluthrin.210-.380-.730 (.790 (. 1985.370-.300-.262) * * * < LOD < LOD .640 (.250 (.300 (.54) .270 (.24) 1.380-.220-. and trans-cyfluthrin.630) .600 (.47 (. 1985. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.200) .610) .150 (.470 (.2dichlorovinyl)-2.12 (.220-.120-.200) .380-.740-1.380) . and ciscyfluthrin.340) . ciscypermethrin and cis-cyfluthrin. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.210) 90th .630 (.44 (.2-Dichlorovinyl)-2.13 (. 1999).900 (.68) .790-1.240) .or trans-3-(2. cis-permethrin.2-dimethylcyclopropane carboxylic acid formed in the environment from the degradation of these pesticides (George.630-.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-..68) .630) .300-.910-5.Pyrethroid Pesticides Cyfluthrin the cis-metabolite is found in the urine.1 and 0.220) .310) .250-. Biomonitoring Information Urinary levels of cis.2-dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.2dichlorovinyl)-2.790-1.880 (.600) .820 (.890 (. The chemical trans-3(2.155-..270-.08) 947 1193 1004 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * .740-2.700) . Similarly.110-.460 (.410) .500 (.600-1.680) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .230) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Kuhn et al.490-.68 (.28) 671 680 518 701 591 957 Limit of detection (LOD.510 (.670 (.510 (.160 (.340) . Generally.1.370 (.180) .670-1.07 (.350) .120-. cis-3-(2.2-dimethylcyclopropane carboxylic acid Metabolite of cis-Permethrin.740) 1.2-dichlorovinyl)- CAS No. trans-permethrin.2-dichlorovinyl)-2.330 (.110 (<LOD-. but can also reflect exposure to trans-3(2.490-1.11) .200-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. In the body.770) . the presence of trans-3-(2.160 (. 52315-07-8 CAS No.730 (.202 (.510 (.400-.460-1.490-1. The presence of cis-3-(2.740 (. cis-cypermethrin.2-dichlorovinyl)2.440 (.710) .270 (. but it can also reflect exposure to cis-3-(2.210) .170 (.380 (.35) .470-1.300 (.270 (.420-.77 (.120-.280-. more of the trans-metabolite than Urinary cis-3-(2.960 (. < LOD means less than the limit of detection.680-3.and trans-isomers.690) .28) 468 580 667 831 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .920) 1.240) .120-.870) 1.220-.43) .710-1.490-.200) < LOD < LOD < LOD .670-2.21) .530 (.2dimethylcyclopropane carboxylic acid in urine not only reflects the metabolic transformation of any of the three pesticides.610) .950-2.2-dichlorovinyl)-2. 1999).260 (.890 (.730 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from trans-permethrin.110-.52645-53-1 General Information Several pyrethroid pesticides are formulated as a mixture of cis.140 (.80) .50) .53) .S.220-.650-1.200-.2-dimethylcyclopropane carboxylic acid that is formed in the environment from the degradation of these pesticides (George.570 (.2-dimethylcyclopropane carboxylic acid is a metabolite formed from cis-permethrin.680 (.770-1. which may vary for some chemicals by year and by individual sample. The cis-isomer of permethrin has more potent insecticidal activity than transpermethrin.670-1.08) .

Studies in Germany of 396 children and adolescents (Becker et al.260-. median urinary levels of trans-3-(2.600 (.430-. In these volunteers. urinary trans-3-(2. Other studies have provided evidence that urinary levels of cis. 2004).21) .640-.580) . 2006).440-.320) .80) .390 (.190) .S.370-. Schettgen et al. These studies indicated that intake is mainly from the diet and that dermal absorption contributes little to intake (Heudorf et al.780) 1.580-1.11 (. 2005) In a small group of indoor pest-control operators. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. population from the National Health and Nutrition Examination Survey.320-.450-1.560) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.270 (.49) .270) .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 .370-.2dimethylcyclopropane carboxylic acids at the 95th percentile that were similar or slightly less than the 95th percentiles in the U.2-dichlorovinyl)-2. 164 Fourth National Report on Human Exposure to Environmental Chemicals .59 (1. the median and 95th percentile of urinary levels of cis-3-(2.920 (.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.900 (. 2005).250) .S.450-.640-1. In the same residents.540) .11) .230-. 2005).680-1.080-. representative NHANES 2001-2002 subsample (CDC.160 (<LOD-. urinary levels of cis-3-(2.and trans-3-(2.and trans-3(2.380 (..Pyrethroid Pesticides 2.220 (.182) * * * < LOD < LOD .12-2.500 (.540 (.550-1. In a study of volunteers.440 (.550) .690-1.410) . 2002).150-.290 (.200-. though the 95th percentile levels increased several fold after exposure to nearby pest control operations (Leng et al.390-.380) . 2006) and 1177 urban adults and children (Heudorf et al.710 (.440 (.590) . 2006.570) .2-dichlorovinyl)-2.290) .830) ..750 (.2dichlorovinyl)-2.200 (.700-2.33 (.430 (.260 (.840 (. post- Urinary cis-3-(2.840 (..2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of cis-Permethrin.230-.510-1.150-.. 2006. 2005).190) .11) 1.700) .2dimethylcyclopropane carboxylic acid at the 95th percentile were about half the 95th percentile in the NHANES 20012002 subsample (CDC.280-.800 (.250 (<LOD-.700) .430-1.2-dichlorovinyl)-2.67 (.290-. 2001.590 (.340) .220 (.300 (. Cyfluthrin.370-.890 (.750-1.530 (.250) 90th .. 2005)..350 (.200-.24) .450 (.180-.250) .350) .230-.300) .260 (.530 (.2-dimethylcyclopropane carboxylic acids in children were related to residential pesticide use and house dust levels (Becker et al.29 (.340) .67) .2-dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid did not increase at 24-72 hours after exposure to nearby pest control operations (Leng et al.2dichlorovinyl)-2.14) 671 680 518 700 591 957 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.880) .290) . 2004.550-1.220) .710-3.520) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .170) < LOD < LOD < LOD .170 (.780 (.360-1.560) 1.200) .59) .12 (.810 (.300 (.640) 1. 2003).400 (.270) .190 (.640 (..08) 468 580 667 830 816 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD . Survey Geometric mean (95% conf. Lu et al.2-dimethylcyclopropane carboxylic acid did not increase.. 2001) showed urinary levels of cis.470-1.170 (.420 (. Urinary levels of the two chemicals in adults were similar to those in children in these studies (Heudorf et al.2-Dichlorovinyl)-2.390-. 2002).550) .250-.300) .180 (.230 (.540 (.150-.130-. 2003).11) .280 (.37) .140-..2-dimethylcyclopropane carboxylic acid levels at the 95th percentile were about one-third of the 95th percentile in the NHANES 20012002 subsample (CDC.240 (<LOD-. and cis-Cypermethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.440-..250-.120 (.2-dimethylcyclopropane carboxylic acid reflect recent exposure to either their parent pyrethroid pesticides or their environmental degradates. In a study of urban residents in Germany (Berger-Preiss et al.680-1.260 (.250-.33) .31) . the levels at 24-72 hours were slightly less than the 95th percentile in the NHANES 2001-2002 subsample (CDC.270-.300-. 2006).138 (.640-1.03) 1.550 (.260) .340-.680 (.210-.400-1.59) . Estimated daily pyrethroid intakes based on urinary levels in the German children were below the acceptable daily tolerances (Heudorf et al.11) 947 1193 1004 1345 99-00 01-02 99-00 01-02 99-00 01-02 * * .380-.890) .104-.

56) 2.520-.800-1.28 (2.940 (.09 (.49-3.58) 961 1184 1015 1341 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . trans-Cypermethrin. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.07 (1.400 (<LOD-.700-1.700) .730) .7) 2.97-11.440 (<LOD-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.19 (3.48) 4.10) 2.490 (<LOD-.5) 2.830-1.840-1.560 (.54) 4.2-dichlorovinyl)-2.500) .77) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD .560 (.41-14.49-5.470 (.19) 1.95) 3.68) 2.670) .39-5.40 (1.410-.77) 2. which may vary for some chemicals by year and by individual sample. Finding a measurable amount of cis.03-1.43) 2.66) 691 680 518 690 595 954 Limit of detection (LOD.55-4.500 (.400-.14-6.420 (<LOD-.970 (.41 (1.68-2.60) .55-3. Survey Geometric mean (95% conf.17 (.820) .19 (2.470 (<LOD-. 2005).530) .850-1.11-1.08) 1.25 (1.2-dimethylcyclopropane carboxylic acid Metabolite of Cyfluthrin.49-3.90) 1.2-Dichlorovinyl)-2.27 (1.63) 1.14) 1.610) 1. The maximum post-application urinary levels.710 (.780 (.860) .16) 1.2-dimethylcyclopropane carboxylic acid (Hardt and Angerer.69 (1.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level causes an adverse health effect.68) 1.94 (1.87 (1.and trans-3-(2.670) .4 and 0.42) 1.460-. however.77) 1.66) .23) 2.410-. 2003) were similar to the 95th percentiles for adults in the NHANES 2001-2002 subsample (CDC. population from the National Health and Nutrition Examination Survey.89 (2.4.14-2.03-1.07-3.23 (.460-.01) 4.810-1.20 (.Pyrethroid Pesticides application median urinary levels of summed cis.60) 1.480-.69) 1.77 (1.660) 1.01 (1.490-1.13) .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. Fourth National Report on Human Exposure to Environmental Chemicals 165 .570) 90th 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.50 (1.20 (.2dichlorovinyl)-2.920-1. < LOD means less than the limit of detection. Urinary trans-3-(2.2-dichlorovinyl)-2.520) .26 (.37 (1.560 (.910-1. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.750) .39 (1. were up to 27 times higher than the 95th percentile for adults in the NHANES 2001-2002 subsample (CDC.56 (1.42 (2.91 (1.08-4.410 (<LOD-.11-2.54 (1. Biomonitoring studies on urinary levels of cisor trans-3-(2.17 (.64-4.08-6.84 (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 .25-3.550 (.55-5.620) < LOD 2.410 (<LOD-.56) 2.35) 1.68-3.12-6.17-1.S.910-1.or trans-3-(2.85) 4.76-3.760) . 2005).22 (1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.56 (1.66) 478 576 675 826 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .680-1.81) 2.95) 2.20 (.500-.59 (1.76-4.580 (.28 (1.62 (1.63) 1.60-4.68) 1.

560 (.20-2.410-.60 (1.91 (1.15-3.720-1.15 (1.22) 1.08 (.13) .74) .36) 2.520 (<LOD-.98 (1.850-3.640) .39) 1.87-3.02-1.33-2.670) .11) 691 680 518 689 595 954 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.26 (1.87-8.47-2.30-3.41) 1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 2.33 (1.700-.45-2.S.67 (2.780 (<LOD-.31) 1.87 (1.00) 1.700 (.3) 2.45 (1.29) 1. 166 Fourth National Report on Human Exposure to Environmental Chemicals .39 (1.00) 5.780) .42) 1.47 (1.27-2.750) .81 (2.07-2.800-1.60) 2.440-.30-6.20 (1.15-3.57 (1. and trans-Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.570-.31 (2.35 (1.87) 1.27-2.07-3.570 (<LOD-.00-5.48-2.34-4.760 (.880-1.730) .75 (1.42 (. trans-Cypermethrin.11) .47-2.930-1.530 (<LOD-.19 (1.56-2.12 (.36 (1.33-1.60) 2.15-3.40-2.55 (2.86 (2.22-1.00 (1.580 (.610-.44) 2.57) 3.12-1. Survey Geometric mean (95% conf.68) 3.88) * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD 1.11) 478 576 675 825 823 1123 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD .74) 2.13) 1.Pyrethroid Pesticides Urinary trans-3-(2.07) 2.880 (.19) 961 1184 1015 1340 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.65) 1.500-.15) 2.65 (2.07-1.10) 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 .61) 1.530 (.00) 1.87) 1.28) 2.31 (.80) 1.70 (.08 (.34-3.37 (1.720 (<LOD-.91-11.48 (1.35) 1.56-5.55 (2.55 (2.16 (1.56 (1.580) .820-2.880 (<LOD-1.770) < LOD 2.780) 90th 1. population from the National Health and Nutrition Examination Survey.470 (.660) .64 (1.720-1.89) 2.700 (.07) 2.800-1.19) .900 (<LOD-1.850) .470-.540) .850) 1.91) 1.2-Dichlorovinyl)-2.2-dimethylcyclopropane carboxylic acid (creatinine corrected) Metabolite of Cyfluthrin.480-.22-2.740) .970 (.15) 3.570 (.

Int J Hyg Environ Health 2003. Kolossa-Gehring M. Ranft U.62:101-108. Int Arch Occup Environ Health 2004.209(3):221-233. Environ Health Perspect 2006. Int J Hyg Environ Health 2002. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Drexler H. Leng G. et al. J AOAC 1985.68(6):1160-1163.76(7):492-498. Idel H. Schettgen T. Kuhn K.206(2):85-92. Int J Hyg Environ Health 2006.205(6):459-472.77(1):67-72. Int Arch Occup Environ Health 2003. Berger-Preiss E. Hadnagy W.Pyrethroid Pesticides References Becker K. Angerer J. Leng G. Angerer J. Schulz C.114(9):14191423. Angerer J. Centers for Disease Control and Prevention (CDC). Atlanta (GA). Ball M. Int J Hyg Environ Health 2006. Hoppe HW. Permethrin and its two metabolite residues in seven agricultural crops. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides. Leng G. Angerer J. Bravo R.109(3):213-217. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. Fourth National Report on Human Exposure to Environmental Chemicals 167 . Drexler H.209(3):293-299. Angerer J. Hardt J. Barr DB. Biological monitoring of workers after the application of insecticidal pyrethroids. A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides. Idel H.134(1-3):141-145. Pearson M. Angerer J. Ranft U. Pyrethroid exposure of the general population-is this due to diet? Toxicol Lett 2002. Idel H. Third National Report on Human Exposure to Environmental Chemicals. Heudorf U. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Bartell S. Levsen K. Lu C. Seiwert M. 2005. Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany. Berger-Preiss E. Environ Health Perspect 2001. George DA. Toxicokinetics of pyrethroids in humans: consequences for biological monitoring. Heudorf U. Sugiri D. Heudorf U. Butte W. Bull Environ Contam Toxicol 1999. Heudorf U. Sugiri D. Wieseler B.

39 µg/L. Finding a measurable amount of cis-3-(2.2-dibromovinyl)-2. 2005)..2-dibromovinyl)-2.2-dimethylcyclopropane carboxylic acid in children increased at least 450-fold relative to the non-detectable background levels for several days and mean levels remained slightly above background levels 45 days after the spraying (Ortiz-Perez et al.2-dibromovinyl)-2.2-dibromovinyl)-2. Deltamethrin can degrade to cis-3(2. urinary levels of cis-3-(2. (2004) reported a geometric mean concentration of cis-3(2.1 μg/L) for the NHANES 2001-2002 subsample (CDC. In the NHANES 2001-2002 subsample..5 μg/L) than the detection limit (0.3-0.2-dibromovinyl)2. deltamethrin has been used against mosquitoes that carry malaria.. 2001. Urinary levels for adults and children in these studies were similar (Heudorf et al.2-dibromovinyl)-2.Pyrethroid Pesticides Deltamethrin CAS No.S.2dimethylcyclopropane carboxylic acid formed in the environment. 168 Fourth National Report on Human Exposure to Environmental Chemicals .2-dimethylcyclopropane carboxylic acid were below the limit of detection (CDC. Biomonitoring Information Urinary levels of cis-3-(2.2-dibromovinyl)-2. in detection of cis-3-(2..2-dimethylcyclopropane carboxylic acid is a metabolite of the pyrethroid insecticide deltamethrin.2-dimethylcyclopropane carboxylic acid at the 95th percentile ranged slightly higher (0. In an analysis of 217 urine specimens from a nonrandom sample of United States residents.2-dimethylcyclopropane carboxylic acid of 0.2-dibromovinyl)-2. 1990). 2005).2-dimethylcyclopropane carboxylic acid in the environment (IPCS. 2006) and estimated daily intakes based on urinary levels in children were considered to be below acceptable daily intakes (Heudorf et al.2-dibromovinyl)-2. Baker et al.2-dimethylcyclopropane carboxylic acid in the urine may reflect exposure to deltamethrin or to cis-3-(2.2-dibromovinyl)-2. 2004). Following residential spraying with deltamethrin for malaria protection in Mexico.2dimethylcyclopropane carboxylic acid reflect recent exposure to deltamethrin or its environmental degradate. mean peak urinary levels of cis-3-(2.2-dimethylcyclopropane carboxylic acid in urine does not mean that the level will result in an adverse health effect.. 2006) and 1177 urban adults and children (Heudorf et al. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.. 52918-63-5 General Information 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. 2001) showed that urinary levels of cis-3-(2. The peak mean levels in these children were more than 800-fold higher than the detection limit in the 2001-2002 NHANES subsample. Outside the U. Studies in Germany of 396 children and adolescents (Becker et al. 2005). in some situations replacing the use of DDT. Thus.

2-dimethylcyclopropane carboxylic acid Metabolite of Deltamethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.S.Pyrethroid Pesticides Urinary cis-3-(2.2-Dibromovinyl)-2. Fourth National Report on Human Exposure to Environmental Chemicals 169 . Survey Geometric mean (95% conf.1. population from the National Health and Nutrition Examination Survey. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.1 and 0. < LOD means less than the limit of detection. which may vary for some chemicals by year and by individual sample. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD < LOD size 1698 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th < LOD < LOD < LOD < LOD 75th < LOD < LOD 90th * * 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 415 580 570 831 713 1128 99-00 01-02 99-00 01-02 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 818 1193 880 1346 99-00 01-02 99-00 01-02 99-00 01-02 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 578 680 445 701 527 957 Limit of detection (LOD. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

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

Hoppe HW. et al. Third National Report on Human Exposure to Environmental Chemicals. and genotoxicity in exposed children. Batres LE.113(6):782-786. Environmental Health Criteria 97.109(3):213-217. 2005. Seiwert M. Angerer J. Centers for Disease Control and Prevention (CDC). Metabolites of pyrethroid insecticides in urine specimens: current exposure in an urban population in Germany.209(3):221-233. Angerer J. Environ Health Perspect 2005. toxicokinetics.209(3):293-299.org/documents/ehc/ehc/ ehc97. Current internal exposure to pesticides in children and adolescents in Germany: urinary levels of metabolites of pyrethroid and organophosphorus insecticides.77(1):67-72. International Programme On Chemical Safety (IPCS). Environ Health Perspect 2001. Available at URL: http://www. Carranza C. Lopez-Guzman OD. Angerer J. Heudorf U. Drexler H. Fourth National Report on Human Exposure to Environmental Chemicals 171 . Ball M. Heudorf U. Grimaldo M. et al. Atlanta (GA). Deltamethrin.inchem. Heudorf U. Int J Hyg Environ Health 2006. [online] 1990. Reference values for metabolites of pyrethroid and organophosphorous insecticides in urine for human biomonitoring in environmental medicine. Kolossa-Gehring M. Butte W.htm. Int Arch Occup Environ Health 2004. Schulz C. Angerer J. Int J Hyg Environ Health 2006. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. Torres-Dosal A.Pyrethroid Pesticides References Becker K. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides. 5/26/09 Ortiz-Perez MD.

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

352-.18 (1.81 (1.26) 2. population from the National Health and Nutrition Examination Survey.190-.41-3.1) 3.830-2.69 (1.355) .266-.800 (.530-.44) 5.300 (.780) 4.238-. Fourth National Report on Human Exposure to Environmental Chemicals 173 .1 and 0.12) 4.230-.41-2.260 (.590-.595) .230-.49-2.320) .60) .32-21.364) .321 (.288-.04) .50 (2.730 (.276-.33) .78) 6.610) .300 (.387) .92-3.25) size 1998 2539 Total Age group 6-11 years 12-19 years 20-59 years Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 99-00 01-02 50th .53-3.454 (.290 (.620-1.360) .78 (1.64) 697 680 524 701 603 957 Limit of detection (LOD.820) .27-2.760 (.750-1.240 (.51-3. interval) .200-.227-.05) .32 (2.406) .336 (.362) .25 (2.230 (.83-11.32 (1.8) 3.16) 1.940) 1.71 (1.990) .12 (.33 (2.190-.13) .14-6.340) 75th .200-.35) 2.27-2.35) 2.253-.233-.28) 1.297 (.26-2.63 (3.45 (2. and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.369) .52-4.270 (.38 (2.373) .160-.55 (1.89-71.311 (.69) 3.740 (.570-1.260 (.45-5.79) 3.350-.48-2.54) 1.353 (. Survey Geometric mean (95% conf.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid Metabolite of Cypermethrin.250-.30 (1.21 (2.810) 1.470-.700 (.601) .428-.35 (2.29-1.62-8.250 (.330) .427) .590 (.374) 99-00 01-02 99-00 01-02 99-00 01-02 .560-1.34 (2.670 (.325 (.340) .226-.320) .90) 1.25-7.73) 1.430-.230-.43) 3.507 (.510-.320 (.330) .570-.1.48-2.76 (1.560-.56-5.292-.34-6.320) .300 (.298 (.52-5.49 (1.62) 5.16-1.46) 2.1) 3.180-.190-.280 (.384) .800) 1.277-.271-.230 (.78) 1.35) 1.51-6.292 (.840-1.314 (.210-.42-2.260-.300) .23 (2.315 (.340) 1.46) .26) 2.250 (.710 (.490-.630) .49 (1.288 (.16) 483 580 682 831 833 1128 99-00 01-02 99-00 01-02 .295) .260 (.750) .53) 1.700-1.65-2.200-.25 (2.93 (1.63-3.210-.27-11.600 (.560-.160-.05) 1.13 (.49-2.267 (. Deltamethrin.273 (.510-.35 (1.02-6.490) .270) .640 (.34) 8.33 (1.03 (3.25-1.750) .240 (.38 (2.1) 3.320) .65 (1.30 (.190-.247-.417 (.62-6.246-. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.850) .75 (1.530-.430-.18 (2.960 (.710 (.434) .78) 1.850) .830) 90th 1.586) .250 (.86 (1.01 (1.440) .04-5.520 (.16) 974 1193 1024 1346 99-00 01-02 99-00 01-02 99-00 01-02 .420) .314) .740 (.72 (1.680 (.30) 3.870 (.390) .S.220-.550-.650 (.820) .370) .41 (1.25-4.12) .41) 3.328 (.265-.36) 1.450 (.345) Selected percentiles ( 95% confidence interval) Sample 95th 4.39) 2.

41-4.930) .380 (.264 (.25-2.67) 1.320) .362 (.09) 3.62) .41) 1.510 (.310) .423 (.11 (.329) .365) 99-00 01-02 99-00 01-02 99-00 01-02 .73-4.25-5.91 (2.202-.51-7.52 (1.35-3.370-.590) .253) .16-4.280 (.860 (.580) .290-.81 (1.13 (.280) .86 (1.440-.323 (.49 (1.590-1.49) 3.43-64.220-.150-.275 (.534) .270 (.720) 90th 1.290) .280) .280 (.60) 1.03 (.240-.750-1.17-1.238-.19) 2.490-.11 (.210 (.321-.300-.40 (1.39) 1.44) 2.370 (.00) 1.37) 1.271-.21-4.200-.670) .480-.550 (.312 (.200-.35) 1.160-.15-2.437) .490 (.91-4.640 (.328) .90) 3.240 (.48) 697 680 524 700 603 957 174 Fourth National Report on Human Exposure to Environmental Chemicals .61-2.730) .06-3.02-1.19-6.860-1.220 (.19) 974 1193 1024 1345 99-00 01-02 99-00 01-02 99-00 01-02 .91) .250) .35 (1.329) .40) 2.510 (.63) 1.04 (3.04 (.22 (1.64-5.580 (.810) 1.48 (1.400-.91) 9.250 (.330 (.730-1.37 (1.274-. Survey Geometric mean (95% conf.460-.240-.88-5.10 (2.94 (1.62) 1.350) .49) 1.570) .270 (.80) 4.27) 1.272) .05-3.270-.02 (2.00) 1.730) .44 (1.510 (.330) 1.500) .401) .677) .760) .36 (1.74) 3.60-4.700-1.09-2.21 (1.420-.25) 2.240 (.52) 2.13-1.230-.230) .54 (1.630) .234 (.560 (.261 (.190-.73) 1.278) .55 (1.400-.Pyrethroid Pesticides Urinary 3-Phenoxybenzoic acid (creatinine corrected) Metabolite of Cypermethrin.55) 3.299-.83 (1.390-.178-.229-.72 (1.590) .210-.173-.240 (.280 (.350 (.03-1.670) 3.610 (.311 (.96 (1.590) .387) .250 (.07-5.440-.00) 5.36-6.261-.274 (.09 (.200-.75-8.480 (.17 (.460-.0) 3.640 (.225-.07) 2.63-3.400) .224-.410) .309) .240-.550 (.13-1.53 (1.210 (.280-.309 (. Deltamethrin.227 (.240-.19 (2.43 (2.190-.304) Selected percentiles ( 95% confidence interval) Sample 95th 3.550 (.372) .740) .270) . and Permethrin Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.330) .272 (.330) .240 (.357) .S.960-1.378 (.200-.92) 483 580 682 830 833 1128 99-00 01-02 99-00 01-02 .216-.49-2.09-2.226-.720 (.410-.270) .32 (2.335-.490 (.530-.840-1.316 (.290) . population from the National Health and Nutrition Examination Survey.84 (1.246 (.43 (1.330) 75th .43) 1. interval) .35) .450 (.67 (1.95) 1.930) 1.380-.67 (1.530-.83) 1.300-.860-1.440-.446) .230-.190 (.540 (.650) .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 .

Levsen K. Hardt J. Pearson M.76(7):492-498. et al. Batres LE. Idel H. Bartell S. Sugiri D. Godbold J. Environmental health assessment of deltamethrin in a malarious area of Mexico: environmental persistence. urban cohort. Grimaldo M. Idel H. Atlanta (GA). et al. Int Arch Occup Environ Health 2003. Berger-Preiss E. Angerer J. Kolossa-Gehring M. Int J Hyg Environ Health 2003. Lopez-Guzman OD. Olsson AO. Hadnagy W. Bravo R.Pyrethroid Pesticides References Baker SE. Berger-Preiss E. Sugiri D. toxicokinetics. GerES IV pilot study: assessment of the exposure of German children to organophosphorus and pyrethroid pesticides.113(6):782-786. Becker K. et al. Liu Z. Berkowitz GS. Barr DB. Hoppe HW. Leng G. Environ Health Perspect 2006.114(9):14191423. and genotoxicity in exposed children. Biological monitoring of workers after the application of insecticidal pyrethroids. Isotope dilution highperformance liquid chromatography-tandem mass spectrometry method for quantifying urinary metabolites of synthetic pyrethroid insecticides. Indoor pyrethroid exposure in homes with woollen textile floor coverings. Fourth National Report on Human Exposure to Environmental Chemicals 175 . A longitudinal approach to assessing urban and suburban children’s exposure to pyrethroid pesticides.206(2):85-92. Lu C. Obel J.209(3):221-233. Seiwert M. Int J Hyg Environ Health 2002. Carranza C. Ranft U.111(1):79-84. Exposure to indoor pesticides during pregnancy in a multiethnic. Ortiz-Perez MD. Ranft U. Deych E. Ball M.46(3):281-288. Centers for Disease Control and Prevention (CDC). Angerer J. Pyrethroids used indoors—biological monitoring of exposure to pyrethroids following an indoor pest control operation. Lapinski R. Environ Health Perspect 2005. Barr DB. Arch Environ Contam Toxicol 2004. 2005. Int J Hyg Environ Health 2006. Third National Report on Human Exposure to Environmental Chemicals. Leng G.205(6):459-472. Torres-Dosal A. Environ Health Perspect 2003.

080) .108-.330 (.200 (.130 (. ceramics.130-.130-.180 (.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 .330 (.130 (.330) .280-. see Data Analysis section) for Survey years 99-00. and 0.270 (.360) .120) .140 (. 7440-36-0 General Information Antimony is found in ores or other minerals.110) .04.260) .110-.490) . People are exposed to antimony primarily through food and. and excretion of antimony vary depending on its oxidation state.130) .126-.080 (<LOD-.180-.400 (.154) . +3.100-.280) . Dermal contact with soil.190 (.169 (.200-.310) .410) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.230) .330) .310 (. respectively.130-. interval) .240 (.150-.430 (.230-.400 (.280-.160) .220 (. metal bearings.160-.132 (.390) .119) .190) .190 (.150) .220) 95th .120) .170 (.470) .109-.150-.119-.340 (.100) .090 (<LOD-.400) .320) 787 683 618 554 667 723 768 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.390-.190 (.190) .175 (.350-.140) .440) .105 (.170-.093 (.500) .120) .390 (.130-.164-.170) .190) . and glass.230 (.180) . coal-fired plants.125 (.160 (.310 (.200-.460 (.090-.240) .600) .112-.132 (.210 (.250-.160 (.170-.140) .130) .160 (.170-.230-. and 03-04 are 0.180 (.360 (.220) .310-.Metals Antimony CAS No.300-.220-.110-.180 (.220) .115-.140 (.178) .120-.180-.250 (.250 (.160-.200 (. 176 Fourth National Report on Human Exposure to Environmental Chemicals .240-.340) .126 (.390-.280) .350) . often combined with oxygen to form antimony trioxide or with sulfur to form stibnite.350 (. Urinary excretion appears to be greater for pentavalent antimony Urinary Antimony Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.230) .230) .160-.123 (.360-.190-.136) * .250 (.280-.250-.090) 75th .260 (.098-.400) .350 (.200 (.230-.260) .145 (.130 (.110 (.350 (. It is used in metal alloys.079-.210) .158 (.230 (. population from the National Health and Nutrition Examination Survey.154) .320-.157) .170-.490 (.260-.210 (.143 (.131-.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 .156-.420) . distribution.190-.310 (.136-.110-.200) .290-.150) 90th .120-.160-.270 (.180-. storage batteries.148-.120) .04.150 (.220-.150-. The absorption.140) .150 (.130-.280) .360 (.130 (.117-.140 (.120-.114) .090 (.140) .120 (.095 (. fireworks.240 (.140 (.430 (. from air and drinking water.390-.207) .220-.200) .117-.190) .137) . It is also used in paints.350) .095-.210) .280) .320 (.128 (.134 (.176 (.090-.120-.130 (.070 (<LOD-.220 (.120-.370) .150-.080) .280-.230 (. to a lesser extent.270) .130 (.260) .146 (.220) .310-.099 (.100 (.280 (.320) Total .161) .130) .300 (.200 (.510) .190) .190 (.170-.460 (.350) . Antimony can exist in one of four valences in its various chemical and physical forms: -3.400-.270-.190-.142 (. enamels.115) . and +5. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.320-. ammunition.07.500) .250-.145) Selected percentiles ( 95% confidence interval) 50th .160) .070-.200 (.350-.120-.200-.S.220-.180-.210-.190-.300) .710) .260-.360) .400) . Workplace exposures can occur at smelters.103) .300-.200) . Stibine is a metal hydride form of antimony used in the semiconductor industry. Antimony enters the environment from natural sources and from its use in industry.560) .100 (.080-. and pewter.180 (.280-.250) .330-. castings.370-. < LOD means less than the limit of detection.160) .210-.470 (. Two antimony compounds (sodium stibogluconate and antimony potassium tartrate) have been used as antiparasitic medications. 01-02.300 (. or other substances containing antimony is another means of exposure.570) .320 (.320-.150) .210) .190 (.530) .137) .150 (.120 (.135) * .320-.410-.240 (.130-.440) .130-.180) .200-.390) .280 (.310) . water.100-.270) .087-.320) .160) .350) .120 (.330) .110-.410) .134-.340 (.120-.144) .180-.300) .133) * .220-.128 (.160) .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 .260 (.200 (.130 (.180 (.141-.460 (.270 (.250-.154-. and as a fire-retardant in textiles and plastics.240 (.350 (. sheet and pipe metal.160) .270 (.310 (.184) .120 (.170 (.130) < LOD .122 (.390) .070 (<LOD-.460) .230-.120-.470) .400 (.130 (.440 (.430 (. solder.330-.150-.300-.140) . 0.300) .180 (.220-.210) . 0.150) .290 (.290-.260 (.200) .210) .108 (.390) . and refuse incinerators that process or release antimony.330) .350-.120 (.240 (. which may vary for some chemicals by year and by individual sample.350 (.330 (.120-.240-.230-.088-.197) .190-.140-.140) .

192 (.242-.200-.154-.228 (.352 (.119 (.130) .173) . and gastrointestinal symptoms such as vomiting.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.438) .727) .125-.276 (. Ming-Hsin et al.317) .143) .248-.338) .103-.193) .333) .245) .148-.310 (.471) .186) . Dysrhythmias and T-wave changes on electrocardiogram have also been noted after both therapeutic (Berman.124 (.130 (.132 (.280-.127) .133) .071-.255) .278) .267-.127 (. and kidney have been demonstrated in high dose animal studies depending on the dose.195 (.146-.135) .119-.122 (.106-.429 (.125 (.098-.313-.225) .137 (.078 (.226 (. An elimination half-life of approximately 95 hours has been estimated after occupational exposures (Kentner et al.199-. Acute antimony poisoning may cause a metallic taste. 1986).084) .086) 75th . interval) .250-.148-.102-.143) .121 (..120 (.209) .235-.164) .300 (.111 (.318-.120 (.156-.122 (.092) .405) .250 (.417) .318-.269 (.S.068 (.176 (.124-. abdominal pain.095-.107-.161) .333 (.118 (.104-.160 (.178-.211) .288 (.150-.425) .120 (.250-.139 (.109 (.148) * . The toxicity of stibine after acute inhalational exposure is similar to that of arsine.085) .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 .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 . 1995).124) .138-.135 (.100 (.213 (.123) .421) .128-.209) .225 (.117-.278 (.181) .167 (.115 (. 1958) and occupational exposures (Briegner et al.124-.109 (.192-.194-.089) .320) .333 (.076-.280 (.430) .203) .236 (.217 (.151) .081) .115-.333-.163 (.220) .171) . 1986).074 (.134) .107-.106-.170 (..127) .266 (.149) .229-.227-.200-.333-.205-.200-.126) .077) .111-.238) . 1954).107-.112 (.138 (.429) .129) .138) * .308-. Inorganic antimony salts irritate the mucous membranes.310) .741 (.108-.143) 90th .261) .182 (.103-.214) .228 (.146-.152) .172-.310) .298 (.153 (.277 (.195-.244-.080 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 177 .286 (.191 (.196 (. 1953).123 (. 1944).117-.127) .192) .132) .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 . and eyes. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.130) .127) .241-.193 (.095-.116 (.Metals than for trivalent compounds (Elinder and Friberg. and route of exposure (Elinder and Friberg.149-.343 (.108-.320-.080 (.097-.238) .179-. 1988.447 (.114 (.173-.079 (<LOD-.208 (.271-.183) .161) .173 (.143) Selected percentiles ( 95% confidence interval) 50th .185 (.152) .255-.380 (.204-.163 (.385 (.295 (.181) .371 (.181) .187) .222 (.317) .272) .069-.265-.076-. Pulmonary edema may occur in severe cases of inhalation exposure (Cordasco et al.156 (. skin.485) .116-.082) .247) .189 (.320 (.265 (.308) .250) .159-.444) .414) .198) .352) .159-.098-.153-. population from the National Health and Nutrition Examination Survey.082 (<LOD-. diarrhea.104-.200) .113) .315) .167-. 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.268) .230-.480) .300) .108-.082) .259 (.146) . myocardium.30) .081 (<LOD-. Human health effects from antimony at low environmental doses or at biomonitored levels from low environmental exposures are unknown.147-.257) . Acute inhalation of antimony has been associated with irritation of the respiratory tract and impaired pulmonary function (Renes.143 (. and ulcers (Werrin.113-.333-.120 (.086 (.230) 95th .068-.417) .115 (.146-.364 (.338 (.102-.207) .741) .140) < LOD . liver.112 (.092-.391) .144-.267 (.176 (.139 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.333-1.159-.250-.233) .135) .167 (.167 (.185 (.112-.185-.173 (.109-.145) .096-.115 (.224 (.129 (.118 (.176-.500) . species.209-.087) .075 (.108 (.338 (.281-.129 (.357-.320-.098) .238 (.267) .135) .138-.400 (.333 (.175 (.121 (.233-.263-.114 (..126-.294) Total .164-.114 (.471 (.206-.208-.317) .126 (.164 (.239-.233 (.129) * .188) .150-..203) . Histopathologic inflammatory and degenerative changes in the lung.250-.321) .256 (.391) .131 (.162-.263 (.135 (.188-.250 (.119-.209 (.099-.069-.105-.195-.099-.115) .131) .357) .253 (.373) . 1973).320 (.115-.130) .113-.140) .075 (.136) .364 (.117-.121) . 1962).444) .300) .241-.131-..147) . resulting in hemolysis with abdominal and back pain (Dernehl et al.248) .253-.061-.178 (.228-.

)1954. Pilgrim L. O’Regan M. Chin Med J 1958. et al.. Stead FM. 1998) or compiled reference ranges (Hamilton et al. et al..106:33-39. 2004. Chia-Yu H. Weltle D. Konings J. Hamilton EI.html. Mechanism and treatment of cardiac arrhythmias in tartar emetic intoxication. Wu M-T. Pietra R. plasma and urine and a critical evaluation of reference values for the United Kingdom population. J Trace Elem Med Biol 2002. clinical efficacy. Cordasco EM. Gebel TW. 1998. Cullen A. 1995. Biological assessment of exposure to antimony and lead in the glass-producing industry. Earlier measurements in general populations (Minoia et al. 1990. Schacke G. 1998). Liao Y-H. Handbook on the toxicology of metals. Sabbioni E. 1991. Finding a measurable amount of antimony in urine does not mean that the level of antimony causes an adverse health effect. 2nd ed.. population. pp.. Semisch CW. References Berman JD. Wade A. Trace element reference values in tissues from inhabitants of the European community I. 26-42. Bolten C. arsenic. Kiberd B. Briegner H. Ludersdorf et al.. Dunkelberg.. Cheng-Wei L.16: 33-39. Apostoli P. environmental levels) and health effects is available from ATSDR at: http://www. Chemotherapy for leishmaniasis: Biochemical mechanisms. Yang C-Y. Antimony trioxide is rated by IARC as a possible human carcinogen.67:119-123. and future strategies. Mahieu P. Review of elements in blood. Industrial Medicine 1944. J Occup Environ Med 2004. Schaller KH. Centers for Disease Control and Prevention (CDC). J Clin Pathol 1998. Kuo-Juie Y. Iavicoli I. Elinder CG. Luedersdorf R. Dezateux C.atsdr. Element reference values in tissues from inhabitants of the European community. and a drinking water standard has been established by the U. Gallorini M. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. and hydrogen sulfide. gov/toxpro2. A study of 46 elements 178 Fourth National Report on Human Exposure to Environmental Chemicals . 1987).e. Levels of urinary antimony in infants appeared to be similar to those reported by CDC (2005) for young children (Cullen et al. Rev Infect Dis 1988. Chen J-R. Bailly R. Leinemann M. HH. 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. Fuchs A. Suchenwirth R. Environ Health Perspect 1998. Shao-Chi C.S. Arsine. 2005. Third National Report on Human Exposure to Environmental Chemicals. et al. Experimental and human studies on antimony metabolism: their relevance for the biological monitoring of workers exposed to inorganic antimony.64(2):182-185. eds. indium. Nordberg GF.. Pulmonary edema of environmental origin. 1994) have reported values slightly higher than those in this Report. Minoia C. Antimony.13:361-362.Metals to antimony have been established by OSHA and ACGIH..158:165-190. Sabbioni E. Urinary antimony was not associated with locally elevated soil levels in a study of more than 200 German residents (Gebel et al. Stone FD. Ming-Hsin H. Ho C-K. Urinary antimony in infancy.cdc. Skulsukai G. Lenert G. Lauwerys R. Ju-Sun P. 20012002. VI. Pozzoli L. Delves HT. Industrial Medicine and Surgery (Dec. Biomonitoring of a worker population exposed to low antimony trioxide levels. respectively. Sci Total Environ 1994.521-523. Stasney J. Matthews T. 1997). In: Friberg L. which may be due to methodologic. gallium. Dernehl CU. Van der Venne MT. Stocks J.10(3):560-586. Industrial antimony poisoning. even when exposure levels were below workplace air standards (Bailly et al. Vouk VB. External and internal antimony exposure in starter battery production. Paschal et al. 2002. Information about external exposure (i.. and antimony in optoelectronic industry workers.76(2):103-115. EPA. Atlanta (GA). Nau CA. stibine. Int Arch Occup Environ Health 1987.51:238-240.. 1986. Iavicoli et al. Mayer P. Br J Ind Med 1991. Costeloe K. Biological monitoring of exposures to aluminum. and 2003-2004. Several investigations of airborne antimony exposures in workers have found urinary levels that are many times higher than those seen in NHANES 1999-2000. Dezateux et al. Chest 1973. Petrucci F. Kentner M.48:93-97. Buchet JP. Kentner et al. Liao Y-H et al. Delves HT. Alimonti A. Arch Dis Child 1997. New York: Elsevier. Mayne P. Biomonitoring Information Levels of urinary antimony reflect recent exposure.46:931-936. Caroli S.. Roland H.76:432436. Friberg L. or exposure differences. Antimony in blood and urine of infants. Carelli G. Piatnek DA. Yu H-S. Human biomonitoring of arsenic and antimony in case of an elevated geogenic exposure..59:469-474. Int Arch Occup Environ Health 1995.

Antimony poisoning in industry. Morrow JC. Pirkle JL. Sci Total Environ 1990. Paschal DC. Trace metals in urine of United States residents: reference range concentrations.95:89-105. Renes LE. Fourth National Report on Human Exposure to Environmental Chemicals 179 . and serum of Italian subjects. Quarterly Bulletin of the Association of Food and Drug Officials 1962.76(1):53-59. et al. Werrin M. Ting BG. Environ Res 1998. Sampson EJ. blood.Metals in urine. Industrial Hygiene and Occupational Medicine 1953.99-108. Chemical food poisoning. Jackson RJ. 27:38-45.

6 (32.4 (7.77) 6.6) 11.30) 17.70) 8. In the last century. interval) 8. copper arsenates.8) 7. gaseous hydride manufactured in small quantities for use in the semiconductor industry.1-18.4-65.5 (40.25-9. General population exposure to inorganic arsenic can occur through consumption of drinking water and.90-11.3-19.90-8. Arsenic trioxide is approved to treat acute promyelocytic leukemia.5) 66.90-7.10-7. lead hydrogen arsenate. arsenic compounds.3-111) 78. Since the 1940s. and monosodium methyl arsenate were used as pesticides but contemporary uses are restricted.0 (15.5 (23. arsenites.6-141) 53.5-178) 46.8) 33.1) 1281 1276 03-04 03-04 03-04 9.000 metric tons annually.20 (8.9-46. Arsenic and its compounds have had many uses in the past and present as medicines.2) 15.8) 7.8) 30. particularly arsenic trioxide.1) 7.9 (8.10 (6. Arsine (AsH3) is a reactive. Survey years 03-04 Geometric mean (95% conf.5) 95th 65.13-8.6 (15.50-14. Also. Water sources contain mostly inorganic arsenate. though in some locations arsenite may be prevalent (WHO. arsenocholine.0 (43.1) 290 725 1542 03-04 03-04 9.6) 618 722 1074 Limit of detection (LOD. chromated copper arsenate (CCA) has been used to treat outdoor timbers and pressure-treated woods to prevent wood rot.5 (36.0-60. mostly for use in wood preservation (ATSDR. mental disorders.80) 6.10) 10. to a lesser extent.41 (7. Arsenic trioxide (As2O3.1 (32.2 (41.1 (38.29 (8. the smelting of copper. The United States no longer produces arsenic from mining but imports about 22. referred to as inorganic arsenic compounds. Various arsenic compounds were used in paint pigments and for tanning animal hides.10-10. semiconductors. and in lead-acid storage battery grids.55 (7.0-19. and produce. Groundwater Urinary Total Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. pesticides.00 (6. cacodylic acid.5-19.5) 43. In nature. black.5-41. meats.3-15.5 (34. see Data Analysis section) for Survey year 03-04 is 0.9) 21. 2001).2-61. Although it is still widely used in the United States.57) Selected percentiles ( 95% confidence interval) 50th 7. as alloy in metal bearings.00-9. Arsenic is measurable in most soils.2 (13. lead.7) 24.8) 29.7 (11. or rarely as elemental metalloids (yellow. CCA-treated wood has been restricted since 2003 and no longer can be used in residential applications such as decks.84) 8. from coal burning.2 (51. arsenic as elemental metalloids may be used in some ammunition.74.9 (17.4) 40.6-35. retaining walls.8 (48. Gallium.4) 60. and foods. 180 Fourth National Report on Human Exposure to Environmental Chemicals .02-8. and arsenates (oxidation states of -3.6-43.84) 8.9) 68. such as arsenopyrite (FeAsS) and realgar (As4S4). aluminum.90 (5.97) 8.5 (14. grain. alloys.6 (9.66-8.5-52. ocean and fresh waters. and gray forms).8) 34.3) 10.12 (6. psoriasis.7) 65. Roxarsone and other organic arsenicals are anticoccidial agents added to poultry feed.27) 9. +3 and +5).S.90) 75th 16. it is found in over 200 crystalline or mineral forms.Metals Arsenic CAS No.4 (48.8) 17.6 (13. and as homicidal poisons.2-93.0 (14. and.90-14.0 (22.90 (7. Various forms of inorganic arsenic can occur in groundwater from natural sources or as a result of soil application or industrial waste.34-9.80-9.50 (8.8-61.2) 46.9-34. sodium arsenite. a trivalent compound known as white arsenic) is a common natural and commercial form that can be released into the air during volcanic action.4 (31. population from the National Health and Nutrition Examination Survey. and other metals. Arsenic can combine with such non-carbon chemicals as sulfur and oxygen to form arsenides.8-77.1) 15.2-20. cancers.7) 90th 37. to a lesser extent. trimethylarsine oxide.90-8. and as a cosmetic to lighten complexion.2 (12.9-62.70 (6.0 (11. and indium arsenides are used in the semiconductor industry.4) 13.90) 16.2-17.90 (7.3) 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. and play sets.7-95.7-83. 2005). 7440-38-2 General Information Arsenic is an element that is widely distributed in the earth’s surface in small amounts. solders.80 (5.19-9.4 (26.5) 41. Before the 20th century. and arsenosugars.40) 7.4 (24.1-40. were used as treatments for syphilis.12-10.70-9.30 (7.08 (5. Arsenic can also combine with organic substances in nature to form such organic arsenic compounds as arsenobetaine.30 (6.34-10.

44) 6. selenium.0) 14.8 (12. interval) 8.4 (42. 2001.1 (11.7 (9.0 (31.59) Selected percentiles ( 95% confidence interval) 50th 7.23-7.93-9.7 (25.3-64. WHO.4 (26. 2007.8-32.96) 12.76 (6.86-17.75) 13..32 (5.06 (4. so exposure to the general population is extremely limited. shellfish.2) 90th 30.18 (5.7 (11. In aquatic sediments.7-17. Steinmaus et al.1) 8.24 (7.3-41.61 (7. NRC.93-8.2 (12. Smelter workers can have significant inhalational exposures to airborne arsenic trioxide for which air standards have been established.64 (7. Though modest bioconcentration occurs in some aquatic life. Inorganic arsenic is well absorbed from the gastrointestinal tract and absorbed to a lesser degree through inhalation.40) 8. 2001).47 (6.8-75. Fish.7) 95th 50. Gamble et al.3) 9. 2007.45) 5.1) 24.2-15..9-56.28-7.11 (5.13) 8. Chowdhury et al. EPA. 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. have caused clinical arsenic poisoning. After absorption.50 (6. Smoking tobacco is also a source of inorganic arsenic. trimethylarsine oxide (TMAO).0-26.4) 32.3) 6.2) 15. In aquatic organisms..7-34.6 (17.8 (27.12-10.3 (24.01) 11. gallium arsenide and indium arsenide.31 (6. cacodylic acid and monosodium methyl arsenate.66-8. TMAO is also formed in the environment from microbiological action and is a metabolite of arsenic in certain mammals. 2001.5) 17. though some reduction may occur in the gut prior to absorption.1 (14. Tseng.33 (6. Extremely high groundwater arsenic levels. and some other seafood can contain organic forms of arsenic including arsenobetaine.6 (35. 2001).88) 7.6 (10.3-53.6-17. arsenocholine is converted to arsenobetaine and also to small amounts of TMAO (Christakopoulos et al. 2001).99-9. These organic forms of arsenic from seafood are absorbed and quickly excreted in the urine (WHO. are used in enclosed ultraclean operations within the semiconductor industry.7-18.9 (45.7-188) 27. 2001).9) 13.4 (12.44-11.1) 58.1) 6.S.35) 7.4 (24.8 (11.1-36.0) 12.0) 1281 1276 03-04 03-04 03-04 8. Children may have additional exposures from ingestion of contaminated soils (e.47 (7.25 (6. and contact with CCA-preserved wood structures.0) 42. Inorganic arsenic and its metabolites have elimination half-lives of approximately 2–4 days (Lauwerys and Hoet.75 (5.8 (20.S.47-6. 2003.6) 45.5) 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 8.51) 75th 14.0 (17. with trivalent inorganic arsenic (arsenite) being more toxic than pentavalent inorganic arsenic (arsenate) (NRC.10-16.7-35.0) 33.38-10.1) 7.04) 7.8 (21.9) 53. The semiconductor dopants.20-9.9) 618 722 1074 Fourth National Report on Human Exposure to Environmental Chemicals 181 .4 (11.66 (7. but is poorly absorbed dermally (WHO. 2006.. 2001). 1988).5-120) 40. age.07-9. Arsenate is reduced in the body to arsenite (oxidation state +3). 2007.25-9. dust. Ingestion of arsenosugars in kelp and algae can also lead to the excretion of DMA. Survey years 03-04 Geometric mean (95% conf.10-8.0) 26. 2001).5) 290 725 1542 03-04 03-04 8. 2001). U. dose level.8-62.7) 28.2-46.58-10.81-9. population from the National Health and Nutrition Examination Survey.. arsenocholine.0-69. Direct exposure to DMA and MMA may result from use of the two pesticides. 2006. WHO.Metals sources of drinking water often have measurable arsenic and several regions of the United States have naturally higher arsenic levels than the U.41) 6.0-38.g.0-18.3-62.4) 54.01) 7. mine tailings).S.5 (9.4 (40. 2001).30-9.3 (27. Arsenite is then oxidatively methylated to the monomethylarsonic acid (MMA) and dimethylarsinic acid (DMA) with subsequent excretion primarily in the urine (NRC..33-10.5-17.66-8. EPA’s maximum contaminant level (Hughes.8) 27.8) 22.00 (6. and folate status (Chen et al. arsenic does not show biomagnification in the food chain (WHO. and arsenosugars.88 (5.4-64. as observed in Bangladesh where millions of people have been exposed. 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. inorganic arsenic is widely distributed within the body.2) 40. organic arsenic can be converted back to methylated and inorganic arsenic. Inorganic forms of arsenic demonstrate high acute toxicity. kelp.04 (5.

Taiwan. Bredfeldt et al. 2001.Metals +3) shows greater toxicity than arsenite itself (Aposhian et al. 2004). Acute unintentional inhalation of arsine gas can produce hemolysis of red blood cells. Although arsenate is reduced in the body to arsenite. 2001). interference in signal transduction pathways.10 (<LOD-1. < LOD means less than the limit of detection. Arsenic has many actions demonstrated in cellular studies. 2001..30) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.S. respectively.80) 1.20 (<LOD-1.S. and peripheral neuropathy may also occur with large doses or after surviving an acute overdose. and diarrhea. and endothelial injury (Kumagai and Sumi. hypertension. including inhibition of numerous enzymes.10 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. 2006. 182 Fourth National Report on Human Exposure to Environmental Chemicals . and bladder cancer (IARC. can cause peripheral sensorimotor neuropathies..30) 1.. hepatotoxicity. Laboratory studies using inorganic arsenic have shown chromosomal aberrations. 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 1.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.. With chronic exposure.50) 621 725 1078 Limit of detection (LOD.S. and hyperpigmentation of the skin (NRC. gluconeogenesis. vomiting.50) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 1. WHO. and DNA repair inhibition (Cohen et al. peripheral vascular disease. which can lead to dehydration and shock. arsenic trioxide) includes hemorrhagic gastritis with nausea. and altered gene expression.20 (<LOD-1.. Such actions may lead to decreased energy production. Bangladesh. lung. 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.60) 1. 2001).0. which may vary for some chemicals by year and by individual sample. fatty acid oxidation. Chile). 2006) or when exposure occurs in smokers (Chen et al.10 (<LOD-1.50) 1.. Cardiac arrhythmias.60) 1. food residue.EPA has established drinking water. some of these effects may take years to develop. Chronic elevated arsenic intakes have been associated with diabetes. 2004. 2001).20 (<LOD-1. increased oxidative stress. 2004).g. 2007).. Studies of arsenic at levels typical of U. WHO.10 (<LOD-1.10 (<LOD-1. hyperkeratosis. Chronic arsenic exposure in humans is considered to be a cause of skin. population from the National Health and Nutrition Examination Survey. Acutely. NRC. drinking water have not been associated with increased cancer rates (Schoen et al. NRC. 2007. 2007. U. but additional or confirmatory research is needed (Kapaj et al.EPA. Cohen et al.20 (<LOD-1.. renal failure. The U. arsenite will inhibit cellular pyruvate dehydrogenase by binding to the sulfhydryl groups of dihydrolipoamide. Cellular glucose uptake. apoptosis. 2000. OSHA and ACGIH have established workplace standards and guidelines for arsenic exposure and monitoring. Survey years 03-04 Geometric mean (95% conf. leading to a decrease in adenosine triphosphate energy production. Acute toxicity resulting from the ingestion of large amounts of trivalent arsenic (e. 2001).. substitution in phosphate metabolism.g. noncirrhotic portal hypertension. 2001). cell transformations. 2001).S... see Data Analysis section) for Survey year 03-04 is 1. cytotoxicity. Raml et al. The organic forms of arsenic occurring in seafood have little known toxicity. WHO. hematocytopenias. 2006. Chronic human intake of arsenic at less than acutely toxic doses. The risk of lung cancer appears more pronounced when large environmental exposures start in childhood (Smith et al. and production of glutathione may be affected as well. and it also will inhibit succinate dehydrogenase. and by uncoupling oxidative phosphorylation (NRC. 1998. 2006) and newly discovered thioarsenic metabolites may also be as toxic (Naranmandura et al. and childhood neurodevelopmental effects in observational human studies.. it may have its own separate toxic action by substituting for phosphate in glycolysis and other pathways. WHO. including drinking water sources with elevated arsenic levels (e. 2006.

Survey years 03-04 Geometric mean (95% conf.S. 2006).80 (<LOD-4.. Caldwell et al. 2006. DMA produced bladder cancer in some chronic rat studies (Cohen et al...41) 3. 2007. 1986). 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 Sample size 3. Pellizzari and Clayton 2006)... environmental levels) and health effects is available from ATSDR at: http://www.. 2005) and Urinary Arsenic (V) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. 2001). IARC and NTP recognize inorganic arsenic and arsenic compounds as human carcinogens.75 (<LOD-2.61 (<LOD-3..S. 2001)...75 (<LOD-2. population (Rubin et al. Vahter et al.19) 3.e.. 1998. Pellizzari and Clayton..95) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine. 2000. the median total urinary arsenic in about 200 people was approximately four times higher than that of the U. 2001). 2006). Caldwell et al. In animal studies..S.70) 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD 2. 1992. Consequently.. Compared with this Report. 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. Josyula et al. 2000). 2006.. but generally only at maternally toxic doses (WHO. Levels of total urinary arsenic in the U. Shalat et al.cdc. urinary arsenic levels have been accepted as a good biomarker of dose (WHO. In the German Environmental Survey III of 1998. and the FDA has established a bottled drinking water standard. Meza et al. Fourth National Report on Human Exposure to Environmental Chemicals 183 . Shalat et al. 2007.. median urinary total arsenic levels in 4052 adults varied with seafood intake. 1999).04 (<LOD-3. Though CCA-treated wood contains several thousand times more arsenic than untreated wood. 2008). 1999. and were about two-fold lower than those for the U. population in NHANES 2003–2004 (Schulz et al.33 (<LOD-3. In a Nevada town where groundwater levels were naturally elevated. Calderon et al.00) 1.33 (<LOD-3.. Valenzuela et al..50) 1. 2004.50) 2568 95th 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2. 2006).89) 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 2.18) 3. 1999. had decreased since the prior 1990– 1992 survey.. although urinary arsenic levels were not associated with CCA contact (Shalat et al. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.69 (<LOD-3.S. though air levels of arsenic fume and dust are correlated with urinary arsenic levels at higher occupational inhalational exposures (Jakubowski et al.Metals compounds.atsdr. Additional information about external exposure (i. 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. WHO.. 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.. 2008. 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. 2008).18 (<LOD-3. Pellizzari and Clayton.html. Offergelt et al.. 2003. Daily variation in creatinine-corrected urinary arsenic is relatively small when intake is constant (Calderon et al. 2004.. arsenic has been fetotoxic and teratogenic. 2006. higher mean or median total urinary arsenic levels have been reported among people living in specific western areas of North America (Calderon et al. gov/toxpro2.. 2006). 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.

5 (14.900 (. 2005. arsenite..20 (4.1) 45.900-1.31-1. geometric mean levels were about 70-fold higher than for the U.60) 1.7) 15.8. with DMA..50-6. 1990.40-7. vasospasm. Levels of DMA and MMA increase in approximate proportion to the intake of inorganic arsenic.. MMA.0 (26.30) 2.9 (7.8-40.20 (2.80 (. Detectable levels of MMA reported in NHANES 2003–2004 were found only at the upper percentiles and. methylation capacity.1-51.20-3. 1996. when seafood organic arsenic is subtracted).70-21. 2005. 2008.600 (.4) 23. WHO.3) 1284 1284 03-04 03-04 03-04 1.66 (1.7) 13. Chowdhury et al.1) 18.Metals other areas of the world (Ahsan et al.. 2001. Valenzuela et al.10) 8. 2005.70 (3.S.93) 1. 2000.0-23.00-1.9-23. population showed a higher contribution of arsenobetaine (Caldwell et al.20) 7. population in the NHANES 2003–2004 subsample.700-1. and peripheral neuropathy) have been associated with urinary levels as low as 50–100 μg/L in chronically exposed populations (ACGIH.S. China.0) 29. 2007) with higher levels of arsenic in the drinking water. and two methylated metabolic products.5 (26. When seafood intake is avoided.50) . Caldwell et al.80 (4. arsenobetaine. and TMAO were detected in only 7.29 (1. arsenocholine.80-5.800) 1. Blom et al.3) 95th 35.20) 3.800-4. interval) 1.20 (1.8) 35.. 1985.5) 29. For residents of Inner Mongolia. population (Ahsan et al. 2008).43-1.05) < LOD ..37 (1. Arsenate. DMA and MMA.60-3.55 (1.70-21. Also. Great Lakes region residents had median urinary DMA levels that were slightly less than median levels in NHANES 2003-2004 (Caldwell et al.70) 6.700-1.. 2000..00 (1.90-7... and duration of exposure are also considered important. 1. and other factors such as nutrition.48-2.00-6.3-39.40) 75th 5..9) 13. Aposhian et al. DMA and MMA compose most (about 75%) of the total arsenic species measured in urine. Individually measurable species resulting from inorganic arsenic exposure are arsenate.19 (.S.800-1.83) Selected percentiles ( 95% confidence interval) 50th 1.1-25.50) . which may vary for some chemicals by year and by individual sample.00 (.5) 621 725 1078 Limit of detection (LOD.6 (11.40-6.. Urinary Arsenobetaine Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.68) . Tseng et al.. After recent seafood ingestion.8-50.6 (25. Total arsenic measured in the urine includes all species of inorganic and organic arsenic. dermal keratosis.90-29.6-44.20-25.2 (6.g.5) 32.00-4..6) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 * * 1. The higher percentiles of total urinary arsenic levels in the U.28) 1.20 (.0 (27. < LOD means less than the limit of detection.0) 4. DMA has been the predominant metabolite composing the majority of measurable inorganic-related arsenic in the urine (i..6.. Survey years 03-04 Geometric mean (95% conf. and TMAO.70 (5.30) 10. Some noncancer effects of arsenic (e.3) 35.10) 4.74 (1. arsenite. 184 Fourth National Report on Human Exposure to Environmental Chemicals .80) 1. 2003).871-1.2-38. and urinary DMA represented about 67% of the total urinary arsenic (Hopenhayn-Rich et al. 2007). 2008.800 (.45 (1. population (Sun et al.1-94. a control population of 696 Tacoma residents had median urinary DMA levels similar to those for NHANES 2003–2004 (Kalman et al.11-1.. In most human studies. population from the National Health and Nutrition Examination Survey. In the residents of a Chilean town who consumed water with high levels of arsenic.3 (9.4) 31. These associations are stronger at higher urinary levels..2-35. Caldwell et al.6.40) 5. 2008). 2001)..9 (6. In the late 1980s.10 (4. 2000. as evidenced by trace or nondetectable levels of arsenobetaine and arsenocholine in the urine.800 (.20) 18.400-. and arsenobetaine being the main contributors to the total urinary arsenic levels (Caldwell et al.4 (16. Caldwell et al.S.S.8 (17.4-35.7 (13. 2008).5) 292 728 1548 03-04 03-04 1.7 (21. see Data Analysis section) for Survey year 03-04 is 0.17-1.30 (1.e. arsenocholine.3% of a representative sample of the U.500-1. 2008). in NHEXAS 1995–1996. Caceres et al. arsenobetaine and arsenocholine will greatly increase the level of total urinary arsenic and comprise the highest percentage of the total urinary arsenic level.4.00) 3.50) 90th 16.00-12.20-190) 31. Measurable organic arsenic species in this Report are three biologically generated environmental forms. and 0. respectively.6 (13.30 (2. 2006). 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. 4. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.3 (21..62) 2. Sun et al. Pellizzari and Clayton.8 (12.7-22.80 (3. median levels of urinary DMA were about 40-fold higher than the adult median reported in NHANES 2003– 2004.

10 (.16 (.. 2001).80-153) 17.4-82. 2008).61-6. not to imply a safety level for general population exposure.73-6.28) 1.531 (.. 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.S.30) 1.05 (.2 (12.62-6.12) < LOD .47 (2.6 (9.1-18. 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.5) 26.15-1.0) 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.400-.5 (18.25-7.93 (1.0 (9.2 (12. WHO.11 (.6 (6.67) 4.00 (3.64-29.S.6) 19. Information about the biological exposure indices is provided here for comparison.32-7.45) 1. 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.3 (10.8) 29.2 (13.4) 32.6-29. 1998.78 (3.1 (26.40 (1.91) 90th 16.55) 1.83) 8.959-1. population from the National Health and Nutrition Examination Survey.79 (1.1) 26.25 (. 2007). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.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 * * 1.901-2.5-20.50-15.54 (1.4-21.05) 1.76-27. 2008).65 (1.83) 2.9) 14. In recent years.6-32.786-1.5) 17.29 (4.30-1.5 (18.19-2.938-1.7) 9.91 (4.78-5.39-3. 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. Caldwell et al.6-46.4 (24.. Urinary Arsenobetaine (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.9-18. Fourth National Report on Human Exposure to Environmental Chemicals 185 .9 (25.43) 14.612-1.40) 1.Metals as with DMA.2 (4.0-36.51) 5.9 μg/L.44 (1.82) Selected percentiles ( 95% confidence interval) 50th 1. 1992.43) 75th 5. interval) 1..21) 5.72) 12. The 95th percentile of the U.18-1. 2003.14 (1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.833-1.68 (1.51-2.47 (1.82) 4. Vahter et al.3) 95th 29.37-2.67) 1. which is below the ACGIH BEI (Caldwell et al.70) 5.877 (.88 (5..15-1.50-7.3 (10. 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..1-36. Survey years 03-04 Geometric mean (95% conf.15-4. 2006.53 (..9) 32.58 (3.29-14.4-28. Finding a measurable amount of arsenic in urine does not mean that the level of arsenic causes an adverse health effect.88) 2.3) 1284 1284 03-04 03-04 03-04 1.9 (13. Sun et al.13-39. these levels were much lower than those found in other studies where environmental exposures were highly elevated (Chowdhury et al.36) 2.4) 292 728 1548 03-04 03-04 1.3-24.81 (4. population for the sum of inorganic related species was 18. Offergelt et al.909-1.80) .4 (11.638) 1. 2001).7) 17. 1986.4) 13.7) 30.00 (1..

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

20 (<LOD-1. population from the National Health and Nutrition Examination Survey.00) 1. which may vary for some chemicals by year and by individual sample.95 (<LOD-2. Survey years 03-04 Geometric mean (95% conf. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. population from the National Health and Nutrition Examination Survey.00 (<LOD-2. < LOD means less than the limit of detection.29) < LOD 621 725 1078 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.40 (<LOD-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Survey years 03-04 Geometric mean (95% conf.00 (<LOD-3.S.Metals Urinary Arsenous (III) Acid 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 1.44) 2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th < LOD 90th < LOD 95th < LOD Sample size 2568 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.S. see Data Analysis section) for Survey year 03-04 is 1.76) < LOD 292 728 1548 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1284 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 3.08 (<LOD-4.80) < LOD 621 725 1078 Limit of detection (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. Fourth National Report on Human Exposure to Environmental Chemicals 187 . Urinary Arsenous (III) Acid (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.

00-5.00-4.70) 5.90) 2.89 (3.00-12.24) 3.9) 13.00) 5.57-5.3 (8.90 (3.95-4.18 (6.86 (2.82-5.00-3.4 (7.69-3.29-4.00) 12.65-6.00-7.0) 621 725 1078 Limit of detection (LOD.00-4.0) 9.78 (4.00-11.00 (3.00) 6.00) 6.0 (12.05) 3.33) 3.9 (11.00 (6.34) 3.48 (3.70-3.55 (2.74 (2.0) 12.00-11.73) 6.Metals Urinary Dimethylarsinic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.0-25.00) 90th 11.88 (4.0) 16.00-7.0-19.72 (4.98) 4.00-3.27 (3.95 (4.81 (5.86-7.61-11.0) 17.05) 10.00-10.0) 13.0 (11.44 (2.20-12.00-15.9 (7.67) 9.03-6.71 (4.00 (3.1 (8.46 (4.60-3.31) 4.5) 95th 13.0 (9.50-15.00 (5.S.73 (3.45) 8.15) 4. Survey years 03-04 Geometric mean (95% conf.33-4.S.39-3.84-8.69-6.0) 14.00) 4.11 (3.32 (8.8) 7.44) 5.69 (3.17-4.00-4.00 (5.0) 13.0-18.1-15.22) 4.0) 16.0 (9.6-18.1-18.16 (4.17-6.59 (6.16-11.0 (10.00) 9.14) 3.00-4. Urinary Dimethylarsinic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.11) 4.03 (3.00 (5.0 (9.00 (7.0 (10.00 (6.77 (3.00-7.30) 3.05) 5.00-11.4) 621 725 1078 188 Fourth National Report on Human Exposure to Environmental Chemicals .10) 3. population from the National Health and Nutrition Examination Survey.17 (2.0 (14.9) 5.00 (6.8) 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 3.84-18.7) 12.27 (2.00-8.34-4.20) 11.0) 11. population from the National Health and Nutrition Examination Survey. Survey years 03-04 Geometric mean (95% conf.91) 75th 5.0 (8.38 (3.12-4.00-4.00) 3.60-6.0-16.78) 4.0 (13.74) 90th 9.45 (8.00) 75th 6.79 (3.24-4.00 (7.3 (8.30 (7.80-6.86-21.00) 6.19) Selected percentiles ( 95% confidence interval) 50th 3.37 (2.00-12.34 (3.48 (2.9) 12.00-13.50 (4.00 (3.80) 7.12 (3.00) 4.00-9.82-9.37 (3.0 (10.32-10.92-12.0 (10.92) 3.0-17.0-16.32 (4.7-16.16 (2.71) 3.5 (11.00 (3.67) 8.60-4.14) Selected percentiles ( 95% confidence interval) 50th 3.20-4.7) 1284 1284 03-04 03-04 03-04 4.00-7.80) 2.49) 10. interval) 3.00-4.0) 292 728 1548 03-04 03-04 4.0) 95th 16.42) 3.95-3.82) 3.00 (3. see Data Analysis section) for Survey year 03-04 is 1.00) 7.6 (9.71-4.71 (3.7 (10.27-2.94) 3.50-5.0 (13.0) 10.6) 1284 1284 03-04 03-04 03-04 4.00) 3.57 (3.65-8.5) 12.09 (7.00 (5.7) 13.49-4.0-17.80-3.45) 3.3 (7.94-3.85 (3.0 (8.0) 11.97-3.1-22.31-4.70-12.2) 10.9) 11.60-7.34-4.06) 5.70 (3.70-4.25 (4.08 (2.0) 9.80-5.80 (4.27-5.0) 17.6) 292 728 1548 03-04 03-04 3.69 (3.00 (5.00 (4.7.13-4.61-16.00) 6.00-22.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2568 03-04 03-04 03-04 4.00-15.00-15.28) 2.10) 6.0-12.0 (12.34 (3.52) 3. interval) 3.62) 4.90) 5.8) 7.95-6.00 (3.0) 9.

58) 2.70-2.10 (1.30-1.85) 2.20) 2.60) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.93) .36) 1.80) 1.81) 1.80 (1.80 (1.30) 2.53) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.50 (1.60-2.10 (1.80) 1.10 (<LOD-1.80 (2.10-3.50 (2.18-1.70) 2.20 (1.90) 1.50) 1.10 (.80-2.90) 2.30-1.S.90) 2.30 (2.70-2.80 (1.18-1.35-3.07 (1.14-1.00) 2.53) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.85) 1.62) 2.00) 2.60) 2. which may vary for some chemicals by year and by individual sample.00) 1.10) 95th 2. Survey years 03-04 Geometric mean (95% conf.00 (<LOD-1.57) 95th 2.50-2.00-4.50 (<LOD-1.S.53) 292 728 1547 03-04 03-04 * * < LOD < LOD 1.00 (1.50) 621 725 1077 Limit of detection (LOD.88-2.43-3.07-3.77) 1.40-3.40-2.60) 1283 1284 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.31 (1.00-2.31-3.20-1.33 (1.30 (1.86) 3.61) 2.30) 90th 1.40-3.22) 3.20 (1.816 (<LOD-.82-2.30 (1.00 (2. see Data Analysis section) for Survey year 03-04 is 0.71-2. interval) Selected percentiles ( 95% confidence interval) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites * 50th < LOD 75th 1.00-1. population from the National Health and Nutrition Examination Survey.86 (2.53-2.79) 2.20 (1.45) 3.63 (<LOD-1.30) 1.70-2.80 (1.86 (2. Urinary Monomethylarsonic Acid (creatinine corrected) Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.00 (<LOD-1.84-3.985) 1.16 (2.20-3.73-2.61-3. < LOD means less than the limit of detection.82-2.34) 2.46-2.33 (1.30) 1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.36 (1.40) 1.52 (2.50 (1.80) Sample size 2567 03-04 03-04 03-04 * * * < LOD < LOD < LOD 1.20 (1.40 (2.96-2.900-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.60) 1.60) 2.05-1.88 (1.80-2.37 (1.28 (1.60 (1.15-1. population from the National Health and Nutrition Examination Survey.00-2.70-2.54) 90th 2.90 (1.07) 2.9.17) 2.Metals Urinary Monomethylarsonic Acid Metabolite of Arsenic Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.86) 2.10-1.40-2.30 (1.20 (1.20 (1.40) 1.00) 1.10 (.00-1.11-1.30-2.40 (1.22 (1. Fourth National Report on Human Exposure to Environmental Chemicals 189 .00 (2.10) 2.90 (2.75) 621 725 1077 < LOD means less than the limit of detection for the urine levels not corrected for creatinine.70-3.40) 2.53 (1.46 (1.00) 1.28 (1.853-1.88 (1.10-1.60 (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. Survey years 03-04 Geometric mean (95% conf.23) 1.

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

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Occurrence of monomethylarsonous acid in urine of humans exposed to inorganic arsenic. Gurzau ES. Burbacher T. Rahman MM.36(2):99-133. Scand J Work Environ Health 1985. Cohen SM.

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54-8.36 (4. are high in barium (Genter.93 (4.30 (1.61 (2.41-1.12) 6. In nature.39) 4. Certain foods.53) 692 683 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.12-1.61 (3.36 (1.07 (2.20-8.80-5.36-1.50 (4.72) 4.77-3.55-7.30) 5.57) 3.80 (5.48-4.40 (1. depilatories.93-8.50 (1.36) 5. population from the National Health and Nutrition Examination Survey.87-3.81-2.76-2.15 (6.72) 1.52 (1.43 (1.35-4.20-8.70-2.46-1.09 (1.71-9.94-6. Workers employed by industries that make or use barium compounds can be exposed to barium dust.21-8.51) 2.08 (6.71) 95th 6.29) 5. water.22) 6.78) 1. were relatively well absorbed following inhalation (60-80% of a dose) or ingestion (11-32 % of a dose).72) 75th 3.87) 7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80 (1.26) 5.21 (1.80-7.26) 2. 2001).34 (1.65) 1.69 (1.12.g.50 (4.63 (1.96-2.30-5.38) 8.50 (4.27) 2.67) 6.54-1. Barium compounds are used by the oil and gas industries to make drilling muds.56) 1.41) 1.91 (2.81-2.75) 2.11 (3.35 (1.71) 1.80-3.40 (4.50-6.8) 9.54 (6.50 (1.06-2.30) 4.90) 4.35-1.12 (2.50) 1.05% of the earth’s crust.19-1.34) 2.05-2.49) 2.39 (1.53-5.00 (1.4) 9.65-5.30-3.18) 3.54 (2.32-7.49) 4. fireworks. interval) 1.71) 2.9) 5.70 (1.50-1.37-1. and ceramics.48 (6. Barium salts have also been available as rodenticides.86 (4.20 (3.76 (3.40 (5.40) 3. 01-02.30-1. Ingested soluble barium General Information Elemental barium is a silver-white metal which comprises approximately 0.63) 1.39-1. soluble forms of barium. Fourth National Report on Human Exposure to Environmental Chemicals 193 .99-5.10-4.97 (1.32-1. respectively.40) 7.44-2.90-2.56 (1.39 (1.90) 2.76-3.53) 2.40-13.50 (2.53) 1.24-1.50 (1.12 (2.87 (6.46) 1.46) 1.90) 1. it combines with other chemicals such as sulfur or carbon and oxygen.63 (2.80 (2.04-2.57-7.48-4.21-2.76) 1.24 (4.66) Selected percentiles ( 95% confidence interval) 50th 1. such as brazil nuts.90-9.60-2.70-8.73-5.50-1.81-3.51) 7.Metals Barium CAS No. and 0.61 (1. bricks.95 (4.12. rubber.54) 1.56 (1.11 (3.15 (1.80) 7.65-1.10-5.36-1.24-1.59-11.26-1.54) 2.86-4. see Data Analysis section) for Survey years 99-00.20-5. 0.30) 2.76-7.63 (8.14-1.49) 11.75-3.06-1.30) 5.00) 1.60 (2.11 (2.80) 6.99 (4.18 (6.90 (1.70) 7.86-5.44 (1.87-7.66 (4.80-2.40 (1.70-6.30 (2.03 (1.45) 7.01 (4.25-1.35-1.80 (2. glass.50 (5.31.50) 2. 7440-39-3 Medically.88) 7.88 (5.88) 1.51 (1.82-6.64) 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 2.64 (1.61-8.22-1.2) 6.27 (1.45 (1. The general population can be exposed to low amounts of barium in air.61 (1. barium sulfate is used as a contrast medium for taking radiographs of the gastrointestinal tract.38 (1.26-7.87-14.. and 03-04 are 0.77) 1.92) 2.64-3.70) 1.73 (6.82) 2.49 (1.30 (3.30) 8.01-7.12) 7.70) 4. Urinary Barium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.32) 8.54-1.60 (1.63 (5.56) 4.87-9.20-1.14 (6.65 (5.70-2. In single dose animal studies. Barium compounds are also used commercially in paint.73) 1.90-13.48) 1.48) 1. such as barium chloride.57 (5.00 (2.50 (1.00-8.38 (1.91) 6.30 (5.60-6.1) 9.35 (2.56 (6.8 (6.60) 3.70) 1.43 (5.86 (4.51) 1.4) 7.00-3.30 (5.16) 5.78) 1.70-3.49) 8. tiles.80) 1.20-6.15-1.20 (1.91) 2.31-2.40 (5.61 (5.27 (1.30-2.35 (3.10 (3.70-5.37) 5.40 (1.20) 2.73) 3.82) 1.30) 3.31 (2.37) 1.93-2.68 (1.15) 5.98) 1.00) 6.80 (1.60-3.78-3.25 (1.55-3.40 (5.70) 3.15 (2.16 (1.88) 4.40) 7.60) 4.65) 3.59) 3. Some barium salts are freely soluble in water.50) 4.65-8.8) 5.09 (2.80 (1.30-1. Small amounts of barium can be released into the air during mining and other industrial processes.00) 1.S.74) 3.90 (4.22-1.00-76.50-6.20 (4.39) 1.43) 2.60-10.35) 5.60-6.43) 6.28) 90th 5.10 (4.10) 5.04-6.73 (5.37 (4.71 (2.43) 297 368 290 621 762 725 1262 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 1.10 (2.42 (1.34 (2.70) 5.52 (4.10) 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 1.30-2.30) 5.15-1.20-8.60) 1.49-1.85) 1.47-1. and food.34 (1.65) 1.10) 3.54) 1.50) 2.70 (5.50 (1.60) 1.63) Total 1.20-1.62 (1.78-2.47-1.19) 2.21 (1.85 (2.29-1.20-1.50 (6.11-1. whereas others are practically insoluble (e.00) 4.74-3.85) 1.90 (6.49-9.74-2.47) 4.84) 5.14-6.02 (7.38) 2.62) 1.86) 6.56 (2.28-1.62) 1.18-1.77 (3.15-11.37-8.41-3.62 (1.4) 6.33 (1.90) 2.29-5.43 (1.20-1.44-5.17-1.95-6.63) 1.25-11.87 (5. barium sulfate and barium carbonate).50 (3.08-8.

Toxicity from soluble barium salts is rare.30 (1.76) 1.23-2.27-1.65 (2.48 (1. 1989).84) 2.39 (2.19-1.56 (1.68 (3.40 (1.28 (1.24 (3.46) 1.97) 1. population from the National Health and Nutrition Examination Survey.86) 5.37 (1.47) 1. 1990).22-1. 1985.32 (1.73-4.24-1.49-1.26-1.20-2.58) 75th 2.28) 5.30 (1.30) 2.24-1. Wones et al. 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.24-6.72) 4.60 (1.56) 4.55 (1.33 (5.73-2.38-5.74) 1.39) 4.33 (1.77) 1.36 (3.0) 5.68 (3.59 (1.36-1.64 (1.98 (2.3) 6.41) 5.33) 1.23-5.99) 1.37) 2.47 (2.58 (2. Symptoms following acute high dose include perioral paresthesias.52 (3.50 (4.42) 1.21 (1.57-10.49-1.74) 1.53-21.91 (3.03) 2.00 (5.40-1.10) 6.60 (5.75) 1.16-1.2) 6. Urinary Barium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.01 (4.11) .02) 4. NTP.76) 2.26-4.27-3.56 (1.10-2.76) 2.46-22.58-6.75) 1.10) 3.921 (.26-1.00 (2.60 (1.38 (4.79-5.54 (2.90-2.02-5.24-3.59 (1.04 (2.45-8. about 75 % of a dose of soluble barium was eliminated within 3 days (Reeves.915 (.06) .59) 1.710-1.48-3.50) 1.69 (5.891 (.62 (2.43-6.3 (6.78 (2.38) 4.48 (1.34) 1.28-7.32) 2. water solubility. 1986).22-1.86 (2.76 (2.51-3.4 (5.48) 2.38 (1. 2001). diarrhea.58) 4. but can occur after intentional or accidental ingestion of barium carbonate in rodenticides (Genter.37 (1.963 (.04) 5.832-1.01) 1.61 (4.31-1.62 (4. The health effects of exposure to barium compounds depend on the dose.29-3.50) 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 1.88 (6.38) 1.96) 4.80) 3.77-5.02 (3.24-11.64 (1.62 (1.31-1. Following intravenous injection in animals.23-1.47 (5.68) 3. Barium blocks cellular efflux of potassium resulting in profound hypokalemia.24-6. vomiting.03-1.13-3.85-5.52) 2.70) 1.01 (5.54) 2.97-4.68 (2.12) 2.97 (5.91 (3.38-7.96 (4.73) 2. in urine.61) 2.55 (5.03) 3.29-1.703-1.39-1.38) 1.27) 692 682 618 540 667 723 765 1132 1074 Non-Hispanic blacks Non-Hispanic whites 194 Fourth National Report on Human Exposure to Environmental Chemicals .13-2.51 (1.03-1.11-2. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.91) 2.83) 2.75) 2.64) 7.75-3.14-2.91-2.96 (4.53) .880-1.27) 7.05-1.39 (2.45-1.70) 4.60) 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 (4.10 (6. chemical form.49 (1.51 (1.08-2.31) 5.42) 1.55) .62) 2.45-6.36-1.77) 1.96) 4.82) 1.77) 5.33 (1.09) 6.20-8. 1984. interval) 1.60 (2. weakness.08-1.00 (3.39 (2. 1994.00-1. paralysis.41 (1.10-1.25) 4.89 (2.54 (1.66 (1.20) 4.75) 2.34 (1.33-1. Perry et al.88 (2.53 (2.58 (4.87) 1.45 (1.29-4.45 (3.47) 10.55 (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 1.19-1.51 (3.38 (1.19-1.02) .97 (4.39-5.49-1.39-1.96) 4.76 (3.36 (3.72 (2.56-3.42 (4.76-3.29 (3. and cardiac dysrhythmias.16 (1.57-5.83) 3.76 (4. Human health effects from barium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.25-11.64 (1.41 (1.84-2.881 (.20 (1.69-9.50) 2.57 (6.63) 1.00) 4.32 (2.68) 1.57) 2.22-2.40 (1.33-4.0) 6.28-11.77) Total 1.45-1.59) 1.24) 3.36 (1.32 (1.99 (2.70) 10.15-4.35-1.29-4.34-1.28-1.4) 5.36 (5.77) 1.47-8.81-6.51) 4.38-1.75-22.74 (5. a benign condition that may occur among barite ore miners.2 (3.80) 4.79) 1.55-5.27 (2.63-4.55-6.64 (1.48 (1.36-2.82) 1.48-5.11) .44 (1.47) 1.31 (1.65 (5.41 (2.04) 1.00) 1.S.72) 6.52) 7.49 (1.46) 2.57-7.754-1.24 (5.36 (1.06) 2.00) 4.44-2.51) 4.64) 7.52) 1.19-2.80-6.38 (4.60 (2.52-10.00 (3.59-7.81-6.35-3.47) 4.905 (.39-10.34-5.58) 1.44-2.Metals was eliminated primarily in feces and to a lesser extent.33) 6.31-1.50) 1.39 (3.51) 6.81-7.92) 2. hypertension.84-5.00) 6..96-6.99 (4.26) 4.68-3.45) 95th 6..26-1.32) 2.26-1.29) 1.20-1.777-1.55 (4.18 (1.45) 1.03) 1.97-3.43) 1.52-4.59) 2.18 (1.92 (4.89) 90th 4.71 (5.22-4.29-7.96) 7.40 (1.0) 7. Insoluble barium salts.34-3.29 (1.16) 11.54) 1.46 (2.00-7.25 (1.35-1. and route of exposure.37-2.46) 3.41) 4.28-6.56) Selected percentiles ( 95% confidence interval) 50th 1. Barium is not rated for human carcinogenicity.84 (3. Chronic accumulation of inhaled barium dust in the lung tissue may cause baritosis.86-7. are not absorbed when administered.68-3. Chronic high doses in animals resulted in kidney damage (McCauley et al.8) 4.2) 5.. such as those used in medical radiographic procedures.37-1.48-1.67-6.

Minoia C. Perry HM. A study of 46 elements in urine. eds. the welders had no obvious adverse clinical effects (Zschiesche et al. Fourth National Report on Human Exposure to Environmental Chemicals 195 . ed. p.atsdr. Magnesium. Pietra R. and radium In: Bingham A.cdc. 1998). 1985. environmental levels) and health effects is available from ATSDR at: http://www. In Friberg L. patient population and literature reference intervals for urinary trace elements. 84-94.. Apostoli P. Vol 2: Specific Metals. In: Inorganics in drinking water and cardiovascular disease. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Exposure to soluble barium compounds: an interventional study in arc welders. 1990. 1986.Metals Workplace standards for external air exposure to various barium salts have been established by OSHA. Powell C. 2000) to levels in NHANES 1999-2000 and 2001-2002. eds. References Brenniman GR. Sci Total Environ 1990. PS. et al. et al. and serum of Italian subjects. p.S.niehs. Weltle D. Third National Report on Human Exposure to Environmental Chemicals. National Toxicology Program (NTP). pp. In: Calabrese EJ. Kopp SJ. Cohressen B. Levy. and 2003-2004 (CDC. Biomonitoring studies of levels of barium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of barium than are found in the general population.28(3):373-388. Princeton NJ: Princeton Scientific Publications. Frohman. Calabrese EJ. Gallorini M. Available at URL: http://ntp. Princeton (NJ): Princeton Scientific Publications. Lack of effect of drinking water barium on cardiovascular risk factor.gov/ntp/htdocs/LT_rpts/tr432.296(1-2):71-90. Stadler BL. Vouk VB.html. Welders of barium-containing electrodes had median urinary levels of barium that were 60 times higher than the median levels in this Report. ed.nih.76(1):53-59. Int Arch Occup Environ Health 1992. p. Biomonitoring Information Levels of urinary barium reflect recent exposure.gov/toxpro2. Finding a measurable amount of barium in urine does not mean that the level of barium causes an adverse health effect. [online]. Clin Chim Acta 2000. 221-252 Komaromy-Hiller G. LA. Schaller KH. Wones RG. Morrow JC. New York: Elsevier. New York: John Wiley & Sons. Sabbioni E. 10326-27-9) in F344/N rats and B6C3F1 mice (drinking water studies).. Centers for Disease Control and Prevention (CDC). Barium. 4/8/09 Paschal DC. EPA. Atlanta (GA). calcium.. Jr. Advances in modern toxicology. Barium levels determined in clinically submitted specimens were broadly comparable (Komaromy-Hiller et al. Howerton K. Sampson EJ.64(1):13-23. Urinary concentrations in acute poisonings are often hundreds to thousands of times higher than in this Report... NTP. Trace element reference values in tissues from inhabitants of the European community I.gov:8080/cs. technical report on the toxicology and carcinogenesis studies of barium chloride dehydrate (CAS no.95:89-105. Zschiesche W. Minoia et al. Information about external exposure (i.html?charset=iso-88591&url=http%3A//ntp. Perry EF. Comparison of representative ranges based on U. Nordberg GF... et al. Hypertension and associated cardiovascular abnormalities induced by chronic barium feeding. Pirkle JL.e. 1994.. Jackson RJ. Patty’s toxicology..pd f&qt=barium+chloride+dehydrate+1994&col=020rpt&n=3&la= en. 2005.S. Trace metals in urine of United States residents: reference range concentrations. Epidemiological study of barium in Illinois drinking water supplies. 2nd Ed. 1984. Paschal et al. blood. 2005.197210. 1992). Studies reporting urinary levels of barium in general populations have found values generally similar to those reported in NHANES 1999-2000.nih. 2001-2002.85:355-359. Pozzoli L. Reeves AL.niehs. Costa R. Genter MB. and a drinking water standard has been established by U. Investigations into the effect of drinking water barium on rats. Inc. J Toxicol Environ Health. 2001. et al. 5th ed. Environ Health Perspect 1990. Ash KO. 231-249. Handbook on the Toxicology of Metals. 1989. barium. strontium. Douglas BH. Environ Res 1998. McCauley PT. Ting BG. Laurie RD.

and refined beryllium is used in mirrors and special metal alloys for the automobile. population from the National Health and Nutrition Examination Survey. Exposure to beryllium occurs mostly in the workplace. Burning coal and oil can produce small amounts of beryllium dust that can be released into the air.140 (<LOD-. or drinking water containing the metal. see Data Analysis section) for Survey years 99-00. 7440-41-7 General Information Pure beryllium is a hard gray metal. and 03-04 are 0. In studies of laboratory animals. aircraft. and 0. electrical. coal. Two types of minerals. 196 Fourth National Report on Human Exposure to Environmental Chemicals . interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . and volcanic dust. soil.13. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. A half-life of 450 Urinary Beryllium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. inhaled insoluble beryllium sulfate was retained in the lungs and nearby lymph nodes.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. beryllium is used in instruments. computer. nuclear. eating food. the lightest of all metals. are mined for commercial recovery of beryllium. which may vary for some chemicals by year and by individual sample. and dental bridges.Metals Beryllium CAS No.13. Beryllium compounds are commercially mined. and machine-parts industries. and from breathing tobacco smoke. bertrandite and beryl. Beryllium is also used in the production of sports equipment such as golf clubs and bike frames. x-ray machines. less than one percent of the inhaled dose was slowly absorbed into the blood and eventually incorporated into the skeleton. respectively. 01-02.130 (<LOD-.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 . 0.130 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result. Low-level beryllium exposure in the general population can occur through breathing air. and can be found in mineral rocks.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 . In medicine.S.13. < LOD means less than the limit of detection. near some hazardous waste sites.

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

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. 2000. Sabbioni E. Comparison of representative ranges based on U. They reported urinary beryllium levels ranging from 0.15 μg/L in workers exposed at the recommended threshold limit value (Apostoli and Schaller.13 μg/L. Sci Total Environ 1994. Environmental Health Criteria. Costa R. less than 0. et al. and 2003-2004. Finding a measurable amount of beryllium in urine does not mean that the level of beryllium causes an adverse health effect. Sci Total Environ 1990. blood.S..158:165-190.. Clin Chim Acta 2000. Element reference values in tissues from inhabitants of the European community. Ash KO.html. Schaller KH.cdc. and the fact that most NHANES participant levels were undetectable.org/documents/ehc/ehc/ ehc106. Pirkle JL. Hamilton et al. Clin Chest Med 2002. Int Arch Occup Environ Health 2001. patient population and literature reference intervals for urinary trace elements.S. Howerton K. HLA-DPB1 and chronic beryllium disease: a HuGE review. Third National Report on Human Exposure to Environmental Chemicals. Ting BG. International Programme on Chemical Safety (IPCS).S. References Apostoli P. and serum of Italian subjects.296(1-2):71-90.23:827-839. In other studies. Apostoli and Schaller (2001) stated that detection limits in earlier studies were inadequate to estimate nonoccupational exposures.inchem. Sampson EJ. 198 Fourth National Report on Human Exposure to Environmental Chemicals . Beryllium [online]. Minoia C. population are lower than levels in workers. population were generally undetectable in NHANES 1999-2000. A study of 46 elements in urine.. Weston A. 3/27/08 Komaromy-Hiller G.1 μg/L). Environ Res 1998. it is likely that urinary beryllium levels in the U. 1998). Am J Epidemiol 2003. 106. Van der Venne MT. Pietra R. 0.157:388-398. Apostoli P. environmental levels) and health effects is available from ATSDR at: http://www.gov/toxpro2. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Gallorini M. and the 95th percentile for males in NHANES 2001-2002.e.12 to 0.atsdr. urinary levels for general populations have been either undetectable or had different detection limits than in this Report (KomaromyHiller et al. 1990. Biomonitoring Information Urinary beryllium levels represent recent and accumulated exposure. Genetic and exposure risks for chronic beryllium disease. Pozzoli L. Andrew M. Atlanta (GA) 2005. Trace metals in urine of United States residents: reference range concentrations. Review of elements in blood. 20012002. Paschal DC. VI.htm. Levels of beryllium in urine for the U. (1994) noted that analytical methods used in several general population studies appeared to have limits of detection that were insufficiently low (i. 2001). et al. Maier L. Hamilton EI. 1990. McCanlies EC. which approximate this Report’s limit of detection.. Minoia et al. Paschal et al.74:162-166. Urinary beryllium--a suitable tool for assessing occupational and environmental beryllium exposure. Kriess K.e.Metals (i.. Given these results. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Available at URL: http://www. Trace element reference values in tissues from inhabitants of the European community I. Morrow JC.95:89-105. Centers for Disease Control and Prevention (CDC). Jackson RJ. Sabbioni E.76(1):53-59.

70) 1.300-.300 (.326 (.500 (.800) .500-.300-.20 (.275-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.300-.10 (1.200 (.395 (. and incineration of municipal waste materials.500-.600 (.400 (.400 (.500) .10) 1.600 (.300) .00 (.00-1.300) .60) Total * .80) 1. during refining of lead and copper from sulfide ore.300-.300) .200 (.00 (.500 (.600) 90th 1.50 (1.400 (.40-1.40 (1.70) 1.382 (.600) .600-. Important sources of airborne cadmium in the environment are burning fossil fuels such as coal or oil.50) 1.30-1.500-.300-.700) .60 (1.20) 1.300) .00 (.600) .700) .300) .424) * .266-.500-.366) * * . EPA.10) 1.500) .00) .00 (1.600 (.500-.20) 1.500-.300 (<LOD-.500) .449) Selected percentiles ( 95% confidence interval) 50th .00 (.50-1.398) < LOD < LOD < LOD < LOD < LOD < LOD .20) 1. Fourth National Report on Human Exposure to Environmental Chemicals 199 .500 (.400) .400-.300-.10) 1.400 (. plastic stabilizers.600 (.400) .400) .400-.400 (.300 (.200) .30-1.60-1.20-1.500-.300-.300-.00-1.400) .30) .200-.900-1.300 (.500) .362-.20-1.300) .700) . or copper smelters (U.Metals Cadmium CAS No.400) .900-1. and nonferrous alloys.usgs.500-.700-1.400-.800-1.600 (.10 (1.300 (.60 (1.14.400 (.393 (.900 (.10) 1.30-1.10 (1.200) .600 (.300) .400) .216-.400 (.60 (1.80 (1.30) 1. < LOD means less than the limit of detection.50 (1.30) 1.40-1.900-1.400) .600) .500 (.400 (.500 (.30) 1.700) .400-.400) .400 (.40 (1.200 (<LOD-. lead. respectively.600) 1.400 (.800 (.40 (1.300-.20) 1.500 (.00-1.300-.367-.441) * .378-.235 (.50 (1. malleable.400 (.500 (.200-.300 (. Since 2001.20) 1.304 (.40) 1.200-.00 (.400-.400) < LOD .400-.300) 75th .20) . coatings and plating.255) .300-.40 (1.400) .500-.600-.500-.900 (.00 (1.368-. interval) .900-1.300-.300 (.10 (1.289-.376-.300-.500-.600) .470) * .600) .400) .400 (.40 (1.304-.70) 1.20-1.300-.309-.20-1.600 (.10) 1.80) 1.300-. 7440-43-9 General Information Cadmium is a soft.800) 1.300 (.00-1.283 (.300-.3.421 (. 01-02. as zinc sulfide) and to a lesser extent.300 (.30 (1.412 (.60) 1.300 (.600 (.300-.500 (.700 (.20-1.00-1.900-1.600 (.400) < LOD . cadmium use has declined in response to environmental concerns (http:// minerals.60 (1.40 (1.600 (.20) 95th 1.500 (.300 (.359-.900-1.00-1.00-1.386-.500-.20) 1.400) . population from the National Health and Nutrition Examination Survey.10) 1.200 (<LOD-.300-.400 (.50-1.300) 1.420 (.3.460) .10 (. Blood Cadmium Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.500-.S.300) .00-1.300) .500-.500-.300-.300-.468 (.600) .200 (.426-.60 (1.300-.700) .30-1.10 (1.300 (<LOD-.500) .400) .600) . U. see Data Analysis section) for Survey years 99-00.400-.20) 1.300 (.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 . Other uses include pigment production.20 (1.400-.10 (1.500-.700) .900-1.30-1.00) .S.300 (.331) . which may vary for some chemicals by year and by individual sample.20-1.513) .60) 1.700) 1.600 (.400) .300-.600) .452) .425 (.300 (.400-.427) * .403 (.400) .300) . 0.700-1.90) 1.900-1.00 (.00 (.800-1.400) < LOD .700-1.600 (.60) 1. and 0. bluish-white metal that is obtained chiefly as a by-product of processing zinccontaining ores (principally sphalerite.400) < LOD < LOD < LOD .361-.400 (.50) 1.400 (.00-1.50-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .700) .600) .344) .900-1.500) .700) . Cadmium also may be emitted into the air from zinc.600 (.300) .800) .400 (.900-1.00 (.50) 1.400-.10 (1.400-.296-.10) 1.333 (.gov/minerals/pubs/commodity/cadmium).10) 1. The predominant commercial use of cadmium is in battery manufacturing.600-.304 (.40 (1.500) .70) 2742 2268 2085 1842 2219 2292 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.600 (.320) Sample size 7970 8945 8372 Age group 1-5 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * .600-1.300 (<LOD-.500-.337) .400 (.200-.00 (.70) 1.500-.20-1.403) .50-1.313 (.800 (.40) 1.300 (.00 (.20) .S. and 03-04 are 0.200-.300) .50 (1.378 (.20) 1.300 (<LOD-.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 .

140 (.114-.090) .01-1. however. **All results are corrected for molybdenum oxide interference in the ICP-MS method.200-.06.306 (.196-.092) .203) .886-1. The gastrointestinal absorption of dietary cadmium is about 5% in adult men and 10% or higher in women (Diamond et al.339) .148-.456-.860) 1.233) .25) 1.260 (.800 (.210 (.972 (.507) .990) .220 (.077 (.28-1.500) 90th .253-.82) 1. potatoes.858 (.545 (.466 (.229) .260-. Renal tubular and glomerular damage.870) .48 (1. To a lesser extent.481) .308) . 200 Fourth National Report on Human Exposure to Environmental Chemicals .232) .06-1.733-.06.479) . rice.310) .820-1.766 (.25 (1.192-.090) .426 (.390-.060-.980) .366-.20) 1.150-.289-.839 (.733) .980-1.890-1.141 (.136) . calcium.270 (.183-.09-1.455 (.101) .519) .189) .310 (.219 (.450 (.170-.02-1.087-.30-1.216 (.520-.284) .223 (.249-.580) .255) .126) .38) .078 (.875 (.06) .061 (<LOD-.551) .208-.452 (.270 (.316 (.320) .260-.589 (.251) .15 (.445 (.202-.247) .150) .191-. zinc. 2003).24) 1.109-.220-.280 (. Urinary Cadmium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.13 (.963-1.490) .843-1.193 (.134) . Cadmium absorption may be increased with iron deficiency (Berglund et al.246) .886) .445 (.135 (.330-.210 (.178-. 2004a.919) .327 (.10 (1. 2003).433-. Kikuchi et al.160) .388-.206) .20 (1.980) .705-.633 (.235) .20-1.980 (. Diamond et al. drinking water is a source for cadmium intake.519) .273 (.06.366) .326) .261-.204 (.192-.Metals 2000).354) .892-1.447 (.151-.210 (.04 (.713) .241) .181 (. The kidney is a critical target and shows the earliest sign of cadmium toxicity.300) .112-.272-.03) . interval) . Horiguchi et al.381-.450 (.283 (.550 (.51 (1.226) .187 (.265 (.200-.061-.482) .281 (.12 (.231) . wheat.800-.282 (.300 (.820 (.229-.160 (. For nonsmokers who are not exposed to cadmium in the workplace.238-.148) .177-.077 (.329 (.01 (.081) .080 (.38) 1.265) . and various seeds.20 (1.551 (.190-.255) .436-.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 .393-.109 (.430-.980-1.530 (.17 (.989-1. population from the National Health and Nutrition Examination Survey.170 (.277 (.226) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .210) .372) .210 (.230) 75th .222) .17 (. an inducible metal binding protein.165-.193-.191 (.** Survey Geometric mean (95% conf.753-.539) .28) 1.22 (1.195-.41 (.202 (.510) .960 (.279 (.06-1.836-1.232 (..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 .171-.806) .180 (.28 (1.170-.257) . 1999.700-.190-.680 (.263) .07-1.336) .510-.38) .13) .100-.175 (.189-.500) .299) . Inhalation of cigarette smoke is a predominant source of exposure in smokers.157) .255) .191-. 2001).440-.237-.623) . and 0.065-.790 (.607) .875) . 2003. and 03-04 are 0.239 (. individual values vary and are affected by factors such as dietary intake of essential nutrients (iron.351-.130 (.72) 1. a factor that may contribute to the higher absorption of cadmium by women (Diamond et al.209 (.440 (.190-.135-..240-.83) 1.890 (.480) . With chronic exposure.714-1.201 (.855-1.115-.313) .74) 1.221 (.207-.194-.686-.394-.640) .210) .818 (.110-.360) .47) 1.238) . 01-02.067-. respectively.462 (.302 (.199 (. About one-third to one half of the total body burden accumulates in the kidney tissues (Nordberg and Nordberg.219 (.390 (.203 (.120 (.17) .559 (. copper) and protein.633-1.848 (.36) 1.390-.977) .940-1.470-.400-.530) .295) .092 (.400-.490) 1.458 (. see Data Analysis section) for Survey years 99-00.128 (..12-1..220) Selected percentiles ( 95% confidence interval) Sample 95th 1.219 (.700-. 1994).S.153-.610) .26) size 2257 2690 2543 Total years 99-00 01-02 03-04 50th . ingestion through food is the largest source of exposure.918-1.230) .220-.17 (.748-1.892 (.366-.322 (. including many food crops such as cereal grains.15) 1. cadmium accumulates in the liver and kidneys where it is bound to metallothionein.880) .198) .221) ..243-.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.290-.233) .20 (1. The estimated half-life of cadmium in the kidney is from one to four decades (ATSDR.175 (.412) .160-.19) 1.492 (.440 (.813 (.210 (. 0.57) 1. whose body burdens of cadmium can be approximately twice that of nonsmokers.200 (.211 (.206 (.790 (.763-.350 (.52 (1.717-.423-.179-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.498-.540) .700-.173) .200 (.220) .285-.34) 1.810-1.227 (.234 (.189-.169-.249) .107-.476-.22 (.741-1.960) 1.596) .240) .387) . 2003).262) .01) .261-. Cadmium is absorbed via inhalation and ingestion.04 (.362) .157-.820) 1.730-.475 (.257-.32 (1.067-.160) .121 (..211-.230 (.38) 1.13-1.817 (.229) .430) .184-.817 (.15) .167-. Cadmium in soil is absorbed by plants.493-.43) 1.214-.

219) Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 * .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.432 (.268 (.941 (.481 (. interval) . At lower environmental exposures.191-.208-.093 (.806-1.182) .850) .104) .414 (.177) .084-.647-.267 (.440) .338 (.130-.181-.232) .388-.16) .828) .438) 90th .** Survey Geometric mean (95% conf.184) .171-.917) .278) .476) .377-.077-.239-.225) .311) .261-.190 (.263-.250) ..433-.325 (.666-.622 (.391-.176 (.112) .228-.224 (.182) .137-. 2004b).100 (.111-.686 (.233 (.865 (.545) .147-.316) .719 (.414-.074-.929) .718 (.256-..288 (.441-.404) .767) .607) .143-.802 (.204-.813-1.104) .446) .725-1.487 (.364) .162 (.202 (.183 (.856) .536 (.350) .215 (.07) .727-.470) .906) .159 (.226) 75th .700 (.421 (. 2004).223) .708-1.168 (. 2002.289) .181) .157-.198) .238-.303) . 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.185 (.418-.631) .440) .404 (.261 (.158-.090 (.229) .210 (.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 ..085 (.318 (.533) ..884) .113-..833-1.255-.147 (.067-.687 (.173 (.163 (.178) .150-.200 (.288) .614) .985 (.184-. 1999).784) ..754) . population from the National Health and Nutrition Examination Survey.242) .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 .227-.234) .282 (.146-.876-1.083-.238) .850) .16) 1.300-.225) .321) .211 (.136-.232) .156 (. 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.293-.484 (.176 (.490 (.304) .779 (.757 (.501 (.874-1.783 (.175-.126 (.190 (.221 (.183) .940 (.12) 1.716) .221-. Staessen et al.296 (.085-.181 (.382) .206-.329 (.340) .473 (.551) ..274) 1.091 (.247-.209) Selected percentiles ( 95% confidence interval) Sample 95th .078 (.856 (..187) .245 (.740 (.096) .650-.175 (.252 (.212 (. **All results are corrected for molybdenum oxide interference in the ICP-MS method.690-.05) 1.192) .219 (.839) .123-.789 (.292) .700) .382-.094) .123-.273 (.235) .500-.09 (.173-.00 (.678 (.191) .412 (.220 (.156-.210) .209) .107) .240) .135) . However.931 (.617 (.166 (.234 (.690 (.962) .148 (.222-.159 (. 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.438-.767 (.712 (.270 (.08) .218) .154-. Horiguchi et al.769 (.316 (.174-.423 (.668-.187-. 2002.280 (. Fourth National Report on Human Exposure to Environmental Chemicals 201 .071 (.191 (.216-.426-. Olsson et al.201-.144-.17) . 2002.156) .830) .818) . most often a result of occupational exposure (Roels et al. a condition known as “itaiitai” (“ouch-ouch”) affected postmenopausal women living in a cadmium-polluted region of Japan.998) .184-.288-.541) .185) .240) .531 (.197-.098) .241) .591 (.199 (.283 (.219 (.434 (.189-.078-.304-.02 (.154 (.795) 1.289) .131-.716-.827) .234-.266) .387-.106) .335 (.168-.10) 1.630-.729 (.826-1.444-. 1999).830-1.423-.143-.075-.909-1.690-.091 (.691-.491-.136-. 2000.084 (.418) .783) .917 (.449) .873 (.199-.645-.331 (.297) .253 (. Jarup et al.091) .207) .38) .518) .537-.352) .00 (.207-.538) .161-.Metals manifested by irreversible proteinuria and progressive reduction in glomerular filtration rate.722-.143) .927-1.253) .07 (.688-.196 (.157-.562-. 1999).205 (.507-.472) .267 (.140-.757) .06 (.979 (.281) . can result from high dose chronic exposure.170-.940-1.178-.168-.075 (<LOD-.792 (.398-.247-.051-.175 (.336-.431) .381-.560-. 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.101) .826-1. 2003.470) .343-.13) .S.818) .194-.086 (.696-.04) size 2257 2689 2543 Total years 99-00 01-02 03-04 50th .559-.208 (.140-. 1996.122 (.663 (.266-. two studies in Japan did not find an association between cadmium in urine and renal biomarkers (Ezaki et al.147-.415) .919 (.210 (.182) .653) .516-.261) .247-.667) .678-.170 (.263 (.387 (. Noonan et al. During the 1950’s and 1960’s.137 (.813-.308) .063-.281) .687-.479 (...950) .693 (. 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.236-.181 (.308 (.163) .097) .674-1.

Ezaki et al.. Staessen et al.46 mg/gram of creatinine) (Ezaki et al.. Noonan et al. Horiguchi et al.. intermediate in former smokers and lower in never-smokers (Becker et al. study subjects living near a former zinc smelter were similar to those from an unexposed community and to those in this Report (Noonan et al. 2002).. Ezaki et al. two studies of women in Japan with lower exposures found no correlation between renal tubular effect markers and blood or urine cadmium levels (geometric means were 1. Zhang et al. 1999). Blood and urine cadmium levels are typically higher 202 in cigarette smokers.. Creatinine-corrected urine cadmium values in U. Wilhelm et al. 2003. 2000. 2004. 2005. 1999. Workplace exposure to airborne cadmium particulates was associated with decreases in olfactory function (Mascagni et al.. Acute and heavy exposure to airborne dusts and fumes. the risk of low bone mineral density increased by nearly three-fold when the blood cadmium exceeded 1.. 2003. decreased bone density was correlated with mean urinary cadmium levels of approximately 1 mg/gram of creatinine (Staessen et al.. Salpietro et al.S. Further research is needed to address the public health consequences of such exposure in the United States. Jarup et al. Wennberg et al... respectively.. 1996. maternal blood or maternal urine and birth weight (Nishijo et al. 2002). Becker et al. Staessen et al... In adults aged 60 years and older. with peak values observed in the fifth to sixth decades (CDC.. 2006). 2003). Waalkes (2003) provides an overview and summarizes potential mechanisms for carcinogenicity... Chronic inhalation exposure to cadmium particulates was associated with changes in pulmonary function and chest radiographs that were consistent with emphysema (Davidson et al. 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)... Komaromy-Hiller et al. Occupational standards are provided here for comparison only.... 2000).. 2003. EPA. 2000. In postmenopausal women. Several studies of populations residing in areas with higher cadmium soil concentrations or with frank cadmium pollution have reported mean blood and urine cadmium levels considerably higher (as much as 10 times higher) than control groups or representative U.. 2005. 2002). approached these values associated with subclinical changes in renal function and bone mineral density... pituitary gland and kidney tumors in animals and has been associated with lung cancer in humans in occupational epidemiologic studies. Horiguchi et al. data (CDC. has resulted in severe. Finding a measurable amount of cadmium in blood or urine does not mean that the levels of cadmium cause an adverse health effect.. 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.cdc. Olsson et al. However.. urinary cadmium reflects both cumulative exposure and the concentration of cadmium in the kidney. Becker et al. Jarup et al. 2002). blood cadmium was also slightly higher in Mexican Americans and participants 20 years and older (CDC. environmental levels) and health effects is available from ATSDR at: http://www. 2002. In this Report the urinary and blood cadmium levels at the 95th and 90th percentiles. Cadmium can produce lung. 2004. Both IARC and NTP consider cadmium a human carcinogen. 2006). 2005. Suwazono et al. 2004). as may occur from welding cadmium-alloyed metals.Metals greater urine cadmium levels may have an increased risk for bone fracture and diminished bone mineral density (Alfven et al. Biomonitoring studies on levels of cadmium provide physicians and public health officials Fourth National Report on Human Exposure to Environmental Chemicals . People who are occupationally exposed may have blood and urine cadmium levels that are higher than those of the general population. 2006. and drinking water and environmental standards have been established by U... 2004. 2003. 2002). 2002. 2002.. 1988). Moriguchi et al. Staessen et al... respectively. not to imply a safety level for general population exposure. Information about external exposure (i. 2005. 2000.. For NHANES 19992000...S. Becker et al.. 2004b. Biomonitoring Information Blood cadmium reflects both recent and cumulative exposures.1 mg/L (Alfven et al.. 2003. 1999). 2003.e.gov/ toxpro2. Olsson et al.. 2004. Workplace standards and guidelines for air exposure to cadmium have been established by OSHA and ACGIH.atsdr. 2002.. 2002. Mannino et al. Surveys of populations not known to have increased cadmium exposure have reported similar urine and blood levels (Becker et al. In the typical environmental exposure. Olsson et al. Blood cadmium levels are about twice as high in smokers compared to nonsmokers (Becker et al. 1996).. 2004b). 2005). 2002) and length at birth (Nishijo et al. Small epidemiologic studies have noted an inverse relationship between cadmium in cord blood. 2002. Friedman et al.26 and 3. Jin et al. Wennberg et al. CDC. potentially fatal pneumonitis (Fernandez et al..S.html. 2006. Animal studies have demonstrated reproductive and teratogenic effects. Women had higher blood and urine cadmium levels compared to men of similar ages..

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Zhang YL.110:1185-1190. Liu QF. Friberg L. et al. Noonan CW. eds. lead.353:1140-1144. Occup Environ Med 2002. Schultz C. Salpietro CD. Roels HA.3:26-41. Roels HA. et al. Effects of exposure to low levels of environmental cadmium on renal biomarkers. or cadmium in controlling occupational and environmental risks of nephrotoxicity. Lundh T. Environ Res 2006. Fan YG. Lijnen P. Zhao YC. Olsson IM. Nogawa K. Nakagawa H. Nakagawa H.html. Hoet P. iron status.533(12):107-120. Cadmium carcinogenesis. Ginucchio G. 2001.84 (Section A):4455. Environ Health Perspect 2002. and mercury in the population of northern Sweden. Lison D. 2004. et al. Merlino MV. Renal effects of cadmium exposure in cadmium nonpolluted areas in Japan.gov/ttn/atw/ hlthef/cadmium. Zhu HD. Cadmium concentration in maternal and cord blood and infant birth weight: a study on healthy non-smoking women. Wennberg M. J Environ Sci Health B 2004.100:330-338. Wang JX.39:2507-2515. Effects of maternal exposure to cadmium on pregnancy outcome and breast milk.59:394-397. Arch Environ Health. Ottosson H. 151-168. Lancet 1999. Campagna D. Nordberg GF. Buchet JP. Kuznetsova T. Revised 2000 [online]. Public health implications of environmental exposure to cadmium and lead: an overview of epidemiological studies in Belgium. and risk of fractures: prospective population study. United States Environmental Protection Agency (U. pp.30(5):395-399. Hazard Summary. J Perinat Med 2002. Relationship between newborn size and mother’s blood cadmium levels. Tanebe K. Ren Fail 1999. Tanebe K. Roels H. age. created 1992. cadmium. Jansson J-H. Int J Hyg Environ Health 2006. Available at URL: www. Bergdahl IA. In: Clarkson TW. Stegmayr B. et al. and mercury in blood or urine of children: Basis for validation of human biomonitoring data in environmental medicine. dietary intake. et al.21(3-4):251-262. Cadmium compounds. EPA). Sager PR. 2000. Thijs L. Biological monitoring of toxic metals. Usefulness of biomarkers of exposure to inorganic mercury. Revised and new reference values for arsenic. Gangemi S. Kobayashi E. Suwazono Y. Gallmans G. Vangronsveld J. Environmental exposure to cadmium. Mueller PW.209:301305.Metals Nishijo M. Environ Health Perspect 2002. Minciullo PL. Effect of environmental exposure to cadmium on pregnancy outcome and fetal growth: a study on healthy pregnant women in China. forearm bone density. Time trends in burdens of cadmium. Environ Res 2000. Sarasua SM. Nordberg GF. 204 Fourth National Report on Human Exposure to Environmental Chemicals . Toyama. Lauwerys R. Saito S. Honda R. Lybarger JA.59(1):22-25. et al. Biological monitoring of cadmium. Kathman SJ. Honda R. Nordberg M. Schwenk M. Lundh T. Cadmium in blood and urine – impact of sex. and former smoking – association of renal effects. Staessen J. 4/8/09 Waalkes MP. lead. Emelianov D. Stelitano A. Okubo Y. Oskarsson A. Japan. Bensryd I. Nishijo M. J Cardiovasc Risk 1996. Nakagawa H.S. Kido T.110:151-155.epa. New York: Plenum Press. lead. Tawara K. Mutat Res 2003. Wilhelm M. Staessen JA. Bruiglia S. Skerfving S.

90-8.21 (4.71 (4.73-11.4) 9.76-6.74-5.7 (10.5-16.00-8.99) 7.35 (4. However.47-8.7) 11. interval) 4.95 (3.13 (8.39) 7.60-6.89-5.4-13.3) 10.90-10.22 (4.40-5.1 (11.7 (9.21) 90th 9.30) 5. 01-02.03-4.10-8.53-11.40-5.01-6.9) Total 4. Fourth National Report on Human Exposure to Environmental Chemicals 205 .2) 11.64-10.30 (6.68 (7.67 (4.26) 4.3) 12.80-10.25-5.12 (4.83) 6.20 (6.17) 4.50 (4.63-4.16-6.80 (8.25) 4.00-10.84) 5.Metals Cesium CAS No.10 (8.9) 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 4.70-5.5) 9.6 (11.22-4. For absorbed cesium salts. and as polymerization catalysts.4) 95th 11.01-8.80) 7.90) 4.55-11.3) 9.0) 12.6) 1226 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4. and clay.1-12. population from the National Health and Nutrition Examination Survey.08 (7.77 (4.98 (7.54) 4.42) 7.20-7. Inorganic cesium compounds are used in photomultiplier and vacuum tubes.6) 10.45-5.88 (8.6 (9.04) 7.70 (9.04 (4.59-5.56) 5.5-13. and 03-04 are 0.4 (10.08 (6.99-6.8 (10. Human health effects from cesium at low environmental doses or at biomonitored levels from low environmental exposures are unknown.40) 7. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.00-9.54-11.82) 5.20) 7.9 (11.63) 6.52-9.7 (9.9 (11. 7440-46-2 General Information Cesium is a silver-white metal that is found naturally in rock.36 (3.33 (5.20-4.34) 9.90 (6.00 (7.64) 5.56 (4.70 (8.09) 5.84-9.1) 9.95) 5.1 (10. although cesium was generally of low toxicity when given to animals.97) 4.24) 4.3) 10.60) 7.6 (9.60) 7.7 (10.17-6.03 (4.77-8. Little is known about the health effects of this metal.9) 12.50) 5. 2004).64) 4.50-7.40) 5.61-6.40) 5.80 (4.80-10.62) 4.43-8. diarrhea. soil.35 (4.47-4.71-5.26) 7.0 (10.14.90) 9.80 (4.32 (3.90-12.44 (8.10-5.37) 7.49 (4.0) 11.34 (4.32-5.70 (6.10 (8. semiconductors.69-6.80 (4.60-7.4) 10.00-4.91 (7. Whether cesium compounds are carcinogenic is unknown.60 (8.90) 5.6 (9.7 (8.71 (8.5) 12.99-11.7-14. 0.62 (5.23-4.96 (6.40-7.55 (7.71-9.0) 11.71-8.20) 8.01) 7.08-5.97) Sample size 2464 2690 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 4.87 (4.70 (6.2-13.59 (5.60-7.4 (9.4) 10.29) 4.80 (8.7) 11.52) 7.50 (4.77 (9.43 (5.46) 7.27 (7.6) 11.8) 11.89) 4.90) 5.12-5.31-8.10-9.91-8.07-11.25 (3.6 (9.8) 12.7) 884 683 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD. nausea.72-7.17 (6.9) 11.26-11.20-5.37) 5.64 (4.8) 11.4) 12.2-12.50) 9.87 (4.27-5.00) 7. Workplace guidelines for cesium hydroxide are available from ACGIH and NIOSH.1-13.99) 9.4) 12.14.23) 9.29 (4.2 (9.20-8.59-5. and high-power gas-ion devices.86-12.5 (10.77 (9.38) 5.49) 75th 7.94) 4. Urinary Cesium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.60-12.15-8.10-7.40-11.8) 9. cesium hydroxide is corrosive and irritating at high concentrations.60-6.2 (9.02 (4.4) 11.45-8.3-13.80-10.87-7.8 (10.53 (6. Case investigations of ingestions of large doses of cesium chloride have reported decreased appetite.56-11.50 (6.3 (8.42-7.59) 7.81) 4.08) 7.13 (5.0-15.84-5.35-5.40-5.93 (4.03 (4.13 (7.1 (9.00-8.14 (4.87 (4.80-13. and cardiac arrhythmia (ATSDR.70 (5.68) 9.80-11.1) 11.7) 10.49 (5.98 (7.74) Selected percentiles ( 95% confidence interval) 50th 4. and 0.09-5.2.90-10.05-5.81-14.80 (8.05) 5.1) 9. Radioactive 137Cs has been used medically to treat cancer.2-14.1) 10.70 (8.57-5.00) 4.7 (10.7 (11.40 (4.3-13.5) 10.8 (11.12-11.S.27) 4.8) 12.49) 4.40-5.20) 4. Most human exposure to cesium occurs through the diet.92-13.3-15.1-12.13-8.71) 4.70) 5.08-5.99-11.9 (11.94 (4.16-6.90-10.20) 5.73-5.33-5.0 (9.36) 3.7) 10.7 (9. photographic emulsions.82-4.00) 6.72) 4.3) 10.9 (10.32) 4.70) 5.8-13.2-13.70 (4.66 (7.90) 7.0) 12.9) 8.26 (3.36 (6.97-7.94-4.30 (6.05-5.81) 4.10 (6.0) 10.0) 12.6 (11.94 (4.30-5.81 (4.86-11.07) 4.9 (11.40-11.1) 11. infrared lamps.5 (8.55 (4.60 (7.63 (4.2-13.4 (9.5-14.0) 9.74 (4.70-8.95-4.80-6.60-5.30) 7.83-4. scintillation counters.12) 5.60) 5.30-10.81) 9.84 (4.86 (7.50 (7.62 (5.3) 10.64-5.33 (6.39-4.84) 8.3 (8.20 (4.42) 6.90-12.87) 5.10 (6. see Data Analysis section) for Survey years 99-00.05) 5.61) 7.79 (4.5-14.56 (4.2) 12.70) 7.97 (7. the body half-life is estimated to be 70-109 days based on 137Cs exposures.8) 12.59-5.90 (4.50 (4.9 (10.8) 9.89) 5. respectively.0-13.64) 5.

03) 5.05) 6.5) 7.74-11.91 (5.40) 7.01-8.46-8.31 (4.93-9.31-6.90-8.94) 7.9 (9..27) 4.9 (10.60 (5.66 (6.67 (5.36-3.61 (7.21 (2.15-4. population.26 (4.33-3.95 (3.77 (6.75 (6.53 (6.18-7.09) 4.54 (4.39) 8.3) 9.96-4.08 (3.80) 6.39) 5.66 (5.99 (3.14-6.6 (9.8) 6.95-12. 1990).13-9. Finding a measurable amount of cesium in the urine does not mean that the levels of cesium cause an adverse health effect.37) 4.16-8..35-11.77) 4.47) 4.09 (4.79) 6.51) 4.21-5.27 (6.27 (8.96-4.89-4.45-6. Komaromy-Hiller et al.64) 5.S.58 (6.22 (3.70) 7.30 (4.00 (8.72 (4.63-6.70) 6.67) 5.66-6.20-4.28) 7.29) 4.70 (7.09) 8.58 (4.13) 7.08-3.63 (4.48) 90th 7.35-7.43) 8.47) 6. 2005.44 (8.07 (5.65-4.07) 8.14-4.41) 4.37-3.41 (5.82) 7.28) 8.99-9.40) 6.84-9.44) 3.03) 6.56-10.42-4.43-6.20-8.67 (6.26 (3.3) 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 3.22) 6.63-6.63) 6.29-3.43 (8.21-3.81 (4.53) 6.16-8.62) 5.15) 95th 8.26-6.41-4.46 (7.56 (4.00-8.88-10.72) 4.05) 3.91) 4.00-10.29) 4.04) 6.9) 10.18 (7.00-4.22-11.13 (3.00-5.28 (5.77 (4.35 (4.74 (5. Urinary Cesium (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.38 (3. Minoia et al.3-15.40-5.33-8.3 (10.36-6.24 (3.60) 3.29) 5.47) 7.29-3. population results shown in this Report (Alimonti et al.30 (7.99) 4.0 (7.75 (7.23 (7.42 (5. 2004).30) 10.12 (3.93-7.24-10.06) 4.30-4.31-4.30 (3.33 (5.04) 5.68-11.91-7.10 (5.5) 9.79-5.20) 5.58) 8.05-3.02-4.44-9.84-11.8 (9.27-4.49) 3.85) 4.91) 5.97) 8.05 (4.17) 4.47) 6.83-7.39 (5.48-6.46-4.52-5.60 (3. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.46 (8.04-11.47 (4.50) 4.43-11.83-6.64 (4.91-9.20-4.98) 5.42-4.Metals Biomonitoring Information Urinary cesium levels reflect recent exposure.17 (6.13-9.98) 5.25) 4.97-4.4) 10.33 (5.91) 5.06) 5.44 (4.36-10.64) 4.92) 3.55 (3.90 (7.83) 8.1) 11.87-4.28 (4.41) 9.12-6.68) 3.0) Total 4.92 (5.27 (6.8) 10.86 (4.48) 7.21-4.17) 9.25) Selected percentiles ( 95% confidence interval) 50th 4.73 (3.77 (7.55) 4.19-3.64) 9. interval) 4.12) 3.46) 6.50) 4.84-9.31 (4.97-5.3 (9.07) 8.56) 4.59) 4.08 (6.43 (4.S.66 (5.06 (3.95-6.56) 3.95) 8.00) 6.91-6..85) 5.50) 4.5) 9.53) 3.6) 6.65 (6.41-7.16-5.10 (3.54 (4.14-7.35) 3.96) 4.75-11.2 (8.68 (4.63 (6.51 (3.55-5.95) 4.11 (5.27-6.38-7.5 (9.51 (3. Urinary cesium levels were similar in a group of forest fire fighters and residents living near the fire area (Wolfe et al.59-8.84-7.95 (5.74) 75th 5.61-3.56) 4.68) 6.15-11.3 (8.71) 6.05-4.99-9.96) 4.50 (5.35 (3.64-6.85-4.00-9.51 (4.8) 5.71 (7.10-4.53 (4.88-4.0) 884 682 618 568 667 723 821 1132 1074 Non-Hispanic blacks Non-Hispanic whites 206 Fourth National Report on Human Exposure to Environmental Chemicals .3) 11.14) 4.60-20.94 (5.30-4.99-4.08 (5.08) 4.S.78) 4.0) 7.2) 11.51 (4.54 (5. Using clinically submitted specimens.78) 4.07-4.03-5.87) 5.58) 3.18-6.14) 4.06 (5.41 (8.18) 8.62-8.17-4.00-5.05-3.50) 8.04-5.30) 10.50 (6. (2000) found urinary cesium levels that were slightly lower than those reported for the U.98 (7.77-5.84-7.98 (6.38) 10.2) 340 368 290 718 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 3.10) 7.14 (6.7) 10.38-12.43 (4.60-10.19-6.78 (3.51 (7.58-5.65-3.57) 3.03-6.74 (4.54 (3.34 (5.91 (5.96 (4.16) 5.64 (8.72-5.24-4.74) 3.43 (3.90-8. Two small studies of European populations reported urinary cesium levels similar to U.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 5.42 (4.73-4.02 (5.63 (7.50 (7.6 (9.20-4.50-5.08) 3.41 (4.82-4. 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.76-9.44-5.90-3.79 (5.81 (4. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.95) 10.15 (7.79) 4.87 (5.10 (3.42-6. and were also roughly similar to those in this Report.45 (4.38 (3.76-6.68) 4.08-7.08) 4. population from the National Health and Nutrition Examination Survey.2 (8.7) 10.47 (7.78 (3.11 (5.79) 9.7-12.

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

270-.420) .454 (.419) Selected percentiles ( 95% confidence interval) 50th .45 (1.294 (.305-.68 (1.330) .430-.460 (.430) . 01-02.570 (.380 (.308-.07.50 (1.390-.48) 1.16-1. respectively.350) 75th .16-1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.301 (.367 (.610 (.930) .590-.05 (.81) 1.372) .28 (1.343 (.430 (.12) 1.790-.28-2.270-.01-1.410 (.450) .377-.398) .388-.950-1.530) . Cobalt compounds are also used in manufacturing battery electrodes.910-1.S.583) .330 (.310 (.22-1.500 (.950 (. 0.890-1.940-1. hard metal (alloys of cobalt and tungsten carbide).52 (1.880 (.390 (.14) .487) .06 (.950 (.690-.469-.339 (. shiny.400-.680) .540) 1.428-.760 (.620-.515 (.379 (.760) .670-.290-.09 (.33 (1.330-. Cobalt occurs naturally in airborne dust.23-2.670-.543) .940-1.22) 1.540-.600 (.418 (.410-.15 (1.920-1.399) .360-.32) 1.26) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.980-1. The cobalt used in U.07 (.463-.16) 1.26-1.620-.640) .850-1.03-1.373-.99) 1.460) .690-.610-. and 03-04 are 0.12) 1.740 (.820 (.530 (. steel-belted radial tires.502) .580 (.09) .390 (.03) 1.380 (. and magnetic recording media.316 (. diamond-polishing wheels.01 (.820 (.393-.940 (.08-1.414) .17 (. and 0.338-.05) 1.550 (.960-1.430 (.465) . seawater.60 (1.07.73) 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 .32-2. Usual human exposure is from food sources.890) .300 (.950-1.660-.350 (.730) 1.570) . Medical uses include joint and dental prostheses and radioactive cobalt in cancer chemotherapy.26) 1.33-1.710) .300-.630 (.59 (1.24 (1.04-1.360-.405-.470) .313) .710) 1.386) .420 (. blue-colored pigments.01 (.17 (1.333-.581) .490-.650-.740-.259-.26) Total .850) .410 (.630-.310-.460) .570) .427-.350-.450-.53) 1.810) .42) 1.440-.480 (.16 (1.06 (.600) .340) .13) 1.430 (.480 (.48) 1.750 (.520 (.316-.355-.520-.550-.398 (.64) 1. It is emitted into the environment from burning coal and oil and car and truck exhaust.690 (.360-.370 (. It is also a component of porcelain enamel applied to steel bathroom fixtures.450) .340-.620) .46 (1.Metals Cobalt CAS No.890-1.09 (.364-. 208 Fourth National Report on Human Exposure to Environmental Chemicals .291-.03) 1.340 (.750 (.04 (.373) .359 (.900-1.523) .369 (.600-.04-1.700) .370-.810-.47) 1.320 (.08) .23) . population from the National Health and Nutrition Examination Survey.270-.17-1. and kitchenware.800-.564) .510) 1.450) .580 (.790) .56) 1.36) 1.700) . and inks.630 (.24 (.470 (.370-.29 (1.17 (1.930 (.348-.334) .460 (.570-.830-1.380-.374 (.900-1.670 (.890) 95th 1.39) 1.660) . and soil.750 (.81) 1.590) .350-.770) .810) .327-.352 (.370) .640) .394) .520) .870-1.410-.336-.570-.331-.20 (1.50) 1. Cobalt may be released into the systemic circulation of patients who receive joint prostheses that are Urinary Cobalt Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. Cobalt is used as a drying agent in paints.22 (1.980) .870 (.410 (.319) .820 (.850-1.370-.410) .404) .870 (.650 (.620-.461 (.371 (.280-.950) .67) 1.520 (.520-.390 (. see Data Analysis section) for Survey years 99-00.07-1.610) .417) .16 (1. 7440-48-4 General Information Cobalt is a magnetic element that occurs in nature either as a steel-gray.670 (.640) .560 (.496) .379 (.930-1.860 (.890-1. and fertilizers.520) .25-1.28 (1.03 (.47) 1.460-. hard metal or in combination with other elements.32 (1.431) .420) .390) .590 (.434 (.410) .47 (1. Among its many uses are manufacturing superalloys used in gas turbines in aircraft engines.880-1.75 (1.26-2.431) .03 (.410 (.500) .540-.550) 90th . industry is imported or obtained by recycling scrap metal that contains cobalt.519 (.15-1.424) .520-.520-.452 (.435 (.680 (. large appliances.65) 1.19) .660) .900) .740-.590-. Cobalt compounds are used as catalysts in producing oil and gas.16) 1.04) 1.32 (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 .580 (.06-1.02-1. and in synthesizing polyester and other materials.520 (.670 (.380-.285 (.350-. varnishes.480-.08.460) .44) 1.790 (.450) .490-.333-.410 (.499 (. interval) .28 (1.03) .S.650 (.430) .800-.680) .710 (.800) .410-.348-.450-.540-.850) 1.610) .920) 1.530-.520 (.340) .73) 1.14-1.840) .32) 1.900) .05 (.47 (1.416) .04-1.540-. automobile airbags.380 (.16 (.21) 1.37-1.01-2.00) .900) .07-1.375 (.340-.92) 1.750-.680 (.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 .

333-.73) 1.335 (.328) .428-.35) 1.455 (.362 (.49) 1. with pulmonary clearance half-lives of from one to two years (Hedge et al.964 (.10) Total .861 (.16 (.33) . 1979).363) .282-.14 (.468) .611) .533 (.534-.257-.346 (.599) .44 (.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 .727 (.329 (.378 (.301-.626-.952 (.348) . an essential human nutrient.529 (.50 (1.495 (.611) .392 (.04-1.905) .293 (.280-.29 (1.593) .353 (.358 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.513-.301) .388 (.29 (1.774 (.384) .857-1.304) .247 (.461) .503-.313-. 1994).Metals fabricated from cobalt alloys (Lhotka et al.425) .417 (.12 (.391) Selected percentiles ( 95% confidence interval) 50th .326-.10-1.393 (.851 (.243-.435-.435 (.667-1. Elimination reflects a multi-compartmental model dominated by compartments with half-lives on the order of several hours to a week.417) .804) 1.600-.313-.990) .700 (.402 (.391 (.00 (. Smith et al.300) .737 (.847) .310) .29) 1.24) .425-.777-. Cobalt is absorbed by oral and pulmonary routes.975 (.387) .879-1.550-.349) .290 (.728) .462) .963-1. and to a lesser extent.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 .938-1.369 (..444 (.976 (.660-.694) .911-1. Recent inhalation exposure to soluble cobalt compounds can be monitored by measuring cobalt in urine or blood (Lison et al.251-.304-.36) 1.278 (.380-.704-.683-.28) 1.297) .442-.481) 90th .738 (.505) .488) .272-.400 (.368 (.313-.850 (.515 (.248-.781-1. cobalt is excreted predominantly in the urine.296) . in the feces.234 (.513 (.273 (.06 (.297-.983-1.361 (.738 (.537 (.615) .644 (.342-.12-1.343 (.54) 1.634-.00 (.833-1.386 (.10) .396) .689 (.736-.306) 75th ..278-.785) .313-.361-.11-1.960 (.60) 1.938) .581) .328 (.277-.479) .963-1.365-.362-.638-1.487-.594) .744) 1.753-.393-.728 (.00) .259) .S.313-.792 (.585) . interval) .647) . Lung retention of relatively insoluble cobalt compounds such as cobalt oxide may be prolonged.25 (.00 (.313 (.917) .895-1.608 (. Once absorbed and distributed in the body. respectively. Human studies with 60Co administered as soluble cobalt chloride have reported oral absorption ranging from approximately 1 to 25 % (Smith et al.50) 1.352) .630-.409) .421) .83) 1.723 (.963) .640) .508-.259-.396) .302-.829) .937 (.513) .426 (.872 (.281) .404-.826-1.355) . Exposure in the workplace may come from electroplating. Cobalt constitutes 4% by weight of vitamin B-12 (cobalamin).361-.16) .861-1.439) .394) .929) .368) .27) 1.662) .60) 1.595) .291 (.616-.309) .750) .543) .352 (.327 (.250) .457) .949) .303-.333 (.850-1.271 (.547 (.844 (.500-. 1972).407) .324) .471 (. Urinary Cobalt (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.259 (.740-1.606 (.429) 1.290 (.257 (.574-.381) .328 (.331-.57) 1.327-.333-.324-. A nutritional requirement for cobalt other than that contained within dietary cobalamin has not been established.467-.372) .786-.344-.15) 1.560-.760-1. 1994.452-.895-1..306 (.983) .29) .237-.792-1.408 (.932-1.469-.294-.679-.419) .388 (.598 (.16 (1.361 (.434-.898 (.339-.955) .352 (.457-..963) .449-.829-1.333-.781) 95th 1.824 (.955) .319-..248-.334) .561) .27) 1.591 (.10 (.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 .582-.289) .00) .707) .630-.407 (.542 (. refining or processing alloys.433) .02 (.55) .353-.463-.479-. Workplace standards and guidelines for external air exposure to cobalt and several of its compounds have been established by OSHA and ACGIH.838 (.279) .471-.298 (.25 (.362) ..00 (.286) .256-.365) .360) .04 (. A portion of cobalt retained for long periods is concentrated in the liver.23 (1.09) 1.523 (.552 (.317 (.756 (.239-.554 (.290 (.03 (.554 (.449) .900-1.476-.821 (.733-1.36) 1.275-.378-.30 (1.337 (.523 (. but with a minor fraction (10-15 %) exhibiting a half-life of several years (Mosconi et al.990-1.848 (. using hard metal cutting tools.16 (.830 (.35) . or using diamond-polishing wheels that contain cobalt metal.667-1.438) .323) .19) .282 (.457 (.563-.842) .00-1.10) 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 .691 (.337) .378-. 2003).750-.29 (1. 1972).562) .753) 1.03-1.33) 1.316 (.548 (.500-. population from the National Health and Nutrition Examination Survey.703-.534 (.632-.296-.757-1.382-.376 (.279 (.314 (.522) .635 (.50) 1.700 (.673-.669) .215-.500 (.17) .378-.343-.11-1.708) .475 (.274-.562) .609) .329-.268 (.15 (.275-.821-3.487-.368) .471-.

Krause et al. White and Sabbioni.. Am J Med 1972. population (CDC. Iavicoli et al. Cobalt-beer cardiomyopathy. Shirakawa et al. MacDonald et al.. 2001. Lisi. Cugell DW. 1994. 2005. References Alexander CS...53:395417. Inhalation toxicity and carcinogenicity studies of cobalt sulfate. Information about external exposure (i.. Hailey JR. Available at URL: http://www.gov/toxpro2. 2003) and produced lung cancer in rats and mice after chronic inhalation (Bucher et al. Morgan WKC..gov/ exposurereport/. Exposure to soluble cobalt salts will produce proportionately higher urinary levels because they are absorbed better. 1998). Toxicol Sci 1999.43(4):299-303. 1992).cdc. Cobalt compounds appear to stimulate erythropoietin production and were formerly used in the treatment of anemia (Goldberg et al. Biomonitoring Information Urinary levels of cobalt decline rapidly within 24 hours after exposure ceases (Alexandersson et al.49:56-67. Atlanta (GA).50(13):95-104.. An industry-wide study of hard metal workers in France observed an increased mortality from lung cancer (Moulin et al. 2003.cdc. 2005 [online]. Urinary measurements mainly reflect recent exposure.. Small studies of patients with hip replacements using metal alloy prostheses reported increased urinary cobalt concentrations. The ACGIH biological exposure index (BEI) for inorganic forms of cobalt (except insoluble cobalt oxides) is 15 mg/L. 1972). Swennen et al. IARC has classified cobalt metal with tungsten carbide and other soluble cobalt salts as possibly carcinogenic to humans.. Third National Report on Human Exposure to Environmental Chemicals.. has been associated with exposure to dusts that contain cobalt..html. 1993). Pharmaceutical preparations of cobalt used in the past as hematinics were associated with the development of overt hypothyroidism (Kriss et al. Lauwerys and Hoet. 1999). an interstitial lung disorder with findings that range from alveolitis to pulmonary fibrosis.. 1988). 1994. environmental levels) and health effects is available from ATSDR at: http://www. Smaller population surveys of European adults reported urinary cobalt levels that were roughly similar U.. Bucher JR.. Occupational exposure to cobaltcontaining dusts has caused occupational asthma (Pisati and Zedda. although substantial occupational exposures have produced elevated urinary levels for many weeks... Alexandersson R. Roycroft JR.. with mean levels that were about 15-20 times higher than in the general U. and this caused outbreaks of cardiomyopathy among heavy drinkers in the mid-1960’s (Alexander et al. biological levels and health effects following exposure to soluble or insoluble cobalt compounds in cobalt blue dyes. Daniel et al. Biomonitoring studies on levels of cobalt provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of cobalt than are found in the general population. Dunstan et al. 1998). not to imply that the BEI is a safe level for general population exposure.atsdr. Rubin A. A clinical and pathological study of twenty-eight cases. Linnainmaa and Kiilunen.e. 210 2006. 2003. Grumbein SL. For workers exposed to cobalt in the air. Sills RC. Lison et al. Perkins DG. Case reports have also suggested a link between occupational cobalt exposure and cardiomyopathy (Jarvis et al. Persons with occupational exposure to cobalt often have urinary cobalt levels that are many times higher than those of the general population. A 1982-1992 surveillance programme on Danish pottery painters. Thomassen et al. Correlations between air exposure levels and urinary cobalt levels in hard metal fabricators are well documented (Ichikawa et al.. “Hard metal” disease. A subclinical decrease in thyroid production was observed in a study of cobalt production workers (Swennen et al. 1988). 1997. 2003). Cobalt compounds are a recognized cause of allergic contact dermatitis (Dickel et al. The respiratory Fourth National Report on Human Exposure to Environmental Chemicals . 1990). 1989). Cobalt was once added as a foaming agent to beer. 1994). 2001. 2005. a distinction is made between soluble and insoluble (oxides and metallic) cobalt (Christensen and Poulsen. 1993).Metals Toxic effects of cobalt have been encountered in workplace settings. population results in this Report (Kristiansen et al. 2001.. usually in combination with tungsten carbide (Cugell et al. Centers for Disease Control and Prevention (CDC). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1997).. 2001). Sci Total Environ 1994. Poulsen OM. 1955). et al.S. 4/3/08 Christensen JM. Haseman JK. 2006. 1985.. Finding a measurable amount of cobalt in the urine does not mean that the levels of cobalt cause an adverse health effect... Information about the BEI is provided here for comparison. Arch Environ Health 1988.S. The extent to which cobalt exposure alone causes interstitial lung disease is unknown (Linna et al... Cobalt compounds elicited numerous genotoxic effects in both in vitro and in vivo assays (De Boeck et al. Blood and urinary concentrations as estimators of cobalt exposure.

Toxic trace element reference levels in blood and urine: influence of gender and lifestyle factors. Biological monitoring of workers exposed to cobalt metal. et al. Long-term clearance of inhaled 60Co. Outcome of occupational asthma due to cobalt hypersensitivity. HoffmannB. Metal ion levels after metal-on-metal proximal femoral replacements: a 30-year follow-up. Sabbioni E. X. De Boeck M. Buchet JP. Pradhan C. Occupationallyinduced “isolated cobalt sensitization. Health Phys 1979. Unwin P. J Bone Joint Surg Br 2006. Iversen BS. Lasfargues G. Thomassen H. Kusaka Y. Gross RT. Cannon SR.58(10):631-634. Meyer zum Buschenfelde K-H. et al. 3rd ed. Health Phys 1972. et al. Arch Intern Med 1990. Pisati G.45:246-247. Heki S. Bacis M. Co-sensitivity between cobalt and other transition metals. Oksa P.Metals effects of cobalt. J Rheumatol 2001. Occup Environ Med 2001. Boca Raton (FL): Lewis Publishers. Cobalt and antimony: genotoxicity and carcinogenicity. Contact Dermatitis 2003. A report of two cases from mineral assay laboratories and a review of the literature.150(1-3):167-171. Bunn HF. Ghat IS. Respiratory health of cobalt production workers. Lauwerys RB.22:359367. oxides. Iavicoli I. Weber A. Hoet P. Am J Ind Med 2003. Vitali MT. Occup Environ Med 1994. Kuska Y. Ichikawa Y. Carnes WH. Cresti R. Schank M. a study of 13 elements in blood and urine of a United Kingdom population. Salvatori S. Falcone G. Lison D.55(4):269-276. Goto S. Robinson C. Thabe H. Mosconi G. Romazini S. Kristiansen J. Alessandrelli M. The effect of the diameter of metal-on-metal bearings on systemic exposure to cobalt and chromium.(1-3):133-139. Int Arch Occup Environ Health. et al.21(2):189-195. Cobalt cardiomyopathy.50(9):835-842. DeSantis V. Biological monitoring of cobalt exposure based on cobalt concentrations in blood and urine. Cobalt excretion in urine: results of a study on workers producing diamond grinding tools and on a control group. Lison D. Fourth National Report on Human Exposure to Environmental Chemicals 211 . Jarvis JQ. cobalt salts. Zobelein P. Moulin JJ. Clin Orthop Relat Res 2003. Bozec C. Dunning SP.36:732-734.28(5):1121-1128. Edmonds CJ. Sci Total Environ 1998. Dunstan E.157:117121.533:135-152. Epidemiological survey of workers exposed to cobalt oxides. J Occup Med 1992. Science 1988. Laippala P. Hedge AG.88(4):443448. Shirakawa T. Wild P. Hypothyroidism and thyroid hyperplasia in patients treated with cobalt JAMA 1955. Regulation of the erythropoietin gene: evidence that the oxygen sensor is a heme protein. Zedda S. Sabbioni E.204:147-160. Sabbioni E. Urinary cobalt as a measure of exposure in the wet sharpening of hard metal and satellite blades. Int Arch Occup Environ Health 1997. Schramel P. Four-year study of cobalt and chromium blood levels in patients managed with two different metal-on-metal total hip replacements. Weyher I. Trace element reference values in tissues from inhabitants of the European Union. Lhotka C. Meier R. Christensen JM.150. et al. Linna A.44:124-132. Sanghrajka AP.148:241-248.87(5):628-631. Chest 1989. Szekeres T.34:620-626.” Contact Dermatitis 2001. Sci Total Environ 1994. Kriss JP. Kraus T. Cleland D. Thakker DM. Am J Epidemiol 1998. The release of metals from metal-onmetal surface arthroplasty of the hip. Zhuber K. and hard metal dust.20(1):25-31. Rorabeck CH. Kiilunen M. Angerer J. J Bone Joint Surg Br 2005.216:253-270.242:1412-1415. Palmroos P. Sci Total Environ 1997. Uitti J. Peltier A. Leghissa P. Fujimura N.95:29-37. White MA. 2001. Molders J. Smith T. J Trace Elem Med Biol 2006. Roto P. Sci Total Environ 1994. Metal-on-metal versus polyethylene in hip arthroplasty: a randomized clinical trial. Blunn G. Schaller KH. Stanescu D. Chess DG. Daniel J. Zweymuller K. Lauwerys R. Lisi P. Br J Ind Med 1993. Dickel H. Kirsch-Volders M. Swennen B. and cobalt metals.150:177-183. Swennen B. Lauwerys R. McMinn DJ.406:282-296. et al. Absorption and retention of cobalt in man by whole-body counting. Buchet JP. Industrial Chemical Exposure: Guidelines for Biological Monitoring. Lison D. McCalden RW. Kato M. Tilley S. Goldberg MA. salt. Barnaby CF. Occupational asthma from cobalt sensitivity in workers exposed to hard metal dust.51(7):447450. Hoher T. Lung cancer risk in hard-metal workers. Radulescu M. Salama A. Mutat Res 2003. Ziaee H. Goto S. Bourne RB.48:172-173. Hammon E. Cobalt-specific T lymphocytes in synovial tissue after an allergic reaction to cobalt alloy joint prosthesis. MacDonald SJ. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds. J Orthop Res 2003. Steffan I. Linnainmaa M.69(3):193-200. Diepgen TL. 1985.

40-2. 212 Fourth National Report on Human Exposure to Environmental Chemicals .75 (1.40-3.34-1.20-3.28.70-1.70) 3.89) 1.30-1.50) 75th 2.25 (1.10-2.50-1.60) 2.60 (3.50) 2. plastics.71-1.30-2.50) 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 2.20) 3.50-5.10-2.g.10-8.50-3.00-2.30-1.20 (2.80) 1.50 (1.50 (1.00) 1.10) 5.86) 1.60 (4.60) 1.80 (4.50) 3.00) 2.20-1.30-1.60 (2.60-6.70) 1.80) 2. brass. 7439-92-1 General Information Elemental lead is a soft.80) 1.30 (2. interval) 1.40 (1.80 (1.70 (2.49-1.40) 2.30 (1.10) 3.90) 5.30 (2. see Data Analysis section) for Survey years 99-00.60 (3.40) 3.90 (2.40 (3.30-5.70-2.00) 1.20 (3.50) 2.30) 2.30 (4.60) 3.30 (2.40-3.60 (2.899-.40) 1.70) 1.80) 1.90 (4.10 (1.30 (1.00-5.30 (2.60) 2.90) 2.00) 1.01 (1.36-1.10-1.00) 4.50-4.00-6.65 (1.3.51 (1.50) 7.10 (2.30) 2.39-1.10-2.50 (2.23 (1.00-4.90 (2. Elemental lead can be combined with other elements to form inorganic and organic compounds.70) 3.50 (2.60) 4.30-1.10-2.70) 4.30-6.900 (.20) 90th 3.69) 1.90) 1.20-4.30-2. and 03-04 are 0.20) 2.40) 1.20-3.50 (2.60-1.36) 1.20-3.00) 3.40 (5.70 (3.50-4.90) 3.10-1.00-4.10-3.60 (1.40 (2. and for radiation shielding.20 (3.60-3.60) 1.60) 5.900-1.40-1.30 (3.30) 2.90) 2.37-1.45 (1.77 (1.87 (1.40-6.3.50-5.80 (4.40-1.25) 1.20 (3.20 (4.37 (1.80-4.80 (1.70) 1.30 (4.30) 95th 5.70-1.50-6.60) 4.60) 2.80 (1. Lead was used in plumbing for centuries and may still be present.20 (3.36-1.00 (6.51) 1.946 (.30-2.83 (1.70-5.50 (2.50 (1.60) 3.52 (1. population from the National Health and Nutrition Examination Survey.48) 1.90 (3.00) 2.20 (1.10-4.00) 5.90-2.56 (1.20) 3.80) 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 1.20 (1.40-1.52-1.70 (3.14-1.70 (1.60) 3.60) 1.43) 1.50) 5.10) 2.50) 1.60) 5.942 (.80 (2.81) 1. blue-gray metal that occurs naturally in soils and rocks.90 (3.90 (3.60-4.70-3.14-1.90) 2.96-2.00-1.20 (1. leaded glass.10-6.14-1.80-3.46 (1. Aerosolized lead is either inhaled or ingested after it is deposited on surfaces and food crops.10) 1.20) 1.20 (3.80-4.70-2.10-3.43 (1.30-1.80 (3.10-1.25 (1.30) 2742 2268 2085 1842 2219 2293 2716 3806 3478 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.50) 4.50-1.30 (2.00-4.30 (1.20 (3.00 (5.20) .60 (2.70) 4.30 (4.90 (1.70-4.70) 4.60) 2.12-1.10-4.40 (1.40-6.00 (3.60 (1. such as lead phosphate and tetraethyl lead. respectively.60-1.50 (4.20-2.50-1.40) 4. 0.60) 3.00) 3.20) 3.70 (5.70) 4. the main source of lead exposure for the general U.10-3.90-2.878-1.00) 4.80 (5.50-2.66) 1.40) 5.80) 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.40-5.69 (1.80 (1.09) 1.70) 1.90) 1.90-4.60 (1.90-3. Since lead has been eliminated from gasoline.70-6.70) 2.10 (1. ammunition.10 (3.80) 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 2.30-4.30-2.72) Selected percentiles ( 95% confidence interval) 50th 1. Lead has a variety of uses in manufacturing: storage batteries.60 (1.62-1.30-1.43-1.40-4.00) 1. Lead is most often mined from ores or recycled from scrap metal or batteries.50 (4.75-2.40 (1. and 0.78 (1.50 (3.10 (2.37 (1.90-4.00) 2.43) 1.90 (1.90-2.90) 2.30 (2.40-2.90-4.70-2.60) 4.900 (.60 (2.62) 1.70 (1.90) 1. malleable.87) 1.45-1.60-1. Before the 1980’s. In the past.10 (2.91) 1.60-2.60 (1.39) 1.80) 2.70-1.40-3. 01-02.00 (4.80-3. solders.50-2.32-1.40 (4.02) 1.70 (2.60) 2.00) 1.70) 1.80 (1.90 (3.30 (2.40 (2.50) 1.70) 3.30) 1.80 (2.90 (3. population was aerosolized lead emitted from combustion engines that used leaded gasoline.S.70 (1.60 (2.75) 1.80-2.90) 2. ceramic glazes.60-4.10) 2.50 (1. bronze).40-1.90-4.80) 3.00) 6.69) 1.50-1.800-1.20 (3.50) 5.55 (1.00 (4.00 (1.20) 4.20 (1.40-1.60) 1.80) 2.55-1.S.80-3.22 (1.60 (3.50) 1.20) 3.30 (1.80 (2.20 (2.66 (1.90-2.10) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80-3.20-3.69 (1.60) 1.17) .00) . metal alloys (e.40) Total 1.10-2.10) 3.10-2.50-3.62 (1.10) 3.53) 1.986) .40) 2.20) 4.40-1.00) 2.10) 4.60) 4.40 (1.60-1.00 (1.20 (1. lead was added to gasoline and residential paints and used in soldering the seams of food cans.20) 5.75-1.80-4.50-2. antique-molded or cast ornaments.52-1.40) 2.80-5.90-6.70 (1.20-1.40-2.55-1.40) 2.04-1.60 (2.50-1.68-1.80 (5.50) 1.80 (1.40) 1.10 (1.31) 1.43 (1.50 (2.20-6.60 (3. dense.80) 2.60 (1.50) 4.70 (2.95) 1.60-2.90) 3.Metals Lead CAS No.20-2.93-2.10) 1.10 (4.10-3.50 (3.30) 5.00 (2.60 (1.00-1.19 (1.32-1.10-6.50-2.

20-2.14-1.600) .70-2.90-2.20 (2. 0.00) 1.20 (1. In the blood.600 (. the primary source of exposure in children is from deteriorated lead-based paint and the resulting dust and soil contamination (Manton et al.915-1.27) 1.579-.60 (1.960-1.695 (.70) 3.10) 2.940 (.630 (.70) 1.20) . or after soluble lead compounds are ingested.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 1.50 (2. lead-contaminated dust in indoor firing ranges.40 (1.40) 1. battery and radiator manufacturing) and recreational sources.810-1.70 (1.19 (1.23-4.30-2.70 (2.1.50-1.70 (2.44-2.731 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2007.22) 1.620 (.700-1.573 (.620) 1.90) 2.30-1.628) 1.10) .80) 2.80) 1.556-.75) 3.35 (.90 (1.70) 1.89) 2.50) 3.40-1.40-5. and contact with soil. Lead is absorbed into the body after fine lead particulates or fumes are inhaled. Small amounts of environmental lead also may result from burning fossil fuels (ATSDR.90-2.51) 884 683 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.04-2.50) 1.800 (.701) .00 (.1.80) 2.40-1.677 (.10 (.66 (2.40) 1.00) 2. Children may also be exposed to lead brought into the home on the work clothes of adults whose work involves lead.690) 75th 1.10-1.33 (2.718) .86 (1.857) .52-1.20-1.616) .20) 1.688 (.02 (.600-.20-2.600-.560-.13-3.540-.30) .59) 1.10 (1.600-.86-2. 01-02.50 (1.60 (1.20 (1.30) 1.50 (1.80) 3.604 (.640 (.50) 1.00-1.00-1.900-1.18-1.30) 2.10-1.800 (.600-.671-.822-1.49 (1.600-.680-. CDC.10-1..730 (.506-.40) 2.564 (.00) .73 (1.80 (1.40) 1.g.50 (2.11 (1.90) 2.20 (2.30-5.900) .752 (.651) .50-2.40) 2. 2000).80-2.00) .591 (.60-1.729-.60 (2.20) 1.40 (1.625 (.10-5.41) 2.00 (1.80-3.708-.745-.800) .749) .558 (.40 (1.S.960 (.66 (2.30-3. which is the site of approximately Urinary Lead Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.80-2.613) .59-2.820-1.50) 1.40-1.86) 1.75) 4.32 (1.70 (2.800-1.90) 1.10-3.815 (.70-3.700) .800) . older plumbing systems with leaded pipes or lead soldered connections.828) Selected percentiles ( 95% confidence interval) 50th .62) Total .700 (.20 (1.900 (.900 (.30) 2.80) 3. dust.10 (1.753 (.13) .20) . and 0.70) 2.70) 3.20) 1.660) ..800) .00 (2.757-.10) 1.862) .920 (.920 (.800 (. absorbed lead is bound to erythrocytes and then is distributed initially to multiple soft tissues and eventually into bone.17 (1.09) 1.910-.30 (1.64) 2. 1991).90-4.80) 2.24-1.590 (.650) 1.600 (.30) 1.00-2.700 (.31 (1.818) .700-.480-.535-.00-2.90-2.931) .595-. bullet fragments retained in human tissue.680) . Fourth National Report on Human Exposure to Environmental Chemicals 213 .900-1.30) 1.955-1.808 (.900) .30-1.20-1.97) 4.30-1.20) .900 (.23) .20 (1.82 (1.840 (.10 (. stained glass framing.600) .640-.21 (2.50) 2. interval) . pewter utensils and drinking vessels.941) .90 (2.691-.579-.20 (1.30) 1227 1335 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 1.790 (.27 (1.40-2.700 (.78-2.90 (2.700 (.50-2.80) 1.78-2.900) .40-3.60-2.990) 1.60) 2.72) 1.900) . Approximately half of the absorbed lead may be incorporated into bone.700 (.49) 340 368 290 719 762 725 1406 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .40-1.90 (2.60-3.30 (2.900-1.40) 2.00) .800) .833-1.04) 2.710-1.12) 90th 2.900) .00-2.605) .30 (3.52-1.90-2.80 (2.33-2.10 (1.800-.04 (.700) 1.33.06) .700 (.800-1. lead-containing folk remedies and cosmetics.82 (2.10-3.935) 1. population from the National Health and Nutrition Examination Survey.10) . respectively.90-3.10-1.642 (.766 (.04) .850 (.641-.60 (1.785) .03-2.700-.540 (.70 (2.31-3. or water contaminated by mining or smelting operations.900) .661-.970-1.960-1.710-.80) 2.553-.14 (1.50 (2.700-.700-.833 (.986) .30) 1.923 (.86) 95th 2.70) 1.04 (. Less common sources of incidental or unique lead exposure are numerous: lead-glazed ceramic pottery.10) 2.795 (.90 (1.636 (.80 (1.80) 2.20 (3.30) 1.738) .00 (1.50-3.20 (1. and 03-04 are 0. see Data Analysis section) for Survey years 99-00.10 (.90 (1.29 (2.90) 2.30-1.659 (.91) 2.90-3.60-2.10-3.14 (1.07-1.674) 1.589-. lead-based painted surfaces undergoing renovation or demolition.10-1.526-.60 (1.680-.00 (1.62-4.800) . However.848 (.07 (.50) 2.40) 3.40 (2.40) 1.500-.00 (1.30) 2.20) .00) 2. imported children’s trinkets and toys.Metals occupational (e.40 (2.40 (1.773) .40) 1.80) 1.50-2.40 (1.52 (1.00) .02) 1.700-. 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.570-.60-3.637-.03 (1.29) 2.40 (2.20-1.11) 2.580-.990) 2.572-.40) 2.00-1.800 (.900-1.78-2.40 (2.20 (2.610 (.800-.625-.10 (1.

For instance.701) .20) .56 (1.05 (1.89-5.681-.41-1.31) 1.765) .588-.623 (.492-.53) 1.27 (1. Schwartz.404 (.709 (.98) 2.03) 1.00 (1. 1993).644 (.50-2.774 (. 1996).17-1.15) 1.65 (1.655-.83 (2.460-.700-.18) 1.601-.Metals 90% of the body lead burden in most adults.05 (.69 (1.48 (1.971 (.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 .11 (1.51) 1.608-.721 (.01 (.25-1.08) .43 (1.46 (2.623 (.638 (.03 (. abdominal pain.06 (1.15-2.375 (.50-2.618 (.617-.71 (1.49 (1.61) 1.946-1.432 (.926 (.870 (.08-2. and through binding to ion channels and regulatory proteins.61) 1.625 (. and iron.25-1.990 (.23 (1.676) . with a half-life of years to decades.64) 95th 2.667) .583-.657) 1.88) 1.29 (1.59-3.645-.73) 2.04-3.918-1.66 (1.622 (.790) . CDC.10) 1.404-.66 (1.89-2.20) .718) .645-.0) 3.644) .79) 1.400) .659-.588-.18) 1.981-1.938-1.28) 2.33) 1. zinc.977) 1.461) .01) . BLLs near 10 µg/dL can affect blood pressure in adults and neurodevelopment in children (Bellinger.988 (.793-1.621 (.469 (.72-2.70 (1.03) 2.02-1.900 (. 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. and paralysis.615 (.658 (.39-1.605-.94-2. 2007).14 (1.718) 1.592-.679) 1.701 (.62) 2.670) 1.88) 2.739) .18 (1.677) .758) .37-1.44 (1.88 (1.707 (.940 (.639 (. 2003.87) 1.85) 1.50 (1.18) .722 (.11) .06 (.65-2. In 1991.47 (1.98-2.19) 1.933) .63) 4.96 (1.603 (.551-.722 (.635 (.03) 2. 1995).06) .667-.882-1.569 (.698) . based on prospective population studies.72-2.594-.33-1.914 (.11 (.655) .742) .712 (.19-5.97-18. population from the National Health and Nutrition Examination Survey.342-.02) 1.734) .55 (1.97) 1.496 (.15-2.682) .03 (.652 (.61) 3.893) .50-2.541-. Lead can cross the placenta and enter the developing fetal brain.33) 2.38 (2.55 (1.64-2.593 (.03-2.725) .14) 1.31 (1.876-1. and approximately 40 to 70% of lead in blood comes from the skeleton in environmentally exposed adults (Smith et al.31 (1.88-2.22) 1. Nash et al.85-2.11 (1.988-1. 1995.702) .535) . The skeleton acts as a storage depot.98 (1.64) 2.648 (.43) 1.920-1.52) 1. seizures.918 (. scant amounts are lost through sweat.72) .07-1.632 (.781-1..38 (2.841-1.606-.20-3.62-3.71-2.85-2.04) 2.763) .22-2.09) 1.35) 2.09-1.00 (.730) 1.83) 1.962 (. and nails (Leggett.85 (1.559-. Approximately 70% of lead excretion occurs via the urine.78 (2.755 (.33 (1.992-1.612-.853-1.914-1.06) 1.92) 2.37-1.79 (1.00 (1.S.07 (.693 (. through the inhibition of certain enzymes.67-4.603-.957-1.997-1.31) 1.62-2..609 (.09-1.26) 2.46 (1.742) Selected percentiles ( 95% confidence interval) 50th .22) 1. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.649 (.44) 1. hair.698) .28-1.963-1.702-.914 (.641 (.681-.97) 1.26) Total . The toxic effects of lead result from its interference with the physiologic actions of calcium.03) 1.34-1.78-4.710) .41) .77) 2.404 (.917-1.851) .07) .36-2.43-1.862-.41 (1. 2004.668-.654) .64 (1.56-3. 1991.662) 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 1.594-.812-1.43 (2.11) 1.12-1.720 (.579-.79) 2.561-.22) .51 (1.696 (.933-1.731-. O’Flaherty.44 (1.607-. kidney injury.667-.50-1.898) .47) 1.703) .753) .22-1.45 (1.828-1.677 (. Additional mechanisms include generating reactive oxygen species and altering gene expression (ATSDR.979 (. Lead is cleared from the blood and soft tissues with a half-life of 1 to 2 months and more slowly from the skeleton.686) .15-3.615 (.40-1.828) .18) 2.608 (.05-1.655) 75th 1.73-2.383-.05-1.74 (1.11-1.639) .17 (.529-. Large amounts of lead in the body can cause anemia.677-.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 .975-1.62-1.746) .671 (.604-.15) 1.82) 1.09-1.63) 1.639 (.679-.53-1.56) 3.708 (.68 (1. interval) .00) .38 (2.603-.510-.88) 2.75 (2.43) 2.587-.61) 1.887 (.47 (2.408-.810 (.03) .03) 90th 1.97 (1.720 (.586-.00 (1.24 (1.10 (1.800-.508) . encephalopathy.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 .436) .. BLLs and associated toxic effects differ in children and adults.03 (.94 (1.688) .50) 1.673) .683-.428) .86 (1. Staessen et al.31 (2.938 (.61) 1.992-1.03 (1.571-.838) .08) . Equilibrated blood lead levels (BLLs) after chronic intake are associated with certain toxic effects.725) .11 (.66) 2.10 (.639 (.796-1.52 (1.75-2.633 (.380-. 1993.702) .28) .56-2.58) 1. with lesser amounts eliminated via the feces.03) .571-.

1998). the geometric mean BLL was 3. A general population survey of adults Germany in 1998 reported a geometric mean blood lead concentration of 3. IARC considers inorganic lead compounds probable human carcinogens. NTP considers lead and its compounds reasonably anticipated to be human carcinogens. Fourth National Report on Human Exposure to Environmental Chemicals 215 . 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. A decrease in BLLs is evident also in adult NHANES results reported over past decades (CDC. 2001).4% in NHANES 1999-2004. Schwartz et al.4% of children had BLLs of 10µg/dL or higher (CDC. Bellinger 2005. almost double the geometric mean of 1.html. and low family income (CDC. premature delivery. 1999). Jones et al. adults in the 19992000 NHANES sample (Apostoli et al.2 µg/dL in males and 3. environmental levels) and health effects is available from ATSDR at: http://www.75 µg/dL in U. 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. the prevalence rate has declined annually since 1994 (CDC. Muntner et al. 1984. Overall. respectively..cdc. 2002.S. 1996.3 million children tested had BLLs of 10 mg/dL or higher (http://www. Payton et al. The Adult Blood Lead Epidemiology and Surveillance program has tracked BLLs reported by states for mostly for occupational but also for non-occupational exposure in U.S.. 1996. Schwartz. 2009).5 per 100. 2003. Jones et al (2009) showed that the prevalence of BLLs of 10 µg/dL or greater decreased from 8. BLLs reflect both recent intake and equilibration with stored lead in other tissues...000 adults. BLLs greater than 10 µg/dL continue to be more prevalent among children with known risk factors.9 µg/dL) and percentage of children with BLLs greater than 10 µg/dL (1.. Borja-Aburto et al. 2007).e. 2003).cdc. particularly in the skeleton. 1995) and associations between increased bone lead concentrations and blood pressure (Hu et al.atsdr. Korrick et al. approximately 11. 1999). and spontaneous abortion (Baghurst et al. though there is greater individual variation in urine lead than in blood and greater potential for contamination.. High dose occupational lead exposure. including minority race or ethnicity. 2000). adult residents.. Pirkle et al.000 higher-risk children and adolescents who were tested from 2001 to 2002 at an urban medical center had higher BLLs than the NHANES sample...6% in NHANES 1988-1991 to 1... Information about external exposure (i.0 µg/dL in females (Soldin et al. Urine levels may reflect recently absorbed lead. Low level environmental lead exposure may be associated with small decrements in renal function (Kim et al. Lanphear et al. 1991. 2000). 2003. More recently. higher than 100-200 µg/dL).. 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. reduce sperm count.6%) were lower than those from NHANES 1991-1994. 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. 2005a).S. 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. adult population has similar or slightly lower BLLs than adults in other developed nations (CDC. 2005b). 2005b. However.. EPA. urban residence.. 2002). 2003. Recent studies have suggested that neurodevelopmental effects may occur at BLLs lower than 10 µg/dL (Canfield et al. Biomonitoring Information Blood lead measurement is the preferred method of evaluating lead exposure and its human health effects. Telisman et al. seizures.S.21% of approximately 3.gov/toxpro2. may alter sperm morphology.S. Many animal studies have established the multiple neurotoxic effects of lead (ATSDR. 2006)..S..7 µg/dL and 4. In occupationally exposed adults. when the geometric mean BLL was 2. residing in housing built before the 1950’s. adults in the 1999-2000 NHANES sample. which is an 84% decline. 1987.. Staessen et al. For example. lead in women may be associated with hypertension during pregnancy. Data submitted through state public health programs from 2006 showed that 1.. and organic lead compounds not classifiable with respect to human carcinogenicity..07 µg/dL (Becker et al.Metals µg/dL or higher as the level of concern in children. 2006). CDC. 1996. usually with BLLs greater than 40 mg/dL. Temporal declines in children’s BLLs have been found in other developed countries (Wilhelm et al.gov/nceh/lead/surv/database/State_ Confirmed_byYear_1997_to_2006... 1995. and peripheral neuropathy generally occurring at much higher levels (e.. 1994). At low environmental exposures. Both drinking water and ambient air standards for lead have been established by the U. with overt encephalopathy. and decrease fertility (Alexander et al.. the national prevalence rate for adults with BLLs 25 mg/dL or higher was 7.g. both the geometric mean (1. 2002a).xls). The U. Surveillance data reported by U.

Kaus S. Baghurst PA. Rotnitzky A. Atlanta (GA). Checkoway H. Am J Epidemiol 1999. Available from URL: http://www. Reese YR.1542/peds:2007-3608. Brody DJ. Weiss ST.10:43-50. Canfield RL. Lead and hypertension in a sample of middle-aged women.101(7):598-616. Trends in blood lead levels and blood lead testing among US children aged 1 to 5 yeas.54(20):513-516. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. Available at URL: http://www. et al. Auinger P. Kim R. Stanek KL. Environ Res 2000. Batuman V. Birth Defects Research (Part A). Hertz-Picciotto I. Angle CR. 2003-2004. Cox C. 4/14/09 Centers for Disease Control and Prevention (CDC).87:1-471. Farias P. 4/14/09 Alexander BH. Age-specific kinetic model of lead metal in humans. Sparrow D. Public Health Rep 2000. Speizer FE. Lead. German Environmental Survey 1998 (GerES III): environmental pollutants in blood of the German population. Hu H. A longitudinal study of low-level lead exposure and impairment of renal function: the Normative Aging Study. Ga. Atlanta. Am J Public Health 1999. Pediatrics 2004.cdc. Dietrich K.275:1177-1181. Weiss ST. Korrick S. Jusko TA. 2002 [online].275(15):1171-1176. Homa DM.205:297-308.htm. Blood lead levels—United States. 4/14/09 Centers for Disease Control and Prevention (CDC). Blanco J. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Leggett RW. Chiodo LM. Ronchi L. Roberts RR. Available at URL: http://www. A prospective follow-up study on psychological effects in workers exposed to low levels of lead. Jacobson JL. The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Krause C. Teratogen update: lead and pregnancy. et al. Acquisition and retention of lead by young children.115:521-529. 4/14/09 Centers for Disease Control and Prevention (CDC). 4/14/09 Centers for Disease Control and Prevention (CDC). Bellinger D. Robertson EF. Caldwell KL. Recommendations from the Advisory Committee on Childhood Lead Poisoning Prevention. Rojas LM. Cory-Slechta DA.89:330-335. Managing Elevated Blood Lead Levels Among Young Children. Hu H. Ganzi A. Hernberg S. Jacobson SW. Scand J Work Environ Health 1984. Pirkle JL. Becker K. Pediatrics 2009. Cox C. Wager C. Schulz C. Meyer PA. The relationship of bone and blood lead to hypertension. Henderson CR.htm. Blood lead reference values: the results of an Italian polycentric study. Bavazzano P. Rotnitzky A. Semen quality of men employed at a lead smelter. Preventing Lead Poisoning in Young Children. Neri A. Jones RL. van Netten C.113(4):1016-1022. Third National Report on Human Exposure to Environmental Chemicals. IARC Working Group on the Evaluation of Carcinogenic Risks to Humans.gov/nceh/lead/publications/ books/plpyc/contents. 2005. Sci Total Environ 2002. Blood lead and chronic kidney disease in the general United States population: 216 Fourth National Report on Human Exposure to Environmental Chemicals . Centers for Disease Control and Prevention (CDC). 1999-2002. Cognitive deficits with blood lead concentrations < 10 µg/dL in US children and adolescents. JAMA 1996. Ewers TG. Seiwert M. Hu H. Inorganic and Organic Lead Compounds. Vimpani FB. Borja-Aburto VH.123:e376-e385. Occup Environ Med 1996. Wigg NR. Neurotoxicol Teratol 2004.cdc.53:411-416.gov/toxprofiles/tp13.atsdr. Environ Health Perspect 1993.348:15171526. Available at URL: http://www. Mantere P. Lanphear BP. Muntner P. et al.150(6):590-597. Kaufman JD. CDC. MMWR Morb Mortal Wkly Rep 2005a. Bellinger D. Sparrow D. 1991 [online].73:409-420. Toxicological profile for lead.Metals Biomonitoring studies on levels of lead provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of lead than are found in the general population. MMWR Morb Mortal Wkly Rep 2006. Vupputyuri S.gov/nceh/lead/ CaseManagement/caseManage_main. gov/mmwr/preview/mmwrhtml/mm5420a5. Luukkonen R. Aro A. Blood lead levels measured prospectively and risk of spontaneous abortion.htm. 1988-2004. N Engl J Med 2003.htm.26:359-371. Lepom P. Korrick SA.cdc. Manton WI.287:1-11. Hänninen H. Atlanta (GA).8(3):395-401. et al. Muller CH. Apostoli P. Aug 2007 [online]. IARC Monogr Eval Carcinog Risks Hum 2006. Coresh J. Neurotoxicol 1987. Available at URL: http://www. Hunter DJ. Kuehnemann TJ.html.82:60-80. et al.cdc.gov/mmwr/preview/mmwrhtml/ mm5532a2.cdc. Neurodevelopmental effects of postnatal lead exposure at very low levels. References Agency for Toxic Substances and Disease Registry (ATSDR).55(32):876-879. Rios C. Adult blood lead epidemiology and surveillance—United States. McMichael AJ. doi:10. Payton M. JAMA 1996. Int J Hyg Environ Health 2002. Lanphear BP. Baj A. 2005b.

9:303-327. Hwang KY. zinc.S. Lauwerys RR. Lee BK. Lead.63:1044-1050.153(5):453464. and hypertension in perimenopausal and postmenopausal women. Toxicol Appl Pharmacol 1993. Environ Health Perspect 1996. Lee SS. et al. 50:31-37. Schwartz BS. JAMA 2003. Schulz D. Hanak B. Schwenk M. blood pressure and cardiovascular disease in men. Sparrow D. Staessen JA. Schwartz J. Kaufmann R. Jurasovic J. Lee GS. blood pressure. Lustberg M. Pirkle JL. et al.327:109-113.118:16-29. Use of endogenous. Fourth National Report on Human Exposure to Environmental Chemicals 217 . Cvitkovic P. Association of blood lead. Physiologically based models for bone-seeking elements. Wilhelm M. Flegal AR. Blood lead concentrations in children: new ranges. Am J Epidemiol 2001.108(1):45-53. Pizent A. population to lead: 1991-1994.104(1):60-66.289(12):1523-1531. Osterloh JD. lead. Arch Environ Health 1995. Kinetics of lead disposition in humans. Kaufmann RB. cadmium. Magder L. stable lead isotopes to determine release of lead from the skeleton. Low-level lead exposure and blood pressure. Exposure of the U. Roels H. J Hum Hypertens 1995. and tibia lead with neurobehavioral test scores in South Korean lead workers. Int J Hyg Environ Health 2006.209:301305. Semen quality and reproductive endocrine function in relation to biomarkers of lead. Low-level lead exposure and renal function in the Normative Aging Study. Rubin R. Paschal DC. and mercury in blood or urine of children: basis for validation of human biomonitoring data in environmental medicine. dimercaptosuccinic acidchelatable lead.Metals results from NHANES III. cadmium. Environ Health Perspect 2000. Smith DR. Kidney Int 2003. Gunter EW. Payton M. Stewar WF. Am J Epidemiol 1994. Nash D. Sherwin R. Weiss ST. Rocic B. Amery A. O’Flaherty EJ. IV. Soldin SJ. Hu H.106:745-750. Gavella M. Soldin OP. and copper in men. Revised and new reference values for arsenic. Hickman T. Telisman S. Brody DJ.140:821-829. Blood lead. Environ Health Perspect 1998. Clin Chim Acta 2003.

800 (.00) 1.40-3. and mercury compounds are still used as preservatives (e.00) . 2007).60 (1.900) 1.927) .02) .50) 5.S. In addition. After elemental mercury is absorbed.S.60-3. which create an episodic potential for volatization and inhalation of mercury vapor. 1999 .00 (1.30-5.400 (.800-1. Accidental spills of elemental mercury. thermometers. Atmospheric elemental mercury can be deposited on land and water. silver-white liquid (quicksilver) obtained predominantly from the refining of mercuric sulfide in cinnabar ore.70 (1.60-5. or oxygen.700-. Apart from methyl mercury.60-2.70 (1.40) 1.20-3.900) .900) 1.g.80 (1.814 (.490 (.80) 4. phenylmercuric acetate) or topical antiseptics (e.40 (3. may contain inorganic mercury.00) 3.800 (.90) 90th 3.20) 2.10-3.484) .12) .60) 2085 2293 3478 Limit of detection (LOD.00 (2. 1998.574) .372) .80 (1. 1994.g.00) 1.700) . Survey years 03-04 Geometric mean (95% conf. sulfur.326 (.300-.40-2.40 (4.80 (3.60-6.689-.20-4.30) 3.40-2.g.60-6.g..500-.70) 911 856 2081 4525 03-04 03-04 .700 (.50-2.800 (. constitutes the main source of dietary mercury exposure in the general population.. sphygmomanometers and barometers.800 (.472-.80) 1.10) . Inorganic mercury compounds such as mercuric oxide are used in producing batteries and pigments and in synthesizing many organic chemicals.500-.700) .60 (1.50-1..800-1.80) 3..40 (3. inorganic..30-2.2.860-1.30) 4132 4241 03-04 03-04 03-04 .40-1.500) .70-2. The ingestion of methyl mercury. synthetic organomercury compounds were once used in pharmaceutical applications.700-.900) 1.919) . it is oxidized in Total Blood Mercury—2003-2004 Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U.50-3.00 (2.40) 3.50) 2. thermostats and switches).90-3.. and organic forms. solid-waste incineration. Other major uses include electrical equipment (e.363-.300) . 1980.900 (.418-.600 (..800-1. Elemental mercury is a shiny.40-1. Some cosmetic skin creams from countries other than the U. electrical lamps.700-.800-1. 218 Fourth National Report on Human Exposure to Environmental Chemicals .20-4.Metals Mercury CAS No.500 (. elemental mercury is used in rituals practiced in some Latin American and Caribbean communities.00 (2.00 (. Metabolism of mercury by microorganisms in aquatic sediments creates methyl mercury.30-4.797 (.903) Selected percentiles ( 95% confidence interval) 50th .300 (.419 (.00 (.400-. with the highest concentrations occurring in the kidneys (Barregard et al. merbromin). Inorganic mercury exists in two oxidative states (mercurous and mercuric) that combine with other elements. Hursh et al.90) 95th 4.30) 3.90 (1.30) 5.285-. Inhalation of elemental mercury volatilized from dental amalgam is a major source of mercury exposure in the general population (Halbach.30) 1. 2002).776 (.600) 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 . 7439-97-6 General Information Mercury is a naturally occurring metal that has elemental (metallic). have often required public health intervention (Zeitz et al.00 (..20 (2. and dental amalgam. thimerosal.700-.703-.714-.00 (.500 (. which can bioaccumulate in aquatic and terrestrial food chains. Elemental mercury is used to produce chlorine gas and caustic soda for industrial applications. such as chlorine (e.781 (. to form inorganic mercury compounds or salts. Kingman et al.886) .877 (. mercuric chloride). and mining and smelting.00) 4.60) 1.50) 4.800-1. population from the National Health and Nutrition Examination Survey. Also. Elemental mercury is released into the air from the combustion of fossil fuels (primarily coal).80 (1. interval) . predominantly from fish and other seafood.90 (4.700-.655-.30 (1.30 (2.70 (3.00-5. 1993)..60 (2.30) 1.30-6. The kinetics of the different forms of mercury vary considerably.90 (1. Poorly absorbed from the gastrointestinal tract. Woods et al. water can be contaminated by the direct release of elemental and inorganic mercury from industrial discharges.400-.70 (4.00-1. see Data Analysis section) for Survey year 03-04 is 0. IARC. and is distributed to most tissues.50) 1.60) 1. Imported folk and alternative medicines occasionally are contaminated with inorganic mercury. elemental mercury is absorbed mainly by inhaling volatilized vapor.563 (.900) 75th 1.979 (.90) 3.672) .753-1.40 (4. an organic form of mercury.

.500-. Vimy et al. Methyl mercury enters the brain and other tissues (Vahter et al.50-2.60 (3.00) 6.60 (3. and a useful marker of exposure in epidemiologic studies (Grandjean et al.10) .30) 3. 1999-2002.70 (1.73) 1.50-12.06-1.269-...30-4. 1998).02 (.667 (.833 (.900 (..0) 4.60 (2.90 (1.800) 1.500-1. National Health and Nutrition Examination Survey.10) 1. 1969.541-.00-2.300) . 2003). Fourth National Report on Human Exposure to Environmental Chemicals 219 .800 (..80 (3.00) 4.. 1971).00) 2.268-.20-3.80) 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.00-2.407) ..317 (.10-3.664-1. excretion of mercury occurs predominantly through the kidney (Sandborgh-Englund et al. 1990).30-6.. interval) Selected percentiles (95% confidence interval) 50th ..200-.700 (.00) .10 (1.824) 1.265-. Myers et al. The fraction of methyl mercury absorbed from the gastrointestinal tract is about 95% (Aberg et al.307 (.80 (1. and the newborn’s levels decline gradually over several weeks (Bjornberg et al.30 (.900-1.27) . 1975.800 (.. Human pharmacokinetic studies indicate that methyl mercury declines in blood and the whole body with a half-life of approximately 50 days..20) .3) 4.01) .700-1.23) .00) 1.35 (1. Suzuki et al. The half-life of inorganic mercury in blood is similar to the slow-phase half-life of mercury after inhalation of elemental mercury.10 (1. 1998).20-2. 2005).820 (.10 (5. Vahter et al. for both acute and chronic exposures.200 (.40-2.800-1.90) 90th 1.400-.318 (.50 (1.738-.300) . population.00 (2.00-1.40-1. Less than 15% of inorganic mercury is absorbed from the human gastrointestinal tract (Rahola et al. 1993). Mercury levels in the cord blood are higher than in the mother’s blood (Stern and Smith.10 (.00 (3.50) 95th 2.00) 1.30 (1.300) .900 (.00-3.377) .90 (1. 1999).60 (1.800) 1.70 (1. with most elimination occurring through in the feces (Sherlock et al.30) 1. a measure of accumulated dose (Cernichiari et al.700-.329 (. Excretion occurs by renal and fecal routes.700-.14.90) 3.50) 1.00 (1.600 (. 16-49 years) Mexican Americans Non-hispanic blacks Non-hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .90) 2.800) . Smith et al.299-.300 (.30 (1.500-.377 (.30-5.20 (2. Transplacental transport of methyl mercury and elemental mercury has been demonstrated in animals (Kajiwara et al.871-1.. thereafter. 1973).369) 1.20-3.200-.200-. 1992).700 (.700 (.300) . 1994.00 (2.300 (.374) . Methyl mercury is incorporated into growing hair.475) .60) 2.40 (1.600) .30-6..70) 4.500-.20) .50) 2. and peak urine levels can lag behind peak blood levels by days to a few weeks (Barregard et al..500 (.800-1.700 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0. Lesser penetration of inorganic mercury occurs through the bloodbrain barrier than occurs with either elemental or methyl mercury (Hattula and Rahola. The slow-phase half-life may be several weeks longer in persons with chronic occupational exposure (Sallsten et al.30 (1.200-.30-4. 1994).7) 4. McDowell et al.90) 2. 1996).944 (.395) .70-6.300 (..800-1.10 (3.726-1.70) 4.50-3.30-6.40) 1.10 (.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) 1.50) 3.60 (1.70) 1. 1996.30-2.. 1995.. 1993). 2004.80-3.90 (4.256-.30) 1.900 (. Miettinen et al.70-5.343 (.600) .90 (4.Metals the tissues to mercurous and mercuric inorganic forms.50) 1.20 (.90 (3.10 (1.70 (1. Jonsson et al.825-1.90) 5.800) 75th . urinary mercury levels decline with a half-life of approximately 1-3 months (Roels et al..800) .697-. 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..06 (.60) 1.40) 2. 1992 and 1999. 1992. Inorganic mercury and methyl mercury are distributed into human breast milk in relatively low concentrations.70-3.20) 1.297-.70-3.200-.900-1. Smith and Farris.300 (.200 (. Sandborgh-Englund et al.00-2.29) . After exposure to elemental mercury.919) .. Geometric mean Survey years (95% conf.S. 1991.80) 579 527 370 436 588 806 Limit of detection (LOD.40) 5.60 (1.200-.500-. 1984.14 and 0.40 (1.30-11.940) Race/ethnicity (females.70-5.10-1.20-3.500 (.700) 2..300) .700-1.10) .00) 7.500-..20-11.00-6. 1994) and then undergoes slow dealkylation to inorganic mercury.300) .60) 3.00 (2.40-2. 2003).800 (.30-3.50 (2.

Acute. 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... Mercury levels in breast milk also decline in the weeks after birth (Bjornberg et al. 1970.700) 2007 2240 3406 Limit of detection (LOD. short-term memory loss. pain in the extremities. 1995.500) ..700-. Overt poisoning from methyl mercury primarily affects the central nervous system. causing parasthesias. 2003)..600-. population from the National Health and Nutrition Examination Survey. Oskarsson et al. 1951. Inorganic mercury exposure usually occurs by ingestion.700) . Occupational exposure to elemental mercury vapor has been associated with subclinical effects on biomarkers of renal dysfunction (Cardenas et al. fatigue.500-.500 (<LOD-. 2000). gingivitis.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-.600) . depression. Stern 2005. 2004. Salonen et al. Bellinger et al.500-. particularly irritability. anorexia.500 (. high-dose exposure to elemental mercury vapor may cause severe pneumonitis. Rissanen et al. 1993). 1998.. At levels below those that cause acute lung injury.500-. Drexler and Schaller.42. 220 Fourth National Report on Human Exposure to Environmental Chemicals ..500-. 1987). Smith et al.600-. In recent epidemiologic studies. 2006. limb deformities. 2000. 2006.600) .600 (. DeRouen et al. Factor-Litvak et al.800) . the most prominent effect is on the kidneys where mercury accumulates and may lead to renal tubular necrosis..500 (<LOD-. typically after a latent period of weeks to months. 2002. The constellation of findings may include anorexia.700 (. 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. 1995.600 (. the existence of a causal relation is unresolved (Chan and Egeland.600 (.600) .600 (. and neurocognitive and behavioral disturbances.800) 792 842 2060 4453 03-04 03-04 * * < LOD < LOD < LOD < LOD .600-.500-. 1963). dysarthria. and cerebral palsy (NRC.S. see Data Analysis section) for Survey year 03-04 is 0.... 1983)..600) . altered physical growth. Large amounts may cause irritant or corrosive effects on the gastrointestinal tract (Sanchez-Sicilia et al. 2004)..500-.500-.700 (. Vupputuri et al. hearing impairment.. sensory impairments. and pinkish discoloration of the hands and feet (Tunnessen et al.700 (. 1996)..600 (. overt signs and symptoms of chronic inhalation may include tremor.600 (. maculopapular rash. hypertension. cerebellar ataxia. Low-level exposure from dental amalgams has not been associated with neurologic effects in children or adults (Bates et al.700 (. Rice.600-.. Sakamoto et al..600) * 03-04 03-04 03-04 03-04 * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD . irritability.700 (.. which may vary for some chemicals by year and by individual sample. insomnia.500-.700-. and progressive constriction of the visual fields. Sakamoto et al. Once absorbed.700 (.600) .. Although recent investigations have suggested a possible link between chronic ingestion of methyl mercury and an increased risk for cardiovascular disease.500-. Acrodynia is a sporadic and predominantly pediatric syndrome historically associated with calomel (mercuric oxide) in teething powders and occasionally other inorganic forms of mercury.800) . and a drinking water Inorganic Blood Mercury Geometric mean and selected percentiles of blood concentrations (in µg/L) for the U. 2004).600) . 2004. 2000. dysarthria.600) . interval) Selected percentiles ( 95% confidence interval) Sample 95th . Workplace standards for inorganic mercury exposure have been established by OSHA and ACGIH. ataxia.600) . and sleep disturbance (Bidstrup et al.800) 4015 4132 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD .Metals may be more efficient for inorganic mercury (Grandjean et al. Smith et al. 2005).600 (. < LOD means less than the limit of detection.600 (. High-level prenatal exposure may result in a constellation of developmental deficits that includes mental retardation. 2005. Survey Geometric mean (95% conf.500 (.600) . * Not calculated: proportion of results below limit of detection was too high to provide a valid result.

520) . average age 33 years.360-.930-1.S.340-.24) 1.13-2. Kingman et al.S.304) . Information about external exposure (i.840-1. 1997. Clinically observable signs of ataxia and paresthesias may occur when blood mercury levels increase to approximately 100 µg/L after methyl mercury poisoning.509) .gov/toxprofiles.epa.14.570) .60) 619 713 1066 Limit of detection (LOD. average age 9.46 µg/L for children.382-..495 (..88 (1.60 (1.23) . total blood mercury increased with age. 2009). 2003).S.67-2..24 (2.16 (1.530) .530-. Grandjean et al. aged 18 to 69 years.870-1. EPA at: http://www.290-.18) 2.20 (1. see Data Analysis section) for Survey year 03-04 is 0. 1995.54 (2.. Urine mercury levels increase as more occlusal surfaces of teeth are filled with mercury-containing amalgams (Becker et al. 2006).254 (. population from the National Health and Nutrition Examination Survey. Schober et al.313-. military veterans (mean age 52.55) 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 . Urinary mercury consists mostly of inorganic mercury (Cianciola et al.610-1. Mahaffey et al.09 (2.52) 2. particularly methyl mercury.00 (.31) 1266 1272 03-04 03-04 03-04 .396-. A cohort of 1127 U.33 (2.370) ..93 (1.61) 1. 1998).23) 2.890 (. and the age-related changes differed across the groups (Caldwell et al.447 (. 2004. Sanzo et al. range 40 years to 78 years) had an average total blood mercury concentration of 2. Total blood mercury levels increase with greater fish consumption (Dewailly et al.840) 1.413-. the total blood mercury concentration is due mostly to the dietary intake of organic forms.405-.05) 1.358 (.440 (.463) . environmental levels) and health effects is available from the U. Fourth National Report on Human Exposure to Environmental Chemicals 221 .e.9 years).01 (.96 (1.05) 3..476 (.29) 1.870-1. In NHANES 19992002.480 (.30) 3.99-6. total blood mercury levels declined slightly in non-Hispanic black and Mexican American children.89) 3. 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.460) . These men had no occupational exposure to mercury but previously had received dental amalgams at military facilities (Kingman et al.160-. 758 children.68 (2.530) . interval) . et al.S. 2002). These distinctions can help interpret mercury blood levels in people. who participated in a 1998 representative population survey (Becker et al. Urinary Mercury—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.90) 2.76-3.gov/mercury and from ATSDR at: http:// www.. 2001. (2000) studied 1216 blood donors in the Czech Republic (896 men and 320 women.400 (. However..67-3.78-2.07 (.88-3.65) 1.360 (.28) 1.00) 1. 2001.08 (1.12 (. Survey years 03-04 Geometric mean (95% conf.60-2...442-.480) 75th 1. Biomonitoring Information In the general population.03-4.200 (. 2003)..Metals standard for inorganic mercury has been established by U.58 µg/L for 4645 adults..213-. During the same survey periods. 1998). total blood mercury geometric mean levels in females aged 16-49 years did not change. the median concentration of blood mercury was 0.441 (.406-. adult women in several ethnic subgroups (Hightower et al. 2000).14) 90th 2.330-.16 (.96 (1.509) . and increased slightly in non-Hispanic white children (Caldwell.31) 2.77-2. slightly higher total blood mercury levels were found in U.330-.940 (.46) 3.42) 95th 3.430 (. Over the NHANES 1999-2006 survey periods.840-1.460 (. From 1996 through 1998.14-2.549) .430 (.350-..8 years.420 (.34-3.330 (.410-.280-.85-2.534) .430) . In Germany the geometric mean for blood mercury was 0.55 µg/L.580) .492) Selected percentiles ( 95% confidence interval) 50th .76-3.08 (1.S.433 (.420 (.39-3.76-4.700 (.88) 287 722 1529 03-04 03-04 .770-1. 2009).960 (.416 (.cdc.26 (1.408) . the developing fetus may be the most susceptible to the effects of ongoing methyl mercury exposure (NRC. although non-Hispanic black females had higher levels than non-Hispanic white or Mexican American females. EPA.360-.97) 2.63-2..330-.250) .700-1.19 (2.19 (1. IARC considers methylmercury to be a possible human carcinogen and elemental and inorganic mercury to be unclassifiable with regard to human carcinogenicity. Benes et al. Among the three racial/ethnic groups.atsdr.78 µg/L for adults and 0.66) 3.555) .

463 (.00 (.217 (.16) 1.67 (1.365 (.400-.23-2.79) 1.358) .276 (. 2009).306 (.969-1. 2005).376-. DeRouen et al.39) 1.620-.90) 618 713 1066 222 Fourth National Report on Human Exposure to Environmental Chemicals . and on average. 2006).85) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites Sample size 2537 03-04 03-04 03-04 .04-3. interval) .970 (.309-.619-. Czech (Benes et al.13-2.35 (1.800-1.40-1.687) ..87) 2.480) .21) 1. Information about the biological exposure indices is provided here for comparison. Urine mercury and the number of dental amalgams were correlated.588) . 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.392-.S.464 (.11) 1.196-.. Survey years 03-04 Geometric mean (95% conf.225-.391) .46-2.18-1.31 (1. representative sample of women aged 1649 years reported in NHANES 1999-2006 (Caldwell.56) 1266 1271 03-04 03-04 03-04 .12-3..301-.365 (.32 (1. 1988. 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.443 (. 2003).Metals 2000).S.11) 2.54 (2.616) .447-.07) 1.76 (1.88-2. An expert-panel report recently prepared for the U.289) .00) 90th 1.S.768 (.51-2.11-2. Blood mercury levels of women and children in NHANES 19992006 were also below levels established as occupational exposure guidelines (Caldwell.44) 1.455-.297 (.1 µg/L. 1992).485 (.78-4. Levels in U.06 (.88 (1.343 (.265-.347) . a biomarker of perturbation in renal tubular function.86) 95th 2. population from the National Health and Nutrition Examination Survey.784) 1. Langworth et al.545 (.587 (. 1998).. The ACGIH (2007) currently recommends that urinary inorganic mercury in workers not exceed 35 µg/g of creatinine.599) . and Italian (Apostoli et al.280-.400) .875-1.40 (1.63) 1.785-1. Department of Health and Human Services noted that several studies have observed a modest.667-1. Finding a measurable amount of mercury in blood or urine does not mean that the level of mercury causes an adverse health effect. In the study of U.391-. 2009).13 (1.498) 75th . ACGIH recommends that the blood levels due to inorganic mercury exposure in workers not exceed 15 µg/L..00) 286 722 1529 03-04 03-04 . et al..652) .32-2.09) 1..65 (1. 2006.307-. not to imply a safety level for general population exposure.535) 1.486) Selected percentiles ( 95% confidence interval) 50th .404-.64-2.455) .03) 2.77 (2. among workers with urinary mercury concentrations of 25-35 µg/L or greater (Barregard et al.964-1.696 (. women of childbearing age have generally been much lower than these levels (CDC.476 (.87 (1. 2002) adult population surveys were similar to those in a U..01) 2.362 (.06 (.61) 1. Biomonitoring data will also help scientists plan and conduct research on exposure and health effects.566) .455-.246-.417) ..30) 1.S.208-.333-. mean urinary mercury was 3. military veterans with dental amalgams.990) .30) 2.255 (.S.41-2.385-. reversible increase in urinary N-acetyl-glucosaminidase.384 (.62 (1.275) . et al.522-.88-2.537) . 2002).630) . Urinary Mercury (creatinine corrected)—2003-2004 Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.368) .532 (.67 (1.525 (.447 (.909 (.508 (.714-1. the urine mercury increased by approximately 0. Urinary mercury levels in recent German (Becker et al.28 (..25 (.1 µg/L for each surface with a dental amalgam (Kingman et al.79 (1.472-.

790) .23-1.850-1.832-1.55) 90th 3.25) 2.76) 2.569-.670) 75th 1.28 (1.48 (2.664) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .540 (.846) .502-.10-4.831) .14-1.650) 1.35) .14.21 (2.657 (.69 (1.45) 95th 3. 16-49 years) 99-00 01-02 .557-.03 (.99 (3. interval) Selected percentiles (95% confidence interval) 50th .42-3.3) 5.45 (1.410-.63) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.686) .744) 1.30 (2.42) 2.46-4.579-.05 (3.00) 2.637) .665) Mexican Americans Non-Hispanic blacks Non-Hispanic whites 99-00 01-02 99-00 01-02 99-00 01-02 .45) 2.620 (.92) 3.46) 3.665) .50-4.05 (2.84 (2.30 (1.387-.76-5.00 (3.615 (.15 (2.45-2.95 (2.833) .50 (2.17) 95th 5.709) 75th 1.99) 1.S.578-.656-.85) 4.631-.03) 1.824) .699) 1.691) .45) 2.47) 1.03-2.77) 1.09-1.616-.685 (.16) 5. Urinary Mercury (creatinine corrected)−Females Aged 16-49 Years Old.930) .605-.21-3.39-3.85-3.50 (1.582-.91 (2.831) .06 (. Geometric mean Survey years (95% conf.91-7.98 (5.37 (1.636-.565 (.522 (.650 (.72) 1.42) 90th 2.13 (2.79) 1.35 (1.658 (.740 (.68 (3.553-.56 (1.580-.21 (1.81-6. Geometric mean (95% conf.18 (3.97 (1.07) 1. interval) Selected percentiles (95% confidence interval) Survey years 50th .S.724 (.622-.97) 2.14 and 0.07-2.806) .710 (.41-6.61-6.56) 3.32-3. population.22 (.664) .45-3.719 (.540-.62 (4.426-. 1999-2002.966) .41 (1.32) 2.520-.52) 3.600 (.53) 595 531 381 442 594 826 Fourth National Report on Human Exposure to Environmental Chemicals 223 .516 (.51 (3.51) .772 (.610-.62 (3.27-1.41 (2.32 (1.10-2.520-.723 (.560 (.650 (.09-1.99 (2.44) 3.870) .81 (3.500-.420-.68-3.706 (.97) 2.596 (.27 (1.65) 1.77) 2.809) .94) 1. 1999-2002.83-3.508-.43-1.475-.742-1.38) 4. 16-49 years) 99-00 01-02 . 1999-2002 Geometric mean and selected percentiles of urine concentrations (in µg/L) for females aged 16 to 49 years in the U.910) .709) .00 (2.79) 3.62 (1.632 (.909-1.810) .450-.23-1.27 (2.24-1.87-4.70 (2.04-10.30-2.03 (. see Data Analysis section) for Survey years 99-00 and 01-02 are 0.560-.24) 6.799) .59-5.07-5.721 (.606 (.68) 3.14-2.97) 2.69-3.41 (1.37) 1.580 (.53-3.22-3.13-4.55-3.54) 595 531 381 442 594 826 Limit of detection (LOD.624-. population.39) Sample size 1748 1960 Age group (females) 16-49 years Race/ethnicity (females.18) 3.760 (.655 (.04-1.Metals Urinary Mercury−Females Aged 16-49 Years Old.47) 1.892) .30 (2.99-2.526-.46 (1.710 (.592 (.92) 2. National Health and Nutrition Examination Survey.31-1.31 (1.16-5.710) 1.56) 4.57-4. National Health and Nutrition Examination Survey.76 (1.92) 4.774) .61) 1.84 (2.89 (2.639 (.14) 3.65-4.501-. 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.15-1.

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Takahashi Y.97(2):195-200. The hair-organ relationship in mercury concentration in contemporary Japanese. The contribution of dental amalgam to urinary mercury excretion in children. et al. 226 Fourth National Report on Human Exposure to Environmental Chemicals . Yoshinaga J. Sandler DP. Imai H. Bolger PM. Schober SE. Stern AH. Toxicol Appl Pharmacol 1994.115(10):1527-1531. et al. Kaye WE. Vimy MJ. Smith AE. Hongo T. Amiano P. McMahon KJ. Methyl mercury pharmacokinetics in man: a reevaluation. Matsuo N.79:786789. Woods JS. Aguinagalde FX. Effects of exposure to mercury in the manufacture of chlorine. Estimation and validation of mercury intake associated with fish consumption in an EPIC cohort of Spain. Effects of occupational exposure to elemental mercury on short term memory. Orr MF. Blood mercury levels in US children and women of childbearing age. Toxicol Appl Pharmacol 1996.124:221-229.128(2):25125-25126. Langolf GD. Sinks TH. Smith PJ. Toxicol Appl Pharmacol 1994. Farris FF. DeRouen TA. Leroux BG. Patil LS. Public health consequences of mercury spills: hazardous substances emergency events surveillance system. Goldberg J. Most B. Maternal-fetal distribution of mercury (203Hg) released from dental amalgam fillings. Bernardo MF.2:117-131.289(13):1667-1674. 1999-2000. Azpiri MA. Allen PV.48(4):221229.258(4 Pt 2):R939-945. et al.31:687-700. Arch Environ Health 1993. Osterloh J. 1993-1998. Hislop D. Smith RG. McDowell M. Jones RL. Amurrio A. Smith JC. Hum Toxicol 1984. Acrodynia: exposure to mercury from fluorescent light bulbs. Environ Health Perspect 2002. An assessment of the cord blood: maternal blood methyl mercury ratio: implications for risk assessment. Blood mercury level and blood pressure among US women: results from the National Health and Nutrition Examination Survey 1999-2000. Whittle K. Newton G. JAMA 2003. Dorronsoro M. Vorwald AJ. Nakazawa M. Environ Health Perspect 2003. Fisher HL. Suzuki T. Lorscheider FL. Topping G. Br J Ind Med 1983. Environ Res 2005.111(12):1465-1470. A review of the studies of the cardiovascular health effects of methylmercury with consideration of their suitability for risk assessment. Friberg L. Am Ind Hyg Assoc J 1970. Vahter M. Burbacher T. Baser M. Speciation of mercury in the primate blood and brain following long-term exposure to methyl mercury. Am J Physiol 1990. Hall LL. Pediatrics 1987.110:129-132.40:413-419. Environ Res 2005. The kinetics of intravenously administered methyl mercury in man. Turner MD. Daniels JL.98(1):133-142. Mooney TF. Guo S. Tunnessen WW. Lind B.37:245-252.Metals Sanzo JM. Longnecker MP. Shen DD. Vupputuri S. Sherlock J. Smith JC. Elevation of mercury in human blood from controlled ingestion of methyl mercury in fish. Environ Health Perspect 2007. Public Health Nutr 2001. Stern AH.4(5):981-988. Leitao JG. Mottet NK. Zeitz P. Martin MD.

6) 71.0-100) 63.9 (37.5 (41.8-108) 87.0) 97.8-94. 2001). urinary excretion over six days CAS No.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. respectively.7 (44. 0.7-50.3 (47.1-55.3 (55.6) 71.7-105) 69.6-58.1) 59.9-55.7 (58.6 (40.0) 60. More recently.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 52.0) 55.4-82.2-37.1-63.8 (42.6-42.6 (73.4-52.6 (55.4) 52. chemical reagents in hospital laboratories. 2001.0 (42.8) 39. hydrogenation catalysts.1 (38.S.2) 40.6-55.0-56.3-47.0) 45.0 (81.3-108) 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 47.7) 51.3) 90th 135 (125-146) 124 (117-130) 111 (105-118) 95th 180 (154-216) 165 (145-176) 138 (133-146) Total 45.5 (41.0-71.7-41.7) 78.9-83.3-44.2) 53.3) 54.6-82.0-77.6-96. population from the National Health and Nutrition Examination survey.2-79.7) 78.9 (34.2 (56.5-124) 108 (92.6-46.7) 46. molybdenum is a cofactor for three enzyme classes— sulfite oxidase.1) 82.6 (55.3 (38.5-68.2 (61. interval) 45.0) 54. At a daily oral molybdenum dose of 24 µg.4) 76.0 (46. Fourth National Report on Human Exposure to Environmental Chemicals 227 .0) 62.6) 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 (99.5-52.7 (50.4 (48.5.3) 41.1 (34..5) 85.4) 49.8-106) 88.4 (80.9) 34.3) 65.7-68.3) 83. see Data Analysis section) for survey years 99-00.3 (53. 7439-98-7 General Information Elemental molybdenum is a silver-white.7 (45.7-39.1 (71.1) 46.1 (91.2 (69.8) 44.1-59.9) 62. hard metal widely used to add strength and hardness and retard corrosion in metal alloys.7-51.7) 75th 84. and in pigments for ceramics. semiconductor and battery industries have begun to use molybdenum.7) 57.2 (49.0-62.5-91.2 (55.0) 84.6-62.7 (51. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.4) 45.2-53. 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.2-70.3-91.3 (37. Gastrointestinal absorption of molybdenum averages 8893% for dietary intakes of 22-1490 µg/day.1) 35.7-47.9 (40. lubricants. and xanthine oxidase (Kisker et al.2) 79.5-65.4 (48.7 (37.7 (73.9-55.8 (82.0) 39.4 (72.3) 85.5 (74.7-84.2) 41.5-41.2) 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 (98.6) 53.4 (34.2 (83.1-88.8 (85.5) 47.3 (84.8) 75. inks.4 (79.8-90.3 (55.7) 86.2 (63.5-46.3 (71.9 (32.7-96.9-85.0-110) 90.6) Selected percentiles ( 95% confidence interval) 50th 50.7-73. Compounds of molybdenum are also used as corrosion inhibitors.3 (73. which exert homeostatic regulation over molybdenum balance.2) 37.3 (64.5) 44.0 (76.9-82.7-92.9 (44.0 (42.6-72.0-101) 82.1-52.8 (67.1) 126 (106-147) 109 (94.4) 56. and 03-04 are 0.5) 80.2) 52.5 (43.6) 51. 1996).0 (41.0 (48.3-75.0-65. The recommended dietary allowance for adult men and women is 45 µg/day (IOM. aldehyde dehydrogenase. and the average dietary daily intake of molybdenum is approximately 100 µg/day (IOM.2) 48.5 (48. 01-02.3) 37.9-109) 97.7-60.6) 93.5-52.4-61. In humans.2-59.4) 42. Molybdenum is a nutritionally essential trace element that enters the body primarily from dietary sources.9) 67.9 (73.7-91.7-122) 93.2-42.7) 77. Excretion occurs predominantly via the kidneys.3 (46.2-59.6 (52.1-48.5 (67.3-115) 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.5) 60.9 (78.1-51.2 (40.7) 45.0 (43.5-66.2 (49. and 1.5) 80.0-85.6 (43.2-91.8-49.8.0-53.1) 60.9-56.7 (71.6 (40.1) 57.8) 46.9 (52.5 (37.5 (81.0-38.8) 48.4-75.2) 150 (128-187) 130 (120-141) 119 (112-130) 119 (105-138) 115 (104-128) 101 (97.5 (49.2 (38.8.8) 40.7 (36.1-44.3) 47.1-52.8-46.4) 41.3 (79.9 (33. WHO. and paints. 1997).Metals Molybdenum or ore deposits.

3-68.4) 40.0-41.5 (35.3-44.2-40.6) 39.6 (71.2-96.7 (30. interval) 43.3-43.7) 62.3-102) 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. In industry.5 (39.5 (38.2) 38.2-46.7 (75.4 (44.3-56.1 (33.8) 62.2 (40.2) 58.1) 40.1-34.6) Selected percentiles ( 95% confidence interval) 50th 41.3 (55.2) 37. Biomonitoring Information Molybdenum is an essential element for health.4-39.7-40.2-80.2 (69. dust and other fine particles produced during refining or shaping of molybdenum or molybdenumcontaining alloys are inhalational pathways of exposure.6 (38.3) 43. and urinary levels reflect intake from all sources.2 (73.9-40.4-185) 106 (94.6-45.5) 73.6) 39.4-76.8-118) 81.8 (56.3) 57. Levels of molybdenum Urinary Molybdenum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.8) 39.4 (37. respectively.6 (36.5-60.4 (67.1) 101 (83.2-65.2) 39.1-43.8) 61.8 (37.4 (56.9-68.0) 36.5 (37.6-63.1) 56.5-45.1-79.9 (39.5) 60.5-50.3 (83.8) 38.1-100) 86.2-121) 107 (92.9-45.7) 42.2) 42. EPA.5 (34.4-106) 85.5 (83.5-62.6-88.9) 92.3) 41.6) 48.3) 37.3-52.5 (36.5) 214 (154-1040) 185 (165-219) 160 (129-257) 112 (78.5) 71.5 (80.1-127) 90.4-41.9) 79.6-61.8-46.6) 43.9) 31.6-61.9-61.0) 62. 1961.3) 56.1-41. A long term inhalation bioassay of molybdenum trioxide in mice yielded “some evidence” of carcinogenicity (NTP.9-118) 91.6 (59..3 (71.1 (54. at daily oral doses of 95 µg and 428 µg.7-43.8-52. Based on studies finding adverse reproductive effects in rats and mice.9 (64.2 (36.0-133) 119 (88.9 (73.4) 48.1-67.1-81.2 (40.S.3 (36.7) 53.1 (39.5-46.4 (55.5 (59. 2001).7) 115 (93.1 (38. population from the National Health and Nutrition Examination survey.8 (75. 1993).2) 37.4 (78.2 (33.9-45.9 (79.5-70.7-44.7-93.5 (35.8) 38.5 (40.5 (65.7) 57.7 (77.S.7) 45.7-100) 77.2) 39. of the ingested dose (Turnlund et al.2 (50.Metals was 18% of the ingested dose.1 (44.1) 43.5 (41.1) 37.3 (58.9 (36.5) 90th 108 (97.4) 122 (107-133) 109 (99.0-46.3-45.8-47.2) 43.7 (66.8) 79.9 (35.6-78.5-69.4 (59.0-120) 85. 1995).3-141) 109 (81. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.7-120) 87.8) 45.3 (51.0) 88.4) 61.9 mg/kg/day and established a tolerable upper intake level of 0.4) 58..1 (37. 1997).1 (30.2 (37.1-112) 78.3-115) 98.0-56. 1999).1) 37.9-117) 57.8) 71.7-52.1 (82.7-62.5) 72.5 (39.2-41. Human health effects from molybdenum at low environmental doses or at biomonitored levels from low environmental exposures are unknown.5 (50.2-103) 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 42.3 (71.1-38.8) 37.1 (49.2-49.6-63.0-103) 103 (90.9) 173 (130-243) 159 (129-170) 132 (107-158) 85.9) 41.8-66.8 (36.1-43.0) 39.4 (53.9-42.3) 64.4) 89.2-96.6) 36.1-109) 89.6-76. the Panel on Micronutrients of the Institute of Medicine identified a no observed adverse effect level (NOAEL) of 0.5-119) 90.3 (53.0 (58.4-42.3) 61.9) 44.8-47.7) 112 (95. Molybdenum is generally considered to be of low human toxicity.0) 39.9-41. and molybdenum has not been systematically evaluated for carcinogenicity by IARC.0 (35.9-96. urinary excretion over six days rose to 50% and 67%.4) 116 (101-126) 104 (88.0-46.5-92. One case-control study suggested a possible link between occupational exposure to molybdenum and lung cancer (Droste et al.4-107) 85.9-71.1-45.5 (79.5-97.0 (80.5 (37.4-118) 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 .4) 47.3 (37.3 (36.2 (40.0 (74.1-39. U.1 (42.2) 42.4 (40.8-42.9 (64.7) 75th 63.9) 40.5-35.0) 72.4-66.1 (38.0) 53.0-38.4) 77.9 (39.6 (36.6-41.1-40.7-38.1 (40. and clinical or epidemiologic evidence of adverse effects is limited.2 (52.3-59.4) 44.0) 95th 144 (125-171) 130 (120-149) 120 (107-135) Total 42.7-137) 129 (109-155) 112 (97.5 (78.03 mg/kg/day in humans (IOM.7) 41.2-47.5 (40.8-84.8 (90..3-46.8-67.6 (57.5 (41.2 (57.5-48.0) 38.3 (37.3) 40. Chronic exposure to very high levels may result in higher serum uric acid levels and a gout-like illness (Koval’skiy et al.5 (65.8-65.8 (57.5-99.5) 63.4-120) 101 (84. but available epidemiologic data are scant.9 (49.2) 55.6 (42.1) 65.0) 44.0) 33.9-87.3) 44.5-44.2 (43.1-39.3) 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 85.5 (54.4) 60.9 (40.

vitamin K. 144-154. Am J Clin Nutr 1995. chromium. Atlanta (GA). Sciarra G. Keyes WR.htm. iron. 56:322-327. Trace element reference values in tissues from inhabitants of the European Union. Inductively coupled plasma mass spectrometric determination of molybdenum in urine. iodine. Schindelin H. Third National Report on Human Exposure to Environmental Chemicals. Turnlund JR.. pp. In: Trace elements in human nutrition and health. 2001. A study of 13 elements in blood and urine of a United Kingdom population. Molybdenum 1993 [online]. 2005). Standing Committee on the Scientific Evaluation of Dietary Reference Intakes. Sci Total Environ 1998.216:253-270. Environmental Protection Agency (U. World Health Organization (WHO).nih. 4/14/09 Iversen BS. White and Sabbioni.62(4):790-796. silicon. (DC): National Academy Press.. 1313-27-5) in F344 Rats and B6C3F1 Mice (inhalation studies) 1997 [online]. manganese. 4/14/09 White MA. Kisker C. 4/14/09 Sievers E.S. TR-462. National Toxicology Program (NTP).15(2-3):149-154. molybdenum. Zhurnal Obshchey Biologii 1961. van Sprundel MP.123(1):81-85. Turci R. Food and Nutrition Board. Menne C. Fourth National Report on Human Exposure to Environmental Chemicals 229 .66:233-267. Washington. boron. pp. Yarovaya GA. Weyler JJ. Ann Rev Biochem 1997. White MA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. 1998). Schaub J. X. 2001). Molybdenum in infancy: methodical investigation of urinary excretion.epa. Sabbioni E. Molybdenum-cofactorcontaining enzymes: structure and mechanism.gov/iris/ subst/0425. U. Molybdenum absorption. Occupational risk factors of lung cancer: a hospital based case-control study. copper. and retention studied with stable isotopes in young men at five intakes of dietary molybdenum. arsenic. Available at URL: http://books. Molybdenum. Minoia et al. cfm?objectid=070A72C6-E9C1-AE67-4BFAB97AD0F427E8. Shmavonyan DM. Urinary molybdenum concentrations in infants may be slightly lower than those in other age groups (Sievers et al.. Koval’skiy GA.niehs. these levels were comparable to those reported for adults in smaller European population surveys (Iversen et al. References Centers for Disease Control and Prevention (CDC). nickel. and zinc: a report of the Panel on Micronutrients. Minoia C. Van Meerbeeck JP. Institute of Medicine (IOM). 1996. Dietary reference intakes for vitamin A. 420-441. edu/openbook. Occup Environ Med 1999. 1998. Vermeire PA. Available at URL: http://www.nap. Aprea C. 2005. Peiffer GL.S. Gatti A. J Trace Elem Med Biol 2001. vanadium. 2002. Ronchi A. excretion.S. EPA). 16:1313-1319. Droste JHJ.php?record_id=10026&page=420. Analyst 1998. Sabbioni E. Finding a measurable amount of molybdenum in the urine does not mean that the level of molybdenum causes an adverse health effect. et al. Christensen JM. population were well characterized in NHANES 1999-2000 and 2001-2002 (CDC. Kristiansen J.22(3):179-191. Geneva: WHO. Inductively coupled plasma mass spectrometric determination of molybdenum in urine from a Danish population. Rapid Comm Mass Spectrom 2002. Changes of purine metabolism in man and animals under conditions of molybdenum biogeochemical provinces. Toxicology and carcinogenesis studies of molybdenum trioxide (CAS No. Schleyerbach U. Available at URL: http://ntp. Rees DC.Metals in urine for the U. 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.gov/index.

and high catalytic activity. Platinum-rhodium compounds are also used in glass and glass-fiber manufacture and in hightemperature thermocouples. strength at high temperatures.04.04. 0. Important properties of platinum are resistance to corrosion. population from the National Health and Nutrition Examination Survey. respectively.g. as oxidation catalysts in chemical manufacturing. 230 Fourth National Report on Human Exposure to Environmental Chemicals . Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 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. Human health effects from platinum at low environmental Urinary Platinum Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U. and 0. and iron. 7440-06-4 General Information Platinum is a silver-gray. however. 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. lustrous metal found naturally in extremely low amounts in the earth’s crust and is typically associated with sulfide-ore bodies of nickel. < LOD means less than the limit of detection.. 1998). 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. cisplatin. 01-02. copper. dental alloys.. and 03-04 are 0.07. and as drugs (e. thick-film circuits printed on ceramic substrates.S.Metals Platinum CAS No. carboplatin) in the treatment of cancer. Platinum compounds are used in electrodes. Higher environmental soil concentrations of platinum from vehicular emissions have been found near roadways (Farago et al. jewelry. Platinum-rhodium and platinumpalladium crystals are used as catalysts in petroleum refining and in vehicular catalytic converters to control exhaust emissions. see Data Analysis section) for Survey years 99-00.

or recommended for the metal form by NIOSH (Czerczak and Gromiec. The pharmaceutical cisplatin is an animal carcinogen and reasonably anticipated to be a human carcinogen as determined by NTP. 1969.. population from the National Health and Nutrition Examination Survey. intravenous medicinal use. Fourth National Report on Human Exposure to Environmental Chemicals 231 . whereas soluble platinum compounds (e.. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.g.. oral). 1975a. platinum metal and insoluble salts are very poorly absorbed (<1% of a dose) and cleared from the body within a week after a single dose. route of exposure (e. Saindelle et al. 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. 2000). When ingested or inhaled. metallic. or organometallic). 1975b). Platinum metal and insoluble salts can produce eye irritation. interval) Selected percentiles ( 95% confidence interval) Total * * * 50th < LOD < LOD < LOD 75th < LOD < LOD < LOD 90th < LOD < LOD < LOD 95th < LOD < LOD < LOD Sample size 2465 2689 2558 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 340 368 290 719 762 725 1406 1559 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1227 1334 1281 1238 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 884 682 618 568 667 723 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites < LOD means less than the limit of detection for the urine levels not corrected for creatinine. The carcinogenicity of other platinum compounds remains uncertain. Toxicity is determined by the type of compound (e...e. environmental levels) and health effects is available from Urinary Platinum (creatinine corrected) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U.g. Most absorbed platinum accumulates in the kidneys and is excreted in urine (Moore et al. cutaneous. Information about external exposure (i. inorganic salt.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. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.. Workplace air standards for external exposure are established for soluble salts of platinum by OSHA and ACGIH. 1969). inhalational. Platinum metal is biologically inert. and duration of exposure.g.S..

04 µg/L) in this Report. et al. Urinary platinum levels associated with dental gold alloys.. German environmental survey 1998 (GerES III): environmental pollutants in the urine of the German population. Thornton I. Raab W. Analyst 1998. Uptake of antineoplastic agents in pharmacy and hospital personnel.inchem. Crocker W.. Stilianakis NI. Wilhelm M. Boos KS. Herr et al. 3/31/08 Moore W Jr. In: Bingham E. Kelly J. Iavicoli I. Schulz C.9:152-158. Ewers U.inchem.org/documents/ehc/ehc/ ehc125.70(3):205-208. Urinary excretion of platinum from platinum-industry workers. Biological monitoring of hospital pharmacy personnel occupationally exposed to cytostatic drugs: urinary excretion and cytogenetic studies. Schierl R. Nowak D. 232 Fourth National Report on Human Exposure to Environmental Chemicals . ruthenium. Duneman L:Long-term urinary platinum. Moore W Jr. 2003. New York: John Wiley & Sons.. 2004) or less than 0. Finding a measurable amount of platinum in the urine does not mean that the level of platinum causes an adverse health effect. Grimm CH. Blanks R. Available at URL: http://www. 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. Gromiec JP. Begerow J.19:685-691. Bocca B. 1997. Platinum. Neuendorf J. Hall L. Farago ME. 1991 [online]. eds. Kazantzis G.4(1):27-36. 2001). Parrot JL. International Programme on Chemical Safety (IPCS).55(2):138-140. Ruff F: Histamine release by sodium cholorplatinate. References Becker K. Angerer J.207(1):69-73. 5th ed. Schierl R. Turfeld M. Schierl. Kuster W.10:63-71. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. J Expo Anal Environ Epidemiol 2003. One study found that traffic-control officers had no greater urinary platinum concentrations than office-based control subjects (Iavicoli et al.htm. 2004). Part 1: monitoring of urinary concentrations. Rommelt H. Schierl R. Biomonitoring studies on levels of platinum provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of platinum than are found in the general population. Patty’s Toxicology. International Journal of Hygiene and Environmental Health 2003. and in blood and urine in the United Kingdom. Kavanagh P. et al. Int Arch Occup Environ Health 2003.htm. Cohrssen B. Revised and new reference values for some trace elements in blood and urine for human biomonitoring in environmental medicine. Senofonte O. 1998). Schulz C.Metals the International Programme on Chemical Safety at http:// www. Pethran et al. Biomonitoring Information Urinary platinum levels reflect recent exposure. Kulka U. Br J Pharmacol 1969.. Hebert R. pp. 2003. Arch Environ Health:1969. Several studies have shown that background concentrations in general populations were usually less than 0. Levels of platinum in urine for the U.S. Environmental Health Criteria 125. 2003.org/documents/ehc/ehc/ehc125. Huber R. Environ Res 1975a. Hysell D.76(1):5-10.123(3):451-454. Schierl R. Int Arch Occup Environ Health 1997. Stara J: Preliminary studies on the toxicity and metabolism of palladium and platinum. et al. and platinum. Hauff K. Nickel. et al. Powell CH. population were below the limit of detection (0. Alimonti A. Saindelle A...56(3):283-286. which elevate urinary platinum by five to twelve-fold (Begerow et al. palladium. Platinum-industry and precious-metal workers had urinary concentrations about one-thousand times higher than general populations (Schierl et al. Jankofsky M.. Biomonitoring of traffic police officers exposed to airborne platinum.. Arch Environ Health 2001. van de Weyer C. Pethran A. 2003). Herr CE. Herr et al. Ruff F: Platinum and platinosis. Platinum concentrations in urban road dust and soil.. Influences on human internal exposure to environmental platinum. 2004.13(1):24-30. Int J Hyg Environ Health 2004. Occup Environ Med 2004. Seiwert M. Campbell K. Seifert B.61(7):636-9. Ensslin AS. Kaus S. palladium.35:313-321. Carelli G.. Saindelle A. osmium. Biomarkers 1999. Stara J: Biological fate of a single administration of 191Pt in rats following different routes of exposure. Fruhmann G. Occup Environ Med 1998. 1998).. Petrucci F. 289-380. Hysell D. Wilhelm et al. Environ Health Perspect 1975b. 206:15-24. 1999. 2000. Schierl et al. Gold-platinum dental restorations were correlated with increased urinary platinum concentrations. Czerczak S. Allergy and histamine release due to some platinum salts. rhodium. Pethran A.01 µg/L (Becker et al. Gieler U. and gold excretion of patients after insertion of noble-metal dental alloys. Fries HG.005 µg/L (Iavicoli et al.

300 (.270-.350-.250 (. the latter being the current major industrial consumer of thallium in this country.330-.370 (. however.210 (.180) 75th .360 (.390) .148-.220) .400-.350-. representing distribution into other tissues.170-. Human health effects from thallium at low environmental CAS No.173-.220) . Fourth National Report on Human Exposure to Environmental Chemicals 233 .250-.370-.260 (.159 (.400) 95th .240-.220 (.163) .160 (.167 (. In addition.320) .290) .430 (.330) .430-.290 (.430 (.240-.320 (.217) .490) .157-.155 (.260-.181-.270 (.173) . Thallium disappears from the blood with a half-life of several days.220 (.165 (.290) .147-.460) .260-.370 (.400 (.300 (.197 (.200) .180-.149 (.360 (. It is still used in relatively small amounts in pharmaceutical and electronics manufacturing.200 (..290) .184 (. 0.360 (.200 (.430-.400-.330) .480) .590) .200 (.210) .370) .420) .167-.360-.160-.360-.170) .02.154-.250-.330) .360-.240) .167-.420-.390-.218) .159 (.185-.220 (.470) .410-.230 (.133-.170-.340 (.260 (.400-.400) .330-.162-.270-.300) .350-.159 (.270 (.250-.370-.200-.370 (.230) .350 (.560) .420) .200) .480) .380 (.185 (.390-.400-.470 (. it has not been specifically mined or refined in the United States since 1984.280 (.172 (.490) .190 (. 2005).440) . 7440-28-0 General Information Elemental thallium is a blue-white metal found in small amounts in soil and in sulfide-based minerals.410-.180 (.170-.420-.440) .190 (.350) .180) .340-.290 (. Thallium exposure occurs primarily from industrial processes such as coal-burning and smelting.160 (. In the United States.420) .202 (.170-.440 (.360 (.400-.460) 336 362 290 697 746 725 1380 1545 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .450 (.260-.170) .187-.430 (.310 (.390-.350-.200-.243) .S.480) .390) .470) .330-.196) . and 03-04 are 0.250-.420) .440-.170-.200) .450 (.450 (.270 (.173) .280 (.150-.490) Total .160-.500) .146 (.450 (.510 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.02.171 (.200) .390) .410 (.380-.360-. 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.380 (.180-.510) .440) .170 (.330-.140-.500) .230) .380) .200 (.179-.350-.400) .320) .220) .160 (.172) .440 (.145-.370) .280-.430) .420-.520) .176 (.200) .02.460-.240) .520 (.320-.201 (.137-.192) Selected percentiles ( 95% confidence interval) 50th .270 (.490) .225) .280) .350-. interval) .145 (.170-.182-.160-.150-.220 (.230-.520) .630) .153-. see Data Analysis section) for Survey years 99-00.290 (.450) .158) .340-.180 (.310 (.390-.290) .300 (.450 (.180-.490 (.250-.370 (.300-.340) .290 (.550 (.400 (.450 (.370 (.450 (.420-.430) .360-.210 (.300) .300) .200-.390 (.280 (.390) .260) .150-.180 (.200) .197-.520) .220) .290 (.220-.280) .410-.350) .175) .430 (.420 (.410 (.160-.240) .250) .430-.200 (.280-.220) .370-.480) . and 0.210-.147-.200 (.410 (.188) .290-.460) 861 675 618 561 657 723 801 1114 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.410-.135-.400 (.330) .450 (.330-. thallium readily crosses the placenta and also distributes into breast milk.250-.410-.183) .250-.370 (.218) .250-.380-.300) .150-.170-. In the past.370 (.480) .340-.270) .177) .460 (.260-.360) .150-.170) .230-.500 (.410-.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 .170 (.440 (.240-.190-.Metals Thallium depilatory cosmetics.230) .156) .230-.310-.330-.201 (.410 (.410 (. respectively.340) .145-.260 (.590) .470) .470 (.178) .420) .191 (.370-. thallium was obtained as a by-product of smelting other metals.310 (.150-.260-.134-.420) .217 (.440 (.172 (.400 (. Elimination from the body tissues occurs slowly through urine and feces (Blanchardon et al.147-.190 (.202 (.400) . 01-02.239) .410) .350 (.400 (.330-.450 (.160 (.160-. From these and other sources.180-. population from the National Health and Nutrition Examination Survey.640) .270-.340-.310) .500) .420) .170 (.410 (.390 (.156) .230) .183) .400) .200-.320) .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 .190 (.190 (.290-.270 (.250 (.290) 90th .215) .220) .196) .206) .160 (. thallium is produced in a fine particulate form that can be absorbed through inhalation or ingestion.270) .690) .290 (.280) .156-.190 (.202) .144 (.220 (.

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

Investigation of a working population exposed to thallium. 2005) and are shown with results from NHANES 2003-2004 in this Report.35(1):4-9. Int Arch Occup Environ Health 1980. Schmidt M. Urinary concentrations of 100 μg/L in asymptomatic workers (500 times higher than median levels in the U. 7/15/09 Blanchardon E. 1998. Challeton-de Vathaire C. 1980. Environ Res 1998.47(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.atsdr. Trace element reference values in tissues from inhabitants of the European Union. Long term retention and excretion of 201Tl in a patient after myocardial perfusion imaging. Investigations of thallium-exposed workers in cement factories. 1981. Apostoli P. 1985). Kramer U. Fourth National Report on Human Exposure to Environmental Chemicals 235 . and serum of Italian subjects. Nearby residents were exposed by eating garden plants that had been contaminated by the thallium. et al. Atlanta (GA).265 people living near a thallium-emitting cement plant in Germany.5 μg/L. Minoia C. population) are thought to correspond to workplace exposures at the threshold limit value of 0. References Agency for Toxic Substances and Disease Registry (ATSDR). Morrow JC. Sampson EJ.Metals (CDC. 1998). Marcus RL. These urine levels are generally comparable to levels observed in earlier studies of general populations (Brockhaus et al. A study of 13 elements in blood and urine of a United Kingdom population. Toxicological profile for thallium.html. Sabbioni E. Martin J-C...cdc. et al. Cassot G. blood. Pozzoli L. White MA. et al. Paschal DC.113(1):47-53.95:89-105. Soddemann H.1 mg/m3 (Marcus. Schaller KH. Minoia et al. 2005. 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. Int Arch Occup Environ Health 1981. (1981) studied 1. Paschal et al. Seventy-eight percent of the urine specimens in that study contained greater than 1 μg/L.. Sci Total Environ 1990. Intake and health effects of thallium among a population living in the vicinity of a cement plant emitting thallium-containing dust. Ewers U. Celier D. 1990.S. X. Sabbioni E. Wiegand H.216:253-270. Trace metals in urine of United States residents: reference range concentrations. Gallorini M. White and Sabbioni. Finding a measurable amount of thallium in urine does not mean that the level of thallium causes an adverse health effect. Pietra R. Third National Report on Human Exposure to Environmental Chemicals. Valentin H. 1992 [online].. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Manke G. Raithel HJ.gov/toxprofiles/tp54. Available at URL: http://www. A study of 46 elements in urine. Brockhaus A. Boisson P. Schaller et al. Jackson RJ. J Soc Occup Med 1985. with concentrations ranging up to 76. Ting BG.76(1):53-59. Trace element reference values in tissues from inhabitants of the European community I. Sci Total Environ 1998. Centers for Disease Control and Prevention. Radiat Prot Dosim. Buhlmeyer G. Pirkle JL. Dolger R. Brockhaus et al. 2005.48(4):375-389.

their illness may stem from exposure to cobalt mixed with tungsten carbide rather than to tungsten alone. Human health effects from tungsten at low environmental doses or at biomonitored levels from low environmental exposures are unknown.130) .350) .380-.078-.310-.204) .084-.S.290) . see Data Analysis section) for Survey years 99-00.360-.530 (.340) .210 (.060 (.650) .240-.450-.070 (.320 (.490) .090) .090 (.360 (.101 (.110) .510-1.092 (.370 (.53) .360 (.100 (.770 (.160-.058-.095-.04. Evidence is lacking for the carcinogenicity of tungsten.260 (.080 (.070 (.500 (.360) .160 (.260-.400 (.110-.520) .070) .560) . population from the National Health and Nutrition Examination Survey.230 (.300 (.290-.370-.110 (.120) .350 (.150) .210 (.210 (.430 (.250) .069-.135) .080-.300 (.220) .082-.310) . Tungsten is used mainly for producing hard metals.570 (.101-.097-.290) .113 (.113 (.130) .100) .190-.066-.090-.120-.100) .200 (. and it has not been classified with respect to its carcinogenicity by either IARC or NTP.190-.180-.620) .060-.070-.260-.096-.230) .140) 90th .830) .350-1.113 (.190) .110-.113 (.092 (.158 (.150-.160) .400-.470) .110 (.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 .111-.280 (.370 (.330-.120-.230-.180-.510-.460 (.170) .270-.630) .380 (.090) .320-.230-.170-.060-.120) .110) .093 (.310-.105) .071 (.088 (.082) .090) .087) .450 (.340-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.056-.130-. Tungsten compounds are used as lubricating agents.670) .120-.470) .430) . and for producing ferrotungsten.330 (.077-.220) .070-.100-.210 (.060-.080-.093) .400) .420-.550) .140 (.430 (.120) .130) .620) .080) .200) .810) .180-.330) .310-.110 (.550 (.430-.050-.100) Selected percentiles ( 95% confidence interval) 50th .520) .060 (.126) .430-.380 (.800) .120-.350) .530 (.290-.076 (.100-.070) .140 (.400 (.470-.320) .330) . Little information is available on the toxicity of tungsten.380-.160 (. 236 Fourth National Report on Human Exposure to Environmental Chemicals .380) .080) .122) .084 (. filaments for incandescent lamps.090-.082 (.300-.090-.410 (. respectively.090-.04.210) .050-.080) 75th .090-.107 (.390) . Urinary Tungsten Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.180) .104) .110-.560) .062 (.400 (.100 (. 01-02.130 (.074-.100 (.120) .470 (.430 (.620 (.310 (.460 (.290 (. and 0.470 (.190 (.120) .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 .080-.080) . and as catalysts in the petroleum industry.130 (.140 (.160-.137 (.390 (.410-.420-.04.082 (.123-.151) .270-.200-.140 (.116) .070) .071-.00) . 0.360-.Metals Tungsten CAS No.080 (.090) .240 (.790) .460 (.230-.133) .480) Total .073-. interval) . Occupational exposure is from dusts released during grinding or drilling of hard metals.073) .140-.690) .180-.100) .064-.400 (.050-.180) .320 (.160-.160-.270-.110 (.270 (.590) .260 (.340-.160 (.280 (.550) .950) .080 (.170 (.050-.096 (.130-.270 (.230) .150 (.100 (.070 (.090-.250) . Most background environmental exposures to tungsten are from the soluble forms such as tungstate salts that may occur in drinking water.132) .210-.100-.120-.087-.073 (.073-.250) .460) .084) .270 (.260) .560 (.560) .065-.260-.180) .230-.065 (.250) .520) .105 (.360 (. which is used in the steel industry.370-.250) .510 (.300) .180) .093-.140-.088) .130) .170) .210 (.091) .270-.080 (.130-.580) . bronzes in pigments.070-.340-.370) .800) .070) .170 (.530 (.109) .380-.190-.130) .076 (.250-.370 (.280-.060 (.190 (.490 (.130-.060 (.220 (.410) 790 680 618 562 649 723 802 1117 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.220-.060 (. which are used in rock drills and metal-cutting tools.310-.250-.160 (.350) .160) .100) .320-. mainly as scheelite (CaWO4).070-.069) .180 (.500 (.220) .081 (.090-.120-.110 (.170) .090 (.060-.150 (.080 (.440) .380-.056-.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 .300) 95th .068) .092) .070-.190-.060-.120) .095-.330-.060-.550) .640 (.460) .170) .150 (.160 (.290-.100) .062 (. 7440-33-7 General Information Tungsten is a steel-gray to tin-white metal that occurs naturally in the earth’s crust.310-.570 (. Although workers occupationally exposed to tungsten carbide may develop serious lung disease (“hard metal disease”).500) .560) .090 (. and 03-04 are 0.060 (.120 (.086 (.250) .090-.300 (.180 (.

(1987) found possibly due to methodologic.169 (.091 (. Workers involved in grinding operations that released tungsten metal into the air had elevated urinary levels that Levels of urinary tungsten reflect recent exposure.333 (.258-.218 (.187) .359 (.284) .379 (.071 (.634 (.082) .103-.253) 95th .364 (.136-. 1997).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 .28) .214) .215) .098-.354) .462) .106 (.190) .049-.S.075-.436) .317 (.063-.075) .270 (.122 (.094-.083-.084 (.168 (.167) .186 (.358) .146) .287) . Using neutron activation analysis to 2000.317) .079) .077) .465) .122-.158) .167-.286-.201) .067-.272-. In whereas the tungsten-worker group had mean urine levels a Nevada community where tungsten was measured and 35 times higher.091) . similar to those in this Report (Schramel et al.267-.090-.139) .154) .331-.082 (.157) .333 (.143 (.145 (.347 (.197 (.275 (.078 (.197) .116 (. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.060-.151 (.063-. 2001-2002.139 (.299 (.054-.111 (.144-.340 (.108) .071 (.105 (.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 .224) .184 (.300-.086) .201 (.065 (.120) .333-.117) .150-.098-.093-.124-.136 (.094) .065 (.265 (.060 (. 2005).465) .216-.410-.386) .133) 90th .167) .554) .077) .216 (.085) . population from the National Health and Nutrition Examination Survey.797) .088) .095-.070 (.199 (.S.063-.739) .146 (.317-.205-.058-.222) .301) .198) .253 (.071-.250 (.119 (.216-.237) .439 (.130 (.071 (.091 (.068-.085-.065-.122-.285) .180-.079) .061-.138 (.133) .426) .091) .080 (.091) .116) .148 (.153) . and 2003-2004 (Paschal et al.605) .197) .197-.086) .(Kraus et al.206-.333 (.179-.073 (.083 (.148) .070 (. population.075) . 2003. population (CDC.056-.. 1998).392) .136-.459) .098 (.315-.130-.158 (.155-.074-.582) .063-.064-.158) .353 (.109 (.154) .068 (.222-.079) .426) .084) .727) .117 (.181 (. A study of 14 unexposed adults yielded values that were similar to the 95th percentiles in this Report.080-.059 (.333) .061-. or exposure that a control group of non-metal workers had mean levels differences.216-.104-.074) .240-.482 (.139-.133) .092) .060-.412 (. 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.353 (.138 (.329-.056-.107-.267) .067 (.279 (.S.077-.125) .108-.074-.484 (.061-.667 (.497 (.279 (.109-.066 (.083) .245-.120) .131-.059-.300-.359 (.431) .Metals Workplace air standards for external exposure have been established by ACGIH and recommended by NIOSH.100) .215 (.071) .341 (.091) .069-.261-.233-.188-.100) .093) .116-.088) .258 (.198-.176-.119-.231 (.158) .073 (.073 (.203-.057-.069 (.084 (.333) .354-.081-.214-.065-.067 (.121 (.098-.072-.555 (.283) .057-.179-.065-.078 (.439 (.344-.138) .073 (.078) .124 (. population in the NHANES 1999-2000 slightly higher values than those found in NHANES 1999.308) .326) .255 (.329 (.439) Total .071) .383 (.169) .484) .237-.089 (.086) .062 (. Patients with medically-inserted tungsten found at increased levels in drinking water.087 (.199 (.100 (.431) ..176-.385 (.072-.453) .150 (.436-1.105 (. 2001).086-.375) .090-.216 (.301) .255-.308) . Biomonitoring Information median urinary levels were as much as 15-fold higher than median levels in the U. Nicolaou et al.294 (.077-.083 (.381) .072 (.096) .211 (.293 (.167-.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 .237) .069 (.081) .174) .089) .085 (.200-.075 (.146 (.083) .452-.136-.126-.278-.306) .081 (.098) .079) .087) .055-.161) .053-.094) .302-.066 (.121-.250-.152-.339 (.063 (.078-.125 (.095) Selected percentiles ( 95% confidence interval) 50th .099-.078) .082) .360 (.164 (.084) .074 (.143-.063 (.153-.300) .250 (.667) .079 (.500) .170-.059-..538) .074) 75th .880) .333-.333 (.080-.209-.059-.075 (.065) .174 (.081 (.217-.414) .208-.200-.301) .231-.255 (.253-.165) .071) .064-.279 (.302-.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 .144 (. interval) .079 (.217-.075-. A were more than 900 times higher than the overall geometric nonrandom subsample from NHANES III demonstrated mean of the U.054-.080 (.136-.300 (.823) .339 (.150-.431) . measure urinary tungsten.

Trace metals in urine of United States residents: reference range concentrations. Centers for Disease Control and Prevention.69(3):219-223. palladium. Paschal DC. cadmium. J Trace Elem Electrolytes Health Dis 1987. The determination of metals (antimony. Nicolaou G. Nevada Exposure Asssessment. 2005. Catheter Cardiovasc Interv 2004. Feuerbach S. Third National Report on Human Exposure to Environmental Chemicals. thallium. References Bachthaler M. Mosconi G. lead. Churchill County (Fallon). Atlanta (GA).(2):73-77. bismuth. Kraus T. 4/15/09 Centers for Disease Control and Prevention. Seghizzi P.58(10):631-634.. Finding a measurable amount of tungsten in the urine does not mean that the level of tungsten causes an adverse health effect. platinum. Pietra R. Ting BG. Schaller KH. Exposure assessment in the hard metal manufacturing industry with special regard to tungsten and its compounds.gov/nceh/clusters/Fallon/study. Paetzel C. Wendler I. tellurium. Urinary tungsten levels in many patients were hundreds-fold higher than observed in this Report.htm. Link J. et al. Environ Res 1998. and hair (Bachthaler et al. 238 Fourth National Report on Human Exposure to Environmental Chemicals . 2004). Angerer J. Pirkle JL. Available at URL: http://www.Metals blood. Weber A. tin and tungsten) in urine samples by inductively coupled plasma-mass spectrometry. Schramel P. Angerer J. [online] 2003. Cassina G. Zobelein P. mercury. Int Arch Occup Environ Health 1997.cdc. Jackson RJ. Lenhart M. Morrow JC.76(1):53-59. Schramel P. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. Manke C. 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. Multielement determination of metals in biological specimens of hard-metal workers: a study carried out by neutron activation analysis. Cancer Clusters. urine. Sampson EJ. Corrosion of tungsten coils after peripheral vascular embolization therapy: influence on outcome and tungsten load. Occup Environ Med 2001.62:380-384. Sabioni E. National Center for Environmental Health.

007-.018 (.036-.012-.020-.027) .040) .042 (.019-.036 (.040-. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.024-.034-.013-.007-.017-.033) .024-.007) .011) .008 (.009 (.016-.065) .008) .045) .027 (.010) .011 (.022 (.019-.054) .006 (.028 (.016) .030 (.016) .010 (.007 (.008 (.037-.012-.056) .011) .007) .009) .015 (.009) .009 (.006-.060 (.017-.010) .009-.019 (.045) .006-.013 (.035-.037) .018) .020-.032 (.052 (.040) .007 (. It usually occurs as an oxide and is extracted from ores containing less than 1% natural uranium.007) .Metals Uranium CAS No.033 (.007-.013) 90th .033 (.009 (.009-.006 (.021) .020 (.031 (.008) .022-.72%).029-.011-. the primary exposure sources for nonoccupationally exposed persons are dietary (especially root vegetables) and drinking water.012-.020) .037) .005.016-.053) . 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.031 (.021 (.046 (.025-.009-.013 (.011-.021 (.046 (.014 (.012 (.011-.023-. Fourth National Report on Human Exposure to Environmental Chemicals 239 . DU has been used by the military in armor-piercing ammunition and as a component of protective armor for tanks.020-.015 (.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 .031 (.010 (.023 (.031 (.026) 95th .039) .009) .020-.024 (.010 (.048 (.008 (.279) .010) .007-.030 (.007-.028-.008) .046 (.043) .009) * .014 (.006-.006-.014 (.009) .028 (.035) .012-.007-.033-.031 (.013 (.009 (.009) Selected percentiles ( 95% confidence interval) 50th .013-.044 (.072) . and 234U.006-. see Data Analysis section) for Survey years 99-00.019-.010-.008 (.016) .010) * .009) .026) .017) .016) .015-.008 (.009-.048) .005-.007-.008 (.034) .010 (.019-.007 (.023-.007 (.053 (.064 (.009-.008-.008-.009-.012 (.010-.008 (. Exposure to DU may occur in military personnel from retention internal shrapnel that contains DU or exposure to dust generated from ammunition Urinary Uranium Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.012 (. 0.010) .027-.027 (.027 (.007-.026 (. 7440-61-1 General Information Uranium is a silver-white metal that is extremely dense and weakly radioactive.008 (.023 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.009) .065) .006-.007-.021-.012) .010) .004.016) .009) .055 (.008-.030) .041 (. 235U (about 0.067) .049) .010-.014 (.030 (.054-.006-. human exposure occurs primarily by inhaling dust and other small particles. nuclear fuel.013) .026 (.009 (.S.026-.017) .020-. 01-02.028 (.009-.042) .023-.029-.011-.008 (.018) .010 (. population from the National Health and Nutrition Examination Survey.050) .008-.067) .005-.016) .038) .011) .023) .007-.011-.008 (.024-.007-.023-.008 (.009) .007 (.011-.005-.026-.041 (.051) .018) .009-.037) Total . interval) . including nuclear weapons.006 (.011) .046-.023) .007 (.005-.012) .034-. Variable concentrations of uranium occur naturally in drinking water sources.009-.027 (.014 (.009 (.027) .009) .009) .017) .012-.069) .015 (.022-.028-.049) . Thus.009) . and 03-04 are 0.009) .062) .036) .011) . Natural uranium is a mixture of three isotopes: 238 U (greater than 99%).073) .010-.009 (. respectively.005-.023 (.017-.014 (.006-.029 (.017-.007-.046) . or processing.027-.036) 883 683 618 568 667 722 822 1132 1074 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.013 (.007-.114 (.007-.006-.016-.007-.012 (.030-.004.026) .006-.008 (.063) .010) .018 (.088) .158) .011) .016 (.007) .021) .031-.007 (.008-.013-.006-.007 (.018-.017) .127) .040-.007) .038) 340 368 289 719 762 725 1405 1560 1543 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 .007-.023) . and 0.012 (.008-.008 (.008 (.017) .021-.010-. In workplaces that involve uranium mining.012 (.008) .013 (.007 (.011 (.017-.010) .010) .008-.006 (.035) .010-.009 (.037 (.011) . Uranium has many commercial uses. Since the 1990’s.036) .022) .021 (.040 (.009) .007 (.006-.050) .027-.021) .022-.015) .009 (.008 (.015) .009 (.039) 1227 1335 1280 1237 1355 1277 Females Race/ethnicity Mexican Americans 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 .008-.027) .038 (.012-. in some ceramics.018) .012) .007-.017-.010) * .007 (.008 (.040 (.008 (.009-.017 (.015 (.026 (.039-.011-.020) .047 (.013 (. and as an aid in electron microscopy and photography.012) .043 (. milling.007-.027) .046 (.054) .013 (.008) .007) 75th .037) .006-.017 (.036 (.066) .036-.039) .056) .

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

NRC. Metivier H. Workplace air standards and guidelines for external exposure to soluble and insoluble uranium compounds have been established by OSHA and ACGIH.S. A cohort of 46 U.. McDiarmid M.S. the median urinary concentration was 0. Komaromy-Hiller et al. in that the levels were below their respective detection limits (Byrne et al. Eighty-five percent of those levels were above the 95th percentile of the NHANES 1999-2000 population.. Pullat VR. 2004).S. Thomas RG. 2006).066 μg/g creatinine (Gwiazda et al.e. References Bhattacharyya MH. Horan P. Karpas et al. Third National Report on Human Exposure to Environmental Chemicals. Mil Med 2003. Dietz LA. 2003.html. IARC and NTP have no ratings for uranium human carcinogenicity.78:143-146. Hamilton et al.62:562-566. Nuclear Regulatory Commission (NRC) has set an action level of 15 μg/L urinary uranium to protect people who are occupationally exposed (U. Durakovic A.. Health Phys 1992. In the same study. 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. (Kurttio et al... eds. urinary levels of uranium were as high as 9. Older studies have demonstrated urinary uranium concentrations that are consistent with levels in the U. In 17 U. and no consistent effects on multiple endpoints of kidney function were found... 1-49..S. Radiation protection dosimetry. Stradling GN. environmental levels) and health effects is available from ATSDR at: http://www. Breitenstein BD. 1992. Benedik L. but in whom no shrapnel was embedded.65 μg/L). Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.110 to 45 μg/L (Ejnik et al. Six workers in a depleted uranium program showed concentrations of 0..168(8):600-605. 2000). 2004).. et al. Biomonitoring studies on levels of uranium provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of uranium than are found in the general population. Atlanta (GA). 41 (1). 1994. 2002.. Information about external exposure (i. 2004). Galletti. Uranium content of blood. 1978).atsdr. Drinking water and other environmental standards have been established by U. 2006). Guidebook for the treatment of accidental internal radionuclide contamination of workers.55 μg/L (median 0. with emphasis on quality control. In: Gerber GB. Fourth National Report on Human Exposure to Environmental Chemicals 241 . the median urinary uranium concentration was 2.. 2006). 2002). Health Phys 2000. 28 soldiers who may have been exposed to DU by inhalation. Hamilton MM. 1991. A previous nonrandom subsample from NHANES III (n = 499) (Ting et al. Squibb K.. respectively. Carmichael AJ. Urinary uranium measurements in 103 Canadian military personnel showed mean urinary levels slightly less than geometric mean in this Report (Ough et al. Boyd P. 2004). Muggenburg BA. Zimmerman I.162 μg/L) (Orloff et al. Sci Total Environ 1991.S.. or wound contamination. McDiarmid et al.gov/ toxpro2. 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. 2006. The U. soldiers who had been injured and had embedded DU shrapnel for as long as eight years.011 μg/L (McDiarmid et al. 2000). Dang HS. Tolmachev et al. 2005. 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. Recent studies of veterans have been conducted to examine concerns about DU exposure during military conflicts. Pillai KC. In two studies of a Finnish population with high natural uranium concentrations in their drinking water. soldiers evaluated before. although slightly increased during and after deployment. In a much larger study of 446 Gulf War veterans who were concerned about past exposure to DU.107:143-157. Centers for Disease Control and Prevention (CDC). 1999) and other small populations have shown urinary concentrations that are similar to those in NHANES 1999-2000.1992. the geometric mean urinary uranium concentration was 0. Finding a measurable amount of uranium in urine does not mean that the level of uranium causes an adverse health effect. EPA.. Kent (England): Nuclear Technology Publishing. 2006).61 μg/g creatinine. pp. (May et al. Volf V. ingestion. Ejnik JW.Metals injury associated with elevated urinary uranium levels (Kurttio et al.1996. population. and 2003-2004 (Dang et al.078 μg/L (ranging up to 5. 2001-2002.cdc.S. had a mean urinary uranium concentration of 0. Byrne AR. urine and hair of exposed and non-exposed persons determined by radiochemical neutron activation analysis. during.... Determining the normal concentration of uranium in urine and application of the data to its biokinetics. Biomonitoring Information Levels of urinary uranium reflect recent and accumulated exposure. Determination of the isotopic composition of uranium in urine by inductively coupled plasma mass spectrometry. In a study of 105 persons exposed to natural uranium in well water. Vol.

Kane R.91(2):144-153. Engelhardt SM. et al. McDiarmid M. Ejnik J. et al. VI. Scott K. J Toxicol Environ Health A 2004. Oliver M. Roth P. and inexpensive method for determination of uranium in urine and fresh water: comparison with LIF. Nuclear Regulatory Commission (NRC) Guide 8. Orloff KG. Int Arch Occup Environ Health 2006. U. Health Phys 1996.87:51-56. Ash KO. Metcalf S.110(4):337-342.S. Gwiazda RH. Kalinsky V. Ting BG.296(1-2):71-90.S. concentration and daily excretion of uranium in urine of Japanese. Howerton K. Wilson PD. Comparison of representative ranges based on U. Pirkle JL.79(1):11-21. Health Phys 2004. NRC). Health Phys 2003.82(4): 527-532. Element reference values in tissues from inhabitants of the European community. Tolmachev S. Health Phys 2004.S. July 1978. Uranium daily intake and urinary excretion: a preliminary study in Italy. Health Phys 2002. Am J Kidney Dis 2006. Auvinen A. Makelainen I. Andrews WS. Hollriegl V. Inductively coupled plasma mass spectrometry as a simple. Sabbioni E. Salonen L.81:45-51. Karpas Z. Cordero S. Smith D.86:12-18. Kurttio P. Gucer P.22–Bioassay at uranium mills. Squibb K. Marko R. Kidney toxicity of ingested uranium from drinking water.71(6):879-85. Salonen L. Saha H. Pinto V. Katorza E.94:319-326. 242 Fourth National Report on Human Exposure to Environmental Chemicals . Sci Total Environ 1994. Nuclear Regulatory Commission (U. Saha H. Shelly T. Roiz J. et al. Lewis BM. Environ Res 1999. Komaromy-Hiller G. U. Lorber A.47(6):972-982. Komulainen H. Biokinetic modeling of uranium in man after injection and ingestion. Ough EA. Squibb K. Environ Res 2004. Kuwabara J. Uranium and thorium in urine of United States residents: reference range concentrations.S. Marino R. Li WB. Costa R. Halicz L.85:228-235. plasma and urine and a critical evaluation of reference values for the United Kingdom population. Renal effects of uranium in drinking water. Biological monitoring and surveillance results of Gulf War I veterans exposed to depleted uranium. et al. Mistry K. Hancock RG. D’Annibale L. Paschal DC. Detection of depleted uranium in urine of veterans from the 1991 Gulf War. Kurttio P.44:29-40. Cremisini C. Englehardt SA. Auvinen A.Metals Galletti M. Wahl W. Jarrett JM. Health Phys 2006. Washington (DC): NRC. Harmionen A. Radiat Environ Biophys 2005. Clin Chim Acta 2000. Jackson RJ. rapid.158:165-190. Oberbroekling KJ. Noguchi H. Bennett LG. McDiarmid MA. Oeh U. Pekkanen J. Biologic monitoring for urinary uranium in Gulf War I veterans. Military deployment human exposure assessment: urine total and isotopic uranium sampling results. Paretzke HG. Human exposure to uranium in groundwater. Van der Venne MT. Hamilton EI. et al. Environ Health Perspect 2002.67(8-10):697-714. Charp P. Karpas Z. Review of elements in blood. McDiarmid MA. May LM. An examination of uranium levels in Canadian forces personnel who served in the Gulf War and Kosovo. Sampson EJ. Heller J. patient population and literature reference intervals for urinary trace elements. et al.

0 (11.30 (2.40 (8.10-4.0) 11.38) 5. Perchlorate has been characterized as a mobile and persistent ground and surface water contaminant.5 hours and has a small estimated volume of distribution (Crump and Gibbs. 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.30 (5.00) 3.60-7.80-4.0 (11.90-9.10-7. and reducing agents.20-3.80) 12.0) 14.40) 3. Perchlorate is excreted unchanged from the human body with an estimated elimination half-life of about 7. 7601-90-3 General Information Perchlorate is an inorganic chemical containing one chlorine and four oxygen atoms. and limited applications in pharmaceutics.0-17. and electroplating.90 (5.70-11.0 (9. Large doses of perchlorate have been used as a medicine to treat hyperthyroidism and to diagnose disorders related to thyroid or iodine metabolism.0) 15. fabric dyeing.90-9.66) 3.30-19.60 (4.90 (5.80 (7.40-4.16) 3.50 (5.19-4.89-3. milk.0 (11.0-18.70-3.00-6.0) 13.62 (3. interval) 3.44-4.0 (8.68) 4.50) 5.0 (12.0) 8.84) 14.10 (7.01 (2.20) 4.90-11.0-17.35 (3.05 and 0.50 (3.40 (3.75 (3.60 (4.40) 6.70-3.Perchlorate Perchlorate (Urbansky.10-11.40 (5.0) 13.70) 3.0) 13.0) 15.10) 5.29-3.55) Sample size 2820 2522 01-02 03-04 01-02 03-04 01-02 03-04 4.39-4.70-5.90) 6.18-3.32 (3.50-11.0-23.20 (2.76 (3. laboratory analysis.0) 708 617 681 652 1228 1092 Limit of detection (LOD.0-14.0) 11.0) 10.70-6.20 (2.90 (3.50-4.0) 9. certain catalytic metals.40 (5.87-3. lettuce) can be the main sources of intake for humans (FDA.70 (3.10-12.0) 19.96 (3.0 (8. Other manufactured uses include fireworks.80 (6.40-13.20-11.0 (11.08-3. The ammonium salt of the perchlorate ion has been manufactured in the military defense and aerospace industries primarily for use as an oxidizer in solid propellant systems for rockets and missiles.05.76) 4.20 (4.90 (2.40) 3.40) 3.80-12.20-12.20) 7.19 (3.56) 3.51 (3.60) 3.0-20.11) 4.0 (11.30-7.0) 13.g.05 (2.80-8.54 (3.60 (7.50-7.40-5.40 (4.07-4.10) 12.40) 90th 10.47-4.0 (9.0) 14.00-6. 2001-2002 performed on surplus samples (variable unavailable of NHANES website) Fourth National Report on Human Exposure to Environmental Chemicals 243 .90-11.80-6.09) 3.80 (3.40-6.90-12.40) 2.40-11.0) 14.0 (9.0) 1335 1229 1485 1293 01-02 03-04 01-02 03-04 01-02 03-04 4.67-5.S.0 (11.30-7.90-3.0-29.0) 13.0) 9.10 (5.20 (5.30 (5.0-15. matches.0 (8.00-5. 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.20-4.0 (8.10-11.70 (3.10 (2.0 (11.0) 9.50-4. In addition.12) 3.00) 4.65) 3.22-5.60) 5. and certain plants with high water content (e.40-4.00) 3.0 (12. It is normally found and produced as the anion of a sodium.50) 5.49-3.0-19.30 (2.03) 3.90-10.0) 16.75-3.90-3.40 (5.20 (6..40) 4.90 (4.10) 5.0-17. Perchlorate was added to the U.70-9.93-4.90) 5.50 (8.0-18.0-17.0-17.26 (2.70 (3.88) 3. see Data Analysis section) for Survey years 01-02 and 03-04 are 0.20 (4.0-17.40 (4. or ammonium salt.50) 3.40 (3.0) 9.51 (3.30) 6.20 (8.0) 9. leather tanning.70-12.0) 9.70-7.93-3.79 (2.30-6.46) 3.0 (9.0) 10.22 (2.80) 7.02 (3. Drinking water.0 (12.10) 3. Perchlorate is stable under most environmental and physiological conditions.80 (3. Animal and human studies have shown that perchlorate can inhibit thyroid hormone production (NAS.0 (11.20 (7.45-4.90 (5. potassium.74-3.90-6. 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.10) 3.50) 11..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. 1998).30-17. but has strong oxidant properties in the presence of concentrated acids.20-4.0 (11.0 (10.0 (9.0) 8.S.0) 10.93 (4.11) 3.00) 5.0) 13.0) 13.31) 2.0-18.0) 13. Survey years 01-02 03-04 Geometric mean (95% conf.0) 12.00) 7.0 (9.50) 6.81) Selected percentiles ( 95% confidence interval) 50th 3.0 (8.80) 3.S.21 (2.0) 95th 14.60) 8.50-3.0) 11.10 (6.80-15. 2005).30) 6.0 (12.0) 374 314 828 721 1618 1487 01-02 03-04 01-02 03-04 4.0 (9.20) 3. 2005). 2007).81-16.80-4. 2002).40-7.0 (11.EPA.0-15.80) 75th 6. population from the National Health and Nutrition Examination Survey.0 (13. small amounts of perchlorate can form naturally in the atmosphere (Dasgupta et al.10 (6.60-6.

S.00 (4. Also.87 (7.30) 5..25 (3.56-3.50) 2..51 (3.S.26) 4.0-19.70 (4.60 (3. Short term human studies of the effect of perchlorate on RUI have been used for risk estimation (Greer et al.60) 8.02-4.50) 6.93-5.60-6.39) 2.41-9.0 (9..82 (5.33-12.50-3.12 (6. and the presence of other substances known to affect thyroid function (e. 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.86) 4. levels.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 .22-6.70) 10.09 (7.00-2.93-7.20 (4.60-8.5) 8.60-5.3) 8.87) 2..0 (11..S.10) 6.80 (4.24-2. dietary iodine intake. 2006. 2000). age.1) 8.33-6. Lawrence et al. although iodine intake was higher than U.4) 13.35) 3.30) 3.35 (4.26 (3.43) 6.71 (5.70-3.0) 1335 1220 1483 1284 01-02 03-04 01-02 03-04 01-02 03-04 3.50) 2.00) 9.36 (8.0-14.61-10.30-5.00) 3. Though it produces follicular cell thyroid tumors in animal studies at goitrogenic doses. nitrate. urinary perchlorate at environmental exposure levels were inversely associated with thyroxine levels and positively associated with levels of thyroid stimulating hormone (Blount et al.72 (3. levels and sufficient in most participants (Tellez et al.0-14.0) 13.6) 12. perchlorate is negative in most genotoxic assays (U.90-20.50-9.40-10. In the U.0 (9. medications). 2005).S.EPA.20) 3. Lamm and Doemland.90-11.10) 13. Steinmaus et al.89 (2.10-3.8 (11. Many factors may be important in consideration of perchlorate action on the thyroid: dose.0) 11. During gestation and infancy.70 (2.90-3.20) 8. up to 68% RUI has been demonstrated.5 (13.20 (6.1-16.2) 8.0) 12.40) 5.77 (3.50) 9.00-3.07 (2..0-17.39-4.6) 20.90 (2.90 (7.00) 4.05 (4.84) 2. 2002).95 (2. 1999. Greer et al.50) 95th 12. 2002. NAS.1 (8.20-4.22-4.08 (3.90-15.41) Sample size 2818 2504 01-02 03-04 01-02 03-04 01-02 03-04 5.30 (5.20-3.03 (2.20-3. congenital hypothyroidism is a condition for which nearly all newborn blood is screened.04-3. However.76 (3.70 (2. 2007).08) 3.0) 374 313 827 715 1617 1476 01-02 03-04 01-02 03-04 3. but without effects on serum levels of thyroid stimulating hormone or thyroxine (Braverman et al.09) 3.39 (3.04-3.46-4.83 (5.18-3.90 (4.90 (2.58) 2.EPA. 2005).75) 3.60-15.25) 5. gender.6-17.30 (3.99-3.3) 12.42 (3.73) 3.93-5.20 (2.61 (5.60-11.70) 2.90-2.1-22.0) 9.4 (8.29-6.4-16.80 (7.22-4.70-5.44-6.25) 5.0) 13. 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.80 (7.20 (7.52-9.S.91) 4.0) 12.00 (6.40) 3.40 (3. 2005.50 (3.89-3.30-5.4) 8.20-9.30 (6.Perchlorate inhibition (RUI).44) 3. it is known that maternal and congenital hypothyroidism adversely effects neurological development and decreases learning capability.0) 4.64-3.02) 3.51-4.87-3.g.70-4.54 (2.70-15.60-3. Li et al. suggesting its tumorgenic effect is a result of a chronic increase in thyroid stimulating hormone indirectly resulting from iodine uptake inhibition.40) 17.14 (2.10 (4.4 (10. menopausal status.S.98) 3.87) 7.0) 12.20-10.53 (2.46 (3.50) 5.64) 5.15-12. 2003.0 (8.93-8. U.12-2.99 (5. 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.2) 8.30) 90th 9.3) 11. women with urinary levels of iodine less than 100 micrograms per day.19-6..0 (8.0 (10.90) 5.0) 9.60) 3.0) Total Age group 6-11 years 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites 3.67) 5.10) 3.50 (6. 2002.74) 7.0) 7. in a representative sample of U.0) 6.0-44.10-7.1 (11.25) 5. 2001.30-10.16-3.. chronicity of exposure.87 (5.32) 5.7 (11. interval) 3.60-11.0) 10.59) 3.0) 12.50-5.90-9.10 (2. 2005.19-10.29) 2.80-3.40 (7.1-14.33 (7.52 (8.22 (2.0 (11.60) 10..34-3.35 (2.81-3.00 (2.10) 4. population from the National Health and Nutrition Examination Survey.0) 14.1-13. Survey years 01-02 03-04 Geometric mean (95% conf.66) 3.30) 75th 5.96) 2.47) 2.60-8.10 (4.93) 3.3 (10.60-5.37-13.76-3.40 (4.24 (4.80-3.0 (11. thiocyanate.46-13.37 (4.40 (3.80) Selected percentiles ( 95% confidence interval) 50th 3.S.56 (3.10 (6.54 (3.45) 3. 2005).3-14.4 (11.0 (9.61-5..00-11.45-2.4 (11.20 (3.97-5.10 (1. 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.21 (2.

most of the population is considered to be below the U. Additional information about exposure and health effects is available from the U. He X. newborn thyroid function. Health Implications of Perchlorate Ingestion. Environ Health Perspect 2002.gov/toxpro2. The effect of perchlorate. Blount et al.113(11):A732.Perchlorate be unlikely to occur without overt perturbation of thyroid homeostasis. Kelsh MA. 2001-2002. Erratum in: Environ Health Perspect 2005..atsdr. Thyroid 2000. J Expo Sci Environ Epidemiol 2007. 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. Washington (DC): National Academy Press. 2005. Health effects assessment for environmental perchlorate contamination: the dose response for inhibition of thyroidal radioiodine uptake in humans.45(10):1116-1127. Gibbs JP. CFSAN/Office of Plant & Dairy Foods. J Occup Environ Med 2000.fda.40(21):6608-6614. Pino S. Lawrence J. Erratum in: J Occup Environ Med 2004. Braverman LE.S. Braverman LE. Doemland M. Lamm SH. Deyhle GM. Crump KS. National Academy of Sciences (NAS). Kirk AB. Blount BC. (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.114(12):1865-1871. Finding a measurable amount of perchlorate in urine does not mean that the level of perchlorate causes an adverse health effect. Low dose perchlorate (3 mg daily) and thyroid function. Long-term environmental exposure to perchlorate through drinking water and thyroid function during Fourth National Report on Human Exposure to Environmental Chemicals 245 . Crump KS. Pirkle JL.html and from ATSDR at: http://www. EPA reference dose (Blount et al. Greer SE. Environ Health Perspect 2007. J Occup Environ Med 2003. Perchlorate in the United States. Lamm SH.90(2):700-706. References Blount BC. Primary congenital hypothyroidism.10(8):659-663. 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. et al.gov/Food/FoodSafety/ FoodContaminantsAdulteration/ChemicalContaminants/ Perchlorate/ucm077653. Page Last Updated: 05/28/2009. Food and Drug Administration (FDA).html. J Clin Endocrinol Metab 2005. 6/2/09 Greer MA. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. epa.htm.S. Li Z.gov/safewater/ccl/perchlorate/perchlorate. Benchmark calculations for perchlorate from three human cohorts.113(8):10011008. Braverman LE. When these NHANES 2001-2002 urinary levels of perchlorate are used to calculate daily oral intakes for the U. Skeels MR. Lawrence JE. Biomonitoring Information Urinary perchlorate levels reflect recent exposure.115(9):1333-1338. Pino S. Landingham CB. Lau EC. Pirkle JL..cdc. Goodman G.. Abarca CR.11(3):295. Urinary perchlorate and thyroid hormone levels in adolescent and adult men and women living in the United States. Osterloh JD. Caldwell KL. Mauldin JP.17(4):400-407. 2005). population. 2005). Valentin-Blasini L. Li FX. Cross M. Howd R. Miller MD. Steinmaus C. Daaboul JJ. thiocyanate. 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. Buffler PA. and environmental perchlorate exposure among residents of a Southern California community. Neonatal thyroxine level and perchlorate in drinking water.41(5):409-411. Has perchlorate in drinking water increased the rate of congenital hypothyroidism? J Occup Environ Med 1999. Impact of smoking and thiocyanate on perchlorate and thyroid hormone associations in the 2001-2002 national health and nutrition examination survey. May 2007. 2007).46(5):509. Dasgupta PK. et al. Barnard JC.EPA at: http://www. Environ Health Perspect 2006. Thyroid 2001. and nitrate on thyroid function in workers exposed to perchlorate long-term. et al. Pleus RC.42(2):200-205. Compared to a previous study of pregnant women in three Chilean communities with varying perchlorate levels in the drinking water. Analysis of relative source contributions to the food chain. Biomonitoring studies of urinary perchlorate provide physicians and public health officials with reference values so that they can determine whether or not people have been exposed to higher levels of perchlorate than levels found in the general population.110(9):927-937. Rutherford GW. Chacon PM. Also. Jackson WA. Available at URL: http://www.S. Lamm SH. Richman K. Byrd D. Magnani B. Osterloh JD. Preliminary Estimation of Perchlorate Dietary Exposure Based on FDA 2004/2005 Exploratory Data. Blount BC. National Research Council of the National Academies. Lamm S. Dyke JV. Perchlorate Exposure of the US Population. Environ Health Perspect 2005. Environ Sci Technol 2006. Tellez RT. Sesser DE. Valentin-Blasini L. et al.

Perchlorate pregnancy and the neonatal period.9(3):187-192. Revised 2/11/05.15(9):963-975. Thyroid 2005.S.S. U. 1988. Integrated Risk Information System (IRIS). Drinking Water Contaminant Candidate List. EPA).S. Urbansky TF. Perchlorate as an environmental contaminant. 246 Fourth National Report on Human Exposure to Environmental Chemicals . Environmental Protection Agency (U. Doc. EPA). cfm?substance_nmbr=1007.epa. No. EPA/600/F-98/002 Washington (DC).1/15/06 U. Environ Sci Pollut Res Int 2002. Environmental Protection Agency (U. Perchlorate.S.gov/iris/quickview. Available from URL: http://cfpub.

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

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

2001.500) 90th .500) . 2004). 2007b. 2007a. population. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.00) . population from the National Health and Nutrition Examination Survey.40) .10 (.50) . development in offspring was stunted and hypothyroxinemia was observed. thyroidal).00 (.Perfluorochemicals and testicular tumors in high dose animal testing (Biegel et al. Serum Perfluorodecanoic acid (PFDeA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. or increased cancer rates (Alexander et al. 2007b). PFOS. 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.00) .400 (<LOD-.800 (. see Data Analysis section) for Survey year 03-04 is 0.. PFOA.3.. possibly related to lung immaturity (Lau et al.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 .600 (.. Olsen et al.. 2003.900 (.00) . Two recent cross-sectional human studies observed a negative correlation of birth weight with serum levels of PFOA (Apelberg et al.400-. Thibodeaux et al. hepatotoxicity. 2004a. At high but non-toxic maternal doses of PFOS. Fei et al. Due to marked intergender differences in the elimination of PFOA in rats and substantial differences in the half-life of PFOA in rats. 2003a.500 (..400-1.400 (<LOD-.500-1.20) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . Late gestational exposure to PFOS in animal studies has also demonstrated early neonatal lethality.800 (.500-3. PFOA.. However.10) * 03-04 03-04 * * < LOD < LOD < LOD .. Harada et al.. developmental and teratogenic effects were demonstrated in offspring..500) . and there was no clear evidence of excess all-cause or diseasespecific mortality.. 1999.500-1.500-. reproductive.700 (. Survey Geometric mean (95% conf. monkeys. 2003a.400 (<LOD-. 2007. A study of workers chronically exposed to primarily PFOA showed no biochemical evidence of hepatotoxicity or hormonal changes (adrenal.400-1..800) 1.10) .. Roughly similar levels of PFCs in serum have also been measured previously in other samples of the U. 2003).. EPA.500-1.20) .600-2. 2003. EPA. and no substantial age trends were seen within adults ages 20-69 (Olsen et al. 2004. 2005). < LOD means less than the limit of detection. Cook et al.. Olsen et al..900 (. animal and human serum PFOA levels have been compared: serum levels associated with toxic effects in animals are 66-11. 2003a.400-1.700) . Biomonitoring Information Serum levels of PFCs (particularly PFOA and PFOS) tend to reflect cumulative exposure over several years. perfluorohexanesulfonate (PFHxS). 2004b).400-1.300 (<LOD-.500) .80) 640 1454 03-04 03-04 * * < LOD < LOD . In comparing three separate reports on adults.400) .600 (. 2004. Animal studies of PFOS have demonstrated weight loss. the median PFCs values tend to be roughly similar in these age categories (Olsen et al.400-1.108 times higher than background serum levels in humans (Butenoff et al.600 (.800 (. elderly and children. and humans. 2007). 2003).S.800) 1. which may vary for some chemicals by year and by individual sample. 2003a). Olsen et al.. Serum PFOS levels associated with toxicity in test animals were 310-1550 fold higher than 95 percent of the levels found in a study of adults (Olsen et al. Slightly higher levels of PFOS and PFOA in males than females have been noted in several other studies (Calafat et al. U.S.900 (.400-.S.800 (.500-1. PFOS. In such studies. 2003).500) .S. 2003. 2004).500 (. At doses causing maternal toxicity.300 (<LOD-...10) . and changes in thyroid hormone concentrations (Grasty et al. 1992.. interval) Selected percentiles ( 95% confidence interval) Sample 95th . 2007a. the potential to estimate risks to humans from animal doses is uncertain. and other PFCs have not been classified as to human carcinogenicity by IARC or NTP. Effects on serum liver enzymes in limited observational studies of human occupational exposures are unclear. Twelve different PFCs were measured in the sera of NHANES 2003-2004 participants.80) 485 538 962 Limit of detection (LOD. 2005). Kennedy et al.500 (<LOD-1..300-1. 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. Fourth National Report on Human Exposure to Environmental Chemicals 249 . 2003a). Lau et al..300 (<LOD-. U.

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

300 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.400 (.500-. Fourth National Report on Human Exposure to Environmental Chemicals 251 .600 (. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 485 538 962 Limit of detection (LOD. interval) Selected percentiles ( 95% confidence interval) Sample 95th .900) < LOD .300 (<LOD-.600) < LOD . Serum Perfluoroheptanoic acid (PFHpA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U. Survey Geometric mean (95% conf.300-.400) .900) < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD . see Data Analysis section) for Survey year 03-04 is 0.3.600) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .S.500 (<LOD-. Survey Geometric mean (95% conf. which may vary for some chemicals by year and by individual sample.500) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD . 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.Perfluorochemicals Serum Perfluorododecanoic acid (PFDoA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.400 (<LOD-. < LOD means less than the limit of detection.0.400 (<LOD-.500) 485 538 962 Limit of detection (LOD. population from the National Health and Nutrition Examination Survey. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 1.S. < LOD means less than the limit of detection.

90) 1.72) 1.80-4.90-2.80-7.50) 6.00-6.20-1.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.60-4. Survey Geometric mean (95% conf.00) 1.40 (1.80) 3.80 (1.40) 640 1454 03-04 03-04 1.56-1.1) 485 538 962 Limit of detection (LOD.00 (1.70) 1.70) 2.01 (1.10 (4.50 (6.70) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th 1.09 (.60-3.10) 5.900-1.10) 6.90 (1.60-2.721-1.10 (.20) 485 538 962 Limit of detection (LOD.10 (4. population from the National Health and Nutrition Examination Survey.14 (.900-1.0) 1053 1041 03-04 03-04 03-04 1.70-2.80-3.51) 1.50 (1.900 (.30-6.80) 1.30-9.50 (6. Survey Geometric mean (95% conf. 252 Fourth National Report on Human Exposure to Environmental Chemicals .67-2.50 (4.80-6.90) 90th 5.80 (1.54) .60-2.70-10.697-1.80 (4. see Data Analysis section) for Survey year 03-04 is 0.30) 3.700-1.700 (.80-2.900-1.3.04) .70-7.30 (6.00 (1.834-1.S.800 (.42 (1.30 (7.20 (1.0) 8.60-2.966 (.20 (1.72 (1.586-.80) 4.70 (2.60-4.87-2.00) 3.00) 2.20 (6.00 (.10-9.50 (1.30 (1.90) 8.40-3.50) 2.40) 1.80) 5.861 (.40) 640 1454 03-04 03-04 2.Perfluorochemicals Serum Perfluorohexane sulfonic acid (PFHxS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.30 (1.40) 2.984 (.20 (1.90-19.816-1.30 (3.60 (1.10) 6.90) 1.20-2.17-1. Serum Perfluorononanoic acid (PFNA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.80-4.30 (1.10) 1.60) 2.00-7.10-5.10) 75th 1.00) 1.50-6.30) 3.40) 4.50) 2.90 (4.00-1.70-6.00 (1.90-10.20-1.826-1.60 (1.50-3.60) 1.900) 1.10) 75th 3.963 (.92 (1.900-1.80-8.90 (4.73-2.20) .70-2.00-8.20 (6.50 (1.40 (1.10) 8.80-7.40 (2.90 (1.10) 4.77-2.60 (1.809) 1.900 (.40 (1.05-2.600-.40) .10-9.900-1.16) .50-10. see Data Analysis section) for Survey year 03-04 is 0.20) 03-04 03-04 2.80-12.50 (2.20) 2.00-1.5) 8.80) 90th 2.27) 1.852 (.70) 2.835-1.93 (1.12) .30) 03-04 03-04 .20-3.44 (2.10) 4.30) .60) 3.70 (1.30-2.60) 9.3 (9.20-1.00 (1.62-2.17 (1.1.00 (2.26) 2.60 (6.10) 1.5) 5.689 (.90 (2.10 (1.20 (1.50-6.30 (2.50 (4.86 (1.70) 1.10 (.90 (1.6) 7.40-1.40) 1.50 (1.30 (2.14) Selected percentiles ( 95% confidence interval) Sample 95th 3. population from the National Health and Nutrition Examination Survey.20-1.60-3.60-7.30) 3.00 (.10) 1053 1041 03-04 03-04 03-04 .10 (. interval) 1.800-1.80-4.90) 1.90 (1.16) Selected percentiles ( 95% confidence interval) Sample 95th 8. interval) .S.00 (5.20) 1.900-1.90) 3.03) 1.912-1.08) 2.80-8.40-1.70-5.30 (1.70) 13.70) 3.91) 2.30-12.60-8.80-3.20) 1.40 (1.

95 (3.3-61.4 (28.6 (19.60-13.10 (6.30-8.4) 75th 30.40 (4.0) 03-04 03-04 19.47 (4.96 (3.5-21.60) 8.9 (19.2-57.6 (35.3 (44.50 (4.70) 4.70 (5. Survey Geometric mean (95% conf.8-30.70-7.0-70.35) 3.40) 5.2) 30.11 (2.7 (35.8-78.30 (3.40-6. see Data Analysis section) for Survey year 03-04 is 0.7-69.2-22.2 (16.50) 7.20) 5.6) 9.7-53.3-22.9-23.9) 9.85-4.60 (4.20) 4.50-13.3 (35.7-30.50) 4.5) 9.99-3.10-3.70 (5.2 (19.6) 1053 1041 03-04 03-04 03-04 3.4 (19.60-14.3) 42.60-6.8-22.90 (5.0) 21.30) 6.7 (19.6-24.90-4. Fourth National Report on Human Exposure to Environmental Chemicals 253 .9) 22.2 (21.80) 8.80 (6.00) 3.1-36.8-22.65-4.0) 36.0) 90th 41.0 (20.80 (7.2 (18.2 (28.1) 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 4.27) Selected percentiles ( 95% confidence interval) Sample 95th 9.7-49.6) 7.0) 23.4 (19.30-6.67-4.60) 03-04 03-04 3.4) 21.20) 7.50-4.89 (3.4-42.0-66.1-35.7 (7. population from the National Health and Nutrition Examination Survey.1 (19.30 (3.0-20.5-23.40) 3.1-33.7 (43.6-50.91) 3.90 (7.20-4.00 (5.0) 43.9) 27.70-9.90 (7.5) 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 21.90-12.5) 8.47-4.90-4.4-25.8-35.82) 4.0) 21.3) 28.2 (27.1 (24.6 (42.9 (17.4 (23.1) 15.S.70) 6.9 (22.80 (6.20 (4.6-45.53) 3.8 (37. interval) 3.9) 22.37 (2.S.10 (3.9-38.84-3.60 (3.5) 1053 1041 03-04 03-04 03-04 14.1 (23.6 (44.1-25.3) 41.70 (3.5) 19.4 (17. population from the National Health and Nutrition Examination Survey.8 (45.8 (34.10) 5.40-6.40-14.90) 6.5 (28.4.20) 10.40-17.1-24.3 (28.50-6.4) 56.3) Selected percentiles ( 95% confidence interval) Sample 95th 54.5-33.20) 5.7 (35.40) 75th 5.70-5.70) 3.5-62.0) 485 538 962 Limit of detection (LOD.3) 485 538 962 Limit of detection (LOD.60-9.07-4.6) 18.30) 7.2) 45.3 (35.00 (3.6) 42.90 (7.8-81.20 (4.6) 21.7 (13. Survey Geometric mean (95% conf.Perfluorochemicals Serum Perfluorooctanoic acid (PFOA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.21-3.8) 46.40 (6.9-19.9 (13.2) 30.70-10.20) 7.20-9.80-4.40) 90th 7.2) 640 1454 03-04 03-04 4.0-16.00 (5.50 (3.27) 4.5 (28.80 (5.18 (3.5) 18.1.8) 32.5) 7.30-5.79) 4.70-7.60 (5.4-17.80-9.8) 27.3 (17.60 (6.1-52.20-5.30 (5.60 (6.7-23.30-3.6) 35.7) 39.10 (3.4) 640 1454 03-04 03-04 23.5) 57. interval) 20.6) 62.1) 57.5) 32.0 (27.40-10.4) 20.7-33.80-12.8-22. Serum Perfluorooctane sulfonic acid (PFOS) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.30-11. see Data Analysis section) for Survey year 03-04 is 0.7 (43.60 (7.

500) < LOD 485 538 962 Limit of detection (LOD.S. population from the National Health and Nutrition Examination Survey.200-.300 (. Survey Geometric mean (95% conf.S.300 (.500) .400 (<LOD-.500) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .300 (.200-.300 (. which may vary for some chemicals by year and by individual sample. see Data Analysis section) for Survey year 03-04 is 0.300) * 03-04 03-04 * * < LOD < LOD < LOD < LOD .200-.200-.2.200-.300 (.200-. < LOD means less than the limit of detection.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.300 (. see Data Analysis section) for Survey year 03-04 is 0.300 (.500) 485 538 962 Limit of detection (LOD.300 (. Survey Geometric mean (95% conf.300 (.300 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.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 .300-. interval) Selected percentiles ( 95% confidence interval) Sample 95th < LOD size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .4.300 (.300 (.200 (<LOD-. which may vary for some chemicals by year and by individual sample. 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. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.300) .300) .300) .300) .300) .500) .400) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .300 (.300) . 254 Fourth National Report on Human Exposure to Environmental Chemicals .300-.200-.300-.200-.200-.500) .200-.300-. interval) Selected percentiles ( 95% confidence interval) Sample 95th . < LOD means less than the limit of detection.300 (.300) .

800) . < LOD means less than the limit of detection.10-1.700) 1.600 (<LOD-1. population from the National Health and Nutrition Examination Survey.900-1. see Data Analysis section) for Survey year 03-04 is 0.60) 485 538 962 Limit of detection (LOD.30 (1.900-1.90) .10) .700) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD .6.10) 1.800 (<LOD-.40) 640 1454 03-04 03-04 * * < LOD < LOD < LOD < LOD .10-1.10 (1.400 (<LOD-1.40) < LOD < LOD . interval) Selected percentiles ( 95% confidence interval) Sample 95th .00 (.700 (<LOD-.40) 1. which may vary for some chemicals by year and by individual sample.20-1.50 (1.10) .900 (<LOD-1.900) 485 538 962 Limit of detection (LOD.900-1.700) 90th 1.10-1.900-1.10-1. see Data Analysis section) for Survey year 03-04 is 0.80) 1.600) .700 (<LOD-.3. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1.300-2.S.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.900-1. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700 (<LOD-. which may vary for some chemicals by year and by individual sample.S.700 (<LOD-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.700) .30 (1.70) 1.10-1.600 (<LOD-.600 (<LOD-1.900-1.10) * 03-04 03-04 * * < LOD < LOD .600 (<LOD-1.30) size 2094 Total Age group 12-19 years 20 years and older Gender Males Females Race/ethnicity Mexican Americans Non-Hispanic blacks Non-Hispanic whites years 03-04 50th < LOD < LOD 75th < LOD 90th * 03-04 03-04 * * < LOD < LOD < LOD < LOD < LOD .00 (.300 (<LOD-1.700 (<LOD-.900) 1.20) 1.400 (<LOD-. Survey Geometric mean (95% conf.30) .900) .700 (<LOD-.60) 640 1454 03-04 03-04 * * < LOD < LOD .00-1.10 (.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 .300 (<LOD-.50 (1.10 (.80) 1. < LOD means less than the limit of detection.900 (.80) 1053 1041 03-04 03-04 03-04 * * * < LOD < LOD < LOD < LOD . population from the National Health and Nutrition Examination Survey. Serum Perfluoroundecanoic acid (PFUA) Geometric mean and selected percentiles of serum concentrations (in µg/L) for the U.30) 1. Survey Geometric mean (95% conf.700 (<LOD-2.900-1.10) 1.500 (<LOD-.00 (.700) 1.00) < LOD .30 (1.20 (1.30) 1. Fourth National Report on Human Exposure to Environmental Chemicals 255 .00 (.800) .10 (.

Calafat AM. Olsen GW. Calafat AM. Environ Sci Technol 2005. Apelberg BJ. et al. Murray SM. Occup Environ Med 2003. Herbstman JB. Induction of Leydig cell adenomas by ammonium perfluorooctanoate: a possible endocrine-related mechanism. Gaylor DW. Ingall GB. Cook JC.39(3):363-380. Calafat AM. O’Connor JC. Environ Sci Technol 2005. Hurtt ME. Toxicol Appl Pharmacol 1995. Mabury SA. Kamiyama S. Jarnberg U. Serum concentrations of 11 polyfluoroalkyl compounds in the U. Androgenic deficiency in male rats treated with perfluorodecanoic acid. Polyfluoroalkyl chemicals in the U. Perkins RG. 2007b. Saito N. Seneviratne HR. Koizumi A. Fei C.115(11):1677-1682. Loganathan BG.113(2):209-217. Environ Res 2005. Environ Health Perspect 2007. Butenhoff JL. Prenatal window of susceptibility to perfluorooctane sulfonate-induced neonatal mortality in the Sprague-Dawley rat. Edwards EA. McLaughlin JK. Rev Environ Contam Toxicol 2003.Koizumi A. Olsen GW. Tarone RE. Witter FR. population: data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and comparisons with NHANES 1999-2000. Environ Health Perspect 2007.41:2237-2242. Caudill SP. Hekster FM.115(11):1596-1602. Butenhoff JL. Taniyasu S.68(6):465-471. Birth Defects Res B Dev Reprod Toxicol 2003. Perfluorochemicals in pooled serum samples from United States residents in 2001 and 2002. Bignert A. Kennedy GL Jr. sex and geographic factors on levels of perfluorooctanesulfonate and perfluorooctanoate in human serum over the last 25 years. O’Connor JC. Perfluorooctanesulfonate and related fluorochemicals in human blood from several countries. Harada K. Moore JA. et al. Inoue K. Chem Biol Interact 2000. Mortality of employees of a perfluorooctanesulphonyl fluoride manufacturing facility. Chlorinated. Seacat AM. Mandel JH. J Environ Monit 2005. population: Data from the National Health and Nutrition Examination Survey (NHANES) 1999–2000.S. Halden RU. Mandel JS. Toxicol Appl Pharmacol 1992. Fillmann G. J Occup Health 2004. Caudill SP. Watanabe T. Inoue K. Yoshinaga T. Kannan K. Yamashita N. et al. brominated. Guruge KS.39(23):9057-9063. Kawashima Y. Bookstaff RC.60(10):722729. Yoshinaga T. Needham LL. Toxicol Sci 2001. Katakura M. Perfluorinated organic compounds in human blood serum and seminal plasma: a study of urban and rural tea worker populations in Sri Lanka. Wijeratna S. Dinglasan MJ.S.39(1):80-84. Suzuki E. Environ Sci Technol 2004.115(11):1670-1676. Laane RW.39(23):9101-9108. Aguilar-Villalobos M. Kuklenyik Z. Needham LL. Environ Sci Technol 2005.134(1):18-25. Moore RW. Perfluorinated compounds in the plasma of loggerhead and Kemp’s ridley sea turtles from the southeastern coast of the United States. Cook JC. Calafat AM.46(2):141-147. Kuklenyik Z. Hurtt ME.40:21282134. Characterization of risk for general population exposure to perfluorooctanoate.7(4):371-377. Day RD. Peterson RE. Rogers JM. Kuklenyik Z. Kannan K. Cord serum concentrations of perfluorooctane sulfonate and perfluorooctanoate in relation to weight and size at birth. Mechanisms of extrahepatic tumor induction by peroxisome proliferators in male CD rats.179:99-121. Corsolini S. et al. Cook JC. Environ Sci Technol 2006a. Reidy JA. et al. and ex vivo studies. Grey BE. Rodricks J. Crit Rev Toxicol 2004. Renal clearance of perfluorooctane sulfonate and perfluorooctanoate in humans and their species-specific excretion. Yun SH. Chemosphere 2006b. et al. Saito N. Kuklenyik Z. Temporal trends of PFOS and PFOA in guillemot eggs from the Baltic Sea. Reidy JA.and perfluorinated acids. Lau CS.38(10):2857-2864. The toxicology of perfluorooctanoate. Taniyasu S. Morikawa A. Environ Health Perspect. Mohotti KM. Keller JM. Hurtt ME. Grasty RC. and perfluorinated contaminants in livers of polar bears from Alaska. Needham LL.124(2):119-132. Olsen GW. in vivo. Biegel LB. Effects of ammonium perfluorooctanoate on Leydig cell function: in vitro. Reidy JA.34(4):351-384. Evans TJ. Liu RC. Mandel JH. Bandai N. Tully JS. et al. Biegel LB.104(2):322-333. The influence of time. Environ Sci Technol 2004. de Voogt P. Falandysz J. Frame SR. Fluorotelomer alcohol biodegradation yields poly. Perfluorinated chemicals and fetal growth: A study within the Danish National Birth cohort. Regul Toxicol Pharmacol 2004. Frame SR. Calafat AM. Kannan K. Environ Sci Technol 2007a.99(2):253-261.1968--2003.38(17):4489-4495.63:490496. Induction by perfluorinated fatty acids with different carbon chain length of peroxisomal beta-oxidation in the liver of rats.Perfluorochemicals References Alexander BH. Holmstrom KE. Kumar KS. Sasaki S. Yamashita N.60(1):44-55. Wong LY. 256 Fourth National Report on Human Exposure to Environmental Chemicals . Kudo N. Burris JM. Tully JS. Arendt MD. Olsen J. Harada K. Perfluorinated chemicals in selected residents of the American continent. Environmental and toxicity effects of perfluoroalkylated substances. Ye Y. Needham LL. Reidy JA. Toxicol Appl Pharmacol 1990.

perfluorooctanoate andother fluorochemicals in human blood. et al. Kannan K. Dietary exposure of Canadians to perfluorinated carboxylates and perfluorooctane sulfonate via consumption of meat.41(9):799-806. EPA). Rogers JM.perfluorohexanesulfonate. Church TR. Ehresman DJ. Lundberg JK. Biochim Biophys Acta 1993. Preliminary evidence of a decline in perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations in American Red Cross blood donors. Grey BE.54(11):1599-1611. J Occup Environ Med 2003b. I: maternal and prenatal evaluations. Thomford PJ. Hansen KJ. Historical comparison of perfluorooctanesulfonate. J Occup Environ Med 1999.113(5):539-545.37(12):2634-2639.198(2):231-241. Sterchele PF. Burlew MM. Hansen KJ.74(2):382-392. Serum concentrations of perfluorooctanesulfonate and other fluorochemicals in an elderly population from Seattle. Moisey J. Butenhoff JL.115(9):1298-1305.51(8-12):658-668. Rogers JM. Subchronic toxicity studies on perfluorooctanesulfonate potassium salt in cynomolgus monkeys. 1/15/06 Vanden Heuvel JP. Butenhoff JL. Olsen GW. Olsen GW. Huang HY. Biol Pharm Bull 2003. fate and transport of perfluorocarboxylates. Ellefson ME.gov/opptintr/pfoa/pfoara. A survey of perfluorooctane sulfonate and related perfluorinated organic compounds in water. Hanari N. Mandel JH. Taniyasu S.S. fish. U.. Burris JM. Butenhoff JL. et al. Stanton ME. (Erratum in: Environ Health Perspect. Gamo T. Preliminary Risk Assessment of the Developmental Toxicity Associated with Exposure to Perfluorooctanoic Acid and its Salts. Burris JM. Yamashita N.82(1):359. and humans from Japan. Church TR. Helzlsouer KJ. et al. fatty acid binding protein and peroxisomal beta-oxidation by peroxisome proliferators. Larson EB. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Nesbit DJ.68:105–111. Olsen GW. Hansen KJ. Toxicol Appl Pharmacol 2004. 2003a. Froehlich JW. Toxicol Sci 2002. Lau C. Fourth National Report on Human Exposure to Environmental Chemicals 257 . Environmental Protection Agency (U. Environ Sci Technol 2003. Ehresman DJ. Mandel JH.111(16):1892-1901. Olsen GW. Environ Sci Technol 2006. and food items prepared in their packaging. van Belle G. Peterson RE. et al. Butenhoff JL. J Children’s Health 2004b. Miller JP. Petrick G. fast foods. Half-life of serum elimination of perfluoroo ctanesulfonate. birds. Olsen GW. Mandel JH. Thibodeaux JR. Available from URL: http://www.S.2(1):53-76. and perfluorooctanoate in retired fluorochemical production workers. Kawashima Y. Buck RC. fish. Environ Health Perspect 2005. Bronson R. Thibodeaux JR.74(2):369-381. Environ Health Perspect 2003a.1177(2):183-190. Olsen GW. Induction of triglyceride accumulation in the liver of rats by perfluorinated fatty acids with different carbon chain lengths: comparison with induction of peroxisomal betaoxidation. Lau C. Cao XL et al. (Erratum in: Toxicol Sci 2004.40(1):32-44. Seacat AM. Rogers JM. Seymour C. Korzeniowski SH. Sources. Cousins IT. Seacat AM. Horii Y.Perfluorochemicals Kudo N. II: postnatal evaluation. htm. Mar Pollut Bull 2005. Zobel LR.55:3203-3210. Mandel JH. Chemosphere 2004a. Olsen GW. Serum perfluorooctane sulfonate and hepatic and lipid clinical chemistry tests in fluorochemical production employees. A global survey of perfluorinated acids in oceans. Prevedouros K.) Tittlemier SA. Church TR. Yamashita N.26(1):47-51. Barbee BD. et al. Mair DC. Toxicol Sci 2003. Burris JM.68(1):249-264. et al. Taniyasu S. 2003. Chemosphere 2007b. Burris JM. Butenhoff JL.111(16):1900) Olsen GW. Grey BE. Hansen KJ. J Ag Food Chem 2007. Kannan K. Washington. Exposure to perfluorooctane sulfonate during pregnancy in rat and mouse. Reagen WK. Epidemiologic assessment of worker serum perfluorooctanesulfonate (PFOS) and perfluorooctanoate (PFOA) concentrations and medical surveillance examinations. Butenhoff JL. Coordinate induction of acyl-CoA binding protein. Burris JM. Hansen KJ.epa. The developmental toxicity of perfluoroalkyl acids and their derivatives. Horii Y. Richards JH. Quantitative evaluation of perfluorooctanesulfonate (PFOS) and other fluorochemicals in the serum of children. Hanson RG. Olsen GW. Perfluorooctanesulfonate and other fluorochemicals in the serum of American Red Cross adult blood donors. Hanson RG.45(3):260-270. Lundberg JK. Case MT. Pepper K. Toxicol Sci 2003. 2007a. Environ Health Perspect.

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

Silva MJ. which may be a pathway to the development of liver toxicity and cancers in these animals. and extent of metabolite conjugation to glucuronide (Albro et al. J Chromatogr B 2004. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Rhodes et al. 2007). Corbett JT. Herbert AR. 2005). Albro PW and Lavenhar SR. Available at URL: http://www. Also. Food Addit Contam 2001. 2005.21:13-34. 1986). reducing estrogen production. Massey RC.. Vol. Drug Metab Rev 1989. In Staples CA (ed).. Silvapathasundaram S. environmental levels) and health effects is also available for some phthalates from ATSDR at: http://www. and Sertoli cell abnormalities in the male animals and. Available at URL: http://www. atsdr. 4/20/09 Albro PW.805:49-56. Coldham NG.45:19-25. dibutyl phthalate (DBP). Calafat AM. Mackay D.. Dirven HA. 1982. 2000b.e. Environ Health Perspect 1982. variation also occurs in the same person during repetitive monitoring (Fromme et al. Hauser et al.atsdr. 2004..gov/ toxprofiles/tp9.html. Springer. 2002). Springall C. 227-262.. 2004. Population estimates of concentrations of specific phthalate metabolites may differ by age.cdc. 1985.cdc.gov/toxprofiles/ tp135. van der Broek PH. In animals. 4/20/09 Agency for Toxic Substances and Disease Registry (ATSDR). Scotter MJ. 2006). Cousins IT. 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.gov/ reports/index.cdc. Toxicological profile for di-n-butyl phthalate update [online]. However.. but there are known species-related differences in the hydrolysis of diester phthalates. NTP-CERHR. 2003. at higher doses.html). Hauser et al. Assessment of critical exposure pathways. 2007. Lovekamp-Swan and Davis. interactions with macromolecules and species differences in metabolism of DEHP. gender. Metabolism of di(2-ethylhexyl) phthalate. and benzylbutyl phthalate (BzBP) during the fetal period produced lowered testosterone levels. 2004. ovarian abnormalities in the female animals (Jarfelt et al. Phthalate urinary metabolite levels in men evaluated at an infertility clinic were associated with several measures of sperm function and morphology (Duty et al. Schroeder JL.html. phthalates produced anti-androgenic effects by reducing testosterone production and.. phthalates have been shown to induce peroxisomal proliferation in rodents.. 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. Jordan S.. Toxicological profile for di(2-ethylhexyl)phthalate update [online].New York. 2004). Clark K.html.nih. The Handbook of Environmental Chemistry. Connor C. These differences may contribute to species-specific differences in toxicity (ATSDR. High doses of di2-ethylhexyl phthalate (DEHP). Peck and Albro. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. The proportions of each metabolite for a given phthalate may vary by differing routes of exposure (Liss et al. 2006). Information about external exposure (i. 2002. Pharmacokinetics. The monoester metabolites are thought to mediate toxic effects for some of the phthalates. 2001.. Slakman AR. pp.Phthalates and metabolites have been tested. 1982).. effects that may be mediated by inhibiting testicular and ovarian steroidogenesis. Castle L..atsdr. efficiency of intestinal absorption. Kessler et al. at very high levels. McDonnell DP. 2003. peroxisomal proliferation may not be a relevant pathway in humans (Rusyn et al.3.gov/toxpro2. Sauer MJ. 2000c.. 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... Anderson WA.18(12):10681074.niehs. testicular atrophy. 2001). Hoppin et al. McKee et al. Automated solid phase extraction and quantitative analysis of human milk for 13 phthalate metabolites. Matthews HB. Determination of four metabolites of the plasticizer di (2-ethylhexyl) phthalate Fourth National Report on Human Exposure to Environmental Chemicals 259 . and race/ethnicity (Silva et al. 2002). Dave M. 105:734-742. Biomonitoring Information Urinary levels of phthalate metabolites reflect recent exposure to the parent phthalate diester. 2001. Environ Health Perspect 1997. Part Q: Phthalate Esters. 2000a. References Agency for Toxic Substances and Disease Registry (ATSDR). Evaluation of a recombinant yeast cell estrogen screening assay. Variation occurs from person to person in the proportions or amounts of a metabolite excreted after similar doses (Anderson et al. but similar findings were not present in young Swedish men with comparable or higher median levels of urinary metabolites (Jonsson et al.. Jongeneelen FJ. Needham LL. 2004.

Anal Bioanal Chem 2005. Draft Update Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP).nih. Park S. Nielsen J. Koch HM. Research Triangle Park (NC). Reprod Toxicol 2004.html. Andersson A-M.nih.html.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Davis BJ. et al. Drexler H. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. consumer milk. Singh NP.110(5):515-518. Monograph on the Potential Human Reproductive and Developmental Effects of Din-Butyl Phthalate (DBP). Ryan L. Wang P. Mechanisms of phthalate ester toxicity in the female reproductive system. Brock JW. Hoppin JA.210:21-33. 2000a [online].46(11):643-647. Zhang S.niehs. Occurrence and daily variation of phthalate metabolites in the urine of an adult population.112(17):1740]. Scand J Work Environ Health 1985. Lovekamp-Swan T. Suzuki T. Environ Health Perspect 2004. A variety of environmentally persistent chemicals including some phthalate plasticizers are weakly estrogenic. Hauser R. Monograph on the Potential Human Reproductive and Developmental Effects of Di(2-ethylhexyl) Phthalate (DEHP). 2006 [online]. Ryan L. Research Triangle Park (NC).26(8):1219-24. Boehmer S. Hanaoka T. Yokoyama Y.112(17):1734-1740. Available at URL: http://cerhr. 6/2/09 NTP-CERHR. Skakkebaek NE.gov/chemicals/dehp/dehp-eval. Numtip W. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Kalita JC. Jarfelt K.11(5):381-387. Meeker JD. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Reynolds T. White R. Pan G. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Harris CA. Kano I.html. Silva MJ. Epidemiol 2005. Jacobsen H.nih. Milligan SR.106(1):23-26. NTP-CERHR. McKee RH. Park MG. Estimation of estrogenic and anti-estrogenic activities of some phthalate diesters and monoesters by MCF-7 cell proliferation assay in vitro.gov/chemicals/ phthalates/dbp/dbp-eval. Butala JH. Richthoff J. Yoshimura M. et al. et al. Ladefoged O. Determination of phthalate monoesters in human milk. Phthalate ester exposure—air levels and health of workers processing polyvinylchloride. Skerfving S. Parker MG. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). Environ Health Perspect 1998. Calafat AM. David RM.64(8):555-560. Relative potency of xenobiotic estrogens in an acute in vivo mammalian assay.19(4):505-515. Sumpter JP. Mortensen GK. Brock JW.nih. Tsukino H. Albro PW. Meeker JD. Akesson B. Am Ind Hyg Assoc J 1985. Fromme H. gov/chemicals/dehp/dehp-eval. Baird DD. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. J Androl 2004. Available at URL: http://cerhr. Stringer WT. 6/2/09 NTP-CERHR. Chahoud I. Kessler W.22(3):688-695.16(4):487-493. Available at URL: http://cerhr.18(1):122. Int Arch Occup Environ Health 1993. Sumpter JP. Calafat AM. Chen Z. Antiandrogenic effects in male rats perinatally exposed to a mixture of di(2-ethylhexyl) phthalate and di(2-ethylhexyl) adipate. Hartle RW. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Jonsson BAG. Grote K. 6/2/09 NTP-CERHR. Silva MJ. Research Triangle Park (NC). Available at URL: http://cerhr. 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 . Research Triangle Park (NC). Environ Health Perspect 1997. Hum Reprod 2007. Leffers H. Biol Pharm Bull 2003. Duty SM.niehs. Bolte G. et al. Environ Health Perspect 1995. The estrogenic activity of phthalate esters in vitro. Silva MJ.382:10841092. Jobling S. Filser J. Csanády G.195:142-153. Urine phthalate determinations as an index of occupational exposure to phthalic anhydride and di (2-ethylhexyl) phthalate.html. Angerer J.103:582-587. Henttu P. 2000b [online]. Toxicol Appl Pharmacol 2004.niehs. Gans G. Reproducibility of urinary phthalate metabolites in first morning urine samples. Duty S. 6/2/09 Okubo T. Blood burden of di(2-ethylhexylphthalate (DEHP) and its primary metabolite mono(2-ethylhexyl) phthalate (MEHP) in pregnant and non-pregnant rats and marmosets. Balasubramanian AV. Kano K. Reprod Toxicol 2005. Hass U. Liss GM. Temporal variability of urinary phthalate metabolite levels in men of reproductive age [published erratum appears in Environ Health Perspect 2004. and infant formula by tandem mass spectrometry (LC-MS-MS). Main KM.105:802-811. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Dalgaard M.niehs. Environ Health Perspect 2003.Phthalates in human urine samples. 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Toxicol Sci 1998. Wu ZF. The plasticizer diethylhexyl phthalate induces malformations by decreasing fetal testosterone synthesis during sexual differentiation in the male rat. Batten PL. et al.36:459-479. Barr DB. Ostby JS. Environ Health Perspect 2006. Caudill SP. Bratt H. Peck CC. Matthews JB. Parks LG.114(11):1643-1648.S. Pratt IA. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Toxicol Sci 2000. Meek MD. Albro PW. Klinefelter GR. Zacharewski TR. Rusyn I. Environ Health Perspect 2004. Modes of action and species-specific effects of di-(2-ethylhexyl)phthalate in the liver. Rhodes C.65:299-308. Orton TC.45:11-17. et al. Toxic potential of the plasticizer di (2-ethylhexyl) phthalate in the context of its disposition and metabolism in primates and man. Cunningham ML. Jackson SJ. Silva MJ. Fielden MR. Comparative pharmacokinetics and subacute toxicity of di(2-ethylhexyl)phthalate (DEHP) in rats and marmosets: Extrapolation of effects in rodents to man. 112(5):A270]. et al. Barlow NJ. Examination of the in vitro and in vivo estrogenic activities of eight commercial phthalate esters. Environ Health Perspect 1982. Reidy JA. Urinary levels of seven phthalate metabolites in the U. Malek NA.46:282-293. Peters JM. Clemons JH. Crit Rev Toxicol 2006. Environ Health Perspect 1986. Hodge CC.Phthalates phthalate (DEHP): a cross-sectional study in China.58:339349. Lambright CR.112(3):331-338. Abbott BD. Fourth National Report on Human Exposure to Environmental Chemicals 261 .

3 (33.8 (21.4 (13.1-214) 166 (116-191) 145 (110-213) 88.5-84.9-27.6) 50.8) 63.5) 214 (108-399) 235 (183-330) 255 (146-365) 125 (93. People exposed to BzBP will excrete mono-benzyl phthalate (MBzP) and small amounts of mono-n-butyl phthalate in their urine.5 (13.4-62.6-18.2) 12.4) 75th 35.5 (66.8-48.8 (14.2-155) 91.8 (80. 85-68-7 General Information Benzylbutyl phthalate (BzBP) is a solvent and additive used in products such as adhesives.5-14.4-24.2-16. and to a lesser extent.4 (31.3-34. NTPCERHR.1-38.7-82.6) 15.8) 28.6) 29.0) 32.2) 32. Biomonitoring Information The median levels of MBzP in NHANES subsamples from 1999-2000.5-62.7 (51.3-43.6-72.7 (70. residents (Blount et al.0) 33.6-79.9 (21.1-120) 52.2-183) 101 (78.5) 55.3-122) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.3-18.4) 65.6-38.1 (13.9 (12.3-125) Total 15. including MBzP.8.1) 31. 2000).7-172) 103 (74.4) 49.1) 14.6 (13.7 (13.8) 33.6 (32.1) Selected percentiles ( 95% confidence interval) 50th 17.5-33.1) 68.1-35. because it is not bound to products in which it is incorporated.0-26.5 (55.2) 69.S.1) 13.0 (14.1.1-39.8 (10.2) 78.8 (30.4 (68. 01-02.0 (11.8) 24.6) 95th 103 (94.9 (13.7-58.6) 14.7) 38.3) 54.3 (44.7-17.9 (16.3 (12.9) 43.2-16.7 (11.4 (53.0 (15. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9-30.4) 81.6-29.3-27.4 (29.7-35.3 (54.5-94.4 (59.9) 12.1-116) 122 (93..2-40.8-16.9-49.5-36.Phthalates Benzylbutyl Phthalate CAS No. particularly male animals (McKee et al.0 (23.S.5) 65. and 03-04 are 0.0 (34.3-21.6) 24.8) 14.9 (28.9-14.5) 27.7-13.8-17.3-18.1) 32.2 (10.5) 82.7-119) 99. and 0.8) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 16. and 2003-2004 were generally similar those reported in U. 2004.4 (10.7-16.7-15.4) 71.3) 15.2-20.9-190) 86.1) 29.5) 16.5-40.1 (14.6-43. it can be released into the ambient air during use or disposal of the products.4-16.2-116) 122 (102-143) 101 (84.8-14.2 (11.5-41.1-18.4) 108 (96.4 (32.1) 67.8 (12.6 (13.8-16.4-15.2) 14. sealants.3) 94.3) 13.8 (86.3-161) 99.6) 13.4) 129 (98.4) 14.2-115) 113 (91.3 (29.1 (20.4) 80.9) 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. population from the National Health and Nutrition Examination Survey.1-15.5) 30. 0.1 (58.7 (82.7-170) 169 (134-198) 152 (99.4 (48.9) 49.4 (27.2-31.4-92.6) 14.3. Food crops take up BzBP.6) 35.2) 33. 2001-2002.9) 11.5) 15.6 (53.2 (19.6-132) 103 (84.8 (71.6-39.4) 35.6) 16. BzBP can be released into the environment during its production and.5 (47.6-92.7 (80.0-55.6) 67.5-145) 138 (106-241) 143 (127-179) 120 (99.3-88.6-17.1 (13.6) 13.4) 51.0) 70.3 (12. car care products.8-14.3) 23.1 (55.9 (11.4 (32.1-16.8-121) 79. 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 (63.9-16.9 (70.9) 18.9-62.5-36.6 (13.2) 22..1-15.2) 13.0-85.3 (30. 262 Fourth National Report on Human Exposure to Environmental Chemicals .0 (20.8-18.6-116) 122 (102-142) 101 (85.9 (12.3-82.9) 13.3-75.7 (15.8-133) 89.4 (10.1 (32.0 (30. see Data Analysis section) for Survey years 99-00.8 (50.5-18.3-91.8 (71.8-72.7 (12.1) 12.4-127) 80.0-130) 101 (86.0-106) 58.6) 35.3 (12.6) 63.0 (55.2) 17.4) 33.5 (57.5 (76.4) 38. can produce developmental and reproductive toxicity in rodents.6-150) 94.7) 40.8-17.8 (53.0 (30.1 (14.2-17. and diet is the major source for general population exposure.5 (67.2-38.9 (22. some personal care products.1-61.2) 15.5) 23.1-16. interval) 15.7-16.3) 13.1) 76.0) 90th 67.7-16.7) 23.5 (61.0 (43.2 (14.8 (38.8-35.3 (22.6 (12.9) 15.3) 63.0 (33.0 (12.7-14.5) 15.3 (13.5 (27.1-43.4-25.5-35.4) 35.6) 37.1 (10.2-19.4 (53.2-33.2 (19.9 (39.6 (21.0) 16.6 (13.2 (47.0 (27.9-28.0 (15.6) 25.8-13.8-98.4-120) 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 13.5-25.8 (28.9-47.0 (26.7 (53.8-64.9-87.8-76.0) 24.8-41.2) 14.3 (29.9) 14.0) 23.1 (19.3-74.5 (26.6 (66.3) 37.2 (43. respectively.9) 14. High dose BzBP and its monoester metabolites.6-92.2) 66.0) 20. 2000).4) 12.2-39.1-90.7-25.4) 98.0) 34. IARC considers BzBP not classifiable with respect to human carcinogenicity.5-97.3-130) 122 (88. vinyl tile.3-12.6 (41.2 (25.

9 (54.2-13.3-38.6 (15.8-15.3-64.3-73.5 (42.5-26.Phthalates York City (Adibi et al.4-14.8-173) 195 (121-305) 229 (99.0) 49.0) 60.5 (56.3) 12.6 (57..5-58..7 (54.0) 13.4-42.5) 17.6 (30.6-40.0 (67. and in a small sample of German residents (Koch et al.0-27.1) 17.1 (41.9-14.4 (10.5-38.9 (24.5 (9.3 (24.0 (62. 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.6-13.9) 11.7-20.4) 44.2 (27.7-19.3 (60.7-14.9) 42.4) 15.9-16.3) 55.1) 35.0) 24.5-31.2) 26.5) 16.8-14.0 (38.9) 12.4 (11.2-13.8) 53.2-12.8) 56. In NHANES 1999-2000.9-13.8) 15.2) 12.1) 23.1-27.7 (59.3) 36. Finding a measurable amount of MBzP in the urine does not mean that the levels of MBzP or the parent compound cause an adverse health effect.7 (11.8-60.73-12.6-12.9) 12. 2005).4 (34.8) 68.2-17.9-104) 62.4 (46.1 (21. median urine levels of MBzP were about one-half the median levels in NHANES subsamples from 1999-2002 (Wittassek et al.0) Selected percentiles ( 95% confidence interval) 50th 13.4) 13. 2003).5) 20.3 (15.9) 52.3) 18.3) 89.1 (43.4) 21.7) 11.9 (15.1 (23.7) 56.4-116) 73.1-12.4-60.5-99.1-35.9-115) 57.8) 46..7 (19.5-213) 49.6 (34.5-26.9 (10.4-102) 70.8 (12.3) 90.7) 25..95-14.7-123) 77.8 (49.4 (13.3) 73.4) 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 12.8) 11.9 (39.8 (64..6 (14.5-29.3-34.1 (21.3) 14. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.3 (38.8 (57.4 (63.8-64. 2002).1-12.4-23.8 (46.7 (14.5-61.1) 27.9-83.6-26.9-69. A small study of African-American women in Washington.8) 13.7 (55.4) 17.1 (21.3) 13.2) 11.1 (14.4-17.5-16.4-90.6 (11.3 (12.0 (41.1-14.8) 54.7 (12. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9 (24.8-42.9 (55.3-11.7 (21.7-397) 70.7-61.5 (49.6) 73.7 (38.4-142) 134 (116-176) 136 (85.1) 142 (99.6 (30.6) 75th 25.0 (12.5 (35.3 (39.1) 12.4) 12.4 (33.3) 14.1) 24.4) 104 (89.2) 67.0 (12.1) 24.8 (50. 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. 2002. population from the National Health and Nutrition Examination Survey.5-58.8-13. Hauser et al.2 (69.0-51. DC reported median urinary MBzP levels that were about twice the levels of adults and females reported in NHANES 1999-2002 (CDC.0 (10.5 (11.S.9-23.8-14.1 (9.4-99.0) 24.1-29.4-15.4 (11.6) 25.0 (33.5-13.2-117) 95.0-53.3) 67.6 (36.8-85.6 (24.6 (19.2) 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 12.7) 46. In an annual sample of German university students.6) 58.8-69.3) 16. interval) 14.4) 14.9 (9.6-15.5) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Fourth National Report on Human Exposure to Environmental Chemicals 263 .7 (18. 2007).7) 38.9) 11.3 (13. Hoppin et al.1-125) 86.5) 46.7-69.6-99.9 (12.1 (13.0) 11.5) 41.0) 12.5) 95th 77.5) 10.4 (12.1 (53.9) 24.6-20.7-15.1 (19.9-62.4 (11. and females compared to males (Silva et al.2 (56.1-79.1 (13.5-23.1 (46.6-116) 74.6) 38.9 (10.9) 64.8-80.7-19. the adjusted geometric mean levels of urinary MBzP were significantly higher in several subgroups: children compared to adolescents and adults.2-78.0-26.9-40.2) 11.5-76.8-16.6) 30.8 (13.4 (25.5) 78.4 (21.8) 33.4) 60.1) 80.5-42.9) 100 (80.7 (13..8) 34.0-48.8-48.7 (11. 2007).2-26.8) 80.0 (13.7-15.9 (29.5 (12.3 (23.4-19.0-109) 65.0) 15.8-27.0 (41.9 (51.2 (40.5 (10.2-49.7-31.7 (13.8-15.8 (30.4-79.8 (69.5 (48..4 (60.2-15.6) 53.3) 21.0 (11.8 (11.6 (11.8) 71.2-57.6-86. in men attending a Boston infertility clinic (Duty et al.8) 108 (75.8 (10.9) 12.9) Total 14.4) 13.7) 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 40.1 (18.1-58.4) 50.1 (34. 2003).0-15.7) 19.3) 13.9 (43.8-13.7 (11.2) 32.0-90.6 (51. 2005.7-90. Weuve et al.2-51.4-18.4) 51.3) 13.3) 37.6) 12.8-39.5) 23.2) 15.6-47.9 (15.1) 39. 2004).4) 28..2-15.6 (22.9-28..3 (35. 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.7 (23.9 (12.4-27. in young Swedish men (Jonsson et al.5-79..1 (11.0 (49.6-81.6) 12.3) 29.6 (11.6) 13.69-11.7-56. 2006).8) 53.9 (22.8-34.1 (21.4) 25.8) 24.4-93. 2004.7-14.7-29.1 (25.2) 11.4) 90th 50.4-14.3-16.4 (74.5-57.8-13.7-12.5 (10.8) 26.9-13.4 (69.5) 13.2 (41.4 (26.7-20.8) 16.2-21.8) 33. adolescents compared with adults.1-120) 77.5) 14.1 (15.

Schettler T.25(2):293-302. Ryan L. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Caudill SP. Drexler H. Silva MJ. Needham LL. et al. et al. Barr DB. Butala JH. Sampson EJ.108(10):979-982. Brock JW. Jedrychowski W. Reidy JA. Sanchez GN. Reprod Toxicol 2004. Helm D. Wittassek M. Reproducibility of urinary phthalate metabolites in first morning urine samples.Phthalates References Adibi JJ. Angerer J. 4/20/09 Silva MJ. Duty S. Meeker JD. Prenatal exposures to phthalates among women in New York City and Krakow.112(3):331-338. Silva MJ. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. J Androl 2004. Environ Health Perspect 2004. Rossbach B. Jonsson BAG. Research Triangle Park (NC). Environ Res 2003.S. et al. Giwercman A. Caudill SP. Third National Report on Human Exposure to Environmental Chemicals. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. Richthoff J. Phthalate monoesters levels in the urine of young children. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study.nih. Davis BJ. Hauser R. Brock JW. Duty SM. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Perera FP. Eckard R. Silva MJ. Environ Health Perspect 2006.gov/ chemicals/phthalates/bb-phthalate/bbp-eval. Blount BC. Rylander L. Bull Environ Contam Toxicol 2002. Pirkle JL. Hu H. Hoppin JA. Weuve J. Needham LL.114(9):1424-1431.22(3):688-695. Malek NA. Koch HM. David RM. Hilborn ED. Koch HM. Levels of seven urinary phthalate metabolites in a human reference population.68:309-314.111(14):1719-1722. Green RA. Singh NP. Brock JW. Atlanta (GA). 112(5):A270]. Poland. Environ Health Perspect 2002.18(1):122. Hum Reprod 2007.niehs. 2005. Jacek R. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. et al.html. et al. Calafat AM. 264 Fourth National Report on Human Exposure to Environmental Chemicals . McKee RH.93:177-185. NTP-CERHR.16(4):487-493. Wiesmuller GA. Monograph on the Potential Human Reproductive and Developmental Effects of Butyl Benzyl Phthalate (BBP). et al. et al. 2000 [online]. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Chen Z. Camann DE. Barr D. Calafat AM. Urinary levels of seven phthalate metabolites in the U. Baird DD. Environ Health Perspect 2000. Silva MJ. Available at URL: http://cerhr. Hagmar L. Int J Hyg Environ Health 2007. Gans G.110(5):515-518. Hodge CC. Dobler L. Centers for Disease Control and Prevention (CDC). Environ Health Perspect 2003. Ryan L. Caudill SP.210(3-4):319-333. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Epidemiol 2005. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004.

7-20.2 (11.4) 22.6 (14. 2005).90 (4.1) 22.91) 4.3 (11.90 (4.7 (16.00-6.81 (3. Compared with the median for 6 to 11 year olds in NHANES 1999-2004 (CDC.5) 25.20-6. in a small sample of pregnant women in New York City (Adibi et al.68 (2.8 (9.2-22. 2000).20-2.80-5.90 (3.50) 8.80-5.50 (3. NTP-CERHR.30-6.6 (13.60) 3.7 (17.50) 18.20 (7.00 (7.5) 14.66) 2.0) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.00-4.85-6. 2007).3-48. CDC.20) 4.43) 6. Neither IARC nor NTP has evaluated dibutyl phthalates with respect to human carcinogenicity..90 (6.10) 2.5) 18.0) 20.25) 01-02 03-04 01-02 03-04 01-02 03-04 4.44-2.1-20.33 (2.94) Selected percentiles ( 95% confidence interval) Sample 95th 17. When total DBP metabolites have been measured.1) 25.7) 15.6 (13.2-33.3-19.19-3.00) 4.30-13.6) 16.40-4.70 (2.20-12.0 (13. Small amounts of mono-3-carboxypropyl phthalate are also produced from di-n-butyl phthalate.6) 10.60 (4.50) 7.80 (3..0-25.30) 5.40-12.5 (11. exposure to benzylbutyl phthalate (BzBP) will also result in small amounts of mono-n-butyl phthalate appearing in the urine.6 (10.3-24. in men attending a Boston infertility clinic (Duty et al.6 (11.5) 19.46 (3.56 (5. Following oral administration of DBP to humans.70-8.40 (7.80 (5. 84-69-5 General Information Dibutyl phthalates (both di-n-butyl and di-isobutyl phthalates. 2001-2002 and 2003-2004 subsamples were similar to MBP levels reported in U.50-4.0 (11.50) 2.10) 3. Median MBP levels in two European studies were about two to six times higher than median levels in this Report (Jonsson et al.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.10 (3.7-31.17) 4.5-16.90-4.0) 12.0 and 0. NIOSH and ACGIH have established guidelines for workplace air exposure to di-n-butyl phthalate.30) 10.2-14. pharmaceutical coatings.0 (19.5) 23.6-14.40-3.0) 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 2.90-2.97-7.00) 7.1-25.30-2.59) 3.40-3.3) 3.55 (3.50) 90th 12.1) 16. Survey Geometric mean (95% conf.3-30.9-14.4-12.40-9.60 (5.17 (2.28-5.40 (2.20-12.9) 10.70-4..46) 2.. People exposed to dibutyl phthalates will excrete mono-n-butyl phthalate (MnBP) and mono-isobutyl phthalate (MiBP) in their urine.1-12.3-20.3 (19.7) 4..90) 12.3) 33.20 (6. Koch et al..10-9. and insecticides.6) 17.4-27. mostly as MnBP (Anderson et al.9-23.6 (10. population from the National Health and Nutrition Examination Survey.5 (17. 2005).30-7.S. 84-74-2 Di-isobutyl Phthalate CAS No.30-3.6) 26.3 (18.80 (2.8) 677 652 703 699 1216 1088 Limit of detection (LOD.0) 24.7) 7.56-4.50) 5.0-14.40 (6.24-8.8) 40.5) 12.S.5-29. interval) 2..97) 2. about 65% to 80% of a dose is eliminated in urine within 24 hours.40-17.26 (2.30-11.20 (3.20) 7.97) 4.4 (14.80 (2.7 (7.30 (4.80 (5.0-18.70) 3.40-4. DBP can produce reproductive toxicity in male rodents (McKee et al.7) 14.1 (8. 2000.37) 6.6-26.6-18.7 (18.67 (5.0-38.5-16.30 (1. In addition.90-4. residents (Blount et al.3 (16.4) 12.90-7.22) 3.10 (4.7 (17.3 (13.9 (16.5) 22.56) 3.00 (5.63) 3.00) 4.3 (13. and also in some printing inks. 2004.5 (27. they have been referred to as monobutyl phthalate (MBP). Biomonitoring Information Median concentrations reported in the NHANES 19992000.00) 6.6-34.73-5.3) 18.80) 75th 5.7 (9.5) 18.6-20. Fourth National Report on Human Exposure to Environmental Chemicals 265 .10) 8.40) 5.30) 10.6) 12.70) 5.3.55) 2.72-3.0) 13.10 (4.46-5. 2004.82-3..71 (2.22 (3.7-18.5-24. 2003).50-10.00-11.9 (16.11-3.30) 6.4) 5.70-4.40-5. 2001).Phthalates Di-n-butyl Phthalate CAS No. 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. 2003). Hauser et al.00) 10.10) 11.40 (3.07 (3. 2005).6 (14.6 (9.02) 4.60-6.30-6.8) 21. Studies of children found age-related differences in urine MBP levels.50-2.6 (29. see Data Analysis section) for Survey years 01-02 and 03-04 are 1.0 (13.00-9.60 (8.49-2.0) 9.1-17.7-31.3 (16.2) 5.50-6. and in a small sample of Japanese adults (Itoh et al.3-43.20-9.5 (20.6) 17.84) 4.50 (6. OSHA has established a workplace air standard for external exposure to DBP. 2005.7) 18.40 (2.2 (12.60 (2.46 (2.3-18..96) 3.2 (8.56 (3.4 (20.1 (13.73 (2.10) 9.10-9.30 (3.70 (5.9) 15.30) 2.10-2. referred to as DBP) are industrial solvents or additives used in many personal care products such as nail polish and cosmetics.6) 16.48 (2.5 (10.00-6.

96 (3. An analysis of NHANES 2001-2002 showed similar age.02-10.10-5.62 (6.26 (2.1-12.08-2.99) 7.45) 3.44 (3. to about two to fourfold higher (Fromme et al.86-4.51) 2.1) 10.33-9.58-3.89-5. 2006).95) 10. up to four and 13 fold.76 (3.13 (2.07 (2.20 (2.94) 6.46-11.52) 3.4) 7.61-3.51) 5. 2005).26-2.7 (13.02 (7.95-3.1) 15.52-3.0) 393 342 742 729 1647 1534 01-02 03-04 01-02 03-04 2.3) 13.78-8.94 (5.8-36.86) 6.73 (5.28-13..0) 7. than adults in NHANES subsamples during the same time period.32) 7.64-7.68) 5.6) 11.6) 13.82 (4.21) 10.04) 7.04-5.28 (4. 2005).11 (5.05) 2.81 (6.1 (10.31) 2.31 (2.18-4.78) 9.. In an analysis of NHANES 1999-2000.7) 19.43) 3.6-19.84 (8.0 (12.7-28.8) 10.20 (2..2) 8. 2004).69-7.03 (5.35) 3.22 (2.33 (2.57-4.31) 2.72) 5.01-2.7) 10.18) 4.6 (12.83 (2.18 (4.8 (10.7) 1371 1250 1411 1355 01-02 03-04 01-02 03-04 01-02 03-04 3.9-40.00-7.2) 24. 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.18) 3.57 (3. 2002.15) 3.82) 4.53-4.54) 2.1) 677 652 703 699 1216 1088 266 Fourth National Report on Human Exposure to Environmental Chemicals .3) 16.21 (5.5) 13.84 (4.34 (3.15-4. 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. Studies measuring urinary MnBP have reported variable median values compared to the NHANES 2001-2002 and 2003-2004 subsamples.4-16.56-15.09-2.37) 3. Between 1998 and 2003.89 (3.17) 90th 8.79-6.39-3.56) 2.66 (8.5 (11.7 (11.5-19.94-12.36-7.0) 11.67-5.8-18.03-7.19 (2.53-5.29-3.65-4.9-26.58-4.43) 3.62-12.3 (13.11) 5.97-2.03-11.33 (3.9 (15.38 (6.80-3.76-3.8 (8.79-8.91-6.9 (9.and gender.47-12.3 (17.56-4.72-7.S.30) 2.18-10.89) 6.55-6.66) 4.1 (11.3) 13.64-10. Differences in urinary MBP population estimates by gender have also been shown (Silva et al.75 (6.57 (3.25) 5.7 (9.00-3.20-3.56) 5.9 (11.6 (8.0-18.66) 10.43) 3. while MnBP declined (Wittassek et al.59 (4.47 (3.99-4.81 (3.0) 3.39) 5.20-2.79 (4.2-15.00-3. the adjusted geometric mean levels of urinary MBP were significantly higher in children aged 6 to 11 years than in either adolescents or adults (Silva et al.69 (2.36-2. ranging from more than one-tenth the NHANES median (Itoh et al.92 (7.08) 75th 4.42) 2.80 (3.8-18.74-3.30 (6.88 (2.6 (15.6 (9.24) 3. samples from German university students had consistently higher median urine levels of MnBP and MiBP.2 (10.13-6.5) 15.31 (7.51) 15.9) 12.1) 7.9-16.1) 13.54 (4.7) 3. population from the National Health and Nutrition Examination Survey.1-25. interval) 2.78) 8.52 (2.00) 01-02 03-04 01-02 03-04 01-02 03-04 4.29-8.4) 15.07-5.8 (9.27-12.85 (2.2 (11.related differences in the adjusted geometric mean levels of urinary MiBP and MnBP (CDC.. 2007). Survey Geometric mean (95% conf. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.32 (3.64-7..18 (1.74 (4.32 (7.65 (4.6-19.73) Selected percentiles ( 95% confidence interval) Sample 95th 12.2) 9. 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. 2007).66) 2.68) 3.1-15.0 (8.0 (10.93-6..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 2.52-20..11-2. Over this time.3) 28.76-3.80) 7.53-3.75 (4.14 (4.41 (2.68 (2.1) 4.04) 3.17-12.95) 2.1-24.98 (2.7 (21.0) 15.65-11.76-15.81) 9.20-4.4 (12.17 (2.69) 6.8-13. Weuve et al.38-10.46 (2.3) 18.1) 11.20 (7.54 (2.69) 4. the students’ median values for MiBP levels remained relatively unchanged.5 (9.Phthalates for neonates was lower (by about half) and the median for toddlers was higher (by about sixfold) (Brock et al.7) 11.6 (8. 2004). respectively.2-13.4) 23.47-5.81) 4.46) 3.00 (3.33) 3.6 (10.

6 (32.0-19.3 (56.0 (18.9-22.6) 35.4 (25.6-29.9) 75.6) 39.8) 62.5 (59.8-111) 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 23.3 (42.5 (74.5) 95.2) 42.2-56.3) 24.7 (18.9-28.3-145) 85.2-114) 73.3-40.5) 31.5) 78.4-159) 107 (84.2-49. see Data Analysis section) for survey years 99-00.9) 36.4 (71.5-60.6 (48.5-117) 95.6 (61.6 (16.7-34.2-93.6) 38.6 (26.6 (65.4-20.7-42.9) 21.4-31.8) 58.7) 92.1-24.5) 19.5) 20.3) 18.4 (35.6-24.2) 62.1 (19.0-24.0 (23.8-42.3) 36.7-106) 69.1) 20.3) 23.5 (29.0-21.4-25.3-60.3-21.3-67.2 (17.1 (36.6-20.4) Selected percentiles ( 95% confidence interval) Sample 95th 150 (121-169) 108 (94.5) 21.4 (35.4) 52.9.2-22.0-73.2) 32.2-23.9-101) 77.4) 22.8) 48.1) 46.3 (51.6) 71.5) 24.0) 120 (98.1 (19.2 (19.1) 17.3 (60.2 (75.4 (35.1 (62.7-34.0) 20.3) 40.6 (90.4 (36.2) 38.7 (22.6-29.9-33.4-60.3 (17. interval) 24.4-42.5) 36.1 (19. respectively.5-53.9-114) 116 (97.0-24.3 (30.2 (59. Fourth National Report on Human Exposure to Environmental Chemicals 267 .5) 34.1 (51.6-44.0) 27. Survey Geometric mean (95% conf.7-117) 118 (108-143) 93.2 (20. *In the 1999-2000 survey period.7-24.7-20.1 (26.8-132) 95.0) 21.1-22.7 (43.8) 75th 51.3 (23.0) 84.1-29.6) 20.2-159) 92.0 (30.9 (17.6-31.2-63.0) 38.7 (18.4-44. 1.9) 18.7 (19.3) 26.7) 52.0) 117 (104-131) 112 (84.7-91.4) 20.6-49.0-51.6 (55.5-43.7 (24.6) 46.4 (19.1 (28.9-53.5) 36.S.9-79.0-58.3 (23.1-51.8-165) 167 (143-197) 138 (110-184) 144 (115-168) 142 (111-161) 107 (89.1) 30.2) 68.4 (38.0-26.2 (74.6-143) 127 (99.7) 42.8-22.5 (30.1) 25.1-80.1 (31.8) 43.2) 26.7 (64.0 (15.8) 23.7 (51.7-42.6-33.5) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.6-40.1 (18.0 (45.6-113) 108 (90.9) 46.3 (37.4) 59.1 (21.3-96.0 (78.8 (19.7-111) 64.6) 17.1) 31.1-82.7-53.7 (16.6 (19.7-121) 97.3-85.6 (44.9) 26.1 (34.2 (25.6-36.2) 20.0) 31.3) 21.6 (22.9-92. referred to as monobutyl phthalate (MBP).3 (36.7) 28.9-87.4-18.2 (18.6-69.1 (41.1 (16.1-20.5) 85.8-123) 101 (90.4 (72.9-42.7-26.2-21.5) 37.6-37.9) 71.1) 47.7 (38.7-124) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites 99-00* 01-02 03-04 Limits of detection (LOD.0 (25.7 (33. population from the National Health and Nutrition Examination Survey.1) 23.5) 40.1 (17.5-47.1 (19.2 (78.3-136) 137 (107-162) 119 (90.8-119) 90.2 (79.6) 21.3) 19.4 (21.5) 26.2) 90th 98.5-121) 106 (94.2 (21.4 (84.1-75. and 03-04 are 0.2 (21.5 (28.5) 47.4.1-27.7-127) 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 22.1.0 (36.2 (58.3-24.2-33.9 (20.7) 74.2-32.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.5-42.5) 17.7-92.4) 64.2-24.4 (35.3 (30. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value. and 0.9) 29.0 (31.6) 166 (127-279) 159 (110-290) 191 (150-243) 165 (121-227) 148 (106-185) 134 (110-158) 143 (117-161) 95.7) 124 (98.0) 30.0-19.1) 19.5 (59.5-47.5-44.8-25.7 (28.9-22.8-29.1) 36.0 (72. 01-02.9 (17.8 (57.5) 65.3-76.1 (54.4-26.7-116) 95.1) 23.7 (70.0 (17.9 (79.6-48.5-27.8) 19.0 (20.1 (58.4 (23.2-87.9 (79.0-32.3-79.1-122) 122 (104-137) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 26.1) 23.6) 80.1-92.

0 (27.3-71.2-73.6 (72.9 (19.4-103) 117 (83.3) 35.2 (35.3) 21.7 (20.0) 75.0) 81.6-44.6) 23.2-28.0 (20.7 (57.4 (18.7-19.5) 134 (93.3 (46.8) 23.8 (17.0 (16.5) 82.0 (70.6-23.0-60.8) 75th 38.6-42.9 (20.4 (33.5-37.4 (17.2-106) 64.2 (83.7) 36.S.6 (31.6) 24.5) 90th 68.2-86.7 (43.0) 55.8 (13.5 (14.2 (16.0 (61.9) 30.6) 24.6) 39.3 (16.2) 74.1) 20.4 (45.3-39.6 (19.6-22.3 (17.3) 33.8 (18.6-28.7) 20.9-68.5-18.6-32.6 (25.1 (21.6-23.3 (52.8) 34.0) 35.7 (28.6) 34.3 (17.7 (19.6 (17.7-20.6-119) 63.5 (64.5) 17.7-23.0) 108 (71.4 (23.0 (18.4) 62.7 (60.6 (41.3 (55.1-62.0) 94.7-80.6 (29.5-23.2-108) 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.6-53.7 (14.4 (68.3) 52.5) 60.6) 65.6) 18.2) 31.5-70.3) 17.6-27.3-106) 74.8) 28.6) 38.1 (61.8) 63.7-39.8) 20.1 (34.7 (12.8-32.4 (17.6-16.6) 31. Survey Geometric mean (95% conf.4 (16.3) 59.2-27.3) 20.9-105) 85.9) 52.4 (56.2) 65.3-49.4) 51.5-16.9) 19.6) 64.8) 17.3-38.5 (18.9-49.9-70.3 (76.6) 14.2) 21.1 (29.9 (30.9-100) 86.9) 28.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.8) 34.0) 29.0 (18.8 (18.9) 62.6-44.6 (27.5-30.2-48.9 (37.9-68.7 (73.4-131) 81.5-41.1-21.7-19.3 (28.7-37.0) 19.6-43.6 (25.1) 17.0 (71.0-113) 104 (83.0 (43.4-24.8 (25.6-24.6-128) 96.1) 21.7) 42.1-99.2-22.8) 13.3 (17.1 (32.9 (58.6-50.6-155) 91.8-23.9) 14.3 (42.4) 20.3-26.9) 91.5) 21.3 (69.4) 15.8-43.1-32.8 (50.5-142) 81.4) 16.6) 37.0 (19.5 (15.2 (19.7) 19.5) 84.0) 25.4) 19.3-21.5 (18.3-81.1-128) 97.9-34.4) Selected percentiles ( 95% confidence interval) Sample 95th 97.9 (39.1) 42.0 (26.4 (50.0) 28.3 (21.0 (15.1) 44.0 (69.1-18.0-92.4) 21.8) 40.8) 35.3 (24.1 (46.5) 91.0 (34.2-22.6 (74.9-84.0-38.9) 24.4-47.5 (81.4-135) 71.2-18.2) 159 (102-263) 147 (93. 268 Fourth National Report on Human Exposure to Environmental Chemicals .3-18.8 (22.5-21.0 (52.0 (50.4 (37.0-41.0-90.9 (35.4) 15.6 (57.4 (47.3) 33.8) 17.0-17.4 (19.8 (16.0) 26.1) 20.2) Age group 6-11 years 99-00* 01-02 03-04 99-00* 01-02 03-04 41.7-42.8 (18.1) 22.9) 39.4-72.9) 20.1 (56.2) 59.4 (13.2) 16.4 (53.4 (50.6) 83.7 (27.2-22.9 (30.9-36.5-22.5-142) 89.6-139) 1215 1371 1250 1326 1411 1355 Females Race/ethnicity Mexican Americans 99-00* 01-02 03-04 99-00* 01-02 03-04 21.4 (31.3-40.3-20.5-64.0) 41.2-179) 84.1-83.9 (56.2 (19.7 (16.7-78.6-92.4 (16.9 (30.1) 61.9-56.3-23.1) 53.5-76.8-235) 137 (108-198) 88.3) 19.4-61.3-17.5 (30.8) 20. population from the National Health and Nutrition Examination Survey.2 (38.4-76.1-23.0) 70.4 (31.3-78.9 (64.8 (33.1) 50.4-34.3-32.9 (21.1-99.3) 19.0-47.0) 59.2-16.9) 49.3 (60.4) 53.7-28.2-21.0-19.5) 39.4-65. concentrations of mono-isobutyl phthalate and mono-n-butyl phthalate were measured together and expressed as a combined value.7 (60.9 (73.1 (15.9-38.3) 18. interval) 22.9 (16.3-21.7 (81.8) 30.9 (35.3-114) 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 17.9-26.5-15.8) 19.2-61.3 (52.6) 25.6-19.8 (65.3 (71.4 (20.6 (61.3 (48.9-14.4-164) 96.4 (31.7-26.6-24.1-115) size 2541 2782 2605 Total years 99-00* 01-02 03-04 50th 21.0) 53.8-24.7-21.8) 17.3 (19.1) 35.1) 37.0-75.8-24.3) 67.6-26.2-85.7-51.7 (54.8) 22.6-74.

Environ Res 2003. Drexler H. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Malek NA. Fromme H. Urinary levels of seven phthalate metabolites in the U. Atlanta (GA). et al. Yoshida K.gov/chemicals/ phthalates/dbp/dbp-eval. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Hodge CC. Blount BC. Needham LL. Caudill SP. National Toxicology Program-Center for the Evaluation of Risks to Human Reproduction. Jacek R. Butala JH.112(3):331-338.108(10)979-982. Needham LL. Hauser R. Camann DE. Rossbach B. Bolte G. Duty S. et al. Third National Report on Human Exposure to Environmental Chemicals. Poland. A biomarker approach to measuring human dietary exposure to certain phthalate diesters. Ryan L. Epidemiol 2005. The relationship between environmental exposure to phthalates and computer-aided sperm analysis motion parameters. Helm D. Rylander L. Monograph on the Potential Human Reproductive and Developmental Effects of Di-n-Butyl Phthalate (DBP). J Androl 2004. Gans G. Meeker JD.111(14):1719-1722.93:177-185. Brock JW. Phthalate monoesters levels in the urine of young children. Calafat AM. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. Silva MJ. Sampson EJ. David RM. Springall C. Food Addit Contam 2001. et al. Int J Hyg Environ Health 2005. Drexler H.16(4):487-493. Caudill SP. Hum Reprod 2007. Scotter MJ.22(3):688-695. Exposure to phthalates in neonatal intensive care unit infants: urinary concentrations of monoesters and oxidative metabolites. et al.114(9):1424-1431. Itoh H. 112(5):A270]. Evaluation of the effect ofa governmental control of human exposure to two phthalates in Japan using a urinary biomarker approach. Koch HM. Hilborn ED. Weuve J. Hu H. Levels of seven urinary phthalate metabolites in a human reference population. Jedrychowski W.210(3-4):319-33. et al. Pirkle JL. Calafat AM. Richthoff J. Koch HM. Int J Hyg Environ Health 2007. Silva MJ. et al.25(2):293-302. Environ Health Perspect 2003. Dobler L. Schettler T. Centers for Disease Control and Prevention (CDC). Available at URL: http://cerhr. Hagmar L. Caudill SP. Barr D. McKee RH. Occurrence and daily variation of phthalate metabolites in the urine of an adult population. Int J Hyg Environ Health 2007. Wiesmuller GA.18(12):10681074. Angerer J. Wittassek M. Angerer J. Duty SM. Koch HM. Chen Z. NTP center for the evaluation of risks to human reproduction reports on phthalates: addressing the data gaps [review]. Reprod Toxicol 2004. Internal phthalate exposure over the last two decades—a retrospective human biomonitoring study. NTP-CERHR. Giwercman A.nih. Urinary phthalate metabolites and biomarkers of reproductive function in young men. Sanchez GN. Environ Health Perspect 2000. Brock JW. Boehmer S. Silva MJ.18(1):122. Barr DB. Research Triangle Park (NC). Fourth National Report on Human Exposure to Environmental Chemicals 269 .210:21-33. Bull Environ Contam Toxicol 2002. et al. Jonsson BAG. Singh NP. Environ Health Perspect 2004. Reidy JA.208:237-245. Castle L.Phthalates References Adibi JJ. Environ Health Perspect 2006. 2000 [online]. Perera FP. et al. 4/20/09 Silva MJ.S. Prenatal exposures to phthalates among women in New York City and Krakow. 2005. Eckard R. Massey RC.68:309-314. Masunaga S. Silva MJ. Green RA.niehs.html. Ryan L. Anderson WA.

400-.500 (.300-.200 (<LOD-.500) . 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.70) .2.500 (.20) .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. and 03-04 are 0.300-.400) < LOD 1.400-.9.00 (<LOD-1.500) < LOD 1.10 (.10) .00 (<LOD-1.300 (<LOD-. 01-02.400) 814 677 652 603 703 699 912 1216 1088 Non-Hispanic blacks Non-Hispanic whites Limit of detection (LOD.300-.10 (<LOD-2.700) .600 (.500) 1.00 (<LOD-1.400-. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.500 (.600) .90) . which may vary for some chemicals by year and by individual sample.400) < LOD < LOD .600) < LOD .400) 1.400 (. < LOD means less than the limit of detection.700) .3.500 (.300) 328 393 342 752 742 729 1461 1647 1534 12-19 years 20 years and older Gender Males 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD .400-.200-.70 (1.500) .Phthalates Dicyclohexyl Phthalate CAS No. 84-61-7 General Information Dicyclohexyl phthalate (DCHP) is used to stabilize some rubbers.300-. including nitrocellulose.300) < LOD .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 .500 (.500) 1.400 (<LOD-.200-.400 (.200-.500) < LOD < LOD . and polyvinyl chloride.00-3.400 (. and polymers.600) . population from the National Health and Nutrition Examination Survey.400 (<LOD-.600) .300-.400-.500) . Urinary Mono-cyclohexyl phthalate (MCHP) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.300-.900-1.200-.500) 1. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.400) 1.300-. 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.50) .500) < LOD < LOD .400 (.300-. only levels at or above the 90th percentile could be characterized.500 (.70) .500 (.400 (.500 (.00) .400) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .300) < LOD .200-. 270 Fourth National Report on Human Exposure to Environmental Chemicals .700) .300 (.70 (1.80) .300 (.200-. People exposed to DCHP will excrete mono-cyclohexyl phthalate (MCHP) in their urine.300-. Biomonitoring Information Urinary levels of MCHP are infrequently measured and the limited population-based surveys available to date have reported most levels below the limit of detection. respectively.300 (.300 (.500 (.00-2.500-.300 (. and 0. Neither IARC nor NTP has evaluated DCHP with respect to human carcinogenicity. polyvinyl acetate.400 (.400-. interval) Selected percentiles ( 95% confidence interval) Sample 95th 1. see Data Analysis section) for Survey years 99-00.300-. 0. Survey Geometric mean (95% conf.10 (<LOD-1.S. resins.50) .400 (<LOD-.600) .600) .400-. In this Report.300 (.400 (.10 (<LOD-1.400 (<LOD-.500) .300 (.

18) .360-.500 (.450 (.S.270) < LOD .54-6.240-.11) .470 (.910 (.690) < LOD 2.660) .06) .770) < LOD 2.14 (<LOD-3.800-1.630 (<LOD-.220 (<LOD-.500-.33 (<LOD-3.Phthalates Urinary Mono-cyclohexyl phthalate (MCHP) (creatinine corrected) Metabolite of Dicyclohexyl phthalate (DCHP) Geometric mean and selected percentiles of urine concentrations (in µg/g of creatinine) for the U. population from the National Health and Nutrition Examination Survey.480 (.420-.33) .410 (.690) < LOD < LOD .67 (1.500) size 2541 2782 2605 Total years 99-00 01-02 03-04 50th < LOD < LOD < LOD < LOD < LOD < LOD 75th < LOD 90th .44) .530 (.450 (.740) .420-.00 (<LOD-3.330 (.54) .510-.910 (.260-.950 (.05) .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 . Survey Geometric mean (95% conf.910 (.770-1.17) .690 (.670-1.53) .590 (.420-.530-.690-1.830) 1.43 (1.06) .250 (.940 (.560) 1.16) .380 (.790-1.74) .660) < LOD < LOD .510 (.12-1.770-1. interval) Selected percentiles ( 95% confidence interval) Sample 95th 3.880 (.22 (<LOD-1.500) 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 .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.530-1.310-.34) .620) < LOD .500) 3.490) .370 (<LOD-.530) 1.400-.740) < LOD < LOD .400-.310) < LOD .690) < LOD * * * Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 * * * * * * * * * < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD < LOD 1.590 (<LOD-.350-.710) .16 (<LOD-3.630 (<LOD-.910 (.10) .610 (.670 (<LOD-. Fourth National Report on Human Exposure to Environmental Chemicals 271 .390 (.36-1.00) .290-.770-1.770 (.380-.53) .170-.82 (1.470) 3.54 (<LOD-2.330 (. * Not calculated: proportion of results below limit of detection was too high to provide a valid result.82) .

population from the National Health and Nutrition Examination Survey. 0.8-111) 85.9. Products that may contain DEP include perfumes.1 (71. 2002).3-110) 211 (160-278) 197 (159-243) 225 (187-270) 190 (164-219) 191 (171-214) 205 (176-238) 75. and 03-04 are 1. and also in men attending a Boston infertility clinic (Hauser et al.1-93.7) 71.5) 81. 2003) and African-American women in Washington. DC (Hoppin et al.2. Neither IARC nor NTP has evaluated DEP with respect to human carcinogenicity.3 (82.. Workplace air guidelines for external exposure to DEP have been established by ACGIH and NIOSH. 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. Biomonitoring Information MEP levels in the NHANES 1999-2000. see Data Analysis section) for Survey years 99-00. People exposed to DEP eliminate mono-ethyl phthalate (MEP) in their urine. and hand lotions.3 (74. 2001-2002. a sample of young Swedish males entering the military had median urinary MEP levels that were somewhat higher than males in the NHANES subsamples. respectively.7 (70. 272 Fourth National Report on Human Exposure to Environmental Chemicals .2-102) 95. soaps. and 0. particularly those containing fragrances. colognes. 2007). 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.. shampoos.4 (62.4. 01-02.S. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.9 (61.. 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. In contrast. 84-66-2 General Information Diethyl phthalate (DEP) is a solvent used in many consumer products.Phthalates Diethyl Phthalate CAS No.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. deodorants.9-92.

7-110) 81. 2005). Survey years 99-00 01-02 03-04 Geometric mean (95% conf. 2003) were slightly lower than levels found in NHANES 2001-2002.9-110) 96. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects. with adjusted geometric mean levels of urinary MEP that increased with age (CDC. 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.S. 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. Other population estimates also differed by sex and race ethnicity (Silva et al.6 (65. population from the National Health and Nutrition Examination Survey.5-114) 101 (87. 2004).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 .2 (66.6 (77.0 (66..3-105) 87. 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.0-117) 142 (119-169) 152 (126-184) 168 (141-201) 179 (161-199) 181 (164-200) 197 (174-223) 79. In an analysis of NHANES 1999-2000.5-113) 122 (93.Phthalates 2002 (Brock et al. 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. Analysis of NHANES 2001-2002 showed similar findings. 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. Median MEP levels found in a small sample of German residents (Koch et al..9 (82.. 2002). This age-related trend is opposite the direction seen for other phthalates.

Poland. et al. Bull Environ Contam Toxicol 2002. Drexler H. Duty S. Prenatal exposures to phthalates among women in New York City and Krakow. Ryan L. Hoppin JA. Hauser R. Koch HM. Caudill SP. Jedrychowski W. Third National Report on Human Exposure to Environmental Chemicals. Phthalate monoesters levels in the urine of young children.22(3):688-695. Baird DD. 2005. Urinary levels of seven phthalate metabolites in the U.110(5):515-518. Angerer J. 112(5):A270]. Caudill SP.112(3):331-338. Environ Health Perspect 2004. Jacek R. Perera FP. Hilborn ED. Barr DB. Brock JW. Internal exposure of the general population to DEHP and other phthalates determination of secondary and primary phthalate monoester metabolites in urine. Environ Health Perspect 2002. Silva MJ.111(14):1719-1722. Singh NP. Atlanta (GA). Hodge CC. Camann DE. DNA damage in human sperm is related to urinary levels of phthalate monoester and oxidative metabolites. Meeker JD. Malek NA. Environ Res 2003. Hum Reprod 2007. 274 Fourth National Report on Human Exposure to Environmental Chemicals .Phthalates References Adibi JJ.93:177-185. Needham LL. population from the National Health and Nutrition Examination Survey (NHANES) 1999-2000 [published erratum appears in Environ Health Perspect 2004. et al. Silva MJ. Brock JW.68:309-314. Barr D. Environ Health Perspect 2003. Rossbach B.S. Reidy JA. et al. Davis BJ. Centers for Disease Control and Prevention (CDC). Reproducibility of urinary phthalate metabolites in first morning urine samples. Silva MJ.

0 (19.87-2.0 (9.16 (2.80-4.2-17.9) 27.20 (3.23) 3. as glucuronide conjugates (Albro et al.60) 90th 14.10) 8.4-27.62) Sample size 2541 2782 2605 Age group 6-11 years 99-00 01-02 03-04 99-00 01-02 03-04 99-00 01-02 03-04 5.5-28. 1982.30 (3.40) 4.1) 22.70-2.6 (12.4) 7.92-5.60) 4.80) 9.4 (16.90) 1.5-40. toys.10) 2.0 (21.9 (29.6) 9.69) Selected percentiles ( 95% confidence interval) 50th 3.80 (2.84 (2.70 (7.50-6. Survey years 99-00 01-02 03-04 Geometric mean (95% conf.80-3.00-5.1) 29.44) 4.6 (41.9 (17.0) 23.7 (14.84-4.50-11.6) 15.91-3.00) 3.80 (1.40) 9.80 (4.5 (18. Four metabolites were measured in this Report: mono-(2-ethyl-5-hexyl) phthalate (MEHP).4-20.80-27.6) 14.92-2.4) 13.40 (4.00) 2. 01-02.40-8.83) 2.4) 15.60) 3.40 (6.60) 8.10-3.4) 33.40-1.5 (12.7) 18.80) 6.3-49.60) 10.10-11.75 (3.3 (10.3 (11.4-20.5) 32.1-17.30 (7.5 (20.2) 29.56 (2.40-9.5 (30.3-25.5-36.5) 43.1982). mono-(2-ethyl5-hydroxyhexyl) phthalate (MEHHP) and mono-(2-ethyl5-carboxypentyl) phthalate (MECPP).40-8.3-26.90) 4.00-3.10) 3.37-4.0) 39.90 (3. packaging film.39) 3.70-3.2 (29.1 (8. Fourth National Report on Human Exposure to Environmental Chemicals 275 .6) 5.8 (19.50-5.20 (1.00) 9.1-48.0) 11.70-5.30-6.50-3.5-27.9) 5.40-12.00) 2.00 (2.85) 4.93) 6.15 (1.10 (3.07-4. which is used for many consumer products.70 (1.2 (7.30) 2.41) 3.50 (7.90 (4.50-3. see Data Analysis section) for Survey years 99-00.6 (20.9) 18.2.7-32.60-11.9-57.0 (16. mono(2-ethyl-5-oxohexyl) phthalate (MEOHP).40 (2.27 (3.00 (7.4) 5.2-39.0 (13.10-5.1 (11. Albro and Lavenhar.20 (3.50-8.30-11.4-53.50-2.10-4.31 (3.4-40.0-29.9-28.0) Total 4.00) 1.21 (2.80) 13.70-2.92) 4.1-29.3 (15.9 (15.10 (6.6-60.96-5.0-19.80 (8.70 (1.50 (3.4) 22.30-13.92-2.40-11.3) 28. population from the National Health and Nutrition Examination Survey.6) 95th 23.23 (3.6 (16..60 (5.1 (8.23 (2.40) 11.1-17.30 (4.Phthalates Di-2-ethylhexyl Phthalate CAS No.40) 4.9 (17.90-11.20 (1.0) 23.40-8.90-8.9-48.2) 42.26-2.4 (21.10 (4.8-47.90) 4.43 (3.2 (31.50-14.82) 3.9 (16.8) 17.5 (12.03-2.4-42.9-26.5 (31.9 (13.3) 13.80-9.30-8.2) 4.10) 2. ATSDR.42-5.5) 19.98) 2. and 0.9 (29.79) 2.60 (6.90-4.4) 20.10) 3.50) 4.46) 3. DEHP present in medical devices and parenteral delivery systems results in the diester rather than the monoester form being directly introduced into the blood.70 (8.00-3. After parenteral administration. 117-81-7 General Information Di-2-ethylhexyl phthalate (DEHP) is primarily used to produce flexibility in plastics.9) 13.0-18. Urinary Mono-2-ethylhexyl phthalate (MEHP) Metabolite of Di-2-ethylhexyl phthalate (DEHP) Geometric mean and selected percentiles of urine concentrations (in µg/L) for the U.50-5.50-6.12 (4.7) 22.0) 328 393 342 752 742 729 1461 1647 1534 12-1